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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 which
are 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 in
Strachan'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 (painfull 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 maldevelopment of
peripheral myelin, the myelin sheath
being abnormally thin for axon diameter.
If you are Living at High altitude You need to
move to Los Angles like altitude or Arizona.
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 be
related to a direct effect of transfer to
normal ambient oxygen concentrations.
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