Week 1 Flashcards

Question 1

Q

Free nerve ending stimuli, rapid or slow

Answer

A

Pain (fast and slow) Crude touch Pressure Heat and cold Rapid

Question 2

Q

Markel cells stimuli, rapid or slow

Answer

A

In hairless skin Stimuli is pressure (touch)

| Slow

Question 3

Q

Hair follicle receptor stimuli, rapid or slow

Answer

A

Touch

| Rapid

Question 4

Q

Meissner corpuscle stimuli, rapid or slow

Answer

A

Light flutter (touch, feather)

| Rapid

Question 5

Q

Pacinian corpuscle stimuli, rapid or slow

Answer

A

Vibration

| Rapid

Question 6

Q

Ruffini corpuscle stimuli, rapid or slow

Answer

A

Stretch your leg ورفسيني slowly

| Stretch

Question 7

Q

Forebrain consists of

Answer

A

cerebrum, Diencephalon

Question 8

Q

Hindbrain consists of

Answer

A

pons,
Medulla oblongata,
cerebellum

Question 9

Q

Brainstem consists of

Answer

A

Midbrain,
pons,
Medulla oblongata

Question 10

Q

Central sulcus separates which lobes?

Answer

A

frontal lobe from parietal lobe

Question 11

Q

lateral sulcus

Answer

A

aka sylvian sulcus

| separates frontal and parietal lobes from temporal lobe

Question 12

Q

corpus callosum function

Answer

A

connects the two hemispheres together and it's made from white matter

Question 13

Q

Grey matter

Answer

A

consists of neuronal cell bodies &amp;amp;amp;amp;amp;amp;amp;amp;amp; forms the cortex

Question 14

Q

White matter

Answer

A

consists of the myelinated neuronal fibers (axons)

Question 15

Q

the cortex is separated by

Answer

A

fissures (sulci) (depression)

Question 16

Q

What's insula?

Answer

A

it's a region of the cerebral cortex located deep within the lateral sulcus

it's made up of grey mater

Question 17

Q

What separated the two hemispheres?

Answer

A

longitudinal cerebral fissure

Question 18

Q

what is Diencephalon made up of?

Answer

A

1) Thalamus

2) Hypothalamus: (has mammillary bodies)
3) Subthalamus:
4) Epithalamus (has pineal body)

Question 19

Q

grey mater makes what in the hemispheres?

Answer

A

ganglion or nucleus

- caudata nucleus
- lentiform nucleus
- the cerebral cortex is also formed by grey mater

Question 20

Q

cavities of the CNS and their locations

Answer

A

a) 2 Lateral ventricles: in the cerebral Hemispheres
b) Third ventricle: between the
2 diencephalon
c) Fourth ventricle: between Pons, medulla and cerebellum (in hind brain)
d) Cerebral aqueduct: in midbrain Central canal of spinal cord

Question 21

Q

What's the function of Cerebral aqueduct?

Answer

A

connects 4th and 3rd ventricles

Question 22

Q

Where can you find CSF? (cerebrospinal fluid)

Answer

A

in CNS cavities and Subarachnoid space

Question 23

Q

What are LMN (lower motor neurons) and where do you find them?

Answer

A

nerves that control muscles directly e.g. spinal nerves and cranial motor nerves

In the spinal cord and brain stem
Their axons innervate directly the
striated muscles of the body and head respectively

Question 24

Q

What are UMN (upper motor neurons) and where do you find them?

Answer

A

neurons that come from the brain cortex and brain stem to control the LMN

their cell Bodies Lie in the cerebral cortex and brain stem The axons of UMNs form descending motor pathways

Question 25

Q

receptors for temperature, pain, itch, Pressure/touch, Position sense:

Answer

A

- temperature: Thermoreceptors

- pain: Nociceptors
- itch: Chemoreceptors
- Pressure/touch: mechanoreceptors (respond to distortions in skin eg. phone vibration)
- Position sense: Proprioceptors (obstacle while walking, we can avoid it by moving our legs without looking down)

Question 26

Q

What are Somatosensation

Answer

A

All modalities other than seeing, hearing, tasting, smelling, and vestibular balance.

يعني يكون شي عام
and they are scattered all over the body

Question 27

Q

What's transduction and transmission?

Answer

A

- transduction: encoding of stimuli into electrical signals (translation)

- transmission propagation of this electric signals to CNS

Question 28

Q

What's adequate and inadequate stimuli?

Answer

A

if a receptor is more selective (specific) for a single stimulus energy – its adequate stimulus.

Differential sensitivity: receptors have a LOW threshold for the adequate stimulus, and a HIGH or no threshold at all to others (inadequate stimuli)

Ex: photo receptors are activated by light, that is their adequate stimulus. When you’re being hit on the eye, you can also see light and this is because the high intensity of the stimulus causes the activation of the photo receptors, that would be the inadequate stimuli.

Question 29

Q

What's receptor (generator) potential?

Answer

A

Change in membrane potential because of a stimuli that allowed ions to diffuse through channels

if stimulus is strong, receptor potential reaches AP threshold, AP is
generated

Question 30

Q

ncreasing amplitude of the generator potential results in?

Answer

A

increases in the frequency of AP

Question 31

Q

What adapts the receptor or the neuron?

Answer

A

The receptor

Question 32

Q

What are phasic receptors?

Answer

A

- aka dynamic receptors - alert us to CHANGES in sensory stimuli - responsible for our ability to cease paying attention to constant stimuli (aka sensory adaptation) - like wearing a ring, you only feel the pressure when you put it on (put stimuli) and take it off (stimuli removed which causes another receptor potential) - it's RAPID adaptation - Pacinian’s corpuscle, Meissner’s corpuscle

Question 33

Q

What are Tonic receptors?

Answer

A

- aka static receptors - SLOW adaptation - don't disappear but decrease with time, it only disappears when you remove the stimuli (Generate AP throughout, but diminish slowly. Give continuous info about stimulus) - Imp for when receptors tell you about muscle movements. Eg: when writing, how your finger is continuously moving with movements. If it was the same position for a while, (static) then AP firing could decrease - Proprioceptors, nociceptors, merkel cells

Question 34

Q

Receptors and their stimuli

Answer

A

Question 35

Q

Whats the No adaptation receptor?

Answer

A

- Tonic receptors (static receptor)

- eg. some Nociceptors
- Imp because you want to constantly know that there’s something damaging to the brain (you don’t want to forget about it)

Question 36

Q

Stimulus intensity coding

Answer

A

Question 37

Q

Mechanoreceptors

Answer

A

- Respond to distortion of the
membrane eg. stretch

- eg. lining of the stomach when full or bladder distention or lung inflation
- pressure (membrane stretching) cause opening of NA+ channels causing generator/ receptor potential
- Direct pressure on skin and/or high-frequency vibration detected by Pacinian corpuscles.

Question 38

Q

difference btw direct and indirect activation of mechanoreceptors

Answer

A

- Direct:
stretching the channel itself OR through structural proteins that are part of the channel (intra or extra cellular proteins)

- Indirect:
through membrane structural proteins (protein is NOT related to channel eg. 2nd messengers)

Question 39

Q

What's the pressure receptor

Answer

A

Markel receptor:

- Sustained touch, texture, pressure
- sense a touch that lasts longer
- SLOW adaptation
- eg. Braille (blind people text)
- superficial in glabrous skin (skin that doesn't have hair)

Question 40

Q

What's light touch/ flutter receptor

Answer

A

Meissner Corpuscle:

- Changes in light touch, stroke, Flutter hence ->
- FAST adapting
- superficial in glabrous skin (skin that doesn't have hair)

Question 41

Q

What's vibration receptor

Answer

A

Pacinian Corpuscle:

| - FAST adapting

Question 42

Q

What's stretch receptor

Answer

A

Ruffini Ending:

- skin stretch, sustained pressure
- eg. when holding a big object, your hands are being stretched, collagen fibers will stretch, cause afferent that will let your brain know that you’re holding something thats stretching your hand
- SLOW adapting

Question 43

Q

What's another flutter, light touch receptor

Answer

A

Hair follicle: - flutter, light touch - in hairy skin unlike meissner corpuscle - eg. when wind blow on your skin - FAST adapting

Question 44

Q

How to test Proprioception?

Answer

A

Proprioception = position sense

1. with eyes closed know wether you're moving their fingers/ toes up or down
2. Romberg test: with eyes closed, if their proprioception is not intact, then they will sway, and when they open their eyes, the swaying will stop because vision compensates for proprioceptive loss.

Question 45

Q

What stimulates muscle spindle?

Answer

A

stimulated by stretch

> fibers elongate

> sensed by nerve endings A1 and II (2)

> fire AP

Question 46

Q

What do gamma motor and alpha motor control?

Answer

A

- Gamma motor: control spindle sensitivity

- alpha motor: muscle contraction of skeletal muscles

Question 47

Q

What does 1b afferent do and where is it

Answer

A

- in Golgi tendon organ

- it signals muscle tension to CNS
- the axon of 1b is intertwined with the collagen fascicles
- When the Golgi tendon organ is stretched (usually because of contraction of the muscle), the Ib afferent axon is compressed by collagen fibers and its rate of firing increases.

Question 48

Q

Transduction by Chemoreceptors

Answer

A

<p><p><p><p>For visceral sensations:
- PO2 , PCO2 receptors
- Hunger: food molecules activate
hypothalamic chemoreceptors
- Thirst: osmoreceptors

For pain:
- Lactic acid when exercising open H+ gated ion channels on nociceptive neural endings

For itch:
- histamine

Question 49

Q

Thermoreceptors

Answer

A

Transient receptor potential channel (TRP) each one has different sensitivity:
- TRPV3 in chilli
- TRPV4 in chilli
(for both,
Adequate stimuli: temperature
inadequate stimuli: vanilloid in chilli)
- TRPM8 in menthol (nonselective cation channel expressed in small diameter trigeminal and dorsal root ganglion neurons in which cooling and menthol evoke inward depolarizing currents and intracellular calcium rises

Question 50

Q

Nociceptors

Answer

A

- For pain
- FREE nerve endings respond to stimuli and damaged tissue

Three types:
1. Thermal nociceptors

2. Mechanical nociceptors
3. polymodal nociception

Question 51

Q

polymodal nociception:

Answer

A

High intensity mechanical, chemical or thermal (v. hot or v. cold) stimuli
UNMYELINATED C axons that conduct more SLOWLY (dull, burning pain, diffusely localised, poorly tolerated).

~~~
TRPA1
TRPV1
TRPV2
MS
ASIC (for acid accumulation)

~~~

Question 52

Q

Mechanical nociceptors:

Answer

A

ntense pressure to skin
thinly myelinated axons
stabbing, squeezing, pinching

Question 53

Q

Thermal nociceptors:

Answer

A

activated by extreme temp (v. high or v. low)
in peripheral endings of small
diameter, thinly myelinated

Question 54

Q

somatosensory fibers are fast when

Answer

A

big in diameter and myelinated

Question 55

Q

Proprioception, mechanoreceptors, nociceptors, thermoreceptors which are myelinated which are not?

Answer

A

myelinated: Proprioception and mechanoreceptors NONmyelinated: nociceptors, thermoreceptors

Question 56

Q

Lower motor neuron lesions features:

Answer

A

- Decreased (flaccidity)
- weakness and w time there will be muscle atrophy
- Hyporeflexia (decreased reflex)
- Hypotonia (decreased muscle resistance to passive movement)
- Fasciculations (muscle contraction seen as skin flickering but not strong enough to move the limb)
- found in Ant horn cell
- eg. Polyneuropathy, (GBS) gullian barre syndrome
- flexors and extensors equally affected
- caused by:
1- Poliomyelitis
2- Spinal muscular atrophy
3- Amyotrophic lateral sclerosis (ALS)

Question 57

Q

Upper motor neuron lesions features:

Answer

A

- Increased tone (spasticity)

- Hypertonia
- hypereflexia
- Above anterior horn cell in spinal cord
- eg. stroke, multiple sclerosis
- Early UMNL manifest as LMNL ( you don't get stroke right away when there is an UMNL)
- extensors are weaker in UPPER limbs (triceps)
- flexors are weaker in LOWER limbs
- +ve babkinski
- +ve clonus
- +ve hoffman sign
- superficial (abdominal reflexes) are absent (decrease)

Question 58

Q

Describe Poliomyelitis

Answer

A

- Caused by Polio virus causing anterior horn cells destruction

- mostly asymptomatic
- few have LMN picture
- Diagnosis: RNA of virus in CSF

Question 59

Q

Describe Spinal muscular atrophy

Answer

A

- Caused by genetics (autosomal recessive)

- progressive weakness &amp;amp; atrophy of muscles
- Treated by Antisense oligonucleotide

Question 60

Q

Describe Amyotrophic lateral sclerosis (ALS)

Answer

A

- stephen hawking!

- It's progressive, pattern of weakness affects right arm then left arm then left leg then right leg
- Affects motor neurons in cerebral cortex and brain stem (UMNL) as well as anterior horn of spinal cord (LMNL)

Question 61

Q

in Peripheral neuropathy what does each of the following affect?

- Neuron-opathy
- Plexopathy
- Motor neuron disease
- Radiculopathy
- Peripheral neuropathy

Answer

A

- Neuron-opathy = dorsal root ganglion

- Plexopathy = plexus
- Motor neuron disease = cell body in anterior horn
- Radiculopathy = Root
- Peripheral neuropathy = peripheral nerve

Question 62

Q

Describe Neuronopathy (NOT neuropathy) and an example

Answer

A

- Degeneration of dorsal root ganglia &amp;amp; projections
- Diseases affecting the neuron cell body
Divides to:
- Motor neuron disease (anterior horn affected)
- Sensory neuronopathy
- Ganglionopthy
- eg. herpes zoster (shingles)

Question 63

Q

Describe Radiculopathy and an example

Answer

A

- affects spinal nerve ROOT

- classic presentation is pain, if in the neck it's brachial plexus, or in lower back and goes to lower limbs
- weakness in muscles supplied by that root
- radiating pain along the root dermatome
- DECREASED deep tendon reflex (eg. knee jerk reflex) in corresponding root ONLY
- caused by compression eg. herniated disc (nerve root compressed, muscles supplied by that root damaged

Question 64

Q

Describe plexopathy

Answer

A

- affects plexus (Brachial or Lumbosacra)

- affects sensory and motor (shows both symptoms)
- weakness and numbness
- Caused MOSTly by diabetes mellitus, can be caused by focal mass (pancoast tumor, a lung tumor that affects brachial plexus)
- eg. Hornor's syndrome, happens bcz of disturbtion of brachial plexus (C8 - T1)

Answer 65

A

- Causes are either Hereditary or Acquired
- Hereditary -> Charcot marie tooth disease (IMPORTANT)
- Acquired (MINI-P):
Metabolic or medication (diabetes, vit B12 def., chemotherapy)
Immune
Neoplastic
Infections
Physical (compression)

Answer 66

A

- one peripheral nerve affected

- cranial or spinal nerve
- caused by trauma, compression or entrapment
- loss of function in part supplied (motor, sensory, &amp;amp;/or autonomic)
- eg. spinal nerve example, Carpal tunnel syndrome -> numbness in lateral 31⁄2 digits +/- weakness -> examined by phalen sign and tinel sign
- eg. Cranial nerve 7 -> bell's palsy -> weakness in face muscle, muscle not moving
- treated w/ NSAID, steroids, surgery

Answer 67

A

- Symmetric

- Length dependent
- Long fibers affected first (leg fibers first)
- Starts at the toes and continues going up until it reaches the hands
- example: patient came w/ numbness that started in feet (both sides) toothpicks then started to go to ankles then in both hands

Answer 68

A

- More than one peripheral nerve affected at the same time or one after the other
- ASYMMETRIC
- affect cranial or spinal n.
- examples:
1. Vasculitis of vasa nervorum
2. Sarcoidosis
3. Diabetes mellitus
- Symptoms are motor (weakness) (LMNL features) and sensory (numbness is most imp)
divides to Demyelinating and Axonal neuropathy

Answer 69

A

- they're both divisions of Polyneuropathy

1. Demyelinating neuropathy:
- loss of myelin so signal will be slower
- causes: common in DIABETES MELLITUS

2. Axonal neuropathy:
- damage occurs to axon itself so signal is not able to pass at all
- causes: Guillain-Barre syndrome (GBS) + mostly autoimmune

Answer 70

A

3. Amyotrophic lateral sclerosis

ALS, cause it's mixed

Answer 71

A

3. Hyperreflexia with spasticity

cause it doesn't happen that early (2 hrs) remember that early UMNL manifests as LMNL

Answer 72

A

2. positive hoffman's sign

it's an UMNL sign and

Note: Down-going toes on plantar reflex is a normal response so it's present even in carpal tunnel syndrome

Answer 73

A

1. Filum terminale

| 2. Denticulate ligament

Answer 74

A

- it's an enlargement in the subrachnoid mater

- contains 3 things:
1) CSF
2) cauda equina
3) filum terminale
- we aspirate CSF from here to avoid injuring the spinal cord

Answer 75

A

- Ends with arachnoid at the
2nd sacral vertebrae
- extradural space which separates the spinal cord from the vertebra so it's not attached

Answer 76

A

innervate most of the body and form the brachial and lumbosacral plexus

Answer 77

A

visceral motor

Answer 78

A

gives rise to "pre-ganglionic sympathetic fibers."

Answer 79

A

gives rise to "pre-ganglionic parasympathetic fibers."

Answer 80

A

Posterior column:

1) Fasculus gracilis
2) Fasculus cuneatus

Anterior column:
Spinothalamic tract

~~~
Lateral column:
spinothalamic
Posterior spinocerebellar
Anterior spinocerebellar
Spinotectal
Spinoreticular
Posterolateral (Lissauer’s)

~~~

Answer 81

A

Lateral column:
Lateral corticospinal
Rubrospinal
Lateral reticulospinal

~~~
Anterior:
Anterior corticospinal
Tectospinal
Vestibulospinal
Medial Reticulospinal

~~~

Answer 82

A

Dorsal root ganglia

Answer 83

A

Ventroposterior Lateral (VPL) nucleus of thalamus

(then it goes to somatosensory cortex)

Answer 84

A

Lamina 1 AND 5 only

Answer 85

A

amina 1 TO 5 (1,2,3,4,5)

Answer 86

A

Anterolateral pathway

1st order neuron
Origin: DRG
End: lamina I to V (dorsal root horn)

Do one of two things:
1. Terminate at that segment level and synapse with the 2nd order neuron level

2. Join the Lissauer’ tract (posterolateral tract), which will either ascend or descend 1 to 3 segment levels. Then it will terminate and synapse with the 2nd order neuron.

Function:

- Pain (sharp, prickling and well organized)
- Pressure
- Temperature

Answer 87

A

Origin: lamina I and V (dorsal root horn)
End: VPL of the thalamus

The neuron body of the 2nd order neuron is at either the I OR V lamina.
The axon crosses the spinal cord at the anterior commissure, causing the tract to be contralateral.
The axon ascends the spinal cord at the anterolateral fasciculus of the white matter. It will terminate at the VPL of the Thalamus.

Answer 88

A

Origin: VPL of the thalamus

| End: Primary somatosensory cortex

Answer 89

A

Lateral pathway

Origin: DRG
End: lamina I and V (dorsal horn)

Function:

- Controls pain
- Spinovisual reflex: it brings about the movement of the eyes and head towards the source of information

Answer 90

A

Origin: lamina I and V (dorsal horn)
End: Superior colliculus

The neuron body of the 2nd order neuron is at either the I or V lamina.
The axon crosses the spinal cord, causing the tract to be contralateral.
The axon ascends the spinal cord at the lateral fasciculus of the white matter.
It will terminate at the superior colliculus.

Answer 91

A

Lateral pathway

Origin: DRG
End: lamina VI, VII, and VIII (6, 7, 8,) (dorsal horn)

Function:

- Pain (dull, aching, and poorly localized)
- Influence the level of consciousness

Answer 92

A

Origin: lamina VI, VII, and VIII (dorsal horn)
End: reticular formulation of brain stem and intralaminar nuclei of thalamus

The neuron body of the 2nd order neuron is at either the VI, VII, or VIII lamina.
The axon does not cross the spinal cord, causing the tract to be ipsilateral.
The axon ascends the spinal cord at the lateral fasciculus of the white matter.
It will give multiple synapse.
It synapses contralaterally (it crosses) to the reticular formation of the brain stem, while the axon continues upwards and terminates at the intralaminar nuclei of the thalamus at the same side (ipsilateral).

Answer 93

A

Lateral pathway

Origin: DRG
End: dorsal horn

~~~
Function:
Visceral information (ex. distended stomach)

~~~

Answer 94

A

Origin: dorsal horn
End: VPL

The neuron body of the 2nd order neuron is at dorsal root horn.
The axon travels with the spinothalamic tract.
The axon crosses the spinal cord at the anterior commissure, causing the tract to be contralateral.
The axon ascends the spinal cord at the anterolateral fasciculus of the white matter.
It will terminate at the VPL of the Thalamus.

Answer 95

A

Origin: VPL

| End: somatosensory cortex

Answer 96

A

Spinocerebellar pathway (found laterally)

Origin: DRG at T1 to L1 or2 (UP)
End: Clark’s nucleus (nucleus dorsalis) found at T1 to L1 or 2

Function:
Unconscious proprioception

Answer 97

A

Origin: Clark’s nucleus (nucleus dorsalis) found at T1 to L1/2
End: cerebellum

The neuron body of the 2 order neuron is at Clark’s nucleus (nucleus dorsalis) found at T1 to L1/2.
The axon travels upwards and passes through the inferior cerebellar peduncle to terminate at the cerebellum.

Answer 98

A

Spinocerebellar pathway (found laterally)

Origin: DRG at T12 to L5 (DOWN)
End: Spinal border neurons found at T12 -L5

Function:
Unconscious proprioception

Answer 99

A

Origin: Spinal border neurons found at T12 -L5
End: cerebellum

The neuron body of the 2nd order neuron is spinal border neurons found at T12 -L5.
The axon crosses the spinal cord, causing the tract to be contralateral.
The axon ascends the spinal cord at the lateral fasciculus of the white matter.
It then recrosses in the middle cerebellar peduncle, causing the tract to be ipsilateral.
It will terminate at the cerebellum.

Answer 100

A

Spinocerebellar pathway (found laterally)

Origin: lateral cutaneous (accessory pathway)
End: cerebellum

The neuron body is found in the lateral cutaneous nucleus in the medulla.
This pathway is an accessory pathway as it begins at the middle of another pathway.
The axon travels through the inferior cerebellar peduncle to terminate at the cerebellum.

Function:
Unconscious proprioception

Answer 101

A

Spinocerebellar pathway (found laterally)

Origin: DRG
End: dorsal horn

Function:
Proprioception
(the information conveyed is from cutaneous and proprioceptive organs)

Answer 102

A

Origin: dorsal horn
End: inferior olivary nucleus

The neuron body of the 2nd order neuron is at the dorsal horn.
The axon crosses the spinal cord at the commissure, causing the tract to be contralateral.
The axon ascends the spinal cord at the lateral fasciculus of the white matter.
It will terminate at the inferior olivary nucleus.

Answer 103

A

Origin: inferior olivary tract
End: cerebellum

The neuron body of the 3rd order neuron is at the inferior olivary tract.
The axon crosses the inferior cerebellar peduncle (the crossing then recrossing causes the pathway to become ipsilateral) and terminates at the cerebellum

Answer 104

A

Origin: DRG
End: gracilis nucleus in medulla

The neuron body is found in the DRG.
The central branch of the axon will ascend the spinal cord until it terminates at the gracilis nucleus in the medulla.

Function:
(important) info from below T6

Conscious proprioception Discriminative touch Vibration
Joint movement

Answer 105

A

Origin: gracilis nucleus in medulla
End: VPL

The neuron body is at the posterior medulla in the gracilis nucleus.
The axon will cross to the other side of the medulla (contralateral) and terminate at the VPL of the thalamus.

Answer 106

A

Origin: VPL

| End: somatosensory cortex

Answer 107

A

Function:
(important) info from above T6

Conscious proprioception Discriminative touch Vibration
Joint movement

Answer 108

A

Origin: cuneatus nucleus in medulla
End: VPL

The neuron body is at the posterior medulla in the cuneatus nucleus.
The axon will cross to the other side of the medulla (contralateral) and terminate at the VPL of the thalamus.

Answer 109

A

Origin: VPL

| End: somatosensory cortex

Answer 110

A

Origin (multiple): 1/3 primary cortex, 1/3 supplementary cortex, and 1/3 somatosensory cortex
End: anterior horn or interneurons

The tract begins in the cerebral cortex (1/3 primary cortex, 1/3 supplementary cortex, and 1/3 somatosensory cortex) and descends to the brain through the cerebral peduncle, then to the Pons (where fibers will move around within the Transverse pontine nucleus).
Here the tract divides.
The fibers will descend to the medulla into the pyramid WITHOUT CROSSING (15%); these will form the anterior corticospinal tract, which will travel downwards, and few will cross at spinal segments.
The fibers terminate at any segment level at the medial group of the anterior horn.
Some will synapse with lower motor neurons (3rd order neurons), while others will synapse with interneurons (2nd order neurons).

Function:
Voluntary control of axial muscles

If injured:
Injury to any side of the anterior corticospinal tract does not affect muscle innervations because the supply to muscles is bilateral

Answer 111

A

Origin (multiple): 1/3 primary cortex, 1/3 supplementary cortex, and 1/3 somatosensory cortex
End: anterior horn or interneurons

The tract begins in the cerebral cortex (1/3 primary cortex, 1/3 supplementary cortex, and 1/3 somatosensory cortex) and descends to the brain through the cerebral peduncle, then to the Pons ( where fibers will move around within the Transverse pontine nucleus). Here the tract divides. The fibers will descend to the medulla into the pyramid and CROSS (85% will undergo decussation at medulla); these will form the lateral corticospinal tract, which will travel laterally and downwards.
The fibers terminate at any segment level at the lateral group of the anterior horn.
Some will synapse with lower motor neurons (3rd order neurons), while others will synapse with interneurons (2nd order neurons).

Function:
Voluntary control of distal muscles

If injured:
1. Injury of the tract (after decussation/ after medulla) will cause ipsilateral deficiency of innervation to the muscles innervated by the tract.
Ex. Lesion to left lateral column of spinal cord -> left side of body is paralyzed

2. Injury in the brain (before decussation/ before medulla) will cause contralateral deficiency of innervation to the muscles innervated by that tract.
Ex. Lesion to right hemisphere -> left side of body is paralyzed

The lateral corticospinal tract is closely related to the rubrospinal tract, so injury in that area will probably affect both tracts

Answer 112

A

Responsible for voluntary control of face and body muscles

Answer 113

A

responsible for involuntary control + balance + posture

Answer 114

A

Origin: medial vestibular nucleus in medulla
End: anterior horn of cervical segments

The tract begins at medial vestibular nucleus in medulla and travels through the medial longitudinal fasciculus (fibers which control extra ocular muscle) and terminates at the ventral horn of cervical segments.
Some will synapse with lower motor neurons (3rd order neurons), while others will synapse with interneurons (2nd order neurons).

Function:
Stabilizing head movement Coordinating head movement with eye movement.
Ex. When looking up, we move our neck up as well
Innervates muscles of head and neck

If injured:
Injury to any side of the medial vestibulospinal tract does not affect muscle innervations because the supply to muscles is bilateral

Answer 115

A

Origin: lateral vestibular nucleus in medulla
End: anterior horn

The tract begins at medial vestibular nucleus in medulla and travels through the lateral fasciculus and terminates at the ventral horn.
Some will synapse with lower motor neurons (3rd order neurons), while others will synapse with interneurons (2nd order neurons).

~~~
Function:
Balance
Postural changes to compensate for tilts and movements of the body
Increase activity of extensor muscles
Decrease activity of flexor muscles
~~~

If injured:
Injury of the tract will cause ipsilateral deficiency of innervation to the muscles innervated by the tract.
Ex. Lesion to left lateral column of spinal cord -> left side of body is affected

Answer 116

A

Origin: red nucleus
End: anterior horn, synapsing with the lateral motor neurons

Tract begin at red nucleus (found in midbrain). It CROSSES the midbrain and runs laterally with the lateral corticospinal tract and ends at the lateral group of the anterior horn.
Some will synapse with lower motor neurons (3rd order neurons), while others will synapse with interneurons (2nd order neurons).

Function:
Activate flexor muscle

If injured:
Injury in the tract will cause contralateral deficiency of innervation to the muscles innervated by that tract.
Ex. Lesion to right fasciculus -> left side of body is affected

Answer 117

A

Origin: superior colliculus
End: anterior horn at cervical level of spinal cord

The tract begins at superior colliculus (receives input from optic nerve).
The axon descends and crosses in midbrain.
They enter spinal cord and they will terminate at the cervical level

Function:
Reflex
Turning head in response to visual stimulus

Answer 118

A

Pontine

Origin: pontine reticular formation (brainstem)
End: anterior horn or interneurons

Function:
Walking, running
Activate extensor muscles

Answer 119

A

medullary

Origin: medullary reticular formation
End: anterior horn or interneuron

Function:
Walking, running Activates flexor muscles

Answer 120

A

- Lateral: control distal limb muscles

- Medial: (always bilateral) controls axial/proximal muscles

Answer 121

A

they are upper motor neurons UMN, they come from the brain.

(All the tracts mentioned previously are part of the third order neurons which are lower motor neurons and they send signals directly to the muscles)

Answer 122

A

- Control visceral activities

- UMN:
o Origin: cerebral cortex, hypothalamus, amygdala, reticular formation

o End: lateral horn at T1-L1/2 and S2-S2

o Pathway: originates from cerebral cortex, hypothalamus, amygdala, reticular formation.
The axons descend and CROSS at the midbrain.
They continue down to the lateral horns in the thoracic or sacral segments.

▪ In thoracic region, the lateral horn in the spinal cord gives rise to preganglionic sympathetic fibers

▪ In sacral region, the lateral horn in the spinal cord gives rise to preganglionic PARAsympathetic fibers

Answer 123

A

- Sense Muscle tension

Answer 124

A

- Sense Muscle length (static gamma)
- Sense Muscle rate/ speed (dynamic gamma)

- has three parts:
1. Specialized intrafusal muscle fibers: contain non-contractile region

2. Sensory fibers (Ia, most myelinated) that terminate in non-contractile region of the intrafusal fibers.
- > When the muscle is stretched, the distance between the spirals will increase which will increase the activity of Ia fibers.

3. Motor axons (gamma)

Answer 125

A

- Motor:
gamma
alpha

- Sensory:
Ia (1a)
II (2)

Answer 126

A

1. Alpha: Aα
- Extrafusal innervation
Large diameter axons =
fast transmission

2. Gamma: γ
- Innervates the core of muscle spindle
- Intrafusal innervation
- two types, dynamic and static
- Modulate sensory information in a dynamic or static fashion

Answer 127

A

1. Nuclear chain fibers

2. Nuclear bag neurons

Answer 128

A

1. Nuclear chain fibers: innervated by static γ motor
neurons only.

2. Nuclear bag neurons: innervated by both static
and dynamic γ motor neurons.

Answer 129

A

Extrafusal fibers are innervated by α motoneurons, generate force.

Intrafusal fibers are innervated by γ motoneurons, adjust sensitivity of muscle spindle

Answer 130

A

- stretch reflex -> monosynaptic

- reciprocal inhibition -> polysynaptic

Answer 131

A

- enhances the effect of the active pathway

- suppressing the activity of other, opposing, pathways.
- Activates one pathway and inhibits all the lateral pathways.
- Example: knee jerk reflex.

Answer 132

A

- stops the activity within the stimulated pathway and prevents it from exceeding a certain critical maximum.

- Inhibits the same Pathway.
- Example: autogenic reflex.
- Renshaw cells are inhibitory cells that transmit inhibitory signals to the surrounding motor neurons.

Answer 133

A

- stepping on sharp object

- receptor is on the skin (not inside the muscle)
- polysynaptic
- occurs in response to a tactile, painful, or noxious stimulus. Somatosensory and pain afferent fibers initiate a flexion reflex that causes withdrawal of the affected part of the body from the painful or noxious stimulus.
- reflex produces flexion on the ipsilateral side &amp; extension on the contralateral side (extensor muscles will contract and flexor muscles relaxes). Extension on the contralateral side is called crossed-extension reflex.

Answer 134

A

1. anterior spinal artery for ant. 2/3

2. posterior spinal arteries for post. 1/3
3. great anterior medullary artery of adamkiewicz (from left side of aorta) supplies LOWER part of the spinal cord (IMPORTANT)

Answer 135

A

Dorsal root ganglia

Answer 136

A

CNS

Answer 137

A

Wallerian Degeneration:
myelin AND axon will be destroyed

HOWEVER
Connective tissue especially (endoneurium) AND schwann cells will persist

Answer 138

A

- Clean/ digest the debris in Wallerian Degeneration

- promotes angiogenesis
- type 2 machrophage will produce factors for the regeneration process

Answer 139

A

INJURED:
- chromatolysis: Nissl material becomes less in number, fine, granular, dispersed throughout the cytoplasm
- nucleus moves towards the periphery (eccentric nucleus)
- cell body swells and becomes rounded.
- Synaptic stripping: synaptic terminals are seen to withdraw from
the surface of the injured neuronal cell body and its dendrites

NORMAL:
- centrally located nucleus w/ prominent nucleolus.
Spread out nissel’s substances

Answer 140

A

collection of RER (Rough endoplasmic reticulum) with ribosomes.

Answer 141

A

retrograde degeneration

| (cause going from distal to proximal).

Answer 142

A

Wallerian Degeneration.

Answer 143

A

1) Anti-inflammation

2) Growth factors
3) Stimulate Schwann cell to differentiate and remeylinate

Answer 144

A

- MQ secret vascular endothelium growth factor that promotes angiogenesis - it will make a connection between the distal and the proximal (bridge) - Along this blood vessel the growing/ proliferating Schwann cell &amp; THEN the axons will be guided till it reaches the distal segment

Answer 145

A

axons are attracted by chemotropic factors secreted by Schwann cells in the distal stump.
Growth-stimulating factors exist within the distal stump

Answer 146

A

Inhibitory factors are present in the perineurium to inhibit the axons from leaving the nerve.

Answer 147

A

Ability of Schwann cells to proliferate.
Presence of Basal Lamina/Endoneurium.
MQ

Answer 148

A

Loss of sensibility and voluntary movement below the lesion
bilateral LMN paralysis and muscular atrophy IN the segment of the lesion
bilateral SPASTIC paralysis (UMN) BELOW the lvl of the lesion
bilateral babinski sign

Answer 149

A

due to anterior spinal artery occlusion
bilateral LMN paralysis and muscular atrophy IN the segment of the lesion
bilateral SPASTIC paralysis (UMN) BELOW the lvl of the lesion
the bilateral spasticity is caused by interruption of anterior corticospinal tract
the bilateral paralysis is caused by interruption of tracts other than corticospinal tract
posterior column is preserved (gracilis and cuneatus)

Answer 150

A

bilateral LMN paralysis on the same segment bcs of damage to the anterior grey horn
bilateral spastic paralysis (UMN) below the lesion
bilateral loss of pain, temp and light touch bcs the crossing fibers of spinothalamic are affected

Answer 151

A

aka hemisection
epsilateral babinski sign
epsilateral LMN paralysis/ hypotonia/ ansthesia
epsilateral loss of posterior colmn, so loss of proprioception
epsilateral spastic paralysis (UMN) below the lesion
contralateral loss of pain, temp and crude touch (tactile sense) two to three segments BELOW the lesion

Answer 152

A

when there is an abnormal dilation of the spinal cord lesion
spinothalamic tract will be affected due to its crossing in the anterior white commissure (NO PAIN)
bilateral loss of sensation but ONLY at the site of the lesion and usually in upper limbs
eg. patient comes with repeated burns in fingers w/out being aware
when it develops to anterior grey horn -> wasting of upper limbs muscles (LMN)
if they extend even more and disturb lateral corticospinal region they will cause UMN problems below the lvl of lesion
- eg. patient comes with repeated burns in fingers of both hands w/out being aware, after a while she develops weakness in upper limbs and her gait becomes spastic and disturbed
if the extension of lesion is lateral at T1 symptoms apply to eyes, it will lead to bilateral horner syndrome

-Why not the whole body? bcz the damage below the crossing.

Answer 153

A

caused by polio
anterior grey column is affected
immobilization of lower limbs

Answer 154

A

ALS
both LMN (corticospinal tract)
and UMN (anterior grey horn)

Answer 155

A

will produce UMN manifestations = Spastic paralysis (in both cases)
either in the cortex/ brainstem (motor decussation happens here in pyramids) or in spine

in spine:
EPSILATERAL UMN lesion
- eg. Lesion of the lateral corticospinal Tract (in the spinal cord)
in cortex/ brainstem:
- before decussation so it’s CONTRALATERAL UMN lesion
- Example: vascular lesion of the Cerebral cortex
- Weber’s syndrome: occlusion of a branch of post. Cerebral artery that Supplies the midbrain
damage to the anterior corticospinal tract
No obvious weakness cause it’s anterior

Answer 156

A

occlusion of a branch of post. Cerebral artery that Supplies the midbrain
CONTRALATERAL UMN lesion

Answer 157

A

presence of inhibitory interneurones

- pain (It can open the gate to more pain & amplify it or shut the gate so the pain becomes less

Answer 158

A

respond to high-

threshold, noxious stimuli (C- and A delta-fibres), encoding location and intensity of the pain

Answer 159

A

mildnoxious stimulus leads to an amplified pain response (something that already causes pain but it’s amplified)

Answer 160

A

pain due to a NON-painful stimulus

eg. brush or clothes on their body causes pain

Answer 161

A

expectation of pain when told verbally or non verbally.

e.g. if you’re going to do a surgery again. Before they even touch, you’d be in pain.

Answer 162

A

do NOT transmit noxious stimuli, they just carry touch sensation and they end in deep dorsal horn.

Answer 163

A

transmit noxious stimuli of mechanical & thermoceptive quality (polymodal) ends in both superficially & deep.

Answer 164

A

transmit Nociceptive mechanical, thermoceptive and chemical stimuli (polymodal) end in superficial dorsal horn.
- eg. acidity, spicy food

Answer 165

A

Primary hyperalgesia:
- it’s where you can see the damage
- is due to sensitisation of nociceptors in the periphery (peripheral sensitisation)
Secondary hyperalgesia:
- Area around it that is also painful
- is due to sensitisation of spinal cord dorsal horn neurons (central sensitisation)

Answer 166

A

Inflammation.

> Inflammatory mediators (eg. histamine) acting on their receptors (H1 receptor)
> sensitisation of nociceptors
> peripheral sensitisation

Answer 167

A

Histamine from mast cells -> H1 receptor
Bradykinin from macrophages, mast cells and damaged tissue -> B2/B1 receptors
PGE2 from mast cells -> EP receptors
ATP from platelets and damaged tissue -> P2X3 receptor
H+ from inflammation -> ASIC receptor

Answer 168

A

glutamate - > act on AMPA and NMDA receptors
substance P -> act on NK-1 receptor
5 HT (seretonin) -> act on 5HT3 receptor (BUT if it acts on 5HT1 it is INHIBITORY)

Answer 169

A

GABA -> act on GABA-A and GABA-B
opioid peptides -> act on opioid receptors
Noradrenaline -> act on alpha 2 adrenoceptors (a2-AR)
5 HT (seretonin) -> act on 5HT1 receptor
cannabinoids -> act on cannabinoid receptors

Answer 170

A

for acute pain
fast excitatory synaptic transmission -> sets baselinenociceptive
transmission (acute pain)
Ion channel, once activated, is more selective to Na+ entry than Ca2+ (more Na)
Antagonist =CNQX (cyanquixaline)
AMPA receptors CANNOT be blocked (but NMDA receptors can)

Answer 171

A

for chronic pain
more complicated to activate
ion channel w/ Mg sitting in the middle blocking the channel stoping it from being activated.
Once Mg is removed, Na & Ca can go in & K+ can go out.

Answer 172

A

the cell that the NMDA receptor is on has to be consistently depolarized
so there’s an electrical activity that helps this Mg leave its place for Na & Ca to go in.

Answer 173

A

Neuropeptide from the neurokinin (tachykinin) family
Neurotransmitter in the CNS, released after HIGH intensity noxiousstimulation
Co-released from primary afferent fibres with other peptides
Acts on neurokinin 1 (NK-1) receptor

Answer 174

A

G-protein coupled (NOT an ion channel)
postsynaptic
Increases release of Ca2+ from intracellular stores via generation of inositol trisphosphate (IP3) (Ca2+ increase in the cell)
Involved in mood, stress, anxiety and pain

Both NK-1 and NMDA receptors are involved in central sensitisation

Answer 175

A

Remember: central sensitisation causes pain around the damaged area
pain sensation coming
-> substance P act on NK1 and Glu acts on AMPA
-> Na and Ca go into the cell
-> Primary alpha fibers (prostanoids and NO in spinal cored) start sending another msg that retrogradely diffuse back to c fibers and facilitate more transmitter release
(the previous step happened WITHOUT a stimulus, it’s a cycle of pain/ LOOP of central sensitisation stimulation)
-> more glu and peptides (substance P)
->more Ca released
-> depolarized cell
-> Few times of this and Mg block is removed (NMDA activated)
NMDA and substance P are involved in central sensitisation

Answer 176

A

major inhibitory transmitter in CNS
acts on GABA-A predominantly
forms a tonic control of excitatory transmission
GABA A receptor: ion channel
GABA B receptor: G protein coupled
Once GABA & BZDs bind—> the channel opens, Cl- goes in
fast postsynaptic inhibition bcz Chloride influx hyperpolarises the cell causes inhibition
inhibitory Target of BZDs, barbiturates

Answer 177

A

PAG (periaqueductal grey area)
eg. urgeries done on monkeys w an electrode going into the PAG area -> animal isn’t feeling pain

so: electrical stimulation of PAG—> analgesia
- morphine microinjection in PAG -> analgesia
- if you activate the NMDA receptor (involved in pain) —> also got analgesia.
- Reversed when given antagonist to morphine & antagonist to NMDA receptor.

Answer 178

A

Reciprocal connections back toPAGand other supraspinal sites
Caudal projections back to spinal cord
RVM stimulation both inhibits and facilitates (centralsensitisation) spinal cord nociception (pain)
in inflammatory diseases it inhibits pain
in neuropathic pain it increases pain

Answer 179

A

Noradrenaline

2. Serotonin (5-HT)

Answer 180

A

acting on a2-adrenoceptors has inhibitory effects

Answer 181

A

has both inhibitory and excitatory
5HT1 is inhibitory
5HT3 is excitatory
5HT3 is involved in vomiting.
Ondansetron is an antagonist to 5-HT3
After this channel is activated, it’s permeable to monovalent cations as well as Ca+

Answer 182

A

exists in a (top-down) descending pain modulatory circuit, underlies placebo analgesia and involves areas of the pain matrix as well as endogenous opioid mediated inhibition

Important:

Nalaxone blocks the opioid receptors.
(IMPORTANT) Studies included placebo analgesia CANNOT be experienced if naloxone blocks the oipid receptors (endogenous opioid peptides cannot access the receptors)
if i’m doing a study for placebo and gave the patient nalaxone to block their opiod receptors -> the study is not going to work cause the top down thing doesn’t work anymore
so, top down enogenous pain control involves endogenous opioid peptides.

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