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.