Essay on Peripheral Nervous System | Neurology

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Essay on Peripheral Nervous System

Essay Contents:

1. Essay on the Introduction to Peripheral Nervous System
2. Essay on the Clinical Features of Peripheral Nervous System
3. Essay on the Classification of Peripheral Nervous System
4. Essay on the Aetiology of Peripheral Nervous System
5. Essay on the Common Diseases of Peripheral Nervous System

Essay # 1. Introduction to Peripheral Nervous System:

Although structure and function of the peripheral nervous system (PNS) are relatively simple, the disease affecting this system stands out as a difficult subject in neurology. Faced with the problems affecting the PNS, the physician has to ascertain two things. First, that the peripheral nerves are being affected and, secondly, to find out the exact aetiology.

It is the latter one which is not always easy to establish. In recent years, with the advent of electrophysiological studies in human beings (nerve conduction velocities and electromyographic studies) and better histo- pathological studies of nerve and muscles, more insight has been gained into this aspect.

A rational approach to the disease/disorder of the peripheral nerves should be based on their fundamental structures. The cells of the origin lie in the motor neurons of the spinal cord. The motor roots are composed of the emerging axons of the anterior and lateral horn cells; they terminate on muscle fibres, or sympathetic or parasympathetic ganglion. The peripheral axons of the dosal root ganglion cells constitute the sensory nerve fibres.

The axons thus formed are enveloped by a series of Schwann cells forming the fatty myelin sheath. There is intimate symbiotic relation between the axon and its myelin, although morphologically they are independent. Thus a disease process may involve one without much involving the other.

The motor and sensory fibres are large protoplasmic extension of their respective parent cells in the spinal cord. The long axon depends upon the intact healthy metabolism of the parent cell for its nutrition.

A disorder of function of nerves thus may occur if some insult occurs at the level of parent cell, or dysfunction in metabolism of ensheathing myelin nor if something goes wrong with rich vascular supply by the nutrient arteries to nerve or combination of these factors.

Further these nerves pass through narrow foramens (intervertebral and cranial) and some of these may pass through tight compartments peripherally (e.g. median nerve between carpal ligaments). This explains the susceptibility of some nerves to compression and entrapment.

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Essay # 2. Clinical Features of Peripheral Nervous System:

There are certain general clinical features which may characterize the disease of peripheral nerves. These may be motor, sensory, trophic or autonomic dysfunction.

Motor weakness may be prominent symptom. In generalised polyneuropathies muscles of lower limbs are affected first and more severely than those of hand or forearm. The trunk and respiratory muscle may also get affected. In mononeuropathy corresponding muscles supplied by the nerve affected show weakness. Weakness of muscle may be slowly followed by atrophy. The rule is that tendon reflexes are markedly diminished or completely lost.

Sensory loss occurs when sensory fibres are involved like motor function, sensation tends to be more affected in the distal segments of the limbs. As the disease worsens, the sensory loss may spread to more proximal part and may involve all the modalities of sensation. Vibration sense is more often affected than the touch and position sense. The paraesthesia like numbness and tingling sensation may dominate in symptomatology.

Autonomic Dysfunction:

In diabetes and certain other polyneuropathies, when autonomic nervous system is involved there may be symptom/signs of autonomic dysfunction. This may be in the form of diarrhoea, weak bladder and bowel sphincters and overflow incontinence, sexual impotence, small or medium size unreactive pupils and anhydrosis, etc. In long-standing slowly progressive polyneuropathies, the feet, hands and spine may become deformed.

Work-Up of a Case of Polyneuropathy:

Once the diagnosis of peripheral neuropathy has been thought of on above referred clinical features, attempt has to be made for establishing the possible aetiology. A detailed history of onset, whether acute, subacute or chronic, any preceding history of fever, infectious conjunctivitis, innoculations, vaccinations, any history of antecedental trauma; history suggestive of metabolic disorder, viz. diabetes or porphyria, history of chronic alcoholism or possible toxin or drugs, signs suggestive of malnutrition may help to suggest the diagnosis in a particular case.

Time spent on such a pursuit may be richly awarded. In laboratory work-up appropriate biochemical tests may be done to rule in or out a particular entity suspected. Measurement of nerve conduction velocities and electromyographic studies may shed further light. CSF studies may help and nerve biopsy may further confirm diagnosis in certain setting.

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Essay # 3. Classification of Peripheral Nervous System:

Several ways of classification are possible:

i. Depending upon course of illness- acute, subacute, chronic.

ii. Depending upon anatomical distribution- Mononeuropathy, mononeuritis multiplex, localized radiculopathy, generalised polyneuropathy.

iii. Depending upon type-of function affected- sensory, motor, mixed.

iv. Depending upon pathology- axonopathy (Predominant axon involvement), Schawanopathy (Predominant myelin involvement)

v. Depending upon aetiology

Generalised Polyneuropathies:

In this group, there is a generalised affliction of all nerves. The most common clinical picture is symmetrical involvement of motor and sensory nerves, first manifest at the distal part of limbs as already described. The course of the disease may be acute, subacute or chronic.

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Essay # 4. Aetiology of Peripheral Nervous System:

List of causes is really a long one.

Some of the important ones are as follows:

Heredo-Familial Diseases:

Peroneal-muscular atrophy, Charcot-Marie-Tooth type of neuropathy, hypertrophic interstitial neuropathy (Dejerine-sottas disease), hereditary sensory radiculoneuropathy, Refsum’s disease.

Infections:

Leprosy, herpes zoster, brucellosis, infectious – hepatitis, infectious mononucleosis, typhoid fever, mumps, diphtheria.

Allergic Neuropathies:

Guillian-Barre’s syndrome (Acute infective Polyneuritis), neuralgic amyotrophy, serum neuropathy.

Metabolic:

Diabetes mellitus, uraemia, porphyria, amyloidosis.

Nutritional Deficiency:

Vitamin B₁₂ deficiency, neuropathy alcoholism, beriberi, pellagra, pyridoxine deficiency and malabsorption syndrome.

Toxic:

Lead, arsenic, mercury, gold triorthocresylphosphate, carbon disulphide, benzene derivatives.

Several Drugs:

Dilantin, furadantin, isoniazide, metronidazole, clinoquinol, sulphonamides, stilbamidine, perhexiline, vincristine, Doriden etc.

Collagen Disease & Vascular disorder:

Polyarteritis nodosa and other vasculitis may cause mononeuritis multiplex.

Neoplasm:

Carcinoma of the bronchus and other neoplastic tumours.

Note:

Polyneuropathy may be the first manifestation of malignancy. There are many other rare causes for which larger neurological texts should be referred to.

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Essay # 5. Common Diseases of Peripheral Nervous System:

i. Acute Infective Polyneuritis’ (Guillian-Barre’s Syndrome):

This disease is characterized by the acute and usually febrile onset of rapidly spreading polyneuritis, with or without implication of cranial nerves; there is usually a considerable increase in the protein content of the cerebrospinal fluid without much of pleocytosis.

The disease is encountered in all parts of the world and in all seasons. A mild respiratory or gastrointestinal infection may precede the neuritic symptoms by 1 to 3 weeks. Other preceding events may include viral exanthema and fevers, vaccinations or surgical procedure. The exact cause is not known but allergic pathology is suspected.

After the above antecedent event, weakness occurs, progressing to paralysis, starting in the periphery and sweeping rapidly up to the legs, arms and trunk. Paraesthesias in the form numbness and tingling is quite common, although there may not be an actual sensory loss.

Bilateral facial weakness is quite common; other cranial nerves may also get involved. The paralysis is flaccid, deep tendon reflexes are lost and the plantar responses are usually flexor. Death may occur because of respiratory or bulbar paralysis, unless prompt action is taken for respiratory support. There may be accompanying changes in autonomic parameters.

ii. Polyneuritis due to Leprosy:

This is probably the most common disease of peripheral nerves in the world today. Disease is particularly frequent in India and Central Africa.

It is an infectious neuritis, being due to direct invasion of nerves by acid-fast mycobacterium leprae. It is to be emphasized that the nerves are thickened and in distinction to other polyneuropathies tendon reflexes are usually preserved in leprosy, despite widespread sensory loss. High index of suspicion is required and disease should not be missed, as it is a treatable condition.

Diagnosis:

The protein content of the spinal fluid is often normal for the first few days, then starts rising (100 – 1000 mg per 100 ml), cell count may be normal or slightly raised (albumino- cytological dissociation).

The presence of paraesthesias and sensory changes helps to exclude poliomyelitis. The neuritis of acute porphyria is distinguished by abdominal pain, a rise of blood pressure, mental symptoms, convulsions, and the presence of porphyrinuria.

Diphtheritic polyneuritis is usually preceded by evidence of the local lesions in the nose, throat or skin and before the onset of polyneuropathy there is usually blurring of vision due to weakness of accommodation. Other causes of rapidly ascending paralysis are rabies, antirabies-inoculation reaction and potassium intoxication.

Treatment:

The key to therapy is respiratory assistance at the earliest sign of respiratory embarrassment and careful nursing. The disease may remit naturally in the majority of cases. The possibility of an autoimmune mechanism provides a rationale for use of corticosteroids.

However, there is no convincing evidence about its beneficial effect. According to some, it may retard recovery. Physiotherapy and proper positioning of limbs should begin once the condition of the patient is stabilized.