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Clin Med- P > neuro- NM disorders > Flashcards

neuro- NM disorders Flashcards

1
Q

what is bells palsy? S&S?

A

paralysis of muscles supplied by facial nerve (CN VII), usually unilateral, caused by inflammation w/in facial canal or stylomastoid foramen. (nerve too big or whole too small)
-sudden onset, ipsilateral dry eye (inadequate lid closure), hyperacusis (hearing sensitive), earache, loss of taste, numbness

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2
Q

what is the pathophys of bells palsy? who gets it? what percent resolve spontaneously?

A

idiopathic, possibly linked to HSV-1 (ramsey-hunt syndrome)

  • men more than women
  • possibly family linked- passing down of small foramen? (no genetic basis )
  • 85% resolve spontaneously in a year
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3
Q

studies for bells palsy?

A

none necessary - no labs are determinant

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4
Q

treatment for bell’s palsy

A
  • lubricating eye drops
    -oral prednisone (w/ anti-virals to cover HSV) - 6-10 days
    -surgery if bad
    -
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5
Q

what is guillien-barre syndrome? what causes it?

A

autoimmune disorder where body attacks nervous system: acute inflammation, demyelination by antiganglioside antiBs, ascending paralysis
-often preceded by URI/diarrhea viral illness 1-3wks before (campylobacter)

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6
Q

S&S of GB?

A
  • dysesthesias (feelings in absence of stimuli)
  • parestethias (numbness/tingle)
  • areflexia
  • dec. positional and vibratory sensation
  • back and leg pain
  • ascending weakness
  • resp. muscle paralysis = death
  • labile (easily changed) BP, arrythmias
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7
Q

2 labs/tests for GB?

A
  • CSF- elevated protein w/ normal WBC

- nerve conduction studies (most sensitive)- conduction block is common

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8
Q

txt for GB? 2 effective therapies?

A

no cure
-hospitalize w/ concern for resp. function failure - intubate
–> support body until it is cleared from it
2 effective therapies speed recovery and reduce severity: plasma exchange & IVIG

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9
Q

what is myasthenia gravis? what is is assoc w/?

A
  • MG antiBs blockage of NM transmission at nicotinic receptors
  • ocular, masticatory, facial muscles - easily fatigued, inc weakness at end of day
  • onset: anything that can activate immune system
  • assosciated w/ other autoimmune diseases, thymoma (thymus tumor)
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10
Q

how does MG present?

A
  • any age, females >males
  • ptosis, diplopia, ptosis, chewing/swallow issues, resp. difficulty, limb weakness
  • weakness in PE (not in nerve root/dermatome distribution)
  • activity = weakness
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11
Q

2 ways to distinguish bells palsy from MG?

A
  1. bells- focal neuro deficits like affected pupillary response, MG does not - only has extraocular muscles effected (ptosis)
  2. bells- areflexive, MG-no reflex change
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12
Q

what is the tensilon challenge?

A

Dx of MG: give pt tensilon (which temporarily blocks axn of acetylcholinesterase)
-response in 5min, improvement of muscles = MG!

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13
Q

2 lab tests for MG?

A
  1. serum anti-AChR

2. Xray or CT of chest may show thymoma

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14
Q

5 possible txts for MG?

A
  1. anticholinesterase drugs (pyridostigmine or neostigmine)
  2. thymectomy (w/ thymoma) in pts <60yo (decreases immune hyperfunction)
    3.immunosuppressants
  3. plasmapheresis/IVIG
  4. pt education: heat and exercise may make symptoms worse
    (mostly supportive care, usually well-managed, fatalities from resp complications)
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15
Q

what is multiple sclerosis?

A

chronic, unpredictable, neuro-immuno disease of CNS

  • likely autoimmune cause
  • inflamm, destruction of myelin, glial scarring
  • eventual irreversible axonal loss (in many cases)
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16
Q

what causes MS?

A

likely. .. autoimmune, genetic
- trigger to cause break in BBB (CNS is usually safe from immune system), immune cells can then infiltrate and attacks central myelin
- -> maybe infection or trauma cause…

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17
Q

who gets MS?

A

young, white, females

-common farther away from equator (migration from high risk areas before age 15 = less risk)

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18
Q

how does MS present?

A
  • weak, numb, tired, tingle
  • imbalance, spastic, tremors
  • speech and swallowing impairments
  • diplopia: 90% w/ optis dysfunction
  • sphincter dysfunction
  • depression, cognitive decline
  • symptoms often fleeting
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19
Q

how many general kinds of MS are there?

A

4

20
Q

imaging for MS?

A

MRI - Dx based on lesions and clinical picture
CAN NOT Dx w/ CT, neg. CT DOES NOT rule out MS
-sed rate: very nonspecific, very sensitive

21
Q

PE for MS shows…5 things

A

nystagmus, visual field deficits (diplopia), dysarthria (speech disorder from muscle weakness), sensorimotor deficits, cerebellar signs

22
Q

Txt goals for MS- 5 major points

A
  • preservation of function between flares, and exercise (keep out of wheelchair for as long as possible!)
  • treat symptoms w/ drugs (spasticity, incontinence, fatigue, pain, depression)
  • PT, OT, cooling vest (overheat = flare)
  • high dose steroids for acute flares (# of times needed coincides w/ severity of disease)
  • plasmapharesis for relapsing forms
23
Q

disease modifying drugs for MS…what do they do and when do you take them? downsides? which one was found to improve walking ability?

A

decrease plaque formation and improve life and longevity

  • these are used earlier, rather than just managing symptoms
  • but they have ADRs and drug rxns
  • fampridine
24
Q

ALS/Lou Gehrig Disease : what is it and what are the 3 kinds?

A

degeneration disease that affects upper and lower motor neurons

  • amytrophic lateral sclerosis: sporadic and most common form of disease (bulbar palsy, muscular atrophy, primary lateral sclerosis)
  • familial ALS
  • ALS-parkinson dementia: complex of Guam (specific type- enviro component)
25
Q

who gets ALS?

A

men, after age 40

26
Q

S&S of ALS?

A

focal wasting of muscle groups, fasciculations

-spares cognitive (watching their bodies fail), ocularmotor, sensory and autonomic functions

27
Q

what is amyotrophic?

A

type of ALS, most common, muscles degenerate due to lack of trophic support from nerves

28
Q

what is lateral sclerosis?

A

component of amyotrophic ALS, lateral horn of spinal cord becomes fibrotic as motor neurons die

29
Q

what is sporadic ALS?

A

degeneration of upper and lower motor neurons , toxic levels of glutamate in serum and CSF (increase cell lysis = inc glutamate = inc cell lysis…)

30
Q

what does a muscle biopsy for ALS show?

A

shrunken angulated muscle fibers

31
Q

txt for ALS?

A

no cure, just supportive

32
Q

what is cerebral palsy?

A

motor dysfunction, non-progressive

-a result of CNS insult that occurs prenatally, perinatally or in first 3 years of life

33
Q

up to 15% of infants with low birth weight will have…

A

cerebral palsy

34
Q

what are the major risk factors for cerebral palsy?

A

hypoxia, seizures during prenatal period, and other birth complications

35
Q

S&S of cerebral palsy?

A
  • spastic (40%), contractures
  • mental retardation and aphonia w. quadriplegia and mixed forms
  • normal intelligence and tremors w. hemiplegia or paraplegia
  • scissors gait, to walking
36
Q

what is athetotic CP?

A

CP w/ writhing/chorea movements, speech issues, muscular hypertrophy

37
Q

2 main types of CP?

A

ataxic: normal intelligence, clumsy, difficulty w/ fine movements
mixed: spastic/chorea, mental retardation

38
Q

early warning signs with CP

A

toe-walking, fisting, delay in motor milestones, seizures, hand dominance before age 2 (dominant hand not effected in hemiplegia)

39
Q

what allows you to rule out CP in your Ddx?

A

progression

40
Q

CP txt?

A

drugs for symptoms- spastic, sleep disturbances, irritability, monitor for UTI (sphincter control), botox to release spasm, surgery- tendon release

41
Q

babinski test

A

for UMN lesion - increased tendon reflexes and extensor plantar response

42
Q

tetany

A

painful muscle spasm, from faulty Ca+ metabolism

43
Q

clonus

A

muscle spasm w/ regular contractions

44
Q

fasciculation

A

involuntary muscle twitch (localized and temporary)

45
Q

flaccid paralysis

A

LMN lesion- interruption between muscles and spinal cord

Clin Med- P (124 decks)

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