CAUSES OF BURNING FEET
- Dampness, together with friction, leads to the
sensation of burning, so its important to buy shoes that
let perspiration evaporate.
- Inappropriate socks. Wear socks made of cotton
rather than synthetic fabrics.
- Athletes foot can sometimes spread to cause burning
sensation on the sole of the foot.
- Allergic reaction to shoe material or socks.
- Alcohol is also contributing factor. Long term use
can affect the nervous activity of the feet.
- Diabetes
- Smoking
- Neuroma. A trapped nerve can lead to a hot burning
sensation. (Tight shoes)
- Gout can cause a burning sensation on the side of
the foot.
TREATMENT OF BURNING FEET
- Buy shoes and socks that have adequate ventilation.
-
If you are suffering from athletes foot then treat this
condition.
-
Reduce alcohol and smoking consumption.
-
Herbal products that increase the circulation may help.
-
Do not leave ice packs on your feet. This can lead to
other foot conditions.
In mechanical cases such as tarsal tunnel syndrome,
conservative treatment with arch supports and wider shoes
may successfully relieve discomfort. If burning feet is due
to flat feet, orthotics may help restore the foot’s arch.
Thanks to Dr Foot for above information.
| J Neurol
Neurosurg Psychiatry 1999;67:78-81
( July )
|
Since polished rice was introduced then south east
Asian countries saw a increase in heart disease and
neuropathy. The cause was determined to be the absence of
the nutritional absent husk around the rice which
contained niacin.
| J Neurol
Neurosurg Psychiatry 2000;69:447-452
( October )
Neurological manifestations in chronic
mountain sickness: the burning feet-burning
hands syndrome
P K Thomasa, R H M Kingb,
S F Fengb, J R Muddleb,
J M Workmanb, J Gamboac,
R Tapiad, M Vargasc, O
Appenzellere
a University
Department of Clinical Neurology, Institute
of Neurology, London WC1N 3BG, UK,
b University Department
of Clinical Neurosciences, Royal Free and
University College Medical School, London,
UK, c Instituto
de Investigationes de Altura, Universidad
Peruana Cayetano Heredia, Lima, Peru,
d Departmento de
Ciencias Fisiologicas, Universidad Peruana
Cayetano Heredia, Cerro de Pasco, Peru,
e New Mexico
Health Enhancement and Marathon Clinics
Research Foundation, Albuquerque, NM, USA
|
Burning paraesthesiae may be a troublesome
symptom in several peripheral neuropathies. They are
prominent in Strachan's syndrome,16
a condition originally found in the West
Indies17 but which
has subsequently been encountered under
conditions of nutritional deprivation
such as during the Spanish Civil War,18
in Japanese prisoner of war camps during
the second world war19
and, most recently, in the epidemic of
Cuban neuropathy that occurred in 1991-3.20
The precise nature of the nutritional deficiency in
Strachan's syndrome has not been identified.
None of our patients with CMS showed
evidence of nutritional deficiency or alcoholism.
Burning feet may occur in diabetic sensory
polyneuropathy, particularly in the
syndrome of acute painful diabetic sensory
neuropathy21
when it is associated with severe contact
hyperaesthesia of the skin. Diabetes was
excluded in our patients.
Burning and tingling paraesthesiae distally in
the lower limbs initially suggested the presence of
a small fibre neuropathy
and these
symptoms were reported by all our patients with CMS
and in all except one in the hands. This
symptom was not restricted to the
patients with CMS, however, being reported, in
lesser degree and confined to the feet,
in four out of five control subjects.
There was evidence on neurological examination of a
mild distal sensory polyneuropathy in
three patients with CMS that predominantly
affected small fibre modalities. 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
most probably hypoxic in origin.
The first description of hypoxic neuropathy was
given by Appenzeller et al in 1968,22
who reported a mild distal polyneuropathy
in seven out of eight patients with severe chronic
obstructive airways disease (COAD).
Subsequently Faden et al23
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 et al.24
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
our 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 et al
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.25
Basal laminal thickening around endoneurial
microvessels is seen in many neuropathies but is
most characteristic of diabetic
neuropathy.26 27
The finding of reduced basal laminal thickness
in our patients with CMS is unexpected but not
surprising. One possibility is that it is
not part of a neuropathic process but
represents an adaptive phenomenon to life at high
altitude. Similar adaptive microvascular
changes have previously been found in other
tissues of high altitude native human beings
and animals.28
It is not unreasonable that the finding of
reduced basal laminal thickness in
altitude associated hypoxia of nerves differs from
that occurring in acquired disease associated
hypoxic neuropathies such as that in COAD
examined by Malik et al.24
Whereas thickening of the basal lamina
layer is a non-specific finding in various
diseases of peripheral nerves, thinness of
this structure, on the other hand, is
likely to be a lifelong adaptive process that
has now also been found to occur in the human
sural nerve.
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,22 24
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
normalisation of the packed cell volume is known to
take about 2 months.29
Conversely, it is not rapid enough for it to be
related to a direct effect of transfer to
normal ambient oxygen concentrations.
The duration and the pattern of disappearance of
the symptoms would be consistent with the resolution
of a dysfunction involving a factor
delivered to the periphery by fast axonal transport.
This has a rate of 400 mm/day30
One possibility would be delivery of
nitric oxide synthase. Nitric oxide has a strong
vasodilatory action and its lack at the
periphery could lead to reduced vascular
perfusion. The effect of hypoxia on nitric oxide
synthase gene expression in central and
peripheral neurons has been examined in
rats by Prabhaker et al.31
The expression of neuronal nitric oxide
synthase (nNOS) mRNA was found to be increased by
10.4 (SD 1.3)% in the vagal nodose
ganglia and by 2.0 (SD 1.4)% in the
cerebellum. No significant effect was detected for
endothelial nitric oxide synthase (eNOS).
As CMS is a neuronal maladaptation
syndrome, it is conceivable that the upregulation of
the nNOS synthase gene in response to
hypoxia fails to occur, resulting in a
reduced delivery of nNOS synthase to the periphery.
This would be corrected by transfer to
the higher atmospheric oxygen
concentrations at sea level. The pattern of
reappearance of symptoms on return to
high altitude from sea level would also be
consistent with this interpretation, the
recurrence affecting the hands before the
feet. This is the opposite of the usual pattern for
distal "length related" neuropathy, but
would be in accordance with the depletion
of a factor delivered by axonal transport. Although
this hypothesis for the occurrence of the
burning feet-burning hands syndrome in
CMS is speculative, observations on nNOS
concentrations in peripheral nerve in
patients with CMS with this syndrome would
be of interest.
|
|
Nutritional and Other Neuropathies
Associated with Gastrointestinal Di.sorders
12/28/02
Laurence J Kinsella, MD, FACP
Chief, Division of Neurology and Neurophysiology
Forest Park Hospital
Associate Professor, Neurology
Saint Louis University
Gluten Sensitivity Neuropathy (Celiac Disease)
This is a proposed autoimmune disorder induced by celiac disease.
Wheat, barley, and oats are
composed of gluten that may induce an antibody reaction in
susceptible individuals.
These
antibodies are thought to be directed against Purkinje cells and
other nervous system tissue
leading to a variety of disorders including cerebellar ataxia,
neuropathy, and myoclonus.
Hadjivassiliou reviewed 35 reports of neurologic disorders
associated with celiac disease in 83
patients (mean age 48, M=F). These included ataxia (29), peripheral
neuropathy (29), myopathy
(13), ataxia with myoclonus (9), myelopathy (4), and dementia (6).
The same author has reported
up to 40% of patients with idiopathic peripheral neuropathy have
anti-gliadin antibodies
(Hadjivassiliou, 2002).
The neuromuscular manifestations include sensorimotor axonal
neuropathy, axonal motor, and
mononeuropathy multiplex. All patients were found to have anti-gliadin
antibodies, either IgG or
IgA. Of all patients with positive antibodies, only 35% have an
abnormal intestinal biopsy,
suggesting that neurologic symptoms may occur without GI symptoms. HLA DQ2 is found in
90% of patients with celiac disease so this offers an additional
confirmatory test. Further study is
needed of this potentially important cause of neurologic illness.
Cobalamin deficiency may be caused by a number of malabsorption
syndromes, most commonly
pernicious anemia, which accounts for well over 80% of all cases of
B-12 deficiency. In up to
10% of patients, the cobalamin deficiency may be due to food
cobalamin malabsorption, which
results from achlorhydria and an inability to separate cobalamin
from food due to inadequate
gastric acidity. A number of other malabsorptive syndromes of the
lower gut, such as bacterial
overgrowth, tapeworm infestation, Crohn's disease, and ulcerative
colitis, may also result in
cobalamin deficiency (Green and Kinsella 1995; Savage and Lindenbaum
1995).
Post gastroplasty neuropathy and Strachan's syndrome remain a
mystery in terms of the exact
etiology but are probably polynutritional in origin, with a heavy
emphasis on thiamin deficiency.
Pyridoxine excess
Toxic doses of pyridoxine may also result in a large fiber sensory
peripheral neuropathy
(Schaumburg et al 1983; Parry and Bredesen 1985; Dalton and Dalton
1987). Mega doses of
pyridoxine may produce a sensory neuropathy after several weeks of
use, generally in excess of 2
grams per day. It has also been reported with longstanding use of as
little as 200 mg a day.
Symptoms of paresthesias, ataxia, and burning feet occur 1 month to
3 years after starting
pyridoxine.
Axonal degeneration, reduced myelin fiber density, and myelin debris
have all been demonstrated
in sural nerve biopsies. After stopping the pyridoxine, few patients
entirely resolved, but most
improved. Individuals who use large doses of B-complex vitamins are
under the false impression
that, because B-complex vitamins are water soluble and, therefore,
are excreted in the urine, it is
not possible to take too much. In fact, 200 mg doses of pyridoxine
are commonly found as
single tablets in pharmacies and are sufficient to cause a sensory
neuropathy after many months
of exposure.
Strachan's syndrome
In 1888, Henry Strachan, a British medical officer stationed in
Jamaica, described a syndrome of
painful peripheral neuropathy, ataxia, optic neuropathy, and
stomatitis among sugarcane workers
(Strachan 1897). Denny Brown and others found similar ailments among
allied troops liberated
from prisoner of war camps after World War II (Denny-Brown 1947).
Other symptoms included
sensorineural deafness, dizziness, confusion, spastic leg weakness,
foot drop, Wernicke's
encephalopathy, and rare cases of neck extensor weakness and
myasthenic bulbar weakness. Poor
nutrition, hard physical labor, and concurrent infection were
thought to be exacerbating factors.
Fischer performed autopsies on a series of Canadian prisoners of
war, the most prominent
pathologic findings were demyelination of the posterior columns of
thoracic and cervical spinal
cord (Fischer 1955).
More recently, an outbreak of optic and peripheral neuropathy
closely resembling Strachan's
syndrome occurred in Cuba from 1992 to 1993 following a loss of food
and fuel imports from
the former Soviet Union (Roman 1994). Fifty thousand people
developed either isolated or
combined optic neuropathy, painful sensory neuropathy, dorsal
lateral myelopathy, sensory neural
deafness, spastic paraparesis, dysphonia, and dysautonomia. Forty-
five percent developed
centrocecal scotoma and optic neuropathy only, often following a
period of weight loss. A
number of possibilities were proposed, including vitamin B-complex
and thiamin deficiency,
cyanide intoxication, viral infections, and mitochondrial deletions.
Heavy alcohol and tobacco use
were found most frequently in those with optic neuropathy
(tobacco-alcohol amblyopia). Clinical
evidence of neuropathy was often lacking despite the severe symptoms
(Thomas et al 1995).
Sural nerve biopsy showed axonal degeneration of large myelinated
fibers. Most patients
responded to supplementation of B-complex vitamins.
Vitamin E deficiency
Vitamin E is fat soluble and found in abundance in vegetable oils
and wheat germ. It is carried
in portal blood to the liver, and alpha- tocopherol transfer protein
binds it and recycles vitamin E
in the liver for incorporation into low density and very low density
lipoproteins. The patients at
risk for development of vitamin E deficiency include those with hypo
or abetalipoproteinemia,
other disorders of the pancreas and liver, such as cystic fibrosis,
protein-calorie malnutrition,
familial vitamin E deficiency, and other malabsorption states
(Jackson et al 1996). Symptoms
include areflexia, cerebellar ataxia, cutaneous sensory impairment,
position and vibratory sense
abnormalities and less commonly, ophthalmoplegia, muscle weakness,
nystagmus, extensor plantar
responses, ptosis, and dysarthria. The peripheral neuropathy is
usually limited to the legs and is
mild, axonal, and sensorimotor in nature (Brin et al 1986).
13. Diagnostic Evaluation
Thiamin deficiency may be assessed by the transketolase assay.
Because the carbohydratemetabolizing
enzyme transketolase requires thiamin pyrophosphate, a deficiency
will lead to an
elevation in the red blood cell transketolase. The assay is most
sensitive when performed with
and without a thiamin pyrophosphate challenge. Serum thiamin levels
are unreliable due to low
sensitivity and specificity. MRI of the brain will occasionally show
an abnormal signal in the
periaqueductal gray matter and midline structures.
Cobalamin deficiency may be due to a variety of disorders, most
commonly pernicious anemia. Approximately 78% of patients with cobalamin deficiency will be
found to have a proven or
probable defect of intrinsic factor production from the gastric
parietal cell (pernicious anemia).
Perhaps 10% of patients have food-cobalamin malabsorption due to
hypo- or achlorhydria, a
disorder that affects from 16-40% of the elderly ( Hurwitz et al,
1997). The rest are due to a
variety of causes including malabsorption from inflammatory bowel
disease, tape worm
infestation, blind loop syndrome, chronic H2 blocker therapy,
gastric bypass, and serum binding
protein abnormalities.
In a patient with signs and symptoms of cobalamin deficiency, one
should begin with a
cobalamin assay. If the serum cobalamin assay result is less than
the lower normal limit, a
measurement of intrinsic factor antibodies should be taken. If this
test is positive, the diagnosis of
pernicious anemia is confirmed, and a Schilling test is not
necessary. In pernicious anemia, some
laboratory evidence of an autoimmune process is often found. Anti-
parietal cell antibodies are
present in 90% and intrinsic factor antibodies in 60% of patients
with pernicious anemia. Antiparietal cell antibodies have a 10% false positive rate. Though
it lacks sensitivity, the test for intrinsic factor antibodies is much more specific.
In patients with serum cobalamin levels in the lower normal range,
but in whom one still
suspects clinical cobalamin deficiency, one should measure levels of
homocysteine and
methylmalonic acid (Snow, 1999; Kinsella and Green, 1995).
Methylmalonic acid may be
measured in serum or urine. The urinary assay is more specific in
patients with renal
insufficiency. If either metabolite is elevated, then serum
intrinsic factor antibodies and gastrin
should be measured. The serum gastrin level is often elevated in
pernicious anemia and is a
marker for achlorhydria, a cause of food- cobalamin malabsorption.
The presence of hypersegmentation may be a sensitive marker for
cobalamin deficiency, even in
the absence of anemia or macrocytosis. If metabolites or the serum
gastrin are elevated, a
Schilling test may be performed to identify cobalamin absorption,
which is usually the result of
autoimmune parietal cell dysfunction that occurs in pernicious
anemia. Technically, patients with
classic pernicious anemia have an abnormal test result when
radioactive cobalamin alone is given
by mouth (Part I). This abnormality is corrected when the test is
repeated with intrinsic factor
(Part II). Abnormally low secretion of cobalamin in the Part II
Schilling test indicates an
intestinal cause for the cobalamin malabsorption, such as
inflammatory bowel disease. The Part II
Schilling test may be repeated, after giving antibiotics or
vermacides to exclude bacterial
overgrowth ("blind loop syndrome") or fish tapeworm infestation due
to diphyllobothrium latum,
rare causes of cobalamin deficiency through competition for
intraluminal cobalamin.
A normal Part I test in a patient with cobalamin deficiency may be
observed in total vegetarians.
It may also occur in patients with food-cobalamin malabsorption who
show normal absorption of
crystalline cobalamin but are unable to digest and absorb cobalamin
present in food due to
achlorhydria. This defect can be identified using a modified
Schilling test in which radioactive
cobalamin is administered with food (Carmel, 1990).
Pyridoxine deficiency will cause elevations in serum homocysteine
and cystathionine, and assays
are commercially available. Urinary assays for xanthurenic acid and
other pyridoxine metabolites
may be performed following tryptophan loading.
Vitamin E deficiency can be reliably investigated using the serum
alpha- tocopherol level. Adult
patients without malabsorption and a clinical picture consistent
with Friedrich’s ataxia and
neuropathy should be investigated for an autosomal recessive defect
in the tocopherol transporter
protein gene of chromosome 8. Tocopherol transporter protein
incorporates tocopherol into
chylomicrons. The serum tocopherol levels in these patients may be
in the normal range;
however, they respond to high dose supplementation.
Strachan’s syndrome and are polynutritional in origin; therefore, a
battery of vitamin deficiencies
should be sought, including thiamin, niacin, pyridoxine, and
cobalamin. The pathophysiology of
post-gastroplasty neuropathy is probably multifactorial, due perhaps
to a polynutritional and an
endogenous toxin produced as the result of the abnormal anatomy
created by the surgical
procedure. This toxic hypothesis is supported by the fact that some
have reported a resolution of
the symptoms following reversal of the surgical procedure whereas
nutritional replacement alone
does not. Alternatively, there may be a nutritional factor that
cannot be replaced adequately until
the procedure has been reversed.Pyridoxine deficiency will cause
elevations in serum homocysteine and cystathionine, and assays
are commercially available. Urinary assays for xanthurenic acid and
other pyridoxine metabolites
may be performed following tryptophan loading.
Vitamin E deficiency can be reliably investigated using the serum
alpha- tocopherol level. Adult
patients without malabsorption and a clinical picture consistent
with Friedrich’s ataxia and
neuropathy should be investigated for an autosomal recessive defect
in the tocopherol transporter
protein gene of chromosome 8. Tocopherol transporter protein
incorporates tocopherol into
chylomicrons. The serum tocopherol levels in these patients may be
in the normal range;
however, they respond to high dose supplementation.
~15.
Management
Treatment of suspected thiamine deficiency in the setting of
post-gastroplasty neuropathy,
Strachan’s syndrome, or Wernicke-Korsakoff syndrome begins with
the immediate administration
of 100 mg thiamine intravenously followed by 100 mg
intramuscularly daily for 3 to 5 days and
parenteral multivitamins. Patients are then maintained on 50 mg
thiamin orally along with
multivitamins daily.
For cobalamin deficiency, the total body store of cobalamin is
2000 to 5000 μg, half of which is
stored in the liver. The recommended daily allowance is 6 μg/day,
and the average diet provides
20 μg/day. Treatment may begin with intramuscular injections of
1000 μg of cobalamin for 5
days, then 500 to 1000 μg intramuscularly every month. Oral
replacement is an alternative for
those patients who cannot tolerate intramuscular injections, or
for whom they are impractical.
Because 1% of all ingested cobalamin may be absorbed by passive
diffusion, cobalamin
requirements can be satisfied with oral therapy, even in
patients with pernicious anemia
(Kuzminski, 1998). A daily dose of 1000 μg/day orally will yield
10 μg of absorbed cobalamin,
which exceeds the recommended daily allowance. Sublingual
cobalamin 2000 ug/ day is also
effective and may be superior to IM injections for some patients
(Delpre, 1999). It may be
practical to replenish cobalamin stores first using injections
of cyanocobalamin for 1 week, and
then to maintain patients using a 1000 μg daily oral supplement.
The effectiveness of treatment,
regardless of route, can be confirmed by demonstrating normal
serum or urine methylmalonic acid
levels three to four weeks after beginning B12 replacement.
The management of post gastroplasty neuropathy begins with a
recognition and replacement of
vitamin deficiency, particularly thiamine and B12. However,
vitamin supplementation alone is
rarely successful. A toxic hypothesis is supported by the fact
that some have reported a resolution if the symptoms following reversal of the surgical procedure
whereas nutritional replacement
alone does not.
The management of gluten sensitivity neuropathy is preliminary
given its uncertainty. Further
study of the efficacy of a gluten free diet in patients with
anti-gliadin antibodies and a peripheral
neuropathy is warranted
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