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CNS Physiology > Sensory & Motor Systems Lesions > Flashcards

Sensory & Motor Systems Lesions Flashcards

1
Q

Describe effect of UMNL on muscle state

A

Minimal (disuse atrophy) due to:
Loss of voluntary & reflex muscle activity
No loss of trophic effects on metabolism of the affected muscle as nerve supply is intact

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2
Q

Compare UMNL & LMNL with respect to reflexes

A

UMNL, all superficial are lost except +ve babniski, hyperreflexia in deep
LMNL, all superficial are lost, hyporeflexia in deep

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3
Q

Mention distinguishing characters of acute UMNL from LMNL

A

Widespread, +ve Babniski, No atrophy

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4
Q

Compare characters of corticobulbar & facial nerve lesion

A

CB: upper face is spared, lower face is affected, contralateral
FN: upper & lower face are affected, ipsilateral

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5
Q

Mention acquired causes of polyneuropathy

A
  1. Metabolic as DM
  2. Autoimmune
  3. Toxins
  4. Tumors
  5. Trauma
  6. Nutritional def
  7. Alcohol
  8. Vascular
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6
Q

Describe sensory & motor effects of polyneuropathy

A

S, numbness, tingling, pricking then hypothesia then anesthesia. Glove & stocking sensory loss
M, paresis, paralysis, loss of reflexes, atrophy (LMNL)

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7
Q

Define syrinomyelia

A

Cyst or glial tissue or fluid that accumulates over time causing cavitation around central canal, more common in cervical segments, may progress to thoracic segments and medulla

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8
Q

Describe effect of small lesion in syringomyelia

A

Damage of decussating fibers of spinothalamic tract resulting in sensory loss of pain & temp in upper limbs & upper chest & back (jacket distribution of sensory loss)
Crude touch (partially carries in dorsal column pathway) & other dorsal column senstaions are not lost.

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9
Q

Describe effect of progressive lesion in syringomyelia

A

Sensory as small lesion
Motor, LMNL due to damage of AHCs at level of affected segments & UMNL below level due to damage of corticospinal tract
Autonomic: damage of LHCs, Horner’s syndrome

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10
Q

Describe effect of more progressive lesion in syringomyelia

A

Sensory as progressive
Motor as progressive with addition of cranial nerve nuclei (syrigobulbia)
Autonomic as progressive
Brain stem affection with various kinds of facial palsy, sensory & motor impairments

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11
Q

Tabes dorsalis more commonly affects …..segments

A

Lumbosacral

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12
Q

C/P of late stage syphilis

A

Sensory loss
Sensory ataxia
Stamping gait
Motor effects (deafferenation, hypotonia & hyporeflexia)

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13
Q

First & last sensation lost in tabes dorsalis, why?

A

Vibration first
Slow pain last, as the lesion causes compression from inside to outside, the pain fibers are located centrally.

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14
Q

Define stamping gait

A

Lifting legs very high to hit the ground hard, with opened eyes looking at legs

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15
Q

Define Argyll-Robertson pupil

A

Loss of eye pupil reaction to light while the pupil itself is normal & can respond to other reflexes such as near response reflex
Occurs in more progressive stages of Tabes dorsalis with brain stem affectiondue to damage of pretectal area of midbrain

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16
Q

Describe effects of Brown-Sequard Syndrome

A

At level of lesion: LMNL & Loss of all sensations
Below level of lesion: ipsilateral UMNL, Ipsilateral loss of dorsal column sensations, contralateral loss of spinothalamic sensations.

17
Q

Causes of spinal cord transection

A

Gunshot injuries, dislocation of spine, vascular accident

18
Q

GR: Transection of spinal cord above C5 leads to death

A

Due to interruption of impulses between respiratory center and C3,4,5 (origin of phrenic nerve) leading to respiratory failure.

19
Q

In Transection of spinal cord below C5 respiration is ……while mid-thoracic it is ……

A

Diaphragmatic only
Diaphragmatic & intercostal

20
Q

Describe cause & duration of spinal shock

A

Due to sudden withdrawal of the facilitatory corticospinal, reticulospinal & vestibulospinal impulses thus dec excitability if spinal motor neurons & loss of response to stimulation of afferents
2-6 weeks depending on degree of encephalization of motor function

21
Q

Mention locomotor effects of spinal shock

A
  1. Loss of stretch reflex, atonia, areflexia & fkaccid muscles
  2. Loss of flexor withdrawal reflex & superficial reflexes
  3. Muscle atrophy
  4. Bone demineralization and hypercalcemia which is dangerous on hear & kidnney. Matrix protein degenration
22
Q

Mention autonomic effects of spinal shock

A
  1. Loss of autonomic reflexes resulting in atonia in wall & sphincters of bladder & rectum
  2. Loss of vasomotor control on sympathetic lateral horn cells, resulting in loss of vasomotor tone & hypotension
23
Q

Describe vascular effects of spinal shock

A
  1. Blood flow to paralyzed limb is decreased while venous return is also decreased thus the limb becomes cyanosed with dec nutrition
  2. Bed ulcers may occur especially in dependent areas
24
Q

Mention causes of reflex recovery

A
  1. Denervation hypersensitvity of remaining neurons thus can respond to afferent stimulation
  2. Increased collaterals from existing neurons & more formation of excitatory endings on interneurons & motor neurons.
25
Q

Explain mass reflex

A

Due to denervation hypersensitivity, release phenomenon from inhibitory gamma motor neurons and increased collateral in spinal cord. Large portion of spinal cord is stimulated at the same time with possibility of irradiation and reverberating circuits between these collateral neurons.

26
Q

Mention acute stage thalamic syndrome manifestations

A
  1. Sensory loss of all sensations of opposite side (body & face)
  2. Secondary hyperalgesia due ti release from gate inhibition
  3. Sensory ataxia
27
Q

Mention delayed stage thalamic syndrome manifestations

A
  1. Recovery of crude sensations but they are more crude
  2. Fine sensations are never recovered
  3. 2ry hyperalgesa
  4. Thalamic hyperpathia
  5. Emotional disturbance
  6. Motor ataxia
  7. Paroxysmal attacks of pain due to release from gate inhibition
28
Q

Compare sensory & motor ataxia

A

Sensory, due to loss of proprioception, finger to nose test can be done only with eyes opened, finger move behind & after nose, +ve Romberg, stamping gate.
Motor, due to cerebellar lesion, finger to nose test shows hypermetria even with open eyes, -ve Romberg, zigzag like gate.

29
Q

Distribution of anterior spinal artery

A

It supplies medial part of medulla oblongata and ant 2/3 of the cross sectional area of spinal cord, which is anterior and lateral white columns, anterior & lateral horns, base of dorsal horn.

30
Q

Describe origin of posterior spinal arteries

A

From vertebral or more commonly from its posterior cerebellar branch

31
Q

Distribution of posterior spinal arteries

A

Posterior 1/3 of spinal cord, posterior white column & post horn

32
Q

Describe origin of radicukar arteries

A

Vertebral, ascending cervical, posterior intercostal & 1st lumbar

33
Q

Mention an infectious cause of LMNL

A

Poliomyelitis

34
Q

Describe effects of UMNL on reflex activity

A

-Exaggerated reflexes in opposite side
-Hypertonia due to loss of supraspinal inhibition on gamma fibers, marked in antigravity muscles
-Spasticity of clasp knife character due to Golgi tendon stimulation
-Hyperreflexia of deep reflexes & tendon jerk, clonus occurs which rpare repeated cycles of stretch-inverse stretch reflex
-Loss of superficial abdominal reflexes
-Positive babniski sign

35
Q

Describe effects of UMNL on voluntary movements

A

-Generalzied contralateral hemiplegia, if the lesion is below level of medulla it will be ipsiltaeral
-Imrovement of gross movements of axial & proximal muscles in 2 weeks but distal movement is lost
-This is due to intact ipsillateral corticospinal fibers thatvterminate of medial alpha cells that mediate gross movement
-Patiaent can walk with a gait knwon as circumduction

36
Q

Define fasciulation & fibrillation & causes

A

Fasciculation is jerky, visible contractions of group of muscle fibers it is both seen & felt.
Due to pthalogic discharge of spinal motor neurons
Fibrillation is irregular contraction of individual fibers invisible to eye but is felt & detected elecrhysiologically
Due to denervation hypersensitivity to circulating Ach

37
Q

Describe effects of LMNL

A
  1. Ipsilateral flaccid paralysis
  2. Loss of muscle tone, deep reflexes & superficial reflexes of the affected muscle
  3. Muscle atrophy due to loss of voluntary & reflex activity and due to & trophic effects on metabolism of affected muscle due to damage of nerve supply.
  4. Fasciculations & fibrillations of affected muscle

CNS Physiology (16 decks)

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