Burning Feet Research Articles

Painful sensory neuropathy: prospective evaluation using skin biopsy.

In patients presenting with painful, burning feet with minimal signs of neuropathy, the following questions were addressed: 1) How many of these patients have a peripheral neuropathy? 2) What is the role of skin biopsy in establishing a diagnosis of neuropathy? 3) What conditions are associated with the neuropathy? and 4) What laboratory studies are useful in this patient population? A total of 117 consecutive patients referred for evaluation were prospectively studied. All underwent nerve conduction studies (NCS) and a battery of blood tests, including antinerve antibodies. If NCS were normal, a punch biopsy of the skin of the distal leg was performed to ascertain the intraepidermal nerve fiber (IENF) density. In a subset of 32 patients, the sensitivity of skin biopsy was compared to quantitative sudomotor axon test (QSART) and quantitative sensory tests (QST). Three groups emerged. Group 1, with abnormal NCS (n = 60, 34 F/26 M, mean age 60 +/- 14 years), represented 51% of the cohort. The majority had neuropathies of undetermined cause, but 18 (30%) had associated conditions. Group 2, with normal NCS and reduced IENF density (n = 44, 29 F/15 M, mean age 57 +/- 14 years), represented 38% of the cohort. Three in this group had associated conditions. Group 3, with normal NCS and IENF density (n = 13, 6 F/7 M, mean age 53 +/- 13 years), represented 11% of the cohort; most had no diagnoses but two had MS. In a comparative subset analysis, skin biopsy was more sensitive than QSART or QST in diagnosing a neuropathy. Patients presenting with painful feet are heterogeneous, consisting of both large and small fiber sensory neuropathies. In rare cases, a central cause for pain can be found. Over one-third of patients required a skin biopsy to diagnose a small fiber sensory neuropathy. A limited battery of blood tests facilitated diagnosis, but serum antinerve antibodies were not helpful.

Neuromuscular complications of kidney diseases.

affected than females [2,6 ]. Bolton pointed out that The uraemic syndrome is characterized by overall 60% of patients receiving haemodialysis for uraemia deterioration of biochemical and physiological funchave neuropathy by electrodiagnostic criteria [2]. The tions in parallel with the progression of renal failure. main symptoms are restless legs, spontaneous cramps, Uraemia results in variable symptoms pointing to distal paresthesias, numbness and burning feet, which, damage of multiple organs, due to retention of comhowever, are not necessarily related to the neuropathy, pounds normally cleared by the healthy kidneys [1]. but due possibly to transient disturbances of peripheral The identified mechanisms currently are attributed to sensory receptors, induced by fluctuation in water and increased protein catabolism, reduced excretory electrolytes [2]. Symptoms may occur either prior to capacity and altered water–electrolyte homeostasis [2]. or during a regular haemodialysis programme; the Major neurotoxins accumulating in uraemia are latter could indicate that the achieved control is not urea, creatinine, guanidine compounds, a number of optimal [2,3]. Clinical signs of uraemic polyneuropathy aromatic acids, uric and ossalic acids, myo-inositol, include symmetric muscle weakness, areflexia and ‘middle molecules’, b2-microglobulin, amines and parasensory loss for all modalities, especially pin-prick and thyroid hormone (PTH) [2]. The nervous system, both vibration. An early finding is elevation of the vibratory central and peripheral, may show changes, mimicking threshold [2,3,6 ] (Table 2). exogenous poisoning or drug overdose [1]. Here we review the clinical, electrophysiological and morpholoPathology of uraemic polyneuropathy gical aspects of peripheral nervous system syndromes

Acute secondary erythermalgia and hypertension in children. Erythermalgia Multidisciplinary Study Group.

We studied the clinical symptoms in nine children (seven females and two males; mean age 11.6 years) with severe but transient acute secondary erythermalgia. The classical symptoms at presentation were episodic attacks of painful burning hands and feet which felt warm with congested appearance of the feet. Each attack lasted for a mean period of 25 days (range from 6 to 56 days). The blood pressure was elevated in seven patients. Intravenous sodium nitroprusside was effective in ameliorating the symptoms with drop in blood pressure to normal in five patients; pizotifene, labetolol, prostaglandin E1 and hypnotherapy were effective in each of four separate cases. The episodes of acute secondary erythermalgia were transient in all and did not recur after a mean follow up period of 1.6 years. These cases suggest that acute secondary erythermalgia, however transient, is not rare and can be associated with mild to moderate hypertension which may respond to sodium nitroprusside. A greater awareness of this condition is necessary to make an accurate and timely diagnosis and institute appropriate therapy in order to prevent undue complications.

Neurologic changes in visceral leishmaniasis.

Neurologic changes in visceral leishmaniasis (VL) are rarely reported. From January 1992 to April 1993, 111 patients with VL were seen at Soba University Hospital in Khartoum, Sudan. Fifty-two (46%) patients had neurologic symptoms or signs; the most common symptom was a sensation of burning feet. Four patients had foot drop. Five patients had deafness and one patient had multiple cranial nerves palsies. None of our patients had vitamin deficiency or any of the other known causes of neuropathy. Nerve conduction studies in 15 patients showed evidence of axonal degeneration and demyelination, which were confirmed by histopathology and electron microscopy of nerve biopsies. There was no direct parasitic infection of the nerve and there was no neuritis. In most patients, the sensory symptoms disappeared within two weeks in most of our patients after specific anti-leishmanial treatment. Motor recovery was much slower. Audiographic studies in five patients with deafness showed it to be sensory-neural. Hearing returned to normal after treatment with sodium stibogluconate. Further studies are needed to define the etiology of the nerve pathology in patients with VL.

Cutaneous thermal thresholds in patients with painful burning feet.

Small nerve fibre sensory function was assessed by psychophysical estimates of cutaneous thermal thresholds in 30 patients who presented with the symptoms of painful burning feet. Thresholds were abnormal in 12 and normal in 18 patients although symptoms in the two groups were very similar. Various hypotheses for the mechanism of pain in small fibre neuropathy have been proposed previously and these are discussed, but the cause of symptoms in patients with normal thresholds, is unknown. The possibility exists that these patients have a neuropathic disorder which affects only those unmyelinated fibres involved with pain.

Bilateral burning foot pain: Monitoring of pain, sensation, and autonomic function during successful treatment with sympathetic blockade

We describe a patient with burning pain in both feet associated with local autonomic disturbances following bilateral traumatic sciatic mononeuropathies. The diagnosis of a sympathetically maintained pain was confirmed through a prompt response to sympathetic blockade. Although a mild alcohol-nutritional neuropathy was found, the clinical findings strongly suggested a diagnosis of bilateral causalgia. Clinical evaluation and quantitative sensory testing were performed prior to and after successive unilateral lumbar sympathetic nerve blocks. After unilateral blockade, bilateral improvement was recorded in measures of pain, sudomotor function, and foot temperature. Other measures of autonomic function showed variable responses to sympathetic blockade. Quantitative sensory testing revealed a dramatic alteration in the contralateral limb's thermal sense following unilateral block. This case underscores the potential for bilateral causalgia and provides additional evidence for a central mechanism operating in this disorder. The relationship between bilateral causalgia and the “burning feet syndrome” in alcoholic neuropathy is discussed.

Thiamine deficiency neuropathy

Despite the fact that thiamine deficiency neuropathy is increasing in incidence in our society, it remains an underdiagnosed disorder. The typical complaints of weakness and burning feet are often regarded as trivial by the attending physician. Electrophysiologic studies are sensitive and often provide supportive evidence to aid in the diagnosis. Since chronic pain therapy is often ineffective, a high index of suspicion should be maintained to help ensure early diagnosis and successful intervention.

“Burning feet” syndrome

“Burning feet” syndrome

Neurologic complications after gastric restriction surgery for morbid obesity.

We report the occurrence of neurologic complications in 23 patients who underwent gastric restriction surgery for the treatment of morbid obesity. Complications occurred 3 to 20 months after surgery. All the patients had had protracted vomiting for the first 3 months after the operation. The following syndromes were found: chronic or subacute symmetric polyneuropathy (12 patients), acute severe polyneuropathy (1 patient), burning feet syndrome (2 patients), meralgia paresthetica (3 patients), myotonic syndrome (1 patient), posterolateral myelopathy (2 patients), and Wernicke-Korsakoff encephalopathy (2 patients). The patients suffering from burning feet syndrome and those with Wernicke-Korsakoff encephalopathy showed a clear improvement after parenteral thiamine treatment. As to the rest of the patients, the occurrence of the complications seems to be linked to nutritional causes, although no such deficiencies were detected.

The restless legs syndrome.

The first description of the restless legs syndrome (RLS) is attributed to Thomas Willis in the 'London Practice of Physick' of 1685 (Ekbom, 1960). Here he wrote 'wherefore to some, when being a bed they betake themselves to sleep, presently in the arms and leggs, leapings and contractions of their tendons, and so great a restlessness and tossings of their members ensue, that the diseased are no more able to sleep than if they were in a place of the greatest torture'. In 1861 Whittmaack used the term anxietas tibiarum to describe nocturnal discomfort of the legs, which he considered was a common symptom of hysteria (Ekbom, 1945). The same phenomenon was called 'impatience musculaire' in the French literature (Ekbom, 1944; Bonduelle, 1952) and the leg jitters by Allison (1943). Ekbom's earliest descriptions of the RLS distinguished a common form which he called 'asthenia crurum paraesthetica' from a painful variant 'asthenia crurum dolorosa' (Ekbom, 1946). He identified the first of these in 34 cases. Paraesthesia with deep calf and shin discomfort started only when the legs were at rest and necessitated that they were moved to provide relief. He postulated that pregnancy was an aetiological factor and in some patients he diagnosed prostatitis, testosterone deficiency and the burning feet syndrome due to malnutrition. Ask-Upmark noted the disorder as a late effect of gastrectomy (Ask-Upmark & Meurling, 1955) and on the basis of anecdotal evidence of postural dependence of symptoms, suggested the cause was vascular congestion ofthe spinal cord (AskUpmark, 1959). Some authors doubted the existence ofa distinct syndrome; Purdon-Martin (1946) believed the symptoms were due to acroparaesthesia and Masland (1947) that they were a manifestation of myokymia. By 1960 Ekbom had studied 175 people whom he had identified with restlessness of the legs. He found that 5% of normal psychiatrically stable individuals were disturbed by restless sensations, but also believed it was symptomatic of anaemia, certain infectious diseases, diabetes, cold exposure or those taking phenothiazine drugs (Ekbom, 1945, 1950, 1960). A diabetic patient whose symptoms vanished on the side of a recent leg amputation was presented as evidence for a peripheral origin (Ekbom, 1961) and Bornstein (1961) speculated about abnormal connections with the reticular system. In recent years neuroleptic-induced akathisia has been compared with idiopathic RLS. Akathisia was originally described in its uncommon idiopathic form by Haskovec (1901) and later in relation to Parkinson syndromes (Sicard, 1923) and drugs such as promethazine (Sigwald et al., 1947) and the phenothiazines (Steck, 1954). It is characterized by a state of mental and motor restlessness which is accompanied by an irresistible compulsion to physically move about. Restlessness of the legs is common and similar to that occurring in idiopathic RLS, but inner restlessness of the mind and body is peculiar to akathisia. Confusion between these two conditions explains why promethazine and prochlorperazine have been considered both cause and ineffective remedy of RLS.

Tropical spastic paraparesis: a neuroepidemiological study in Colombia.

A geographic isolate of tropical spastic paraparesis (TSP) in Tumaco, Colombia, is described. Fifty confirmed cases were identified (29 men, 21 women) with an estimated prevalence ratio of 98 cases per 100,000 population. Patients with identified cases ranged in age from 24 to 75 years (mean, 46.5). TSP begins with burning feet, leg stiffness, spastic bladder, and, in men, impotence. Patients exhibited leg weakness, spasticity, hyperreflexia, and scissoring gait. Babinski, Chaddock, and Hoffmann signs could be elicited. Ankle reflexes and vibratory sensation of the feet were decreased. Intellectual function, coordination, and cranial nerves remained normal. TSP is a slowly progressive disorder but so far there have been no deaths from it. Forty cases in this report began between 1971 and 1980; the earliest documented case began in 1952. Living conditions and occupations of the patients were typical for the region. Yaws had occurred in 74% of confirmed cases. No likely etiological neurotoxic or nutritional factors were identified. TSP also has been described in India, Africa, the Seychelles, and Jamaica.

Neuromyelitis optica (Devic disease)_following varicella infection

A 5-year-old white girl was admitted to Milwaukee Children's Hospital with a four-day history of inability to walk. Eleven days prior to admission she developed a febrile illness associated with a vesicular eruption, which was diagnosed as varicella. Two siblings developed a similar exanthem simultaneously. Five days after the onset of her exanthem the patient complained of burning feet. The next day she refused or was unable to walk. Two days later she was noted to have decreased strength in her lower extremities, a stiff neck, incontinence, and blurred vision. There was no history of loss of consciousness or ataxia. Physical examination re~{ealed a well-developed, wellnourished, afebrile white girl covered with crusted lesions. Positive physical findings included posterior cervical lymphadenopathy and positive Kernig and Brudzinski signs. Papilledema was absent. Her abdomen was distended but there was no organomegaly, The patient was alert and well oriented. The optic fundi were normal and cranial nerve dysfunction was not observed. There was a flaccid paralysis of the lower extremities. Rectal sphincter tone was normal. There was loss of pain, pin, and light touch sensations below T~,. Position sensation could not be reliably tested. Deep tendon reflexes were absent in the lower extremities and the Babinski sign was present bilaterally.

Atrophic beriberi: A complication of jejunoileal bypass surgery for morbid obesity

Four months after jejunoileal bypass surgery for morbid obesity, a 37 year black woman who ate a grossly inadequate diet was hospitalized complaining of diffuse abdominal pain, complete loss of appetite, burning feet, generalized weakness and inability to walk without assistance; she had had a weight loss of 100 pounds. Physical findings were limited to the neurologic examination and revealed bilateral glove hypesthesia to midforearms, bilateral stocking hypesthesia to the ankles and partial loss of all sensory modalities. She also had distal muscle weakness with inability to make a firm fist or to stand without assistance. Routine laboratory studies were not diagnostic. She was admitted to the surgical service with a diagnosis of electrolyte imbalance secondary to gastrointestinal losses; she was fed a high-protein diet as tolerated and given intravenous electrolyte therapy, but her neurologic condition deteriorated severely over a two week period. She had a complete loss of deep tendon reflexes in all extremities; the extent of sensory loss increased slightly and motor function disappeared completely below the knees with minimal function in the thighs. Hip motion remained normal. Finger and wrist extension were absent and flexion was very poor, although shoulder and central nervous system functions were all intact. Several serum vitamin studies made at that time showed only a severe depletion of thiamine. Atrophic beriberi secondary to jejunoileal bypass surgery and poor diet was appreciated for the first time. Replacement therapy with thiamine followed by an elemental diet containing all essential nutrients administered through a jejunostomy tube resulted in gradual improvement. Atrophic beriberi should be suspected whenever peripheral neuropathy develops after jejunoileal bypass for morbid obesity.

Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention

80 strictly selected patients with chronic renal insufficiency with plasma creatinine values of 1.4-14.5 mg% were examined for clinical and electrophysiological signs of nephrogenic polyneuropathy. The motor symptoms complained of were cramps in 43.8% of the patients, "restless leggs" in 18.7%, muscular twitchings in 12.5%. It was emphasized that the first two symptoms do not always indicate the presence of polyneuropathy. 30% complained of paresthesias, 5% of "burning feet". The most frequent clinical finding was the impairment of vibration sense in the feet in 37.5% followed by diminshed appreciation of passive movement of the toes in 30%, weakening or absence of the ankle jerk in 23.8% and finally, weakening of the patellar reflex in 5%...

Uremic neuropathy. Monitoring of transketolase activity inhibition in a child.

A girl with chronic glomerulonephritis reached terminal uremia at the age of 111/2 years and developed peripheral neuropathy characterized by burning foot syndrome, sensory loss, severe weakness of the left leg, and bilaterally decreased nerve conduction velocities. Recovery was virtually complete after eight months of intensive hemodialysis. Serial determinations of transketolase activity (TKA) inhibition by the patient's serum were performed. The TKA inhibition by the patient's serum, initially high, returned to normal as clinical evidence of neuropathy disappeared. Nerve conduction velocities remained below normal during the period of observation.

The peripheral nerve function in chronic renal failure. I. Clinical symptoms and signs.

Abstract. A material consisting of 109 patients with chronic renal failure has been examined for the presence of clinical symptoms and signs indicating a peripheral neuropathy. Symptoms were reported by 84 patients (77%). Cramps and the restless legs syndrome were reported most frequently. However, several clinical observations raised doubt whether these symptoms do at all reflect a peripheral neuropathy. Paresthesia (31%) and dysesthesia (18%) were the most common sensory symptoms, whereas actual pain and the burning feet syndrome were rare complaints. Clinical signs of a neuropathy were recorded in 56 patients (51%). This came close to the over‐all incidence in previously reported materials. Impaired vibration sense and reflex disturbances were the earliest and the most frequent findings. As a rule other signs occurred late in the course of chronic renal failure, and they were late manifestations of neuropathy as well.

Hypoglycemia and burning feet.

Hypoglycemia and burning feet.

BURNING FOOT SYNDROME

Medical Journal of AustraliaVolume 2, Issue 10 p. 434-434 Correspondence BURNING FOOT SYNDROME First published: 01 September 1965 https://doi.org/10.5694/j.1326-5377.1965.tb18888.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume2, Issue10September 1965Pages 434-434 RelatedInformation

BURNING FOOT SYNDROME: BILATERAL OCCURRENCE WITH RADICAL CURE.

Medical Journal of AustraliaVolume 1, Issue 21 p. 764-765 Report of Case BURNING FOOT SYNDROME: BILATERAL OCCURRENCE WITH RADICAL CURE N. F. Babbage F.R.C.S. (Edin.), N. F. Babbage F.R.C.S. (Edin.) General Practitioner Epping, New South WalesSearch for more papers by this author N. F. Babbage F.R.C.S. (Edin.), N. F. Babbage F.R.C.S. (Edin.) General Practitioner Epping, New South WalesSearch for more papers by this author First published: 01 May 1965 https://doi.org/10.5694/j.1326-5377.1965.tb72176.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume1, Issue21May 1965Pages 764-765 RelatedInformation

“Kwashiorkor-like” syndrome, associated with burning feet syndrome, in an adult male

A kwashiorkor-like syndrome, associated with “burning feet,” is described in a forty-five year old Negro man, in whom, ten years after a gastrectomy for intractable duodenal ulcer, progressively severe diarrhea developed which resulted in pronounced protein depletion, affecting particularly the endocrine glands, with apparent decline in the trophic hormones. After all possible etiologies were considered, the patient was explored surgically and no abnormality was found. In the process of preparing for surgery the patient was given a large quantity of plasma protein, including 20 units of plasma, and apparently as a result of this therapy his severe protein depletion was corrected. Subsequently, the patient rapidly recovered.The clinical picture was not unlike that described in the syndrome of kwashiorkor, even to the red hair. Eight months after admission to the hospital, and five months after the institution of protein therapy, the patient appears and acts perfectly healthy.