MIGRAINE: A 1950 SYMPOSIUM · MIGRAINE: A 1950 SYMPOSIUM By N. N. IOVETZ-TERESHCHENKO, F.R.C.S. Definition The disease, also called megrim consists of re- curring attacks of severe

MIGRAINE: A 1950 SYMPOSIUMBy N. N. IOVETZ-TERESHCHENKO, F.R.C.S.

DefinitionThe disease, also called megrim consists of re-

curring attacks of severe headache, usually uni-lateral (hence the synonym hemicrania), sometimespreceded by certain abnormal sensations, mostcommonly disorders of vision, and often associatedwith nausea and vomiting (hence the synonymssick headache and bilious headache).

IncidenceIt is estimated to occur in 8 to I2 per cent. of

all patients seen in general practice (Grimes, I93 I).In the United States 2 to 4 per cent. of the totalpopulation suffer from migraine (Moench, 1947).Two factors are to be considered:

i. Sex. It is more frequent in women than inmen in a ratio of four to one according to vonStorch (I947), the attacks being sometimes closelyrelated to menstruation. Pregnancy usually givescomplete relief (Alvarez, I947).

2. Age. It commonly begins in adolescence atabout the age of puberty, but often a history ofprevious ' bilious attacks' in childhood may beobtained (the so-called ' cyclical vomiting' ofchildren appears to be a condition closely allied tomigraine). More rarely the complaint develops inlater years and still more rarely in early childhoodor infancy (Sinkler, I887, refers to a case in achild aged two years). Having once appeared, theparoxysmal headaches usually persist throughoutlife, with a definite tendency to diminish in fre-quency and severity, and even to disappear, afterthe menopause in women and the age of about50 in men.

AetiologyApart from certain clinical resemblances, there

is an association between migraine and epilepsy;they sometimes both occur in the same patient and,in certain instances, epilepsy has disappeared(Wilson, I925) giving place to migrainous attacksand vice versa.

HEREDITYHeredity plays an important role in some go per

cent of cases (M6bius, I894), a family history ofthe disease being obtainable from a large propor-tion of patients. Personality is an important

factor (Wolff, 1940), the individual affected beingusually an ambitious perfectionist in a continuousstate of tension (Whitehorn, I944). The primeand most common cause appears to be a con-stitutional defect transmitted through the germplasm in accordance with Mendel's laws of in-heritance (Buchanan, I920).

PRECIPITATING FACTORSAs in the case of epilepsy, the great majority of

attacks occur without apparent cause. Manyhave been described as predispersing to andas occasional immediate causes of the attacks.

i. Mental strain is the commonest. Thisapparently explains the relative frequency ofmigraine among intellectual (as opposed tomanual) workers and ' highly strung' persons ofexcitable disposition.

2. Eye strain is an important factor, especiallywhen resulting from uncorrected errors of re-fraction, or of muscle balance, or from readingor writing for prolonged periods in a bad light orincorrect posture.

3. Vasomotor disturbances, characterized eitherby spasm of the arteries, causing the temporaryparalysis which may be associated with a mono-plegic or hemiplegic attack, or by paralysis of thevasomotor centre, with consequent capillary en-gorgement.

4. Toxaemia from disorders of digestion orintestinal function (constipation or dietetic in-discretions may initiate paroxysms) or from self-manufactured poisons (dental sepsis, sinusitis orother septic foci such as chronic cervicitis orappendicitis).

5. Allergy is probably responsible for a certainnumber of cases (Unger, I940), many of which aresensitive to some particular kind of food (Wolffand Unger, I944) and some even may be simul-taneously suffering from hay fever or asthma.

6. Hepatic dysfunction (Diamond, 1927;McClure and Huntsinger, 1928; Critchley andFerguson, I933) perhaps with sub-acute hepatitisand/or gall-bladder disease (Chiray and Triboulet,I925; Vallery-Radot and Blamoutier, I927;Friedlander and Petow, I927; Lyon, 1929; Haugand Wohrmann, 1930; Hunt, 1933) is suggested inmany patients (see also Morlock and Alvarez, I940).

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7. A neurotic manifestation may be the explana-tion, as in the case where trauma, often not verysevere, is blamed several years after the event forpersistent paroxysmal headaches which beganafter the accident.

8. Reflexes from pathological conditions in thenose or genital organs have been considered bysome as a cause (this may be brought into linewith the paragraphs on toxaemia and hepaticdysfunction above).

9. Finally, the presence of a gross anatomicaldefect causing stenosis of the interventricularforamen of Monro and associated with chronichyperaemia of the choroid plexus, is the view heldby Spitzer (I9OI) and nobody else.

PathologyNo macroscopic anatomical changes have been

found to account for the disease, except in theexceedingly rare cases having a congenital stenosisof the foramen of Monro.The association of visual disturbances, slowing

of the pulse rate, headache, vomiting and (some-times) cramps or spasms in the cranial and cervicalmuscles of the affected side, with temporaryaphasia and/or hemiplegia, suggests three possibleexplanations:

i. A mechanical obstruction to the outflowof the cerebrospinal fluid from the ventricles,producing for the time being an internal hydro-cephalus.

2. A transient paralysis of the vasomotor centrewith consequent capillary engorgement andoedema of the brain.

3. A spasm of the arteries supplying variousparts of the central nervous system, causing apartial and temporary ischaemia of the part inquestion.The aura is apparently due to vasoconstriction

of the branches of the internal carotid artery, withconsequent anoxia, especially of the occipitalcortex (Schumacher and Wolff, I941). The head-ache seems to be chiefly due to distension and in-creased amplitude of pulsation of the intracranialbranches of the external carotid artery, the wallof the affected arteries becoming rigid and oftenceasing to respond to vasoconstrictor stimuli(Torda and Wolff, I945). In addition spasmodicor sustained contraction of the cervical or scalpmuscles on the affected side results in further painand in cranial tenderness (Simons, Day, Goodelland Wolff, 1943). The pain reaches consciousnessmainly through the fifth cranial nerve (Row-botham, 1942) but also, though to a lesser degree,through the ninth and tenth cranial nerves and theupper three cervical roots (Ray and Wolff, 1940).Abnormal suprarenal function has been sup-

posed to play a part (Hellwig, 1924) and 'periodic

dilatation ' of the stomach has been observedduring severe attacks (Mangelsdorf, I903).Poussepp (I925) considers that swelling of thepituitary and its consequent compression by anabnormally small sella turcica play an importantpart in initiating an attack of migraine.

It may be mentioned here that the blood glucoseis often low at the onset, that there is sometimesan eosinophilia of 5 to 15 per cent. (Gansslen,192I) and that in severe attacks there is completecessation of gastric peristalsis as seen on radio-logical examination.

SymptomsA typical attack consists of (i) an aura; (2) the

headache; and (3) visceral disturbances (nausea,vomiting, occasionally diarrhoea). Any of thesemay occur without the others, the headache beingpractically always present and most frequentlyassociated with nausea.The attack may last from a few hours to several

days, one day being the usual duration. Dis-appearance of the headache may quickly followvomiting, or it may subside more gradually, thepatient going to bed at night with the headache toawake cured with only, perhaps, some sense ofweakness or fatigue. The attacks may recur atintervals of a few days to two or three months, aninterval of three to four weeks being most common.Their paroxysmal character may be a strikingfeature of the attacks, which may occur on thesame day every week or every month.

Migraine equivalents. A few patients havecurious abdominal attacks regarded as anequivalent of migraine (Brams, 1922; Riley, 1932;van rder Scheer, I938) and possibly allergic inorigin. Colic in children may also be reallymigraine (Soltz, Brickner, Riley and Salmon,I935; Curschman, 1939). Meniere's syndrome isbelieved (Atkinson, 1943) to be an occasional sub-stitute for migraine. ' Precordial migraine,'characterized by dull, heavy, left thoracic painwith occasional radiation into axilla or arm, hasbeen described (Fitz-Hugh, I940). A ' psychic'equivalent (moodiness, confusion, anxiety, agita-tion and general restlessness) has also beendescribed (von Storch, 1947) and can be differenti-ated from the psychomotor equivalent of epilepsyonly by a normal encephalogram taken duringsleep.

The aura. An aura is not always present; ifpresent it lasts from a few minutes to half anhour, typically taking the form of a visual dis-turbance.Most frequently there are only vague flashes of

light followed by darkness in the half-field in-volved, or a simple onset of hemianopic dimness ofvision (the part of the visual field affected varying

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from one attack to another). Commonly only ageneral dimness of vision is present. Sometimesapparitions may be seen in the shape of hallu-cinatory visions of animals such as mice, dogs,etc. Rarely a complete ' fortification spectrum'(known as teichopsia) is present: the patientnotices a blind spot in the centre of his field ofvision (usually in both eyes, rarely in one only),which soon becomes replaced by a bright spot oflight; the area of blindness enlarges in a fewminutes and if the patient turns to a dark part ofthe room he will see an irregularly circular patchof gorgeously sparkling colours; from minute tominute the circle grows larger and larger until itopens out in the form of a horseshoe, the outermargin of which consists of a multicoloured zig-zag line enclosing a central blind area apparentlyfull of movement as of a boiling fluid; the openingas a rule is to one side and away from the centreand the area of recovered vision is within the rest-less stirring blind field. In 20 to 30 minutes fromthe beginning of the manifestation, the brillianthorseshoe reaches the periphery of the visual field,every object now becoming visible, but apparentlyoscillating or quivering as iD a dreamThe visual aura may be followed or replaced by

sensory or motor premonitory signs with the samedistribution as that of a hemiplegia. These usuallybegin with tingling in the tongue and lips then inthe face and hand, the part first attacked recoveringas the next one is invaded. More rarely crampsand spasms of the muscles of the affected side andeven occasionally .paresis or paralysis (monoplegiaor hemiplegia) occur. When the right side isaffected there is usually a temporary aphasia (com-pare with Jacksonian epilepsy and Todd'sparalysis).

In some cases there may be hunger, dizziness orexcitement; more commonly there is mental con-fusion and great depression, with fear of impend-ing evil. Rarely there is an unusual sense of wellbeing.

Headache; This is almost invariably present,coming on as a rule immediately after the aura.The side first affected is generally that which isopposite to the visual spectrum. The pain com-monly starts in a localized spot and spreads indiffered directions (i.e. is expansile in character)or becomes general. The pain is often describedas penetrating, sharp and boring in character, andvaries in intensity from so slight as not to inter-fere with mental work, to so intensely severe asentirely to unfit the sufferer from any action what-soever. The pain is usually aggravated by move-ment, light or sound, and the patients are mostcomfortable in the recumbent posture. Occasion-ally the severity is such that the patient passes intoa stupor or becomes delirious.

Visceral disturbances. Nausea and vomiting arecommon, and a certain amount of relief follows,especially if the attack comes on when the stomachis full.

Other manifestations. In a small proportion ofpatients in addition to or instead of the usualnausea and vomiting there may be present tremors,vertigo, dryness of the mouth, excessive sweating,coldness of the extremities and abdominal dis-tension.

Status migrainicus. Very rarely the periodicattacks may fuse into a continuous episode, pro-longed for days, with excessive gastro-intestinalsymptoms.

Physical SignsIn the interval between the attacks no abnormal

physical signs are present except in certain veryrare cases in which there are signs of sclerosis ofthe retinal arteries on the affected side.

During an attack the pulse is usually small,feeble and slow, the hands and feet are cold, theface is pale and drawn (though in some cases,towards the end of the attack, the face flushes andsweating occurs), with sometimes marked differ-ences between the two sides. The temporal arteryon the affected side is often firm and hard and theretinal arteries may be seen to be in spasm. Insome instances there is a spasmodic action, alter-nate dilatation and contraction, of the pupil on theaffected side, a condition known as hippus.

In the comparatively rare type called ophthalmo-plegic migraine the headache is associated with atemporary paralysis of one of the oculo-motornerves, a paralysis which may in the course oftime become permanent (Riley, 1932).

DiagnosisThis is usually easy: the age of onset, the

periodicity of the attacks with intervals of com-plete freedom, the association with nausea andvomiting and, in many cases, the family historyare as a rule sufficient.Some patients may be troubled by the nausea or

vomiting more than by the headache, and ac-cordingly seek relief for these symptoms only(Alvarez, I947), but a careful clinical history willclinch the diagnosis.

DIFFERENTIAL DIAGNOSISRecurring headaches of the migraine type may

also occur in the following conditions:Cerebral tumour, which is sooner or later always

associated with papilloedema and other signs oflocal damage to the brain.

Chronic nephritis. The aura is absent and signsof renal involvement are to be found.

Infection ofnasal sinuses, which must be excluded

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clinically and radiologically in all cases withattacks of severe headache.

Toxic causes, such as uraemia, should and usuallycan be distinguished with comparative ease.

Meningo-vascular syphilis, when the Was3er-mann reaction and other appropriate tests areusually positive both in the blood and in thecerebrospinal fluid.

Cerebral arterio-sclerosis, always accompanied by.other signs of arterial disease.

Hypertension presents as a rule no specialdifficulty in diagnosis.

Temporal arteritis is often accompanied or pre-ceded by general malaise, low fever and leu-.cocytosis, while locally the skin over the painfularea is reddened and the superficial temporalartery is tender and permanently visibly thickened,tortuous and sometimes nodular; excision of the-affected segment of the temporal artery oftenrelieves the pain (Horton, Magath and Brown,1934; Cooke,- Cloake, Govan and Colbeck, 1946;Kilbourne and Wolff, 1946).

Trigeminal neuralgia is distinguished from*migraine in the trigeminal area by the presence of' trigger zones' and the occurrence of pain alongthe lips and tongue.

Histamine cephalgia (Horton, I941) is associatedwith lacrimation and congestion of the, eye, eyelidsand nose on the affected side and is not accom-panied by visceral disturbances.

Temporal, occipital and supraorbital neuralgiasmay be occasionally misdiagnosed as migraine(Harris, I937).

Aniseikonia may occasionally be mistaken for amigrainous aura (Bannon, I940).

Epilepsy may be mistakenly suspected becauseof the presence of an aura, but the momentaryduration of the epileptic aura as opposed to theseveral minutes' duration of the migrainous auraand, moreover, the absence of any disturbances ofconsciousness in migraine should be sufficient toindicate the correct diagnosis on the history alone.

PrognosisThough the condition may last a lifetime it is

not dangerous to life and tends to disappearspontaneously after the natural, but not theartificial, menopause or the age of about 50. Asfar as frequency of the attacks and their severityare concerned, these may be considerably im-proved by treatment.

TreatmentNo treatment is really specific, as can be inferred

from the number of drugs and procedures thathave been used. They may be considered underthe following headings:-

(A) PROPHYLACTICIn the period between attacks:i. Great attention must be paid to the regula-

tion of the patient's mode of life (Fothergill, 1784).The most favourable hygienic conditions, includ-ing a carefully regulated and supervised diet, pre-vention of constipation, correction of anaemia,avoidance of excitement and worry, exercise with-out exhaustion, a congenial occupation and ex-emption from excessive brain work, are oftenhelpful in reducing the frequency and severity ofthe attacks (Minot, I923; Kerppola, 1926;Schnabel, I928; Barborka, '929; Goldzieher andPopkin, 1946). In the case of allergy to foodspecial attention must be paid to the diet.

2. Errors of ocular refraction and/or musclebalance must be corrected by suitable spectacles orexercises, and in the opinion of Hurst (1924) thissuffices to cure many sufferers.

3. The most valuable drug, if taken regularlyover many months, is phenobarbitone, an adequatedose being i gr. three times a day (Soltz et al., 1935).

4. A prolonged course of bromides or of cannabisindica is sometimes effective (Carron de la Carriere,1905)-

5. In hypertensive subjects a course of nitro-glycerin may be useful (Gowers, I907).

6. Potassium thiocyanate (3 to 6 gr. daily) hasbeen effective in keeping free from migraine bothhypertensive subjects and those with a normalblood pressure (Barker, Lindberg and Wald, 1941;Engle and Evanson, I942; Hines and Eaton, 1942).

7. Intravenous injection of o.5 or i gm. ofsodium thiosulphate twice a week for 12 weeks hasbeen of benefit in a few cases.

8. When the migrainous attacks coincide withthe catamenia, administration of an oestrogen (bestgiven as stilboestrol 0.5 mgm. daily in the weekpreceding the expected date of the next period)may be given with profit.

9. When the attacks are pre-menstrual ormenstrual, testosterone propionate (30 to 150mgm.) has helped on occasions (Friedman,Brenner and Merritt, 1946).

I0. Various hormones (ovarian, placental andpituitary) have been tried, the most favourablereports suggesting that not more than 7 per cent.of all patients thus treated are improved (Brown,1929; Blakie and Hossack, I932; Egglestone andWeiss, 1932; Henriksen, 1933; Riley, Bricknerand Kurzrok, I933; Brock, O'Sullivan and Young,1934; Soltz et al., 1935; Glass, I936; Moffat,1937; Dunn, 194I; von Storch, 1941; Trow-bridge, von Storch and Moore, I942; Leyton,1944; Alvarez, 1947).

iI. Thyroid extract has been given (Moehlig,I93I)-

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I2. Bile salts by mouth have been used byHunt (I933) with success.

13. Chondroitin-sulphuric acid (4 gm. daily) hasrelieved some patients from attacks (Crandall,Roberts and Snorf, 1936; Drewyer, 1940).

I4. Reduction of fluid intake to i qt. a day isoften successful (McQuarrie, 1932; Kennedy,1946).

15. Urea (I.3 to 4. gm. a day) has relieved somepatients from attacks (Brown, 1943).

i6. In an attempt to mobilize extracellularfluid thus compensating and inhibiting fluctua-tions in the circulating blood volume, a mixture ofcalcium lactate and potassium chloride has beenused (Pfeiffer et al., 1943).

17. ' Desensitization ' with prostigmin (Pelnerand Aibel, 1942; Pelner, 1943; Patton, I946) orhistamine (Butler and Thomas, 1945; Horton andMacy, 1946) have been favourably reported on.

i8. Oral carbachol (2 mgm. three times a day)has been enthusiastically recommended by James( I945).

19. Vitamin B1, usually given as thiaminechloride (30 to 100 mgm. daily for four weeks,followed by a maintenance dose varying from 30mgm. once a week to ioo mgm. three times aweek) has been stated to have given good resultsin 65 per cent. of a large series of cases (Palmer,1945).

20. Autohaemotherapy has been tried (Durand,1921).

21. Theophylline (9 gr. daily) has been advised(Marin, 1946).

22. Benadryl has been successful on occasions(Gottlieb, 1942; Friedman, Brenner and Merritt,I946; Alvarez, 1947).

23. Oral dihydro-ergotamine (i to 2 mgm. twoor three times a day indefinitely) lessens the fre-quency and severity of the attacks and may in-hibit them altogether (Bartstra, I946; Pollock,I946; Spuehler, 1946; Chapuis, I948; Kral,1948). No side effects have been observed withthis dosage.

24. A galvanic ring, if worn constantly, mayprevent the occurrence of attacks (personalobservation), probably by subconscious auto-suggestion.

(B) SYMPTOMATICDuring an attack:

(a) General measures:-The patient should be kept absolutely quiet in

bed in a darkened room, and alkaline fluids shouldbe given freely by mouth.

Local application of cold to the head is alwayswelcome and may relieve the pain in the lesssevere cases. A tight headband (Schumacher,Ray and Wolff, I940; Sutherland and Wolff,

I940) or holding the breath for two minutes(Freeman, 1946) reduces the intensity of theheadache.

If the symptoms appear at the end of an ex-hausting day, a good meal and a glass of good winewill sometimes abort an attack provided nauseahas not set in. Strong hot coffee may give relief ifthe patient feels faint and nauseated.Sodium amytal by mouth or by injection (i to

71 gr.) is often useful in giving comfort. A rectalsuppository of nembutal (2 or 3 gr.) is a goodadjuvant treatment, especially if nausea andvomiting are troublesome. Lavage of the stomachwith water at 105° F. (40.5° C.), a brisk salinecathartic and irrigation of the colon with salinesolution are sometimes of value at the onset.

If vomiting is severe, rectal infusion of 5 percent. glucose shortens the attack and lessens thesubsequent exhaustion.

(b) Obsolescent ' specific' measures:-i. Sir Lauder Brunton (I894) recommended,

sodium salicylate 15 gr. and potassium bromide30 gr. at the onset.

2. Calcium lactate, 30 gr., if given at the veryonset may abort an attack (Bigiand, 1923; Riggs,.1926).

3. Acetyl-salicylic acid is sometimes effective indoses of 5 tO 20 gr., with or without the additionof 5 gr. of caffeine citrate, when given at the onsetand repeated in one hour (Wolff, Hardy andGoodell, 1941)-

4. An intravenous injection of ascorbic acid (o.s-to i gm.) will terminate many headaches (vonStorch, I947) including migraine.

5. Inhalation of 7 1. per minute of pure oxygenfor periods from 30 minutes to 2 hours has beenvery favourably reported on (Cobb and Fremont--Smith, I93I; O'Sullivan, 1936; Alvarez andMason, 1940; Remond, Davies and Bronk, 1946).

6. Butyt chloral-hydrate, up to 4 gr., giveneither alone or with Tinct. Gelsemii 20 minimsand/or Tinct. Cannabis indica I5 minims, may-afford relief.

7. Adrenalin (o.6 ml. of a I/IOOO solution) givensubcutaneously, may be useful if administered atthe onset but is contraindicated in the presence of'hypertension.

8. Lumbar puncture (Mingazzini, 1917), intra-venous sodium bicarbonate (Sicard, Paraf andForestier, I92I), intravenous hypertonic saline'(Villey and Buvat, I937) and intravenous glucosehave all successfully aborted attacks in a few-patients.

9. Intravenous injection of peptone has helpedsome patients (Auld, 1920; Miller and Raulston,I923; Ball, 1927; Brown, 1929).

io. Intravenous injection of 3 to 30 mgm. of

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amphetamine sulphate at the rate of i mgm. perminute has been successful in stopping a de-veloping attack in a small group of cases (Gott-lieb, 1942);.

iI. Intramuscular injection of ioo mgm. ofmethyl-iso-octenylamine hydrochloride (repeated intwo hours if necessary) is said to have terminatedattacks in occasional patients (Palmer, 1945;Friedmann, Brenner and Merritt, I946; MacNealand Davis, 1947).

I2. Even insulin shock has been advised (Tillim,I944) to stop severe attacks.

(c) Recent ' specific' measures:-i. A large dose of nicotinic acid (ioo to zoo

mgm. intravenously) benefits patients in whomarterial spasms occur during the attack (Enrique,I943; Atkinson, i944; Goldzieher and Po pkin,1946).

2. Ergotamine tartrate by mouth (or better dis-solved under the tongue) in doses of 2 mgm.(repeated hourly if necessary up to a total of iomgm.) is often effective, particularly if given earlyin the attack; it may cause vomiting (preventedby atropine sulphate I/IOO gr.) and should beused with cautionf in vascular diseases. It may begiven also by subcutaneous or intramuscular in-jection in doses of 0.25 to 0.5 mgm. every 2 or 3hours till the headache ceases. It is dangerous ifinjected intravenously, and should not be givenduring menstruation (as it has a powerful utero-tonic action). It is definitely contraindicated in-pregnancy, hepatitis, obliterative vascular diseaseand in renal disorders (Brock, O'Sullivan andYoung, I934; Lennox and von Storch, 1935; vander Scheer, I938; von Storch, I941).

3. Dihydro-ergotamine injected subcutaneouslyor intramuscularly in doses of 0.5 to 3 mgm.(repeated in i or 2 hours if necessary in severe andpersistent attacks) successfully terminates migrain-ous attacks within 2 hours of administration in 8oto 90 per cent. of patients; the effect is mostpronounced and most rapid if it is exhibited earlyin the attack. In the absence of nausea andvomiting and in mild attacks I to 2 mgm. bymouth (repeated up to three times daily) may beeffective. Intravenous injection (not more thano.s mgm.) may be given in very exceptional cases,but is not recommended as it may result in vertigoand precordial pain as well as in exacerbation of theheadache, nausea and vomiting. It has no effecton the uterine musculature and is not contra-indicated in pregnancy or in vascular disease.Occasionally, especially if used in high dosage late

in an attack, it may cause nausea and vQmiting(effect inhibited by atropine sulphate, i/ioo gr.)(Ekbom, I944; Hartman, 1945; Horton, Petersand Blumenthal, I945; Friedman and Friedman,1945; Allan, I946; Clein, I946; Dannenberg,1946; Spuehler, I946; Alvarez, I947; Blumen-thal and Fakler, '947; Dreyfus, 1947; Friedmanand Wilson, I947; von Storch, 1947; Tillgren,I947; Chapuis, 1948).

4. If the pain is unusually severe morphia j gr.or pethidine hydrochloride 200 mgm. may benecessary.

(C) SURGICAL TREATMENTI. In a few selected cases of atypical migraine

affecting chiefly one eye, temple and upper part ofthe cheek, sometimes producing lacrimation andcongestion of the eyeball, temporary or per-manent relief may be obtained by alcohol injectionof the Gasserian ganglion (Harris, 1946).

2. Injection of procaine into or ligation, sectionor resection of the temporal (Nadler, I945;Patzer, Derbes and Engelhardt, 1945; Froucht-man, I945; Freeman, I946; Moore, I946), supra-orbital (Freeman, I946; Moore, I946) and/oroccipital (Freeman, I946) arteries has been success-ful in aborting and inhibiting attacks; unfortu-nately the effect is usually only transient and rarelylasts for more than one year (von Storch, 1947).

3. The middle meningeal artery has beenligated (Dickerson, I933).

4. A periarterial sympathectomy of the externaland internal carotid arteries close to the base of theskull has been performed (Hellwig, I924).

5. Removal of the inferior cervical and firstthoracic sympathetic ganglia has been reported(Dandy, 193 I).

6. Rowbotham (1946) has successfully per-formed a periarterial sympathectomy of the com-mon, internal and external carotid arteries to-gether with division of the external carotid arteryand simultaneous removal of the lower half of thesuperior cervical sympathetic ganglion.

7. Finally, even sub-temporal decompressionhas been carried out in excessively severe cases(Buchanan, I924; Alvarez, 1947).

The writer wishes to thank Dr. S. P. Meadows,F.R.C.P., for attracting his attention to the subject,and Miss Irene Colbert, M.B., Mr. G. F. Home,Miss W. C. Donkin and Mr. T. Bradbeer for theircourtesy and help in obtaining, collecting andchecking references.

BIBLIOGRAPHYALLAN, F. M. (I946), Lahey Clin. Bull., 5, 52.ALVAREZ, W. C. (940), Proc. Staff Meet. Mayo Clin., 15, 380.ALVAREZ, W. C. (I947), Gastroenterology, 9, 754.

ALVAREZ, W. C., and MASON, A. Y. (I940), Proc. Staff Meet.Mayo Clin., I5, 6i6.

ATKINSON, M. (I943), Ann. Int. Med., I8, 797.

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December 1950 IOVETZ-TERESHCHENKO: Migraine 653

ATKINSON, M. (x944), Ann. Int. Med., 21, 990.AULD, A. G. (I920), Brit. Med. J., 1, 567.BAKER, B. M. (I940), Tr. A. Am. Physicians, 55, 294.BALL, F. E. (I927), Am. _7. Med. Sc., 173, 78I.BANNON, R. E; (1940), Am..7. Optometry, 17, ISO5.BARBORKA, C. J. t1929), M. Clin. N. Amer., 12, I639.BARBORKA, C. J. (1930), 7. Am. Med. Ass., gs, I825.BARKER, M. H., LINDBERG, H. A., and WALD, M. H. (1941),

7. Am. Med. Ass., 137, I59I.BARTSTRA, H. K. G. (I946), Ned. Tijdschr. Geneesk., go, I786.BARUK, H. (I93I), Enciphale, 26, 42.BASSOE, P. (I933),.7. Am. Med. Ass., 101, 599.BIGLAND, A. D. (I923), Brit. Med..7., ii, II33.BLAKIE, N. H., and HOSSACK, J. C. (1932), Canad. M. A..7.,

27, 45.BLUMENTHAL, L. S., and FAKLER, B. (1947), Med. Ann. D. C.,

06,IO.BRAMS, W. A. (I922),.7. Am. Med. Ass., 78, 26.BRAVAIS, L. F. (I827), 'Recherches sur les symptomes et le

traitement de l'epilepsie hemiplegique,' Thhse No. iI8, Paris.BROCK, S., O'SULLIVAN, M., and YOUNG, D. (I934), Am..7.

M. Sc., I88, 253.BROWN, J. A. (I943), Brit. Med..3., ii, 201.BROWN, T. R. (192), .7. Am. Med. Ass., 77, 1396.BROWN, T. R. (I929), Tr. A. Am. Physicians, 44, 215.BRUGELMANN, W. (I0og), ' Die Migrane,' Wiesbaden.BRUNTON, T. L. (1894), Pra:titioner, 52, IOI.BUCHANAN, J. A. (1920), Med. Rec., 98, 807.BUCHANAN J. A. (I924), S. G. O., 38, 638.BUTLER, S. and THOMAS, W. A. (194S), 7. Am. Med. Ass.,

128, 173.CARMICHAEL, F. A. (1943) _. Kansas M. So&., 44, 333.CARRON DE LA CARRIERE, G. (I905), Medecin Brux., 15, 305.CHAPUIS, J. P. (I948), Schwez. Med. Wschr., 78, 1125.CHIRAY, M., and TRIBOULET, F. (192S), Presse Med., 33, 313.CLEIN, N. W. (I946), Ann. AUergy, 4, 128.COBB, S., and FiRMONT-SMITH, F. (193I), Arch. Neural. and

Psychiat., 26, 73I.COOKE, W. T., CLOAKE, P. C. P., GOVAN, A. D. T., and

COLBECK, J. C. (1946), Quart. 7. Med., I5, 47.CRANDALL, L. A., and ROBERTS, G. M. (I933), Illinois M. 7.,

63, 513.CRANDALL, L. A., and ROBERTS, G. M. (1933), Proc. Soc.

Exper. Biol. and Med., 30, 704.CRANDALL, L. A., ROBERTS, G. M., and SNORF, L. D.

(1936-I937), Am. 7. Digest, Dis., 3, 289.CRITCHLEY, M., and FERGUSON, F. R. (I933), Lancet, i,

123 and 182.CURSCHMANN, H. (I939), Handbuch d. Inn. Med., 5, isos.DANDY, W. E. (I93I), Bull. Johns Hopkins Hosp., 48, 357.DANNENBERG, TH. (I946), Perm. Found. Med. Bull., 4, 96.DERBES, V. J., ENGELHARDT, H. T., and WATTERS, T. A.

SI945), South M. Y., 38, 533.DIA OND, J. S. (I927), Am..7. M. Sc., 174, 695.DIAMOND, J. S. (I934), M. Re'.., 139, 634.DICKERSON, D. G. (I933), 7. Nerv. and Ment. Dis., 77, 42.DREWYER, G. E. (I940),.7. Michigan M. Soc., 39, 486.DREYFUS, PH. R. (I947), Rev. Med. Suisse Rom., 67, I22.DUNN, C. W. (I94i), Delaware State M. 37., 13, 89.DURAND, G. (192I), Bull gen. de Therap. Paris, 172, iS9.EGGLESTON, C., and WEISS, S. (1932), Am..7. M. Sc., 183, 283.EKBOM, K. A. (i944), Nord. Med., 22, 86I.ENGLE, D. E., and EVANSON, C. 0. (I942), Am. J. M. Sc., 204,

697.ENRIQUE, E. ('943), Rev. Clin. Espan., IO, 53.ESCHBACK, H. (I927) ' Epilepsie und Migrdne,' Bonn.FABRE, E. (I904), La Migraine chez les enfants.'FITZ-HUGH, T. (I940), Intern. Clinics, I, 143.FLATAU, E. (I9I2), ' Die Migrane,' Berlin.FOTHERGILL, J. (1784), 'Medical Observations and Enquiries,

6, 103.FREEMAN, W. (1946),.Y. Am. Med. Ass., 132, 501.'FRIEDLANDER, W., and PETOW, I. (1927), Med. Klin., 23,

1498.FRIEDMAN, A. P., and BRENNER, C. (I94S), N. York State .

Med., 45, I969.FRIEDMAN, A. P., BRENNER, C., and MERRITT, H. H.

(I946),.7. Am. Med. Ass., 132, 498.FRIEDMAN, M. D., and FRIEDMAN, D. A. (I94S), Ohio State

Med. J., 41, 1099.FRIEDMAN, M. D., and WILSON, E. J. (1947), Ohio Med. J.,

43, 934-FROUCHTMAN, R. (Ix94S), Med. Clin. Barcelona, 4, 396.GANSSLEN, M. (1921), Med. Klin. Berl., 7, 1232.GLASS, S. J. (1936), Endorinology, 20, 333.GOLDZIEHER, J, W., and POPKIN, G. L. (1946), J7. Am. Med.

Ass., 131, 103.GOTTLIEB, J. S. (1942), Am. Y. M. Sc., 204, 553.GOWERS, W. R. (1907), 'Borderland of Epilepsy, Faints, Vagal

attacks, Vertigo, Migraine, Sleep symptoms and their Treat-ment,' London.

GRIMES, E. (I93I), Med.3. and Rec., 134, 417.HARRIS, W. (I937), 'The Facial Neuralgias,' London.HARRIS, W. (1946), Brit. Med. 7., L 754.HARTMAN, M. D. (Ix945), Atn. AlUergy, 3, 440.

HAUG, H., and WOHRMANN, W. (1930), Deut. Med. Woch.,26, Io85.

HELLWIG, A.. (I924), Arch. f. Klin. Chir., I28, 26I.HELLWIG, A. (1924), Y. Am. Med. Ass., 82, Io86.HENRIKSEN, K. Z. (933), Acta Psychiat. and Neurol., 8, 701.HINES, E. A., and EATON, L. M. (I942), Proc. Staff Meet. Mayo

Clin., 27, 254.HIRSCH, B. R. (1765), 'Paris Quinti Nervorum Encephali Dis-

qUitio Anatomica,' Vienna.HORTON, B. J., MAGATH, T. B., and BROWN, G. E. (I934),

Arch. Int. Med., 53, 400.HORTON, B. T. (I94I), Y. Am. Med. Ass., II6, 377.HORTON, B. T., and MACY, D. (I946),,M. Clin. N. Am., 30, 8I I.HORTON, B. T., PETERS, G. A., and BLUMENTHAL, L. S.

('942), Proc. Central So^. Clin. Res., 25, 9I.HORTON, B. T., PETERS, G. A., and BLUMENTHAL, L. S.

(I94S), Proc. Staff Meet. Mayo Clin., 20, 241.HORTON, B. T., PETERS, G. A., and BLUMENTHAL, L. S.

(1947) 'Festschrift Prof. Stoll,' Benno Schwabe, Basel, p. 355.HUNT, T. C. (933), Lancet, ii, 279.HURST, A. F. (1924), Lancet, ii, 3.HYSLOP, G. H. (I934), M. Clin. N. Am., I8, 827.JACKSON, J. H. (x863), Med. Times and Gaz., I, 588.JAMES, A. K. (1945), Brit. Med. Y., 1, 663.KENNEDY, F. (I946), Y. Am. Med. Ass., 232, 502.KERPPOLA, W. (I926), Monatschr. f. Psychiat. u. Neurol. 6I, 83.KILBOURNE, E. D., and WOLFF, H. G. (1946), inn. Int.

Med 24, I.KRAL, V. A. (1948), Schweiz. Arch. Neurol. Psychiat., 62, 128.LENNOX, W. G. (I94I), 'Science and Seizures,' New York.LENNOX, W. G., and VON STORCH, T. J. C. (193S), Y. Am.

Med. Ass., x05, I69.LEYTON, N. (I944), M. Press, 211, 302.LIVENIG, E. (1873), 'On Megrim, Sick Headache and some

Allied Disorders.'LYON, G. (Igg), Bull. Med., 43, 1145.MCCLURE, C. ., and HUNTSINGER, M. E. (1928), New Eng.M

. Med., 299, 13I2.MAC EAL, P. S., and DAVIS, D. (I947), Ann. Int. Med., 26, 526.McQUARRIE, I. (1932), Ann. Int. Med. 6, 497.MANGELSDORF, F. (1903), Berl. Klin. Wchnschr., 4o, 1004.MARIN, R. B. (I946), . M. Soc. N. Jersey, 43, 274.MENDEL, G. H. (x866), Verhand. d. Naturf. Vereins in Brunn,

4,3.MILLER, J. L., and RAULSTON, B. 0. (1923), Y. Am. Med.

Ass., 8o, 1894.MINGAZZINI, G. (1917), Policlin. Roma, 24, 269.MINOT, G. R. (1923), M. Clin. N. Am., 7,715.MOBIUS, P. J. (I894), 'Die Migrane.'MOEHLIG, R. C. (193I), Endocrinology, 25, II.MOENCH, L. G. (I947), 'Headache,' Chicago.MOFFATT, W. M. (I937), Y. Am. Med. Ass., I08, 612.MOLONEY, J. C. ('928), Arch. Neurol. and Psychiat., i9, 684.MONRO TERTIUS, A. (82S5), 'Elements of Anatomy of the

Human Body,' 2 363.MOORE, M. T. (1946), J. Am. Med. Ass., 232, 502.MORENAL, L., and DECHAUME, J. (I929), Y. Med. Lyon, zo,

259.MORLOCK, C. G., and ALVAREZ, W. C. (I940), Y. Am. Med.

Ass., 224, 1744.NADLER, S. B. (I945), Y. Am. Med. Ass., 229, 334.O'SULLIVAN, M. E. (1936), Y. Am. Med. Ass., 207, 1208.PALMER, H. D. (I94I), Arch. Neurol. and Psychiat., 45, 368.PALMER, H. D. (194S), Clinics, 4, 531.PATTON, I. J. (1946), Canad. M. A. Y., S4, s88.PATZER, R., DERBES, V., and ENGELHARDT, H. (194S),

Arch. Sung. 50, 296.PELNER, L. (I943) Dis Nerv. System, 4, 177.PELNER, L., and AIBEL, M. E. (1942), 7. Lab. and Clin. Med.,

27, 1546.PFEIFFER, C., DREISBACH, R. H., and ROBY, C., C. (I944),

t. Lab. and Clin. Med., 29, 709.PFEIFFER, C., DREISBACH, R. H., ROBY, C., C., and GLASS,H. G. (I943), Y. Lab. and Clin. Med., 28, 1219.

POLLOCK, L. A. (1946), Rocky Mountain M. Y., 13, 895.POUSSEPP, D. (1925), Rev. Neurol., Paris, 32, 925.RAY, B. S., and WOLFF, H. G. (1940), Arch. Neurol. and

Psychiat., 42, 8I3.REMOND, A., DAVIES, P. W., and BRONK, D. W. (1946),

Fed. Proc., S, 86.RIGGS, C. E. (1926), Minnesota Med., 9, 87.RILEY, H. A., (1932), Bull. Neurol. Inst. N. York, 2, 429.RILEY, H. A., BRICKNER, R. M., and KURZROK, R. (1933).

Bull. Neurol. Inst. N. York, 3, 53.BOWBOTHAM, G. F. (1942), Brit. Med. .-., i, 68S.ROWBOTHAM, G. F. (1946), Brit. Med. Y., i, 319.VAN DER SCHEER, W. M. (1938), Ned. Tijdschr. Geneesk, 82,

_5843.SCHNABEL, T. G. (1928), Ann. Int. Med., 2, 341.SCHUMACHER, G. A., RAY, B. S., and WOLFF, H. G. (1940),

Arch. Neurol. and Psychiat., 44, 701.SCHUMACHER, G. A., and WOLFF, H. G. (94I), Arch. Neuro

and Psychiat., 45, 199.SICARD, J. A., PARAF, J., and FORESTIER, J. (I92I), Bull.

et Mem. Soc. Med. Hop. Paris, IS (3rd S.), 1204.

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654 POSTGRADUATE MEDICAL JOURNAL December 1950

SIMONS, D. J., DAY, E., GOODELL, H., and WOLFF, H. G.(i943), Research Pubi. A. Nerv. and Ment. Dis., 23, 228.

SINKLER, W. (I887-88), Maryland journal, i8, i.SLATER, J. K. (1948), Edinb. Med. J., 5S, 173.SMITH, C. B. (I946), Canad. M. A. J., 54, 589.SOLTZ, S. E., BRICKNER, R. M., RILEY, H. A., and SALMON,

L. A. (I935), Bull. Neurol. 7nst. N. York, 4, 432.SPITZER, A. (I9OI), 'Ueber Migrane,' Jena.SPUEHLER, 0. (1946), Schweiz. Med. Wschr. 76, I259.VON STORCH, T. J. C. (1937), Nervenarzt, IO, 469.VON STORCH, T. J. C. (I937), New Eng. J. Med., 217, 247.VON STORCH, T. J. C. (1938), Y. Am. Med. Ass., III, 293.VON STORCH, T. J. C. (I941), Med. Clin. N. Am., 25, 13I7.VON STORCH, T. J. C. (I947), Amer. Practit., I, 63I.SUTHERLAND, A. M., and WOLFF, H. G. (I940), Arch. Neurol.

and Psychiat., 44, 929.THOMAS, W. A., and BUTLER, S. (1946), Am. _J. Med., I, 39.THOMAS, W. A., and BUTLER, S. (1946), Bull. N. York Acad.

Med., 22, 125.TILLGREN, N. (I947), Nord. Med., 33, 502.TILLGREN, N. (I947), Nord. Med., 34, 937.TILLGREN, N. (I947), Acta Med. Scand. (Suppl.), I96, 222.TILLIM, S. J. (i944), Ann. Int. Med., 20, 597.

TODD, R. B. (I854), 'Clinical Lectures on Paralysis, Diseases ofthe Brain and Other Affections of the Nervous System,'London, p. 28i.

TORDA, C., and WOLFF, H. G. (I945), Arch. Neurol. andPsychiat., 53, 329.

TROWBRIDGE, L. S., VON STORCH, T. .J. C., and MOORE,M. (I942), New Eng. J. Med., 227, 699.

UNGER, L. (1940), J. Alergy, 12, 197.VALLERY-RADOT, P., and BLAMOUTIER, P. (1927), Bull.

et Mem. Soc. Med. Hop. Paris, Si, 925.VILLEY, G., and BUVAT, J. F. (I937), Paris Med., I03, I89.VON WASSERMAN, A., NEISSER, A., and BRUCK, C. (I906),

Dtsch. Med. Wchschr., 32, 745.WEISMANN, S. (1924), 'Des Migraines,' Paris.WHITEHEAD, R. W., and McNIEL, E. E. (I935), Am. J.

Psychiat., 91, I275.WHITEHORN, J. C. (I944), Areh. Neurol. and Psychiat., 52, 197.WILSON, D. C. (l925), Clifton M. Bull., II, 71.WOLFF, A. A., and UNGER, L. (I944), Ann. Int. Med., 20, 828,-WOLFF, H. G. (1940), 'Modern Medical Therapy in General

Practice,' Baltimore.WOLFF, H. G. (I948), ' Headache and other Head Pain,' New York.WOLFF, H. G., IIARDY, J. D., and GOODELL, H. (1941), Y.

Clin. Invest., 2o, 63.

INFECTIONS OF THE FEET IN DIABETESWith Special Reference to Those Due to Gas-Forming Organisms

By E. C. B. BUTLER, F.R.C.S.The London Hospital

It is a common error to regard all infections ofthe feet occurring in diabetic patients as cases ofincipient gangrene. Most of these patients can besafely treated at home or in the out-patient de-partment. Only a minority need admission tohospital, and of these only a small proportion havetrue necrosis or require a major amputation. Theincidence of severe infection has been much re-duced since the introduction of penicillin.

Patients who require in-patient treatment mayfor convenience be divided into two groups,although the dividing line between the two is oftendifficult to determine.Group i consists of those patients who have

signs and symptoms of senile obliterative arterialdisease. The diabetic cases differ only in havinginfection as a constant feature.Group 2 consists of cases of diabetes com-

plicated by infection of the feet, the circulationbeinggood, the popliteal pulse being readily feltand oscillometer tests showing good pulsationbelow the knee.

Group IFollowing mild trauma an infection starts on

one or more toes and similar lesions may arise onthe heel or elsewhere on the foot. Under favour-able circumstances and treatment the infection will

resolve but in other instances it may spread or goon to necrosis, which in turn may remain localizedor involve the remainder of the foot.When spread of the infection occurs there is

little local reaction; formation of pus is unusualand there is no definite line of demarcation be-tween diseased and healthy tissue. On examina-tion, these patients are likely to show signs ofthrombosis in the femoral or popliteal vessels.Popliteal pulsation is absent, oscillometer readingsshow minimal or absent records below the kneeand the limb rapidly becomes blanched when ele-vated. Radiography may reveal widespreadmedial calcification of the main vessels.

TreatmentThe patient is best treated as an in-patient. A

swab from the infected area is sent to the laboratoryso that the invading organisms can be identifiedand their sensitivity established.

Staphylococcus aureus and haemolytic and non-haemolytic streptococci are commonly found; butgram-negative bacilli may also occur. Not in-frequently various types of anaerobic organismsare present and these may cause serious spreadinginfections. Some of these organisms are penicillinresistant and it is a wise precaution to learn with-out delay what drug or combination of drugs is

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