Physiology 🫁 Flashcards

1
Q

what are the components of the sensory nervous system?

A

1- Sensory receptors

2- Afferent fibers

3- Sensory center (special areas in brain or spinals cord)

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2
Q

Definition of Sensory receptors

A

Receptors are specialized microscopic structures located at the peripheral terminations of the afferent nerves.

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3
Q

Functions of Sensory receptors

A

They detect the stimuli and transduce (convert) these stimuli into nerve impulses (detectors and transducers).

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4
Q

Classification of Sensory receptors

A

Anatomical classification: divided into an External and internal receptors

Physiological classification: divided into Mechano-receptors, pain receptor, thermal receptor, chemical, and photoreceptors

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5
Q

what are the properties of Sensory receptors?

A
  • Specificity (Adequate stimulus).
  • Excitability (Receptor potential).
  • Rate of discharge from the receptors (detection of the stimulus intensity).
  • Adaptation of the receptors.
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6
Q

what is Specificity of sensory receptors?

A
  • The receptors show a high degree of specificity as Muller’s law applies:

Muller’s law:
Each type of receptors is highly sensitive to one type of stimuli called the adequate stimulus and its stimulation gives rise to one type of sensation whatever the way of stimulation”.

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7
Q

Examples of Specificity of sensory receptors

A
  • Retinal receptors are highly sensitive to the light waves.
  • Auditory receptors are highly sensitive to the sound waves…etc.
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8
Q

what are exceptions of Specificity of sensory receptors?

A
  • However, the receptors may respond to stimuli other than their specific or adequate ones, provided that these stimuli are very strong; but still the response is the same modality to which the receptor is specialized

Example: Retinal receptors are normally stimulated by the light waves and give rise to sense of vision. But if heavy mechanical stimuli applied to the eye as in heavy blow, the retinal receptors can be stimulated and eye sees flashes of light.

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9
Q

Compare between adequate stimulus & Non-adequaqte stimulus in terms of:

  • Intensity of stimulus
  • Example
A
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10
Q

what does Excitability of Sensory receptors mean?

A

Excitability of receptors is the ability of the receptors to respond to their adequate stimuli.

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11
Q

How do receptors respond to stimuli?

A
  • Most of the body receptors on adequate stimulation show depolarization through the increased permeability of their membranes to Na+.
  • Only the visual receptors (Rods & Cones) when stimulated adequately, they show hyperpolarization (Further details in special sense).
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12
Q

what is the definition of Receptor potential (Generator potential)?

A

is the potential changes that occur in the receptors on adequate stimulation, usually in the form of depolarizations. (Partial)

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13
Q

where is study of receptors potential best demonstrated?

A

It is best studied in pacinian corpuscles

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14
Q

why is study of receptors potential best demonstrated on pacinian corpuscle?

A

i) Easily stimulated by microglass rods under microscope.

ii) Large in size and easily dissected.

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15
Q

Type of Pacinian corpuscle receptors

A

(mechano-receptors present in the skin, deep tissues involved in the sensations of touch, pressure and vibrations).

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16
Q

Structure of pacinian corpuscle

A
  • Pacinian corpuscle is a vesico-elastic structure consists of several concentric layers of connective tissues like an onion surrounding a central nerve terminal.
  • The ending of the sensory nerve is not myelinated, but the first node of Ranvier is also located inside the capsule.
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17
Q

Mechanism of Receptor potential

Revise the notes in this page

A
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18
Q

what is the amplitude of the electronic current directly proportional to?

A

The amplitude of electrotonic current is determined by the amplitude of the receptor potential which by its turn depends upon the intensity of the stimulus.

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19
Q

what is the maximum amplitude of receptor potential?

A
  • The maximal amplitude of receptor potential around 100 mv occurs when maximal opening of Na+ channels is achieved in the receptor membrane.
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20
Q

what does the generation of further action potentials depend on?

A
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21
Q

name of the point of receptor stimulation

A

The nerve terminal is termed the Transducer region

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22
Q

what is the first node of ranvier in pacinian corpuscle called?

A

1st node of Ranvier is called the Spike Generator region.

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23
Q

what are the properties of receptor potential?

A
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24
Q

what is the relation between stimulus intensity & Rate (Frequency) of impulses discharged from the receptors?

A

Relation between stimulus intensity and rate (frequency) of impulses discharged from the receptors is logarithmic according to “Weber-Fischer law”

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25
Q

Statment of Weber-Fischer law

A

The Rate (frequency) of impulses discharged from the receptors through the afferent nerves is directly proportional with the logarithm intensity of the applied stimulus.

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26
Q

Equation of Weber-Fischer law

A

R= Log S x K

  • R= rate of discharge.
  • S= strength of stimulus.
  • K=constant.
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27
Q

Examples of relation between stimulus intensity & rate og impulses discharged according to Weber-Fischer law

A
  • Increase stimulus intensity 100 times leads to increase rate of discharge 2 times only (as log 100 =2).
  • Increase stimulus intensity 1000 times leads to increase rate of discharge 3 times only (as log 1000=3).
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28
Q

what is the significance of Weber-Fischer law?

A

This allows receptors to:

1) Respond to a wide range of stimulus strength.

2) Compression function of the receptors which means that the receptors compress these wide range of stimuli into narrow range of discharge.

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29
Q

How does intensity of stimulus increase rate of discharge?

A
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30
Q

Definition of Adaptation of sensory receptors

A

Decline in the rate of discharge from receptor in spite of prolonged constant stimulation

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31
Q

Compare between Rapidly adapting receptors & Slowly adapting receptors in terms of:

  • Definition
  • Example
  • Other name
  • Physiological significance
A
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32
Q

what is a Sensory unit?

A
  • Single sensory axon with its peripheral branches and receptors.
  • All receptors of the some sensory unit are sensitive to the same type of stimulation.
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33
Q

What is Receptive field?

A
  • Area of skin which is supplied by sensory unit
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34
Q

what is the definition of Coding of sensory information?

A
  • It is the ability of higher centers of the brain to identity the:
  • Type of the stimulus (modality discrimination).
  • Intensity of the stimulus (intensity discrimination).
  • Locality of stimulus (locality discrimination).
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35
Q

what does Modality Discrimination depend on?

A

Peripheral & Central mechanisms

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36
Q

Peripheral mechansim of Modality Discrimination

A
  • Occurs at the level of receptors and depends on muller’s law.
  • So that specificity of receptors represents the first step in the coding of different modalities (types) of stimuli.
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37
Q

Central mechansim of Modality Discrimination

A
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38
Q

what does Intensity Discrimination depend on?

A

Peripheral & Central mechanisms

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39
Q

Peripheral mechanism of Intensity Discrimination

A

Depends on:

  • Rate of impulse discharge from each receptor: the higher the rate of discharge, the stronger is the stimulus.
  • Number of stimulated receptors (recruitement of recepfors): the more the number of stimulated recepfors, the stronger is the stimulus.
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40
Q

Central mechanism of Intensity Discrimination

A

Depends on: number of afferents reaching CNS: the more the number of afferents reaching CNS the stronger is the stimulus.

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41
Q

what does Locality Discrimination depend on?

A

Somatotopic map

  • According to which each area in the body is represented in a specific area in the cerebral cortex with accurate anatomical pathways from the receptor to the center in the cerebral cortex.
  • So when the impulse reaches specific area in the cerebral cortex, the sensation isn’t felt in the cortical neuron but it is referred (projected) to its original site in the body this principle is called law of projection.
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42
Q

what is Sensation?

A
  • Sensation is the conscious awareness of a particular feeling produced by stimulation of a certain type of receptors by its adequate stimulus.
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43
Q

Classification of sensation

A

General:
- Arises from widely distributed receptors all over the body.

Special:
- vision
- taste
- smell
- hearing
- Sense of equilibrium.

Emotional:
- fear
- anxiety
- sadness

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44
Q

Com pare between Somatic sensation, Visceral sensation & Sensation organ in terms of:

  • Arise from
  • Crried by
  • Examples
A
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45
Q

what is the definition of Touch sensation?

A
  • It is a sense or feeling produced by application of light mechanical pressure to the skin
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46
Q

what happens if the intensity of touch increases?

A

if the intensity of the stimulus is increased, it is changing into pressure sense

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47
Q

what are the types of touch?

A

a) Fine touch.
b) Crude touch.

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48
Q

Definition of Crude touch

A

A type of touch sensation which is poorly localized

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49
Q

Stimulus in case of Crude touch

A

Diffuses ill defined object, Touching the skin with a piece of cotton or the touch of clothes.

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50
Q

Receptors of Crude touch

A
  • Free nerve endings & hair end organs or follicle receptors “located in the hair follicles”
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51
Q

Afferents of Crude touch

A
  • A-δ nerve fibers “5-30 meter/second”.
  • C fibers “0.5-2 meter/second”.
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52
Q

Pathways of Crude touch

A

Pathway from the body:
- Ventro spino thalamic tract by A delta fibers
- Spino reticular tract by C fibers

Pathway from the face:
- Trigeminal pathway

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53
Q

whose transmission is faster, crude or fine touch?

A

The transmission of crude-touch is much slower than fine touch

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54
Q

Spatial arrangment of Crude touch

A

the spatial arrangement of the fibers in the pathway is poor

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55
Q

Does Crude touch inform the CNS accurately?

A

the impulses not inform the C.N.S accurately about the size & site of the crude-touch stimulus

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56
Q

Definition of Fine touch

A

It is a type of touch which informs us accurately about the shape, form and site of the tactile stimulus.

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57
Q

Stimulus of Fine touch

A

Well localized object to the skin as tip of pencil, head of a pin, teeth of comb

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58
Q

Receprors of Fine touch

A
  1. Meissner’s corpuscles (rapidly adapting).
  2. Merkel’s discs (slowly adapting)
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59
Q

Afferents of Fine touch

A

A-beta rapidly conducting nerve fibers (30-70 meters/second).

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60
Q

Pathway of Fine touch

A

Fine touch impulses are transmitted by A-beta nerve fibers which travel through the Dorsal column – medial lemniscal system (Gracil & Cuneate tracts).

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61
Q

Types of Fine touch

A

1-Tactile localization
2-Tactile discrimination
3-Stereognosis
4-Texture of materials

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62
Q

Definition of Pressure sensation

A

It is a sensation produced by the application of heavy mechanical stimuli to the skin (which can cause deformation of the different skin layers).

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63
Q

Receptors of Pressure sensation

A

a) Rapidly adapting receptors (Pacinian corpuscles).

b) Slowly adapting receptors (Ruffini multi-branched nerve endings); present in the deeper layers of the skin and responsible for the continuous information of the C.N.S about the pressure stimuli which play a role in the orientation of body position.

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64
Q

Afferents of Pressure sensation

A

as fine touch. (G & C)

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65
Q

Pathway of Pressure sensation

A

as fine touch. (G & C)

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66
Q

Types of Pressure sensation

A

Deep pressure sense:
- Discriminate between different weights without lifting them

Muscle tension sense:
- Discriminate between different weights with lifting them

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67
Q

significance of Pressure sensation

A
  • Maintain posture
  • Diffrentiate between different weights
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68
Q

Defintion of Vibration sensation

A
  • It is a sensation of rhythmic pressure changes produced by the rapid repetitive stimulation of certain mechanoreceptors.
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69
Q

Stimulus of Vibration sensation

A

It can be produced by placing the base of vibrating tuning fork on the skin over bony prominence

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70
Q

Receptors of Vibration sensation

A

i)Meissner’s corpuscles: can respond to frequencies to frequencies up to 200 cycles/second.

ii)Pacinian corpuscles: can respond to frequencies to frequencies up to 700 cycles/second.

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71
Q

Afferents of Vibration sensation

A

as fine touch (G &C)

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72
Q

Pathway of Vibration sensation

A

as fine touch (G &C)

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73
Q

Definition of Proprioceptive sensation

A

Is a sense that allows us to know the position and movement of every part of the body specially joints and limbs.

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74
Q

Receptors of Proprioceptive sensation

A

1) Muscle proprioceptors.
2) Joint proprioceptors.

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75
Q

Pathway of Proprioceptive sensation

A
  • At conscious level
  • At subconscious level
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76
Q

Types of Proprioceptive sensation

A
  1. Sense of position.
  2. Sense of movement.
  3. Muscle-tension sense.
  4. Deep pressure sense.
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77
Q

what are the types of Fine touch?

A

1-Tactile localization
2-Tactile discrimination
3-Stereognosis
4-Texture of materials

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78
Q

what is the definition of Tactile localization (topognosis)?

A
  • It is the ability of the person with his eyes closed to perceive and determine accurately the site of a single point of fine touch.
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79
Q

Definition of Tactile discrimination (2 point discrimination)

A

Its the ability of the person or central nervous system to discriminate 2 points of fine touch applied simultaneously to the skin with the person’s eyes closed provided that the distance between them is greater than the minimal distance.

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80
Q

what is Minimal (Threshold) distance?

A

it is the distance between 2 points of fine touch below it the points are felt as a single point whereas at or above it the 2 points are felt as separate points

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81
Q

what does Minimal (Threshold) distance equal?

A

It equals 1 mm at tip of tongue, 3 mm at tip of fingers, 70 mm at the back.

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82
Q

where is Tactile discrimination more accurate? and why?

A
  • On the extremities than on the proximal parts due to:
  1. Greater number of touch receptors, and subsequently a greater number of afferents
  2. Little convergence of afferents.
  3. Wide area of cortical representation and so good analysis and interpretation of sensory information.
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83
Q

what is the definition of Stereognosis?

A

Is the ability of the person with his eyes closed to recognize a familiar object by touching it e.g. recognition of a key, a pen or a coin.

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84
Q

what is the definition of Determination of texture of materials?

A
  • Is the ability of the person with his eyes closed to recognize the nature of an object/textiles e.g. glasses and wood
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85
Q

which type of sense is Sense of position?

A

static sense

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86
Q

what does sense of position represent?

A

conscious orientation of the relative position of the different parts of the body to each other.

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87
Q

which type of sense is Sense of movement?

A

dynamic sense

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88
Q

what does Sense of movement represent?

A

means conscious orientation of the changes in the relative position of the different parts of the body to each other as regard, onset, termination, direction and the rate or velocity of this change

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89
Q

what are receptors of proprioception?

A
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90
Q

Compare between pathway of proprioception at conscious & subconscious level in terms of:

  • Center
  • Function
  • Pathway
A
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91
Q

Definition of Thermal sensation

A

Is the sensation that enables us to detect temperature change, it includes warm and cold sensation.

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92
Q

Distribution of Cutaneous thermo receptors

A
  • Number of cold receptors is greater than the number of warm receptors by about 3- 10 times.
  • They are distributed in a punctuate fashion where, certain areas of skin contain warm receptors only and others contain cold receptors only with thermally insensitive areas in between.
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93
Q

what are the types of thermo-receptors?

A
  • External (peripheral) thermoreceptors
  • Internal (central) thermoreceptors
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94
Q

Compare between External (Peripheral) thermo-receptors and internal (Central) thermo-receptors in terms of:

  • Types
  • Location
  • Detect
A
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95
Q

Compare between Warm & Cold Receptors in terms of:

  • Morphology
  • Number
  • Afferent fiber
  • Discharge impulse between
  • Maximum discharge
A
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96
Q

Thermo-receptors at zero degree

A

all receptors stop discharge and this is one of the methods of anaesthesia.

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97
Q

Thermo-receptors at 45 degrees

A

the person feels “Paradoxical cold sensation” due to a brisk discharge from the cold receptors “Paradoxical cold sensations”.

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98
Q

Thermo-receptors if temperature is less than 10 degrees

A
  • Stimulate cold pain receptors
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99
Q

Thermo-receptors if temperature is more than 45 degrees

A

Stimulate warm pain receptors

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100
Q

what is the mechanism of stimulation of thermo-receptors?

A
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101
Q

what is the type of thermo-receptors?

A

Biphasic but mainly slowly adapting receptors

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102
Q

Adaptation of thermo receptors

A
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103
Q

Neural pathway of thermal sensation

A
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104
Q

Definition of Pain Sensation (Nociceptors)

A
  • Unpleasant sensory and emotional experience associated with actual tissue damage.
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105
Q

Physiological significance of Pain Sensation

A
  • Protective sense that direct the person to get rid of injurious stimulus.
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106
Q

what are the characters of pain receptors?

A
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107
Q

what is the type of pain receptors?

A
  • They are morphologically one type → free nerve endings.
  • They are slowly adapting and even non-adapting receptors.
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108
Q

Specifity of pain receptors

A
  • Highly specific → respond to tissue damage & classified

according to type of painful stimuli into:

a. Mechanical pain receptor→ to mechanical stimulus.

b. Chemical pain receptor→ to chemical stimuli

c. Thermal pain receptor → respond to excess temperature → (<10°C &>45°C)

d. Polymodal pain receptor → respond to all above painful stimuli.

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109
Q

Threshold of pain receptors

A

high threshold → need strong stimulus that cause tissue damage.

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110
Q

Distribution of pain receptors

A

Widely distributed all over the body:

a. More abundant in the skin.

b. Present in deeper structures (muscles - joints - periosteum).

c. Viscera contains a smaller number of pain receptors and even this few numbers are concentrated in serous membranes e.g. peritoneum, pleura, pericardium & meninges of the brain.

d. Absent from: Liver, lung, brain & bone

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111
Q

when do diseases that affect the viscera start causing pain?

A
  • The diseases affecting the parenchyma of organs, may not produce pain early, but lateral when they invade the serous covering they cause severe pain.
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112
Q

Definition of Pain Threshold

A

The lowest intensity of injurious agent needed to stimulate the pain receptors and produced pain sensation.

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113
Q

what are the methods of determination of the pain threshold?

A
  1. By pricking the skin with a pin.
  2. By compressing the skin against hard objects.
  3. Thermal method “more accurate’’ by applying to skin to a thermostatically controlled metallic rod (Most of individuals begin to feel pain at 45°C and all feel pain at 47 C and this is known as thermal threshold for pain receptors stimulation).
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114
Q

Feeling of pain in different people

A
  • Most people feel pain at similar points but differ in their reaction to pain.
  • Pain threshold is not the same in all individuals.
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115
Q

what is pain classified into?

A
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116
Q

What is the mechanism of stimulation of pain receptors?

A
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117
Q

Definition of Pain producing substance

A
  • Which directly stimulate pain receptor.
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118
Q

Examples of Pain producing substances

A
  • Histamine, serotonin.
  • Bradykinin.
  • Proteolytic enzymes & K ions.
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119
Q

Definition of Pain sensitizers

A
  • Which increases sensitivity of receptors by lowering pain threshold
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120
Q

Examples of Pain sensitizers

A
  • Substance-P
  • PGs-E2
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121
Q

What are neural pathways for pain transmission?

A

1) Fast pain pathway (Neo-spino-thalamic tract).

2) Slow pain pathway (paleo-spino-thaiamic tract).

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122
Q

Significance of Neo-spinothalamic tract

A

a. Rapidly Inform the C.N.S about the injurious agent to initiate rapid protective reflexes as flexion withdrawal reflex.

b. Determining accurately the site of the painful stimuli.

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123
Q

Characters of Neo-spinothalamic tract

A
  • Fast pain is transmitted by neo- spinothalamic tract.
  • Consists of 3 order neurons “A-δ nerve fibres”
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124
Q

1st order neuron of Neo-spinothalamic tract

A
  • From pain receptors →1st order neuron → dorsal horn → end on neurons in laminae I & IV.
  • Its ends release rapidly acting neurotransmitter (Glutamate)
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125
Q

2nd order neuron of Neo-spinothalamic tract

A
  • From dorsal horn cells fibers pass to opposite side in front of central canal→ ascend in the lateral column of the spinal cord till the PVLNT of thalamus.
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126
Q

3rd order neuron of Neo-spinothalamic tract

A
  • From PVLNT, fibres Ascend in the posterior limb of internal capsule to terminate in primary sensory cortex (3. 1 & 2) in the post- central gyrus.
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127
Q

Significance of Paleo-spinothalamic tract

A

a. Continuously inform C.N.S about the presence of tissue damage to direct the person to remove the injurious agents

b. Responsible for strong arousal state due to potent (strong) activation of reticular activating system (RAS)

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128
Q

Characters of Paleo-spinothalamic tract

A
  • Slow pain transmitted by paleo- spinothalamic tract
  • Consists of C non-myelinated nerve fibers.
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129
Q

1st oerder neuron of Paleo-spinothalamic tract

A
  • C-myelinated nerve fibres ends in laminae II & III on dorsal horn
  • Release the slowly acting neurotransmitter (substance- P)
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130
Q

2nd order neuron of Paleo-spinothalamic tract

A
  • From the dorsal horn, fibers arise & Ascend in the lateral column till Brainstem where it relays on the neurons of reticular formation.
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131
Q

3rd order neuron of Paleo-spinothalamic tract

A
  • From R.F, fibers ascend to intralaminar (non specific) nuclei of the thalamus → then fibres arise & ascend to all areas of the cerebral cortex
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132
Q

Definition of Cutaneous pain

A

Pain sensation results from the stimulation of pain receptors in the skin.

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133
Q

Compare between the components of Cutaneous pain (Fast “Pricking” & Slow “Burning”) pain in terms of:
- Localization & Quality
- Spread
- Significance
- Perception and lost in
- Transmission

A
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134
Q

what is the Role of the cerebral cortex in pain perception?

A

1) Coding of sensation i.e. determine type, site, intensity of pain.

2) Lesion in cerebral cortex → pain will be diffuse, ill-defined.

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135
Q

Reaction to cutaneous pain

A
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136
Q

what is Cutaneous hyperalgesia?

A

Increased pain sensitivity in skin area, surrounding to the site of injury.

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137
Q

Types of Cutaneous hyperalgesia

A
  • 1ry hyperalgesia (allodynia)
  • 2ry hyperalgesia
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138
Q

Site of 1ry hyperalgesia (allodynia)

A

Develop in area of erythema (flare) which surrounds 1ry site of injury.

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139
Q

Characters of 1ry hyperalgesia (allodynia)

A
  • Pain threshold is lowered that non-painful stimuli as touch produces pain
  • Develops within 30 - 60 min following skin injury & lasts for several hours or days.
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140
Q

Mechanism of 1ry hyperalgesia (allodynia)

A

Local axon reflex:

  • In which antidromic fibers arise from afferent pain fibers which arise from 1ry site of injury, these antidromic fibers release substance - P & PGs in skin area surrounding 1ry site of injury to ↓ threshold of pain.
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141
Q

Definition of 2ry hyperalgesia

A
  • Develops in normal skin which surrounds area of flare
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142
Q

Characters of 2ry hyperalgesia

A
  • No lowering of pain threshold but mild painful stimuli produce more severe pain than usual.
  • Shorter duration than 1ry hyperalgesia.
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143
Q

Mechanism of 2ry hyperalgesia

A

Convergence-facilitation theory:

  • In which fibers arise from 1ry site of injury & from area of 2ry hyperalgesia converge on the same neuron in dorsal horn in spinal cord or thalamus
  • Fibers from 1ry site of injury produce state of facilitation (excitability) that the response to pain is intensified → that mild pain from normal skin is felt as severe pain →This facilitation occurs mainly at level of SGR but can occur atlevel of thalamus or cerebral cortex
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144
Q

Definition of Deep pain

A
  • Pain sensation due to stimulation of receptors in deeper structure as muscle, tendon, joint
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145
Q

Causes of Deep pain

A
  • Injury or trauma to tissue
  • Inflammation as arthritis & myositis.
  • Ischemia to tissue
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146
Q

Characters of Deep pain

A
  • Dull aching or throbbing
  • Poorly localized
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147
Q

Pathway of Deep pain

A

C-nerve fibers

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148
Q

Definition of Visceral pain

A
  • Pain sensation due to stimulation of receptors in the viscera.
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149
Q

Causes of Visceral pain

A
  • Spasm of smooth muscle in wall of hollow viscera (colic) → (most common cause)
  • Mechanical over distension of hollow visceral wall as stomach (a & b cause ischemia of organ → pain)
  • Inflammation of viscera.
  • Irritation as → HCI in stomach
  • Thrombosis of SMA.
  • Trauma → diffuse cut of viscera
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150
Q

Characters of Visceral pain

A
  • Dull aching or colicky.
  • Poorly localized and referred.
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151
Q

Pathway of Visceral pain

A

Parietal pathway:

  • From parietal layer of serous membrane and some retroperitoneal structures as kidney by type A-delta fiber which join somatic fiber to enter CNS.

Visceral pathway:

  • From viscera and visceral layer by type C-fiber which join autonomic fibers to enter CNS.
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152
Q

Reaction to deep & visceral pain

A
  1. Somatic reactions → reflex spasm of overlying ms (guarding response).
  2. Autonomic reactions → depressor effect due to parasympathetic reaction.
  3. Emotional reaction.
  4. Hyperalgesia.
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153
Q

Definition of Ischemic pain

A

Pain due to decrease Blood Supply to active organ as skeletal ms.

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154
Q

Causes of Ischemic pain

A
  1. Sever arteriosclerosis or sever spasm.
  2. Partial obstruction by thrombosis.
  3. Compression from outside as tumour.
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155
Q

Mechanisms of Ischemic pain

A
  1. During rest with normal Blood Supply → exercising muscle Produce certain substances as K+, lactic acid → which cause local V.D → washout of these metabolites (If not washed will cause pain)
  2. In case of ischemia these substances will accumulate & stimulate pain
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156
Q

Examples of Ischemic pain

A

Muscle spasm → compress blood supply.

Angina pectoris pain → due to atherosclerosis of coronary artery appears on exertion & relieved by rest.

Intermittent claudication → sever pain in calf muscle which appears on walking & relieved by rest occurs in old people with severe atherosclerosis

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157
Q

Definition of Referred Pain

A
  • Pain from viscera is not felt in the viscera themselves but felt in skin area or somatic structures supplied by same dorsal root which innervate diseased viscera.
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158
Q

Causes of Referred Pain

A

Both viscus & somatic structures originate from same dermatome.

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159
Q

Mechanism of Referred Pain

A

(Convergence Projection theory)

  • Pain fibers from diseased viscus & from related somatic structures converge on
    same SGR cell & ascend to same cortical neuron.
  • Since, cortical sensory area is accustomed to receive pain impulses from somatic structures.
  • So, when viscus is injured or diseased → cerebral cortex project pain to somatic structures which are supplied by same spinal dorsal root.
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160
Q

Definition of Neuropathic pain

A

A chronic type of pain caused by damage to or pathological changes in the nerve fibres either in peripheral or central nervous system

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161
Q

Examples of Neuropathic pain

A
  • Trigeminal neuralgia.
  • Any type of peripheral neuropathy e.g. diabetic neuropathy.
  • Phantom limb.
  • Herpes zoster.
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162
Q

Mechanism of Neuropathic pain

A

Peripheral sensitization or ectopic activity:

  • Tissue damage produce abnormal types of Na ion channels which result in unstable sodium channel activity

Central sensitization:

  • Release excitatory amino acids and neuropeptides will produce changes in 2nd order neuron such as phosphorelyation of glutamic receptors or expression of voltage gated Na channels
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163
Q

Characters of Neuropathic pain

A

1) Usually associated by hyperalgesia and allodynia.

2) Usually associated with reflex sympathetic dystrophy (sweating, warmth and/or coolness, flushing, discoloration of skin).

3) Described as excruciating burning or shooting pain.

4) It occurs in bouts or paroxysms (Attacks).

5) Partially responsive to opioid therapy.

6) Hardly to be treated.

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164
Q

what is cardiac pain referred to?

A
  • Referred to Lt Shoulder, inner side of Lt arm, Lt Forearm and little finger (may be in epigastric region).
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165
Q

what is Oesophageal pain referred to?

A

Referred to pharynx, lower neck, middle chest region.

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166
Q

what is Gastric pain referred to?

A

Referred to epigastric region in wall of abdomen

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167
Q

what is Gall baldder pain referred to?

A

Referred to Rt side of epigastric region, Rt shoulder and neck

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168
Q

what is Renal and ureteric pain referred to?

A

Referred to back behind the kidney also, to ant. Abdominal wall & near inguinal region

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169
Q

what is Appendicular pain referred to?

A

Starts in skin area around umbilicus and when peritoneal covering is involved → pain shifts to Rt iliac fossa

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170
Q

Definition of Pain control (analgesia) system

A
  • It is a system concerned with the inhibition of pain impulses transmission at Different levels in pain pathway and produces analgesia.
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171
Q

Activity of Pain control (analgesia) system

A

The activity of this system differs from one person to another and from time to time in the same person.

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172
Q

Location of Pain control (analgesia) system

A

Periaqueductal grey area (PAG) → in midbrain &pons.

Raphe Magnus nucleus & Nucleus para giganto cellularis → in medulla oblongata

Pain inhibitory complex → in dorsal horn of spinal cord.

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173
Q

Definition of Endogenous opioids

A
  • Natural peptide substances produced inside the body (mainly by areas of pain control system) and have the ability to bind opioids receptors (morphine receptors) and produce pain analgesia (relieve pain).
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174
Q

Classes of Endogenous opioids

A
  • Endorphins
  • Enkephalins
  • Dynorphins
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175
Q

Endorphins

  • Derived from
  • present mainly in
  • Most common
A
  • Pre-opio-melano- cortin (POMC)
  • Anterior pituitary and hypothalamus.
  • B-endorphins
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176
Q

Enkephalins

  • Derived from
  • present mainly in
  • Most common
A
  • Pro-enkephalins
  • Brain stem and Spinal cord.
  • leu-enkephalin, encephalin
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177
Q

Dynorphins

  • Derived from
  • present mainly in
  • Most common
A
  • null
  • Brain stem and Spinal cord.
  • null
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178
Q

what are opiate receptors?

A
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179
Q

what do neurons in PAG and Raphe nuclei contain?

A
  • Contain opioids receptors on their surface membrane when stimulated by exogenous or endogenous opioids, this leads to activation of pain control system.
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180
Q

What activates pain control system?

A

activated naturally by severe stress& strong emotions e.g. during severe exercise, battles, fear.

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181
Q

Evidences that pain inhibition can occur at level of brain stem & hypothalamus

A

1- Their stimulation by (electrical stimulus) cause pain relief

2- Injection of encephalin in animal cause pain relief.

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182
Q

Mechanism of action of pain control system

A
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183
Q

Mechanisms for pain control at spinal cord level

A
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184
Q

Comparisons Between Slow and Fast Pain

A
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185
Q

Definition of Synapse

A

Areas of contact between neurons in the CNS.

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186
Q

Types of synapse

A
  • Electrical synapse
  • Chemical synapse
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187
Q

Compare between Electrical Synapse & Chemical Synapse in terms of:

  • existence
  • Nature
  • Function
  • Fatigue
  • Speed
  • Conduction
A
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188
Q

Site of electrical Synapse

A

Present in hippocampus and
retina

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189
Q

what do chemical synapses consist of?

A
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190
Q

Mechanism of synaptic transmission (In brief)

A
  1. Release of neurotransmitter into synaptic cleft.
  2. Action of neurotransmitter on postsynaptic membrane.
  3. Termination of synaptic transmission.
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191
Q

Mechanism of Release of neurotransmitter

A
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192
Q

what are Active zones?

A

The site at which vesicle bind to membrane

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193
Q

Method of release of chemical transmitter

A

exocytosis

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194
Q

what does Number of ruptured vesicles depend on?

A
  • Number of ruptured vesicles depend on concentration of ca
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195
Q

Action of neurotransmitter on post synaptic membrane

A

After release of neurotransmitter → It binds with specific receptors on post synaptic membrane to act by two mechanisms:

  • Ligand-gated ion channels (inotropic)
  • G-protein coupled receptor (Metabotropic)

And explain ….

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196
Q

what are the types of Ligand-gated ion channels (Inotropic)?

A

Cation & Anion channels

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197
Q

what happens to cation channels of synapses on activation?

A
  • When activated , allows Passage of Na+& K+ but Na+ influx more than K+ efflux (about 7.5 time) due to ↑ driving force for Na+→ Depolarization of the membrane.
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198
Q

Neurotransmitter in cases of cation channels in chemical synapses

A
  • Neurotransmitter is called excitatory transmitter
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199
Q

why don’t cation channels in chemical synapses allow passage of anions as cl?

A
  • Channels are lined with -ve Charge which don’t allow passage of anions as Cl-.
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200
Q

what happens to anion channels of synapses on activation?

A
  • When activated , allows passage of Cl- → Cl– influx → Hyperpolarization of the membrane.
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201
Q

Neurotransmitter in cases of anion channels in chemical synapses

A

Neurotransmitter is called inhibitory transmitter.

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202
Q

why don’t anion channels in chemical synapses allow passage of cations as Na & Ca?

A
  • Channels are lined with +ve charge and has small pores , So don’t allow passage of cations as Na+ & Ca2+ .
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203
Q

G-Protein coupled receptors (Metabotropic)

A
  • These receptors are bound to G-proteins, which is composed of 3 subunits {α, β, γ} & α-subunit is bound to GDP.
  • When chemical transmitter binds to receptor → GDP is converted to GTP.
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204
Q

Effects produced when α-subunit with GTP separates

A

Opening of specific ion channels: 2nd messenger gated k+ channels Opens → k+ efflux → Hyperpolarization of post synaptic membrane.

Activation of enzyme system in the cell membrane leads to formation of 2nd messenger as cAMP which control metabolic pathway.

Regulation of gene expression: stimulate DNA to form m.RNA, which form protein (receptors and enzymes).

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205
Q

Termination of synaptic transmission

A

a) By active reuptake into presynaptic terminal.

b) By enzymatic destruction.

c) By diffusion into surrounding interstitial fluid

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206
Q

Compare between Post-Synaptic Potential in terms of:

  • During rest
  • On stimulation
  • Excitability of membrane
A
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207
Q

Properties of Post-synaptic potential

A
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208
Q

what happens to summated EPSP reach firing level?

A

When summated EPSP reach firing level → this will generate an action potential at initial Segment of axon (Axon hillock) because it is rich in voltage gated Na channel

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209
Q

Definition of Presynaptic inhibition

A

Inhibition of presynaptic terminal before nerve impulse reaches post- synaptic membrane.

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210
Q

what is Presynaptic inhibition mediated by?

A

Mediated by inhibitory interneuron which terminates on excitatory presynaptic neuron.

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211
Q

Mechanism of Presynaptic inhibition

A
  • Inhibitory interneuron release Inhibitory neurotransmitter GABA which open Cl channels in presynaptic terminal →↑ Cl- influx which cause hyperpolarization which inhibit voltage gated Ca channel → ↓ Ca++ influx →↓ neurotransmitter release.
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212
Q

Types of inhibition of synapses

A
  1. Post-synaptic inhibition
  2. Recurrent of feedback inhibition
  3. Pre-synaptic inhibition
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213
Q

Significance of Presynaptic inhibition

A
  • Supraspinal inhibition of pain transmission (pain control system).
  • Spinal inhibition of pain transmission.
  • Lateral inhibition.
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214
Q

what are the types of Neurotransmitters of CNS?

A
  • Small M.W rapidly acting Neurotransmitter
  • Large M.W slowly acting Neuropeptides
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215
Q

Examples of Small M.W rapidly acting Neurotransmitter

A

Class I → Acetyl choline.

Class II→ Biogenic amines as:
- Noradrenalin
- Dopamine
- Serotonin
- Histamine

Class III → Amino acids as:
- Glutamate
- GABA
- Glycine
- Aspartate

Class IV→ NO (Nitric oxide)

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216
Q

Examples of Large M.W slowly acting Neuropeptides

A

Substance P: For pain Transmission.

Opioid peptide: as Enkephaline& endorphin for prevention of pain transmission.

Some co-exist:
- With acetyl choline as VIP.
- With noradrenalin as NPY (neuropeptide Y)

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217
Q

Signifance of Small M.W rapidly acting Neurotransmitter

A

Important for fast response as:

  • Transmission of sensory information to CNS.
  • Transmission of motor information from CNS to ms.
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218
Q

Significance of Large M.W slowly acting Neuropeptides

A
  • Prolong action of small M.W neurotransmitter at Post synaptic membrane through G- Protein coupled receptors for days, months or years.
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219
Q

General properties of chemical synaptic transmission

A
  • One-way conduction
  • Synaptic delay
  • Synaptic fatigue
  • Effect of hypoxia
  • Effect of pH
  • Effect of Drugs
  • Post tetanic facilitation & Long term potentiation
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220
Q

Direction of impulse transmission in synapses

A

impulses are transmitted only in one direction from presynaptic to post synaptic Neuron.

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221
Q

why is there one-way conduction in chemical synapses?

A

because no transmitter releasing vesicles in postsynaptic membrane.

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222
Q

Definition of synaptic delay

A
  • It’s time () arrival of action potential to synaptic knobs & occurrence of response of post synaptic neuron
  • It’s the time needed for release & diffusion of neurotransmitter & binding with receptor on post synaptic neuron.
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223
Q

Duration of synaptic delay

A

0.5 m.sec

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224
Q

Significance of Synaptic delay

A
  • It help to calculate number of
    interneurons.
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225
Q

what is synaptic fatigue?

A
  • Decline or even stoppage of synaptic transmission with rapid & strong stimulation of Synapse.
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226
Q

Causes of synaptic fatigue

A

a) depletion of neurotransmitter stores in synaptic knobs

b) progressive inactivation of most post-synaptic receptors

c) development of abnormal concentration of ions on post synaptic neurons

usually fatigue develop gradually and recover slowly.

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227
Q

Significance of synaptic fatigue

A
  • One of mechanisms which stop after discharge in reverberating circuits.
  • Suppress brain activity during epileptic fit
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228
Q

Effect of hypoxia on synaptic transmission

A
  • Marked hypoxia for few seconds → stop transmission & loss of excitability.
  • Marked hypoxia more than 7 sec. → Coma occurs.
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229
Q

Effect of pH on synaptic transmission

A
  • Alkalosis →↑ Excitability & if PH reaches 7.8-8 → convulsion occurs.
  • Acidosis →↓ Excitability & if 7 → Coma occurs as in uremic or diabetic acidosis.
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230
Q

Effect of drugs on synaptic transmission

A
  • Caffeine & theophylline → ↑ neuron excitability.
  • Anaesthesia & hypnotic→↓ neuron excitability
  • Strychnine→↑ neuron excitability.
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231
Q

Compare between (Post-tetanic facilitation = Post-tetanic potentiation) & Long-term potentiation in terms of:

  • Produced by:
  • Lasts for:
  • Cause
  • Function
A
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232
Q

Definition of Spinal Reflexes

A
  • Involuntary programmed response to a stimulus.
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233
Q

Classification of Spinal Reflexes

A
  • Conditioned & Unconditioned reflexes
  • Somatic & Autonomic spinal reflexes
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234
Q

Characters of Conditioned reflexes

A
  • Aquired
  • Not inherited
  • Need training
  • Need intact cerebral cortex
  • Play a role in regulation of GIT , respiratory , CVS functions.
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235
Q

characters of Unconditioned reflexes

A
  • Inherited
  • Not acquired.
  • Don’t need learning
  • Don’t need intact cerebral cortex
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236
Q

Classification of Unconditioned reflexes

A

Hypothalamic reflexes: e.g.
- Reflexes regulating body temperature.
- Reflexes regulating food intake.

Brain stem reflexes: e.g.
- Midbrain reflexes as light reflex.
- Pontine reflexes as salivary reflex.
- Medullary reflexes as most of CVS & respiratory reflexes.

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237
Q

Compare between Somatic spinal reflexes & Autonomic spinal reflexes in terms of:

  • Carried by
  • Innervate
A
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238
Q

Components of spinal reflex

A
  1. Receptor
  2. Afferent Nerves.
  3. Interneurons.
  4. Efferent Nerves.
  5. Effector organ.
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239
Q

Definition of Afferent neuron

A
  • They are pseudo-unipolar neurons whose cell bodies are in DRG & axons divide into:

Peripheral branches: Which terminate in sensory receptor.

Central branches: which enter spinal cord through the dorsal horn

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240
Q

Functions of Afferent neuron

A

Conduction: of impulses from receptor to spinal cord.

Divergence: in which branches of afferent n. divide into many central branches.

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241
Q

Definition of Inter-neurons

A
  • They are numerous , small sized, highly excitable neurons, located in spinal cord grey matter & provide link () central terminal of afferent neurons & efferent neurons.
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242
Q

which reflex doesn’t include Inter-neurons?

A
  • All reflex arcs include interneurons except the stretch reflex.
  • Thus, all reflexes are Polysynaptic (have more than one synapse) except the stretch reflex which is a monosynaptic (has only one synapse) reflex.
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243
Q

Functions of Inter-neurons

A
  1. Convergence
  2. Divergence
  3. After discharge (repetitive) circuits
  4. Inhibitory circuits
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244
Q

Definition of Convergence

A

Large number of afferent neuron or interneuron (more common) converge on one efferent neuron.

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245
Q

Significance of Convergence

A

This helps in spatial summation.

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246
Q

Definition of Divergence

A
  • One afferent or one interneuron (more common) diverge to large number of efferent neurons.
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247
Q

Significance of Divergence

A

This helps in irradiation (wide response)

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248
Q

Definition of After discharge (repetitive) circuits

A
  • Prolonged efferent discharge after stoppage of stimulation of afferent
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249
Q

Cause of After discharge (repetitive) circuits

A

Due to presence of interneurons.

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250
Q

Types of After discharge (repetitive) circuits

A

A. Parallel (Open) chain circuits
B. Reverberating (closed) chain circuits

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251
Q

Mechanism of Parallel (Open) chain circuits

A
  • Afferent neuron stimulates efferent neuron directly & through interneurons which are parallel with afferent neurons
  • A delay of 0.5 m.sec occurs at each synapse in this circuit, thus the impulse reaches the Efferent neuron after variable periods of delay.
  • duration of after discharge depends on number of interneurons in this circuit.
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252
Q

what does duration of after discharge depend on?

A
  • duration of after discharge depends on number of interneurons in this circuit.
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253
Q

Mechanism of Reverberating (closed) chain circuits

A
  • Afferent nerve ends on principal interneuron whose axon either → terminate directly on efferent neuron & send collateral branch

which either:

  • Stimulates principle interneuron again (Reverberating).
  • Stimulates another interneuron which re- stimulates principle interneuron.

So, brief afferent signal causes reverberating of signal for long time → Prolonged after Discharge.

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254
Q

what causes stoppage of Reverberating (closed) chain circuits activity?

A

1) Fatigue of synapse.

2) Inhibition from other neurons.

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255
Q

what are examples of reverberating circuits?

A
  • Reticular activating system (RAS)
  • Respiratory centre
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256
Q

Reticular activating system (RAS)

A
  • Present in brain stem & responsible for wakefulness. (12-18 hours).
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257
Q

Respiratory centre

A

Continues to discharge for life.

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258
Q

Definition of Inhibitory circuits

A
  • convert excitatory input signals into Inhibitory output signals.
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259
Q

Types of Inhibitory circuits

A
  • lateral inhibitory circuits
  • Recurrent (feedback) inhibitory Circuits
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260
Q

Definition of lateral inhibitory circuits

A

In which the most active neuron send a collateral to stimulate an inhibitory interneurons to inhibit the less active or less stimulated neurons

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261
Q

Example of lateral inhibitory circuits

A

Ascending sensory tracts during their course to C.C.

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262
Q

Importance of lateral inhibitory circuits

A

To focus or sharpen reflex response.

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263
Q

Definition of Recurrent (feedback) inhibitory Circuits

A

In which efferent neuron (AHCs) axon send recurrent collateral branches which release acetyl choline to stimulate inhibitory interneurons called renshow cell which release glycine to inhibit:

  • The neighbouring α- motor neurons.
  • The originally stimulated α- motor neuron.
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264
Q

Importance of Recurrent (feedback) inhibitory Circuits

A
  • On neighbouring α-Motor neurons → Focus motor response.
  • On Originally stimulated α-Motor neuron → To limit its discharge (-ve feedback control).
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265
Q

Tyoes of Efferent neuron

A
  • Autonomic efferent neurons (LHCs) → Mediate autonomic reflex.
  • Somatic efferent neuron (AHCs) → Mediate somatic spinal reflex.
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266
Q

what are AHCs divided into?

A
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267
Q

Examples of polysynaptic reflexes

A
  • Flexion-Withdrawal reflex
  • Crossed-Extensor Reflex
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268
Q

Def of Flexion-withdrawl reflex

A

It’s a poly synaptic reflex that moves the affected limb away from painful stimulus.

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269
Q

Stimulus of Flexion-withdrawl reflex

A

painful stimulus

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270
Q

Receptors of Flexion-withdrawl reflex

A

Free nerve ending.

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271
Q

Afferents of Flexion-withdrawl reflex

A

A-Delta nerve fibers

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272
Q

Centre of Flexion-withdrawl reflex

A
  • Afferent neurons affer entering spinal cord divide into many central branches
  • Which synapse with interneurons
  • Through these interneurons, afferent Impulse
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273
Q

Action done by interneurons in Flexion-withdrawl reflex

A
  • Excite motor neuron pool which supply ipsilateral flexors
  • Inhibit motor neuron pool which supply ipsilateral extensors (antagonists).
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274
Q

Significance of Flexion-withdrawl reflex

A
  • Of survival value because it removes limb away from injurious agent. (protective)
  • Pre-potent reflex that suppresses any other reflexes occurring at the same time
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275
Q

Definition of Crossed-Extensor reflex

A
  • It is reflex extension of a limb during fexion of the other limb, as a result of flexion withdrawal reflex.
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276
Q

Pathway of Crossed-Extensor reflex

A

When strong painful stimulus is applied to one limb on one side, afferent fibres cross to Opposite side to synapse with interneurons which either:

  • Stimulate motor neuron pool of extensors.
  • Inhibit motor neuron pool of flexors.
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277
Q

Significance of Crossed-Extensor reflex

A
  • To cause extension of the controlateral limb to support body during flexion of the stimulated limb (supportive)
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278
Q

Properties of polysynaptic somatic spinal reflexes

A
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279
Q

what are other names for strech reflex?

A

(Myotonic reflex - Ms spindle reflex)

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280
Q

Definition of strech reflex

A

Reflex contraction of muscle when it’s passively stretched

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281
Q

Receptor of strech reflex

A

Muscle spindles.

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282
Q

Afferent of strech reflex

A

A-alpha & A-beta nerve fibers. (type Ia and type II)

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283
Q

Center of strech reflex

A

A.H.Cs (alpha-motor neurons).

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284
Q

Efferent of strech reflex

A

alpha-motor nerves.

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285
Q

Response of strech reflex

A

Contraction of the muscle

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286
Q

Definition of muscle spindle

A
  • Specialized fusiform capsulated structures located in the fleshy part of the muscles.
  • They act as length receptors i.e. detect the changes in the muscle length.
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287
Q

Number of muscle spindle

A

Each muscle spindle consists of 4-12 modified muscle fibers called intrafusal muscle fibers which are of 2 types

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288
Q

Types of muscle spindle

A
  • Nuclear bag muscle fibers
  • Nuclear chain muscle fibers
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289
Q

Compare between Nuclear bag of muscle fiber & Nuclear chain of muscle fiber in terms of:

  • Composed of
  • Length
  • Number
  • Sensory (Afferent)
  • Motor (Efferent)
A
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290
Q

Mechanism of stimulation of ms. spindle

A
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291
Q

Central connection of muscle spindle

A
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292
Q

Defintion of stretch reflex

A
  • Reflex contraction of a muscle when it is passively stretched.
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293
Q

what are the types of stretch reflex?

A
  • Dynamic response or dynamic stretch reflex
  • Static response or static stretch reflex
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294
Q

Compare between Dynamic stretch reflex & Static stretch reflex in terms of:

  • stimulus
  • Receptors
  • Afferent
  • Center
  • Example
  • Potentiated by
A
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295
Q

what is the function of strech reflex (Muscle spindle)?

A
  • Generation of muscle Tone
  • Smoothing of muscle contraction (Damping function)
  • Load Reflex (servo-assist function)
  • Proprioceptive functions
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296
Q

Generation of muscle tone by stretch reflex

A
  • Muscle spindles, through the stretch reflex, are responsible for generation of skeletal muscle tone.
  • CNS adjusts muscle tone by varying the level of gama-M N. activity which by its turn affect the frequency of spindle sensory discharge.
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297
Q

Smoothing of muscle contraction (Damping function) by stretch reflex

A

the ability of muscle spindle to prevent oscillation and jerkiness of body movements.

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298
Q

Load reflex (Servo-assist function) by stretch reflex

A

reflex that is responsible for keeping the hand or foot in position when a moderate or heavy load is applied.

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299
Q

Proprioceptive function by stretch reflex

A
  • Muscle spindles provide proprioceptive information to the brain and cerebellum for keeping them continually informed about muscle length and changes in that length.
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300
Q

Intro to Supra-spinal control of stretch reflex

A

AHCs of the stretch reflex (alpha & gama -motor neurons) continuously exposed to supraspinal facilitatory & inhibitory impulses from different areas in brain.

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301
Q

what are supraspinal facilitatory areas?

A
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302
Q

what are supraspinal inhibitory areas?

A
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303
Q

which supraspinal action dominates under normal condition?

A
  • Under normal condition the supraspianl facilitation predominates and the stretch reflex & muscle tone are facilitated.
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304
Q

what are the proprties of stretch reflex?

A
  • Short latent period and total reflex time
  • High localization
  • Graded response
  • Reciprocal inhibition
  • Fatigue resistance
  • No recruitment nor discharge
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305
Q

Why does Stretch reflex has a short latent period?

A
  • The stretch reflex has short latent period that passes between application of the stretch & onset of the reflex contraction

Because:
1. It is a monosynaptic reflex (the only monosynaptic reflex).

  1. The afferent & efferent are rapidly conducting fibers
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306
Q

High localization of Stretch reflex

A
  • Stretch of certain muscle leads to contraction of the same stretched muscle.
  • This is due to limited divergence & absence of interneurons in its pathway
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307
Q

graded response of Stretch reflex

A
  • Strength of the reflex contraction is proportional to the extent of stretch.
  • The greater the degree of stretch the greater the rate of discharge from muscle spindles, vice versa.
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308
Q

Reciprocal innervation of Stretch reflex

A
  • Stretch of certain muscle leads to contraction of that muscle & inhibition of its antagonistic muscle due to reciprocal innervation circuits between the motor neuron pools.
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309
Q

Fatigue resistance of Stretch reflex

A
  • Stretch reflex can be sustained for long periods of time (in antigravity muscles).
  • The delayed onset of fatigue is related to:
    1. Asynchronous (alternative) contraction of different motor units.
  1. The antigravity muscles contain greater number of tonic muscle fibers (slow muscle fibers) which resist fatigue.
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310
Q

why is there no recruitment nor discharge in Stretch reflex?

A

Due to absence of interneurons

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311
Q

Compare between Stretch reflex and inverse Stretch reflex in terms of:

  • Type
  • receptor
  • Stimulus
  • Afferent
  • Efferent
  • Effect
  • Function
A
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312
Q

Definition of Skeletal muscle tone

A
  • It is a state of continuous partial (subtetanic) contraction present in all skeletal muscles during rest.
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313
Q

Mechanism of Skeletal muscle tone

A
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314
Q

Functions of muscle tone

A

1) It is the basic mechanism for postural reflexes which regulate the body posture and equilibrium.

2) Helps production and maintenance of body temperature.

3) Helps venous and lymphatic return.

4) Keeps viscera in position and prevents visceroptosis.

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315
Q

Definition of tendon jerk

A

Rapid contraction followed by relaxation of a muscle due to sudden stretching of that muscle by tapping on its tendon using a medical hammer

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316
Q

Mehcanism of tendon jerk

A
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317
Q

Clinical significance of tendon jerk

A
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318
Q

Stimulus of stretch reflex

A

Passive stretch of the muscle

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319
Q

what are other names of Inverse stretch reflex?

A
  • Lengthening reaction
  • Golgi tendon reflex
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320
Q

Definition of Inverse stretch reflex

A
  • Is reflex relaxation of a contracting skeletal muscle when exposed to excessive stretch
  • It is protective against:
    1. muscle tearing.
    2. tendon avulsion
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321
Q

Stimulus of Inverse stretch reflex

A

Increased tension in the tendon of the muscle due to:

  • severe contraction
  • Overstretch.
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322
Q

Receptor of Inverse stretch reflex

A

Golgi tendon organs (GTO)

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323
Q

GTO:

  • Site
  • Content
  • Stimulation
A
  • present in the tendon of the muscle in series of the muscle fibers.
  • each organ consists of modified fibers mostly elastic fibers “number 6-20”
  • stimulated by increased tension in the tendon “Tension receptors”
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324
Q

afferent of Inverse stretch reflex

A
  • A-alpha nerve fibers (Ib).
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325
Q

Center of Inverse stretch reflex

A
  • impulses from GTO inhibit A.H.Cs via interneurons leading to relaxation of the muscle. (it is a di-synaptic reflex)
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326
Q

Response of Inverse stretch reflex

A

Muscle relaxation

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327
Q

Significance of Inverse stretch reflex

A

protective against:
- muscle Tearing
- tendon avulsion

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328
Q

what is somatic motor system composed of?

A
  • Upper motor neurons (UMN)
  • Lower motor neurons (LMN)
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329
Q

where are the Cell bodies of UMN?

A

In higher motor centers (motor cortex & brain stem).

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330
Q

What do the axons of UMN form?

A

descending motor tracts.

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331
Q

where are the cell bodies of LMN?

A

lie in the spinal AHC and the cranial motor nuclei

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332
Q

what do the axons of LMN form?

A

motor fibers in the peripheral nerves to skeletal muscle

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333
Q

Site of cortical motor areas

A

The cortical motor areas located precentral gyrus in the frontal lobe.

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334
Q

what do cortical motor areas include?

A

– 1) The Primary motor area (area 4).

– 2) The Premotor area (area 6).

– 3) The Supplemental motor area.

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335
Q

Site of 1ry motor area (area 4)

A
  • the precentral gyrus of the frontal lobe.
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336
Q

Body representation of 1ry motor area (area 4)

A

Contralateral: the muscles of left side controlled by the right motor cortex and vice versa.

Inverted: the muscles of the face are controlled by the lowermost part of area 4 & muscles of lower limbs controlled by the upper most part of area 4.

Size: Muscles involved in fine movements (hand & tongue) are represented by relatively large areas than those involved in gross movements (trunk).

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337
Q

Connection of 1ry motor area (area 4)

A

through pyramidal tract:

  • Initiation of voluntary movements done by the limb muscles of the opposite side
  • Facilitation to the tone of the distal limb muscles
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338
Q

what does a lesion in 1ry motor area (area 4) cause?

A

1) Loss of voluntary movements (paralysis or weakness) in one limb (monoplegia) on the opposite side.

2) Hypotonia and weak tendon jerks.

3) Babinski’s sign: (dorsiflexion of the big toe)

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339
Q

Site of Premotor area (area 6)

A

In the frontal lobe just anterior to the primary motor area 4.

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340
Q

Body representation of premotor area (area 6)

A

1) contralateral
2) inverted.

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341
Q

Connection of premotor area (area 6)

A

1) Primary motor area & supplemental motor area.

2) Basal ganglia & cerebellum.

3) With supplemental motor area Give 30% of the axons of pyramidal tract.

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342
Q

what does a lesion in premotor area (area 6) cause?

A

1) Impairment of complex movements or paresis.

2) Hypertonia and exaggerated tendon jerks.

3) Babinski s sign (fanning of the outer 4 toes).

4) Loss of automatic or associative movements.

5) Motor aphasia (inability of articulation).

6) Motor apraxia (inability to perform the learned skillful movements).

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343
Q

Site of supplemental area (4s)

A
  • In the frontal lobe just anterior & above the premotor area 6.
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344
Q

Body representation of supplemental area (4s)

A
  • Bilateral and horizontal with face Anterior and leg posterior
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345
Q

Connection of supplemental area (4s)

A

1) initiate complex movements involve both sides of the body (as both hands to perform a motor act together).

2) with the premotor area (6):

  • provide postural background for the performance of fine skilled movements by hands and fingers.
  • shares in the planning and programming of the complex movements.
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346
Q

what does a lesion of supplemental area (4s) cause?

A

Nothing as it is bilateral

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347
Q

function of premotor area (area 6) with supplemental motor area

A

shares in planning of complex movements.

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348
Q

function of premotor area (area 6) with basal ganglia

A
  • postural adjustment of the trunk and proximal limb for the performance of the distal voluntary movements.
  • initiate the automatic associative movements (subconsciously) as swinging of arms during walking.
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349
Q

what are special areas and functions of premotor area (area 6)?

A

Broca’s area: active in the dominant hemisphere (the left side in right handed persons). controls the muscles involved in speech.

Frontal eye movement area: control voluntary movements of the eye.

Head rotation area: directs the head towards visual objects.

Area of hand skills (Exener’s area): controls skilled movements of the hand and fingers as writing.

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350
Q

what are the types of descending motor tracts?

A
  • Pyramidal tract
  • Extrapyramidal tracts
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351
Q

Course of pyramidal tract

A

One tract passes through the pyramid of the medulla so called pyramidal tract.

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352
Q

what do pyramidal tracts include?

A

Corticobulbospinal tract.

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353
Q

Course of Extra-pyramidal tract

A

Group of tracts not pass through the medullary pyramid so called extrapyramidal tracts.

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354
Q

what do extra-pyramidal tracts include?

A

– 1) Rubrospinal tract
– 2) Reticulospinal tracts
– 3) Vestibulospinal tracts
– 4) Tectospinal tract

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355
Q

Functional classification of descinding motor tracts

A
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356
Q

what are another names for pyramidal tract?

A

corticobulbospinal

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357
Q

Origin of pyramidl tract

A
  • Motor areas 60 %. (Primary motor area “area 4” 30%, Premotor & Supplemental motor areas 30%.)
  • Somatosensory areas give 40 % of fibers.
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358
Q

Stations of pyramidl tract

A

CBS tract pass through

1) the genu & anterior 2/3 of posterior limb of internal capsule).

2) the middle 3/5 of the cerebral peduncles of midbrain

3) form several bundles in the basis pontis

4) collect in the upper medulla forming the pyramid.

5) In spinal cord as lateral & ventral coticospinal tract.

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359
Q

what are 3 pyramidal tracts?

A
  • Corticonuclear tract
  • Corticobulbular tract
  • Corticospinal tract
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360
Q

where does corticonuclear tract terminate?

A
  • Fibers terminate on the 3, 4, & 6th cranial nerves nuclei bilateral
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361
Q

where does corticobulbar tract terminate?

A

Fibers terminate on the 5, 7, 9, 10, 11 & 12th cranial nerves motor nuclei.

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362
Q

which cranial motor nuclei recieve bilateral supply?

A

All cranial motor nuclei receive bilateral supply from the pyramidal tract except the lower parts of the 7th & & 12th nuclei, receive only contralateral supply.

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363
Q

Course of corticospinal tract

A
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364
Q

Functions of pyramidal tracts

A

pyramidal tract perform the following functions:

1) Initiation of voluntary skilled movements: speech (Corticobulbar tract) , and movements of hand and fingers (Lateral corticospinal tract).

2) Has a Role in automatic movements as chewing, swallowing (corticobulbar) and postural movements (medial corticospinal tract).

3) Facilitatory to muscle tone of flexor muscle of the limbs.

4) Inhibits primitive withdrawal reflex as dorsiflexion of big toe in planter reflex (Babinski sign).

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365
Q

Origin of Extra-pyramidal tracts

A

Mainly from area (6) and some fibers from area (4) → descends to corpus striatum → Globus pallidus→ from the globus pallidus fibers pass to:
1. Red nucleus
2. Reticular formation
3. Vestibular nuclei
4. Tectum of midbrain.
5. Inferior olive.

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366
Q

what are examples of extra-pyramidal tracts?

A

1) Rubrospinal tract.
2) Reticulospinal tract tracts.
3) Vestibulospinal tracts.
4) Tectospinal tract.
5) Olivospinal tract.

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367
Q

Origin of Rubrospinal tract

A

Red nucleus in midbrain (receive fibers from ipsilateral cortical motor area (cortico-rubro-spinal tract).

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368
Q

Course of Rubrospinal tract

A

Cross to opposite side & descends contralateral.

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369
Q

Termination of Rubrospinal tract

A

in the cervical spinal cord, so it functions in upper limb.

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370
Q

Function of Rubrospinal tract

A

1- Control of distal muscles of upper limb responsible for skilled movements. Rubrospinal & lateral corticospinal tract are called lateral motor system.

2- Facilitatory to the muscle tone of the distal limb muscles.

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371
Q

Origin of tecto-spinal tract

A

superior (mainly) & inferior colliculi in the midbrain.

372
Q

Course & termination of tecto-spinal tract

A

descends contralateral (crossed) to the spinal motor neurons of the neck muscles only.

373
Q

Function of tecto-spinal tract

A

reflex turning of the head in response to sudden visual or auditory stimuli.

374
Q

Origin of lateral reticulo-spinal tract

A

medullary (inhibitory) reticular formation.

375
Q

Decend of lateral reticulo-spinal tract

A

descends bilaterally

376
Q

Function of lateral reticulo-spinal tract

A

inhibits the tone in the antigravity muscles.

377
Q

Origin of medial reticulo-spinal tract

A

Pontine (facilitatory) reticular formation.

378
Q

Descend of medial reticulo-spinal tract

A

descends ipsilaterally

379
Q

Termination of medial reticulo-spinal tract

A

facilitates motor neurons of antigravity muscles that support body posture against gravity.

380
Q

Origin of lateral vestibulospinal tract

A

lateral vestibular nucleus.

381
Q

Descend of lateral vestibulospinal tract

A

descends ipsilateral, to AHCs of the antigravity muscles.

382
Q

Function of lateral vestibulospinal tract

A

Facilitatory to the antigravity muscles to maintain body posture & equilibrium on exposure to acceleration.

383
Q

Origin of medial vestibulospinal tract

A

medial vestibular nucleus.

384
Q

Descend of medial vestibulospinal tract

A

descends bilaterally: to AHCs of neck & upper limb muscles

385
Q

Function of medial vestibulospinal tract

A

facilitatory to muscle of head & upper limb & adjust their position on exposure to acceleration.

386
Q

Origin of Olivospinal tract

A

from inferior olivary nucleus in MO & descends ipsilateral.

387
Q

Function of Olivospinal tract

A

facilitatory to skeletal muscle tone

388
Q

what does a Lesion in extrapyramidal tract cause?

A

the effects of lesion in extrapyramidal tracts lead to:

1) Difficulty in initiation of voluntary movements but not paralysis.

2) Impairment of orienting and balancing of reflexes

3) Alternation in muscle tone (may increase or decrease)

4) Characteristic appearance of abnormal involuntary movements

5) Babinski’s sign reappear (Fanning of toes)

389
Q

Connection of primary motor area (Area 4)

A
390
Q

what are the functions of premotor area (Area 6)?

A
  • with supplemental motor area
  • with Basal ganglia
  • Inhibition of the muscle tone
  • Area 6 contain special functional areas
391
Q

Causes of UMNL

A

damage of upper motor neuron in the higher center or the descending motor tracts.

392
Q

Example of UMNL

A

Strokes due to damage of both pyramidal and extrapyramidal fibers.

393
Q

Paralysis and weakness in UMNL

A
  • Widespread: affecting half of the face, upper &lower limbs (hemiplegia).
  • Below the level of the lesion.
394
Q

Muscle tone in UMNL

A

Increased (Hypertonia or spastic paralysis).

395
Q

Tendon jerk in UMNL

A

Exaggerated or hyperreflexia

396
Q

Planter reflex in UMNL

A

Show +ve Babiniski’s sign (dorsiflexion of big toe ± fanning of other toes).

397
Q

Abdominal reflex in UMNL

A

Absent or Lost on the affected side.

398
Q

Muscle state in UMNL

A

No wasting but late slight disuse atrophy

399
Q

Signs of denervation in UMNL

A

absent

400
Q

Response to electric stimulus in UMNL

A

(Normal)

Faradic current —> tetanic contractions

Galvanic current —> normal response
- cathodal closing contraction is stronger than anodal closing contraction (CCC > ACC)

401
Q

Causes of LMNL

A

damage of the lower motor neurons (the spinal AHCS and the cranial motor nuclei or their axons).

402
Q

Examples of LMNL

A

Damage of lower motor neurons as
poliomyelitis or trauma to the nerve.

403
Q

Paralysis and weakness of LMNL

A
  • Localized: Restricted to the muscles supplied by the affected segment.
  • At the level of the lesion.
404
Q

Muscle tone in LMNL

A

Decreased (Hypotonia or flaccid paralysis)

405
Q

Tendon jerk in LMNL

A

Absent in the affected muscle

406
Q

Planter reflex in LMNL

A

Absent if the involved muscles affected.

407
Q

Abdominal reflex in LMNL

A

Absent if the involved muscles affected.

408
Q

Muscle state in LMNL

A

Early & marked wasting (Atrophy)

409
Q

Signs of denervation in LMNL

A

Fasciculation & fibrillation

410
Q

Response to electric stimulation in LMNL

A

Abnormal

Faradic current —–> no response

Galvanic current —-> reactions of degeneration
- ACC > CCC

411
Q

what is the site of basal ganglia?

A

It is a group of nuclear masses of gray matter deep to the cerebral cortex and lateral to the thalamus “Within the cerebral hemisphere”.

412
Q

what does the basal ganglia consist of Functionally?

A
  1. Caudate Nucleus.
  2. Putamen.
  3. The globus pallidus.
  4. The subthalamic nucleus (STN).
  5. The substantia Nigra (SNr) located in the mid brain.

(1,2 is corpus striatum)

413
Q

what are neural connections of Basal ganglia?

A
  • With the cerebral cortex in the form of circuits (Cudate & Putamen)
  • Internal connections
  • Connections with the brain stem
414
Q

Caudate circuit

A
415
Q

Putamen circuit

A
416
Q

Internal connections between basal ganglia

A
417
Q

what is the significance of internal connections between basal ganglia?

A

The internal connections form circuits for processing the information that enter it before giving out its projections.

418
Q

Connections of basal ganglia with brain stem

A
419
Q

How are signals transmitted from the basal ganglia to the spinal centers?

A

through such connections (Basal ganglia with nuclei in brain stem) to the spinal centers via extrapyramidal tracts where they affect the muscle tone and voluntary movements.

420
Q

what are chemical transmitters in Basal ganglia?

A
  • Dopamine
  • GABA
  • Ach
  • Glutamate
  • Others: norepinephrine, serotonin and enkephalin
421
Q

Dopamine pathway

A
  • From substantia Nigra to the caudate nucleus and putamen (corpus striatum).
  • It is an inhibitory pathway.
422
Q

GABA pathway

A
  • From the corpus striatum to the globus pallidus and substantia Nigra.
  • It is an inhibitory pathway.
423
Q

Ach pathway

A
  • From the cortex to the corpus striatum.
  • It is an excitatory pathway.
424
Q

Glutamate pathway

A
  • Provide most of the excitatory signals that balance out the large inhibitory signals transmitted by Dopamine, GABA and serotonin pathways.
425
Q

what are the functions of basal ganglia?

A
  • The basal ganglia constitute an accessory motor system that functions in close association with the Cerebral Cortex and corticospinal motor control system.
  1. Planning and programming of motor actions (caudate circuit)
  2. Executing patterns of learned movements (putamen circuits)
  3. Postural regulation
  4. Initiation of automatic associative
  5. Regulation of muscle tone
426
Q

Planning and programming function of basal ganglia (Caudate circuit)

A
  • B.G. plays a role in cognitive control of motor activity i.e. converting the generated thoughts in the mind into voluntary motor acts.
427
Q

what is the function of (Planning and programming function of basal ganglia) done in association with?

A
  • Motor cortex that provide the plane of the motor act and the cortical association areas that provide information about the relation of different parts of the body to each other and to the surrounding environment.
428
Q

Executing patterns of learned movements (Putamen circuits)

A
  • The B.G. may control the rapid and automatic repetition of certain skilled movements as writing, typing … etc and certain aspects of speech.
429
Q

what happens to execution function of basal ganglia if it is damaged?

A
  • If damaged the act will be done in a crude manner as it is done for the first time.
430
Q

Postural regulation function of basal ganglia

A
  • The B.G assists in providing a postural background, which is necessary for the performance of voluntary movements done by the distal muscles.
  • The B.G. adjusts tone in the proximal muscles through the reticular spinal tract.
  • The B.G. acts as a bridge that links the lateral motor system (CBST) to the medial motor system.
431
Q

Initiation of autonomic associative movemnts by basal ganglia

A
  • Movements done at subconscious level as swinging of the arms during walking and facial expressions that reflect the emotional state of the subject.
432
Q

Regulation of muscle tone by basal ganglia

A

The final output of the B.G. is inhibitory to muscle tone.

433
Q

what are the disorders of basal ganglia?

A
  • Parkinson’s Disease
  • Chorea
  • Athetosis
  • Hemiballismus
434
Q

Nature of Parkinson’s disease

A
  • It is the most common degenerative disease of the brain.
435
Q

Etiology of Parkinson’s disease

A
  • Results from degeneration of Dopaminergic neurons in substantia nigra with resultant decrease in dopamine release in corpus striatum.
  • Most cases of parkinsonism are idiopathic and occur more commonly in old ages.
436
Q

what is Parkinson’s disease characterized by?

A
  1. Tremors.
  2. Rigidity.
  3. Akinesia & bradykinesia
437
Q

Pattern of tremors in Parkinson’s disease

A
  • Regular rhythmic alternating contractions in the antagonistic muscles of the hands & fingers.
  • It takes the characteristic pill rolling pattern.
438
Q

when do tremors occur in Parkinson’s disease? and what increases/decreases it?

A
  • Static —> occurs during rest and disappear during movements
  • exaggerated by emotional excitement and disappear during sleep.
439
Q

Rigidity in Parkinson’s disease

A
  • Marked increase in the muscle tone “hypertonia.
440
Q

what does hypertonia in Parkinson’s disease mostly affect?

A
  • Affects both flexors and extensors but more in flexors
441
Q

Characters of rigidity in Parkinson’s disease

A

resists the passive movements.

442
Q

Patient’s altiltude in Parkinson’s disease

A

The patient attains the flexion altitude.

443
Q

what is akinesia?

A
  • Difficulty initiating voluntary movements
444
Q

what is bradykinesia?

A

Slow movements

445
Q

Manifestations of akinesia and bradykinesia

A
  1. Slow Gait with short, shuffling steps.
  2. Slow monotonus Speech.
  3. Loss of automatic associative movements with loss of expressive face “Mask face” and loss of swinging of the arms
446
Q

where is the lesion in chorea?

A

caudate nucleus

447
Q

Types (Causes) of chorea

A
  • Huntington’s chorea.
  • Rheumatic chorea .
448
Q

Charaters of chorea

A
  1. Spontaneous rapid involuntary dancing movement which may involve many parts of the body as face, arms, head, legs & trunk
  2. Hypotonia & pendular knee jerk
449
Q

Where is the lesion in case of athetosis?

A

globus pallidus

450
Q

what causes athetosis?

A

Wilson’s disease

451
Q

Characters of athetosis

A
  1. Continuous slow snake-like movements or writing movements of a hand, an arm, the neck or the face.
  2. Hypertonia
452
Q

where is the lesion in cases of hemiballismus?

A

subthalamus

453
Q

Causes of hemiballismus

A

Vascular lesion

454
Q

Characters of hemiballismus

A
  • Involuntary, intense violent movements involving large areas of the body
455
Q

Histologocal division of cerebellum

A
456
Q

Anatomical division of cerebellum

A
457
Q

Functional division of cerebellum

A

Functionally, the cerebellum is divided into:

  • Vestibulo-cerebelum
  • Spino-cerebellum
  • Cerebro-cerebellum (pontocerebellum)
458
Q

what is vestibulo-cerebellum called?

A

Archicerebellum

459
Q

what does vestibulo-cerebellum consist of?

A

flocculo-nodular lobe which is closely related in its functions with the vestibular system.

460
Q

what is vestibulo-cerebellum connected with?

A

Vestibular apparatus

461
Q

what is spino-cerebellum called?

A

paleocerebellum

462
Q

what does spino-cerebellum consist of?

A

vermis and the intermediate zones of the cerebellar hemispheres.

463
Q

what is spino-cerebellum connected with?

A

spinal cord

464
Q

what is cerebro-cerebellum called?

A

neocerebellum (Pontocerebellum)

465
Q

what does cerebro-cerebellum consist of?

A
  • lateral zones of the cerebellum and almost all of its afferent signals originate from the cerebral cortex and reach it through the pons.
466
Q

what is cerebro-cerebellum connected with?

A

cerebral cortex

467
Q

what are the functions of the cerebellum?

A

Generally, the cerebellum adjusts the timing and sequence of movements involved in regulation of equilibrium, posture and voluntary motor acts.

  • Regulation of equilibrium (F.N.L)
  • Regulation of body posture
  • Regulation of voluntary movements
  • Motor learning
  • rapid ballistic movements
468
Q

mechanism of Regulation of equilibrium (F.N.L)

A

Disturbed equilibrium or altered head position –> ++ Vestibular receptors –> Vestibulo- cerebellum –> Corrective signals

469
Q

what are corrective signals in case of Regulation of equilibrium (F.N.L)?

A

1- V.S.T & R.S.T —> motor neurons of axial muscles & proximal limb muscles —> maintain body posture.

2- M.L.B (III, IV & VI cranial nuclei) —> coordinate eye movement with head movement —> maintain clear vision —-> help keep equilibrium.

470
Q

which part of cerebellum causes Regulation of body posture?

A

vermal zone.

471
Q

Mechanism of Regulation of body posture

A
  • It receives information from proprioceptors about position and movements then sends –> output –> Fastigeal N. —> V.S.T & R.S.T —> controls the tone of antigravity muscles —> maintain posture against gravity effect.
472
Q

How does the cerebellum regulate the volunatry movements?

A

Cerebellum ensures smooth progression or coordination of movements through the following mechanisms:

  1. Servo-comparator function
  2. Predictive and damping functions
  3. Planning and timing function of the cerebellum
473
Q

Mechanism of servo-comparator function

A

The spino-cerebellum is informed about:

a) The intended plan of movement from the motor cortex (via cortico-ponto-cerebellar tract)

b) The performance of movement from muscles (via spino-cerebellar tracts)

  • The spino-cerebellum compares the intention of the motor cortex with the performance of the muscles. If not appropriate, the spino-cerebellum sends corrective signals to the motor cortex
474
Q

pathway of corrective signals in case of servocomparator function

A
  • via interposed N-thalamo-cortical tract), which by its turn through descending CBS tract adjust the muscle activity
475
Q

what does Predictive and damping function of the cerebellum mean?

A
  • Damping means ending of the movements without oscillation at the proper site
476
Q

How does the cerebellum perform this function? (Predictive and damping function)

A
  • The cerebellum assesses the rate of movement, calculates the time needed to reach the intended point & then transmits inhibitory impulses to the motor cortex to stop the movements at the exact intended point without oscillation.
  • The cerebellum sends signals to stop the movement at the intended point, & preventing the overshoot.
477
Q

what does damage to cerebellum cause?

related to this function—-> Predictive and damping function

A

overshooting of movements.

478
Q

Planning & timing function of the cerebellum

A

The cerebro-cerebellum:

  1. Receives afferent impulses from the cortical association areas (the site of ideas for voluntary movements).
  2. Sends efferent impulses to the motor area of the cortex that initiates movements.
479
Q

what is the main function of cerebro-cerebellum?

A
  • The cerebro-cerebellum plans for the next movement while the present movement is occurring.
  • The cerebro-cerebellum provides proper timing for each movement.
480
Q

what is the importance of the predictive function of cerebro-cerebellum?

A
  • Such predictive function is necessary for smooth transition from one movement to the next and joining of sequential movements.
481
Q

what does a Lesion of the cerebro-cerebellum cause?

A

inability to judge the movement in a given time.

482
Q

Motor learning function of cerebellum

A
483
Q

Role of cerebellum in rapid ballistic movements

A
484
Q

what happens When a complex voluntary movement done for the first time?

A
  • The movement usually inaccurate, and the cerebellum detects the mismatch between the motor plan and performance, and tries to correct it by sending a more accurate plan to the motor cortex.
485
Q

Site of manifestations in cerebellar lesions

A

Lesions of each side of the cerebellum manifest their effects on ipsilateral side of the body (the same side of lesion).

486
Q

what are cerebellar lesions?

A
  • Flocculo-nodular Lobe disorders
  • Neocerebellar Syndrome
487
Q

manifestations of Flocculo-nodular Lobe disorders

A
  • These disorders impair equilibrium.
  • This is manifested by swaying during standing and unsteady wide based gait (waddling gait).
488
Q

what causes Neocerebellar Syndrome?

A

Due to cerebellar hemispheric (paravermal and lateral zones) lesion.

489
Q

Manifestations of Neocerebellar Syndrome

A

The principal motor dysfunctions caused by hemispheric lesions include:

a- Hypotonia: decrease muscle tone due to decreased supraspinal facilitation of stretch reflex.

b- Asthenia: leading to weakness of movements.

c- Ataxia (asynergia): incoordination of voluntary movements in absence of UMN and LMN lesions.

490
Q

what are manifestations of ataxia?

A
  • Dysmetria
  • Intention (Kinetic) Tremors
  • Decomposition of Complex movements
  • Rebound phenomenon
  • Dysdiadochokinesia
  • Nystagmus
  • Scanning speech
  • Unsteady Gait
491
Q

Descripption of dysmetria

A

The moving limb usually overshoots the intended point (hypermetria), due to failure of “comparator” and “damping” functions.

492
Q

what causes Intention (Kinetic) Tremors?

A
  • Occur during voluntary movements, due to hypermetria of movements.
493
Q

explain mechanism of Intention (Kinetic) Tremors

A
  • The cerebral cortex detects this overshooting & tries to correct it by a movement in opposite direction, but this corrective movement also overshoots needing a new correction, and so on.
494
Q

describe Decomposition of Complex movements

A
  • Voluntary movements is carried out as several successive steps, because of inability to adjust the precise timing of contraction of different muscles.
495
Q

describe Rebound phenomenon

A
  • When the patient flexes his forearm strongly against a resistance, then the resistance is suddenly removed, the patient cannot stop movement at proper time, and may thus strike his body, due to failure of the “damping” function.
496
Q

describe Dysdiadochokinesia

A
  • The patient is unable to perform rapid successive opposite movements, e.g. supination & pronation of the hands,
497
Q

what causes Dysdiadochokinesia?

A

due to failure to adjust the precise timing for “onset” and “termination” of movements.

498
Q

what is Nystagmus?

A
  • represents the kinetic tremors of the extraocular muscles during movements of the eye.
499
Q

what is Scanning speech (Dysarthria)?

A
  • Speech becomes slow and decomposed.
  • Each word is fragmented and pronounced as several separate syllables.
500
Q

Unsteady Gait of ataxia

A

The gait is unsteady as a result of the dysmetria and kinetic tremors of the lower limb muscles.

501
Q

Definition of thalamus

A
  • It is an ovoid gray mass located in diencephalon.
502
Q

what separates the two thalami?

A
  • 3rd ventricle
503
Q

what connects the two thalami?

A

interconnection by a narrow band called interthalamic adhesion

504
Q

what divides the thalamus?

A

divided internally by laminae of white matter into many separate nuclei

505
Q

Compare between specific and non specific nuclei of the thalamus in terms of:

  • Definition
  • Examples
A
506
Q

Specific Thalamic Nuclei

A
  • Consist of Anterior nuclei & Medial nuclei & Lateral nuclei
  • Project to specific cerebral cortical areas
507
Q

Classisification of Specific Thalamic Nuclei

A

Classified into:
- Specific Relay Nuclei
- Specific Association Nuclei

508
Q

what do Specific Relay Nuclei project to?

A

project to 1ry cortical areas

509
Q

what do Specific Relay Nuclei include?

A
  • MGB → 1ry auditory cortex
  • LGB → 1ry visual cortex
  • VA nucleus → premotor area
  • VP nucleus → 1ry somatic sensory cortex
  • VL nucleus → try motor and premotor areas
510
Q

what do Specific Association Nuclei project to?

A

project to cortical association areas

511
Q

what do Specific Association Nuclei include?

A
  • Anterior nuclei (AN) → limbic association cortex
  • Lateral dorsal (LD) nucleus → limbic association cortex
  • Lateral posterior (LP) nucleus → parietal somatic sensory association cortex
  • Dorsomedial (DM) nucleus → prefrontal association cortex
  • Pulvinar (P) → sensory association cortex in parietal, temporal, & occipital lobes
512
Q

Thalamic nuclei

A
513
Q

what are thalamic functions?

A

1- Sensory functions (sensory relay station, Gating of ascending sensory information & Thalamus as a sensory center)

2- Motor functions

3- Association and integration

4- Arousal function

514
Q

what happens to All Ascending sensory pathways before reaching cerebral cortex?

A

relay in thalamus especially those carrying fine epicritic sensations from opposite side of body

515
Q

relay and termination of Somatic sensory pathways from the body

A

relay in V.P.L then to primary somatic sensory cortex

516
Q

relay and termination of Somatic sensory pathways from the head and face and taste

A

relay in V.P.M then to primary somatic sensory cortex

517
Q

relay and termination of vision fibers

A

optic fibers from both retinae reach L.G.B. and projected to visual cortex

518
Q

relay and termination of hearing pathway

A
  • auditory fibers from both ears relay in M.G.B. before reaching auditory cortex
519
Q

relay and termination of olfaction pathway

A
  • recently, olfactory pathway has found to pass through dorsomedial nucleus to orbitofrontal cortex
520
Q

Gating of ascending sensory information

A
  • Cortico-fugal impulses are transmitted back from cerebral cortical sensory areas to thalamic relay nuclei which already project to these areas
521
Q

what is the type of cortico-fungal impulses?

A

inhibitory

522
Q

Significance of cortico-fungal impulses

A
  • it decreases transmission through these nuclei particularly when sensory input is very high & sensory system is overloaded with sensory input
523
Q

Thalamus as a sensory center

A
  • Discrimination of many sensory impulses occurs in thalamus, but sensations felt are of crude protopathic nature
524
Q

Examples of impulses that are discriminated at the thalamus

A
  • diffuse pain, crude touch & extremes of temperature change.
525
Q

Motor functions of the thalamus

A
  • V.A. & V.L. nuclei relay motor signals from B.G. & cerebellum to motor & pre-motor areas of frontal lobe to control their functions.
  • V.P.L nucleus relays tactile & proprioceptive signals to motor cortex, This provides sensory information about position & movements of different parts of body.
  • Non-specific nuclei adjust general level of excitability of motor cortex.
526
Q

Association and integration function of the thalamus

A
  • Anterior & medial nuclei together with hypothalamus & limbic system play a role in integrating visceral & somatic motor responses evoked during emotional reactions with incoming sensory signals.
  • Reciprocal connection () D.M. nucleus of thalamus & pre-frontal areas may play a role in coding, storing & recalling of memory.
527
Q

arousal function of the thalamus

A
  • through Non-specific thalamic nuclei
  • receive excitatory signals from R.A.S of brain stem
  • project it to almost all areas of cerebral cortex, producing & wakefulness.
528
Q

what is wakefullness (Arousal)?

A

State of consciousness in which the person is aware of:

  • Various sensory stimuli
  • His feelings, thoughts and ideas
  • Enables the person to pay attention to external stimuli & focus his mind
529
Q

what does RAS consist of?

A
  • RAS consists of excitatory or facilitatory reticular formation RF (in pons & midbrain) with its upward projections to non-specific thalamic nuclei, from which excitatory signals project diffusely to all areas of neo-cortex, causing generalized activation of brain
  • This activation of brain produces arousal & wakefulness
530
Q

what are factors affecting RAS?

A
  • Reticular Formation
  • Sensory signals
  • Cortical feedback signals
  • Transmitters
  • Drugs
  • Feed-back signals
  • Reticular inhibitory area
531
Q

Compare between factors Increasing/Decreasing consciousness

A
532
Q

Feedback signal from cerbral cortex and their relation with consciousness

A
  • From the cerebral cortex that are sent back to RAS, whenever the cortex becomes activated by thinking or motor activity
  • This corticofugal feed-back activates RAS which in turn sends more excitatory signals to the cortex to enhance its activity
533
Q

where is reticular inhibitory are located?

A
  • located in medulla oblongata
534
Q

what happens when RIA is excited?

A
  • When this area is excited, it inhibits the RAS possibly by increased secretion of serotonin at certain sites in the reticular formation
535
Q

what regulares Normal wakefulness - sleep cycles?

A
  • Normal wakefulness - sleep cycles may be regulated through the alternating reciprocal activity in between the RAS and the reticular inhibitory area
536
Q

Definition of sleep

A
  • State of unconsciousness from which person can be aroused
537
Q

what is the duration of sleep?

A
  • sleep-wakefulness cycles consists of:

In adults: 8 hours of sleep & 16 hours of wakefulness

In infants & children: More hours of sleep are required about 18 hours in infants

In elderly: Less hours of sleep are required about 6 hours in old ages

538
Q

what are types of sleep?

A
  • 2 types of sleep alternate with each other
  • Each characterized by different EEG patterns
539
Q

Compare between non-REM sleep (SWS) and REM sleep in terms of:

  • Order
  • % of sleep hours
  • EEG
  • Rapid eye movement
  • Dreams HR, BP, Respiration & brain activity
  • Muscle tone
A
540
Q

Duration of each sleep cycle

A

On average takes about 90 – 100 minutes

541
Q

How many sleep cycles take place during ordinary night sleep?

A

There are 4 – 5 sleep cycles during ordinary night sleep

542
Q

events during Phase of SWS

A
  • Sleep pass through 4 stages of gradual increasing depth & slowing of EEG waves (stages 1, 2, 3, and 4)
  • Then order of sleep stages reversed till stage 1 & then passes to REM phase
543
Q

Events of REM sleep

A
  • Lasts 5 – 30 min, show gradual prolongation of REM sleep periods till end of night
  • Represents 20 – 25% of total sleep time
544
Q

what are basic theories of sleep?

A
  • Sleep is caused by active inhibitory process (active theory) (most accepted) or due to fatigue of the RAS (passive theory)
  • Stimulation of many areas of brain lead to sleep (sleep centers)
545
Q

what are the mechanisms of sleep?

A

Slow wave sleep:
- Role of Raphe nuclei in the lower pons and medulla

REM sleep:

  • on neurons: cholinergic neurons at ponto-mesencephalic junction
  • off neurons: Noradrenergic neurons in locus ceruleus & serotoninergic neurons in raphe nuclei
546
Q

what intiates SWS (Terminates REM sleep)?

A
  • ++ of Raphe nuclei in pons & medulla
  • Hypothalamic suprachiasmatic nucleus (SCN)

(Also REM off neurons)

547
Q

what is serotonin associated with?

A
  • Serotonin the transmitter associated with induction of sleep, So Drugs that blocks serotonin synthesis Leads to insomnia
548
Q

what synchronizes sleep/wake rhythm with light-dark cycles of day?

A

Hypothalamic SCN

549
Q

Initiation of SWS

A
550
Q

what initiates REM sleep?

A
  • REM sleep on neurons
  • increased activity of cholinergic neurons in upper brain stem RF
  • send excitatory signals to RAS, thalamus & Cerebral cortex —> REM sleep
551
Q

Mechanism of REM sleep

A
552
Q

Circadian nature of sleep

A
  • Cycle between sleep and wakefulness:
  • Exact mechanism for cyclical sleep wakefulness cycle is not yet definite
  • Hypothalamic suprachiasmatic nucleus (SCN): synchronizes sleep/wake rhythm with light-dark cycles of day
553
Q

Suggested possible mechanism of sleep

A

Wakefulness for several hours —> fatigue of RAS —-> - - of +ve feedback cycle —->↑↑ promoting effects of sleeping center —> sleep

554
Q

Suggested possible mechanism of wakefullness

A

When sleep centers are inactive —> ↑↑ spontaneous activity of RAS —-> activates cerebral cortex & peripheral nervous system —-> +ve feedback stimulation of RAS —->wakefulness

555
Q

Physiological significance of sleep

A

Adequate periods of sleep are essential for restoration of :

1) Normal levels of brain activity

2) Normal (balance) among the different functions of the CNS

(Prolonged periods of wakefulness or sleep deprivation leads to: deterioration of the higher brain functions)

556
Q

Site of the hypothalamus

A
  • Hypothalamus is located at the base of the brain, just above pituitary gland and below the thalamus, on either side of the 3rd ventricle.
557
Q

what are hypothalamic nuclei?

A

A. Anterior nuclei
B. Posterior nuclei
C. Lateral nuclei
D. Medial nuclei

558
Q

Hypothalamic connections

A
559
Q

what are the functions of the hypothalamus?

A
  • Regulation of autonomic nervous system
  • Regulation of body weight and food intake
  • Regulation of blood glucose level
  • Regulation of body temperature
  • Regulation of body osmolality and volume of body water
  • Hypothalamus and response to stress
  • Regulation of endocrine glands
560
Q

Regulation of autonomic nervous system by hypothalamus

A
561
Q

How does the hypothalamus regulate body weight and food intake?

A
  • Hypothalamus help in adjusting the food intake (source of energy input) to match the energy expenditure (production).
  • Hypothalamus controls the food intake by two centers called APPESTATE (feeding center and satiety center):
562
Q

Compare between feedking center and satiety center in terms of:

  • Site
  • Stimulation
  • Lesion
A
563
Q

How does the hypothalamus regulate blood glucose level?

A
  • Hypothalamus contains glucoreceptors in the lateral hypothalamic region stimulated by hypoglycemia.
564
Q

How does hypoglycemia trigger counter-regulatory mechanisms by hypothalamus?

A
565
Q

Regulation of body temperature by hypothalamus

A

(in cases of exposure to cold and hot weathers):

566
Q

How does the hypothalamus regulate body osmolarity & Volume of body water?

A
567
Q

How does hypothalamus respond to stress?

A
568
Q

Regulation of endocrine glands by hypothalamus

A
  • Hypothalamic control of anterior pituitary gland: (vascular control)
  • Hypothalamic control of posterior pituitary gland: (Nervous control)
  • Hypothalamic control of suprarenal medulla:(Nervous control)
569
Q

mechanism of Hypothalamic control of anterior pituitary gland

A
  • Through the hypothalamo-hypophyseal portal-like circulation between the hypothalamus and the anterior pituitary (adenohypophysis)
570
Q

what are Releasing factors (hormones) secreted by hypothalamus?

A
  • Thyrotropin (TSH. RF).
  • Corticotropin (ACTH. RF)
  • Gonadotropin (GTH. RF)
  • Growth H. RF
571
Q

what are Inhibiting factors (hormones) released by hypothalamus?

A
  • Prolactin inhibiting factor (PIF). PIF is now known to be Dopamine.
  • Growth inhibiting factor (GIF) GIF is now known to be Somatostatin (SS)
572
Q

Mechanism of Hypothalamic control of posterior pituitary gland

A

through hypothalamo-hypophyseal tract

573
Q

where does hypothalamo-hypophyseal tract arise from? and where does it end?

A
  • arises from S.O and P.V nuclei and ends in the posterior pituitary (neurohypophysis).
574
Q

what do S.O & P.V nuclei secrete?

A
  • The S.O nucleus secrets ADH and P.V nucleus secrets oxytocin.
575
Q

Mechanism of Hypothalamic control of suprarenal medulla

A
  • SRM is controlled by hypothalamic fibers that affect the adrenaline-secreting center in the medulla oblongata, which is turn affect the activity of SRM, that secretes adrenaline and noradrenaline in the blood stream.
576
Q

what are body functions that undergo diurnal variation across 24 hours of day?

A
  1. Wake-sleep cycle
  2. Cyclic rhythm of the body temperature
  3. Blood pressure
  4. Secretion of hormones as: cortisol., growth H., melatonin, prolactin.
  5. Bronchomotor tone.
577
Q

what is the master clock (Biological clock) that is responsible for regulation of various biological ryhthms?

A

the supra-chiasmatic nucleus (SCN) of hypothalamus which receive information about light and darkness directly from the retina of the eye.

578
Q

what is the definition of limbic system?

A

The limbic system consists of those parts of the brain that are of great importance in:

  1. Initiation of emotions.
  2. Regulation of emotional behavior
    - The limbic system is interconnected group of cortical and subcortical nuclei within the brain
579
Q

Structure of limbic system

A
580
Q

Connections of limbic system

A
  • With cerebral cortex
  • Internal connections
  • With reticular formation and autonomic centers in the brian stem
581
Q

Connection of limbic system with cerebral cortex

A
  • Through connection with cerebral cortex, the limbic system receives processed sensory information from the cortical association area about various stimuli in the internal and external environments
582
Q

Significance of Connection of limbic system with cerebral cortex

A

For deciding the nature of appropriate internal and external response initiated by the limbic system.

583
Q

Internal connections of limbic system

A
  1. A closed circuit called Papez circuit connects the thalamus and hypothalamus with the limbic system.
  2. Stria-terminalis which connects the amygdaloid with the hypothalamus.
  3. Few connections exist between limbic system and the neocortex (cortical tissues other than the limbic cortex) specially from the frontal lobe to the adjacent limbic areas.
584
Q

Connection of limbic system with RF and Autonomic centers of brain stem

A
585
Q

what are the functions of limbic system? (Role of limbic system in motivation and motional behaviour)

A

Limbic system is primarily concerned with emotions, motivation, and emotional behavior and plays an essential role in learning and memory.

  • Control of the feeding behaviour
  • Fear and rage reactions
  • Sexual behavior and reproduction
  • Punishment and reward response
  • Olfaction
586
Q

Feeding behaviour of limbic system

A
  • This is one of the functions of the amygdaloid nuclei.
587
Q

Fear and rage reactions by limbic system

A
  • The limbic system receives information from different association areas of the cortex about various environmental stimuli.
  • Many limbic centers especially the amygdale, evoke protective emotional reactions (.e.g. fear or rage reactions).
588
Q

Sexual behaviour and reproduction by limbic system

A
  • Hypothalamus plays a control role on the onset of puberty as well as it contains sensory neurons that respond to gonadal hormones —> powerful control upon the sexual function and activity.
589
Q

Punishment and reward respons by limbic system

A
  • Stimulation of certain areas in limbic system —> pleasure and satisfaction (reward effect).
  • Stimulation of certain areas in limbic system –> displeasure, rage, fear, escape (punishment effect) —> avoidance of these punishing stimuli.
590
Q

Olfaction by limbic system

A
  • The limbic system is concerned with perception and discrimination of different odours.
  • It stores the olfactory memories and controls the emotional responses to olfactory stimuli.
591
Q

Definition of vision

A
  • Vision is a complex process through which an image of the external environment is formed on the photosensitive retina of the eye.
  • This image is conducted as a nerve impulse to the brain where it is interpreted and recognized.
592
Q

Structure of eye

A

The eye is the organ of vision which consists of 2 parts:

  • Eyeball
  • Extraocular accessory structure
593
Q

Nature of light

A

Light is a form of radiant energy, consisting of electromagnetic waves

594
Q

what happens When light rays strike a surface?

A

When light rays strike a surface, they are either;

  1. Reflected (white objects reflect all light).
  2. Absorbed (black objects absorb all rays).
  3. Transmitted through it, with or without refraction.
595
Q

What is Refraction?

A
  • It is the bending of light rays when they travel in 2 transparent media with 2 different refractive indices, provided that they travel at angulated interface
596
Q

what does Light refraction depend on?

A
  • The refractive index of the media (RI)
  • The Interface
597
Q

what is The refractive index of the media (RI)?

A
  • It is the ratio of velocity of light in air to the velocity in that medium.
598
Q

what is RI of different structures in the eye?

A
  • RI of cornea = 1.38
  • RI of aqueous humour = 1.33
  • RI of vitreous humour =1.34
  • RI of lens =1.40
599
Q

what is The Interface?

A

whether the strike surface is plane , convex or concave

600
Q

what is The power (or strength) of lenses measured in?

A

in diopters

601
Q

what is the power of a lens having a focal length 0.1 meter?

A

= 1/ 0.1 = 10 diopters.

602
Q

Refractive index and power of:

  • Cornea
  • Aqueous Humour
  • Lens
  • Vitreous humour
A
603
Q

what is The Outer Layer of the Eye?

A

consists of 2 parts; anterior transparent one sixth called the cornea and posterior opaque five sixth called the sclera.

604
Q

what is the cornea?

A

The cornea is the transparent anterior 1/6 of outer coat of the eyeball.

605
Q

Diameter and thickness of the cornea

A

It is 11 mm in diameter & 1.0 mm in thickness.

606
Q

Nutrition & metabolism of The Cornea

A
  • Energy of the cornea is needed for maintenance of its dehydration and transparency.
  • Normally the cornea is avascular i.e. contains no blood vessels , so the cornea can obtain oxygen and glucose from the following;
    a. Tears → supply O2 from the atmosphere.
    b. Aqueous humour → supply glucose.
    c. The blood capillaries surrounding the corneo-scleral junction→ supply both O2 and glucose.
  • The cornea contains ascorbic acid & glutathione which act as H2 acceptors in anaerobic metabolism.
607
Q

why is Energy of the cornea needed?

A
  • for maintenance of its dehydration and transparency.
608
Q

How does the cornea obtain O2 and glucose?

A

Normally the cornea is avascular i.e. contains no blood vessels , so the cornea can obtain oxygen and glucose from the following:

  • Tears → supply O2 from the atmosphere.
  • Aqueous humour → supply glucose.
  • The blood capillaries surrounding the corneo-scleral junction→ supply both O2 and glucose.
609
Q

Significance of ascorbic acid & glutathione in the cornea

A
  • Act as H2 acceptors in anaerobic metabolism.
610
Q

Transparency of the cornea

A
  • The cornea is a transparent structure. This is essential for passage & refraction of light entering the eye to form a sharp image on the retina.
611
Q

what are the Causes of transparency of the cornea?

A
  • Anatomic factors
  • Physical factors
612
Q

Anatomic factors of transparency of the cornea

A
  • Regular & uniform arrangement of the epithelial cells & lamellae.
  • Absence of blood vessels & myelinated nerve fibres.
613
Q

Physical factors of of transparency of the cornea

A
  • The refractive index of various layers of cornea is the same.
  • Relative corneal dehydration
614
Q

why is the cornea kept dehydrated?

A

to avoid corneal cloudiness.

615
Q

Mechanism of corneal dehydration

A

Corneal dehydration occurs by 2 mechanisms:
- Osmotic pump
- Metabolic pump

616
Q

Osmotic pump of the cornea

A
  • The aqueous humour & tears are hypertonic relative to corneal tissue, so they draw water from the cornea.
617
Q

Metabolic pump of the cornea

A
  • is an active process using energy produced by corneal metabolism especially of endothelium. It pumps water from the cornea to aqueous humour.
618
Q

what are the Factors maintaining corneal transparency?

A
  • Vitamin A
  • Vitamin B2 (Riboflavin)
  • Moistening of the corneal surface by tears: Dryness of the cornea disturbs its transparency.
  • Metabolic pump of the endothelial cells: It leads to dehydration of the cornea so prevents corneal cloudness.
619
Q

Role of Vit. A in corneal transperancy? and what does its deficiency cause?

A
  • It is essential for maintenance of healthy corneal epithelium.
  • Its deficiency leads to keratinization & opacity of the cornea
620
Q

Role of Vitamin B2 (Riboflavin) in corneal transparency

A
  • It is important for tissue respiration especially the avascular structures as the cornea.
621
Q

what does deficiency of Vitamin B2 (Riboflavin) cause to corneal transparency?

A
  • Its deficiency leads to hypoxia which is compensated by corneal vascularization which disturbs its transparency.
622
Q

Functions of the cornea

A
  1. It is transparent structure allowing the passage of light rays into the eye.
  2. It is the most important refractive media of the eye. It acts as a powerful convex lens (+ 39-43 diopters) having 70% of total diopteric power of the eye. Its refractive index is 1.38.
  3. The regular curvature of the corneal surface helps the formation of sharp clear images on the retina.
  4. Protective functions of the cornea: it protects the delicate intraocular structures because:
    - is tough.
    - absorbs UV rays.
    - is the initiator of Corneal reflex which is a protective reflex.
623
Q

What is the sclera?

A

It constitutes the posterior opaque 5/6 of the outer coat of the eye.

624
Q

Covering of the sclera

A

It is covered anteriorly by the conjunctival membrane.

625
Q

Color of the sclera

A

Normally, it is whitish in adults & bluish in infants & young children.

626
Q

Transperency of the sclera

A

It is opaque due to marked irregularity of its fibres.

627
Q

Functions of Sclera

A
  1. It protects the delicate inner eye structures
  2. It gives attachment to the external ocular muscles.
628
Q

Functions of the iris

A
  • The pigments of iris absorb all light rays which enter into the eye except though which pass through the pupil.
  • It prevents light from falling on the peripheral parts of the lens. Thus it prevents spherical and chromatic aberration.
  • It regulates the amount of light which enters into the eye
  • Pupillary constriction increases the depth of focus i.e. the distance of the object can be changed but its image is still focused on the retina without change in accommodation.
629
Q

what is Spherical aberration? and what decreases it?

A
  • The peripheral part of the lens has a greater curvature than the central part, so light rays
    passing through the peripheral part comes to a focus nearer to the lens than that of the central rays resulting in a blurred image.
  • Pupillary constriction decreases this defect as the light rays pass only in the central part of the lens.
630
Q

what is Chromatic aberration? and what decreases it?

A
  • The peripheral part of the lens acts as a prism which analyses the white light into the
    different colours of the resulting in a blurred image surrounded by coloured halos.
  • This is prevented by constriction of the pupil.
631
Q

How does the iris regulate the amount of light which enters into the eye?

A

by regulating the size of the pupil.

Exposure to light → parasympathetic stimulation → contraction of constrictor pupillae → pupillary constriction (miosis) → ↓ the amount of light entering the eye.

Exposure to dark → sympathetic stimulation → contraction of dilator pupillae →pupillary dilatation (mydriasis).

632
Q

Functions of the ciliary body

A

This contains the ciliary muscle & the ciliary processes.

1) The ciliary muscle is essential for accommodation.

2) The ciliary processes secrete the aqueous humour into the posterior chamber & give attachment to the suspensory ligament of the lens.

633
Q

Functions of the choroid

A

1) It is a vascular layer which provides blood supply to the eye.

2) The pressure inside its vessels maintains the intraocular pressure.

3) It contains melanin pigments which absorb light & prevent its reflection inside the eye which
cause blurring of vision.

634
Q

what is Crystalline Lens?

A

It is avascular, transparent biconvex elastic structure.

635
Q

Lens Structure

A
  • The crystalline lens is enclosed in an elastic capsule (becomes hard with advances of age). It consists of concentric layers of modified fibrous cells (with the older at the center).
  • The crystalline lens is held in place by a circular lens ligament (zonule) which is attached to the ciliary body.
636
Q

what causes Lens transparency?

A

It is due to:

a. Uniform arrangement of lens fibres.

b. Absence of blood vessels.

c. Dehydration maintained by an active process.

d. Constancy of its chemical composition.

e. The refractive indices of the various materials in the lens are nearly equal.

637
Q

Importance of lens metabolism

A

maintain its transparency. The lens obtains oxygen and glucose from aqueous humour, because it is avascular.

638
Q

Metabolism of lens

A
  • Glucose is metabolized mainly anaerobically to lactic acid. Some aerobic metabolism can occur in which glutathione and ascorbic acid act as hydrogen acceptor.
639
Q

Importance of glutathione in lens

A
  • Protects lens protein against damage from free radical, so its removal by dialysis or its decrease e.g. in old age will cause damage of lens proteins by free oxygen radical and loss of lens transparency or cataract formation.
640
Q

Functions of the lens

A
  1. It provides about 30% of the total diopteric power of the eye. Its R.I. is 1.4.
  2. It protects the retina by absorbing ultraviolet waves.
  3. Accommodation to near vision: the lens enables the eye to see far and near objects clearly by the mechanism of accommodation that changes its power from 20 to 32 D.
641
Q

Lens During rest (far vision)

A

ciliary muscle is relaxed so it pulls on the zonule that flattens the lens .

642
Q

Lens on near vision

A

On near vision, ciliary muscle is contracted so it releases the pull on the suspensory ligaments, making the lens thicker.

643
Q

what happens If the ciliary muscles become paralyzed?

A

a condition called cycloplegia, focusing no longer occurs, and it is impossible to read a book.

644
Q

what is accommodation?

A
  • Accommodation is the ability of the eye to keep the image of an object focused on the retina as the distance between the object & retina varies
645
Q

what is Accommodation Reflex?

A
  • Accommodation Reflex (Near Response) is the changes occurring in the eye as a result of retinal blurred image of the near object.
646
Q

Response in Accommodation Reflex

A

1- Constriction of the pupils.

2- ↑ refractive power of the lens (more spherical; becomes very convex instead of moderate convexity). When ciliary muscle contract; this releases tension on suspensory ligaments leading to more spherical (rounder) lens and this increases its.

3- Medial convergence of the eyes due to contraction of medial recti muscles. This will make the image of the near object falls on the fovea of each eye and prevent diplopia [double vision].

647
Q

what is Range of accommodation?

A
  • It is the distance between the far point of distinct vision (normally infinity) and the near point of distinct vision.
  • The near point is the shortest distance at which the eye can see clearly and at which the accommodation is maximum.
648
Q

what happens to Range of accommodation by aging?

A
  • It recedes by aging due to the decrease of the lens elasticity and ciliary muscle power.
649
Q

what is Amplitude of Accommodation?

A

Is the difference in diopters between:

1- maximal diopteric power of the lens during maximum accommodation in near vision= 32 diopters

2- minimal diopteric power of the lens during minimum accommodation in far vision= 20 diopters.

650
Q

what is the value of Amplitude of Accommodation?

A

Normally the amplitude of accommodation = 32-20=12 diopters.

651
Q

what happens to Amplitude of Accommodation by aging?

A

This difference (amplitude) decreases with advance of age due to gradual loss of lens elasticity.

652
Q

what is Near Point? and what happens to it by aging?

A
  • it is the nearest point to the eye at which the object can be seen clearly.
  • It becomes far with age due to ↓ lens elasticity.
653
Q

What are problems associated with lens?

A
  • Aphakia
  • Presbyopia
  • Cataract
  • Errors of Refraction
654
Q

what is Aphakia?

A
  • means absence of the lens from the eye. It may be congenital or after surgical removal.
655
Q

what is Presbyopia?

A
  • means failure of accommodation to near objects due to gradual diminution of lens elasticity with advancing age.
656
Q

what causes Presbyopia?

A
  • means failure of accommodation to near objects due to gradual diminution of lens elasticity with advancing age.
657
Q

How is Presbyopia corrected?

A
  • corrected by convex lens for near vision only.
658
Q

what is Cataract?

A

means loss of lens transparency.

659
Q

what causes Cataract?

A

due to degenerative changes resulting in denaturation of lens proteins.

660
Q

What causes degenerative changes resulting in denaturation of lens proteins?

A

Ultraviolet rays
- which cause coagulation of lens protein in presence of calcium.

Diabetes mellitus:
- in which the disturbance in glucose metabolism makes the lens protein more coagulable by light.

Old age (senile cataract):
- in which glutathione is absent from the lens.

661
Q

How is cataract treated?

A

removal of the lens.

662
Q

what are Errors of Refraction?

A
  • Myopia (short-sight)
  • Hypermetropia (Far-sight)
  • Astigmatism
663
Q

what is Emmetropic (Normal) eye?

A
  • is the eye in which parallel rays converge to a focus on the retina.
664
Q

what is Ammetropic eye?

A
  • is the eye in which parallel rays can not converge to a focus on the retina
665
Q

what is Myopia (short-sight)?

A
  • It is a condition in which image of near objects fall on the retina but images of far objects focus at a point in front of the retina .
666
Q

what causes Myopia (short-sight)?

A
  • In most cases, it is due to abnormally long eyeball.
  • Occasionally, it is due to abnormally great curvature of cornea or lens.
667
Q

Correction of Myopia (short-sight)

A
  • corrected by biconcave lens (Divergent lens).
668
Q

What is Hypermetropia (Far-sight)?

A
  • It is a condition in which image of far objects fall on the retina but images of near objects converge to a point behind the retina .
669
Q

What causes Hypermetropia (Far-sight)?

A
  • In most cases, it is due to abnormally short eyeball.
  • Occasionally, it is due to abnormally small curvature of cornea or lens.
670
Q

Correction of Hypermetropia (Far-sight)?

A
  • The condition is corrected by biconvex lens.
671
Q

What is Astigmatism?

A
  • It is a condition in which the curvatures of the cornea or to less extent the lens are not the
    same in all planes
    , so that rays fall on the eye are not focused in one focus on the retina but some rays in one plane are focused on the retina while those in other plane do not, This causes blurring of vision.
672
Q

Correction of Astigmatism

A
  • Corrected by cylindrical lens with its longitudinal axis perpendicular to the plane to be corrected.
  • Contact lenses are the only correction possible when the cornea is abnormal.
673
Q

what is Aqueous humor?

A
  • It is a transparent colourless alkaline fluid that fills the anterior and posterior chambers of the eye.
674
Q

Mechanism of formation of Aqueous humor

A
  • It is formed continuously by the ciliary epithelium by facilitated diffusion and active transport mechanisms at a rate 1-2 μL/min.
  • Sodium is secreted actively.
  • Chloride and bicarbonate follow Na passively.
  • Water is pulled by osmosis.
675
Q

Composition of Aqueous humor

A

In relation to plasma, the composition of the aqueous humour is:

  • Nearly protein free (contains about 100-200 mg/L).
  • Na+ concentration is higher.
  • Bicarboante concentration is higher.
  • Vitamin C concentration is 10-20 times higher.
676
Q

Circulation and drainage of aqueous humour

A
  • After its formation it flows between the suspensory ligaments of the lens into the posterior chamber .
  • Then, it passes through the pupil into the anterior chamber.
  • Lastly, it passes through the irido-corneal junction (filtration angle) into the spaces of Fontana to the canal of Schlemm which encircles the anterior chamber at the cornea-scleral junction.
  • Finally the aqueous passes from the canal of Schlemm to the aqueous veins to the systemic
    veins.
  • There is a balance between its rate of production and the rate of drainage.
677
Q

Functions of aqueous humour

A
  1. It is one of the important refractive media of the eye.
  2. It nourishes the avascular cornea and lens.
  3. It also buffers the acid produced by the anaerobic metabolism of the cornea and lens.
  4. It has a mechanical function to keep the eyes rigid and to maintain its refractory power.
  5. It maintains the intraocular pressure constant by means of its steady formation and drainage.
678
Q

what is the normal Intraocular Pressure (I.O.P.)?

A

15-20 mmHg.

679
Q

what causes Intraocular Pressure (I.O.P.)?

A
  • due to the resistance of flow in the narrow channels of drainage.
680
Q

What measures Intraocular Pressure (I.O.P.)?

A
  • measured by a tonometer.
681
Q

What keeps the Intraocular Pressure (I.O.P.) constant?

A
  • pressure is kept constant by a perfect regulation of the rate of drainage of aqueous to be equal with the rate of its secretion.
682
Q

what does a rise/drop in Intraocular Pressure (I.O.P.) cause?

A
  • A rise in pressure distends the spaces of Fontana so increases the outflow, while a drop in pressure collapses the spaces of Fontana, so decreases the outflow.
683
Q

Importance of I.O.P

A
  • A normal I.O.P. is essential for the focusing mechanism of the eye, excessive drop in I.O.P. leads to relaxation of suspensory ligament of the lens and increased its convexity and vice versa.
  • Therefore, it is important for proper accommodation of the lens.
684
Q

what is Glaucoma?

A
  • a disease in which there is excessive increase in I.O.P, either due to ↑ in production of aqueous humor, or ↓ its drainage [due to obstruction of Corneoscleral angle].
685
Q

Effects of Glaucoma

A

1- Sever pain.

2- Disturbances of focusing mechanism especially for near vision.

3- Pressure on retinal vessels → pressure atrophy of optic disc (nerve) → blindness.

686
Q

Treatment of Glaucoma

A

it is treated either by:

1- Carbonic anhydrase inhibitors.

2- Parasympathomimetics [pupilloconstrictors].

3- Surgical opening of Corneoscleral angle (trabeculectomy).

687
Q

What is Vitreous humour?

A
  • It is a transparent gelatinous material filling the space between the posterior surface of the lens and the retina.
688
Q

what encloses Vitreous humour?

A

It is enclosed in a membrane.

689
Q

what separates Vitreous humour from the lens?

A
  • It is separated from the lens by a narrow space (retrolental space).
690
Q

what traverses the Vitreous humour?

A
  • Also, the vitreous is traversed from the posterior surface of the lens to the region of optic disc by a canal (hyaloid canal) which acts as a lymph channel.
691
Q

Functions of Vitreous humour

A
  1. It is one of the refractive media of the eye.
  2. It supports the retina.
  3. It supports the crystalline lens and prevents it from falling back.
  4. It maintains the spherical shape of the eye.
692
Q

Definition of retina

A
  • the innermost photosensitive layer of the eyeball.
693
Q

what characterizes the retina?

A
  • It contains about 55 types of cells and 70% of total sensory receptors of the body.
694
Q

Histology of the retina

A
  • Histologically, it is formed of 10 layers.
695
Q

What are the layers of physiological importance in retina?

A
  • 4 layers have special importance.

a. Layer of pigmented epithelium.
b. Layer of rods and cones.
c. Layer of bipolar cells.
d. Layer of ganglion cells.

696
Q

What is retinal pigmented epithelium?

A
  • It is a monolayer of pigmented epithelial cells, its outer side is in contact with the choroid and its inner side with the rods and cones.
697
Q

Function of retinal pigmented epithelium

A
  • It contains large amounts of melanin pigments which absorb light and prevent its reflection inside the eyeball which cause glare.
  • Pigmented epithelium produces a sticky extracellular matrix material that keeps the outer segments of rods and cones straight and aligned.
  • It participates in the process of the breakdown and resynthesis of the photopigments.
  • It helps the continual renewal of the outer segment by ingesting the old outermost tips of the rods and cones.
  • It stores large amount of vit. A needed for photopigments recycling.
698
Q

What are the types of photoreceptors?

A
  • two types; rods and cones.
699
Q

Structure of photoreceptors

A

Each rod or cone is formed of:
- An outer segment
- An inner segment

700
Q

What is the outer segment of photoreceptors?

A
  • They are modified cilia which are long cylindrical in rods and short conical in cones.
701
Q

What does the outer segment of photoreceptors Contain?

A

They contain a great number of disc-shaped shelves which are composed of folds of the cell membrane. The disc membrane contains;
- Photosensitive pigments e.g. rhodopsin.
- G protein called transducin.
- c GMP phosphodiestrase (PDE).

702
Q

What does The membrane of the outer segment of rods and cones contain? And what is it selective for?

A
  • The membrane of the outer segment of rods and cones contains cGMP-gated ion channels
  • selective for Na+, Ca++ and Mg++.
703
Q

Structure of outer segment of photoreceptors

A
  • They are modified cilia which are long cylindrical in rods and short conical in cones.
  • They contain a great number of disc-shaped shelves which are composed of folds of the cell membrane. The disc membrane contains;
    1. Photosensitive pigments e.g. rhodopsin.
    2. G protein called transducin.
    3. c GMP phosphodiestrase (PDE).
  • The membrane of the outer segment of rods and cones contains cGMP-gated ion channels selective for Na+, Ca++ and Mg++.
704
Q

What does the inner segment of photoreceptors contain?

A
  • They contain nuclei and mitochondria.
  • They have synaptic body that synapses with bipolar cells.
  • The membrane of inner segment contains an active Na+-K+ pump.
705
Q

Structure of inner segment Of photoreceptors

A
  • They contain nuclei and mitochondria.
  • They have synaptic body that synapses with bipolar cells.
  • The membrane of inner segment contains an active Na+-K+ pump.
706
Q

Compare between cons and rods in terms of:
- Number
- Shape
- Distribution
- Photosensitive pigments
- Connection
- Function

A
707
Q

What do Bipolar Cells represent?

A
  • They constitute 1st order neurons in visual pathway.
708
Q

Function of Bipolar Cells of retina

A
  • transmit signals from photoreceptors to ganglion cells
709
Q

What do ganglion cells represent?

A
  • 2nd order neurons in visual pathway
710
Q

What do ganglion cells of retina transmit?

A
  • ganglion cells transmit signals from bipolar cells to brain through the optic nerve.
711
Q

What are lateral cells of retina?

A

horizontal and amacrine cells.

712
Q

Site of horizontal cells of retina

A
  • lie between photoreceptors and bipolar cells
713
Q

Role of horizontal cells of retina

A
  • Lateral connection between photoreceptors and bipolar cells
  • Responsible for lateral inhibition giving a stop to lateral spread of excitation →↑visual accuracy.
714
Q

Site of amacrine cells of retina

A
  • lie between bipolar cells and ganglion cells.
715
Q

Role of amacrine cells of retina

A
  • Lateral connection between BC & GC
  • 30~ types
  • Helping to analyse visual signals before leaving retina
716
Q

what are special areas of the retina?

A

Fundus Oculi

717
Q

Definition of Fundus oculi

A
  • the part of the retina which can be seen by ophthalmoscope
718
Q

What is the only part where arterioles are readily visible?

A
  • Fundus Oculi
719
Q

Examination of Fundus oculi

A
  • Examination of the fundus oculi is important for the diagnosis of diseases affecting blood vessels (diabetes mellitus and hypertension).
720
Q

Site Fovea centralis (Macula lutea)

A
  • At the posterior pole of the eye 3 mm lateral to optic disc
721
Q

Size of Fovea centralis (Macula lutea)

A
  • The macula is a small yellow area (4.5 mm in diameter).
  • It contains in its centre, an oval depression called the fovea centralis.
722
Q

Structure of Fovea centralis (Macula lutea)

A
  • The fovea cones are very thin and densely packed
723
Q

Functions of Fovea centralis (Macula lutea)

A
  • It is the area of acute vision and it contains only cones
  • Fovea is the most sensitive spot in
    retina because:
  1. All layers are shifted aside leaving outer segments of photoreceptors to be hit directly by light
  2. High density of small diameter Cones with long outer segments
  3. 1:1 convergence (cone-bipolar cell ganglion cell)
  4. Wide presentation in occipital primary visual area
724
Q

Site of Optic Disc (Blind spot)

A
  • It is located 4 mm medial to fovea centralis
725
Q

Size of Optic Disc (Blind spot)

A
  • It is 1.5 mm in diameter
726
Q

Structure of Optic Disc (Blind spot)

A
  • It contains no photoreceptors, so it is a blind spot
727
Q

Functions of Optic Disc (Blind spot)

A
  • It is the site of exit and entry of blood vessels and optic nerves to the retina.
728
Q

Clinical importance of Changes in the appearance of the optic disc

A
  • Depression may be exaggerated due to loss of ganglion cell axons (optic atrophy)
  • protruded because of edema (papilledema) caused by an increase in the intracranial pressure
729
Q

Definition of Phototransduction (Mechanism of Vision)

A

It is a process by which light is converted into signals in the rods & cone cells and photosensitive ganglion cells of the retina of the eye.

730
Q

Steps of Phototransduction (Mechanism of Vision)

A

It consists of 4 steps:

  1. Decomposition of photosensitive pigment in rods & cones
  2. Excitation of the photoreceptors by activated rhodopsin and generation of photoreceptor potential
  3. Termination of excitation
  4. Regeneration of photopigments.
731
Q

what does Rhodopsin (visual purple) consists of?

A

protein (scotopsin) and pigment (11-cis retinal).

732
Q

what does Light covert the angulated 11-cis retinal to?

A

Light coverts the angulated 11-cis retinal to straight all-trans retinal

733
Q

what does conversion of 11-cis retinal to straight all-trans retinal enhance?

A

enhance splitting between scotopsin & all-trans retinal

734
Q

what is rhodopsin converted to?

A

bathorhodopsin (in nanoseconds) → lumirhodopsin (in microseconds) → metarhodopsin I (in milliseconds) → metarhodopsin II (activated rhodopsin).

735
Q

Decomposition of photosensitive pigment

A
  • Rhodopsin (visual purple) consists of protein (scotopsin) and pigment (11-cis retinal).
  • Light coverts the angulated 11-cis retinal to straight all-trans retinal → enhance splitting between scotopsin & all-trans retinal, thus rhodopsin is converted to bathorhodopsin (in nanoseconds) → lumirhodopsin (in microseconds) → metarhodopsin I (in milliseconds) → metarhodopsin II (activated rhodopsin).
  • Metarhodopsin II splits slowly (in seconds) into scotopsin and all-transretinal by rhodopsin
    kinase enzyme.
736
Q

Gneration of photoreceptor potential in light (ionic basis)

A
  • The activated rhodopsin activates G- protein transducin which in turn activates phosphodiestrase enzyme→ breakdown of cGMP → closure of cGMP dependent Na+ channels → decrease Na entry to outer segment (with Na+ & K+ still pumped out of inner segment) → hyperpolarization of rod to -80 mv → decrease transmitter (glutamate) release in synaptic terminal → stimulation of bipolar cells → excitation of ganglion cells that respond by generation of action potential in optic nerve → visual pathway.
737
Q

Gneration of photoreceptor potential in dark (ionic basis)

A
  • In dark, the intracellular concentration of cGMP is high → open cGMP dependent cation channels in the outer segment of the photoreceptor cells.
  • Na+ (mainly) & Ca++ (small fraction) enter the outer segment & diffuse into the inner segment where it is pumped out.
  • The flow of Na+ between outer and inner segments form a current flow called dark current of about – 40 mV (depolarization) → continuous release of synaptic transmitter (glutamate) from the synaptic terminals → hyper polarization of bipolar cells by opening of Cl- channels → inhibition of ganglion cells → no action potentials in optic nerve.
738
Q

what inactivates rhodopsin?

A

Within a second the activated rhodopsin is inactivated by the enzyme rhodopsin kinase

739
Q

what does inactivation of rhodopsin lead to?

A

reversal of all reactions → regeneration of cGMP → reopening of Na+ channels → termination of excitation.

740
Q

Termination of excitation

A

Within a second the activated rhodopsin is inactivated by the enzyme rhodopsin kinase → reversal of all reactions → regeneration of cGMP → reopening of Na+ channels → termination of excitation.

741
Q

what convers All-trans retinal into 11-cis retinal?

A
  • All-trans retinal is taken up by pigmented epithelium where it is converted to 11-cis retinal by isomeraze then sent back to rods to recombine with opsin.
742
Q

Difference between excitation in cones and rods

A
  • Excitation in cones is similar to rod except no involvement of pigmented epithelium
743
Q

Definition of Retinal Adaptation

A
  • It means that the retina can change its sensitivity according to the intensity of light.
  • So, retinal sensitivity increases in dark and decreases in light (i.e. automatic adjustment to the changes in illumination).
744
Q

Value of light and dark adaptation

A
  • It provides an automatic adjustment to the changes in illumination; the eye can change its sensitivity as much as 500,000-1000, 000 times.
  • The difference between star light and sun light is about 10 billion times, yet the eye can function to both illuminations.
745
Q

Definition of Dark adaptation

A
  • It is the ability of the retina to become more sensitive to faint light.
746
Q

what happens When a person enters a dark room after being previously exposed to bright light?

A
  • When a person enters a dark room after being previously exposed to bright light, he cannot see anything at the start in spite of the rapid pupillary dilatation. After a few minutes, he becomes accustomed to the dark and can see well, i.e. the retina become more sensitive to light.
747
Q

what type of process is Dark adaptation?

A
  • Dark adaptation is a slow process during which regeneration of the photosensitive pigments (rhodopsin and iodopsin) occurs.
748
Q

Duration of Dark adaptation

A

30 minutes

749
Q

How much does the sensitivity of the retina increase in drak adaptation?

A

the sensitivity of the retina increases by 10,000 - 100,000 times.

750
Q

Phases of Dark adaptation

A

Dark adaptation occurs in 2 phases:

Cone adaptation:
- It is due to regeneration of iodopsin which leads to a slight increase in the retinal sensitivity and completed within 5 minutes.

Rod adaptation:
- It is due to regeneration of rhodopsin which leads to a marked increase in the retinal sensitivity and completed within 30 minutes.

751
Q

Changes occurring during the dark adaptation

A

1- Dilatation of the pupils which allows more light to enter the eye and stimulates more rods.

2- Regeneration of the pigments in the rods and the cones which increases the retinal sensitivity to the dim light.

3- Decreased visual acuity so that the fine details and colours of the object cannot be seen.

4- The blue-green part of the spectrum becomes the most luminous part.

752
Q

Definition of Light Adaptation

A
  • It means a decrease in the retinal sensitivity which occurs in bright light.
753
Q

what happens When a person moves from a dark place to bright light?

A
  • When a person moves from a dark place to bright light, at the start even moderate light seems to be very intense and uncomfortable.
  • After about 5 minutes, this sensation disappears due to the decrease in the retinal sensitivity, which results from degeneration of the photosensitive pigments (rhodopsin and iodopsin).
754
Q

Changes occurring during the light adaptation

A

1- Constriction of the pupils (miosis) to reduce the amount of light entering the eye.

2- Breakdown of the pigments in the rods and cones, so photopigments are decreased.

3- Decrease in the retinal sensitivity due to a parallel decrease in the amounts of the photosensitive pigments of the rods and cones.

4- The yellow green part of the spectrum becomes the most luminous part.

755
Q

what is the visual pathway composed of?

A
  • bipolar cells (1st order neuron)
  • ganglion cells (2nd order neuron)
  • fibers of the optic radiations from LGB (3rd order neuron)
756
Q

First order neuron of Visual pathway

A

Bipolar cells

757
Q

Second order neuron of Visual pathway

A

ganglion cells, Axons of which form of the optic nerve

  • optic nerve: reaches the optic chiasma, where the nasal fibers cross to the opposite side, while the temporal fibers Pass in the same side to form the optic tract (ipsilateral Temporal fibers + contralateral nasal fibers of retina)
758
Q

Third order neuron of Visual pathway

A

cells in LGB of thalamus

  • From which of the fibers of the optic radiation is arise, and terminate on the visual cortex in the occipital lobe
759
Q

Function of retinal cells in Visual pathway

A

They start the analysis of the visual image.

760
Q

Function of Photoreceptors in Visual pathway

A
  • They transmit signals to the outer plexiform layer, where they synapse with bipolar cells and horizontal cells.
761
Q

Role of bipolar cells in Visual pathway

A
  • They constitute direct pathway between photoreceptors and ganglion cells.
  • They release excitatory chemical transmitter glutamate.
762
Q

Types of bipolar cells in Visual pathway

A

They are 2 types:

  • Depolarizing bipolar (on-bipolar) cells which depolarize when the photoreceptors are hyperpolarized
  • Hyperpolarizing bipolar (off-bipolar) cells which depolarize when the photoreceptors are
    depolarized ( not exposed to light)
763
Q

what are lateral cells in Visual pathway?

A

Horizontal & Amacrine cells

764
Q

Horizontal cells in Visual pathway

A
  • They form a lateral connection between photoreceptors & bipolar cells
  • They represent lateral inhibitory pathway in the retina which is essential mechanism to allow high visual accuracy in transmitting contrast borders in the visual image.
765
Q

Amacrine cells in Visual pathway

A
  • They form a lateral connection between bipolar cells & ganglion cells
  • They are about 30 types.
  • They help the analysis of the visual signals before leaving the retina.
766
Q

Number of ganglion cells of Visual pathway

A

They are about 1.6 millions cells.

767
Q

what are the only retinal neurons that respond to stimulation by a full action potential?

A

Ganglion cells

768
Q

what are the types of ganglion cells?

A

are 3 types of ganglion cells

  • Magnocellular (M) (10%)
  • Parvocellular (P) (80%)
  • Coniocellular (10%)
769
Q

what are Magnocellular (M)?

A
  • They are large ganglion cells.
770
Q

Function of Magnocellular (M)

A
  • They are concerned with gross analysis of visual image & location of objects in visual field and motion
771
Q

what are Parvocellular (P)?

A
  • They are small ganglion cells.
772
Q

Function of Parvocellular (P)

A
  • They are responsible for fine detailed vision (shape & texture) and color vision
773
Q

what are Coniocellular?

A
  • They are medium in size.
774
Q

Function of Coniocellular

A
  • They are concerned with controlling pupillary reflexes.
775
Q

what are the functions of ganglion cells in visual pathway?

A

Ganglion cells have the following functions:

  • Detection of 2 point discrimination in the visual scene
  • Detection of the contrast in the visual scene
  • Detection of the movement and its orientation in the visual scene
  • Colour analysis
776
Q

what is Lateral Geniculate Body (LGB)?

A

It is a thalamic relay nucleus that present at the dorsal end of thalamus

777
Q

Structure of Lateral Geniculate Body (LGB)

A

consists of C-shaped 6 defined layers.

778
Q

Function of Layers 1, 2 of LGB

A

receive from large M ganglion cells → magnocellular division.

779
Q

Function of Layers 3, 4, 5 & 6 of LGB

A

from small P ganglion cells → parvocellular division.

780
Q

Function of Layers 2, 3, 5 of LGB

A

receive signals from ipsilateral retina.

781
Q

Function of Layers 1, 4, 6 of LGB

A

receive signals from contralateral retina.

782
Q

what are the Functions of LGB?

A
  1. It plays a part in fusion of retinal images from the 2 eyes.
  2. It plays a part in stereoscopic vision by comparing the visual images from both eyes and detection of minimal differences.
  3. Magnocellular neurons are concerned with perception of white and black shape and motion.
  4. Parvocellular neurons are concerned with perception of color vision and accurate point-point spatial information.
783
Q

Visual Cortical Areas (Visual pathway)

A
  • They are present in the occipital lobe and include areas 17,18, and 19;
784
Q

Site of 1ry Visual Area (area 17)

A
  • It surrounds the calcarine fissure on the occipital lobe
785
Q

Arrangment of neurons of 1ry Visual Area (area 17)

A
  • Its neurons arranged in the form of columns (1x1x2 mm) forming 6 distinct layers.
786
Q

Representation of retina in area 17

A
  • Peripheral part is represented in anterior part
  • Macula is represented in posterior part
  • Upper part of retina is resented above calcarine fissure
  • Lower part of retina is represented below the calcarine fissure
787
Q

Functions of area 17

A
  1. Perception of the visual sensations without understanding the meaning of the images.
  2. Perception of the colours.
  3. Fusion of the 2 images formed on both retinae.
  4. Perception of luminosity.
788
Q

Site of 2ry Visual Areas (areas 18 and 19)

A
  • They lie on the occipital lobe around 1ry visual area and extend to the parietal & temporal lobes
  • Areas 18 is called area V-2, more distant 2ry visual areas are assigned V-3, V-4 and so on
789
Q

Functions of area 18

A

It is also known as visuopsychic area which is concerned with:

  • Recognition the nature of the objects and correlates their colours
  • Interpretation of visual sensations
  • Localization of object in space i.e. depth perception
790
Q

Functions of area 19

A

It is also known as the occipital eyefield area.

  • It shares area 18 its functions.
  • It controls the different types of eyeball movements.
791
Q

Def. of Colour Vision

A
  • It is the ability of the eye to perceive the different types and characters of colours.
792
Q

what are types of colors?

A
  • Primary & Secondry colors
793
Q

Definition of Primary colours

A
  • When they are mixed together in the same proportion they give white colour
  • When mixed by different proportion they give other colours
794
Q

Examples of Primary colours

A

They are red, green, and blue

795
Q

Def. of Complementary colours

A
  • These colours when mixed together they give white colour e.g. deep blue and yellow; red and cyano.
796
Q

Examples of Complementary colours

A
  • deep blue and yellow; red and cyano.
797
Q

Characters of colours

A
  • Colors have three attributes: hue, intensity, and saturation.
798
Q

Definition of Hue

A

means the wave length e.g. red light (wavelength 723-647 nm), green light (575-492 nm), and blue light (492-450 nm).

799
Q

Definition of Intensity

A

means the purity of the colour i.e. it is pure or mixed with other colours.

800
Q

Definition of Brightness

A

means the amount of light in the colour

801
Q

what are Mechanisms of colour vision?

A
802
Q

what is the most accepted theory of colour vision?

A

Young-Helmholtz or trichromate theory

803
Q

what does Young-Helmholtz theory explain?

A

explains the mechanism of colour vision at the level of receptors.

804
Q

Assumptions of Young-Helmholtz theory

A
  • It postulates that there are 3 kinds of cones; each containing a different photopigment and
    maximally sensitive to one of the three primary colors.
  • Equal stimulation of the 3 cone systems produces white sensation while unequal stimulation produces another colour e.g. yellow colour is perceived when red cone stimulated by 83%, green cone by 83%, and blue cone by 0%.
805
Q

what is Binocular Vision?

A

It is the ability to see an object with 2 eyes without double vision (diplopia).

806
Q

Requirements of binocular vision

A
  • The visual fields must overlap to a great extent.
  • A nearly normal refractive power in both eyes.
  • Intact neuromuscular apparatus that allow the eyeball to move so that both images of the
    object fall at the corresponding points of both retinae.
  • Intact visual cortex where fusion of images occur.
807
Q

where does fusion at the level of primary visual area occur?

A
  • The 2 images of an object placed in the area of binocular vision (one from each retina) are fused at the level 1ry visual area (17) into a single image
808
Q

what are corresponding points?

A
  • The retinal points at which the images of an object must fall to be seen binocularly as a single image
809
Q

Site of corresponding points

A
  • They are located at the nasal side of one retina and the temporal side of the other retina
  • The foveae centralis of both eyes are the normal corresponding points.
810
Q

Advantages of binocular vision

A
  • It increases the visual field horizontally from 160 to 200 degrees.
  • It corrects the minor defects in one eye by the other eye e.g. blind spot of one eye is corrected by the other eye.
  • It is important for stereoscopic vision (3 dimensions of object height, width, and depth). It can be perceived by monocular vision but it is better recognized by binocular vision (due to the more accurate perception of depth).
  • It improves the depth perception.
811
Q

Assumptions of Duplicity Theory of Retinal Function

A
  • This theory states that retinal function is double in nature depending on the properties of its 2 photoreceptors.
  • It assumes the existence of 2 different inputs from the retina (one from rods & the other from the cones) to the CNS, each input works maximally under a different condition of illumination.
  • Cones are used for bright day light (photopic vision) while rods are used for dim night light (scotopic vision).
812
Q

Compare between photopic and scotopic vision in terms of:

  • Receptors
  • Site
  • Threshold
  • Sensitivity to light
  • Accuracy
  • Colour vision
  • Adaptation
A
813
Q

Evidence for the duplicity theory

A
  • Nocturnal animals such as rats have rods only in their retinae, while those adapted for day- life such as chickens have cones only.
  • The peripheral parts of the retina which contain mainly rods are proved to be colour-blind while the central part is most sensitive to colour.
  • Vitamin A deficiency which causes dysfunction of the rods due to deficient formation of rhodopsin, leads to night blindness (nyctalopia) but does not affect day vision.
  • The eye shows both dark and light adaptation.
814
Q

Objections to the duplicity theory

A
  • Guinea pigs have only rods in their retinae but they can see during day-time and can also differentiate some colours.
  • Snakes have only cones in their retinae but they can see at night and cannot differentiate various colours.
815
Q

Modification of this theory

A
  • Rods are the main (instead of only) receptors of scotopic vision, but they share also in photopic vision (may give some colour sensation, probably blue) e.g. in guinea pigs.
  • Cones are the main receptors for photopic vision, but they share also in scotopic vision e.g. in snakes.
816
Q

what is Audition or hearing?

A
  • is the sense that allows us to communicate and hence interact with other organisms throughout the world.
817
Q

what is adequate stimulus for hearing?

A
  • Sound waves
818
Q

Nature of sound waves

A
  • longitudinal pressure waves consisting of alternating phases of compression and rarefaction
  • They require a medium for its transmission (air, water or solid).
819
Q

what describes sounds?

A
  • described in terms of their velocity, frequency, intensity, and wave form.
820
Q

what causes difference in velociy of sound?

A
  • differs according to the medium conducting it.
821
Q

Velocity of sound

A
  • It is about 344 meter/second in air, 4 times in water and 7 times in bone greater than that of air.
822
Q

what is Frequency (pitch) of sound? and what is it measured in?

A
  • Frequency (pitch) is the number of waves that pass a certain point in a second. It is measured in cycles/second or Hertz (Hz).
823
Q

what is Intensity (amplitude) of sound?

A
  • amount of sound energy passing through a given unit of area per unit of time (dyne/cm2).
  • It determines the loudness of the sound (the greater the amplitude, the louder will be the sound).
824
Q

what is intensity of sound measured in?

A
  • The intensity of sound is measured in Bells
825
Q

what is the intensity of normal speech?

A

about 60-65 dB.

826
Q

Frequencies heard by the ear

A
  • The human ear can perceive frequencies range between 20-20,000 Hz with maximum sensitivity between 1000-4000 Hz.
827
Q

what is the frequency of voice of average male and female?

A
  • The pitch of the average male voice in conversation is about 125 Hz and that of average female voice is about 250 Hz.
828
Q

Definition of Threshold of audibility

A
  • Threshold of audibility is the lowest intensity just gives a sound sensation.
  • It equals the intensity of standard sound or zero decibel.
829
Q

Sound intensities & response to it

A
  • Sounds intensities of about 120dB produce discomfort
  • while those of 140dB are painful
  • those of 160 dB (as sound of jet plane) have a very high energy (increase body temp. and may damage the delicate tissues of the ears).
830
Q

Physiological Anatomy of the Ear

A

The human ear consists of 3 parts:
a. External ear.
b. Middle ear.
c. Inner ear.

831
Q

what does the extrnal ear consist of?

A

The external ear consists of:

a. Ear pinna.

b. External auditory meatus.

832
Q

what is The Ear Pinna (Auricle)?

A
  • It is the cartilaginous external flap and its extension (the tragus).
833
Q

Functions of The Ear Pinna (Auricle)

A
  • It collects and directs sound waves into the external auditory meatus.
  • It also plays an important role in sound localization especially in the vertical (Actually it is horizontal) plane
834
Q

what is The External Auditory Meatus?

A
  • It is an oblique tortuous skin-lined canal of about 2.5cm length in the temporal bone.
835
Q

what is present at the end of The External Auditory Meatus?

A
  • The tympanic membrane (ear drum) exists at the end of the canal and completely separates the external ear from the middle ear.
836
Q

Functions of The External Auditory Meatus

A
837
Q

Anatomy of Middle Ear

A
838
Q

Functions of the Middle Ear

A
  • The primary function of the middle ear is to transfer sound from the external ear to the inner ear.
  • All middle ear structures are designed to perform this function.
839
Q

what is The Tympanic Membrane?

A
  • It is a thin semi-translucent membrane, conical in shape with its concavity directed laterally.
840
Q

Surface area and thickness of The Tympanic Membrane

A
  • Its surface area is about 55 mm2 and its thickness is about 0.1 mm.
841
Q

Functions of The Tympanic Membrane

A
  1. It acts as a resonator that reproduces the vibrations of the sound source i.e. vibrates in and out according to the frequency and intensity of the sound introduced.
  2. It is highly damped i.e. its vibration stops when the applied sounds stop, this prevent the unnecessary sound prolongation.
  3. It is aperiodic i.e. it has no natural frequency, but takes up the characteristics of the vibrations applied on it.
842
Q

Function of the Ossicular System

A
  • Amplification and Impedance Matching
843
Q

what causes loss of sound energy in middle ear?

A
  • The fluid has great inertia than air, therefore, the transmission of sound waves from air in the external ear to endolymph in the inner ear results in a great loss of energy.
844
Q

what is the amount of sound energy lost in middle ear?

A
  • More than 97% of a sound’s energy would be reflected at the surface of water (i.e. sound of loud speaker would be lowered to just whisper).
845
Q

How could This impedance or resistance to sound transmission be matched?

A

This impedance or resistance to sound transmission can be matched by 2 mechanisms:

  • The areal ratio of the tympanic membrane and the oval window
  • The lever system of the bony ossicles
846
Q

The areal ratio of the tympanic membrane and the oval window

A
  • The surface area of the drum (55 mm2) is about 17 times greater than that of the foot plate of the stapes (3.2 mm2).
  • This areal ratio produces an amplification sound waves about 20-fold at the oval window.
847
Q

The lever system of the bony ossicles

A
  • The bony ossicles are arranged in such a manner that they function as a series of levers.
  • The handle of the malleus is about 1.3 times that of long process of the incus.
  • This lever action of the malleus and incus increases the force of movement of the stapes about 1.3 times.
848
Q

Efficiency of lever action of ossicles and areal ratio of the tympanic membrane and oval window (The impedance matching device)

A
  • The lever action of ossicles and areal ratio of the tympanic membrane and oval window amplify the sound pressure at the oval window about 22 times.
  • The efficiency the impedance matching device is not 100%, but it is about 50 to 75% for sound frequencies between 300 and 3000Hz.
849
Q

where do both oval and round windows open respectively?

A
  • The oval window opens into the scala vestibuli and the round window opens into the scala tympani.
850
Q

what happens if sound waves, strike the two windows simultaneously (as that occur when the transformer action of the middle ear is not present)?

A
  • If sound waves, strike the two windows simultaneously (as that occur when the transformer action of the middle ear is not present), the effect could be the same as that produced by making equal pressure on the two ends of an open U tube filled with water i.e. there would be no displacement of fluid, this is called cancellation effect.
851
Q

Role of ear windows when intact

A
  • In intact ear, sound energy is applied to the ear drum whose vibrations are transmitted to the ossicular bones to the oval window then through the scala vestibuli and scala tympani to the round window.
  • Therefore, when there is condensation phase, at the oval window there will be rarefaction phase at the round window i.e. the two windows vibrate reciprocally in response to sound energy.
  • So the round window serves as a relief hole in the bony cochlea.
852
Q

Role of the round window in sound transmission

A
853
Q

what is the Eustachian Tube?

A

It is a tube that connects the middle ear with the nasopharynx.

854
Q

Functions of Eustachian Tube

A
855
Q

what happens during ascent of an airplane?

A

the external pressure is decreased and the Eustachian tube is closed (Actually it is passively opened) to equalize the pressure on both sides of the drum.

856
Q

what happens During rapid descent of an airplane?

A

May cause Otitic Barotrauma

  • the external pressure increases and pushes the drum inwards and may rupture it unless the person swallows.
857
Q

what is the function of middle ear muscles?

A
  • Tympanic (attenuation) reflex
858
Q

Definition of Tympanic (attenuation) reflex

A
  • This is a reflex contraction of both tensor tympani and stapedius muscles in response to sounds of high intensity and low frequency (above 80 dB and below 1000 Hz).
859
Q

Mechanism of Tympanic (attenuation) reflex

A
  • The tensor tympani muscle pulls the handle of the malleus inward while the stapedius muscle pulls the stapes outward.
  • These two forces cause the entire ossicular system to develop a high degree of rigidity and greatly reduce the transmission of loud sound.
  • This reflex has a long latent period (about 40 m.sec).
860
Q

Latent period of Tympanic (attenuation) reflex

A
  • This reflex has a long latent period (about 40 m.sec).
861
Q

Importance of Tympanic (attenuation) reflex

A
862
Q

Site of the Inner ear

A
  • It is situated in the petrous portion of the temporal bone (bony labyrinth)
863
Q

Structure of the Inner ear

A
  • The membranous labyrinth is separated from the bony labyrinth by perilymph (as ECF) the sacs contain endolymph (as ICF).
  • It consists of 2 parts:
    a. The cochlea, which is the organ of hearing.
    b. The vestibular apparatus, which is concerned with posture and equilibrium.
864
Q

what divides the choclea?

A
  • The cavity of the cochlea is divided by 2 membranes, vestibular and basilar into 3 compartments (or scalae): scala vestibuli, scala media, and scala tympani.
865
Q

what do scala vestibuli and scala tympani contain?

A
  • The scala vestibuli and scala tympani contain perilymph, which has a high [Na+].
866
Q

How do scala vestibuli and scala tympani communicate?

A
  • They communicate with each other at the apex of the cochlea through a small opening called “the helicotrema”.
867
Q

what does scala media contain?

A
  • The scala media contains endolymph, which has a high [K+]
868
Q

what is scala media bordered by?

A
  • It is bordered by the basilar membrane, which is the site of the organ of Corti.
869
Q

Structue and function of vestibular membrane

A
  • The vestibular membrane is a thin structureless membrane
  • Moves easily and transmits the vibrations from scala vestibuli to scala media.
870
Q

Structure of basilar membrane

A
  • The basilar membrane, on the contrary, is a fibrous membrane and carries the “Organ of Corti”.
871
Q

what is organ of corti? and where is it located?

A
  • The organ of Corti is the sense organ of hearing.
  • It is located on the basilar membrane.
872
Q

Structure of organ of Corti

A
  • It contains the receptor cells (inner and outer hair cells), they are the mechanoreceptors for auditory stimuli.
  • Cilia protrude from the hair cells and are embedded in the tectorial membrane.
  • The hair bundle consists of a large one on one side of the bundle (called kinocilium) while the others are falling away in height to the opposite side (called stereocilia).
  • Inner hair cells are arranged in single rows and are few in number.
  • Outer hair cells are arranged in parallel rows and are greater in number than the inner hair cells.
873
Q

Spiral ganglion

A
  • The spiral ganglion contains the cell bodies of the auditory nerve [cranial nerve (CN) VIII], which synapse on the hair cells.
874
Q

Mechnism of hearing

A
  1. Transmission of sound waves in the outer and middle ear.
  2. Transmission of sound waves in the cochlea (the traveling wave)
  3. Receptor potential and generation of cochlear nerve impulse: “Generation of action potential (MechanoTransduction)”
875
Q

what does Inward movement of the footplate of stapes do?

A
  • increases the pressure in the scala vestibuli.
876
Q

what does increase in the pressure of the scala vestibuli result in?

A

displacement of the cochlear membranes (vestibular and basilar) towards the scala tympani increasing its pressure

877
Q

What does displacement of the cochlear membranes (vestibular and basilar) towards the scala tympani increasing its pressure cause?

A

causing the round window to bulge in the middle ear.

878
Q

Transmission of sound waves in the cochlea (the traveling wave)

A
  • Inward movement of the footplate of stapes increases the pressure in the scala vestibuli.
  • This results in displacement of the cochlear membranes (vestibular and basilar) towards the scala tympani increasing its pressure and causing the round window to bulge in the middle ear.
  • Rapid movements of the tympanic membrane in response to sound waves result in traveling waves that move in the basilar membrane from base to apex.
879
Q

what does Up and down movements of the basilar membrane create?

A
  • create a shearing force in the tectorial membrane that leads to depolarization or hyperpolarization of the receptor cells.
880
Q

what does the opening of K+ channels at the apex of the hair cells cause?

A
  • Because endolymph which surrounds the apex of the hair cells has a higher concentration of K+ than that inside the hair cells, the opening of K+ channels at the apex of the hair cells causes depolarization whereas its closure causes hyperpolarization.
881
Q

what does Bending of the stereocilia away from the kinocilium cause?

A
  • Bending of the stereocilia toward the kinocilium opens the apical channels leading to influx of K+ with cellular depolarization and activation of Ca2+ channels, opening them causing Ca2+ influx, that triggers the release of an excitatory transmitter, probably glutamate, This stimulates the postsynaptic terminals of the sensory neurons.
  • Bending of the stereocilia away from the kinocilium closes the apical channels leading to cellular hyperpolarization and inhibition of Ca2+ channels and release of chemical transmitter.
882
Q

what alters the rate of impulse
discharge along the cochlear nerve?

A
  • hyperpolarization and depolarization of hair cells alter the rate of impulse discharge along the cochlear nerve
883
Q

Receptor potential and generation of cochlear nerve impulse: “Generation of action potential (MechanoTransduction)”

A
  • Up and down movements of the basilar membrane create a shearing force in the tectorial membrane that leads to depolarization or hyperpolarization of the receptor cells.
  • Because endolymph which surrounds the apex of the hair cells has a higher concentration of K+ than that inside the hair cells, the opening of K+ channels at the apex of the hair cells causes depolarization whereas its closure causes hyperpolarization.
  • Bending of the stereocilia toward the kinocilium opens the apical channels leading to influx of K+ with cellular depolarization and activation of Ca2+ channels, opening them causing Ca2+ influx, that triggers the release of an excitatory transmitter, probably glutamate.
  • This stimulates the postsynaptic terminals of the sensory neurons.
  • Bending of the stereocilia away from the kinocilium closes the apical channels leading to cellular hyperpolarization and inhibition of Ca2+ channels and release of chemical transmitter.
  • Thus hyperpolarization and depolarization of hair cells alter the rate of impulse
    discharge along the cochlear nerve.
884
Q

How is sound encoded?

A

The frequency that activates a particular hair cell depends on the location of the hair cell along the basilar membrane.

a. The base of the basilar membrane (near the oval and round windows) is narrow and stiff. It responds best to high frequencies.

b. The apex of the basilar membrane (near the helicotrema) is wide and compliant. It responds best to low frequencies.

885
Q

Structure of the vestibular apparatus

A

A. 3 semicircular canals.
B. 2 small sacs called utricle & saccule.

886
Q

what does each Semi-circular canals (SCC) contain?

A

Each canal contains endolymph & has an enlargement at one of its ends called the ampulla and contains receptors called crista ampullaris

887
Q

Openings of the ampulla of Semi-circular canals (SCC)

A
  • The ampulla of the canal then opens in the utricle by 5 openings.
888
Q

Arrangment of Semi-circular canals (SCC)

A

semicircular canals are arranged at right angles to each.

889
Q

what are the 3 Semi-circular canals (SCC)?

A
  • One horizontal (lateral) canal.
  • One anterior vertical (superior) canal.
  • One posterior vertical (posterior) canal.
890
Q

Co-planar (corresponding) canals

A
  • Each SSC of one side has another SCC on the opposite side lying in the same or parallel plane called the co-planar canal.
891
Q

what are Utricle and saccule?

A
  • 2 small sacs or cavities.
  • Each one contains specific receptor called Macula
  • The macula of the saccule lies in the vertical plane and the macula of the utricle lies in the horizontal plane
892
Q

Structure of Crista ampullaris

A

Consists of a ridge of epithelial cells, These cells are of 2 types:

Hair cells:
- its upper border show ciliary projections. Its base and lateral borders are surrounded by the vestibular nerve endings. The ciliary projections are embedded into a gelatinous covering called cupula.

Supporting cells:
- in between hair cells.

893
Q

Structure of Macula

A
  • Macula has a basic structure similar to crista but the gelatinous layer contains many calcium carbonate crystals called “Otoconia” forming a membrane called “otolith” membrane.
894
Q

Vestibular Hair cells

A

Their upper border show ciliary projections which are of 2 types:

  • Stereocilia; short, numerous, thin. and motile
  • Kinocilium; long, single, thick and tough.
895
Q

Stimulation of vestibular hair cells

A
  • When there is no deflection of cilia, the vestibular hair cells initiate a resting level of impulses along the vestibular nerve.
  • Bending of the stereocilia towards the kinocilium —> opening of mechanosensitive potassium channels —-> depolarization of the haircells —-> increase in the release of the chemical transmitter —-> increase impulse discharge.
  • While bending away from it —> closing of potassium channels —–> hyperpolarization of the hair cells —> release of the chemical transmitter —-> impulse discharge
896
Q

Orientation of hair cells in cristae

A
  • Position and arrangement of stereocilia in relation to the kinocilium is the same in all hair cells of the same crista.
  • In Horizontal SCCs; the Kinocilium towards the utricle.
  • In Vertical SCCs; the Kinocilium away from the utricle.
897
Q

Orientation of hair cells in maculae

A
  • The position of the kinocilium and stereocilia differ from one group of hair cells to another in the same Macula
898
Q

Nervous connections of the vestibular apparatus

A
  • The mother cells of the vestibular nerve fibers located in the vestibular ganglion.
  • The central branches of these fibers enter the brain stem and end on thevestibular nuclei.
899
Q

Functions of the vestibular apparatus

A

Functions of Utricle and saccule = function of Maculae:

  • Detection or orientation of the absolute position of head in space
  • Detection of linear acceleration
  • Initiation of reflexes that maintain body posture

Functions of semicircular canals (SCCs):

  • Perception of angular acceleration (rotation)
  • Initiation of reflexes that maintain body posture
900
Q

Functions of Utricle and saccule = function of Maculae

A
  • Detection or orientation of the absolute position of head in space
  • Detection of linear acceleration
  • Initiation of reflexes that maintain body posture
901
Q

Explain Detection or orientation of the absolute position of head in space function of maculae

A
902
Q

Explain Detection of linear acceleration function of maculae

A

Responsible for perception of linear acceleration as regard:

1- Onset of acceleration.
2- Deceleration (Stoppage).
3- Change in the rate of acceleration.

903
Q

Explain Initiation of reflexes that maintain body posture function of maculae

A
  • When the head position is changed it initiates reflexes that maintain body posture during the change of head position.
  • During acceleration the tone increases in muscles on the same side of acceleration & opposite changes occur on deceleration.
904
Q

Functions of semicircular canals (SCCs)

A
  • Perception of angular acceleration (rotation)
  • Initiation of reflexes that maintain body posture
905
Q

perception of angular acceleration (Rotation) by SCC

A

SCC is responsible for perception of angular acceleration (rotation) as regard:
1- Onset of acceleration.
2- Stoppage of acceleration.
3- Change in velocity of rotation.

906
Q

Events in SCC Without acceleration

A
  • The rate of discharge from both S.C.Cs is equal i.e. symmetrical.
907
Q

Events in SCC With onset of rotation from left to right

A
  • Due to inertia of the endolymph, the cupula of right crista will be displaced towards the utricle i.e. bending the stereocilia towards the kinocilium —> increases the rate of discharge from the right crista.
  • At the same time, the rate of discharge from the left crista is decreased by opposite mechanism —> asymmetrical discharge from both horizontal S.C.Cs with excessive discharge from the right —-> Sense of rotation to the right side.
908
Q

Events in SCC During constant speed rotation

A
  • After 20 seconds, Endolymph will gain the same speed and the cupulae return to the original position, and the rate of discharge return to basal level.
909
Q

Events in SCC On deceleration

A
  • Due to momentum of endolymph, the cupulae on the side of rotation will bend the stereocilia away from the Kinocilium —> decrease the rate of discharge.
  • At the same time, the rate of discharge increases from the Cristae of the opposite side —> false sensation of counter-rotation (Vertigo).
910
Q

Initiation of reflexes that maintain body posture by SCC

A

during exposure to acceleration or deceleration.

911
Q

what causes asymmetrical and excessive SCC stimulation?

A
  • When the person exposed to unusual pattern of motions e.g. after prolonged & rapid rotation.
  • In certain diseases e.g. Menier’s disease,
912
Q

Definition of Autonomic reactions (motion sickness)

A
  • Vertigo (sense of rotation of either the subject or his surroundings)
  • Autonomic reactions (Motion Sickness)
  • Nystagmus
  • Changes in the muscle tone
913
Q

Symptoms of Autonomic reactions (motion sickness)

A
  • The exposure to unusual pattern of motions leads to a group of manifestations called (Motion Sickness).
  • These manifestations include: bradycardia, hypotension, nausea & vomiting and profuse sweating.
914
Q

Cause of Autonomic reactions (motion sickness)

A
  • This is due to the effect of vestibular apparatus on the autonomic centers in the brain stem reticular formation
915
Q

Changes of musce tone due to excessive SCC stimulation

A
  • Stimulation of Crista on one side leads to increase muscle tone in the muscles on that side; at the start of rotation.
  • This change in muscle tone tends to maintain equilibrium, but after stoppage of rotation this change in muscle tone may disturb equilibrium.
916
Q

Definition of Nystagmus

A
  • Means oscillatory movement of the eye balls.
917
Q

Causes of Nystagmus

A
  • Spontaneous
  • Optokinetic
  • Rotational
918
Q

what causes spontaneous nystagmus?

A
  • Irritation of the labyrinth as in Minier’s disease.
  • Neocerebellar Syndrome.
  • Severe defective vision (e.g. in blind).
919
Q

what causes rotational nystagmus?

A

Due to rotation and occurs:

I) At the onset of rotation (for 20-30 sec.).

II) Post-Rotational nystagmus (for 20-30 Sec.)

920
Q

what causes opyokinetic nystagmus?

A
  • During looking out from a moving vehicle, e.g. train, it is initiated by impulses from the retina as the objects are moving across the field.
921
Q

Duration of rotational nystagmus

A

20-30 seconds

922
Q

Duration of post-rotational nystagmus

A

the same

923
Q

Compoinents of rotational nystagmus

A

Fast: in same direction of rotation

Slow: In opposite direction of rotation

924
Q

Compoinents of post-rotational nystagmus

A

the opposite

925
Q

Significance of Rotational nystagmus

A
  • maintain clear vision to keep equilibrium
  • The slow component, keep eyes fixed on certain scenes in field
  • When the eyes movement becomes extreme, The fast component makes eyes move rapidly in the direction of rotation to re-fix on a new scene in field
926
Q

Significance of post-Rotational nystagmus

A
  • impair clear vision, which disturbs equilibrium
927
Q

Compare between rotational & post-rotational nystagmus in terms of:

  • Duration
  • Components
  • Significance
A