Nutritional Disorders of Nervous System

The following points highlight the five major nutritional disorders of nervous system. The nutritional disorders are: 1. Burning Feet Syndrome 2. Spinal Ataxia 3. Cerebellar Cortical Degeneration 4. Vitamin B₁₂ Neuropathy 5. Spastic Paraplegia.

Nutritional Disorder # 1. Burning Feet Syndrome:

a. The earliest symptom is aching, burning or throbbing in the feet. This becomes more intense and is followed by sharp, stabbing, shooting pains, which may spread up as far as the knee like an electric shock, causing excruciating agony. They come on in paroxysms and are usually worse at night.

b. Most patients get some relief by walking about, and sufferers may spend the night limping up and down outside their quar­ters.

c. Some patients manage to get relief by wrap­ping their feet in cold wet cloth or sitting with their feet in a pail of cold water. Con­tinuous pain and loss of sleep produce a thin, exhausted, irritable patient.

d. The tendon jerks may be normal but may be exaggerated.

e. The syndrome has been associated with the prolonged consumption of a diet deficient in protein and the B group of vitamins.

f. Patients who suffer from it may also de­velop the orogenital syndrome or nutri­tional amblyopia, but rarely beriberi.

g. The syndrome can be seen sometimes in chronic alcoholics and patients with dia­betic and other neuropathies, and rarely in other disorders.

Nutritional Disorder # 2. Spinal Ataxia:

a. Patients living on unbalanced diets for long periods develop neurological signs which indicate that the principal lesion is in the dorsal columns of the spinal cord involving particularly proprioceptive sen­sation. The gait is unsteady and the pa­tient is unable to stand upright without swaying when the eyes are closed. Vibra­tion sense in the legs is often lost.

b. In tropical ataxic neuropathy, Vitamin B₁₂ plays only a secondary role. In the fully developed syndrome there is sensory spi­nal ataxia, retro-bulbar neuropathy or op­tic atrophy and sometimes bilateral nerves deafness.

Signs indicating mild involve­ment of the lateral or pyramidal tracts may be found. Epidemiologically the condi­tion is found in people who regularly con­sume large amounts of cassava. Cassava contains a cyanogenic glycoside, Linamarin, which can be broken down to yield free hydrogen cyanide by enzymes in the plant tissue if it is crushed or left standing in water.

c. The cyanide is detoxified by sulphur con­taining amino acids, which convert it to thiocyanate, and by hydroxy-cobalamin which forms cyanocobalamin. Patients with tropical ataxic neuropathy have in­creased plasma concentration and urinary excretion of thiocyanate with increased Vitamin B₁₂ and reduced cystine in the plasma.

The condition can be prevented in part by cooking methods which wash out the glycoside or boil off the HNC.

Nutritional Disorder # 3. Cerebellar Cortical Degeneration:

This condition in which the characteristic clinical feature is ataxia of the legs arises from degenera­tive changes limited to the anterior superior part of the vermis of the cerebellum. It is associated with alcoholism and poor nutrition but the response to vitamin thereby and nutritional rehabilitation is less consistent that in the Wernicke-Korsakoff syn­drome.

Nutritional Disorder # 4. Vitamin B₁₂ Neuropathy:

a. Early symptoms are tingling, coldness and numbness in the extremities due to periph­eral neuropathy.

b. Motor weakness and ataxia appear later and become increasingly severe as the cord is involved.

c. The physical signs depend on the relative involvement of the peripheral nerves and the dorsal and lateral columns of the cord.

d. In severe cases, ataxia is the outstanding feature with loss of reflexes especially in the lower limbs. Sometimes the pyrami­dal tracts are involved, and spasticity, in­creased reflexes and an extensor plantar response are present.

e. If the brain is affected, there may be an organic psychosis and this may be the first evidence of Vitamin B₁₂ deficiency.

Nutritional Disorder # 5. Spastic Paraplegia:

a. If khesari dal (pulse) eaten in excessive amount and for a long period, it gives rise to lathyrism.

b. The onset of lathyrism is sudden and is often preceded by exertion or exposure to cold. A patient may go to bed well and wake up paralyzed; or he may fall down at the plough. Sometimes backache and stiff­ness of the legs precede the onset of the paralysis by a few days. The condition is a spastic paralysis of the lower limbs, due presumably to precisely localised lesion of the lower parts of the pyramidal tracts.

The motor nerves to the muscles of the trunk, upper limbs and sphincters are spared. The sensory nervous system is not involved. In mild cases there is only stiff­ness and weakness of the legs and exag­gerated knee and ankle jerks. In more se­vere cases, the patients walk with bent knee on tiptoe. The legs are often crossed; a ‘scissors gait’ develops and walking is only possible with the aid of sticks.

In se­vere cases, paraplegia in flexion follows, and walking becomes impossible. The pa­tient can only move about by pushing himself along, supporting his body on his hands, buttocks and heels. The paraple­gia is typically spastic with greatly in­creased ankle and knee jerks and with clonus.

The final stage of the disease is completely incapacitating and the suffer­ers may move to the cities where they are easily recognised amongst the beggars.

c. Epidemic lathyrism is mainly a disease of famine. When the price of wheat rises, many of the poor increase their consump­tion of the pulse and cases of lathyrism arise. Prevention requires change in agri­cultural and economic policies. The toxin can be extracted from khesari dal (pulse) by heating it in four volumes of water for an hour.

d. There is no specific treatment. All patients need a good diet.