Peripheral Neuropathy Flashcards

1
Q

What are the 3 main disorders relating to peripheral neuropathy

A
  1. Trigeminal neuralgia
  2. Idiopathic facial palsy (Bell’s palsy)
  3. Acute inflammatory demyelinating polyneuropathy
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2
Q

Define: trigeminal neuralgia

A

It is the abbraviation of primary trigeminal neuralgia
- transcient recureent paroxysmal pain in the territory of the trigeminal nerve

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3
Q

What is the etiology of trigeminal neuralgia

A
  • peripheral hypothesis: compression of trigeminal nerve before it enters the lateral surface of the pons
  • central hypothesis (sensory): abnormal discharge may be in nucleus of spinal tract of trigeminal nerve or brainstem
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4
Q

What is the mechanism of trigeminal neuralgia

A

compression –> demyelination –> hyperexcitable and electrically couples with smaller unmyelinated or poorly myelinated pain fibres in close proximity

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5
Q

List the main clinical findings of trigeminal neuralgia

A
  • middle aged and elderly people are most affected
  • 60% of cases are in women
  • sudden lacinating facial pain
  • trigger points
  • spontaneous remission
  • symptoms may be confined to distribution of trigeminal nerve on one side only
  • neurological examination may show no positive signs
  • CT and radiology is normal
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6
Q

How is trigeminal neuralgia diagnosed?

A
  • brief episodes of stabbing facial pain
  • pain is in territory of the second and third division of the trigeminal nerve
  • pain is exacerbated by touch
  • sensory deficit cannot be differentiated
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7
Q

What is the differential diagnosis for trigeminal neuralgia

A
  • secondary trigeminal neuralgia
  • glossopharyngeal neuralgia
  • atypical facial pain
  • post therpetic neuralgia
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8
Q

What is the treatment plan for trigeminal neuralgia

A
  1. Pharmacologic treatment
    - carbamazepine
    - phenytoin
    - baclofen
    - gabapentin
    - pregabalin
  2. microvascular decompression
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9
Q

What is Idiopathic facial palsy (Bell’s palsy)

A

idiopathic facial nerve paresis of LMN type that has been attributed to an inflammatory reaction involving the facial nerve near the stylomastoid foramen in the bony facial canal

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10
Q

List the clinical findings of Bell’s palsy

A
  • paresis usually comes on abruptly (may worsen over the next day)
  • pain around ear only lasts a few days
  • face feels stiff and pulled to one side; ipsilateral restriction of eye closure and difficulty with eating and fine facial movement
  • disturbance of taste
  • hyperacusis
  • full recovery within several weeks or months in 80%
  • incomplete paralysis in first week is a favorable prognosis sign
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11
Q

How is Bell’s palsy diagnosed

A
  • sudden onset of LMN facial palsy
  • hyperacusis or impaired taste may occur
  • no risk factors or pre-exisitng symptoms that may cause palsy
  • no lesions of herpes zoster in external ear canal
  • normal neurologic examination except for facial nerve
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12
Q

List some of the differential diagnoses of Bell’s palsy

A
  • Ramsy Hunt syndrome
  • Acoustic Neuroma
  • Infection
  • Bilateral facial weakness
  • Hemifacial spasm
  • belpharospasm
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13
Q

What is the treatment of Bell’s palsy

A
  • Protecting eye during sleep (eyedrops)
  • corticosteroids appear to shorten recovery period and improve functional outcome (within 5 days of onset)
  • Hunt syndrome (acyclovir + prednisone)
  • acupuncture and rehabilitation to help function recovery
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14
Q

What aspects of Bell’s palsy have poor prognosis

A
  • advanced age
  • hyperacusis
  • severe initial pain
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15
Q

What is acute inflammatory demyelinating polyneuropathy (AIDP)

A

Guillian-Barre syndrome
- acute, frequently severe and fulminant polyradiculoneuropathy that is autoimmune in nature

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16
Q

Etiology of GBS

A
  • around 75% are preceded by 1-3 weeks of infection (respiratory/GI)
  • Campylobacter jejuni, herpes virus, cytomegalovirus or Epstein-Barr
  • recent immunisation/immunodeficiency
17
Q

Pathogensis of AIDP

A

autoimmune pathogenesis: cellular and humeral mechanism: T cell mediated immunopathy designed experimental allergic neuritis, antibodies directed against non-protein determinants

molecular mimicry mechanism: non-self antigen that misdirect to host nerve tissue

18
Q

List the clinical findings of AIDP

A
  • areflexic motor paralysis with or without sensory disturbance
  • ascending paralysis (rubbery legs)
  • tingling dysesthesia in extremities, maximum weakness reached within 2w
  • legs usually more affected than arms
  • deep tendon reflexes usually disappear within first few days of onset
  • cutaneous sensory deficit is usually relatively mild
  • bladder dysfunction
  • autonomic nerve disorder: hypotension and cardiac dysrhythmias
  • pain
19
Q

How is ADIP diagnosed

A
  • acute or subacute progressive polyradiculoneuropathy
  • usually ascending, symmetric weakness
  • paraethesis
  • acute dysautonomia
  • elevated CSF total protein without pleocytosis
  • demyelination by EMG
20
Q

What is the differential diagnosis for ADIP

A
  • acute myelopathy
  • botulism (pupillary reactivity lost early)
  • diphtheria (early oesophageal disturbance)
  • porphyria (abdominal pain, seizure, psychosis)
  • vascular neuropathy
  • neuromuscular disorders (MS)
21
Q

What is the treatment plan for ADIP

A
  • after 2w of first motor symptoms, immunotherapy is no longer effective
  • high dose of I.V immunoglobulin or plasma exchange
  • Glucocorticoids are ineffective