Burning feet are a troublesome symptom in several diseases that affect the nerves called the peripheral neuropathies. They are prominent in Strachan's syndrome, a condition originally found in the West Indies but whichare encountered under conditions of nutritional deprivation such as during the Spanish Civil War, in Japanese prisoner of war camps during the second world war and, most recently, in the epidemic of Cuban neuropathy that occurred in 1991
.The precise nature of the nutritional deficiency inStrachan's syndrome is most likely nutritional. Patients with CMS (Chronic Mountain Sickness) showed evidence of nutritional deficiency or alcoholism.Burning feet may occur in diabetic sensory polyneuropathy, particularly in the syndrome of acute painful diabetic sensory neuropathy when it is associated with severe contact hyperaesthesia (painful sensations) of the skin.
Burning and tingling sensation or paresthesias ( altered sensations) in the legs initially suggest the presence of a small fibre neuropathy and these symptoms were reported by all patients with CMS and in the hands. This symptoms are not restricted to the patients with CMS,and can be seen with other diseases. In CMS that nerves affected are predominantly affected small fibres. The biopsy findings indicated the presence of a modest demyelinating neuropathy without a
reduction in total myelinated fibre density and a reduced unmyelinated axon density in one biopsy. This altitude associated neuropathy is probably hypoxic in origin.
The first description of hypoxic neuropathy was given by Appenzeller et al in 1968,who reported a mild distal polyneuropathy in seven out of eight patients with severe chronic obstructive airways disease (COAD). Subsequently Faden documented the presence of mild sensory loss and reflex depression in the legs in four out of 23 patients with chronic respiratory insufficiency.
The most detailed description of the underlying neuropathological changes in hypoxic neuropathy has been provided by Malik Nerve biopsies obtained from six patients with COAD showed the presence of demyelination and remyelination, a reduced density of unmyelinated axons, and an increased thickness of the basal laminal layer around endoneurial capillaries. The findings in patients with CMS conform to this apart from the lack of basal laminal thickening. It is of relevance that experimental hypoxia seems to have a selective effect on myelination in peripheral nerve. Benstead found that in rats reared under hypoxic conditions there is a selective mal development of peripheral myelin, the myelin sheath being abnormally thin for axon diameter.
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The relevance of the mild sensory neuropathy in patients with CMS to the occurrence of the burning feet-burning hands syndrome is questionable as patients with neuropathy related to COAD do not experience this symptom, and there was no clinical evidence of neuropathy in seven out of our 10 patients with CMS,all of whom experienced burning feet and burning hands. Some other explanation is therefore necessary. In this connection, the improvement of the burning feet and hands on transfer to a lower altitude is of particular interest. The improvement took place over 2 weeks for the lower limbs and 1 week in the upper limbs. On returning to high altitude, the symptoms recurred in the hands before the feet. This fairly rapid time course suggests that the regression is not related to structural restitution.
The time course is also too rapid for it to be due to a reduction in blood viscosity, as normalization of the packed cell volume is known to take about 2 months. Conversely, it is not rapid enough for it to berelated to a direct effect of transfer to normal ambient oxygen concentrations.
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