Background: Burning feet syndrome (BFS) has been described anecdotally in the literature for over 200 years. Described subjectively by patients as burning, prickling and unremitting with nocturnal exacerbations, the condition draws parallels with the burning dysaesthesia found in diabetic peripheral neuropathy, and appears to display a similar chronicity. Despite being a common symptom, especially among the elderly, its etiology in non-specific and often marked by a lack of objective clinical signs. Historically, burning feet syndrome has been recorded in situations of poor nutrition, including malnourished African populations in the early 20th century, South American plantation workers in the 1920s and during food shortages in the Spanish Civil War. Perhaps the best described and largest outbreak of burning feet occurred amongst prisoners of war (POWs) of the Japanese during the 2nd World War in South East Asia and the Far East. In this review we summarise reports of the condition, in particular amongst Far East POWs (FEPOWs), using both the available literature as well as a unique and previously unknown contemporary study carried out in a POW camp. Materials and Methods: During his stay in the Tandjung Priok POW camp, Nowell Peach recorded 54 cases of burning feet seen over a 4 month period during captivity. This data was concealed from his captors and survived to return home with him. Results: 54 prisoners presented over a 4 month period with a mean age of 28 years and mean duration of symptoms of 12 weeks. Neurological signs were meticulously documented. All were on an inadequate diet, 20 (38%) were on less than a full ration. Accompanying tropical infections were common including malaria (73%), dengue (45%) and dysentery (41%). Discussions: The Peach survey confirmed the frequency of burning feet amongst FEPOWs and was unusual in that the neurological examination and conditions endured were documented in captivity. A paucity of physical signs was noted, and a suggestion that burning feet could be precipitated by intercurrent infection. Conclusions: Burning feet syndrome can be regarding as an antique medical condition as chronic malnutrition becomes less common. This hidden study carried out during captivity provides remarkable new insight into the disease which is now essentially unknown to modern practitioners.
Keywords: Burning feet syndrome, diabetic neuropathy, far east prisoners of war, nutritional neuropathy
|How to cite this article:
Welch E, Peach N, Parkes M, Gill GV. Burning feet syndrome: An old tropical syndrome revisited. Ann Trop Med Public Health 2013;6:65-70
|How to cite this URL:
Welch E, Peach N, Parkes M, Gill GV. Burning feet syndrome: An old tropical syndrome revisited. Ann Trop Med Public Health [serial online] 2013 [cited 2016 Aug 15];6:65-70. Available from: https://www.atmph.org/text.asp?2013/6/1/65/115206
Burning feet syndrome (BFS) has been described anecdotally in the literature for over 200 years. Subjectively described by patients as burning, prickling, and unremitting with nocturnal exacerbations  – its more modern symptomatic equivalent may be diabetes – related painful symmetrical sensory neuropathy.  The condition draws parallels with the burning dysesthesia found in diabetic peripheral neuropathy, and appears to display a similar chronicity. Despite being a common symptom, especially among the elderly, its etiology is non-specific and often marked by a lack of objective clinical signs. 
Historically, burning feet syndrome has been recorded in situations of poor nutrition.These have included malnourished African populations in the early 20 th century,  South American plantation workers in the 1920s,  and during food shortages in the Spanish Civil War.  Perhaps the best-described and largest outbreak of burning feet occurred amongst prisoners of war (POWs) of the Japanese during the second World War in south-east Asia and the Far East. ,,, In this review, we will summarise reports of the condition, in particular amongst Far East POWs (FEPOWs), using both available literature, as well as a unique and previously unknown contemporary study carried out in a POW camp.
|Far east POWs and ‘burning feet’|
In late 1941 and early 1942 about 100,000 allied troops (mainly British, Australian and Dutch) were captured by the Japanese in locations including Singapore, Hong Kong, Java, and Sumatra. During the next 3½ years, the POWs were moved to various other locations, including Japan, to work in the dockyards and factories; and Thailand and Burma to construct the notorious “Death Railway”. As well as undertaking hard physical work and exposure to tropical infections (e.g., malaria, dysentery, cholera, dengue etc), there was a universal shortage of food which was of poor quality and low in protein and vitamins.Overall, about 25% of POWs died in captivity,  and many survivors suffered persisting ill health – including post-traumatic stress disorder in about 35%,  and long-term infection with the nematode worm Strongyloides stercoralis in 15%. 
|Burning feet in captivity|
FEPOWs from all areas of incarceration frequently complained of burning feet. In some locations, these were known as “electric feet” (to describe the shooting neuropathic pains) or “happy feet” (in relation to moving and stamping around to try to relieve the pain). Shortly after release in 1945, some POW medical officers recorded their experiences of the condition ,,, in captivity. Later, BFS in FEPOWs was to be described as persisting many years after release. ,,,,,,
In 1946, Page published an account of his experiences of the condition during internment in Hong Kong and Java. His study of 2,000 cases was based on observations alone – “as there were no adequate means of studying the cases on scientific lines, no definite cause could be attributed”.  A month after this article appeared, Cruickshank produced a similar review of 500 cases he had personally observed in Changi POW camp.  Both reports described typical symptoms starting three to five months after capture, and consisting of a dull ache below the metatarsal heads, initially at night. As the condition progressed, the pain became unremitting, stabbing, and burning – often preventing sleep and eased by exercise. Thus, Churchill recorded that “it always became worse at night and in bad cases led to serious insomnia… in many camps it was usual to see these men wandering unhappily between the huts or tents at any time of the night”.  As well as burning in quality, other descriptions of the pain included shooting or stabbing, and sometimes “like toothache”. Nocturnal worsening was universal, and as well as moving the feet and walking, immersion in cold water sometimes gave partial relief. ,,
Clinical signs were variably reported. According to Cruickshank “some feet were red, some pale, some somewhat bluish, but when the feet of 50 patients with painful feet were compared with those of 50 persons without painful feet, an equal variety of hue was found in the skin of the controls”.  Hyperhidrosis and hypersensitivity were often noted, reflexes showed no consistent pattern – brisk in some, absent in others. ,
In his immediate post-war account (1945), Churchill noted that “Happy Feet” was a common condition, occurring in 27 of the 500 FEPOWs he studied on deficiency diets. Similar intractable tingling, aching or shooting pains were described, lasting for periods of between one month and two years.  Weight loss was noted in many, and limb weakness in 8 cases. In mild cases, treatment with rice polishing was sometimes effective. In 11 cases, marmite and nicotinic acid were given orally with no improvement to symptoms. In 7 patients to whom subcutaneous nicotinic acid was given-immediate resolution of symptoms was achieved. 
The etiology of BFS was universally presumed to be due to vitamin deficiency secondary to malnutrition. Diet varied between camps but was rice-based, with small amounts of vegetables and occasional meat or fish. Peach documented a diet consisting of twice daily rice pap and vegetable stew at night. The only source of protein at one of the camps were the maggots that infested the rice supplies.  Simpson linked the symptoms of burning feet and retrobulbar neuritis to long term vitamin deficiency, documenting his experience in a 1946 report in the Lancet.  Remarkably, he presented his work in 1946 to the University of Durham for a successful MD degree thesis.  In his camp of approximately 2000 men, 300 were affected with the condition. Therapeutic trials treating patients withvitamin A and thiamine were ineffective, but administration of daily ‘kachang hijau’ beans (in the Dutch East Indies known as kadjang idjoe; today widely known as mung beans)- a substance rich in vitamins B1 and B2, improved burning feet symptoms in 4-6 weeks. ,
A typical FEPOW ration was predominantly polished rice, with small amounts of vegetables, oil, sugar and salt.Tiny amounts of vegetables meat or fish were sometimes given.Though varying between POW camp, the diet was about 25% deficient in calories, and grossly short of all B vitamins. ,
|The secret burning feet survey of nowell peach|
The Liverpool School of Tropical Medicine (LSTM) has seen over 2,000 ex-Far East POWs since their release for tropical disease investigation. ,,, With declining numbers of survivors, in the last decade the LSTM has been investigating historical aspects of the FEPOW experience and related medical issues.As part of this project, a series of oral history interviews were conducted between 2007 and 2010 by an LSTM researcher (MP). One of these was with former Flight Lieutenant Nowell Peach, a medical officer with the Royal Air Force Volunteer Reserve, initially in Malaya. He later moved to Singapore and then Java, where he was taken prisoner.  Nowell Peach was interviewed on three occasions between 2007 and 2008.
During his stay in the Tandjung Priok prisoner of war camp in Java, Peach kept meticulous records of the cases of burning feet in men who presented to him between November 1942 – March 1943. This data was carefully concealed from his captors and survived to return home with him in late 1945. He immediately resumed his civilian surgical career and attained his Part 1 Fellowship of the Royal College of Surgeons in the early summer of 1946. He did not publish his “Burning Feet” study. When interviewed as part of our oral history enquiry over 64 years after compiling his study, he produced a bundle of original medical notes that he had recorded. It was extraordinary for such detailed records to have survived, given that record keeping of any kind was strictly forbidden under the Japanese regime, frequently at risk of execution. The existence of this set of records serves as a reminder of the hardships these men faced, and provides a unique new research source into the intriguing POW problem of burning feet.
Lt Peach compiled data on 54 prisoners (all male) presenting to him with burning feet, and detailed clinical information was recorded onto typed proformata [Figure 1], which were then hidden. The mean age was 28 years (range 20-47), and mean duration of symptoms 12 weeks (range 2 – 56). [Table 1] shows the neurological findings in the group of patients, as well as accompanying tropical infections. As in other reports, the pain was described as aching, burning, or shooting. All these men were on an inadequate diet, but 20 (38%) were not even on a full ration (standard Japanese procedure was that if a POW could not work, their rations were cut).
|Table 1: Neurological and other findings in 44 prisoners of war (POWs) with burning feet syndrome
Click here to view
|Figure 1: Proforma used to collect data on each prisoner of war (POW) with burning feet syndrome
Click here to view
The Peach Survey confirmed the frequency and symptomatology of burning feet amongst Far East POWs. As with other surveys, it also suggested that intercurrent infection (usually malaria or dysentery) could precipitate burning feet. ,,, The Peach study was unusual in that the patients were meticulously examined neurologically. Though broadly this confirmed a paucity of physical signs (for example, over 80% had no sensory loss), some did have abnormalities of both sensation and motor function.The difficulty is, however, that in their generally malnourished state, these signs could have been due to a background sensorimotor neuropathy of “dry” beriberi, rather than to the specific neuropathy of BFS.
|FEPOW aftermath – burning feet persistence|
Nutritional neuropathy showed remarkable persistence in former FEPOWs after repatriation despite resuming an adequate diet supplemented with vitamins, and peripheral neuropathy was found to persist in Canadian repatriates 9 years after release from Hong Kong. 
A report from Queen Mary’s Hospital, Roehampton (in south London) detailed clinical observations in a total of 4,684 FEPOWs seen between 1946 and 1968.  A total of 238 (5.1%) had persisting peripheral neuropathy, though it was not recorded what proportion of these were painful. A study from the Liverpool Tropical School published in 1980,  examined the health of 602 FEPOWs seen a mean 30 years since repatriation in 1945. There were 34 (5.6%) men with persisting syndromes of nutritional neuropathy (including peripheral sensory neuropathy, optic atrophy, nerve deafness, and spinal cord syndromes). Of these, 23 (1.7%) had “symptomatic peripheral neuropathy” – probably BFS. A larger and more detailed study from Liverpool was of 898 FEPOWs seen a mean 32 years since repatriation.  A similar proportion (5.5%) had symptomatic nutritional neuropathic syndromes, and 24 had peripheral sensory neuropathy – 11 of whom had burning feet. Thus, permanent symptoms of painful peripheral neuropathy of the burning feet type were present in 1.2% of FEPOWs. The Liverpool survey recorded individual case histories, including one of a 57-year-old man who had been interned in Rangoon. He was assessed 30 years later in Liverpool, and it was recorded that “he was regularly kept awake at night by the pain in his feet, and he would walk around the house to gain relief”. 
Interestingly, detailed neurological investigation of a small group of FEPOWs with single neurological syndromes, showed evidence of much more widespread damage to other parts of the nervous system.  This suggests that the persisting nutritional neuropathic syndromes seen in FEPOWs may not just be permanent but may be anatomically more widespread than previously appreciated.
|Burning feet through the ages|
Neurological syndromes involving a peripheral neuropathy in association with optic atrophy have been described in undernourished subjects around the world for decades [Table 2]. At the end of the nineteenth century, Strachan first reported a number of cases of “burning feet” and “dimness of sight” in Jamaica, which he initially ascribed to malaria before a nutritional deficiency was suggested. , When similar symptoms were reported in starved Canadian POWs held in Japan during the second World War, it was suggested the condition be named “Strachan’s Disease”.  This nomenclature has been debated, with an alternate suggestion of ‘Strachan and Madan disease’ since the same combination of symptoms were described by Cuban physician Domingo Madan during the Cuban War of Independence at the same time as Strachan published his work. ,
Further reports of “Footburning” were documented throughout the early twentieth century in malnourished inmates of Zomba jail in Malawi  and also in labourers on a sugar plantation in British Guiana.  Neurological symptoms, including ataxia, paraesthesiae, and burning feet were recorded in Chinese immigrants to Malaya in 1940 and attributed to a diet of polished rice.  German prisoners of war in the Middle East were recorded to suffer from “obscure neuropathy” during outbreaks of dysentery when nutrition was poor. 
|Table 2: Historical reports of burning feet syndromes associated with malnutrition similar to those experienced by far east POWs (FEPOWs)
Click here to view
More recently, an epidemic of optic neuropathy and painful sensory neuropathy occurred in Cuba, affecting over 45,000 individuals. The clinical picture was consistent with a Strachan’s syndrome which was undoubtedly related to nutritional deficiency.  A similar epidemic of undetermined aetiology, but again thought to be due to a micronutrient deficiency, affected large numbers of young adults in coastal Tanzania.  Isolated case reports of optic and peripheral neuropathy have also been published – the most recent account, in a vegan Afro-Caribbean patient with evidence of dietary deficiency. 
|Etiology of burning feet|
The exact nutrient deficiency responsible for nutritional neuropathic syndromes has been debated. Painful dysesthetic neuropathy appears distinct from the traditional peripheral parasthesia seen in cases of thiamine deficient beri-beri – which was also prevalent in POW camps, especially during outbreaks of dysentery ,,, and responded to treatment with “marmite” or local plant extracts. , “Burning feet” has been attributed to a lack of nicotinic acid, ,,, riboflavin,  pyridoxine,  and thiamine  – though it is probable that deficiency of multiple B vitamins contributes. ,,
The syndrome of painful dysesthetic neuropathy is commonly described in diabetic patients as burning, prickling, and unremitting, with frequent nocturnal exacerbations. Contact hypersensitivity or allodynia is typically described, with symptoms ranging from mild involvement in a toe, to continuous pain involving both feet or legs.  Diabetic neuropathy can present acutely in the setting of poor glycemic control or sometimes after the rapid initiation of treatment -known as “insulin neuritis”, and in such instances the outcome is generally good. , In the majority of cases, diabetic neuropathy is a chronic condition.  Thus, a 5-year follow-up study of community patients with neuropathic symptoms demonstrated that remission of symptoms can occur over time, but the majority of patients continue to experience pain, which is often inadequately treated. 
It can be seen from the description above that painful diabetic neuropathy and burning feet syndrome share much in their characteristics, symptomatology and potential persistence. Clearly, however, they have very different underlying causes.The cause of neither syndrome is absolutely certain – diabetic neuropathy may be due to both microvascular and metabolic insults. , BFS is typically nutritional in origin, probably due to multiple deficiencies of the B complex of vitamins. ,, Presumably both diseases lead to similar neuronal damage, and similar clinical symptomatology.
BFS can now be regarded as an “antique” medical condition as chronic under-nutrition becomes less common. The “lost” study of Nowell Peach, secretly recorded during imprisonment in the Far East in the early 1940s, provides a remarkable new insight into this disease, which is now essentially unknown to modern medical practitioners. Our descriptive review has also drawn attention to the clear clinical similarities between BFS and painful diabetic neuropathy – the latter being a condition very much seen today.
Dr. Peach died in January 2012 age 98. His obituary, written by Meg Parkes is available here: .
|1.||Makkar RP, Arora A, Gupta AK, Mukhopadhyay S. Burning feet syndrome.AustFam Physician 2002;31:1006-9.|
|2.||Tesfaye S, Malik R, Harris N, Jakubowski JJ, Mody C, Rennie IG, et al. Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis). Diabetologia 1996;39:329-35.
|3.||Stannus HS. Pellagra in Nysaland.Trans RSoc Trop Med Hyg 1911;5:112-9.|
|4.||Sharples LR. The condition of “burning feet” or “foot burning” in labourers on sugar plantations in the Corentyne District of British Guiana. J Trop Med Hyg 1929;32:258-360.|
|5.||Peraita M. Deficiency Neuropathies in Madrid during the Civil War.Br MedJ 1946;2:784.|
|6.||Page JA. Painful feet syndrome among prisoners of war in the Far East.Brit Med J 1946;2:260-2.
|7.||Cruickshank EK. Painful feet in prisoners of war in the Far East – review of 500 cases. Lancet 1946;2:368-72.|
|8.||Churchill MH. Dietary deficiency diseases among prisoners of war. J R Army Med Corps 1945;85:294-8.
|9.||Simpson J. Burning feet in British prisoners of war in the Far East. Lancet 1946;1:959-61.
|10.||Kinvig C. River Kwai Railway.The story of the Burma-Siam railroad.London: Brassey’s; 1998.|
|11.||Robson D, Welch E, Beeching NJ, Gill GV. Consequences of captivity: Health effects of far East imprisonment in World War II. Q J Med 2009;102:87-96.|
|12.||Gill GV, Welch E, Bailey JW, Bell DR, Beeching NJ. Chronic strongyloidesstercoralis infection in former British Far East Prisoners of War.Q J Med 2004;98:789-95.|
|13.||Gill GV, Bell DR. Persisting nutritional neuropathy amongst former war prisoners. J Neurol Neurosurg Psychiatry 1982;45:861-5.|
|14.||Gill GV, Bell DR. Persisting tropical diseases amongst former prisoners of war of the Japanese. Practitioner 1980;224:801-3.|
|15.||Gill GV, Bell DR. The health of former prisoners of war of the Japanese. Practitioner 1981;225:531-8.|
|16.||Fisher M. Residual neuropathological changes in Canadians held prisoner of war by the Japanese. Can Serv Med J 1955;11:157-99.|
|17.||Adamson JD, Judge CM. Residual disability in Hong Kong prisoners of war. Can Serv Med J 1956;12:837-50.|
|18.||Venables GS, Welch JL, Gill GV. Clinical and subclinical nutritional neurological damage in former war prisoners of the Japanese.Trans R Soc Trop Med Hyg 1985;79:412-4.|
|19.||Peach N. Java 1942-5: Extracts from the diary of a medical officer. Br Med J 1990;301:1469-71.|
|20.||Simpson J. A syndrome of painful feet and retrobulbar neuritis occurring amongst British Prisoners of War in the Far East. MD Thesis, UK: University of Durham; 1946.|
|21.||Walters JH, Caplan JP, Hayward EW. A FEPOW Survey. Report to the DHSS from Queen Mary’s Hospital, UK: Roehampton; 1971.|
|22.||Grierson J. On the burning feet of natives. Trans Med Phys Soc Calcutta 1826;2:275-80.|
|23.||Strachan H. Malarial multiple peripheralneuritis. Sajous Ann Universal Mad Sci 1888;1:139-51.|
|24.||Strachan H. On a form of multiple neuritis prevalent in the West Indies. Practitioner 1897;59:477-84.|
|25.||Madan D. Notas sobre una forma sensitiva de neuritis periferica. Ambliopia por neuritis optica retrobulbar.Cron Med Quir Habana 1898;24:81-6.|
|26.||Santos Fernandez J. Ambliopia por neuritis periferica debido a autointoxicacion de origen intestinal por alimentacion defectuosa. Cron Med Quir Habana 1900;26:330-4.|
|27.||Pallister RA. Ataxic paraplegia occurring amongst Chinese in Malaya.Trans RSoc Trop Med Hyg 1940;34:203-11.|
|28.||Spillane JD, Scott GI. Obscure neuropathy in the Middle East. Lancet 1945;2:261-4.|
|29.||Gopalan C.The burning feet syndrome. Ind Med Gaz 1946;81:22-6.|
|30.||Thomas PK, Plant GT, Baxter P, Bates C, Santiago LR. An epidemic of optic neuropathy and painful sensory neuropathy in Cuba: Clinical aspects. J Neurol 1995;242:629-38.|
|31.||Huertas R, Del Cura MI. Deficiency neuropathy in wartime: The “Paraesthetic-Causalgic syndrome” descried by Manuel Peraita during the Spanish civil war. J Hist Neurosci 2010;19:173-81.|
|32.||Plant GT, Mtanda AT, Arden GB, Johnson GJ. An epidemic of optic neuropathy in Tanzania: characterization of the visual disorder and associated peripheral neuropathy. J Neurol Sci 1997;145:127-40.|
|33.||Nightingale LM, Paviour DC. Nutritional optic and peripheral neuropathy: A case report. Cases J 2009;2:7762.|
|34.||Dunlop EE. Medical experiences in Japanese captivity.Br Med J 1946;2:481-6.|
|35.||Pavillard SS. Bamboo doctor. London: Macmillan and Co Ltd; 1960.|
|36.||Crawford JN, Reid JA. Nutritional disease affecting Canadian troops held prisoner of war by the Japanese. Can J Res 1947;25:53-85.|
|37.||Lai CS, Ransome GA. Burning feet syndrome. Case due to malabsorption and responding to riboflavin. Br Med J 1970;702:151-2.|
|38.||Vilter RW, Mueller JF, Glazer HS, Jarrold T, Abraham J, Thompson C. The effect of vitamin B6 deficiency induced by desoxypyridoxine in human beings. J Lab Clin Med 1953;42:335-57.|
|39.||Bozzeti F. Long term parenteral nutrition. Br Med J 1979;1:487-8.|
|40.||Cockerell OC, Ormerod IE. Strachan’s syndrome: Variation on a theme. J Neurol 1993;240:315-8.|
|41.||Tesfaye S, Kemplar P. Painful diabetic neuropathy. Diabetologia 2005;48:805-7.|
|42.||Krentz AJ. Acute symptomatic diabetic neuropathy associated with normalization of haemoglobin A1.J RSoc Med 1989;82:767-8.|
|43.||Daousi C, Benbow SJ, Woodward A, MacFarlane IA. The natural history of chronicpainful peripheral neuropathy in a community diabetes population.Diabet Med 2006;23:1021-4.|
East Cumbria GP Training Programme, Cumberland Infirmary, Port Road, Carlisle, CA2 7HY
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2]