In this group are neuropathies which are as a result of toxic substances like Arsenic, Lead, mercury, thallium and Triorthocresyl phosphate (‘IOCP) etc.

Arsenic neuropathy

It may be acute when a very heavy dose of arsenic has been ingested either accidentally or for medicinal purposes. In the acute phase patient gets nausea, vomiting, diarrhea and severe abdominal pain.


Symptoms pertaining to nervous system include headache, drowsiness and convulsions. Signs of peripheral neuropathy appear 1-4 weeks after acute intoxication. Skin becomes dry, scaly and occasionally hyper pigmented.

Arsenic or Arsenite is contained in insecticides, pesticides and certain rat poisons as well as weed killers. Earlier on Arsenic compounds were used for medicinal purposes, Accidental poisoning occurs when a person comes in contact with these substances.

Chronic arsenic poisoning is generally as a result of its slow administration mainly for intent to kill some body slowly.

Symptoms besides chronic ill health, include a form of mixed sensory motor neuropathy where sensory symptoms predominate. Patient complains of tingling, buming, lancinating pains in limbs, cramps in calf muscles and hyperalgesia.

Glove and stocking type of anesthesia is present with impairment of all type of sensory modalities. Muscular weakness is usually more prominent. Bilateral foot and wrist drops may be seen. Tendon reflexes are diminished or absent.

Cranial nerves are not affected though autonomic disturbances may be seen in the form of flushing and sweating. Skin changes such as pigmentation and exfoliation are present. Hyperkeratosis of skin of palms and soles is often found. Transverse lines may appear over the nails.

Diagnosis of arsenical poisoning is made by estimation of levels of arsenic in hair and nails. Arsenic levels of more than 0.1 mg per 100 rhg of hair and in the urine excretion of more than 0.1 mg per liter of urine are highly suggestive of arsenic poisoning.

Prognosis in cases of arsenical neuropathy is good provided, it is recognized early.


It is by dimercaprol which is given in a dose of 2-3 mg/ kg body weight intramuscularly every 6 hourly for 24 hours and then 12 to 24 hourly for 10 days. Dimercaprol chelates arsenic by producing an insoluble complex which is excreted by the kidneys.

Penicillamine administered orally in a dose of 100 mg/kg body weight per day in four divided doses for 5 days is another mode of treatment in both acute and chronic arsenic poisoning. Side effects of penicillamine include rash, thrombocytopenia leucopenia and nephrotoxicity.

Besides these two drugs, neuropathy be managed symptomatically.


TOCP is a constituent of aviation oils, or fluids used to keep the machine guns cools. But ill effects of this are produced when rape seed oil is adulterated with TOCP by unscrupulous people. Very often epidemics of this toxicity occur.

Being colorless, odorless, soluble in organic solvents and vegetable oils, makes it an ideal substance for adulteration. After ingestion, immediate symptoms are gastrointestinal disturbances with pain, cramps, nausea, vomiting and diarrhea. After a period of 10- 15 days following gastrointestinal symptoms, patient complains of cramps in calf muscles, parasthesiae in the distal part of limbs and feeling of heaviness.

Within few days the patient becomes bed ridden and there is rapid wasting of the affected muscles. Dorsiflexors and peronei become weak and flaccid foot and toe drop develops. This weakness may extend to upper limbs resulting in rapid weakness and wasting involving small muscles of the hands producing a claw hand.

Variable degree of sensory disturbances are seen in the lower limbs. Impairment of pinprick and touch is present over the feet. Deep tendon reflexes are diminished or absent in lower limbs but may be normal or exaggerated in upper limbs.

Routine biochemical tests are normal. CSF shows mild increase in protein with normal cell count. Electrophysiological studies show evidence of neurogenic paresis with spontaneous activity and reduced interference pattern. There is no treatment for TOCP neuropathy. Disease is self limiting and in mild cases complete recovery may take place. In severe cases residual neurological deficit persists for a long time.

Genetic neuropathy

This presents as an autosomal dominant disorder and may present as purely sensory or sensoriniotor forms.

Charcot-Marie-Tooth disease or peroneal muscular atrophy is one form of hereditary motor sensory neuropathy (HMSN-1). It occurs in the second or third decade and presents with wasting and weakness in the anterior and posterior tibial muscles and muscles of lower half of thigh giving an inverted champagne, Bottle appearance, Weakness is predominant in the peronei and ankle dorsiflexors. Wasting generally stops at mid thigh level. Despite wasting patient is able to walk. Foot drop and Pes cavus appear. Fasciculations may appear while deep sensations are effected.

The phenotype of this disorder is due to two different disorders HMSN-1 and 2. The main difference is that HMSN-1 is a demyelinating neuropathy while HSMN-2 is due to axonal degeneration.

The neuropathic form is associated with duplication of a strand of chromosome 17. It is frequently associated with distal involvement of hands and feet.

Another form of Hereditary neuropathy is Dejerine sottas Disease which is a recessive disorder seen at first decade of life. This is severe degree of motor and sensory demyelinating neuropathy with sensory impairment being more marked. Children suffering from it may be mentally retarded and are often bed ridden by the age of 20-30 years. Nerves in such cases are hypertrophied, thickened and are well palpated.

Prognosis of genetic neuropathies is poor.


It refers to conditions where there is patchy or focal destruction of normally formed myelin sheaths accompanied by an inflammatory response. There is relative sparing of other elements of nervous tissues like axons though some degree of axonal damage may occur.

Demyelinating disorders encompass number of conditions – primary such as multiple sclerosis. Devic’s disease and secondary which include post infectious or Post immunization acute disseminated encephalomyelitis following measles, chicken pox, small pox and after vaccination, against rabies, smallpox.

These disorders have to be distinguished from conditions where there is defect in the formation of myelin at birth due to an inherited enzymatic defect. This is referred to as dysmyelination, also known as leukodystrophies.