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B&B Part 1 > B&B Week 1 > Flashcards

B&B Week 1 Flashcards

1
Q

what are the 3 divisions of the CNS?

A

brain
brainstem
spinal cord

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2
Q

what are the the two divisions of the forebrain?

A

telencephalon

diencephalon

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3
Q

what structures comprise the telencephalon?

A
  1. cerebrum (cerebral hemispheres)

2. basal ganglia

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4
Q

what are the functions of the basal ganglia?

A

associated with a variety of functions, including:

  1. voluntary motor control
  2. procedural learning related to routine behaviors or “habits” (bruxism, eye movements, cognitive, emotional functions)
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5
Q

what structures make up the diencephalon?

A

“anything with -thalamus in it”

  1. thalamus
  2. hypothalamus
  3. subthalamus
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6
Q

what is the function of the thalamus?

A

relaying sensation, spatial sense, and motor signals to the cerebral cortex, along with the regulation of consciousness, sleep and alertness

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7
Q

what is the function of the hypothalamus?

A
  1. certain metabolic processes and other activities of the autonomic nervous system
  2. synthesizes and secretes certain neurohormones, often called hypothalamic releasing hormones, and these in turn stimulate or inhibit the secretion of pituitary hormones
  3. hypothalamus controls body temperature, hunger, thirst, fatigue, sleep and circadian cycles
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8
Q

what is the function of the subthalamus?

A

relay station

takes in sensory info and then passes it on to the cerebral cortex

cerebral cortex also sends info to the thalamus which then sends this info to other systems

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9
Q

what are the two main divisions of the brain stem?

A

midbrain and hindbrain

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10
Q

what are the three divisions of the hindbrain?

A

medulla, pons and cerebellum

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11
Q

what is the function of the midbrain?

A

associated with vision, hearing, motor control, sleep/wake, arousal (alertness) and temperature regulation

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12
Q

what is the function of the pons?

A

involved in motor control and sensory analysis

i.e info from ear enters brain in the pons

it has parts that are important for the level of consciousness and for sleep

some structures are linked to the cerebellum and are thus involved in movement and posture

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13
Q

what is the function of the cerebellum?

A

regulation and coordination of movement, posture and balance

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14
Q

in what two ways can the PNS be classified?

A

by direction

by function

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15
Q

describe how the PNS may be classified by direction

A

there are two types of neurones carrying nerve impulses in different directions:

  1. sensory neurons are afferent neurons with relay nerve impulses toward the CNS
  2. motor neurons are efferent neurons which relay nerve impulses away from the CNS
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16
Q

describe how the PNS may be classified by function

A

PNS is structurally and functionally divided into the somatic and the autonomic nervous system

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17
Q

what is the function of the somatic nervous system?

A

responsible for coordinating the body movements and also for receiving external stimuli

system that regulates activities that are under conscious control

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18
Q

what are the divisions of the autonomic nervous system?

A

sympathetic division
parasympathetic division
enteric division

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19
Q

what is the function of the sympathetic division of the ANS?

A

responds to impending danger

responsible for increase in HR and BP along with the sense of excitement one feels due to the increase of adrenaline in the system (fight or flight)

slows digestive system so more blood is available to carry oxygen to vital organs such as brain, heart and muscles

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20
Q

what is the function of the parasympathetic division of the ANS?

A

resting and relaxed state

constricts pupil, slows heart, dilates blood vessels, stimulates digestive and genitourinary tracts

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21
Q

what is the function of the enteric nervous system?

A

manages every aspect of digestion from esophagus to stomach and small intestine and colon

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22
Q

describe the orientation of the nervous system (i.e anterior, rostral etc…)

A

look on diagram on page 3 of B&B notes

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23
Q

what are the biggest peripheral nerve fibers?

A

A-alpha

13-22 micrometers in diameter

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24
Q

how does diameter correlate with conduction velocity in peripheral nerve fibers?

A

as the diameter gets bigger, conduction velocity gets faster

i.e A-alpha nerve fibers have the biggest diameter and have the fastest conduction velocity

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25
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of A-alpha peripheral nerve fibers?
A
  1. 13-22 micrometers
  2. 70-120 m/sec
  3. alpha-motoneurons, muscle spindle PRIMARY endings, golgi tendon organs, TOUCH

*afferents in muscle spindles (Ib) and tendon organs (Ib)

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26
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of A-beta peripheral nerve fibers?
A
  1. 8-13 micrometers
  2. 40-70 m/sec
  3. tough, kinesthesia, muscle spindle SECONDARY endings

*mechanoafferents of skin (II)

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27
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of A-gamma peripheral nerve fibers?
A
  1. 4-8 micrometers
  2. 15-40 m/sec
  3. touch, pressure, temperature

*muscle spindle efferents

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28
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of A-delta peripheral nerve fibers?
A
  1. 1-4 micrometers
  2. 5-15 m/sec
  3. pain, CRUDE tough, pressure, temperature

*skin afferents (temp and “fast” pain)–(III)

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29
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of B peripheral nerve fibers?
A
  1. 1-3 micrometers
  2. 3-14 m/sec
  3. preganglionic autonomic

*sympathetic preganglionic, visceral afferents

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30
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of C peripheral nerve fibers?
A
  1. 0.1-1
  2. 0.2-2
  3. pain, touch, pressure, temperature, postganglionic autonomic

*skin afferents (“slow” pain) and sympathetic post ganglionic afferents (IV)

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31
Q

list the peripheral nerve fibers in order of descending size and conduction velocity

A 
A-alpha
A-beta
A-gamma
A-delta
B
C
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32
Q

in addition to the (i.e A-alpha) classification system for peripheral nerve fibers, what is another classification system?

A

roman numeral system

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33
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of Ia peripheral nerve fibers?
A
  1. 12-20 micrometers
  2. 70-120 m/sec
  3. muscle spindle PRIMARY endings
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34
Q

are C fibers myelinated?

A

no

A and B are

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35
Q

in the roman numeral classification system for peripheral nerve fibers, what fiber type correspond to the following numerals?

  1. Ia
  2. Ib
  3. II
  4. III
  5. IV
A
  1. Ia–> A-alpha
  2. Ib–> A-alpha
  3. II–> A-beta
  4. III–> A-delta
  5. IV–> dorsal root C
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36
Q

characterize the various roles of A-alpha peripheral nerve fibers

A

can be divided into somatic motor and proprioception functions

in the proprioception functions, you have Ia fibers that work in the muscle spindle and Ib fibers that work in the golgi tendon organ

note that both Ia and Ib fibers are A-alpha nerve fibers

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37
Q

what peripheral nerve fiber is the motor fiber to muscle spindles?

A

A-gamma

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38
Q

what peripheral nerve fiber does fast pain?

A

A-delta (III)

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39
Q

what peripheral nerve fiber does cold?

A

A delta (III)

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40
Q

what peripheral nerve fiber does preganglionic sympathetic?

A

B

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41
Q

what peripheral nerve fiber is most numerous?

A

C (IV)

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42
Q

what peripheral nerve fiber does slow pain?

A

C (IV)

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43
Q

what peripheral nerve fiber does hot?

A

C (IV)

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44
Q

what peripheral nerve fiber does the golgi tendon organ?

A

A-alpha (Ib)

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45
Q

what peripheral nerve fiber does the muscle spindle (proprioception)?

A

A-alpha (Ia)

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46
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of Ib peripheral nerve fibers?
A
  1. 11-19 micrometers
  2. 66-114 m/sec
  3. golgi tendon organs

aka A-alpha

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47
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of II peripheral nerve fibers?
A

aka A-beta

  1. 5-12 micrometers
  2. 20-50 m/sec
  3. touch, kinesthesia, muscle spindle SECONDARY endings
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48
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of III peripheral nerve fibers?
A

aka A-delta

  1. 1-5 micrometers
  2. 4-20 m/sec
  3. pain, crude touch, pressure, temp
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49
Q 
what are the:
1. diameter
2. conduction velocity
3. general function 
of IV peripheral nerve fibers?
A

aka C fibers

  1. 0.1-2 micrometers
  2. 0.2-3 m/sec
  3. pain, touch, pressure, temp
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50
Q

what are sensory receptors?

A

specialized neurons found in the periphery of our bodies which as as transducers

they convert energy from a stimulus into action potentials (APs are the unit of communication used by the nervous system)

sensory systems extract 4 elementary attributes of a stimulus: modality, intensity, duration, location

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51
Q

what are the 4 elementary attributes about a stimulus that sensory systems extract?

A

modality
intensity
duration
location

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52
Q

with regard to the attributes of a stimulus that are extracted by sensory systems:

what is a modality?

A

a type of physical phenomenon that can be sensed… i.e photons (light), chemicals, temp, pressure (sound, touch)

it depends on the type of receptor and where the fiber terminates in the brain

energy in each modality is able to open ion channels in the receptor which is SPECIFIC for that modality

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53
Q

with regard to the attributes of a stimulus that are extracted by sensory systems:

how do sensory systems “read” intensity of s stimulus?

A

the amount of sensation varies with the strength of the stimulus

this is mediated by:

  1. frequency coding/temporal summation
  2. population coding/spatial summation
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54
Q

with regard to the attributes of a stimulus that are extracted by sensory systems:

how do sensory systems “read” duration?

A

perceived duration depends on the rate of adaptation

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55
Q

with regard to the attributes of a stimulus that are extracted by sensory systems:

how do sensory systems achieve localization of a stimulus?

A

precise mapping onto the somatocensory cortex

properties of the sensory system that enable discrimination of location are:

  1. receptor density
  2. size of the receptive fields
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56
Q

how do sensory receptors generate APs in response to a stimulus?

A

the energy contained in the stimulus is used by the receptor to change the membrane potential

this change in potential is the receptor/GENERATOR potential

in most cases, the receptor potential is a DEPOLARIZATION (with + ions flowing in, mostly Na+) of the receptive portion of the sensory axon, caused by application of the sensory stimulus

the exception to this is the photoreceptors (rods and cones) of the eye, in which the receptor potential is a HYPERpolarization

when the receptor potential reaches a threshold, an action potential is generated.

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57
Q

what types of sensory receptors are there?

A

mechanoreceptors
chemoreceptors
thermoreceptors
photoreceptors

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58
Q 
what is the 
1. stimulus
2. mechanism
3. receptor potential
4. example
of mechanoreceptors?
A
  1. mechanical deformation of the receptor
  2. stretching of the receptor membrane opens ion channels
  3. depolarization
  4. pacinian corpuscle
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59
Q 
what is the 
1. stimulus
2. mechanism
3. receptor potential
4. example
of chemoreceptors?
A
  1. chemical
  2. binding of chemical to receptor activates a signalling cascade that opens ion channels
  3. depolarization
  4. taste cells
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60
Q 
what is the 
1. stimulus
2. mechanism
3. receptor potential
4. example
of thermoreceptors?
A
  1. temperature
  2. change in temperature alters the permeability of the membrane to ions
  3. both depolarization and hyperpolarization but the NET effect is depolarization
  4. sensory neurons in the dorsal root ganglia
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61
Q 
what is the 
1. stimulus
2. mechanism
3. receptor potential
4. example
of photoreceptors?
A
  1. electromagnetic radiation (light)
  2. Dark: cGMP levels are high and cGMP-gated Na+ channels are open//the cell is depolarized, resting potential is -40mV//tonic release of neurotransmitter
    Light: rhodopsin in the outer segment of the rod is stimulated by a photon of light//causes activation of a signalling cascade culminating in decreased cGMP levels//cGMP-gated Na+ channels close//K+ channels are unaffected, cell becomes hyperpolarized to -70mV//decrease in neurotransmitter release
  3. dark–> depolarized//light–>hyperpolarized
  4. rods and cones of eye
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62
Q

what is an upper motor neuron?

A

refers to those motor neurons that have cell bodies in the motor cortex or the brain stem

serve to carry motor information down via descending tracts to be delivered to lower motor neurons

apply to the corticospinal tract, corticobulbar tract and rubrospinal tract

lesions in the descending motor systems can be located in the cerebral cortex, internal capsule, cerebral peduncles, brain stem or spinal cord

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63
Q

what is a lower motor neuron?

A

refers to those motor neurons that have cell bodies in the spinal cord including (i.e alpha or gamma motor neurons)

serve to relay motor info from UMNs to the motor end plate

LMNs innervate muscle fibers

lesions of LMNs can be located in the cells of the anterior gray column of the spinal cord or brain stem or in their axons, which constitute the ventral roots of the spinal or cranial nerves
*based on the diagram in the notes, LMNs include the interneuron, and peripheral nerve

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64
Q

how do UMN lesions and LMN lesions compare in terms of:

muscle signs

A

UMN:

  • weakness
  • increased muscle tone
  • increased spasticity
  • little to no muscle atrophy

LMN

  • weakness
  • decreased muscle tone
  • flaccid paralysis of the involved muscles
  • presence of muscle atrophy and fasciculation
  • usually a single or small group of muscles involved
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65
Q

how do UMN lesions and LMN lesions compare in terms of:

deep tendon reflexes

A

UMN–> hyperreflexia

LMN–> hyporeflexia

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66
Q

how do UMN lesions and LMN lesions compare in terms of:

cutaneous reflexes

A

UMN–> absent

LMN–> normal

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67
Q

how do UMN lesions and LMN lesions compare in terms of:

babinski sign

A

UMN–> positive (extensor, big toe up)

LMN–> negative (no response or flexor, big toe down)

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68
Q

how do UMN lesions and LMN lesions compare in terms of:

bing sign

A

UMN–> positive (extensor, foot up)

LMN–> negative (flexor, foot down)

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69
Q

how do UMN lesions and LMN lesions compare in terms of:

clonus

A

UMN–> present

LMN–> absent

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70
Q

how do spinal cord injuries present in terms of UMN vs LMN sx?

A

present as a LMN disorder at the level of the injury and like a UMN lesion caudally (below the lesion)

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71
Q

what is spinal shock?

A

acute UMN lesions may cause flaccid paralysis with decreased tone and decreased reflexes (LMN lesion characteristics) initially before developing spastic paresis gradually over hours to months (more UMN lesion characteristics)

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72
Q

what is Wallerian degeneration?

A

when peripheral nerves are injured, there is peripheral nerve axon degeneration, i.e when the transected distal axon stump is not viable and loses continuity with the cell body and axoplasmic transport systems

distal stump initiates wallerian degeneration within minutes of injury

  1. AXONAL factors–> calcium influx at axonal injury site triggers protein synthesis and growth cone formation (actin-supported extension of a developing or regenerating axon seeking its synaptic target) –> axon fragments into small pieces–> growth factors like neuroregulin are released–> initiates schwann cell dedifferentiation and proliferation
  2. SCHWANN CELL involvement–> myelin sheath breaks down into droplets–> proliferation of undifferentiated schwann cells and these phagocytose myelin droplets–> increased dedifferentiation of ensheathing SCs which form a SC tube around the basal lamina of the regenerating stump
  3. IMMUNE involvement–> breakdown of blood-nerve barrier–> macrophage infiltration to engulf debris from degenerating axons
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73
Q

how does axonal regeneration occur after injury? what factors are involved?

A
  1. axon initiates growth–> transected proximal stump almost immediately initiates axonal regeneration–> multiple growth cones form each with several filopodia expressing cellular adhesion molecules
  2. basal lamina required–> LAMININ and FIBRONECTIN interact with growth cone adhesion molecules to guide axon sprouts
  3. schwann cells–> ensheathing schwann cells encapsulate the basal lamina/sprouting axons forming SC tube/column–> this tube guides growth cones toward innervations target –> the tube/schwann cells secrete growth factors and guidance molecules within the tube–> myelinating SC remyelinate each axonal outgrowth as it grows

**note that nerve regeneration is not perfect–> some axons do not find their innervation target leading to persistent deficits, the remyelination is not as extensive, and the rate of regeneration is 1-4 mm/day

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74
Q

what is a localized mononeuropathy? what are some examples?

A

fits specific peripheral nerve or nerve root distribution in the limb

i.e carpal tunnel
i.e nerve trauma site
“makes sense”

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75
Q

what is a regional neuropathy? what are some examples?

A

involves all nerve in a compartment of distal to a certain level of the limb

i. e compartment syndrome
i. e occluded major artery territory

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76
Q

what is a generalized polyneuropathy? what are some examples?

A

involves multiple sites, transient or otherwise

i.e patchy in MS

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77
Q

what % of diabetics will develop neuropathy within 25 years of diagnosis?

A

50%

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78
Q

what axons are affected first in diabetic neuropathy?

A

longest axons are affected first, resulting in a glove and stocking pattern of sensory and motor deficits

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79
Q

RE: neuropathies

define numbness

A

loss of sensation

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80
Q

RE: neuropathies

define dysesthesia

A

abnormal sensation on stimulus

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81
Q

RE: neuropathies

paresthesia

A

burning, pricking, tingling with NO stimulus

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82
Q

what are some examples of sensory neuropathy symptoms

A 
numbness
dysesthesia
paresthesia
neuropathic pain
loss of proprioception/balance
sensory loss results in injuries to extremities (i.e ulceration in diabetic foot)
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83
Q

what are some symptoms of motor neuropathy

A

weakness, depressed reflexes, muscle atrophy

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84
Q

what are some symptoms of autonomic neuropathy

A

can include orthostatic hypotension, diarrhea, impotence, incontinence

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85
Q

what is the etiology of diabetic neuropathy?

A

multifactorial etiology resulting in mixed axon loss and/or segmental demyelination (affects BOTH myelinated and unmyelinated axons)

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86
Q

what is the pathogenesis of diabetic neuropathy?

A
  1. vascular–> hyperglycemia causes hyperglycosylation of proteins–> causes constriction and capillary wall thickening and neural ischemia
  2. neuronal–> unmetabolised glucose enters the polyol pathway–> this forms sorbitol in neurons–> this stresses the neuronal membrane via osmotic water influx//in addition, there is oxidative stress from disrupted glucose metabolism
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87
Q

what is the etiology of compression neuropathy?

A

trauma, inflammation, tumour, entrapment in fibro-osseous tunnel (i.e carpal tunnel)

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88
Q

what is the pathogenesis of compression neuropathy?

A
  1. axon loss and segmental demyelination can occur
  2. pressure and stretch directly damage nerve membrane, black axonal flow and cause axon thinning
  3. ischemia in nerve following blood vessel compression
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89
Q

what is the procedure of an EMG?

A

apply a depolarizing electrical pulse to a peripheral nerve and measure the chance in electrical activity in the target muscle

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90
Q

what is the CMAP? (re: EMGs)

A

compound muscle action potential

represents summation of action potential from several muscle fibers in the same area

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91
Q

what does a decrease in CMAP amplitude on an EMG indicate?

A

usually due to axon loss or severely demyelinated axons (that will result in AP failure)

demyelination can also cause a decrease in amplitude through temporal dispersion

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92
Q

what does an increase in distal motor latency (which is the time from stimulation to onset of wave) usually indicate on am EMG?

A

usually due to axon demyelination

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93
Q

what does CMAP temporal dispersion on an EMG usually cause?

A

usually due to unequal demyelination of adjacent nerve fibers

this will result in some APs to arrive sooner than others which causes phase cancellation

in a normal nerve, responses arrive at the recording electrode almost together

in the case of unequal demyelination the responses arrive at different times causing phase cancellation leading to temporal dispersion (i.e lower amplitude with multiple peaks on wave)

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94
Q

how can an EMG be used to calculate conduction velocity?

A

measured by stimulation of the peripheral nerve at two sites and then applying the calculation:

difference in latency/difference in distance

decreased velocity is due to demyelination

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95
Q

what is the F wave?

A

EMG

measuring the M wave (response to the stimulation of alpha motor neuron) gives info about the peripheral segment of the nerves but yields no info on the proximal nerve roots

the F wave results from an antidromic AP that travels back to the nerve root via the alpha motor neuron, into the anterior horn cell, depolarizes the cell and causes an AP to shoot back out the axon into the target muscle

F wave latency therefore gives info on the proximal nerve root

it is useful in guillain barre because in the initial stages of the disease the proximal nerve roots are often affected before the distal parts of the nerve

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96
Q

in what disease are F waves of EMGs particularly useful in diagnosis?

A

guillain barre, because proximal nerve roots are often affected before distal parts of the nerve and the F wave gives info on this

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97
Q

MAKE SURE TO GO OVER ANATOMY

A

DO IT

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98
Q

what part of embryonic development of the CNS occurs in weeks 1 and 2?

A

development of the bilaminar embryonic disc

embryo goes from the 2–> 4–> 8 cell stage

forms the morula then the early blastocyst (with an inner cell mass and the trophoblast)–> then the late blastocyst

the inner cell mass goes thru segregation, delamination and hypoblast formation to form the epiblast on the outside, blastocoele and hypoblast on inside

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99
Q

what part of embryonic development of the CNS occurs in week 3?

A

gastrulation

  • establishes 3 germ layers, axial orientation of the embryo and induces NEURAL PLATE
  • primitive streak formed from migration of epiblasts to form a clump, which then migrates through the primitive groove to form mesoderm and endoderm layers
  • primitive streak migrates rostral to caudal and gives rise to the neural plate
  • epiblast also directly creates the ectoderm layer
  • hypoblast gives rise to endoderm of yolk sac and extra-embryonic mesoderm (no embryonic endoderm input)
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100
Q

what part of embryonic development of the CNS occurs in week 3 and 4?

A

neurulation

  • formation of NEURAL PLATE, NEURAL FOLDS and NEURAL TUBE are induced by notochord signals (sonic hedgehog)
  • cranial neural tube closure involves both median and lateral hinge points creating a diamond shaped tube which gives rise to brain ventricles in the neural canal (spinal cord neural tube only has a median hinge point)
  • neural crest cells migrate from the neural tube–> these are extremely pluripotent stem cells for cranial and sensory nerves
  • neural tube closure occurs in a wave like pattern starting in several locations–> anancephaly results if it doesn’t zip at wave in brain region and spina bifida if doesn’t zip at wave in spinal region
  • neuropores are the final points of closure–> anterior closure failure is life threatening whereas posterior failure just causes defects
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101
Q

what part of embryonic development of the CNS occurs in week 4 and 5?

A

brain development

develops from neural tube section cranial to 4th somites

3 primary brain vesicles: forebrain (prosencephalon), midbrain (mesencephalon) and hindbrain (rhombencephalon)

as the brain grows it bends and forms 3 flexures–>

  1. cephalic flexure (midbrain)
  2. cervical flexure (separates brain from spinal cord)
  3. pontine flexure (separates hindbrain)
    - -> these flexures create two secondary brain vesicles –> the forebrain divides into the telencephalon (cerebrum) and diencephalon (-thalamus)//the midbrain doesnt divide and becomes the mesencephalon//the hindbrain divides into the metencephalon (pons, cerebellum) and myelencephalon (medulla)

cerebral hemispheres rapidly enlarge and separate into lobes, glia, and neurons proliferate

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102
Q

what sections of the neural tube form the brain?

A

develops from neural tube section cranial to the 4th somites

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103
Q

list the 3 primary brain vesicles in brain development in the embryo

A
  1. forebrain/prosencephalon
  2. midbrain/mesencephalon
  3. hindbrain/rhombencephalon
104
Q

name the flexures formed by the developing brain and their locations

A

week 4/5

as the brain grows it bends and forms 3 flexures–>

  1. cephalic flexure (midbrain)
  2. cervical flexure (separates brain from spinal cord)
  3. pontine flexure (separates hindbrain)
105
Q

does the developing spinal cord form flexures like the developing brain does?

A

no

106
Q

how do the flexures formed in the developing brain relate to structure and function in the brain?

A

the flexures alter the orientation of sensory (dorsal) areas (alar plate) and motor (ventral) areas (basal plate)

107
Q

how does the position of the spinal cord change with development?

A

at the beginning of the third month–> coccyx

at birth–> L3

adult–> L1/L2
-remnants of pia matter–the filum terminale–are surrounded by filum of the dura // angulated spinal nerves from cauda equina

108
Q

list the characteristics of an action potential

A
  1. all or nothing event
  2. triggered when membrane potential reaches threshold
  3. initial depolarization (voltage gated Na+ open)
  4. return to RMP with hyper-polarization (voltage gated K+ channels open)
  5. APs are regenerative events
  6. APs are driven by a positive feedback cycle once threshold is reached
  7. generator potentials leading up to APs are graded–> larger stimulus results in a larger depolarization
109
Q

describe the state of the Na+ and K+ channels in the following phases of an AP:

  1. resting phase
  2. rising phase
  3. falling phase
  4. afterhyperpolarization
A
  1. both closed
  2. Na+ channels open, K+ channels closed
  3. Na+ time dependent gate closed, K+ open
  4. both voltage and time dependent gates closed, K+ open
110
Q

what is the absolute refractory period of an AP?

A

voltage gated Na+ channels have not reset yet

no AP can be generated

approx 1.5 ms after initial stimulus

111
Q

what is the relative refractory period of an AP?

A

number of voltage gated Na+ channels that have reset is less than the number at RMP, but sufficient to generate an AP

threshold is elevated therefore a greater than normal stimulus is required to generate an AP

approx 2.5 ms after initial stimulus

112
Q

how do APs propagate?

A

by passive (electrotonus) and active propagation

113
Q

what is electrotonus and how does it propagate an AP?

A

passive propagation

positive charge introduced into axon will depolarize that region

positive charge is attracted to adjacent negatively charged region of membrane and is repulsed by the next positive charged to be introduced

suffers from electronic decay (passive leaking of + charge)

electrotonus is dependent on axial resistance and membrane resistance (length constant)

114
Q

how can you increase the distance travelled by an AP under passive propagation?

A

larger diameter of axon (less axial resistance)

introduce myelin to increase membrane resistance and prevent leaking of charge

115
Q

what is active propagation of an AP?

A

voltage gated channels along the axon regenerate the depolarization

116
Q

how does membrane capacitance influence rate of AP propagation?

A

the greater the amount of capacitance, the more charge that can be stored and therefore more charge is required to change the membrane potential

capacitance is directly proportional to surface area and inversely proportional to the distance between conductive plates

myeline serves to increase the distance between conductive plates and therefore reduce capacitance and increase the rate of AP propagation

117
Q

what is saltatory conduction of APs?

A

on myelinated axons, active AP propagation “hops” from node of ranvier to node of ranvier

between nodes, the AP travels passively as the capacitance of the membrane is low, the charge time of the membrane is short, and depolarization propagates rapidly

at the nodes of ranvier, there is active propagation as the membrane capacitance is greater where there is no myelin, the charge time of the membrane is longer and the action potential slows

118
Q

what is ataxia?

A

incoordination and unsteadiness due to the brain’s failure to regulate the body’s posture and regulate the strength and direction of limb movements

119
Q

what often causes ataxia? where is the lesion (PNS or CNS)?

A

often a consequence of disease in the brain, specifically in the cerebellum, which lies beneath the back part of the cerebrum

location of lesion is the CNS

motor deficit

120
Q

what is numbness/parasthesia?

A

parasthesia is sensation of tingling, burning, pricking or numbness of a person’s skin with no apparent long term physical effect

“pins and needs”

121
Q

where is the location of the lesion in numbness/parasthesias?

A

PNS

sensory deficit

122
Q

list the clinical features required for diagnosis of guilllauin barre

A
  1. progressive weakness of both arms and legs
  2. areflexia
  3. clinical features supportive of diagnosis:
    - progression over days to 4 weeks
    - relative symmetry of signs
    - mild sensory sx or signs
    - cranial nerve involvement (bifacial palsies)
    - recovery beginning 2-4 weeks after progression ceases)
    - autonomic dysfunction
    - absence of fever at onset
123
Q

what are two lab features supportive of GB diagnosis?

A

elevated CSF protein with less than 10 cells/uL

electrodiagnostic features of nerve conduction block or slowing

124
Q

what is the workup for GB syndrome?

A
  1. exclude other possible causes based on clinical hx, exam and lab tests
  2. lumbar puncture (may be normal in first week or two of the illness)–> typical findings include elevated CSF protein with few mononuclear leukocytes (albuminocytologic dissociation) in 80-90% of patients…. elevated CSF cell counts is an expected feature in cases associated with HIV seroconversion
  3. EMG/NCS–> may be normal in the first 10-14 days of the disease. the earliest electrodiagnostic abnormality is prolongation or absence of H-reflexes
    - EMG/NCS evidence of demyelination (prolonged distal latency, conduction velocity slowing, conduction block, temporal dispersion and prolonged F waves) in two or more motor nerves confirms diagnosis of ACUTE INFLAMMATORY DEMYELINATING POLYRADICULOPATHY (AIDP) in the appropriate clinical context
125
Q

what is the earliest electrodiagnostic test abnormality in GBS?

A

prolongation or absence of H waves

126
Q

what lab test should be done in the context of suspected GBS?

A
  1. CBC–> may reveal early leukocytosis with left shift. Electrolytes are tested to exclude metabolic causes
  2. heavy metal testing
  3. urine porphyria screen
  4. creatine kinase
  5. HIV titers
  6. neuroimaging of the brain and spinal cord if diagnosis is uncertain–> nerve root enhancement may be seen on the MRI of the lumbosacral spine
  7. antibodies against ganglioside GQ1b may be present in up to 90% of patients with Miller-Fisher syndrome (triad of areflexia, ataxia, ophthalmoplegia)//IgG antibodies against ganglioside GM1 may be associated with AMAN (acute motor axonal neuropathy)//there are no antiganglioside antibodies commonly associated with ADIP
  8. in equivocal cases (especially if peripheral nerve vasculitis is a concern) a nerve biopsy may aid in confirming the diagnosis of GBS–>sensory nerve biopsies demonstrate segmental demyelination with infiltration of monocytes and T cells into the endoneurium; axonal loss is commonly seen in sensory nerve biopsy specimens with GBS
127
Q

what might you see on a nerve biopsy of a patient with GBS?

A

sensory nerve biopsies demonstrate segmental demyelination with infiltration of monocytes and T cells into the endoneurium; axonal loss is commonly seen in sensory nerve biopsy specimens with GBS

128
Q

what might a person with antibodies against ganglioside GQ1b have?

A

Miller-Fisher syndrome (ataxia, areflexia, ophthalmoplegia)

129
Q

what signs and symptoms in a patient might suggest GBS?

A

muscle weakness and abnormal sensation

areflexic (specific for LMN disorder)

conduction studies:

  • increased distal motor latency, decreased conduction velocity, CMAP temporal dispersion suggesting demyelination
  • F wave latency suggests possible proximal nerve root involvement

increased protein without increase cellularity in CSF

130
Q

why do UMN lesions cause hyperreflexia?

A

less descending inhibition

131
Q

what is the etiology of GBS?

A

caused by an autoimmune destruction of myelin and/or axons in the peripheral nervous system

exact mechanisms are unclear, but damage is probably due to aberrant immune responses to various components of the axon membrane or its myelin sheath

in about two thirds of cases of GBS, an antecedent infection 1-4 weeks prior to the onset of neuro sx can be discerned–>most commonly:
Viruses–> CMV, HIV, EBV, HBV
Bacteria–> CAMPYLOBACTER (most common!!!!!!), mycoplasma, H. influenza
Drugs–> gold, penicillin
Other–> surgery, delivery, lymphoma

132
Q

what is the prognosis for someone with GBS?

A

approx 85% of people with GBS achieve a full functional recovery within several months to a year, although minor findings on exam (such as areflexia) may persist and patients often complain of continued symptoms including fatigue and neuropathic pain

133
Q

what is the mortality rate for GBS in optimal settings?

A

less than 5%

death usually results from secondary pulmonary complications

134
Q

what is a poor prognostic marker in GBS?

A

outlook is usually worse in patients with severe proximal motor and sensory axonal damage

such axonal damage may be either primary or secondary in nature but in either case successful regeneration cannot occur

other poor prognostic markers:

  • advanced age over 65
  • a fulminant or severe attack (reach plateau by 7 days)
  • a delay in the onset of tx
  • ventilator support required
  • prominant axonal involvement
135
Q

what % of people with GBS (typical GBS) have one or more late relapses?

A

between 5-10%

such cases are then classified as chronic inflammatory demyelinating polyneuropathy (CIDP)

136
Q

what is the treatment for GBS?

A

either high dose IV immune globulin (IVIg) or plasmapheresis can be initiated (are equally effective for typical GBS)

a combo of the two therapies is not significantly better than either alone

functionally significant improvement can occur towards the end of the first week of tx but may be delayed for several weeks (patients who improve early may also relapse however)

occasional patients with very mild GBS who have plateaued before seen may be managed without IVIg or PE

137
Q

what is IVIg often the initial therapy chosen for GBS?

A

ease of administration and good safety record

138
Q

how must a worsening case (w tx) of GBS be managed?

A

most patients would require monitoring in a critical care setting with particular attention to:

  • vital capacity
  • heart rhythm
  • BP
  • nutrition
  • DVT prophylaxis
  • CV status
  • early consideration of tracheotomy (after 2 weeks intubation)
  • chest physiotherapy

frequent turning and assiduous skin care are important as are daily ROM exercises to avoid joint contractures and daily reassurances as to the generally good outlook of the disease

139
Q

what % of patients with GBS require ventilatory assistance?

A

30%

sometimes for prolonged periods of time

140
Q

what embryonic structure gives rise to the motor neurons to skeletal muscle?

A

pharyngeal arches

141
Q

what are neurons?

A

basic unit of structure of the CNS

excitable cells in the CNS

transmit signal via chemical or electrical transmission

classified according to morphology

142
Q

describe the pathway of information in a neuron in the CNS

A

neurons receive info from their dendrites

signals travel to the cell body

signalling down the axon via a synapse to other neurons

a chain of neurons is a pathway (i.e the visual pathway)

a bundle of axons is a tract (i.e the optic tract)

143
Q

what are microglial cells?

A

immune function of CNS

144
Q

what are astroglia?

A

interact with neurons at the synapse–> can modulate synaptic transmissions

are an important part of the B/B barrier

regulate what comes into CNS and what doesn’t

145
Q

what are oligodendrocytes?

A

do myelination in the CNS

146
Q

what are polydendrocytes?

A

precursor cells of the CNS

147
Q

what part of the neuron receives APs?

A

primary dendrites

148
Q

what happens to the AP at nodes of ranvier?

A

it is regenerated via active propagation

149
Q

what are 4 characteristics of APs? how do they achieve these 4 characteristics?

A

unidirectional–> achieved through refractory period

fast–> decrease in capacitance of axons via myelin and decrase in resistance via increased axon diameter

efficient–> APs generated only at nodes of ranvier not along entire length

simple–> all or none response, binary system

150
Q

what are neurotransmitters and what do they do?

A

released by presynaptic neurons at a chemical synapse

binds to neurotransmitter receptors which are coupled to

  1. ion channels–> ionotropic receptors
  2. intracellular signalling cascade–> metabotropic receptors (will often open a channel downstream)

they can result in either excitatory or inhibitory signals

151
Q

where are neurons located in the brain?

A

located in grey matter

  • cortical band
  • deep nuclei of forebrain
  • central grey in spinal cord

fibre tracts connect neurons in different areas

152
Q

what is grey matter? white matter?

A

grey–> where the neurons are

white–> where the tracts are

153
Q

what three parts does the neural tube divide into?

A

prosencephalon
mesencephalon
rhombencephalon

154
Q

what does the prosencephalon divide into?

A

telecephalon

diencephalon

155
Q

what does the telencephalon become?

A

cerebral hemispheres

156
Q

what does the diencephalon become?

A

thalamus
hypothalamus
subthalamus

157
Q

what does the mesencephalon become?

A

midbrain (mesencephalon doesn’t further subdivide)

158
Q

what does the rhombencephalon divide into?

A

metencephalon

myelencephalon

159
Q

what does the metencephalon become?

A

pons

cerebellum

160
Q

what does the myelencephalon become?

A

medulla

161
Q

what is a nerve?

A

bundles of fascicles containing many axons

162
Q

what is a motor unit?

A

a motor neuron and the muscle fibers it innervates

basic functional unit of motor control

163
Q

what are the two different kinds of somatic motor neurons?

A
  1. alpha motor neurons
    - skeletomotor–> innervates extrafusal muscle fibers
  2. gamma motor neurons
    - innervates intrafusal fibers (within muscle spindle)
164
Q

what do small motor units do? large ones?

A

small–> i.e 10 fibers per motor neuron–> fine movements i.e eyes

large–> i.e 1000s of fibers per neuron–> gross movements ie leg muscles

165
Q

what are muscle spindles?

A

stretch sensitive mechanoreceptors

found in virtually all skeletal muscle

small, elongated structure scattered among and PARALLEL to the contractile extrafusal fibers

connective tissue sheath surrounding intrafusal fibres

provide information about muscle length and velocity of contraction to the CNS via discharge pattern of muscle spindle

166
Q

in what muscles are muscle spindles particularly dense?

A

in muscles concerned with fine, manipulative tasks (i.e intrinsic hand muscles)

highest density in neck muscles

167
Q

what are intrafusal fibers?

A

inside muscle spindle

modified muscle fibers lacking myofibrils in the center

1/3 length of extrafusal fibre

168
Q

how many types of intrafusal fibers are there?

A

3–> related to how they are innervated

types:
Bag2
Bag1
Chain

169
Q

what types of intrafusal fibers are the largest?

A

bag2

170
Q

describe Bag2 intrafusal fibers

A

largest

no striations in middle region and swells to enclose nuclei

171
Q

describe chain intrafusal fibers

A

half as long as bag, smaller diameter

has a row of nuclei in the middle (“chain”)

172
Q

what does a typical spindle contain in terms of types of intrafusal fibers?

A

1 Bag1
1 Bag2
4 chain fibers

but there is much variation

173
Q

what is the muscle spindle sensory innervation?

A
  1. large diameter group Ia afferents–> enters capsule and branches; unmyelinated terminals wrap around fiber–> annulospiral ending on nucleated bag1, bag2 and chain fibers
  2. smaller group II afferents that enter with Ia afferents –> unmyelinated spray terminals on one end of fiber–> Bag2 and chain fibres
174
Q

what is the motor innervation for muscle spindles?

A

gamma or fusimotor neurons

2 types:

  1. static –> Bag2 and chain
    - when you’re at rest, postural
  2. dynamic–> Bag 1
    - tuning things around movement
175
Q

what types of intrafusal fibers fo static gamma neurons innervate in the muscle spindle? dynamic?

A

static–> bag 2 and chain

dynamic–> bag 1

176
Q

what type of information do Group Ia fibers in the muscle spindle give? II?

A

Ia: velocity and length info about the muscle

II: only length info

177
Q

how does the activity of gamma motor neurons affect the muscle spindle?

A

activity of gamma dynamics increases velocity sensitivity

activity of gamme statics increases length sensitivity

178
Q

what is responsible for muscle tone? how?

A

muscle spindles

they fire action potentials when the muscle is at resting length

signals alpha motor neurons in the ventral horn –> tonic excitation causes contraction in muscle extrafusal fibres resulting in resting muscle tension (“muscle tone”)

firing rates of the gamma motor neurons can change in different situations

179
Q

what is the stretch reflex?

A

involves the muscle spindle

muscle stretch initiates contraction–> monosynaptic and polysynaptic excitatory connections between group Ia and II afferents and alpha motor neurons

180
Q

what is a myotatic unit?

A

collection of nervous pathways controlling a single joint

181
Q

what is a monosynaptic stretch reflex?

A

one sensory neuron and one somatic motor neuron

182
Q

what is reciprocal inhibition?

A

relaxation of antagonist muscle during contraction of the agonist

divergent pathways in spinal cord and inhibitory interneurons –> i.e when quad flexes, hamstring relaxes allowing leg to extend

mediated by Ia inhibitory interneuron –> receives convergent input from corticospinal tract and other descending pathways–> there is flexible control

183
Q

what is the epineurium?

A

surrounds entire nerve

184
Q

what is the perineurium?

A

encapsulates bundles of axons called fascicles (has blood supply)

185
Q

what is the endoneurium?

A

contained within the perineurium and consists of axons

186
Q

what is the blood-nerve barrier?

A

exists between inner perineurium and endothelial cells of the microvasculature within endoneurium

there is a filtering that happens between all components of the nervous system and the blood supply

187
Q

if you have a dull, aching, burning pain, what muscle fiber types is likely involved?

A

C

188
Q

what peripheral nerve classification scheme is typically used for motor neurons?

A

ABC

189
Q

what is the ABC system based off of? the numeral system?

A

ABC is based on conduction velocity and numeral is based off of diameter

190
Q

what is the numeral system exclusively used for?

A

sensory axons

191
Q

what do axons require to be viable? why?

A

require cytoplasmic continuity with the soma for viability

antrgrade and retrograde axoplasmic transport

192
Q

what are the two types of schwann cells associated with axons?

A

myelinating and ensheathing

ensheathing ones maintain the basal lamina that surrounds the axon and the myelin

193
Q

what is the mildest form of peripheral nerve damage?

A

segmental demyelination

aka grade I injury or NEUROPRAXIA

schwann cells are compromised i.e in an ischemic or inflammatory environment –> this might not mean much for sensory info because APs are still propagating but this matters for motor as it affect synchronocity of APs to muscle groups

complete demyelination of a segment results in slower APs and Na+ channel redistribution from the node of Ranvier

complete demyelination of several adjacent segments results in AP failure (need demyelination of multiple segments because Na+ channel redistribution cannot cover for the AP loss thru propagation thru unmyelinated axons)

194
Q

what does remyelination require in a damaged peripheral nerve?

A

trophic factors and cytokines released by damaged schwann cells and affected axons

this reciprocal signalling triggers the proliferation of undifferentiated schwann cells

some of these new schwann cells differentiate into myelinating cells and wrap around the bare axon (takes time)

195
Q

what is the M wave on an EMG?

A

a CMAP

evoked by peripheral nerve stimulation of alpha motor neurons

generated during muscle contraction

demyelination causes prolonged M wave latency and maybe temporal dispersion –> if several segments are demyelinated you get AP loss and thus reduced M wave amplitude

196
Q

what is grade II and III peripheral nerve injury?

A

ii–> axonotmesis
III–> neurotmesis

cutting of axon itself resulting in a gap in the axon

transected distal axon stump is not viable as it loses continuity with cell body and axoplasmic transport systems

distal stump initiates wallerian degeneration within minutes of injury

197
Q

how does axon loss affect the M wave on an EMG?

A

reduces amplitude

198
Q

are all motor nerves myelinated?

A

yes

199
Q

are all sensory and autonomic nerves myelinated?

A

no

200
Q

what types of nerve fibers are associates with the autonomic system?

A

A-delta and C

201
Q

what types of nerve fibers are associated with motor neurons?

A

A-alpha

202
Q

what are “negative” sensory symptoms?

A

numbness, hypoesthesia

arise because you are NOT getting info

203
Q

what are “positive” sensory symptoms?

A

tend to be more problematic

spontaneous pain–> parasthesias, burning pain, shock like pain (often pinched nerves ie sciatica)

evoked pain–> allodynia (normally non painful stimuli) and hyperalgesia (normally painful stimuli is extra painful)

204
Q

what added symptoms in addition to a neuropathy/neuropathic pain would be suggestive of autonomic involvement?

A

bladder
erectile dysfunction
orthostatic hypotension
change in sweating (increased or decreased)
postprandial bloating, diarrhea, nausea, vomiting

205
Q

is there is a motor neuropathy, what nerves are affected first?

A

longest and thinnest–> you get tripping, stumbling symptoms or inability to fine motor skill things

its a length dependent problem which is why you get distal weakness

206
Q

what patterns of neuropathy are suggestive of a problem in the
1, spinal cord
2. brain
3. peripheral neuropathy

A
  1. problems from a specific spinal level downwards
  2. problems are all on one side of the body
  3. glove and stocking
207
Q

how do you know whether a peripheral neuropathy is axonal or demyelinating?

A

axonal neuropathies are length dependent (i/e long thing axons affected first), slowly progressive, sensory more than motor sx, lose ankle jerks–> example is diabetic neuropathy

demyelinating neuropathies affect the arms and legs, are rapid, affect both motor and sensory and result in areflexia–> example is GBS

208
Q

what is an example of a hereditary neuropathy?

A

charcot marie tooth 1A

209
Q

what happens if a peripheral nerve is injured and the gap is too wide for the nerve to regenerate itself?

A

you get fibrosis and fibrotic scare tissue around the regenerating end that cannot find the other end of the damaged axon to bind to and then you get a neuroma

all neuromas come from cut peripheral nerves

210
Q

when you are repairing and injured nerve, why do you have to trim the bruised/damaged ends?

A

otherwise the scar tissue remains blocking regeneration

211
Q

what nerve is often used as a nerve graft?

A

sural nerve

212
Q

how long before there are irreversible muscle changes as a result of a peripheral nerve injury?

A

about 12 months–> without nervous input, muscles start degenerating

the nerve gives it trophic factors that “keeps the muscle going”

the muscle would remain non-contractile even if the axons reached it later

213
Q

what is early management for compression syndromes?

A

non operative

i.e splint and activity modification

214
Q

what are exteroreceptors?

A

respond to stimuli from outside the body

215
Q

what are intero- and proprioceptors?

A

provide info about whats happening inside the body and position

216
Q

what nerves carry the special senses?

A

cranial nerves

217
Q

what are the special senses and what specific cranial nerves carry each of them?

A

olfaction–> CN I
vision–> CN II
taste–> CN VII and IX
hearing and balance–> CN VIII

218
Q

what is a pacinian corpuscle?

A

a mechanoreceptor with stretch sensitive ion channels

in the center of the corpuscle is an inner bulb with a single afferent unmyelinated nerve ending

219
Q

what are the two spatial aspects of the sensory experience?

A

the ability to locate the site of the stimulus (precise mapping onto the somatosensory cortex) and the ability to distinguish two closely placed stimuli

220
Q

what is the two point discrimination test?

A

used to check ability to distinguish between two points pushing on the skin

helps assess nerve damage

i.e on the back about 30-40 mm is the smallest distance we can distinguish between but on the fingers we can distinguish between 1-2 mm because of increased receptor density

you need to have at least on sensory receptor in between the two stimulated receptors in order to distinguish two different stimuli (two adjacent receptors will read as one stimulus)

221
Q

what is lateral inhibition?

A

in the sensory system (i.e pushing on two points on the back) lateral inhibition blocks the lateral spread of excitatory signals and therefore increases the degree of contrast in the sensory pattern perceived in the cortex

222
Q

what is the pharyngeal apparatus?

A

a group of structure which contribute to form the head and neck

it consists of four parts:

  1. pharyngeal arches
  2. pharyngeal pouches
  3. pharyngeal grooves
  4. pharyngeal membranes
223
Q

what are the pharyngeal arches?

A

part of the pharyngeal apparatus

paired ridges of tissue which each contain four things:

  1. a muscle component
  2. cartilage
  3. cranial nerve
  4. aortic arch
224
Q

what are the pharyngeal pouches?

A

part of the pharyngeal apparatus

paired segments of balloon-like pockets separating the pharyngeal arches internally

225
Q

what are the pharyngeal membranes?

A

part of the pharyngeal apparatus

formed when the epithelia of the grooves and pouches approach each other

226
Q

how many pharyngeal arches are formed during the embryonic period? what problems can arise?

A

each arch is covered externally with ectoderm and internally by endoderm

there are 6 arches formed during the embryonic period but the 5th and 6th arches are rudimentary and are not visible on the surface of the embryo

most of the head and neck congenital anomalies originate during transformation of the pharyngeal apparatus into its adult derivatives

227
Q

where do neural crest cells originate from?

A

neural tube

228
Q

what do the neural crest cells do?

A

migrate into the ventral part of the pharyngeal arches and form different tissues in this region including cartilage, bone, dentins, tendon, dermis, meninges, sensory neurons and ganglia

the muscles and vascular endothelia are derived from original mesenchyme

229
Q

what forms the bones, muscle, dermis and connective tissue in the dorsal region of the head?

A

paraxial mesoderm

230
Q

what plays the major role in the formation of the face, nasal cavities, mouth, pharynx, larynx and neck?

A

pharyngeal arches

231
Q

what is the first pharyngeal arch? what are its two portions and what do they give rise to?

A

mandibular arch

  1. maxillary prominence–> gives rise to maxilla, zygomatic bone and squamous part of the temporal bone
  2. mandibular prominence–> gives rise to the mandible

this arch has the main role in the formation of the face

232
Q

what is 1st arch syndrome?

A

a pattern of anomalies arising from insufficient migration of NCCs into the 1st pharyngeal arch

deformed auricle of external ear, defect in cheek between the auricle and mouth, hypoplasia of the mandible, macrostomia (large mouth)

233
Q

what cranial nerve supplies the 1st pharyngeal arch?

A

CN V (V2 and V3 only)

supply the sensory innervation of the head and part of the neck and motor innervation of the muscles of MASTICATION

234
Q

what cranial nerve supplies the 2nd pharyngeal arch?

A

CN VII

235
Q

what cranial nerve supplies the 3rd pharyngeal arch?

A

CN IX

236
Q

what cranial nerve supplies the 4th and 6th pharyngeal arch?

A

CN X

4th–> superior laryngeal branch of vagus nerve
6th–> recurrent laryngeal branch of vagus nerve

237
Q

what is another name for first arch cartilage?

A

meckels cartilage

238
Q

what does the first arch cartilage form?

A

two of the middle ear ossicles (malleus and incus) and mainly the horseshoe shaped primordium of the mandible and guides its early morphogenesis

the cartilage disappears as the mandible develops around it by intramembranous ossification

239
Q

what is another name for 2nd arch cartilage?

A

reichert cartilage

240
Q

what does 2nd arch cartilage form?

A

one of the middle ear ossicles (stapes), the styloid process of the temporal bone and a part of the hyoid bone

241
Q

what does the 3rd arch cartilage form?

A

ossifies to form the rest of the hyoid bone which is not formed by the 2rd arch cartilage

242
Q

what do the 4th and 6th arch cartilages form?

A

fuse to form the laryngeal cartilages (except for the epiglottis which is derived from mesenchyme)

243
Q

what do the 1st pair of pharyngeal grooves become?

A

persist as the external acoustic meatus (only grooves to persist to adulthood)

244
Q

what does the 1st pharyngeal membrane become?

A

the tympanic membrane

it is the only pharyngeal membrane that persists

245
Q

what does the 1st pharyngeal pouch become?

A

tympanic membrane, tympanic cavity and auditory tube

246
Q

what does the 2nd pharyngeal pouch become?

A

endodermal lining of the second pouch forms the surface epithelium and lining of the tonsilar crypt

the mesenchyme around the crypt differentiates into lymphoid tissue and forms the lymphatic nodules of the palatine tonsil

247
Q

what does the 3rd pharyngeal pouch become?

A

inferior parathyroid gland and thymus

248
Q

what does the 4th pharyngeal pouch become?

A

develops into the superior parathyroid glands and the ultimopharyngeal body–> this fuses with the thyroid gland and its cells give rise to parafollicular cells which produce calcitonin–> these cells differentiate from NCCs that migrate from the pharyngeal arches into the 4th pair of the pharyngeal pouches

249
Q

what is the first endocrine gland to develop in the embryo?

A

thyroid

250
Q

what does the thyroid develop from in the embryo?

A

from a median endodermal thickening in the floor of the primordial pharynx and forms the thyroid diverticulum

as tongue grows, the developing thyroid descends, passing ventral to the developing hyoid bone and laryngeal arches (connected to tongue by thyroglossal duct)

after final stage of development, it takes its final shape with R and L lobes in the front of the neck and the thyroglossal duct degenerates and disappears

the proximal opening of the thyroglossal duct persists as a small blind pit called the foramen cecum of the tongue

251
Q

what happens if the thyroglossal duct doesnt degenerate?

A

may persist and form a cystin the anterior part of the neck

it is painless and a moveable median mass (which is how you differentiate from a cervical cyst)

following the infection of a cyst, a perforation of the skin occurs forming a thyroglossal duct sinus

252
Q

what muscles are formed by the first pharyngeal arch?

A

muscles of mastication

tensor tympanic

tensor veli palatini

253
Q

what muscles are formed by the second pharyngeal arch?

A

muscles of facial expression

stapedius

stylohyoid

posterior belly of digastric

254
Q

what muscles are formed by the third pharygeal arch?

A

stylopharyngeus

255
Q

what muscles are formed by the 4th and 6th arches?

A

soft palate msucles ecept tensor veli palatini

pharyngeal constrictor muscles

laryngeal muscles

B&B Part 1 (4 decks)

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