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Alasdair - Neurology > Peripheral polyneuropathy > Flashcards

Peripheral polyneuropathy Flashcards

1
Q

Sensory findings in peripheral polyneuropathy

A

Bilateral, symmetrical
Glove and stocking distribution: length dependent
Reduced tendon reflexes (loss of ankle jerks in DM)
Signs of trauma or joint deformity (Charcot’s joints)
Loss of proprioception - positive Romberg’s test

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2
Q

Motor findings in peripheral polyneuropathy

A

Bilateral, symmetrical

LMN weakness: wasting, fasciculations, reduced tone, hyporeflexia

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3
Q

Completion of neurone exam in peripheral neuropathy

A

Review drug chart
Dipstick for glucose
Gait + Romberg test
Cranial nerve exam

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4
Q

Causes of peripheral polyneuropathy

A 
Mainly sensory:
DM
EtOH
B12 deficiency
CRF (uraemia) and Ca (paraneoplastic)
Vasculitis
Drugs e.g. isoniazid, vincristine
Mainly motor:
HMSN/CMT
Paraneoplastic (Ca lung, RCC)
Lead poisoning
Acute - GBS and botulinum
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5
Q

Specific history for peripheral polyneuropathy

A

Time course
Precise symptoms: ataxia - B12, painful dysesthesia - EtOH, DM
Associated events: D+V - GBS, weight loss - cancer, arthralgia, CTD.
Travel, EtOH, drugs.

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6
Q

Investigations for peripheral polyneuropathy

A 
Dipstick: glucose
Bloods: DM (glucose, HbA1C), EtOH (FBC ± film, LFTs, GGT), CRF (U+E), B12, folate, vasculitis (ESR, ANA, ANCA), thyroid disease (TFTs).
Imaging: CXR for paraneoplastic.
Nerve conduction studies
Electromyography
Genetic (PMP22 gene in CMT)
Nerve biopsy
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7
Q

Nerve conduction studies interpretation

A

Demyelination - reduced conduction speed, axonal degeneration - reduced conduction amplitude

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8
Q

General management of peripheral polyneuropathy

A

MDT
Foot care and careful shoe choice
Splinting joints can prevent contractures

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9
Q

Specific medical management for peripheral polyneuropathy

A

Optimise glycemic control (DCCT, UKPDS trials)
Replace nutritional deficiencies
Avoid EtOH or other precipitants
Vasculitis: steroids/immunosuppressants
Neuropathic pain: amitriptyline, gabapentin
GBS: IVIg

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10
Q

Signs on inspection for diabetic neuropathy

A

Finger-pricks from BM monitoring
Peripheral vascular disease
Charcot joints
Bilateral loss of ankle jerks (sensory neuropathy)
Mononeuritis multiplex - foot drop
Distal sensory loss in stocking distribution

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11
Q

Completing diabetic neuropathy exam

A

Examine the fundi
Examine the upper limbs and cranial nerves: sensory neuropathy, mono neuritis multiplex (CN3, CN6, ulnar nerve).
Urine dip: glucose, proteinuria.

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12
Q

Specific history for diabetic neuropathy

A

Pain, especially at night
Glycaemic control
Complications of insulin
Other micro- and macro-vascular complications

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13
Q

Pathophysiology of diabetic neuropathy

A

Metabolic: glycosylation, ROS, sorbitol accumulation
Ischaemia: loss of vasa nervorum

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14
Q

Investigations for diabetic neuropathy

A

Urine: glucose, ACR
Blood: glucose, HbA1c, U+E

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15
Q

Management of diabetic neuropathy

A

MDT
Good glycemic control
Amitriptyline, gabapentin
Capsaicin cream

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16
Q

Describe femoral neuropathy

A

AKA diabetic amyotrophy AKA proximal diabetic neuropathy.
Painful asymmetric weakness and wasting of quadriceps with loss of knee jerks.
Diagnose by nerve conduction studies and electromyography.

17
Q

Features of autonomic neuropathy

A

Postural hypotension - treat with fludrocortisone
Gastroparesis - early satiety, GORD, bloating
Diarrhoea - treat with codeine phosphate
Urinary retention
Erectile dysfunction

18
Q

Synonyms to Charcot-Marie-Tooth syndrome

A

Hereditary Motor and Sensory Neuropathy (HMSN), peroneal muscle atrophy

19
Q

Charcot-Marie-Tooth syndrome findings on examination

A

Inspection:
Pes cavus
Symmetrical distal muscle wasting - claw hand, champagne bottle leg
Thickened nerves: especially common peroneal around fibula
Motor:
High-stepping gait (foot drop)
Weak foot and toe dorsiflexion
Absent ankle jerks
Sensory:
Variable loss of sensation in a stocking distribution

20
Q

Specific history in Charcot-Marie-Tooth syndrome

A

Family Hx

21
Q

Pathophysiology of commonest types of CMT

A

CMT1 (=HMSN1) is the commonest form
Demyelinating
AD mutation in peripheral myelin protein 22 gene (PMP22)
CMT2 (=HMSN2) is the second most common.
Axonal degeneration, also autosomal dominant.

22
Q

Investigations for CMT

A

Nerve conduction studies

Genetic testing

23
Q

Differentiating between CMT1 and CMT2 with nerve conduction studies

A

CMT1 is demyelinating - nerve conduction studies will show reduced velocity
CMT2 is axonal degeneration - nerve conduction studies will show reduced amplitude

24
Q

Management of CMT

A

MDT
Foot care and careful shoe selection
Orthoses e.g. ankle braces

Alasdair - Neurology (16 decks)

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