Polyneuropathy Flashcards
What is polyneuropathy?
Generalised disease of the peripheral nerves due to damage to the axon and/or myelin sheath (peripheral neuropathy)
How can polyneuropathy present?
Predominantly motor loss or predominantly sensory loss
What are some conditions that cause predominantly motor loss polyneuropathy?
Guillain-Barre syndrome
porphyria
lead poisoning
hereditary sensorimotor neuropathies (HSMN)- Charcot marie tooth
chronic inflammatory demyelinating polyneuropathy (CIDP)
diphtheria
What are some conditions that cause predominantly sensory polyneuropathy?
diabetes
uraemia
leprosy
alcoholism
vitamin B12 deficiency
amyloidosis
RF for diabetic neuropathy?
Smoking
hypertension
older age
longer duration of diabetes
greater degree of hyperglycaemia
How does sensory polyneuropathy typically present?
Starts with the distal lower limbs
Progresses to glove and stocking distribution
Diabetic neuropathy presentation?
Sensory loss in glove and stocking distribution with lower legs affect first
Management of diabetic neuropathy?
First line: amitriptyline, duloxetine, gabapentin, pregabalin
If the first-line drug treatment does not work try one of the other 3 drugs
Tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain.
Feature of gastrointestinal autonomic neuropathy in diabetes?
Gastroparesis- erratic glucose control, bloating and vomitting (metoclopramide, domperidone)
Chronic diarrhoea- often occurs at night
GORD0 due to decreased lower oesophageal sphincter pressure
What is Guillain-Barre syndrome?
Rapidly progressive predominantly motor, immune mediated demyelination of peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)
Pathogenesis of GBS?
cross-reaction of antibodies with gangliosides in the peripheral nervous system
correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated
anti-GM1 antibodies in 25% of patients
Presentation of GBS?
Initially patients present with back/leg pain
Progressive, symmetrical weakness of all the limbs.
Classically ascending weakeness
Reduced or absent reflexes
Very mild sensory symptoms
Other features incl:
Resp muscle weakness
Cranial N involvement- Diplopia, bilateral facial N palsy, oropharyngeal weakness
Autonomic involvement (urinary retention, diarrhoea)
Less common: papillodema
Investigations for GBS?
Lumbar puncture: Rise protein with a normal WBC count in 2/3s
Nerve conduction studies:
Decrease motor nerve conduction velocity
Prolonged distal motor latency
Increase F wave latency
RF for GBS?
Preceding viral illness
Preceding bacterial infection
Preceding mosquito borne infection (ZIKA)
Hep E infection
Management of GBS?
IV immuneglobulin- 400 mg/kg/day intravenously for 5 days with supportive treatment OR Plasma exchange with supportive treatment
If renal failure or IgA deficiency: Plasma exchange + supportive treatment
What is chronic inflammatory demyelinating polyneuropathy?
Immune- mediated neuropathy in which weakness is main symptom.
Develops sub acutely over weeks- months
Must have progressed or relapsed for longer than 8 weeks.
Who gets uraemic neuropathy?
People with advanced renal failure
What is Charcot-Marie-Tooth disease?
Most common hereditary peripheral neuropathy.
Results in predominantly motor loss
No cure, managed with occupational and physio
Features of Charcot-Marie-tooth?
History of frequently sprained ankles
Foot drop
High arched feet
Hammer toes
Distal muscle weakness
Distal muscle atrophy
hyporeflexia
stork leg deformity
Who is at risk of B12 deficiency?
> 65 y/o, vegan/vegetarian diet, chronic GI illness, PPI, H2 receptor antagonists, metformin, anticonvulsants
Features of B12 deficiency?
Parasthesisia/ polyneuropathy
Ataxia
Postive rhombergs test
glossitis
angular cheilitis
What is the most severe form of b12 deficiency?
Subacute combined degeneration of the spinal cord.
What are the features of subacute combined degeneration of spinal cord/
Dorsal columns +lateral corticospinal tracts affected
Joint position and vibration sense lost first and then distal paraesthesia
UMN signs in the legs- extensor planters, brisk knee reflexes and absent ankle jerks
If untreated stiffness and weakness persist
