electrodiagnostic criteria for polyneuropathy and demyelination: … · tive treatment for...

48ournal ofNeurology, Neurosurgery, and Psychiatry 1995;59:482-486

Electrodiagnostic criteria for polyneuropathy anddemyelination: application in 135 patients withGuillain-Barre syndromeJ Meulstee, F G A van der Meche, and the Dutch Guillain-Barre Study Group

Department ofNeurology, UniversityHospital Dijkzigt andErasmus UniversityRotterdam, TheNetherlandsJ MeulsteeF G A van der MecheCorrespondence to:Dr J Meulstee, Departmentof Neurology, UniversityHospital Dijkzigt andErasmus UniversityRotterdam.Dr Molewaterplein 40.Room BA-402. NL 3015GD The Netherlands.

Received 24 February 1995and in revised form4 July 1995Accepted 1 1 July 1995

AbstractSince the development of effective butexpensive therapeutic strategies for thetreatment of Guillain-Barre syndrome,early confirmation of the diagnosis hasbecome very important. Electro-diagnostic criteria were developed for thediscrimination of polyneuropathy and inparticular for demyelination. The sensi-tivity and specificity of these criteriawere determined in 135 patients withGuillain-Barre syndrome in an earlystage of the disease, along with 45 healthyvolunteers.The algorithms used to develop our

criteria consisted of sets of selectedelectrodiagnostic variables, each of themrelevant to the detection of polyneuropa-thy. Each set was applied on all of threeconsecutive electrodiagnostic examina-tions within one month of disease onset.Application of the best set resulted in 85%of patients with Guillain-Barre syndromefulfilling the criteria for polyneuropathyat the first examination (mean timeinterval six days of disease onset),whereas none of the healthy volunteersfulfilled the criteria (sensitivity 85%,specificity 100%).The set of criteria for the detection of

demyelination was fulfilled by 60%during the first examination (by 66%and 72% during the second and thirdexamination). Application of criteria fordemyelinating polyneuropathy as definedby others resulted in substantiallylowered incidence (3O/o46%).

It is concluded that these criteria forthe electrodiagnostic delineation ofpolyneuropathy are the most sensitive todate, with respect to the early confirma-tion of the diagnosis of Guillain-Barresyndrome.

(J Neurol Neurosurg Psychiatry 1995;59:482-486)

Keywords: Guillain-Barre syndrome; demyelinatingpolyneuropathy; electrodiagnostic criteria

The Guillain-Barre syndrome is an acutepolyradiculoneuropathy which may lead tosevere tetraparesis. The precise aetiology isunknown but immune mechanisms areinvolved. In the recent past several therapeu-tic regimes have emerged, all of which help toreduce the duration and severity of the diseaseas well as the incidence and duration of respi-

ratory dependency.' Therefore, it is of majorimportance to have a firm diagnosis as early aspossible. Clinical diagnostic criteria have ingeneral been shown to be reliable in recentlyconducted clinical trials.45 Electrodiagnostictests may, however, in some cases be neces-sary in the differential diagnosis of Guillain-Barre syndrome. Moreover, in cases ofclinically defined Guillain-Barre syndrome,electrodiagnostic studies and, more specifical-ly, nerve conduction studies may show signsof demyelination, and thus further characte-rise clinically defined Guillain-Barre syn-drome as demyelinating Guillain-Barresyndrome. This may, in the future, prove tobe of help in the selection of specific treat-ments. In the present study we constructedtwo sets of electrodiagnostic criteria, based onthe findings in patients included in the DutchGuillain-Barre study.3 The first set can beused to prove the existence of a polyneuropa-thy. The second set was designed to test thepresence of electrodiagnostic signs of demye-lination. In addition, we tested several, previ-ously published sets of electrodiagnosticcriteria constructed for demyelinatingpolyneuropathies.468

Patients and methodsPatients tested in this study were all includedin the Dutch Guillain-Barre trial which testedthe efficacy of intravenous immunoglobulin vplasma exchange in 147 patients.3 Patients(mean age 47-5 (SD 19-2)) entered the study ifthey fulfilled the criteria for acute Guillain-Barre syndrome,4 were not able to walk 10metres independently, and could enter thestudy within two weeks of onset of thepolyneuropathy. The predefined outcomemeasure was improvement at four weeks by atleast one grade on a seven point scale ofmotor function. Patients were followed up forsix months. The main conclusion was thatimmunoglobulin treatment was at least aseffective as plasma exchange and thatimmunoglobulin is a practical, safe, and effec-tive treatment for Guillain-Barr& syndrome.The results of electrodiagnostic tests were notpart of the inclusion criteria. Electrodiag-nostic tests were scheduled within two days ofentry, one week later, and one month later.The methods of electrodiagnostic testing

have been discussed in detail elsewhere.9 Inshort: motor nerve conduction studies wereperformed on ulnar and median nerves in theforearm. Shortest F response latencies weremeasured after 20 stimuli. Sensory nerve

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Electrodiagnostic criteria for polyneuropathy and demyelination: application in 135 Guillain-Barre patients

conduction velocities of ulnar and mediannerves were measured antidromically. Ampli-tudes and duration of the evoked motor andsensory responses were measured with surfaceelectrodes. The peroneal and sural nerveswere tested when relevant. With concentricneedle electrodes, small hand muscles andanterior tibial muscles were tested for the pre-sence of denervation potentials and therecruitment pattern on maximal voluntaryeffort. All tests were performed unilaterally.

Electrodiagnostic variables used for thedevelopment of criteria were: distal motorlatency (DML), motor nerve conductionvelocity (m-NCV), F response latency, com-pound muscle action potential amplitude(CMAP amplitude), and duration after distalstimulation, ratio of distal v proximal CMAPamplitude, ratio of distal v proximal CMAPduration, compound sensory nerve actionpotential amplitude (CSNAP amplitude),sensory nerve conduction velocity (s-NCV),recruitment pattern, and presence of denerva-tion potentials. Some values were not scoredin individual patients; however their clinicalcharacteristics were not different. In 135patients at least one complete electrodiagnosticexamination (EMG) was performed (table 1).An electrodiagnostic variable was defined asabnormal if it fell outside our laboratory's lim-its of normal (outside 95th percentile). Theselimits of normal were obtained in 45 healthyvolunteers (range of ages 37-7 (SD 11-6))(table 2). We defined abnormal CMAPamplitude reduction as present if the observeddecrease in CMAP amplitude exceeded theupper limit of normal; in cases where theCMAP amplitude after distal stimulation was

Table 1 Variables usedfor the development of criteria forthe electrodiagnostic delineation ofpolyneuropathy

1 DML > ULN2 m-NCV < LLN3 F wave latency >ULN ifm-NCV is normal4 s-NCV ULN if distal CMAP > 5 mV (hand) response,> 3 mV (foot), or CMAP amplitude decay of 1 mV ifdistal CMAP < 5 respectively 3 mV

7 Distal CMAP-duration > ULN8 Increase ofCMAP duration > ULN9 Distal CSNAP amplitude < LLN10 Recruitment pattern 0 or SP11 Presence of denervation potentials

DML = distal motor latency; ULN = upper limit of normal;m-NCV = motor nerve conduction velocity; LLN = laboratorylimits of normal; s-NCV = sensory nerve potential; CMAP =compound muscle action potential; CSNAP = compound sen-sory nerve action potential; SP = single pattern.

Table 2 Normal values

Ulnar Median Peroneal Sural

DML* 2-2 ms 3-0 ms 4-3 ms -m-NCVt 60 m/s 60 m/s 50 m/s -CMAP amplitudestt 15-5 mV 12-3 mV 6-0 mV -Reduction*§ 16% 11% 41% -CMAP surfacett 33 mV/ms 29 mV/ms 11 mV/ms -Reduction*§ 11% 8% 34% -CMAP duration*t 8-1 ms 7-2 ms 6-7 ms -Increase*§ 12% 12% 19% -F-latency*t 32-3 ms 31-2 ms 59-6 ms -s-NCVtt 60 m/s 60 m/s - 50 m/sSNAP#4 1OPV 10,uV - 10,V*Upper limits and tlower limits based on 5th and 95th percentile values in 45 healthy volun-teers; tafter distal stimulation; §in the trajectory of forearm-lower leg. Skin temperature 35°C.

< 5 mV, we defined CMAP amplitude reduc-tion as abnormal if the difference betweendistal and proximal stimulation was at least 1mV. Recruitment pattern was defined asabnormal if no pattern or a single pattern wasobtained on maximal voluntary effort.

Electrodiagnostically a nerve can bedefined as abnormal if a minimal number ofvariables exceed the normal limits; however,no consensus exists on the number ofrequired abnormal variables per nerve and therequired number of abnormal nerves withregard to the electrodiagnostic definition ofpolyneuropathy. Due to the nature of poly-neuropathy a minimal number of two abnor-mal nerves would seem to be required. Byvarying the number of abnormal variables pernerve, and the number of required abnormalnerves, we designed different sets. An optimalset would result in a high sensitivity andspecificity, yet still be feasable in clinical prac-tice. Therefore, the number of requiredabnormal variables per nerve was variedbetween three and five out of 11 tested, andthe number of required abnormal nerves waslimited to two or three. The sensitivity andspecificity of both polyneuropathy sets andsets for demyelination were tested in 135patients with Guillain-Barre syndrome and 45healthy subjects. Only the results of the firsttwo EMGs were used to compute the sensiti-vity of polyneuropathy criteria, as these are ofrelevance for early diagnosis.

In addition to criteria for polyneuropathy ingeneral, the following findings, characteristicof demyelination, were evaluated: severe slow-ing of conduction, abnormal dispersion, andabnormal reduction in CMAP amplitude.7910We considered signs of demyelination to bepresent in a peripheral nerve if at least one ofthe aforementioned criteria was fulfilled. Thepolyneuropathy was considered to bedemyelinating if two or more nerves showedsigns of demyelination (table 3). Patients inwhom less than two nerves were tested wereexcluded; the number of patients with at leasttwo completely tested nerves is presentedthroughout the results section. In addition, wecalculated the incidence of several previouslydesigned sets of criteria for demyelinatingpolyneuropathy in the same group of patients.Here again, a correction for bias due to absentvalues was performed and true incidence wascalculated as the ratio between sufficientlytested patients and patients with elec-trodiagnostic abnormalities.

Table 3 Criteria for primary demyelinationProposed and tested set: one of the following abnormalities inat least two nerves should be demonstrated.

1 DML>150%ofULN2 m-NCV < 70% ofLLN3 F wave latency > 150% ofULN4 Abnormal CMAP amplitude decay > ULN5 Abnormal distal temporal dispersion: distal GMAP

duration > 300% ULN6 Abnormal temporal dispersion: distal to proximal

CMAP duration ratio > 150% ofULN

DML = distal motor latency; ULN = upper limit of normal;m-NCV = motor nerve conduction velocity; LLN = labora-tory limits of normal; s-NCV = sensory nerve potential;CMAP = compound muscle action potential; CSNAP = com-pound sensory nerve action potential; SP = single pattern.



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Table 4 Duration ofweakness (days) at the moment ofEMG

Range 5%-95% (days) Median (days)

EMG I 2-15 6EMG II 9-22 13EMG III 29-49 34

ResultsThe median duration of weakness was 6, 13,and 28 days respectively, at the moment ofthe three subsequent EMGs (table 4). Noelectrodiagnostic differences were foundbetween the two treatment modalities.

Over 25 criteria sets were applied to allthree EMGs. In these sets the definition of anabnormal nerve was varied by changing thenumber of required abnormal variables (threeto five). The definition of a polyneuropathywas varied by changing the number of abnor-mal nerves (two or three). The best resultswere obtained when an abnormal nerve wasdefined by the presence of at least threeabnormal variables, and polyneuropathy whenat least two nerves were abnormal. Within thisset the criteria were met in 85% after the firstEMG and in 93% after the second EMG. Innone of the healthy volunteers were these cri-teria met (table 5). Theoretically, bias towardsa reduced sensitivity could be expected frominsufficiently tested nerves. Therefore, wedefined a nerve as sufficiently tested when atleast five, six, or seven variables were tested. Itseems that missing values did not significantlyinfluence sensitivity when at least five vari-ables per nerve were tested (table 5).

At the first EMG most nerves were abnor-mal: ulnar nerve 88%, median nerve 90%,and peroneal nerve 70%. The same trend wasobserved in the second EMG, but here theincidences were higher. In the 45 normal sub-jects these percentages were always zero.

Evidence for demyelination, as defined bythe proposed criteria, was seen in 54%, 72%,and 51% in the ulnar, median, and peronealnerves respectively, in the first EMG. In 60%,signs of demyelination were present in at leasttwo nerves simultaneously (table 6). In subse-quent EMGs these incidences increasedmaximally with an additional 17%. None of45 healthy volunteers had signs of demyelina-tion in more than one nerve according to theproposed set.

Applying previously published criteria forprimary demyelinating polyneuropathies,yielded low incidences, varying from 3% to36% at the first EMG, 8% to 39% at thesecond EMG, and 13% to 46% at the thirdEMG (table 7).

DiscussionWe designed a set of electrodiagnostic criteriafor detection of polyneuropathy and a set fordetecting signs characteristic of demyeli-nation, and applied these in 135 patients withclinically defined Guillain-Barre syndrome.This is the first study in which such a largegroup of patients has been followed upprospectively according to a standard EMGprotocol. During follow up, the clinicaldiagnosis of Guillain-Barre syndrome was notchanged in any patient; it is assumed, there-fore, that in the patients the diagnosis wascorrect.The first set for the diagnosis of polyneu-

ropathy was compiled from electrodiagnosticvariables available from the test protocol.Because the normal limits for these variablesare based on 95th percentiles, the applicationof individual variables would have a falsepositive rate of 5%, by definition. Therefore,the major advantage of requiring a minimalnumber of three abnormal variables per nervein several nerves was that the false positiverate was reduced to zero in all 45 healthy sub-jects and therefore the specificity was 100%.The sensitivity of this set was tested in twoEMGs, performed at the moment of entry(EMG I) and one week later (EMG II)-thatis, at an early stage of the disease. The num-ber of variables per nerve required for nerve tobe scored as abnormal was chosen rather arbi-trarily; however, different combinations allyielded a high incidence of polyneuropathy.The set which scored best was the one thatrequired three abnormal variables in twodifferent nerves (85% in EMG I and 93% inEMG II) (table 5). Ulnar and median nervescontributed slightly more than the peronealnerve (about 88%, 90%, and 70% respec-tively in EMG I, table 5). No such sets of cri-teria are as yet available in the medicalliterature for comparison.

Electrodiagnostic criteria, usually appliedfor the detection of demyelination, are DML,m-NCV, F response latency, and CMAPreduction and duration of CMAPs, becausethese variables are related to nerve conductionslowing and conduction block.67 9-11 In thepresent study, the threshold value that woulddiscriminate had to be chosen arbitrarily, ashas been done by others478 Nevertheless, theproposed set yielded a high incidence of signsof demyelination (60%, 66%, and 72% inconsecutive EMGs) (table 5). Again, ulnarand median nerves contributed most (table2). The best explanation of the lower yield,compared with those for polyneuropathy,

Table 5 Incidence of abnormal nerves related to the required number of abnormal variables within a nerve

EMG I EMG II

Ulnar Median Peroneal > One nerve Ulnar Median Peroneal > One nerve(%/. (n)) (% (n)) (% (n)) (% (n)) (% (n)) (% (n)) (% (n)) (% (n))

3 out of 5* 88 (124) 90 (125) 70 (57) 85 (127) 93 (124) 93 (126) 77 (64) 93 (128)4 out of 5 71 (124) 78 (125) 39 (57) 64 (127) 81 (123) 85 (126) 20 (55) 78 (127)5 out of 5 50 (124) 50 (124) 27 (56) 40 (126) 63 (123) 66 (125) 33 (51) 50 (125)5 out of 7 53 (116) 52 (122) 30 (50) 42 (118) 64 (122) 68 (120) 37 (46) 53 (121)

*The first number gives the required number of abnormal variables, the second the required number of evaluated variables;n = number of adequately tested patients.



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Table 6 Incidence ofmotor nerves with at least one sign ofdemyelination according to theproposed set of criteria

Nornalcontrols EMG I EMG II EMG III(% (n)) (%l (n)) (% (n)) (% (n))

Ulnarnerve 9 (45) 54 (124) 69 (121) 74 (109)Median nerve 7 (45) 72 (120) 75 (130) 68 (130)Peroneal nerve 11 (45) 51 (53) 52 (50) 56 (39)Two or more nerves 0 (45) 60 (124) 66 (124) 72 (109)

n = number of adequately tested patients.

Table 7 Incidence ofdemyelination according to previously published sets of criteriaapplied to the present patients with Guillain-Barri syndrome

EMG I EMG H EMG III(% (n)) (% (n)) (l (n))

Barohnetal6 3 (119) 8 (116) 13 (101)Albers and Kelly7 5 (122) 11 (117) 15 (104)Asbury and Cornblath4 22 (74) 39 (57) 46 (63)Albers et al" 36 (72) 28 (64) 41 (59)This study 60 (124) 66 (124) 72 (109)

n = number of adequately tested nerves.

lies in the fact that many patients withGuillain-Barre syndrome have (near) normalm-NCVs" 13 and, as a consequence, willescape detection if the limiting value ofNCV isset at a lower value. We think, however, thatthe proposed set is reasonable to use for thedetection of demyelination, but a firmerconclusion can only be drawn if this set of cri-teria is tested in a group of patients with pureaxonal disorders. In some patients withGuillain-Barre syndrome an "axonal form"may exist, as reflected by excitable nerves. Inthe present study there were seven suchpatients. This may be the result of severedemyelination, but a primary axonal formprobably also exists. Obviously, these patientsdid not fulfil the proposed set of criteria fordemyelination.

Various sets of electrodiagnostic criteria forthe detection of demyelination have beendeveloped by others.468 When possible weapplied these criteria to our patient popu-lation (table 7). The criteria developed byBarohn et at6 and Albers and Kelly7 weredesigned for patients with chronic inflamma-tory demyelinating polyradiculoneuropathy.Application to our data resulted in a muchlower yield. This may be explained by the factthat characteristics of demyelination are oftenfar more pronounced partly due to the longerduration of the disease. The criteria devel-oped by Albers et all and Asbury andCornblath,4 and designed for Guillain-Barresyndrome are less stringent and therefore givea higher yield (table 7). Albers et al reportedcriteria for demyelination derived from aretrospective study on patients with Guillain-Barre syndrome." Their patients were exam-ined electrodiagnostically at weekly intervals,which enables comparison with our group.Electrodiagnostic examination at time pointscomparable with consecutive EMGs (I, II,and III) yielded incidences of 50%, 50%, and68% in eight, 18, and 25 patients respectively.The study of McLeod is less comparable inthis respect (duration of illness 1-125 days),but an incidence of 50% was reported.'4

Several studies have shown the demyelinat-

ing nature of nerve pathology in Guillain-Barre syndrome.'0 15-17 Feasby et al'8 were ableto relate conduction block to pathologicaldemyelination in nerve biopsies. Also, experi-mental conduction block-whether inducedmechanically'9 or immunologically20-isassociated with demyelination. These studiessuggest that significant demyelination will berevealed by conduction block and conductionslowing. In some nerves, however, these elec-trodiagnostic signs of demyelination are notfound, despite the fact that demyelination issuspected on the basis of clinical findings.This may occur when lesions are patchy alongthe nerve outside the segment which can betested in routine studies. Furthermore,conduction block in the thinner segment ofmotor fibres may be difficult to detect, as longas a few large motor units with thick axons-the principal constituents of the CMAP-are free from demyelination. This has beenshown by morphological and physiologicalstudies.'2 18 Another reason why patients withdemyelination may pass undetected using theproposed criteria is that many patients withGuillain-Barre syndrome have a very low distalCMAP amplitude.9 As other causes, such asaxonal degeneration or motor end platedysfunction, cannot be discriminated fromdistal demyelination, low CMAP amplitudescannot be applied as a criterion of primarydemyelination. Therefore, the patients withpredominant distal demyelination will escapedetection and may, in any set, cause a seriousunderestimation of the incidence of demyeli-nation.

In conclusion, in the 135 patients withGuillain-Barre syndrome studied, the pro-posed set of criteria for polyneuropathy had asensitivity of 85% and a specificity of 100%.The polyneuropathy was demyelinating in72% or 36% respectively, using two sets ofcriteria for demyelination. This set should betested in other categories of demyelinatingand pure axonal neuropathies.

1 Guillain-Barre Syndrome Study Group. Plasmapheresisand acute Guillain-Barre syndrome. Neurology 1985;35:1096-104.

2 French Cooperative Group on plasma exchange inGuillain-Barre syndrome. Efficiency of plasma exchangein Guillain-Barre syndrome: role of replacements fluids.Ann Neurol 1987;22:753-61.

3 Van der Meche FGA, Schmitz PIM and the DutchGuillain-Barre Study Group. A randomized trialcomparing intravenous immune globulin and plasmaexchange in Guillain-Barre syndrome. N Engl Jf Med1992;326:1123-9.

4 Asbury AK, Cornblath DR. Assessment of current diag-nostic criteria for Guillain-Barre syndrome. Ann Neurol1990;27(suppl):S21-4.

5 Van der Meche FGA, Meulstee J, Kleyweg RP. Currentdiagnostic criteria for Guillain-Barre syndrome. AnnNeurol 1991;30:851-2.

6 Barohn RJ, Kissel JT, Warmolts, Mendell JR. Chronicinflammatory demyelinating polyradiculoneuropathy.Arch Neurol 1989;46:878-84.

7 Albers JW, Kelly J. Acquired inflammatory demyelinatingpolyneuropathies: Clinical and electrodiagnosticfeatures. Muscle Nerve 1989;12:435-51.

8 Bromberg MB. Comparison of electrodiagnostic criteriafor primary demyelination in chronic polyneuropathy.Muscle Nerve 1991;14:968-76.

9 Van der Meche FGA, Meulstee J, Vermeulen M, Kievit A.Patterns of conduction failure in the Guillain-Barresyndrome. Brain 1988;111:405-16.

10 Brown WF. In: Brown WF, Bolton, eds. Clinical electro-myography. 2nd ed. Boston: Butterworth-Heinemann,1993.



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11 Albers JW, Donofrio PD, McGonagle TK. Sequentialelectrodiagnostic abnormalities in acute inflammatorydemyelinating polyradiculoneuropathy. Muscle Nerve1985;8:528-39.

12 Brown WF, Feasby TE. Conduction block and denerva-tion in Guilain-Barre polyneuropathy. Brain 1984;107:219-39.

13 Arnason BGW. Acute inflammatory demyelinatingpolyradiculoneuropathies. In: Dijck PJ, Thomas PK,Lambert EH, Bunge RP, eds. Peripheral neuropathy. Vol 2.3rd ed. Philadelphia: WB Saunders 1993:1437-97.

14 McLeod J. Electrophysiological studies in Guillain-Barresyndrome. Ann Neurol 1981;9:20-7.

15 Asbury AK, Arnason BG, Adams RD. The inflammatorylesion in idiopathic polyneuritis. Medicine 1969;48:173-215.

16 Saida K, Saida T, Brown MJ, Silbergberg DH. In vivodemyelination induced by intraneural injection of anti-galactocerebroside serum. Am Pathol 1979;95:99.

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19 Denny-Brown D, Brenner C. Paralysis of nerve induced bydirect pressure and by toumiquet. Archives of Neurologyand Psychiatry 1944;51: 1-26.

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Migraine

Descriptions of migraine in the literature have provedremarkably elusive. Even where the term has beenused, for example with Mrs Ordyntsev, doubt arises asto the certainty of the diagnosis. Madame Goesler, inPhineas Redux, feigns an attack to avoid an uncom-fortable situation; perhaps a device neurologists shouldrecall when dealing with an intractable case! At leastpresent day sufferers have the consolation of moreeffective remedies than Hoffman's drops.

George Eliott, 1858, Scenes of clerical lifeJust before the appointed hour of eleven, Caterinacame down into the drawing-room, looking so unusu-ally ill as to call forth an anxious inquiry from LadyCheverel, who, on learning that she had a severeheadache insisted that she should not attend service,and at once packed her up comfortably on a sofa nearthe fire, ...

"Well, my dear Miss Sarti, and how do you feelnow?-a little better, I see. I thought you would be, sit-ting quietly here. These headaches, now, are all fromweakness. You must not overexert yourself, and youmust take bitters. I used to have just the same sort ofheadaches when I was your age, and old Dr Samsonused to say to my mother, "Madam, what your daugh-ter suffers from is weakness."

Fedor Dostoyevsky, 1868, The idiotMrs Odyntsev, I was told, had migraine, was running atemperature, and was delirious.

Leo Tolstoy, 1868-9, War and peaceThe countess had a headache brought on by all thenoise and turmoil, and was lying down in the new sit-tingroom with a vinegar compress on her head ...

Natasha ran into the house, and went on tiptoethrough the half-open door into the sitting-roomwhere there was a smell of vinegar and Hoffman'sdrops.

Anthony Trollope, 1874, Phineas ReduxShe almost plotted some scheme of a headache, bywhich she might be enabled not to show herself tillafter dinner. "I am so blind that I can hardly see out ofmy eyes," she said to the maid, actually beginning thescheme.

Saki, 1911, The way to the dairyThey contrived, whenever possible, to excuse them-selves from participation in their aunt's deplored gai-eties; the Brimley Bomefield headaches becamefamous ...

"It's time you went home and had those headachesseen to by a specialist," was her comment on the situa-tion.

Arnold Bennett, 1918, The pretty lady"Do not be vexed. I have my migraine-am good fornothing. But I gave the order that thou shouldst beadmitted. "

Thomas Mann, 1947, Dr FaustusAdrian had not asked for a physician, because hewanted to interpret his sufferings as familiar andhereditary, as merely an acute intensification of hisfather's migraine. It was Frau Schweigestill who at lastinsisted on calling in Dr Kurbis, the Waldshut districtphysician, the same who had once delivered thefraulein from Bayreuth. The good man would not hearof migraine, since the often excessive pains were notone-sided as is the case with migraine but consisted in araging torment in and above both eyes, and moreoverwere considered by the physician to be a secondarysymptom. G D PERKIN

Regional Neurosciences Centre,Charing Cross Hospital,Fulham Palace Road,London W6 8RF, UK

NEUROLOGY IN LITERATURE



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