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Neuro Rehab II > CIDP > Flashcards

CIDP Flashcards

1
Q

Types of physical therapy for CIDP

A

pool, stretching, yoga, pilates

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2
Q

In CIDP, in some instances, treatment of ___ is occasionally all that is needed.

A

pain
Neuropathic pain meds: choose based on co-morbidities:
1. TCAs: migraines, depressed, pain at night, poor sleep, avoid in cardiac conduction problems.
2. Neurontin: additional muscle/joint problems, multiple meds or medical problems.

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3
Q

May be spontaneous remission in ____ of CIDP patients

A

one third; two-thirds or three-fourths go into remission with immuno suppression. 95% have good control

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4
Q

3 thoughts with regard to immunosuppression with CIDP patient’s before starting:

A
  1. need to suppress then maintain
  2. consider co-morbidities
  3. severity of symptoms need to be weighed.
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5
Q

4 different routes of immunosuppression in CIDP:

A
  1. prednisone: 60mg x 2 months, 40mg x 2 months, 20mg x 2 months, then slowly decrease on alternating days.
  2. IVIG; 2g/kg over 3-5 days, or 0.4mg/kg for 5 days. Can give 0.4mg/kg “booster” every 4-6 weeks. Problems with habituation and availability. (IVIG now reserved for crisis patients: rare)
  3. Plasma exchange
  4. Steroid sparing: Less likely to use than in myasthenia gravis, Azothioprine (imuran), Mycophenolate (cellcept)
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6
Q

which co-morbidity might have a role in CIDP?

A

hypothyroidism; always borderline. check homocystiene in this case.

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7
Q

Classic Criteria for CIDP diagnosis: 8

A
  1. Progression over 2 months (more like 3)
  2. weakness/coordination over sensory symptoms
  3. Symmetric involvement
  4. Predominantly distal but with proximal involvement
  5. Reduced (absent) stretch reflexes throughout.
  6. Increased CSF protein but with normal cells
  7. NCS with demyelinating polyneuropathy
  8. Nerve biopsy with segmental demyelination with or without inflammation present.
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8
Q

Differentiating factor for CIDP vs CMT Type I is?

A

NCS - dispersion and conduction block. Often absent conduction velocity in the legs but can be found yet slow in the arms.

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9
Q

Pathology smear in CIDP

A

cells attemtping to replicate and reyelinate. Sural N biopsy used to be done, not so much anymore

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10
Q

what should be ruled out when assessing CIDP?

A

Chronic Meningitis - CSF counts.

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11
Q

CIDP vs GBS?

A

GBS starts at nerve root, CIDP periph

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12
Q

What will be seen on NCS for CIDP? (5)

A
  1. Lowconduction velocity
  2. Absent F wave
  3. Dispersed CMAP
  4. Prolonged latencies
  5. Partial conduction block
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13
Q

What will be seen in CSF for CIDP?

A

high protein, normal cells

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14
Q

What will be seen on sural n biopsy for CIDP?

A

Standard histo: can see onion bulbs but should not be the dramatic whorls of CMT1
Inflammation variable

Teased fiber, segmental demyelination, then myelin

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15
Q

CIDP profiles:

  1. Age at oneset:
  2. ___% motor symptoms
  3. ___% sensory symptoms
  4. Motor and sensory symptoms
  5. Cranial N involvement:
  6. Bulbar dysfunction
  7. CSF protein > 45mg/dl
  8. Relapsing vs progressive
A
  1. Age 2-90
  2. 80-100%
  3. 64-95%
  4. same
  5. 10-20%
  6. 2-10%
  7. > 90%
  8. progressive more common.
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16
Q

CIDP epidemiology

  1. Incidence
  2. prevalence
  3. associated infection in _____
  4. Pathogenesis:
  5. Affects what part of nervous systom?
A
  1. 1-2/100,000 (any age but highest in 40-60s)
  2. 2-9/100,000
  3. 1/3; mainly viral
  4. both cellular and humoral demyelinating process
  5. nerve roots and peripheral nerves (polyradiculoneuropathy)
17
Q

CIDP largely affects ___ fibers

A

large nerve fibers; can see some nerve root hyperintensity and contrast enhancement
On autopsy, can see swollen edematous n roots

18
Q

CIDP stands for

A

Chronic inflammatory demyelinating polyneuropathy

19
Q

CIDP:

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Motor>sensory, weakness: proximal and distal, symmetrical; sensory loss: distal. Onset 1-80 years. Chronic or relapsing.
  2. Motor + sensory, Slow NCV, conductionblock, prolonged F waves
  3. Ab targets B-tubulin, heparan sulfate, MPZ, PMP22, Ab class: IgM or IgG; frequency: rare. Heparan sulfate 20%
  4. 15%
  5. T-cell suppression: corticosteroids, Cyclosporine A, MTX, IVIG, PE
20
Q

Multifocal CIDP

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Motor > sensory, weakness distal > proximal, Asymmetrical arms > legs, sensory loss multifocal, Onset: 15-75yr
  2. Motor + sensory, Slow NCV, Conduction block, Prolonged distal latency, Prolonged F waves
  3. ?
  4. ?
  5. T-cell suppression: Corticosteroids, IVIG
21
Q

Multifocal motor Neuropathy (MMN)

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Motor only, Weakness: distal > proximal, asymmetrical, arms>legs. Onset 25-60yrs, slowly progressive
  2. Motor only: conduction block, axonal loss, EMG no paraspinous denervation
  3. ab target: GM, ganglioside, aB class IgM. Frequency 30-80%
  4. 20%
  5. IVIG, B-cell suppression: cyclophosphamide, rituximab
22
Q

Anti-MAG neuropathy

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Sensory > motor. Distal, symmetrical, gait disorder & tremor. Onset: > 50yr. Slowly progressive
  2. Motor + sensory, prolonged distal latency, slow NCV, No conduction block, axonal loss
  3. Ab target: MAG. Ab class: IgM, Frequency 100%
  4. 85%
  5. B-cell suppression: cyclophophamide: Rituximab
23
Q

Antisulfatide Neuropathy

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Sensory > motor, distal, symmetric. Onset > 45yrs
  2. Motor + sensory, slow NCV, Prolonged distal latency, axonal loss
  3. Ab target: sulfatide, Ab class IgM
  4. 90%
  5. IVIG, B-cell supression: cyclophosphamide
24
Q

GALOP syndrome

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Gait disorder, sensory>motor, distal, symmetrical tremor. Onset > 50yr
  2. motor + sensory, slow NCV, prolonged distal latency, no conduction block, axonal loss
  3. Ab target: sulfatide in lipid membrane. Ab class: IgM
  4. 80%
  5. IVIG: B-cell suppression: cyclophophamide
25
Q

Anti-GM2 & GalNAc-GD1a neuropathy

  1. Clinical Features
  2. Electrophysiology
  3. Serum Autoantibody
  4. M Protein (serum)
  5. Treatment
A
  1. Sensory > motor, distal, symmetrical, limb and gait ataxia, onset: adult
  2. Motor + sensory, slow NCV, prolonged distal latency, conduction block
  3. Ab target: GM2 & GalNAc-GD1a, Ab class IgM
  4. common
  5. IVIG

Neuro Rehab II (6 decks)

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