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Peripheral neuropathy Flashcards

1
Q

What is the definition of polyneuropathy?

PAthophys: can be from two things?

A

symmetric distal sensory loss with burning, or weakness

PP: can be axonal or demyelinating

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2
Q

Pathogenesis of Guillain-Barre Syndrome (GBS)‏

A

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

  1. Demyelinating is more common in the US
  2. Motor axonal is more common in Asia
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3
Q

GB is Preceded by infection such as?

2

A
  1. usually Campylobacter jejuni or respiratory tract infection, others are CMV and EBV
  2. Small percentage result from immunizations, surgery, trauma and bone marrow transplant
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4
Q

What do the antibodies attack and what does this cause?

A

Causes generation of antibodies to gangliosides that cause axonal injury or immune response to myelin

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5
Q

GBS clinical features?
1. What kind of muscle weakness and decreased what?

  1. Weakness starts where?
  2. What causes respiratory distress?
  3. Describe the sesnory effects of the disease?
  4. Often sevre pain where?
  5. What does Dysautonia (70%) cause? 7
A
  1. Symmetric muscle weakness w/ absent or decreased DTRs
  2. Weakness usually starts proximal legs, begins arm and facial muscles—10% patients
  3. Severe respiratory muscle weakness requiring ventilator support—30% patients
  4. Paraesthesia’s in hands/feet common (80%), sensory abnormalities on examination frequently mild
  5. Often prominent severe back pain
    • tachycardia,
    • urinary retention,
    • HTN alternating w/ hypotension, -orthostatic hypotension,
    • bradycardia,
    • ileus,
    • loss of sweating
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6
Q

How should he be taken care of in the hospital?

A

Hospital Course: The patient was admitted to the ICU where his VS and cardiac rhythm/BP were closely monitored

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7
Q

How would we treat?

2

A

Therapy for GBS is either plasmapheresis or IV immune globulin
-Our patient received IVIG for 5 days

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8
Q

Supportive treatment or for complications?

4

A
  1. Heparin,
  2. IV proton pump inhibitors
  3. compressions stalkings,
  4. turns
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9
Q

GBS diagnosis?

3

A
  1. Lumbar puncture
  2. Neurophysiology studies:
    - Eletromyography
    - Nerve conduction studies
  3. Glycolipid antibodies to gangliosides
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10
Q

What would the LP show?

2

A
  1. Elevated cerebrospinal fluid (CSF) protein

2. Normal WBC count in the CSF

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11
Q

Features make GBS doubtful?

4

A

1, Sensory level (shouldnt have any sensory level)

  1. Marked, persistent asymmetry of weakness
  2. Severe and persistent bowel and bladder dysfunction
  3. More then 50 white blood cells in the CSF
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12
Q

What is Bell’s Palsy?

What anatomical features are affected?
4

A

Acute peripheral facial palsy of unknown origin

  1. Fibers for motor output to the facial muscles
  2. Parasympathetic fibers to the lacrimal, submandibular, and sublingual salivary glands
  3. Afferent fibers for taste from the anterior 2/3 of the tongue
  4. Somatic afferents for the external auditory canal and pinna
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13
Q

Epidemiology

1. Risk is three times greater when?

A

Risk 3 x greater in pregnancy

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14
Q

Pathogenesis: BP

3

A
  1. Herpes simplex most common cause of Bell’s palsy
  2. Other infectious causes—EBV, adenovirus, rubella, mumps, influenza B, herpes zoster, and coxsackie virus
  3. Ischemia may be a cause
    In pregnancy—3rd trimester due likely to fluid retention
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15
Q

Bell’s Palsy clinical presentation:

6

A
  1. Sudden onset—over hours: unilateral facial paralysis
  2. Eyebrow sagging
  3. Inability to close the eye
  4. Disappearance of the nasolabial fold
  5. Mouth drawn to the non affected side
  6. Decreased tearing
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16
Q

Physical exam for BP: What are we looking for?

A
  1. Assess facial movement
  2. General physical and neurologic exam
  3. Attention to external ear for vesicles or scabbing
  4. Attention to parotid for mass lesions
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17
Q

Bells palsy course:

  1. Onset?
  2. Max paralysis is when?
  3. Recovery by when usually?
A
  1. Onset over hours to 1-2 days
  2. Progressive w/ maximal paralysis within three wks of onset
  3. Recovery of some degree of function by 6 months
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18
Q

Keys to a doubtful Bells palsy? 3

If we see these what should we do?

A
  1. If onset prolonged
  2. Relapsing course
  3. Paralysis persists or physical signs atypical

Then need to do imaging studies—high resolution CT or MRI with gadolinium

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19
Q

Bell’s Palsy Differential Diagnosis

8

A
  1. Lyme disease
  2. HIV
  3. Bacterial Otitis media
  4. Cholesteatoma if onset of palsy is gradual
  5. Sarcoidosis
  6. Sjogren’s syndrome (unusual)
  7. Tumors
  8. Stroke
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20
Q

BP Management?

4

A

Eye care: poor lid closure

  1. Eye drops
  2. Patch/glasses/Tape
  3. Eye ointment at night
  4. Early short term glucocorticoid therapy
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21
Q

When should you start steriod therapy in BP?

SHould we use Antivirals?

A
  • Should begin within 3 days of symptoms

- Antivirals no longer thought to be helpful so not added to treatment

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22
Q

What does the patient need to know:

  1. Caused by? 2
  2. As the nerve swells what happens? 2
  3. How long will it take to recover?
A
  1. Caused by inflammation of the facial nerve:
  2. Usually caused by a virus
  3. it becomes compressed and it’s protective covering breaks down
  4. Takes time to recover
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23
Q
  1. What is Myasthenia Gravis?
  2. What are the autoantobodies against?
  3. What decreases because of this?
A
  1. Autoimmune disorder characterized by weakness and fatigability of skeletal muscle
  2. Autoantibodies against acetylcholine receptors (AChR-Ab)
  3. Decrease in number of acetylcholine receptors because of AChR-Ab binding
    - -Destruction of receptors by a compliment-mediated process
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24
Q

Which specific cells bind to the AcH receptors?

Most patiens have what kind of abnormalities?

A

T-cells bind to acetylcholine receptors and activate B cells

Most patients w/ MG have thymic abnormalities: hyperplasia or thymoma

25
Q

What is the age distribution in myasthenia gravis?

2

A

Bimodal distribution:

  • Early peak 2nd and 3rd decades (female predominance)
  • Late peak 6th-8th decade (male predominance)
26
Q

MG—Clinical Manifestations
KEY symptoms? 3

Ocular symptoms? 3

Bulbar symptoms? 3

A

KEY Symtoms:

  1. Fluctuating skeletal muscle weakness
  2. Worsened by contractile force
  3. True muscle fatigue not tiredness

Ocular:

  1. Ptosis, can be bilateral or unilateral
  2. EOM often involved leading to diplopia
  3. Ptosis increases w/ sustained upward gaze or by holding up the opposite eyelid

Bulbar:

  1. Weakness w/ prolonged chewing, jaw weakness at rest
  2. Oropharyngeal muscle weakness–dysarthria and dysphagia (imminent risk of aspiration can produce “myasthenic crisis”)
  3. Nasal regurgitation of liquids
27
Q

MG—Clinical Presentation cont

Facial Symptoms? 4

Neck and limb symptoms? 3

Respiratory symptoms? 1

A 
Facial: 
1. Patient appears expressionless
“Lost his or her smile”
2. Weakness of orbicularis oris muscle: “myasthenic sneer”
3. Weakness of orbicularis oculi

Neck and limb:

  1. Weight of head overcome extensors resulting in “dropped head syndrome”
  2. Limbs proximal weakness—arms more affected legs
  3. Wrist & finger extensors and foot dorsiflexors involved

Respiratory:
1. when respiratory muscles weaken produces respiratory insufficiency and pending respiratory failure which is life-threatening

28
Q

MG—Clinical Course
1. Early symptoms are worse when? 3

  1. Max extent of disease after how long?
A
  1. Early on symptoms transient, OK in am
    - worse later in day or
    - when tired or
    - have exercised
  2. Maximal extent of the diseases seen 77% pts 3 yrs
29
Q

MG–Diagnosis

2

A
  1. Serologic testing immunologic assays:
  2. Eletrophysiologic studies:
    - Repetitive nerve stimulation studies
    - Single fiber electromyography:
30
Q

What would we see on the following:
1. Serologic testing immunologic assays: 3

  1. Eletrophysiologic studies:
    - Repetitive nerve stimulation studies
    - Single fiber electromyography:
A
    • Detect circulating AChR-Ab
    • Seronegative MG—40-50% will have Ab to muscle specific receptor tyrosine kinase (MuSK)
    • Small percentage double seronegative
    • This is the most sensitive for MG
31
Q

Differential diagnosis:
2

For generalized disease that we would consider?
5

A
  1. Thyroid ophthalmopathy
  2. Brainstem and motor cranial nerve pathology
  3. Generalized fatigue
  4. Motor neuron disease (ALS)
  5. Botulism
  6. Penillinase-induced myasthenia
  7. Congenital myasthinic syndromes
32
Q

Treatment for MG

4

A
  1. Anticholinesterase agents:
  2. Chronic immunotherapies:
  3. Rapid immunotherapies:
  4. Surgery—
33
Q

Describe what we would use in each of the following categories:
1. Anticholinesterase agents: 2

  1. Chronic immunotherapies: 2
  2. Rapid immunotherapies: 2
  3. Surgery: 1
A
  1. Pyridostgigmine (Mestinon)
  2. For symptomatic treatment (SE-Cholinergic)
  3. Moderate doses corticosteroids
  4. Immunosuppressive medications
  5. Plasmapheresis
  6. IV immunoglobulin
  7. thymectomy for thymoma
34
Q

What is the definition of polyneuropathy?

2

A
  1. Symmetric distal sensory loss

2. With symptoms of burning and eventually weakness

35
Q

Etiologies of polyneuropathy?

6

A
  1. Diabetic polyneuropathy most common—up to 50% diabetics will develop it
  2. Patients w/ AIDS—12%
  3. Vitamin B 12 deficiency
  4. Toxins: alcohol, chemotherapy, heavy metals
  5. Other vitamin deficiencies less common
  6. Uremia
36
Q

What are the two types of pathophysiology of polyneuopathy and describe them?

A
  1. Axonal: most common—injury related to axonal length

2. Demyelinating: seen more in autoimmune and to some extent in diabetic polyneuropathy

37
Q

Clinical presentation of polyneuropathies?

A
  1. Slowly progressive sensory loss feet 1st
  2. Dysesthesias: burning, pain
  3. Mild gait abnormalities
  4. As progresses mild weakness in lower legs and hand symptoms begin—”stocking and glove”
  5. Severe cases affect the intercostal nerves, sternum, top of the head
38
Q

Polyneuropathy—Physical Exam
1. Findings on sensory exam?

  1. Reflexes?
  2. Motor exam?
  3. Vibratory?
  4. Proprioception?
A
  1. sensation decreases
  2. Decerased reflexes or absnet
  3. 5/5 initally weakened in later stages
  4. big toes first to lose, then the malleous of the ankle, then the knee
  5. Can’t sense proprioception
39
Q

Polyneuropathy—Diagnosis

DDx?

A

Progressive numbness and weakness in the lower extremities may be a result of a spinal cord process

40
Q

What would make us do a workup for a polyneuropathy pt?

  1. What would we do? And what would this show (2)?
  2. Labs? 7
A

If there is no clear etiology or symptoms are severe and rapidly progressive then a more complete diagnostic workup is indicated

  1. Electrodiagnostic testing:
    - Reduced amplitude of evoked compound actions potentials
    - Preservation of nerve conduction studies

Labs:

  • CBC,
  • ESR,
  • TSH,
  • glucose,
  • Vitamin B12 level,
  • antinuclear antibodies,
  • UA
41
Q

Diabetic Neuropathy Risk factors?

5

A
  1. Duration and severity of hyperglycemia
  2. Increased triglyceride level
  3. BMI
  4. Whether the patient smokes or not
  5. Presence of HTN at baseline
42
Q

Pathogenesis of Diabetic Polyneuropathy

5

A
  1. Accumulation of advanced glycosylation end products—
  • strong cross-linking activity w/ collagen,
  • increase vascular permeability,
  • monocyte influx contributing to vascular injury
  1. accumulation of sorbitol—interferes w/ cell metabolism
  2. Increased oxidative stress—accumulation of reactive oxygen species therefore reduced antioxidant defense
  3. Nerve ischemia
  4. Peripheral nerve repair is impaired in diabetes
43
Q

What is affected by the damage from Diabetic Polyneuropathy?

3

A
  1. Results in length-dependent “dying back” axonopathy
  2. Involves the distal portions of the longest myelinated and unmyelinated sensory axons
  3. Relative sparing of motor axons
44
Q

Clinical presentation of Diabetic neuropathy?

4

A
  1. Loss of vibratory sensation and altered proprioception
  2. Impairment of pain, light touch and temperature
  3. Decreased or absent reflexes occur early in the disease
  4. More widespread loss of reflexes and motor weakness are late findings!!
45
Q

Diabetic Polyneuropathy
DDx?
6

A
  1. Other forms of neuropathy are more common in diabetics!!
  2. Chronic inflammatory demyelinating polyneuropathy
  3. Vitamin B12 deficiency
  4. Hypothyroidism
  5. Uremia
  6. *Acute painful neuropathies associated w/ rapid glycemic control, unintended severe weight loss or intentional weight loss
46
Q

Treatment and Prevention of Poly neuropathy?

3

A
  1. tight glycemic control for treatment and prevention
  2. Stop smoking
  3. Lose weight
47
Q

Polyneuropathy—Symptomatic Rx

5

A
  1. Gabapentin (Neurontin): reduces pain, well tolerated
  2. TCAs: such as amitriptyline and desipramine (SE?)
  3. Carbamazepine (Tegretol) and phenytoin (Dilantin) have varying success
  4. Pregabalin (Lyrica) : targeted for diabetics but is worth trying for patients regardless of etiology
  5. Duloxetine (Cymbalta)

has the advantage of being an antidepressant as well as helping control pain

48
Q

Pathogensis of alcoholic polyneuropathy?

4

A
  1. Axonal neuropathy complicated by demyelination when there is coexisting nutritional deficiency
  2. Reduction in the density of small myelinated and unmyelinated fibers w/ normal thiamine status
  3. Alcohol is a direct neurotoxin
  4. Correlates best w/ lifetime alcohol consumption
49
Q

Alcoholic polyneuropathy treatment?

A

Stop drinking alcohol

50
Q

Vitaman 12 deficiency polyneuropathy: Adequate absorption of cobalamin depends on? 5

A
  1. Dietary intake
  2. Acid-pepsin to liberate Cbl from binding proteins
  3. Pancreatic proteases to free Cbl from R factors
  4. Secretion of IF by parietal cells to bind Cbl
  5. Ileum w/ Cbl-IF receptors
51
Q 
Vitamin B12 (Cobalamin)‏
pathophysiology?

Symptoms? 6

A
  1. Defect in myelin formation leading to subacute degeneration of dorsal (posterior) and lateral spinal columns
    • Paresthesia’s,
    • ataxia w/ loss of vibration and position sense,
    • can progress to severe weakness,
    • spasticity,
    • clonus and
    • paraplegia
52
Q

How do we diagnose B12 deficiency?5

A
  1. Serum B12 level,
  2. serum gastrin,
  3. parietal cell antibodies,
  4. anti-intrinsic factor antibodies, 5. check for H pylori
53
Q 
Vitamin B12 (Cobalamin)‏ treatment?
3
A

1, IM B12 injections 1000microgms twice weekly for 2 weeks

  1. Weekly injections for 2 months
  2. Then monthly injections for life or until deficiency resolves
54
Q
  1. Vitamin E deficiency
    polyneuropathy is also called?
  2. symptoms? 4
  3. What is it seen with 2 and what is it not common with?
  4. Diagnosis? 1
  5. Treatment? 3
A
  1. Spinocerebellar syndrome
  2. Variable peripheral nerve involvement:
    - ataxia,
    - hyporeflexia,
    - proprioceptive
    - vibratory loss
  3. seen with
    - chronic cholestasis and
    - pancreatic insufficiency (fat malabsorption–steatorrhea)

Rarely caused by dietary inadequacy,

  1. Diagnosis:
    - serum alpha-tocopherol divided by the sum of serum cholesterol + triglycerides

Treament:

  • large oral doses (200 IU/kg/d) or -IM doses of alpha-tocopherol are used then
  • daily oral vitamin E
55
Q

Thiamine Deficiency seen in who?

4

A
  1. anorexia nervosa,
  2. malnutrition,
  3. alcoholism,
  4. bariatric surgery patients
56
Q

What is dry beriberi? (associated with what) 4

A

neuropathy associated w/

  1. calf cramps,
  2. muscle tenderness, and
  3. burning feet,
  4. autonomic neuropathy may be present
57
Q

What is wet beriberi?

2

A

high-output CHF + neuropathy

58
Q

Diagnosis of thiamine deficiency? 2

Treatment?

A
  1. Diagnosis: urinary thiamine, serum thiamine

2. Thiamine 50-100mg IV, IM or orally

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