PERIPHERAL NEUROPATHY.pptx

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.

3. APPROACH I dentify where the lesion I dentify the cause D etermine the proper treatment.

4. Identification of lesion A ccomplished 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.

5. Cause identification M ost blood tests should be deferred until the results of electromyography (EMG) and nerve conduction study (NCS) testing are known. D istinction 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.

6. Treatment T wo aspects to the treatment of polyneuropathy treatment of the underlying disease etiology and alleviation of symptoms related to the illness   Drugs used are gabapentin , duloxetine , amytryptylline , pregabalin , carbamazepine , phenytoin , topiramate , baclofen , mexiletine , and dextromethorphan

7. 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

8. 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.

9. 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.

10. 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.

11. Thiamin (vitamin B1) Dietary deficiency causes beriberi . Its principal features are polyneuropathy and cardiac failure. Thiamin deficiencyalsoleadstoanamnesticsyndrome ( Wernicke–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 .

12. 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 .

13. Guillain-Barre Syndrome GBS is the most common acute polyneuropathy . I t is usually demyelinating but occasionally axonal. GBS is monophasic – it does not recur. A lso known as acute inflammatory or postinfective neuropathy, acute inflammatory demyelinating polyradiculoneuropathy .

14. 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.

15. Clinical features of weakness of distal limb muscles and/or distal numbness. P rogress 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.

16. 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 .

17. 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

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

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