PERIPHERAL NEUROPATHY

1. PERIPHERAL NEUROPATHIES
Dr. Navin Adhikari
IM Resident Second year.

2. INTRODUCTION
• Polyneuropathy, peripheral neuropathy, and
neuropathy are frequently used interchangeably.
• Polyneuropathy is refers to a generalized, relatively
homogeneous process affecting many peripheral
nerves, with the distal nerves usually affected most.
• Peripheral neuropathy is a less precise, synonymously
with polyneuropathy, but can also refer to any disorder
of the peripheral nervous system including
radiculopathies and mononeuropathies.
• Neuropathy can refer even more generally to disorders
of the central and peripheral nervous system.
• Mononeuropathy refers to focal involvement of a
single nerve, usually due to a local cause such as
trauma, compression, or entrapment.

5. APPROACH
• Identify where the lesion
• Identify the cause
• Determine the proper treatment.

6. Identification of lesion
• Accomplished by obtaining a thorough history,
neurologic examination, While gathering this
information, seven key questions are asked
the answers to which help identify the pattern
of involvement.

12. Cause identification
• Most blood tests should be deferred until the results of
electromyography (EMG) and nerve conduction study (NCS)
testing are known.
• Distinction that can be made by clinical neurophysiology is
whether a neuropathy is due to axon loss or demyelination.
• As an example, thyroid function studies are unlikely to be
useful if the neuropathy has prominent demyelinating
features.

18. Treatment
• Two aspects to the treatment of
polyneuropathy
1. treatment of the underlying disease etiology
and
2. alleviation of symptoms related to the illness
Drugs used are gabapentin, duloxetine,
amytryptylline, pregabalin, carbamazepine,
phenytoin, topiramate, baclofen, mexiletine,
and dextromethorphan

19. Diabetes Mellitus
• Distal symmetrical sensory polyneuropathy-
common form of diabetic neuropathy and
manifests as sensory loss beginning in the toes
that gradually progresses over time up the legs
and into the fingers and arms
• mononeuropathy and multiple mononeuropathy:
isolated peripheral nerve lesions (e.g. carpal
tunnel syndrome)
• Diabetic Radiculoplexus Neuropathy (Diabetic
Amyotrophy or Bruns-Garland Syndrome)
• Autonomic neuropathy

20. • Uraemia- Progressive sensorimotor
neuropathy develops in chronic uraemia.
Response to dialysis is variable; the
neuropathy usually improves after
transplantation.
• Thyroid disease - A mild chronic sensorimotor
neuropathy is sometimes seen in both
hyperthyroidism and . Myopathy also occurs in
hyperthyroidism.

21. • Porphyria. In acute intermittent porphyria
there are episodes of a severe, mainly
proximal neuropathy in the limbs, sometimes
with abdominal pain, confusion and coma.
Alcohol, barbiturates and intercurrent
infection can precipitate attacks.
• lead – motor neuropathy
• arsenic and thallium – polyneuropathy,
initially sensory.

23. • Alcohol polyneuropathy, mainly in the lower
limbs, occurs with chronic alcohol abuse. Calf
pain is common. The response to thiamin
treatment is variable, even with complete
alcohol abstention. Recurrence and
progression occur with even small amounts of
alcohol.

24. • Thiamin (vitamin B1) Dietary deficiency causes
beriberi . Its principal features are
polyneuropathy and cardiac failure. Thiamin
deficiencyalsoleadstoanamnesticsyndrome(Werni
cke–Korsakoff psychosis, see below). Alcohol is
the commonest cause in western countries.
• Pyridoxine (vitamin B6) Deficiency causes a
mainly sensory neuropathy. In practical terms this
is seen as limb numbness developing during
antiTB therapy in slow isoniazid acetylators (p.
925). Prophylactic pyridoxine 10 mg daily is given
with isoniazid.

25. Vitamin B12 deficiency
• Deficiency causes damage to the spinal cord,
peripheral nerves and brain.
• Subacute combined degeneration of the cord
(SACD). Combined cord and peripheral nerve
damage is a sequel of vitamin B12.
• Initially there is numbness and tingling of fingers
and toes, distal sensory loss, particularly
posterior column, absent ankle jerks and, with
cord involvement, exaggerated knee jerks and
extensor plantars.

26. Guillain-Barre Syndrome
• GBS is the most common acute
polyneuropathy .
• It is usually demyelinating but occasionally
axonal.
• GBS is monophasic – it does not recur.
• Also known as acute inflammatory or
postinfective neuropathy, acute inflammatory
demyelinating polyradiculoneuropathy.

27. • Paralysis follows 1–3 weeks after a trival infection
• Campylobacter jejuni and cytomegalovirus
infections are common causes.
• Infecting organisms induce antibody responses
against peripheral nerves. Molecular mimicry, i.e.
sharing of homologous epitopes between
microorganism liposaccharides and nerve
gangliosides (e.g. GM1), is the possible
mechanism.

28. • Clinical features of weakness of distal limb
muscles and/or distal numbness.
• Progress proximally, over several days to 6
weeks. Loss of tendon reflexes is almost
invariable.
• In mild cases there is mild disability before
spontaneous recovery begins, but in some
20% respiratory and facial muscles become
weak.

29. • Diagnosis is established on clinical grounds and
confirmed by nerve conduction studies, these show
slowing of conduction in the common demyelinating
form.
• CSF protein is often raised to 1–3 g/L, cell count and
glucose level remain normal.
• In the Miller Fisher syndrome antibodies against
GQ1b (ganglioside) have a sensitivity of 90%.
• Differential diagnosis includes other acute paralytic
illnesses, e.g. botulism, cord compression, muscle
disease and myasthenia.

30. Management of GBS
• Paralysis may progress rapidly (hours/days) to require
ventilatory support.
• It is essential that ventilation (vital capacity, blood
gases) is monitored repeatedly to recognize emerging
respiratory muscle weakness.
• Subcutaneous heparin should be given to reduce the
risk of venous thrombosis.
• Immunoglobulin given intravenously within the first 2
weeks reduces duration and severity of paralysis
• Plasma exchange is also of proven benefit in shortening
disability

31. • No role of steroids.
• Recovery begins, with or without treatment,
between several days and 6 weeks from the
outset.
• Prolonged ventilation may be necessary.

34. References
• Harrison's Principles of Internal Medicine,
20th Edition
• Davidsons Principle and Practice of Medicine
• Kumar & Clark's Clinical Medicine, 7th Edition
• Uptodate 2020