F. C. DE BEER*
INTRODUCTION CSF-examination in patients with migraine generally is a non-contributory and therefore futile gesture, both during and outside the attacks. Early authors agreed that CSF-pressure is quite often increased during an attack and that a spinal tap may bring relief,lV7 but that the CSF-composition, in particular protein- and cell-content, is only most exceptionally abnormal.7-s Accordingly, unless specific diagnostic or scientific considerations require its execution (which e.g., may obtain in cases of complicated, invariably same-sided, migraine) the procedure is not warranted. Even in this restricted category of patients and also during their attacks, the reported yield of abnormal findings is meagre (and, at that, transient) in spite of the multitude of patients examined. i”-ls Interestingly, Wolffs casei developed during one of her attacks Weber’s brainstem-syndrome (oculomotor deficit on the right, and hemiparesis on the left side); without knowing this, Whiteho~se and Bleecker reported another instance of migrainous Weber-syndrome,2~ All this constitutes solid evidence, that the association of migraine with abnormal CSFcomposition essentially is not a mutally causal one. This, of course, leaves hors de COPZCOU~S the perfectly feasible instance of the precipitation of (a) migraine attack(s) in a (n5~-)migraineur by a lesion or pathological process that, simultaneously, gives rise to CSF-abnormalities. The assertion, viz. that compositional CSF-changes
1984. Vol. 86-l.
A critical analysis ispresented of the problem whether the migraine attack causes CSFpleocytosis or vice versa, on the basis of a series of 3 cases, including one of Tolosa-Hunt syndrome due to sarcoidosis, the other two ultimately showing chronic leptomenin~tis. The evidence leads to the conclusion that migraine does not cause pleocytosis and pleocytosis does no& cause migraine: both are common correlated by an underlying denominafor. Key words: Migraine, Tolosa-Hunt syndrome chronic sarcoidosis, pleocytosis, CSF meningitis.
should cause migraine-attacks, seems scarcely tenable in view of the untold cases of meningitis, and subarachnoid haemorrhage with severe headache, nausea and vomiting, but without migraine~atta~ks. An individual constitutionally predisposed to react to various adverse stimuli with migraine-attacks (such an individual being denoted as a migraineur) is of course also liable to develop migraine-attacks when leptomeningeal irritative lesions are present. The increase of CSF protein per se is, within wide limits, a result rather than a source eo
of irritation. In spite of these considerations, the flurry of, mostly anecdotal, reports that have recently appeared on complicated migraine and CSF-
Year of Ref. publino. cation
M F M
1954 1960 1960 1962 1963
7 24 25 9 35
CSF pressure mmH,O
46 52 39
+ + +
h.c h h
22 IX 30 42 42
+ + + +?
b h (Fam.) Weber sy. 0
Weber sy. h(Fam.) -_ h
290 I60 _
M F M
M M F F M
I6 I7 I7 27 35
_ _ _ -
h.c act act act h
70 II0 270 210 290 210 _ 200 230 200
F M 1981
F 1982 1982 1982
21 23 I7
F M M
38 33 21
+ _ +
h h ac
_ 240 140 N _ _
Table I. Summary of reports on complicated migraine and CSF pleocytosis (MN: mononuclear cells. lymphocytes; PN: polymorphonuclear cells. o. ophthalmoplegic migraine; h: hemiplegic migraine; f: facioplegic migraine: b: basilar migraine: c: confusion: act: migraine accompagnee. migr: history of migraine).
pleocytosis21-32 (see Table 1) apparently implies a resurrection of the dilemma formulated in this paper’s stubtitle. The recent reports constitute sufficient impetus to reconsider the 34
Cells per mm3
Died I month later; men. tuberc Angioma mesenceph. bilat. infarction int. caps.
IXS(PN) 50 45 35
lO(PN) qMN) 49(.MN) 74tPN) 4 5
F M F M F F F F
Protein mg/ 100 ml.
51 I65 86 85 80 70 65 _ 40 54 30 41 _ I20 95 30 217 II8 II0 87 90 56 184 I65 88 IO1 I5 II2 II0 32 81 I I6
70 44 II8
N _ _ _
Hemangioma IVth ventricle also invol. mov. and ataxia
also char. atheto-dystonic.
28(MN) 197(PN) 40(MN) 300 54(MN) 272(PN) 18(MN) I8 20 30 350( MN) 85(MN) 155(MN) 37(MN) 73(MN) 23O(MN) 90(MN) 50(MN) 50(MN) 188(MN) 8(MN) 2OO(MN) 96(MN) 24(MN) 17(MN) 96(MN) 193(MN) 32 histiocY’ 8(PN) 8’XMN) 8(MN) 27(MIV)
Died by respiratory
questions whether CSF-changes are caused by the migraine-attack, or vice versa, or whether both epiphenomena are caused by a (viral) The unwary physician meningoencephalitis. might, by these reports, be incorrectly induced to accept, that migraine in certain patients may produce CSF pleocytosis. The cases presented below are intended as a contribution to the clarification of the matter.
I .92 1.62
3.12.75 1.3.76 5.7.76 19.1.77 25.3.78 24.5.78 25.6.78 7.8.78 19.2.79 30.8.79 20.3.80 23.9.8 1 22.10.82
107 75 73 155 74 102 75 40 77 77 47 90 71
1.50 1.24 1.78 I .69 1.61 1.64 1.56 1.15 1.29 1.08 1.26 1.35 1.08
‘able 2 CSF findings
1.04 0.95 1.00 0.34 0.54 0.68
0.303 0.33 0.308 0.156 0.232 0.306 t
0.291 0.351 0.3 0.464 0.4 0.464 0.402
1.24 2.18 1.21 1.29 0.88 1.13
2 bands I band >20 bands
in case I.
CASE PRESENTATION l.Male, born April 1928. This sales-manager, without medical antecedents, started to develop infrequent attacks of throbbing headache, localised at the vertex (L > R), and associated with bilateral paraesthesiae and numbness of the hands and tongue, inability to speak, nausea, and right-sided hemianopia, at the age of 47. Occasionally, the neurological spectrum included a gait-disturbance or a dreamy state. The attacks lasted from 2 to 12 hours; the neurological symptoms +: 30 min. The 45 year-old patient never had migraine-attacks before; migraine does not occur in the family. The repetition of the attacks (2 to 3 per year) induced him to seek advice at the out-patient departments of neurology and internal medicine. With the exception of cryptorchidism, physical examination was unremarkable, as were X-rays of skull and thorax, EEG, EMG, EKG, and intelligence (I.Q. 135). One thing was found to be abnormal and remained so: the CSF (see Table 2) repeatedly showing increased protein and pleocytosis (“chronic meningitis”). Three years later, in 1978 the patient was admitted because he developed a left frontoparietal infarction (with coma, right hemiparesis including a central facial nerve paresis, expressive aphasia and agraphia, and bilateral extensor plantars) during one of his daily swims. The coma cleared in 3 days, the
hemiplegia improved moderately over the course of 1% years. The CT-scan revealed the infarction (Fig. lA/B); four-vessel angiography only yielded a hypoplastic left vertebral artery. Cardiovascular check-up remained unremarkable. Ophthalmologist: no vasculitis. The diagnosis was assumed to be chronic lymphocytic meningitis e cau~a ignota, with cerebral infarction, presumably due to arteritis, and symptomatic migraine accompagnee attacks. An extensive programme was carried out to detect the cause, in particular tuberculosis, sarcoidosis, syphilis, SLE, panarteritis nodosa, viral, and fungal disease, and lastly malignancy or autoimmune disease. Routine blood- and urinanalysis, minerals, lipid-spectrum, liver- and kidney functions, bone-marrow, radionuclide liver/spleen scan, Rose/Latex, cold agglutinins, cryoglobulins, paraproteins, Australia-antigen, Ziehl-Nielsen, Paul-Bunnell, Anti Nuclear Factor, 5 nucleotidase, V-GT, and PPD were negative, with constant exceptions: 1) a raised SLDH (particularly subfractions 2 and 3) 2) hypophosphataemia, and 3) a slight tendency to eosinophilia. Extensive tests (and cultures) for toxoplasma, cryptococcus neoformans, listeria monocytogenes, psittacosis, LCM, CMV, HVH, HSV A and B, various enterovirus, mycoses and fungi, TBC and syphilis remained negative. Following discharge, regular check-up at the out-patient department learned that the attacks changed their character slightly in that the 35
Fig. I 8 Pat. no. I. 197X. Infarction left frontal area Contrast-enhanced CT f:ig. i b Patient no. I, 1978. The frontal infarct extends over the main area supplied hj rhc middle cerebral artery. On the right side old small infarction in the posterior frontal area off the island of Rril. Non-contrast enhanced CT. Fig. I c Pat. no. I, 1978. Middle cerebral artery M, segment calcification on the left side. Non-contrast-enhanced CT. Fig. i d Patient no. 1. 197X Bilateral middfe cerebral artery Mi calcification. Fig. I E Patient no 1. 1982. Coronal CT cut revealing bilateral M, calcification predominant on the left side and ballooning left ventricle t;nrophy).
Fig. 2 A. Patient no. 1; 1979 Isoelectric focussing of CSF (left side) and serum (right side). Nine oligoclonal bands are to be noted, of which two are marked. 2. B. Enlargement of 2A. + other extra bands are faintly outlined.
Patient no. 1; i982. Fig. 2 C. Isoelectric focussing of CSF and serum two years later. Just over 30 bands can be distinguished and the alkaline IgG-domain. 2 D. Enlargement of alkaline IgG-domain. At least 15 extra-bands are discernable as compared with serum IgG.
hemianopic scotoma (always on the right side) now was associated invariably with left-sided (!) cheirooral paraesthesia. The attack-frequency remained 2 to 3 per year. The CSF- and blood abnormalities remained constant over the years. In 1979, two marked and seven slight extra (oligoclonal) IgG bands in the CSF were noted (Fig. 2A and B). CT-scans obtained in 1980 and 1982 revealed calcification of both M 1 segments of the middle cerebral arteries, a phenomenon overlooked on the 1978 CT-scan (Fig. lC, D). In 1980, during clinical observation in another neurological University department, the following serological virus-tests were negative: influenza A + B, parainfhienza I-III, adenovirus, rickettsioses, psittacosis, m. pneumoniae, polio I-III, LCM, measles, parotitis epidemica, CMV, HS, varicella; also negative were the direct Coombs test antigen, and the cultures (serum, CSF, nose-secretion,
feces) for mycoses, yeasts, virus, and bacteria. A clinical check-up in September 1982 revealed: 1) the same CSF hyperproteinorrhachia, 2) enormous intrathecal IgG-synthesis (see Figs. 2C and D), 3) unchanged lymphocytic pleocytosis with atypical lymphocytes in all forms, plasma-cells, and stemcells, 4) unchanged increased SLDH (high subfraction 2), 5) unchanged MI(Fig. lE), and 6) hypophosphataemia. Negative were: liver-biopsy, jejunalbiopsy (to exlude Whipple-disease), musclefascia biopsy (to exclude panarteritis and other collagen diseases). Serum C, (105 mg%) was normal, C, (32 mg%) slightly raised, A.C.E., lysozyme and RAST-asp. score were normal, as were T3, T4, 25OH vit. D,, lipids, ANF and Latex-Rose tests. Visual evoked potentials showed asymmetry at the expense of the rightside, as did the cornea1 reflexes. The DVI-examination revealed patent 37
Fig. 3. Tolosa-Hunt syndrome. Occlusion of superior orbital vein on the left side, dilatation of homologous \ein on the right.
carotids, vertebrals, and medial cerebral arteries, the latter showing a better flow on the left (!) side than on the right. 2. Male, born 16th February 1935. Sydenham’s chorea at the age of 12. In 1969 injury compression fracture with L1; examination otherwise normal, including CSF with exception of a raised total protein of 61 mg/dl. In 1970, the patient started to develop attacks of severe headache, nausea and vomiting on the left-side lasting about 1 week, and followed by either third or sixth nerve palsies which resolved in 3 to 5 weeks’ time. These episodes occurred 4 times in 1970, 1971. 1973. 1974 resp. and were associated with unilateral and exophthalmos of I-4 mm. (Hertel) occasionally complete ptosis. CSF protein was consistently raised over these years with slight pleocytosis. Serological reactions negative. The diagnosis was posed (elsewhere) of migraine ophtalmopl~gique. Because of the proptosis and CSF-changes the possibility of an intraorbital tumor was analysed, with negative results. Orbital phlebography confirmed the cells/mm”
years later. Still
no drainage of Ich superior
diagnosis, already to be suspected on the basis of the history-data, of Toiosa-Huni .s,yndrome (see Fig. 3-4). No attacks occurred between early 1975 and early 1977. In April 1977 a right-sided attack of retroorbital/temporal pain occurred for 3 days followed by n.Vl palsy lasting weeks. In February, March and November 1978 three attacks lasted 3 weeks each, the first associated with n.Vl palsy on the right. the second and the third on the left side. A third admission to hospital revealed relative lymphocytosis, marked CSF-changes (see Table 3), tendency to anaemia, low serum glucose and serum 1~~globulins. Extensive investigations on viral and microbial origin remained repeatedly negative; rheuma-factors. ANF. Bence-Jones protein, parietal-cell antibodies, muscle and liver biopsies, pentagastrin test and benzidine-reaction were negative. no porphobilinogin or aminolevulinic acid folic acid normal. changes; transketolase, Serum Complement C3 92 mg%, C4 18 mg%, CHSO 263 pg/nl, Clq: 1098, haptoglob. 32 mg%, fibrinogen 580 mg’%. Serum Lysozyme y glob
75 44 24 6
Mo MCI MO Ly/Mo
1.68 1.37 I .46 I.1 I
1979 1980 Table 3 CSF
Fig. 4. Two
(whital vein upon the cavcrnouy \lnu\ but ;)~a\ !‘rcm II it~~rd the sphenoparictal Gnu\.
in case 2.
increased (146%, 162%), slightly was angiotensin converting enzyme (ACE) slightly decreased (24 resp. 22 nmol/nl). Marrowreticular suspected revealed biopsies malignancy, class V. The Kveim-test was weakly positive. The diagnosis was posed of sarcoidosis. Hypopituitarism was shown to be ophthalmoplegia-attacks Painful present. recurred twice in 1979 (n. VI R, n. III L) and twice in 1980 (n. III L). Since then headacheattacks were less severe and no oculomotor nerve palsies were noted to be associated with them; over the last 3 years the patient’s hypopituitarism is substituted by corticosteroid, testosterone and thyroidhormone therapy. 3. Man, born 27th July 1923. Previous medical history unremarkable with exception of mild migrainous attacks since the age of 36. Sister is migraineuse. Mid November 1965 he developed fairly acutely a sensation of stiffness and numbness in the right foot ascending to involve the right body-half and arm with difficulty of speech, nausea and vomiting, lasting % hr. and therefore clearly not epileptic. Two days later attack of right-sided teichopsia, photo/phopulsatile headache, nophobia, nausea and vomitus. This migraine attack recurred 6 times over the next 20 days, without sensory or motor defect. Examination at the outpatient department revealed bilateral papilloedema with a fine haemorrhage in OS at 14.00 o’clock. The left plantar reflex tended to be extensor. EEG: right temporal abnormal activity with bilateral symmetrical theta and delta activity. X-sinus: sinusitis maxillaris frontalis. ENT consultant: usual treatment. Upon admission, carotid angiography revealed slow circulation with patent arterial and venous systems. Radionuelide scanning and ventriculography were normal. Basal ~iste~ography failed to reveal the right olfactory cistern. Mid December another attack of numbness in the right foot and arm occurred followed by a headache attack as described above. Routine laboratory examination, including liver/kidney functions, electrolytes, serumproteins, ketosteroid excretion, PBI and Wassermann, and benzidinetests, was negative, with the exception of ESR 11135 mm, and a relative lymphocytosis of 40%.
Extensive tests and cultures for T.B.C., mycoplasma, toxoplasmosis, listeria, cryptococcus, various virus remained negative. The CSF composition was as follows (Table 4). pressure mmH,O 29.12 6.1 10.I 12.1 21.1 25.1 2.3 6.3
250 250 360 270 210
Protein g/l 0.25* 0.65 0.65 0.25* 0.65 0.65 0.45 0.40
cells/mm’ 48 160 53 48 129 84 15 11
* ventricular fluid Table 4 CSF findings in case 3.
Follow-up (out-patient department) over the next year (1966) revealed slow resolution of the papiloedema, first of the left and then of the right eye with macula-degeneration, slight personality-changes, and only one ~jgrai~e-attach. The follow-up was discontinued in 1968. A check-up in 1982 taught that the patient has remained well since 1968 without further migraine attacks. Conclusion: a man with late onset migraine, with exacerbation of a meningitis, probably sympathetic due to sinusitis, with longlasting papilloedema. No further symptoms during the next 17 years. DISCUSSION In case 1 a non-migraineur started to have sporadic attacks of migraine accompagnee unusually late (age 45). Examination revealed a chronic leptomeningitis e causa ignota, low blood phosphorus and raised SLDH (especially subfraction 2) between age 47 and 56. He developed an infarction in the distribution area of the left cerebral medial artery. Since age 51 he showed progressive intrathecal IgG synthesis with many oligoclonal bands. Extensive clinical analysis for an infective agent or systemic disease failed to detect the cause. Both medial cerebral M, segments developed calcification but the vessels remained patent. The chronic leptomeningitis continues to be present at the moment of writing, i.e. at least 8 years. The meningitis apparently being produced by a chronic vascular auto-immune process, can not 39
be interpreted as a cause for the sporadic migraine attacks. Neither can the sporadic migraine attacks be interpreted as causative for the constant, even progressive CSF-changes. Rather, both chronic lepto-meningitis and sporadic migraine attacks seem to be produced by the substratum of an as yet unidentified pathological process. Case-history # 2 is, to our awareness the first in which a classic, though rather belatedly diagnosed, Tolosa-Hunt syndrome was shown to be caused by intracranial (cavernous sinus) sarcoidosis. This case also showed chronic leptomeningitis over a period of nearly a decade, and the headache attacks were initially erroneously diagnosed as ophthalmoplegic migraine. The CSF changes remained unchanged irrespective of the presence of the attacks. Both tended to normalize upon steroid therapy. The same line of reasoning as applied in case # 1 obtains here: the CSF-changes are clearly not caused by the Tolosa-Hunt phenomenology, nor is, inversely, the latter syndrome caused by the CSF changes, but both are produced or precipitated by the underlying sarcoidosis, involving the anterior cavernous sinus. The third case history exemplifies the exacerbation of the latent migrainous predisposition of a middle-aged man by a 3 (sympathetic) months’ lasting lymphocytic meningitis with raised CSF-pressure and symptomatic migraine accompagnee. This case too allows no other rational interpretation than has been given above. As an additional argument one may consider the clinical fact, that in most cases of improving purulent meningitis or subarachnoid haemorrhage, the headache disappears completely in spite of the presence of still hundreds of cells per cubic millimeter CSF. As argued elsewhere33*34 the migraine attack itself can be elicited by an impressive gamut of heterogeneous exogenous and endogenous factors. Once triggered, it shows a conspicuously stereotyped chain of events. The more the constitution of the patient seems to predominate in the ultimate build-up and precipitation of a migraine-attack, the less (specific) significance the attack-precipitating endo- or exogenous factor will have. In fact, such a person usually is inclined to produce 40
migraine-attacks without apparent “cause”. In such a case, one poses the diagnosis of migraine as a disease and one denotes the person as a migraineur or migraineuse. Usually. one uncovers evidence of hereditary predisposition for migraine in the family of such a person. Usually, the disease manifests as early as childhood or adolescence. Contrariwise, if the exogenous factors do not seem to be pluriform and non-specific, but rather monoform, one is likely to surmise a specific (metabolic) derangement to produce the migraine attack. This applies e.g. in persons who react with a migraine attack to the ingestion of chocolate, sherry or the contraceptive pill. In such individuals the migraine is mostly not complicated. In yet other instances the attacks are “complicated”, manifest fairly late or are phenomenologically unusual. Such attacks must be regarded as symptomatic of e.g. an a.v. angioma, an aneurysm, microembolic mitral-valve prolapse, a brain tumour or abscess, cerebral vasculitis, SLE, or, as has been argued above by means of three examples, a chronic (viral?, auto-immune?) meningitis. In such persons the constitutional inclination to reach with migraine attacks to adverse stimuli is present (as in every human individual), but only slightly. In ophthalmoplegic migraine and painful ophthalmoplegia (Tolosa-Hunt) the causal determinant is so often a structural, recognisable lesion, that one may make a strong case of the thesis that ophthalmoplegic migraine does not inherently belong to the constitutionallv determined disease called “migraine”. The cases recently reported in the American literature, were, almost without exception nonmigrainous. Their migraine-attacks were limited to the period in which they showed CSF pleocytosis. They had a negative family history for migraine and were therefore without a marked constitutional predisposition for it. Some, but not all of recent authors infer, rightly so, that the migraine is symptomatic of a benign intracranial inflammatory process. Finally, the recently reported anecdotal evidence consisted of short-term observations. The case reported in this paper have been followed-up for periods ranging from 8 up to 18 years. On the basis of the clinical examples
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