Journal of Neurology, Neurosurgery, and Psychiatry 1984;47:564-566

Short report

Slimmer's paralysis peroneal neuropathy duringweight reductionKA SOTANIEMI

From the Department ofNeurology, University of Oulu, Oulu, Finland

SUMMARY Ten patients developed peripheral neuropathy while on a reducing diet. One of thepatients sustained a severe polyneuropathy attributable to thiamine deficiency. Nine developedunilateral peroneal paralysis. Electromyography revealed bilateral abnormalities in three of thesepatients. The neuropathy could not be attributed to any factor other than weight reduction. Incontrast to previous reports suggesting a compressive aetiology, the present observations indicatethat metabolic disturbances are the cause of the disorder.

Weight reducing diets introduced and practised formedical requirements, as well as for the timelytrends of high-fashion and body-building, havebecome very popular in recent years. Both pro-longed total starvation' and supplemented fasting,2in which a protein supplement is employed, havebeen prescribed as a treatment of obesity. In addi-tion, people construct dietary regimens by them-selves and may even follow extremely radical reduc-ing diets without medical surveillance. Althoughsupplemented fasting is now recognised as an effec-tive means of achieving substantial weight loss safelywith a minimum of patient discomfort,2 slimmingprocedures may also cause several problems, includ-ing complaints such as headache, nausea, dizziness,fatigability and muscle cramps,23 and a number ofmetabolic disturbances.34 Unfortunately, weightreduction also is occasionally followed by neurologi-cal complications,5-8 which may sometimes mar anotherwise successful outcome of therapeutic orcosmetic slimming. In particular, rapid and self-planned weight reduction may be disastrous.9 Wedraw attention to the features associated with theoccasional neurological consequences of dieting.This report presents ten cases, nine of whomdeveloped peroneal paralysis and one sustained asevere generalized polyneuropathy during a self-planned weight reducing diet.

Address for reprint requests: Dr KA Sotaniemi, MD, Dept ofNeurology, University of Oulu, Oulu, Finland.Received 1 January 1982 and in final revised form 20 January 1984

Case reports

The cases are presented in the table. All the patientsunderwent thorough clinical neurological examinations,radiology of the spine and of the lower extremities, andextensive laboratory investigations to exclude knowncauses of peripheral neuropathy and local or systemic dis-eases. The laboratory investigations (erythrocyte sedimen-tation rate, blood cell count, glucose tolerance test, liverenzymes, thyroid hormone, uric acid, electrolytes, serumtotal proteins, serum albumin, serum creatine, urinalysis,B, vitamin, serum folate, collagen disease screening per-formed in all the cases and cerebrospinal fluid analysis per-formed in most of them) were normal. No other abnor-malities except those given in the table were encountered.None of the patients showed muco-cutaneous signsattributable to nutritional deficiency. All the patients hadbeen neurologically asymptomatic before the onset of theirsymptoms. None of them had taken any medication forseveral months prior to the weight reduction period andnone used slimming pills. Two patients (Cases 1 and 2) hadused multivitamins during the diet. Only one of the slim-mers (Case 1) increased his physical activities, starting jog-ging and weight-lifting while dieting. None reported exces-sive use of alcohol prior to the weight reduction period,and during the period alcohol was particularly avoidedbecause of its supposed appetising effect.The slimming regimen was self-planned in all of the

cases, not being under doctor s surveillance. The diets werecomposed either of vegetables alone or of a reducedamount of usual food with as little fat and carbohydrate aspossible. Case 4 had an extreme diet: she took only onefruit (apple, tomato, orange etc.) a day. This strict diet wasfollowed by thiamine deficiency resulting inpolyneuropathy which made the patient bed-ridden fortwo weeks and caused marked disability for half a year.

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Slimmer's paralysis-peroneal neuropathy during weight reduction

Table Details of cases

Case Previous Weight reduction Neurological Recoveryidentification weight findingsM = man kg Weight lost by Months of Daily MultivitaminF = woman the time when dieting before diet substituton

complications the appearance useappeared of neurological

symptoms

1. M, 28 years 86 16 3 vegetables yes R peroneal paralysis complete, afteronly 6 months

2. M, 35 years 96 14 2,5 vegetables yes R peroneal paralysis essential in 4 months,only slight resid. symptoms

3. M, 50 years 104 20 3 fat-free meat, L peroneal paralysis complete in 2 monthsone piece ofbread

4. F, 16 years 104 44 4 one small no severe generalised disabled for 6 months,fruit polyneuropathy permanent peroneal

weakness5. M, 34 years 95 17 3 reduced no R peroneal paralysis complete in 2 months

amount ofusual food

6. M, 32 years 101 25 4 reduced no R peroneal paralysis complete in 3 monthsamount ofusual food

7. M, 39 years 92 16 4 reduced no R peroneal paralysis persistent peronealamount of weaknessusual food

8. F, 18 years 54 10 2 tea and fruitsno L peroneal paralysis complete in 3 monthsonly

9. F, 32 years 74 12 3 vegetables, no R peroneal paralysis persistent peronealfruits weakness

10. M, 48 years 86 16 4 reduced no L peroneal paralysis complete in 3 monthsamount ofusual food

Her serum thiamine concentration was 0-006 ±g/ml (nor-mal values over 0-01 ,ug/ml). This case has been describedin detail earlier.9

Peroneal paralysis developed gradually over a few daysin all the cases. Two patients (Cases 3 and 7) had onlymotor signs while the others also showed sensory peronealabnormalities.

Routine electroneuromyography (ENMG) showed signsof denervation in the muscles innervated by the clinicallyaffected peroneal nerve but, in addition, three patients dis-played denervation activity also on the clinically asymp-tomatic side. In Case 4, the ENMG revealedpolyneuropathy due to axonal degeneration, peronealabnormalities being the most severe. Two years after theacute phase there was still marked peroneal neuropathybut no other ENMG findings were present.The mean motor conduction velocity of the clinically

affected peroneal nerve was 46-1 m/s (range 39-5-50-8m/s), the mean distal latency was 5 0 ms (range 4-2-5-3ms). The respective values for the clinically non-affectedperoneal nerves were 51-1 m/s (range 44 5-54-0 m/s) and4-3 ms (range 3 6-5O0 ms).

Intensive physiotherapy including electrical stimulationof the peroneal nerve was prescribed as treatment in mostof the cases. No other specific therapy was practised exceptintensive vitamin B treatment in Case 4. Six patients reco-

vered completely in 2 to 6 months, the remaining ones

having slight residual peroneal weakness.

Discussion

Peroneal paralysis is known to be associated with a

number of conditions and illnesses (nerve compres-sion, alcoholism, chronic infection, thyreotoxicosis,paraneoplastic conditions, vitamin B depletion,haemorrhagic diathesis).6 10 However, these andother known causes of neuropathic manifestationscould be ruled out in the present patients (exceptCase 4). Follow-up for at least one year in all thecases has not revealed any additional or relapsingsymptoms. The ENMG also failed to revealperoneal nerve entrapment which is commonly seenin, for instance, peroneal nerve compression at thelevel of the knee. Polyneuropathy could not befound, except in Case 4, the only case with anapparent couse of neurological signs. In this patientthe complications were attributable to a verifiedthiamine deficiency due to prolonged inadequatenutrition. Although thiamine determinations werenot performed in the other patients, the nature oftheir diets made thiamine deficiency less likely.Moreover, thiamine stores built up with normal nut-rition are considered to be sufficient for severalmonths.6 However, it is noteworthy that the clinicalsigns of thiamine deficiency may be delayed in star-vation when the need of the vitamin is minimal dueto low carbohydrate intake." Signs may appearrapidly when carbohydrate is given after a period ofmalnutrition,'2 as occurred in the present Case 4which sustained polyneuropathy a few days afterturning to a high carbohydrate diet after having

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fasted for 4 months.Compressive mononeuropathy is one of the most

common causes of peroneal paralysis. It has beenemphasised that susceptibility to mechanical irrita-tion at the proximal head of the fibula increases afterthe amount of fat around the peroneal nerve hasdecreased due to weight loss.5 10'1' Habitual exces-sive leg-crossing has also been claimed- '° to favourthe development of pressure neuropathy in inactivepersons on reducing diets. In the present patients,however, this kind of involvement seemed unlikely.Although we paid particular attention to thepatients' sitting and lying postures, none of themreported any conditions supporting a compressiveaetiology. Nor could any postural or toxic occupa-tional correlates be established. Furthermore, thepatients were young (mean age 31 years), active andhealthy without any factors predisposing them toneurological manifestations. Local aetiology withmechanical nerve irritation cannot be absolutelyexcluded in the patient who increased his physicalactivities but even he did not show any localisableclinical or ENMG findings.Both the rate and the prolongation of the reduc-

ing diet seem to be involved in the occurrence ofneuropathy, since in the present as well as in thepreviously reported7 cases the signs appeared onlyafter at least two or three months' dieting. In ourpatients, the rate of weight loss exceeded 5 kg permonth and dieting lasted for at least two months.From the arguments and observations discussed

above it is concluded that peroneal paralysis appear-ing in association with weight reduction by dieting isunlikely to be attributable to mechanical causesalone, such as excessive leg-crossing or the relatedcompressive factors previously suggested. It seemsmore probable that neuropathy is due to factors ofmetabolic origin or to metabolic, mechanical or mic-rocirculatory disturbances operating alone, simul-taneously or successively. There are, indeed, anumber of reports on obesity and weight reductionwhich mention disturbances in, for example, lipo-proteins,'4 catecholamines,'5 hormonal activity'6 andelectrolytes,3 '7 and all of these disturbances couldboth be associated with and contribute to nerve dys-function. The fact that the harmful manifestationsappear first in the peroneal nerve shows the predis-posing nature of the anatomical conditions. How-ever, the elucidation of the pathogenesis requiresmore knowledge of the metabolic conditions both inobesity and in weight reduction.To conclude, the clear risk of peripheral

neuropathy should always be remembered both in

Sotaniemi

therapeutic fasting and when counselling about aslimming regimen. Special care should be takenwhen the weight loss exceeds 5 kg a month and isprolonged over several months. Furthermore, slim-ming persons known to have conditions predispos-ing them to neurological disturbances should bekept in particular surveillance. And finally, it isworth noting that the use of multivitamins is notnecessarily effective in preventing slimmer' speroneal paralysis.

References

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2 Vertes V, Genuth SM, Hazelton IM. Supplemented fast-ing as a large-scale outpatient program. JAMA1977;238:2151-3.

Lawlor T, Wells DG. Metabolic hazards of fasting. Am JClin Nutr 1969;22:1142-9.

Editorial. Fasting and obesity. Lancet 1977;i:673.Sprofkin BE. Peroneal paralysis-a hazard of weight

reduction. Arch Int Med 1958;102:82-7.6 Victor M. Polyneuropathy due to nutritional deficiency

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Sherman DG, Easton JD. Dieting and peroneal nervepalsy. JAMA 1977;238:230-1.

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'° Marwak V. Compression of the lateral popliteal (com-mon peroneal) nerve. Lancet 1964;2: 1367-9.

"Farmer TW. Vitamin B, deficiency. In: Vinken PJ,Bruyn GW, eds. Handbook of Clinical Neurology.Amsterdam: North Holland Publishing Company1976:49-57.

2 Sibley WA. Polyneuritis. Med Clin N Amer1972;56: 1299-319.

3 Nagler SH, Rangell L. Peroneal palsy caused by crossingthe legs. JAMA 1947;133:755-61.

4 Streja DA, Boyko E, Rabkin SW. Changes in plasmahigh-density lipoprotein cholesterol concentrationafter weight reduction in grossly obese subjects. BrMed J 1980;281:770-2.

Jung RT, Shetty PS, Barrand M, Callingham BA, JamesWPT. Role of catecholamines in hypotensive responseto dieting. Br Med J 1979;1: 12-3.

16 Kopelman PG, Pilkington TRE, White J, Jeffcoate SL.Impaired hypothalamic control of prolactin secretionin human obesity. Lancet 1979;1:747-9.

' De Luise M, Blackburn GL, Flier JS. Reduced activity ofthe red-cell sodium-patassium pump in human obes-ity. N Engl J Med 1980;303:1017-22.