127

4. Jankovic J, Glaze DG, Frost JD (1984) Effect of tetrabenazine on tics and sleep of Gilles de la Tourette's syndrome. Neurology 34: 688-692

5. Login IS, Cronin MJ, McLeod RM (1982) Tetrabenazine has pro- perties of a dopamine receptor antagonist. Ann Neurol 12: 257- 262

6. Munetz MR, Slawsky RC, Neil JF (1985) Tardive Tourette's syn- drome with clonidine and mesoridazine. Psychosomatics 26 : 254- 257

7. Sacks OW (1982) Acquired Tourettism in adult life. In: Friedhoff A J, Chase TN (eds) Gilles de la Tourette syndrome. Raven Press, New York, pp 89-92

8. Seeman MV, Patel J, Pyke J (1981) Tardive dyskinesia with Tou- rette-like syndrome. J Clin Psychiatry 42 : 357-358

9. Sutula T, Hobbs WR (1983) Senile-onset vocal and motor tics. Arch Neurol 40 : 825-826

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Received July 14, 1987 / Accepted July 16, 1987

Visual hemineglect as cause of impaired contralateral visually guided eye movements

A. Ferbert

Abteilung Neurologie, Klinische Anstalten der RWTH, Pauwelsstrasse, D-5100 Aachen, Federal Republic of Germany

Sirs: It is well established that parieto-occipital lesions may lead to impaired smooth ocular pursuit movements as well as to a disturbance of the slow phase of the optokinetic nystag- mus towards the affected side. These phenomena are present in right as well as in left hemispheric lesions [1, 4, 8]. Insuffi- cient data are available on a possible hemispheric asymmetry of these functions.

Recently, Bogousslavsky [2] reported a patient with a parieto-occipital glioblastoma of the right hemisphere who showed, in addition to the above-mentioned findings, im- paired eye movements to the contralateral side. Whereas vol- untary saccades to the left (independent of a visual stimulus) were normal, visually guided saccades were slow and perform- ed with successive hypometric steps. Smooth pursuit move- ments to the left are not mentioned in the text, but as seen in Fig. 1 D they were almost as impaired as those to the right.

These interesting findings are interpreted by the author as indicating a generation of contralateral visually guided sac- cades in the parieto-occipital region. However, an alternative explanation appears more likely. The patient had no visual field defect, but "there was left-sided visual extinction on simultaneous bilateral visual stimulation". This is clearly a sign suggesting visual neglect in the left hemifield. "Staircase like" eye movements towards the neglected field instead of

smooth pursuit or visually guided saccades have been reported in the literature [3, 5]. Most of these patients had, in addition, hemianopia. However, as hemianopia itself does not cause disturbance of smooth pursuit, optokinetic nystagmus or sac- caddes [5], the impairment of eye movements towards the contralateral side must be attributed to visual hemineglect.

Hemineglect should not reduce the velocity of the saccadic eye movements, as was indeed described in this case. How- ever, this phenomenon might have been the consequence of the low amplitude of the saccades to the left.

One might argue that visual hemineglect was not present in this patient because voluntary saccades were normal towards both sides. However, neglect does not necessarily involve all functions. There may be visual neglect without motor neglect. Saccades, by themselves, may be unimpaired, whereas the vis- ual information for planning saccades may be deficient be- cause of unilateral neglect.

Even in visually guided saccades, visual input is only one of at least two parameters for computing direction and amplitude of saccadic eye movements, the other being eye position [6]. Disturbed processing of the visual input and intact common efferent pathways for saccadic eye movements provide a more likely explanation in this case than two different efferent path- ways, one for voluntary and one for visually guided saccades, the latter being impaired.

Finally, most neuropsychological research is done in pa- tients with stable lesions, several weeks or longer after stroke. Patients with a malignant brain tumour and extensive hemi- spheric oedema are, in my view, ill suited for the demonstra- tion of a relationship between distinct neurological signs and a distinct localization of lesion.

Has this been a case of neglect of the neglect?

References

1. Baloh RW, Yee RD, Honrubia Y (1980) Optokinetic nystagmus and parietal lobe lesions. Ann Neurol 7: 269-276

2. Bogousslavsky J (1987) Impairment of visually evoked eye move- ments with a unilateral parieto-occipital lesion. J Neurol 234: 160- 162

3. Girotti F, Casazza M, Musicco M, Avanzini G (1983) Oculomotor disorders in cortical lesions in man: the role of unilateral neglect. Neuropsychologia 21 : 543-553

4. Lynch JC, McLaren JW (1983) Optokinetic nystagmus deficits fol- lowing parieto-occipital cortex lesions in monkeys. Exp Brain Res 49 : 125-130

5. Meienberg O, Harrer M, Wehren C (1986) Oculographic diagnosis of hemineglect in patients with homonymous hemianopia. J Neurol 233 : 97-101

6. Schiller PH, Sandell JH (1983) Interactions between visually and electrically elicited saccades before and after superior colliculus and frontal eye field ablations in the rhesus monkey. Exp Brain Res 49 : 381-392

7. Sharpe JA, Deck JHN (1978) Destruction of the internal sagittal stratum and normal smooth pursuit. Ann Neurol 4 : 437-476

8. Troost BT, Daroff RB, Weber RB, Dell'Osso LF (1972) Hemi- spheric control of eye movements. II. Quantitative analysis of smooth pursuit in a hemispherectomy patient. Arch Neurol 27: 449-452

Received July 20, 1987 / Accepted July 27, 1987