Visual evoked potentials and pattern electroretinograms in Parkinson\'s disease and control subjects

1243

Letters 2 Al-Ubaidy SS, Nally FF. Adverse reactions to carbamazepine (Tegretol). Br J Oral Surg 1976;13:289-93. 3 Criss WE. Carbamazepine. Ann Intern Med 1973;79:844-7. 4 Simpson JR. Collagen disease due to carbamazepine (Tegretol). Br Med J 1966; 2:1434. 5 Ford JR, Bieder L. Exfoliative dermatitis due to carbamazepine. NZ Med J 1968;68:386-7. 6 Coombes BW. Stevens-Johnson Syndrome

Matters arising Visual evoked potentials and pattern electro-

retinograms in Parkinson's disease and

con-

trol subjects

Sir: We read with interest the report by Nightingale etall on visual evoked potentials (VEPs) and electroretinograms in Parkinson's disease. In that study two checkerboard stimuli, respectively with checks of 25' and 50' angular subtense, over a central field (170 x 140 in size) were presented to 36 patients with idiopathic Parkinson's disease. Inter alia, it was found that "the latency of the P100 and N 150 components were not significantly different between the Parkinson's disease patients and control subjects at either check size". This result contributes to the controversy on the existence of VEP latency abnormalities in Parkinson's disease. In fact, while some authors refer to the occurrence of significantly delayed P100 to sine-wave gratings,2`4 depending on spatial frequency,4 others did not find changes in the latency of checkerboard to generally P100, presentation.5 - 7 Nightingale et al' quoting our suggestion8 that checkerboard might be less effective than grating to identify visual changes due to Parkinson's disease, pointed out that our two stimuli differed not only in pattern form but also in angular subtense and retinal field stimulated. In particular, they argued that under these conditions it would be very difficult to establish whether the two pattern forms have a different diagnostic yield per se.

It should be noted that our goal was to demonstrate that the possibility of obtaining a delayed P100 in a Parkinsonian patient is contingent upon the stimulus employed. We were so aware of the experimental limitations indicated by Nightingale etal' as to state that our data did not "presume to

7 8 9

10

associated with carbamazepine (Tegretol). 11 Fauci AS, Haynes RF, Katz P. The spectrum of vasculitis. Ann Intern Med 1978; Med J Aust 1965;1:895-6. 89:660-76. Mullick FG, McAllister HA, Wager BM, etal. Drug related vasculitis. Hum Pathol 1979; 12 Meckel SE, Jordan RE. Leucocytoclastic vasculitis-a cutaneous expression of 10:313-25. immune complex disease. Arch Dermatol McCoombs RP. Systemic allergic vasculitis. 1982;118:196-201. JAMA 1965;194:1059-64. Cluff LE. Clinical Problems with Drugs. 5th ed. 13 Shalit M, Flugelman MY, Harats N, etal. Quinidine induced vasculitis. Arch Int Med Philadelphia: Saunders Co, 1975:200-1. 1985;145:2051-2. Gammon R. Leucocytoclastic vasculitis. Clin Rheum Dis 1982;8:397-413.

answer the general question as to whether gratings are more effective than checkerboard".8 Accordingly, the effectiveness of the two pattern forms was investigated in a further study9 of which a brief account may be useful here. Checkerboard (with checks of 55' angular subtense) and grating (with a spatial frequency of 2 c/deg) were presented over different retinal areas, that is: (a) central area 100 wide; (b) central area 4° wide; (c) ring area with outer and inner diameters respectively of 100 and 40. The average luminance was identical in all the stimuli, the dark elements presenting a luminance of 0 6 cd/m2 and the light ones 30 cd/m2. Stimuli had no light surround. VEPs were evoked monocularly by pattern reversal at a temporal frequency of 2 Hz. The investigation was carried out in nine patients with Parkinson's syndrome and in nine age matched controls; visual acuity was never less than 20/25. All the Parkinsonian patients were on medication with variable combinations of drugs. Individual latencies of P100 obtained for each stimulus condition were entered into a mixed design of analysis of variance. VEP latencies of Parkinsonians to checkerboard stimuli (55') did not differ from those of controls, although a tendency for the central 4° stimulus to yield a longer latency in the former group was noted. On the contrary, sine-wave grating yielded significantly delayed P100 in Parkinsonians in all the stimulus conditions. In order to assess the incidence of abnormal P100 latencies in Parkinsonian patients as a function of stimulus, the original data9 have been re-examined. Latencies were considered abnormal if they outweighted the cut-off value for each stimulus condition, expressed by the mean + 1-83 times the SD (that is 95% of control population determined by using a one tailed t distribution). Abnormal P100 latencies to checkerboard (55') occurred in one out of 18 eyes (5-5%) with either 100 or 40 stimuli and in no instance with the ring stimulus. Abnormal

P100 latencies to sine-wave grating were found respectively in three eyes (16-7%)

with the 100 stimulus, in nine eyes (50%) with the 40 stimulus and in seven (38-9%) with the ring. Summing up, in Parkinsonian patients the grating has a greater diagnostic yield than checkerboard, no matter what the angular subtense and the retinal projection of the stimulus. However, foveal stimulation seems to be more efficient in identifying the presence of functional damage, irrespective of the stimulus used. We feel that the low sensitivity of checkerboard in identifying visual changes occurring in Parkinson's disease should be considered when evaluating the results obtained by Nightingale et al.' This applies to the 50' element and probably also to 25' element checkerboard, although in this regard, the presence of a significant interaction of retinal field calls for further analysis.9 As to the main problem whether Parkinson's disease is associated with electrophysiological signs of visual disfunction, it should be recalled that in multiple sclerosis the occurrence of VEP changes depend on the pattern employed10 1 so that only the use of different types of stimuli in the same patient enables a satisfactory assessment of visual function. We believe that such approach should be applied also to Parkinson's disease, particularly if one considers that the disorder seems to involve selectively some aspects of visual function, as processing of spatial,4 12 and temporal13 freand foveo-perifoveal quencies relationships.9 This would allow a better understanding of the visual impairment in Parkinsonians. ANTONIO TARTAGLIONE ANGELO ONETO FABIO BANDINI EMILIO FAVALE

Clinica Neurologica dell'Universitti, Via A de Toni, S 16132 Genova, Italy

1244 References

Matters arising Catatonia secondary to acute Chagas' test seemed attributable to immunoencephalitis suppressive treatment. Since catatonia is often caused by an Sir: We have read the contribution by MP underlying brain disease,5 every effort Barnes, etalt with great interest. It empha- should be made to exclude an organic lesion. sises the need to view catatonia as merely a A brain biopsy may be the only means of symptom and not a disease, and that full diagnosing a life-threatening condition. neurological investigation is warranted to GUSTAVO SEVLEVER disclose any organic brain lesion. Our recent ANA HiA TARATUTO M CAROLINA DE LAS CARRERAS experience with a patient suffering from Chagas' (American trypanosomiasis) ROMON LEIGUARDA MARTIN NOGUtS encephalitis presenting with catatonia, Instituto de Investigationes Neurologicas, encouraged us to report our findings. This 25 year old man acutely developed Dr Raul Carrea, abnormal behaviour and intermittent fever Ayaoucho 2166, six months after renal transplantation. He 1112 Buenos Aires, Argentina had been treated with cyclosporin and methylprednisolone. When the psychiatric References symptoms developed, he was on mainte- I Barnes MP, Saunders M, Walls TJ, Saunders I,

I Nightingale S, Mitchell KW, Howe JW. Visual evoked potentials and pattern electroretinograms in Parkinson's disease and control subjects. J Neurol Neurosurg Psychiatry 1986;49:1280-7. 2 Bodis-Wollner I, Yahr MD. Measurement of visual evoked potentials in Parkinson's disease. Brain 1978;101:661-71. 3 Kupersmith MJ, Shakin E, Siegel IM, Lieberman A. Visual system abnormalities in patients with Parkinson's disease. Arch Neurol 1982;39:284-6. 4 Onofrj M, Ghilardi MF, Basciani M, Gambi D. Visual evoked potentials in Parkinsonism and dopamine blockade reveal a stimulusdependent dopamine function in humans. J Neurol Neurosurg Psychiatry 1986;49: 1150-9. 5 Hansch EC, Syndulko K, Cohen SN, Goldberg ZI, Potvin AR, Tourtellotte WW. Cognition in Parkinson's disease: an event related nance doses of both drugs and his renal potential perspective. Ann Neurol 1982;11: function was normal. At age 12 years, he had been seen by a psychiatrist because of 559-607. 6 Halliday AM. The visual evoked potential in social withdrawal and a diagnosis of schizthe investigation of chiasmal and retro- oid personality was made. On admission, he chiasmal lesions and field defects. In: Hall- lay motionless and mute with an expressioniday AM, ed. Evoked Potentials in Clinical less face; he would reply occasionally and Testing. Edinburgh: Churchill Livingstone, appropriately in monosyllabels when ques1982:235-82. maina 7 Dinner DS, Luders H, Hanson M, Lesser RP, tioned. He also had d catalepsy and Klem G. Pattern evoked potentials (PEPs) in tamned astereotyped posture. There were no Parkinson's disease. Neurology 1985;10: abnormalities on neurological examination, except for reduced muscle tone. Initially, 610-3. 8 Tartaglione A, Pizio N, Bino G, Spadavecchia symptoms were attributd to a psychiatric L, Favale E. VEP changes in Parkinson's cause. An EEG showed diffuse slowing. disease are stimulus dependent. J Neurol CSF was clear, with a protein content of Neurosurg Psychiatry 1984;47:305-7. 1-2 g/l and no cells. The complement fixation 9 Tartaglione A, Pizio N, Bo I, Spadavecchia L, achado Guerreiro) test for f Chagas' dis(M Favale E. Spatial properties of pattern as as determinants of visual evoked potential ease was negative. A CT scan was normal. There was of conprogressive clouding changes in Parkinson's syndrome. In: Morocutti C, Rizzo PA, eds. Evoked Poten- sciousness, leading to stupor and coma tials. Neurophysiological and clinical aspects. within two weeks. A frontal brain biopsy Amsterdam: Elsevier Science Publisher BV showed necrotic parenchymal tissue with (Biomedical Division), 1985:321-7. macrophages full of amastigotes positive for 10 Camisa J, Mylin LH, Bodis-Wollner I. The specific Trypanosoma cruzi antiserum effect of stimulus orientation on the visual (Stermberger's PAP Technique), and a few evoked potential in multiple sclerosis. Ann lymphocytes as well as reactive peripheral Neurol 1981;10:532-9. 11 Tartaglione A, Oneto A, Bandini F, Spa- astrocytes. Despite treatment with Nifdavecchia L, Gandolfo E, Favale E. Electro- urtimox (15 mg/kg/day), there was no physiological detection of "silent" plaques in improvement and he died one month after the optic pathways. Acta Neurol Scand 1987 onset of catatonia. (in press). To the best of our knowledge, this is the 12 Bodis-Wollner 1, Mitra S, Bobak P, Guillory S, first report of catatonia induced by Chagas' Mylin L. Low frequency distorsion in disease, and we suggest that it should be spatio-temporal threshold surface in Parkin- included in the list of neurological infections son's disease. Invest Ophtalmol Vis Sci liable to cause catatonia. Chagas' encepha1984;25:3 13. 13 Marx M, Bodis-Wollner I, Bobak P, Harnois litis causes an acute non-suppurative C, Mylin L, Yahr M. Temporal frequency- encephalomyelitis,2 with small inflamdependent VEP changes in Parkinson's matory foci spread uniformly in the white disease. Vision Res 1986;26:185-93. and grey matter. Acute Chagas' disease is mainly restricted to children, but can occur in immunodeficient adults due to contaminated blood transfusion.34 In our

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(Machwad

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3 Leiguarda

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AL. American trypanosomiasis

(Chagas' disease). Acute CNS involvement in

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1978;150:294. 4 Jost L, Turin M, Etchegoyen F, Leiguarda RC, Taratuto AL, lotti R. Meningoencefalitis chagisica en pacientes con tratamiento inmunosupresor por transplante renal. Rev Neurol Argent 1977;3:425-8. 5 Strub RL. Mental disorders in brain disease. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of Clinical Neurology, Vol 46.

Amsterdam: North Holland, 1985:413-41.

Behavioural manifestations of third ventricular colloid cysts

Sir: Dr Arnold Goran, a Diplomate of the American Board of Neurological Surgery, recently referred me to the section entitled "Matters Arising" in the April 1986 issue of J Neurol, Neurosurg Psychiatry. In Dr Winer's reply to Dr Backlund, he makes the statement "unfortunately, in the United States there is difficulty finding a neurosurgical centre which performs CT guided biopsy." patient, the negative complement fixation I would like to strongly disagree with Dr