Physical signs of moderate thiamine deficiency are not easily identified, but when an individual is continuously depirved of thiamin, he builds up an increasing deficiency state that takes shape in the form of fatigue, lack of interest in work, emotional instability, poor memory, irritability, depression, anger, fear, loss of appetite, weight and strength, minor abdominal and cardiac complaints. When deficiency advances, neurologic symptoms appear. These involve the longest nerve pathways and the most distal parts of the lower extremi­ties. Neuritis is characterised by paresthesia (pins and needles) of the toes, followed by a burning sensation in the feet which is particularly pronounced at night.

Thiamine deficiency may also cause defects in the myocardium. The heart may show dilatation and enlargement, especially on the right side.

When this state worsens, the patient suffers from indigestion, constipation, headache and insomnia, irregular and increased heart­beat with just a little exertion. This is followed by cramping of calf muscles and numbness of the feet, loss of vibratory sense, loss of normal reflexes and eventually weakness and secondary muscular atrophy which at first involves the legs and progresses proximally.

Thiamine deficiency is expressed clinically as beri-beri in several distinct forms:

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1. Infantile Beri-beri

This appears in the very first year of life especially between the 1st and 4th month. Vomiting is an early sign in this beri-beri. This is followed by ‘visible cry’ or aphonia (the child cries but no sound is made). The infant, due to oedema, appears to be plump and well nourished. He is constipated, the heart, is large and there is muffled sound. An acute form of the disease may occur which runs to cardiac failure, twitching, coma and death. The infant suddenly becomes cyanosed (blue) due to difficulty in breathing and dies within 24 to 48 hours.

2. Dry beri-beri

In this there is symmetrical tingling, numbness and burning in feet and hands which further leads to peripheral neurophathy. The calf muscle becomes tender, the thighs are affected. In severe cases the upper extremities are affected. There is marked wasting of the extremities resulting in foot drop and wrist drop, loss of knee and ankle jerks and complete loss of sensation at the periphery.

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3. Wet Beri-beri

Oedema and cardiac dis-functioning are the characteristics of wet beriberi which finally leads to cardiac failure. Pathologically there is numbness of the heart, the right side being more affected than the left.

Under the microscope the cardiac muscle fibers are separated by oedema. Clinically, oedema of the extremities develops. Swelling of abdomen (ascites), collection of fluid in the pleural cavities (hydro­thorax) may also occur. Heart failure is manifested by abnormally low excretion of urea (Oliguria), difficulty in breathing (dyspnoea), pal­pitation, acceleration of pulse (tachycardia), engorged neck veins and cardiac enlargement. The electrocardiogram shows rapid heart rate but there are no diagnostic electrocardiography changes.

A combination of dry and wet beri-beri may also occur.

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4. Wernicke’s Encephalopathy

It is a syndrome related to thia­mine deficiency (severe restriction of thiamine intake). This may develop by over-loading with glucose without adequate thiamine intake. This can occur even with any type of severe vomiting. People taking excess of alcohol also show Wernicke’s encephalopathy symptoms.

The disease is characterized by:

i. Occular signs-Paralysis of external recti. Pupils may be small, double vision can occur. This results in weakness of eye movement.

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ll.  Ataxia: Difficulty in walking.

Mental disturbances-Hallucinations, loss of memory (there is difficulty in retaining simple, meaningful material); confusion, agitation and mental apathy are common. Finally this advances to stupor and coma.