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Neurology (inpt) > diseases of peripheral nerves > Flashcards

diseases of peripheral nerves Flashcards

1
Q

what are the main features of myasthenia gravis?

A

weakness and fatigability that is improved with rest

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2
Q

what is the onset of MG like?

A

usually insidious, but can be made evident by a coincidental dental infection that exacerbates the sx

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3
Q

who is normally diagnosed with MG?

A

young women and older men

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4
Q

what is the PP of MG?

A

antibodies directed against the acetylcholine receptor on the muscle surface that can cause an increased rate of receptor distruction leading to weakness

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5
Q

what are the clinical features of MG?

A
  • ptosis
  • diplopia (60% of pts have these two)
  • difficulty in chewing or swallowing
  • respiratory difficulty
  • limb weakness

(2 clinical forms- ocular weakness or genearlized that affects ocular, bulbar,limb and respirator muscles

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6
Q

how often do the sx present? (MG)

A

can fluctuate in intensity during the day, tendency to have longer term spontaneous relapses and remission that may last for weeks

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7
Q

what should the clinical exam reveal? MG

A

weakness and fatigability of the affected muscles that improves with rest

  • normal sensations
  • no reflex changes
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8
Q

how is the diagnosis confirmed? MG

A

clinical improvement after a short acting anticholinesterase (edrophonium)

TENSILON TEST

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9
Q

dx studies fo MG

A
  • chest CT or MRI to r/o coexsiting thymoma
  • electrophysiologic studies-show decremating muscle response
  • serum assay for elevated levels of acetylcholine receptor antibodies (positive in 80-90% of pts)
  • MuSK antibody (muscle -specific tyrosine kinase)
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10
Q

mainstay tx of MG

A

cholinesterase inhibitor-pyridostigmine
prevents destruction of acetylcholine by acetylchoinesterase and allows the transmission of nerve impulses across the neuromuscular junction

-thymectomy

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11
Q

ADR of pyridostigmine

A

-cholinergic crisis, AV block, bradycardia, hypotension
-Skin rash (bromide)
Muscarinic
nausea, vomiting, diarrhea, abdominal cramps, increased peristalsis, increased salivation, increased bronchial secretions, miosis and diaphoresis
Nicotinic
muscle cramps, fasciculation and weakness

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12
Q

what disease is pyridostigmine contraindicated in?

A

urinary or bowel obstruction or use in asthma/COPD pts (iprtropium, tiotropium)

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13
Q

what is a cholingergic crisis?

A 
Increasing muscle weakness
Can be difficult to distinguish from worsening MG
Differentiate with the Tensilon test
Administer edrophonium
If weakness worsens = cholinergic crisis
If weakness improves = myasthenic crisis
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14
Q

how do you tx a cholingergic crisis?

A

with atropine

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15
Q

what are bulblar sx?

A

dysarthria, dysphagia, facial weakness,weakness of mastication

**respiratory compromise

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16
Q

guillian barre syndreom

A

idiopathic polynerupoathy often following minor infections, immuiations or surgical prcecures

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17
Q

what infection is related to GBS?

A

lung and GI infections

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18
Q

what is the most common precipitant of GBS?

A

campylobacter jejuni , can also see EBV, CMV, HIV

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19
Q

what are the CF of GBS?

A

symmetrical extremity weakness that begins distally and ascends, proximal muscles ten to be affected more often than distal muscles

“rubbery legs” that tend to buckle

  • may have sensory deficits
  • pain (deep aching pain)
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20
Q

what will happen to DTRs in GBS?

A

may be decreased or absent

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21
Q

can GS be life threatening?

A

yes, if it involves the muscles of respiration or swallowing- most pts will need ventilation assistance

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22
Q

what willl electrophysiologic studies reveal in GBS?

A

slowing of nerve conduction velocities, both motor and sensory

-denervation or axonal loss

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23
Q

what cranial nerve can also be affected in GBS?

A

facial (if its alone then bells palsy)

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24
Q

what kind of sensory loss can be expected with GBS?

A

proprioception and areflexia

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25
Q

what are some anatomic symptoms that may be seen w/ GBS?

A

-autonomic dysfxn: tachycardia, cardiac irregularities, labile blood pressure, disturbed sweating, impaired pulmonary fxn, sphincter disturbances, paralytic ileus

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26
Q

what other diagnostic testing can bc done with GBS?

A

CSF evaluation: elevated protein, ut cell counts are normal

27
Q

what is the tx of GBS?

A

inpt care-w/ close monitoring of respiratory status- can progress to orthostatic hypootension or arrythmias

PT/OT/ speech therapy

28
Q

what is the most common form of GBS?

A

acute inflammatory demyelilnating polyneruopathy (AIDP)

29
Q

once admitted, what can be done to GBS pts to hlep prevent the progression/decrease recovery time?

A

plasmapheresis

-can also use gabapentin for pain

30
Q

what can be used in pts with cardiovascular instability and in kids w/ GBS insteat of plasmapheresis?

A

intravenous immunoglobulin (IVIG)

31
Q

what is the miller-fisher syndrome?

A

a

variation of GBS

32
Q

what is the prognosis of GBS?

A

most make a full recovery in 1 year, mortality rate is 5%

33
Q

Complex regional pain syndrome (CRPS)

A

aka reflex sympathetic dystrophy

  • most pts don’t have an indentifiable neruologic lesion responsible for the pain
  • 2 mains types: Type I (no cause, no nerve lesion), Type II (definited nerve lesion)
34
Q

what can trigger CRPS?

A

operation, an injury, a vascular event (stroke, MI)

almost 1/3 have an idiopathic cause

35
Q

what is CRPS characterized by?

A

regional pain in the affected limb, retricted mobility, edema, color changes of the skin, and spotty bone thinnig

36
Q

what is the PP of CRPS?

A

thought to be partially secondary to abnormal sensitivity to inflammatory mediators of pain

37
Q

what are the hallmark features of CRPS?

A

severe burning or throbbing pain w/ associated allodynia in the affected region/extremity

  • cyanosis, abnormal sensitivity to cold and warm exposure, abnormal skin temp, atrophy
  • limited ROM
  • bone demineralization
38
Q

what can be other causes of CRPS symptoms?

A

vasculitis, claudication, nerve root impingement, atrophy from disuse, and progressive systemic sclorisis

39
Q

hwat are some diagnostic studies that can be helpful in making the dx?

A

bone scintigraphy, plain XRay, MRI

-regional nerve block can be used for diagnosis, complete relief of pain is consistent w/ CRPS

40
Q

what is PP of CRPS?

A

formation of reflex arc

-increased sensitivity of injured axons

41
Q

what are the three stages of CRPS? (clinical features)

A

Characterized by pain, burning, temperature hyperalgesia, local edema, and restricted mobility
Worsening of the edema, skin thickening, atrophy, and wasting of the muscles in the affected region
Symptoms have worsened to limited range of motion, irreversible skin and nail changes, and demineralization seen on x-ray
The most severe stage
These characteristics can intermingle at any given time

42
Q

what can be done to prevent CRPS?

A

early mobilization after injury

43
Q

what type of meds can be used for pain relief?

A

amitryptyline, nortriptyline, gabapentin, pregabali, or lamotrigine

+/- nsaids

-calcitonin, bisphosphanates, IVIG, regional nerve blocks, or dorsal column
stimulation may be effective

-tender point injections

44
Q

Bell palsy?

A

unilateral facial muscle weakness noted w/o evidence of other neruologic dz

45
Q

what side of the face is most affected by bell palsy?

A

the right side

46
Q

what is the primary cause of bell palsy?

A

HSV activation, but other viruses (herpes zoster,0, trauma, neoplasia, or toxins can be causative too

47
Q

what is the end result of bell palsy?

A

damage to the myelin layer facial nerve

48
Q

what pt population is more likely to get bell palsy?

A

prgo and DM

49
Q

what are the clinical features of bell palsy?

A

facial muscle weakness typically begins abruptly - but it may progress over a matter of hours to 2 days

  • can be complete or incomplete palsy
  • pain in the ipsilateral ear often preceded the facial weakness
  • may see impariment of taste, lacrimation, or hypacusis
50
Q

what will a clinical exam reveal? BP

A

no abnormality byond the motor or fxn of cranial nerve VII

51
Q

when do sx peak for BP

A

weakness peaks at about 21 days, and revcory (partial or complete) in 6 mnths

52
Q

dx of BP?

A
  • clinical

- specific diagnostic testing is only done when the pt has prolonged BP

53
Q

what other conditions do you need to rule out when dz BP?

A

stroke, tumor, lyme dz, AIDS, sarcoidosis

54
Q

tx of BP?

A
  • most resolves spontaneously, but course if varied
  • supportive care like lubricating eye drops
  • prednisone
  • surgery in recalictrant cases
55
Q

what is a poorer prognosis of BP associated with?

A

w/ pts presenting w/ severe pain and complete palsy, hyperacusis, or advanced age

56
Q

Diabetic peripheral neuropathy?

A

most common type of neruopathy dx in the western hemisphere

57
Q

PP of DPN?

A
  • can be the presenting sx in occult DM

- result of vascular insufficiency or nerve infarction

58
Q

CF of DPN?

A

sx more common in the lower extremities than in the uper extremities

  • pain, numbness, dysesthesias (burning) or paresthesias
  • first: reduced deep tendon reflexes (ankle jerk), impaired vibratory sensation
59
Q

what are some autonomic complications related to dm?

A

postural hypotension, cardiac arrhythmias, impaired thermoregulatory sweating, and disturbances of bowel, bladder, gastric and sexual function

60
Q

dx studies of DM PN?

A

serial nerve conduction studies to document the presence, severity, and course of the neuropathy

61
Q

tx of DM PN?

A

tight control of hyperglycemia,

-entrapment neuropathy: may respond to a decompression procedure

62
Q

drug therapy for diabetic polyneuropathy?

A

-deep, constant aching pain: amitriptyline, nortriptyline, desipramine, gabapenting, or pregabalin

  • duloxetine (SSnRI)
  • postural hypotension: may respond to salt supplementation, lower extremity pressure stocking, or meds like fludrocortisone or midodrine
63
Q

midodrine?

A

A1 adrenergic receptors-it an inotrope/pressor

Neurology (inpt) (10 decks)

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