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Peripheral neuropathies Flashcards

1
Q

Definition of polyneuropathy?

Etiologies?

A
  • symmetric distal sensory loss with burning, or weakness
  • etiologies:
    adverse effect of meds, manifestation of systemic disease
    PP: can be axonal or demyelinating
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2
Q

Pathogenesis of GBS?

A
  • acute immune mediated group polyneuropathies, usually provoked by preceding infection
  • acute inflammatory demyelinating polyneuropathy (AIDP) - most common one seen in US and Europe (85-90%)
  • acute motor axonal neuropathy and acute motor and sensory axonal neuropathy- most common in Asia
  • preceded by infection: usually campylobacter jejuni or respiratory tract infection, others - CMV and EBV
  • small percentage result from immunizations, surgery, trauma, and bone marrow transplant
  • causes generation of Abs to gangliosides that cause axonal injury or immune response to myelin
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3
Q

GBS clinical features?

A
  • symmetric muscle weakness w/ absent or decreased DTRs
  • weakness usually starts proximal legs, begins arm and facial muscles - 10% of pts
  • severe respiratory muscle weakness requiring ventilator support - 30%
  • parasthesia’s in hands/feet common (80%), sensory abnorm on exam frequently mild
  • often prominent severe back pain
  • dysautonia (70%) - tachycardia, urinary retention, HTN alt w/ hypotension, orthostatic hypotension, bradycardia, ileus, loss of sweating
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4
Q

Therapy for GBS?

A
  • plasmapheresis or IV immune globulin
  • ventilator if resp muscles failing
  • give proph IV PPI for prevention of GI problems
  • lovenox SQ for prevention of DVTs
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5
Q

GBS dx? features that make GBS doubtful?

A
  • LP:
    elevated CSF protein
    normal WBC count in CSF

-neurophysiology studies:
EMG
Nerve conduction studies

  • glycolipid abs to gangliosides

GBS doubtful:

  • if sensory fxn lost
  • marked, persistent asymmetry of weakness
  • severe and persistent bowel and bladder dysfxn
  • more than 50 WBCs in CSF
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6
Q

What is Bell’s palsy?

Anatomy?

A
  • acute peripheral facial palsy of unknown origin

anatomy:

  • fibers for motor output to facial muscles
  • parasympathetic fibers to lacrimal, submandibular, and sublingual salivary glands
  • afferent fibers for taste from anterior 2/3 of tongue
  • somatic afferents for external auditory canal and pinna
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7
Q

Epidemiology of Bell’s palsy?

A
  • risk is 3x greater in pregnancy (immunosuppressed)
  • 8-10% increased incidence of recurrence ipsilateral or contralateral side
  • DM presents 5-10% of pts
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8
Q

Pathogenesis of Bell’s palsy?

A
  • herpes simplex most common cause of Bell’s palsy
  • other infectious causes: EBV, adenovirus, rubella, mumps, influenza B, herpes zoster, and coxsackie virus, ischemia may also be a cause
  • in pregnancy - 3rd trimester due likely to fluid retention - pressure on nerve
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9
Q

Clinical presentation of Bell’s palsy?

PE?

A
  • suden onset - over hours: unilateral facial paralysis
  • eyebrow sagging
  • inability to close the eye
  • disappearance of nasolabial fold
  • mouth drawn to non affected side
  • decreased tearing

PE:

  • assess facial movement
  • general physical and neuro exam
  • attention to external ear for vesicles or scabbing
  • attention to parotid for mass lesions (tumor?)
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10
Q

Course of Bell’s palsy? Features that pt to it not being Bell’s palsy?

A
  • onset over hours to 1-2 days
  • progressive w/ maximal paralysis within 3 weeks of onset
  • recovery of some degree of fxn by 6 months
  • key features - not Bell’s palsy:
    if onset prolonged
    relapsing course
    paralysis persists or physical signs atypical
    then need to do imaging studies - high resolution CT or MRI with gadolinium
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11
Q

Bell’s palsy diff dx?

A
  • Lyme disease
  • HIV
  • bacterial otitis media
  • cholesteatoma if onset of palsy gradual
  • sarcoidosis
  • sjorgren’s syndrome (unusual)
  • tumors
  • stroke
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12
Q

Management of Bell’s palsy?

A
  • early short term glucocorticoid therapy: should begin within 3 days of sxs, antivirals no longer thought to be helpful so not added to tx
  • eye care: ointment in eye at night to keep it moist, tape it or use eye patch - prevent abrasions
  • during day wear glasses and use eye drops
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13
Q

information to tell pt about Bell’s palsy and recovery?

A
  • caused by inflammation of facial nerve, usually by virus, and as nerve swells ot becomes compressd and protective covering breaks down, it takes time to recover and recovery may be disorganized:
    want to do one thing and your face will do another thing - like trying to smile and your eye tears
  • will have decreased taste
  • really have to take care of your eye - keep it covered and keep it moist
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14
Q

Pathogenesis of myasthenia gravis?

A
  • autoimmune disorder characterized by weakness and fatigability of skeletal muscle
  • autoabs against acetylcholine receptors (AChR-Ab)
  • decrease in number of ACh receptors becuase pf AChR-Ab binding
  • destruction of receptors by a compliment mediated process
  • 10-20% of pts are ab negative, they may have abs directed against another target - muscle specific receptor tyrosine kinase (MuSK)
  • T cells bind to acetylcholine receptors and activate B cells
  • most pts with MG have thymic abnormalities: hyperplasia or thymoma
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15
Q

epidemiology of MG?

A
  • annual incidence of 10-20 new cases per million, prevalence is 150-200 million
  • prevalence has been increasing over the past 5 decades
  • bimodal distribution: early peak 2nd and 3rd decades (female predominance - tends to be hormonal), and late peak 6th-8th decades (male predominance)
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16
Q

Clinical manifestations of MG?

A
  • Key sxs:
    fluctuating skeletal muscle weakness, worsened by contractile force, true muscle fatigue not tiredness
  • ocular:
    ptosis, can be bilateral or unilateral, EOM often involved leading to diplopia, ptosis increases with sustaiend upward gaze or by holding up the opposite eyelid
  • bulbar: weakness with prolonged chewing, jaw weakness at rest,
    oropharyngeal muscle weakness - dysarthria and dysphagia (imminent risk of aspiration can produce myasthenic crisis)
  • nasal regurgitation of liquids
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17
Q

Clinical presentation of MG?

A
  • facial:
    pt appears expressionless
    lost his or her smile
    weakness or orbicularis oris muscle “myasthenic sneer”, weakness of orbicularis oculi

neck and limb:

  • wt of head overcome extensors results in dropped head syndrome
  • limbs proximal weakness: arms more affected legs
  • wrist and finger extensors and foot dorsiflexors involved

respiratory: when respiratory muscles weaken produces resp insufficiency and pending respiratory failure which is life threatening

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18
Q

Clinical course of MG?

A
  • early on sxs transient, ok in am worse later in day or when tired or have exercised
  • max extent of disease seen 77% pts 3 years
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19
Q

Dx of MG?

A

serologic testing immunologic assays:

  • detect circulating AChR-Ab
  • seronegative MG - 40-50% will have Ab to muscle specific receptor MuSK
  • small % double seronegative
electrophysiologic studies:
- repetitive nerve stimulation studies
- single fiber EMG:
more technically demanding
less widely available
*most sensitive test for MG
20
Q

Diff dx of MG?

A
  • thyroid opthalmopathy
  • brainstem and motor CN pathology
- for generalized disease:
generalized fatigue
motor neuron disease (ALS)
botulism
penillinase-induced myasthenia
congenital myasthnic syndromes
21
Q

Tx for MG?

A
  • anticholinesterase agents:
    pyridostgigmine (mestinon)
    for sx tx (SE-cholinergic - diarrhea, increased salivation, decreased HR)

chronic immunotherapies:

  • moderate doses corticosteroids
  • immunosuppressive meds

rapid immunotherapies:
plasmapheresis
IV immunoglobulin

surgery: thymectomy for thymoma

22
Q

Polyneuropathy? Etiologies?

A
  • symmetric distal sensory loss
  • with sxs of burning and eventually weakness

etiologies:

  • diabetic polyneuropathy most common - up to 50% diabetics will develop it
  • pts with AIDs - 12%
  • Vit B 12 deficiency
  • toxins: alcohol, chemo, heavy metals
  • other vitamin deficiences less common
  • uremia: Kidney failure
23
Q

PP of polyneuropathies?

A

axonal: most common - injury is related to axonal length
demyelinating: seen more in autoimmune and to some extent in diabetic polyneuropathy

24
Q

Clinical presentation of polyneuropathies?

A
  • slowly progressive sensory loss: first in feet
  • dysesthesias: burning, pain
  • mild gait abnormalities
  • as progresses mild weakness in lower legs and hand sxs (begin stocking and glove)
  • severe cases affect intercostal nerves, sternum, top of the head
25
Q

Physical exam findings for polyneuropathy?

A
  • sensory exam: decreased ability to distinguish b/t dull and sharp sensation, may have absent sensation
  • reflexes: decreased or absent especially in ankles
  • motor exam: strength, will be normal early on and get progessively weaker
  • vibratory: absent at great toe most likely then later on at malleolus and then up to knee
  • propioception: won’t be able to distinguish b/t up and down, why they will have ataxia
26
Q

Diff dx of polyneuropathy? When is a more complete workup indicated? What are these tests?

A
  • progressive numbness and weakness in lower extremities may be a result of a spinal cord process
  • pts with mild sxs and known underlying reason do not warrant extensive testing
  • if there is no clear etiology or sxs are severe and rapidly progressive then a more complete dx workup is indicated
  • if more complete workup indicated order:
    electrodiagnostic testing - see reduced amplitude of evoked compound action potentials, preservation of nerve conduction studies
27
Q

What labs should be ordered in a pt with suspected polyneuropathy?

A
  • CBC, ESR, TSH, glucose, Vit B12 level, ANA, UA
28
Q

RFs for diabetic polyneuropathy?

A
  • duration and severity of hyperglycemia
  • increased TG levels
  • BMI
  • whether the pt smokes or not
  • presence of HTN at baseline
29
Q

Pathogenesis of diabetic polyneuropathy?

A
  • accum of advanced glycosylation end products: strong cross linking activity with collagen, increase vascular permeability, monocyte influx contributing to vascular injury
  • accum of sorbitol: this interferes with cell metabolism
  • increased oxidative stress: accum of reactive O2 species therefore reduced antioxidant defense
  • nerve ischemia
  • peripheral nerve repair is impaired in diabetes (decreased perfusion)
  • all of this results in length-dependent “dying back” axonopathy
  • involves distal portions of longest myelinated and unmyelinated sensory axons
  • relative sparing of motor axons
30
Q

Most common neuropathy in the western world?

A
  • diabetic polyneuropathy

- 50% of pts with diabetes will develop neuropathy

31
Q

DPN summary?

A
  • loss of vibratory sensation and altered proprioception
  • impairment of pain, light touch and temperature
  • decreased or absent reflexes occur early in the disease
  • more widespread loss of reflexes and motor weakness are late findings
  • screening/scoring systems
  • Complications: falls, ulcers: lead to amputations
32
Q

diff dx of diabetic polyneuropathy?

A
  • other forms of neuropathy are more common in diabetics!
  • chronic inflammatory demyelinating polyneuropathy
  • Vit B12 deficiency
  • hypothyroidism
  • uremia
  • acute painful neuropathies assoc with rapid glycemic control, unintended severe wt loss or intentional wt loss

Tx: tight glycemic control
prevention: tight glycemic control, smoking cessation, wt loss

33
Q

Polyneuropathy sx Rx?

A
  • gabapentin (neurontin): reduces pain, well tolerated
  • TCAs: such as amitriptyline and desipramine
  • carbamazepine (tegretol) and phenytoin (dilantin) have varying success
  • pregabalin (lyrica): targeted for diabetics but is worth trying for pts regardless of etiology
  • duloxetine (cymbalta): has advantage of being an antidepressant as well as helping control pain
  • DON’T give narcotics!
34
Q

Pathogenesis of alcoholic polyneuropathy?

A
  • axonal neuropathy complicated by demyelination when there is coexisting nutritional deficiency
  • reduction in density of small myelinated and unmyelinated fibers with normal thiamine status
  • alcohol is direct neurotoxon
  • correlates best with lifetime alcohol consumption
  • tx: stop drinking!
35
Q

Absorption of B12 factors?

A

adequate absorption of cobalamin (B12) depends on:

  • dietary intake
  • acid-pepsin to liberate Cbl from binding proteins
  • pancreatic proteases to free Cbl from R factors
  • secretion of IF by parietal cells to bind Cbl
  • ileum with Cbl-IF receptors
36
Q

Causes of B12 deficiency?

A
  • not enough intake (veggie diet)
  • stomach: bariatric surgery, decreased stomach acid in older people
  • intestine: celiacs or crohns disease
37
Q

Vitamin B12 deficiency polyneuropathy?

A
  • defect in myelin formation leading to subacute degeneration of dorsal (posterior) and lateral spinal columns
  • paresthesia’s, ataxia with loss of vibration and positon sense, can progress to severe weakness, spasticity, clonus, and paraplegia
38
Q

Dx vit B12 def polyneuropathy?

A
  • serum B12 levels, serum gastrin, parietal cell abs, anti-intrinsic factor abs, check for H pylori
39
Q

Tx of Vit B 12 def polyneuropathy?

A
  • IM B12 injections 1000 micrograms 2x weekly for 2 weeks
  • weekly injections for 2 months
  • then monthly injections for life or until deficiency resolves
40
Q

Vit E deficiency polyneuropathy?

A

Vit E:

  • spinocerebellar syndrome
  • variable peripheral nerve involvement: ataxia, hyporeflexia, proprioceptive and vibratory loss
  • rarely caused by dietary inadequacy, seen with chronic cholestasis and pancreatic insufficiency (fat malabsorption - steatorrhea)
41
Q

Dx of Vit E deficiency polyneuropathy?

A
  • serum alpha-tocopherol divided by sum of serum cholesterol + TGs
42
Q

Tx of vit E deficiency polyneuropathy?

A
  • large oral doses (200 IU/kg/d) or IM doses of alpha-tocopherol are used then daily oral vit E
43
Q

Thiamine deficiency polyneuropathy?
Dx?
Tx?

A
  • deficiency seen in anorexia nervosa, malnutrition, alcoholism, bariatric surgery pts
  • dry beriberi: neuropathy assoc with calf cramps, muscle tenderness, and burning feet, autonomic neuropathy may be present
  • wet beriberi: high output CHF + neuropathy
  • dx: urinary thiamine, serum thiamine
    tx: 50-100 mg IV, IM or orally, give before glucose to prevent encephalopathy
44
Q

GBS has what kind of paraylsis pattern? what isn’t realy affected? LP findings?

A
  • bilateral ascending paralysis with little sensory loss and high protein level in CSF on LP
45
Q

Bell’s palsy is what type of paralysis?

A
  • acute paralysis, unilateral

- eye must be protected!

46
Q

Peripheral neuropathies?

A
  • more chronic, have diff pathophys paths with similar presentation:
  • not a simple neuropathy because there is an underlying cause - tx this

Neuro (19 decks)

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