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Neurology Week 2 > Peripheral Neuropathies > Flashcards

Peripheral Neuropathies Flashcards

1
Q

Polyneuropathy

A

Symmetrical distal sensory loss with burning or weakness.
Med rxn or systemic dz
Can be axonal or demyelinating

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2
Q

Guillain-Barre Syndrome (GBS)

A

Acute immune-mediated group of polyneuropathies, usually provoked by preceding infection.

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3
Q

GBS Patho

A

Acute inflammatory demyelinating polyneuropathy (AIDP)
Can be caused by preceding infxn, immunizations, surgery
Generation of antibodies against galgliosides that cause an immune response against axons

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4
Q

Which bug usually causes GBS?

A

Campylobacter Jejuni

also CMV, EBV

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5
Q

GBS clinical features

A 
Symmetrical muscle weakness
Decreased DTR's
Respiratory involvement
Parasthesias in hands and feet
Severe back pain
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6
Q

Where does weakness usually start in GBS?

A

Proximal legs, arm and facial muscles

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7
Q

Dysautonia

A

Common in GBS

Tachycardia, urinary retention, HTN altering with Hypotension, bradycardia, ileus, loss of sweating.

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8
Q

Therapy for GBS?

A

Plasmapheresis or IVIG

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9
Q

GBS DIagnosis

A

LP: Elevated protein

Neurophysiology studies

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10
Q

Bell’s Palsy

A

Acute peripheral facial palsy of unknown origin

Involves the facial nerve (CN VII)

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11
Q

What does the facial nerve innervate?

A

Facial motor output
Parasympathetics to salivary glands (including lacrimal)
Taste for anterior 2/3 of tongue
Somatics for EAC and pinna.

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12
Q

Bells palsy Epidemiology

A

Risk 3x greater in pregnancy
DM is risk factor
Recurrence is common

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13
Q

Bells palsy patho

A

Herpes virus most likely cause
Can also be other viruses
Ischemia may play a role

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14
Q

Bells palsy clinical presentation

A

Sudden onset over hours**
Eyebrow sagging, cant close eye
Mouth drawn to non-affected side
Decreased tearing**

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15
Q

Bells palsy course

A

Onset over hours to 1-2 days
Maximal paralysis within 3 wks of onset
Some degree of recovery by 6 months
Usually recover fully

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16
Q

Bells Palsy Mgmt

A

Eye care (drops)
Glucocorticoid therapy within 3 days of onset
For severe, valcyclovoir

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17
Q

Myasthenia Gravis (MG)

A

Autoimmune disorder characterized by weakness and fatiguability of skeletal muscle.
Decrease in number of acth receptors

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18
Q

What are the antibodies against in MG?

A

Acetylcholine receptors (AchR-Ab)

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19
Q

MG Patho

A

Acetylcholine receptor antibodies mount immune response via complement against receptors.
T cells bind receptors and activate B cells.

20
Q

Which thymus abnormalities do MG patients usually have?

A

Thymoma or hyperplasia

21
Q

MG Bimodal distribution

A

Females peak in 2nd and 3rd decade

Males peak in 6th to 8th decade

22
Q

MG Clinical Manifestations

A 
Fluctuating skeletal muscle fatigue worsened by contractile force.  
Ptosis, worse w/ upward gaze
Diploplia
Weakness with prolonged chewing
Dysphagia
23
Q

MG Neck and Limb Symptoms

A

Dropped head syndrome from weak neck

Limb proximal weakness Arms > Legs

24
Q

MG respiratory sx

A

Respiratory muscles weaken and leads to respiratory failure

25
Q

MG Course

A

Symptoms ok in morning, worse later in day

Maximal extent of dz seen in 3 yrs

26
Q

MG Dx

A

Detect circulating AChR-Ab

Electromyography

27
Q

MG Tx

A

Pyridostigmine
Corticosteroids
IVIG
Thymus surgery

28
Q

Polyneuropathy Causes

A

Diabetic polyneuropathy most common

AIDS, B12 def, Toxins, Uremia

29
Q

Polyneuropathy Patho

A

Axonal injury is most common

Demyelinating seen in some autoimmune processes

30
Q

Polyneuropathy Presentation

A

Slowly progressive loss of sensation in feet 1st
Dysesthesias, burning, pain
Gait abnormalities
Stocking and glove weakness

31
Q

Risk factors for diabetic polyneuropathy (DPN)

A 
Duration and severity of hyperglycemia
Increased triglycerides
Increased BMI
Smoking
HTN
32
Q

Diabetic Polyneuropathy Patho

A

Accumulation of AGE’s, collagen cross-linking, increased permeability, monocyte influx, vascular injury.
Accumulation of sorbitol, interferes w/ cell metabolism.
Axonopathy

33
Q

What is the most common neuropathy in the western world?

A

Diabetic neuropathy.

50% of DM pts will develop

34
Q

DPN S/S

A

Loss of vibratory sensation and proprioception
IMpaired pain, light touch and temp perception
Decreased/absent DTRs
Widespread losses are a late finding

35
Q

Best pain reliever for Polyneuropathy

A

Gabapentin (Neurontin)

36
Q

Best pain reliever for Diabetic PN

A

Pregabalin (lyrica)

37
Q

Other meds for Polyneuropathy

A 
Gabapentin (Neurontin)
TCA's (amitryptaline)
Carbamazepine (Tegretol) - varying success
Pregabalin (lyrica) - Diabetics
Duloxetine (Cymbalta)
38
Q

Alcoholic Polyneuropathy Patho

A

Axonal neuropathy complicated by demyelination with coexisting nutritional deficiency
Normal thiamine status
Alcohol is direct neurotoxin

39
Q

Vitamin B12 Deficiency

A

Cobalmin

Must have adequate dietary intake and intrinsic factor

40
Q

B12 Patho

A

Defect in myelin formation leads to subacute degeneration of dorsal and lateral spinal columns.

41
Q

S/S of B12 Def.

A

Parasthesias, ataxia, loss of proprioception, weakness, spasticity, clonus, paraplegia

42
Q

B12 Tx

A

IM B12 injections 1000mg twice weekly

43
Q

VItamin E deficiency

A

Spinocerebellar syndrome

Seen in pancreatic deficiency, cholestasis

44
Q

Vitamin E deficiency tx

A

Large oral doses of IM Alpha-Tocopherol

then daily oral vitamin E

45
Q

Thiamine Deficiencies

A

Seen in malnutrition, alcoholism, bariatric surgery

Dri or wet Beriberi

46
Q

Dry beriberi

A

Neuropathy associated with calf cramps, muscle tenderness, burning feet, autonomic neuropathy may be present.

47
Q

Wet beriberi

A

High output CHF and neuropathy

Neurology Week 2 (7 decks)

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