July 1950 BOYD and JEPSON: Primary or Essential Hyperidrosis 37I

FINLAND, M., COLLINS, H. S., GOCKE, T. M., and WELLS,E. B. (I949), Ann. intern. Med., 31, 39.

FINLAND, M., COLLINS, H. S., and PAINE, T. F. (jun.),(1948), J. Amer. med. Ass., 138, 946.

GOCKE, T. M., COLLINS, H. S., and FINLAND, M. (1949),Arch. intern. Med., 84, 857.

GRATER, W. C., and RIDER, J. A. (I949), Tex. St. J. Med., 45,568.

HARNED, B. K., CUNNINGHAM, R. W., CLARK, M. C.,COSGROVE, R., HINE, C. H., McCAULEY, W. J.,STOKEY, E., VESSEY, R. E., YUDA, N. N., and SUBBAROW, Y. (I948), Ann. N, Y. Acad. Sci., 51, i82.

HARVEY, J. C., MIRICK, G. S., and SCHAUB, I. G. (I949),J. clin. Invest., 28, 987.

HERRELL, W. E., and HEILMAN, F. R. (I949), Proc. MayoClin., 24, I57.

KIERLAND, R. R., HERRELL, W. E., and O'LEARY, P. A.(I950), Arch. Derm. Syph., N.Y., 6I, I85.

KNEELAND, Y. '(jun.), ROSE, H. M., and GIBSON, C. D.(1I949), Amer. J. Med., 6, 41.

KNIGHT, V., RUIZ-SANCHEZ, F., RUIZ-SANCHEZ, A.,and McDERMOTT, W. (1949), Amer. J. Med., 6, 407.

LENNETTE, E. H., MEIKLEJOHN, G., and THELEN, H. M.(1948), Ann. N.Y. Acad. Sci., 51, 331.

LOGAN, M. A., METZGER, W, I., WRIGHT, L. T., PRIGOT,A., and ROBINSON, E. A. (I950), Amer. J. Surg., 79, 229.

LONG, P. H., CHANDLER, C. A., BLISS, E. A., BRYER,M. S., and SCHOENBACH, E. B. (1949), J. Amer. med. Ass.,141, 315.

LYNAS, M. A. (195o), Lancet, I, 373.McVAY, L. V., LAIRD, R. L., and SPRUNT, D. H. (1949),

Science, 109, 590.MARKS, J. A., WRIGHT, L. T., and STRAX, S. (1949), Amer.

J. Med., 7, I8o.MEIKLEJOHN, G., and SHRAGG, R. 1. (1949), 7. Amer. med.

Ass., 140, 391.NICHOLS, D. R., and NEEDHAM, G. M. (1949), Proc. Mayo

Clin., 24, 309.OLSHAKER, B., ROSS, S., RECINOS, A. (jun.), and TWIBLE,

E. (1949), New. Engl. J. Med., 241, 287.PAINE, T. F. (jun.), COLLINS, H. S., FINLAND, M. (1948),

J. Bact., 56, 489.

PRICE, C. W., RANDALL, W. A., and WELCH, H. (1948),Ann. N. Y. Acad. Sci., 5, 2Ix.

ROSE, H. M., and KNEELAND, Y. (1949), Amer. 7. Med., 7, 532.ROSS, S., SCHOENBACH, E. B., BURKE, F. G., IRYER,

M. S., RICE, E. C., and WASHINGTON, J. A. (1948),J. Amer. med. Ass., 138, 1213.

RUTENBERG, A. M., and SCHWEINBURG, F. B. (1949),New Engl. J. Med., 24i, 698.

SCHOENBACH, E. B. (I949), J7. Ahter. med. Ass., x39, 450.SCHOENBACH, E. B., and BRYER, M. S. (x949), J. Amer. med.

Ass., 139, 275.SCHOENBACH, E. B., BRYER, M. S., and LONG, P. H. (1948),

Ann. N. Y. Acad. Sci., 51, 267.SCHWACHMAN, H., CROCKER, A. C., FOLEY, G. E., and

PATTERSON, P. R. (I949), New Engl. J. Med., 241, i85.SPINK, W. W., BRAUDE, A., CASTANEDA, M. R., and

GOYTIA, R. S. (1948), J. Amer. med. Ass., 138, 1145.SPINK, W. W., and YOW, E. M. (x949), 7. Amer. med. Ass., I41,

964.STEENKEN, W., and WOLINSKY, E. (I949), Amer. Rev. Tuberc.,

59, 221.STEINBACH, M. M., DOONEIEF, A. S., and BUCHBERG,

A.S. (I949), Amer. Rev. Tuberc., 59, 624.THOMPSON, B. F. (jun.), and SPECTOR, S. (0949), J. Pediat.,

35, 546.WHITTLE, C. H. (1950), Lancet, x, 139,WILLCOX, R. R. (x949), Brit. med. Y., 2, 1076.WILLCOX, R. R., and FINDLAY, G. M. (I949), Brit. med. J.,

2, 257.WONG, S. C., and COX, H. R. (1948), Ann. N.Y. Acad. Sci.,

51, 290.WOODWARD, T. E. (I949), Ann. intern. Med., 31, 53.WOODWARD, T. E., RABY, W. T., EPPES, W., HOLBROOK,

W. A., and HIGHTOWER, J. A. (1949), J. Amer. med. Ass.,139, 830.

WRIGHT, L. T., METZGER, W. I., SHAPERO, E. B., CARTER,S. J., SCHREIBER, H., and PARKER, J. W. (1949), Amer.J. Surg., 78, 5.

WRIGHT, L. T., SANDERS, M., LOGAN, M. A., PRIGO'TA., and HILL, L. M. (1948), 7. Amer. med. Ass., 138, 408

PRIMARY OR ESSENTIAL HYPERIDROSISBy PROFESSOR A. M. BOYD, F.R.C.S., and R. P. JEPSON, F.R.C.S.

The Professorial Department of Surgery, The Royal Infirmary, Manchester

Primary hyperidrosis may be defined as excessivesweating of unknown aetiology. It is a diagnosisof exclusion for although this condition has manycharacteristic features and can usually be diag-nosed from the history alone, secondary andthermoregulatory sweating must first be eliminated.Thermoregulatory sweating occurs mainly on thebody and is a physiological mechanism designed tomaintain the body temperature within a narrowrange. Its features are so distinctive that there areno difficulties in diagnosis. Secondary hyperi-drosis is a symptom of a local or general cause.Thus it may follow, for example, central nervoussystem disease, an irritative peripheral nerve lesion,toxic states or even a glomus tumour. It is un-usual for it to have the strictly symmetrical dis-tribution of primary hyperidrosis, and the presence

of a causative lesion establishes the diagnosis(Wright, I948).The following is a typical case of primary

hyperidrosis:Patient A.H., male, aged I9 years. Occupation:Hotel trainee.The patient developed normally until the age of

eight when he began to sweat excessively on thepalms and soles of the feet. The dorsum of thehands and feet, face and body continued to sweatnormally. The axillae were affected by thehyperidrosis but to a much milder degree. Thesweating was not affected by climatic conditions,and was as excessive in winter as in summer. Thehyperidrosis was precipitated by varying stimuli,but particularly writing and driving a car. Em-barrassment and strange company acted to a less

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from

372 POSTGRADUATE MEDICAL JOURNAL Jldy 195o

.....

*·. ·.0.::/ : : i i

* :' 4 q 3-: i! X ·.f ..... -

*': .'; Kay· ··':. ·l:::.: 3··~8 i;

.···i:..r

FIG. I.

\,4.\ he

>l 0~

FIG. Ia. FIG. Ib.

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from

July 1950 BOYD and JEPSON: Primary or Essential Hyperidrosis 373

TABLE I

Length of Raynaud'sName Sex Age Site History Associated Factors Phenomenon

H.B. F. 47 Hemi-facial I year SinusitisR.A. M. 23 Hands I8 years Neurotic traitsR.D. F. 19 Hands and feet 5 years Neurotic traitsE.D. M. 25 Feet x8 yearsJ.M. M. 26 Hands 4years + mildS.W. M. 38 Hands and feet 12 years Neurotic traits (son also de-

veloped hyperidrosis)P.M. M. 20 Hands o years Neurotic traitsN.J. M. 27 Feet 3 yearsF.B. M. 48 Feet and hands 20 years + mildA.H. M. I9 Hands, axilla and feet i x years Neurotic traitsT.T. M. i9 Hands 5 years Gustatory sweating AcrocyanosisB.N. M. 20 Hands and feet From birthF.L. M. 38 Hands and feet From birth - Mild acrocyanosisB.W. M. 22 Hands and feet From birthF.B. F. Io Hands From birth

extent. Food and drink had no effect and the ex-tremities were always dry on first awakening in themorning. The bursts of hyperidrosis usuallylasted for minutes or hours and were unaccom-panied by any vasomotor phenomena. His handswere normally warm and there was no history ofRaynaud's phenomena or pain in the arm. Hisgeneral health had always been excellent. Thedegree of sweating was quite surprising. Thehands literally dripped with sweat (Fig. I) andhis shoes had to be emptied at intervals. It be-came impossible to write a letter or do any finepen work such as ledger keeping. Socks andshoes were quickly rotted. Psychologically, he wasa well-balanced individual. Social life and per-sonal contact which was necessary in his occupa-tion were made difficult by the hyperidrosis. Nolocal or general abnormality was found on ex-amination, except for the sweating already referredto. Sympathectomy completely relieved the ex-cessive hand sweating.Clinical PictureThe sweating in patients with primary hyperi-

drosis is typically symmetrical and 'emotional'or 'mental' in distribution. The palms areusually most affected whilst the axillae, feet andface are involved to a lesser degree (Figs. Ia, Ib).Occasionally only one part, for example the feet,sweats excessively, but more often all are involvedwith one area predominating.On awakening in the morning the affected area

is always dry. Early after rising it becomes per-sistently moist, with attacks lasting for minutes orhours, in which the involved skin literally runswith perspiration. These characteristic bursts ofexcessive sweating are frequently fired off by ex-

citement, embarrassment or by a physical act de-manding mental concentration, such as driving acar or writing. Often, however, the patient statesthat the attacks begin and end for no apparentreason, being equally severe in winter as insummer. Exercise alone rarely causes anythingbeyond normal thermoregulatory sweating. Itmay be impossible for the patient to write'morethan a line of a letter before the paper becomessoaked with perspiration. This is a serious educa-tional and economic handicap to school children,students or clerks who are compelled to write pro-tected by several sheets of blotting paper. Other-wise the patient is perfectly healthy. AssociatedRaynaud's phenomena or a mild acrocyanosis arenot uncommon but probably the incidence is notgreater than on the population as a whole. Theclammy cold extremities so common in patientswith acrocyanosis or hypersympathotonia (Vealand Shadid, 1949), where evaporation is minimal,are entirely different in the degree of perspiration,and they never show the explosive bursts of sweat-ing so characteristic of primary hyperidrosig.

Sixteen patients with severe primary hyperi-drosis have been operated upon in the last threeyears on the Professorial Surgical Unit of theManchester Royal Infirmary. Their case historiesare briefly summarized in Table I. Certain factsare striking. If one atypical case with unilateralfacial sweating is excluded, the onset of the hyperi-drosis was always before the age of 24 years, themajority occurring at birth or in young adult life.Three patients were females, 13 males. The pre-ponderance of males is in general agreement withpreviously published figures. In only one casecould a family history be obtained (S.W.). Thispatient's son, aged IS, had suffered from palmar

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from

374 POSTGRADUATE MEDICAL JOURNAL July 1950

hyperidrosis since birth. None of S.W.'s otherfive children were affected.

It is important to know something of thenatural history of primary hyperidrosis, for if it isa remitting disease, temporization alone wouldlead to cure. Unfortunately, as far as one can tell,once established the condition remains or pro-gresses. No case has occurred in our experience,nor has a case been discovered in the literature ofa spontaneous cure. Changes of occupation orenvironment may, however, cause a temporary re-mission of the severer symptoms. This mayoccur most unexpectedly, as in case E.P., who ex-perienced far less trouble with hyperidrosis duringhis war-time Army service in the tropics. Thecondition retrogressed, however, to its previousseverity on the patient's return to civilian life.The psychological make-up of the patients in

these cases was investigated with care. Althoughsome were perfectly well adjusted people, manyshowed neurotic traits. It is doubtful, however,if the hyperidrosis was caused or aggravated bythe neurosis. It seems more likely that the un-pleasant features of the hyperidrosis had causedthe patient to withdraw from social activities andbecome introspective. The sweating had withoutdoubt magnified, if it had not initiated many ofthe neurotic traits seen amongst this group.

AetiologyBy definition, a patient with primary hyperi-

drosis is one in whom no local or general cause forthe condition can be found. Nevertheless, manysuggestions as to its causation have been made.Histology (Adson, Craig and Brown, i935) hasfailed to show either numerical or structuraldifferences from the normal sweat pattern. It isalso known (Gurney and Bunnell, 1942) that'biopsy of the skin in regions to which thesympathetic nerves have been severed failed toshow any alteration from the appearance of theglands in normal regions to which the sympatheticnerve supply was intact.' A sympathectomy will,nevertheless, permanently cure the primary hyperi-drosis, in contrast to the great tendency to relapsein Raynaud's phenomenon where the importantlesion is the 'local fault.' The histological ex-amination of the sympathetic ganglia and chainsremoved in our patients have not shown anyabnormality. Wertheimer and Barrie (I947)claim, however, to have found abnormal collagensclerosis and degeneration in excised ganglionictissue. Their histological examination followedprevious novocaine injections and this may havecontributed to the final histological picture.Leslie-Roberts (1934) suggested that the hyperi-drosis was due to the 'abnormal function of

dermal mesenchymal cells.' This has never beenconfirmed.

In summary, there is no evidence of a 'localanatomical fault' in either swest glands or sym-pathetic nervous system in patients with primaryhyperidrosis.

It is theoretically possible that the sweat glandsof the hyperidrotic areas are abnormally sensitiveto locally released chemicals of the acetyl-cholinegroup. Several of our patients were tested beforeand after operation with pilocarpine, mecholyl andfurmethide. They responded just as normal peopleboth in intensity and distribution of sweating.

It is well known that sweat dysfunction canfollow a wide range of organic central nervoussystem disorders, such as encephalitis, hypo-thalamic lesions or spinal cord irritation. Telford(I942) has described two cases cured by removal ofa cervical rib. No neurological lesion was demon-strated in our cases nor has it developed in othercases followed up for longer periods (Haxton,1948). Neverthless, although there is no evidenceof organic nervous disease, 'there is much tosuggest that the abnormal sweating is due to acentral out-flow possibly from the hypothalamicregion. During times of central suppression, suchas in sleep or under pentothal narcosis, the sweat-ing is in abeyance. Patients state that their handsare always dry on awakening in the morning. Inone case pentothal was administered duiing asevere bout of hyperidrosis. This caused anabrupt cessation of sweating. Conversely, stimuliwhich invoke mental tenseness or stress cause ex-cessive perspiration. Sanctorius (I720) wrote ' abody which is at rest while the mind is intenselyagitated has a stronger perspiration and less weightthan a body that is strongly moved whilst the mindis at rest.' It has been suggeste'd that primaryhyperidrosis is a true psychomatic disorder where amental or emotional conflict is translated into aphysical defect. Against this is the very earlyonset of some cases. Three patients could notremember when they were free from hyperidrosis,and in none of our cases could the onset of sweatingbe attributed by the patient to any one psycho-logical experience. It is also claimed (Adson,Craig and Brown, I935) that such symptoms asabnormal fatigue, vasomotor instability and gastro-intestinal functional disorders are commonly as-sociated with hyperidrosis. We have not foundthis to be so, although it is evident that anyneurotic tendencies will be exaggerated by a com-plaint which renders normal social and professionallife intolerable.

Complications of HyperidrosisThe psychological stress under which the patient

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from

July 1950 BOYD and JEPSON: Primary or Essential Hyperidrosis 375

FIG. 2.

labours has already been mentioned. In addition,local complications may arise in the hyperidroticareas. Interdigital and plantar infections areespecially common in the feet. These are oftenfungoid in origin, with a secondary pyogenicbacterial infection, leading to recurrent lym-phangitis' and cellulitis. Most of our cases havebeen referred for sympathectomy by derma-tologists, because the sweating has resisted alllocal measures. Rashes, vesicle formation anddyshydroses are common on the hands. The feetbecome particularly tender, soft and macerated inthe hot weather and through pain or bleeding, maygreatly limit the patient's walking. Axillary sweat-ing is often malodorous. Socks and shoes arequickly rotted by the sweating and renewals maybe an economical imposition in the lower incomegroups.

TreatmentIn the treatment of patients with severe hyperi-

drosis, measures designed to damage the sweatglands, such as radiation, formalin or alum ap-plications, do not cure, rarely alleviate and oftencause considerable damage to the skin. Occasionalcases have been reported cured by novocaine in-filtration of the sympathetic chain (Mandl, I947)or peri-arterial stripping (LeClerc and Berger,1947). These are theoretically uncertain methodsfor permahent relief and we have no experience intheir use.

For hand sweating the second and third thoracicganglia and intervening chain should be resected.

This dries the hand, the arm and the axilla (Fig. 2),and because the stellate ganglion is spared, avoidsthe unsightly and sometimes troublesome com-plications of a Homer's syndrome. The an-terior supra-clavicular approach to the chain(Telford, I942) is most satisfactory. It gives afine cosmetic result and is not so traumatic as theposterior rib-resection exposure which is so oftenfollowed by a good deal of aching and an uglyscar. Both sides may be done at the same opera-tion and the patient discharged from hospitalwithin five days. If facial sweating is present thenthe stellate ganglion must be excised, preferablytogether with the second and third thoracicganglia.

For the lower limb 2 in. of lumbar chain to-gether with two lumbar ganglia should be ex-cised opposite the third lumbar vertebra, throughan extra-peritoneal loin incision. This completelydries the troublesome foot sweating and a varyingarea on the remainder of the leg (Fig. 2), Bothsides may be completed at the same operation;the convalescence is characteristically uneventfuland the patient is discharged on the eighth post-operative day. The highest lumbar ganglion lyingbeneath the crus of the diaphragm is not resectedas its fibres probably only supply the upper thigh.Bilateral removal of the highest lumbar ganglionhas also been condemned because of its possibleeffect on ejaculation in the male. A review ofmany other cases in which the highest lumbarganglion has been resected on both sides does notsupport this view (Rose). If operation is contra-

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from

376 POSTGRADUATE MEDICAL JOURNAL July i950

indicated or refused, paravertebral blocks of thestellate ganglion or the lumbar chain with alcohol(White, i940) or phenol (Haxton, 1948) can beused. These, however, may lead to undesirableside effects such as a persistent neuritis and areprobably better avoided.

ResultsAll the patients in this series have been treated

by sympathectomy. None have recurred althoughthe longest follow-up is three years. Haxton(x948) reporting on Telford's cases has shown thecure to be permanent up to xI years or more post-operatively. No report has been found in theliterature of relapse of hyperidrosis followingadequate sympathectomy. In addition, any as-sociated Raynaud's phenomena or acrocyanosis isimproved by the sympathectomy, especially in thefeet. After some months or years, a very lightmoisture may return on the hands but this is never

troublesome. There are, however, some minorcomplications which follow sympathectomy. Theexcessively dry skin of the hands may crack andbreak. This may be relieved by regular lanolineor Nivea Cream inunctions. Women especiallycomplain that the dry finger-skin catches instockings and that the fingers are too dry to handlesmooth objects such as playing cards. When bothcervical and lumbar sympathectomies have beenperformed, compensatory sweating on the bodymay distress the patient. This is an aggravation ofnormal thermoregulatory sweating being invokedby heat or exercise. Probably these patients shouldavoid warmer climates. Peri-lesionary sweating(Guttman, I947) on the fringe of the sym-pathectomized area may occur, though rarelysufficiently to worry the patient. The gustatorysweating which may follow an upper limb sym-pathectomy (Haxton, 1948) was not seen in thisseries of patient.

BIBLIOGRAPHY

ADSON, A. W., CRAIG, W. McK., BROWN, G. E. (I935),Arch. Surg. Chicago, 3I, 794.

GURNEY, R., BUNNELL, I. L. (1942), J. Cli,. Investigation,21, 269.

GUTTMAN, L. (I947), Postgrad. Med. J., 23, 353.HAXTON, H. A. (I948), Brit. Med, J., 1, 636.HAXTON, H. A. (I948), Brain, 71, x6.LECLERC, F. P., and BERGER (1947), Mimoires de L'Acadimid

de Chirurgie, 73, 05o.LESLIE-ROBERTS, H. (I934), Brit. 7. Derr. Syph., 46, Ia6.

MANDL, F. (I947), 'Paravertebral Block,' W. Heinemann Ltd.,Lonon, pp. 297.

ROSE, 'S SS. Personal Communication.SANCTORIUS (1720), 'Midicina Statica Edz.,' trans. John

Quinsy, London, W. & J. Newton, 344.TELFORD, E. D. (i942), Brit. Med. ., 2, 96.VEAL, J. R., SHADID, J. N. (x949), Surgery, 26, 89.WERTHEIMER, P., BARRIE, J. (x947), Asta Anatomica, 4, 288.WHITE, J. C. (I940), Surg. Gync. Obstet., ?1, 334.WRIGHT, A. D. (1948), 'British Surgical Practice,' Butterworth

& Co., London, 5, 6z.

copyright. on M

arch 25, 2022 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.26.297.371 on 1 July 1950. D

ownloaded from