Movement Disorders Vol. 10, No. 6 , 1995,. pp. 794-802 0 1995 Movement Disorder Society Communications in each parietal lobe, the larger one on the left side (Fig. 2). The electroencephalogram (done during dystonia) showed a few random left focal temporal sharp waves. He refused an ocular and masseter electromyogram study. Brainstem auditory evoked responses (BAEP) at 90 dB and blink reflex (BR) R1 responses were normal and comparable on both sides, but the R2 responses were delayed and of very low amplitude on both sides. During his admission to the hospital, he had a right partial motor seizure (tonic-clonic) affecting the right upper and lower limbs without loss of consciousness. He was treated with sodium valproate 1,200 mg/day orally, which he discontinued after 2 weeks. He had no further seizures but continued to have episodic BS and JCD for another month, after which these symptoms remitted spontaneously. He was seen again 5 months later and still remains free of the BS and JCD. He still has a residual right upper limb weakness, MRC grade 4/5. Blepharospasm and Jaw Closing Dystonia After Parietal Infarcts To the Editor: The association of blepharospasm (BS) and oromandibular dystonia has been termed Meige’s syndrome and usually no other pathology is detected in the nervous system. Rarely, it has been described in association with structural lesions. These structural lesions have been bilateral basal ganglion infarcts (1) and rostra1 midbrain lesions (2). We report a patient who developed blepharospasm and jaw-closing dystonia (JCD) after parietal lobe infarction. Case Report A 43-year-old Omani male patient (heavy cigarette smoker) was well until 1 year previously, when he developed sudden numbness of the right hand that recovered during 2 h. Two days later he developed weakness of the right side of the body that improved during 6 weeks’ time with mild residual weakness of the right hand. Three weeks before admission, he felt increasing weakness of his right hand along with inability to open the mouth. While the weakness of the right hand improved, the inability to open the mouth persisted and fluctuated in severity. When severe, he was not able to ingest food or speak. He also had episodic inability to open his eyes, often increased by bright light. Swallowing was normal. His past history included an episode of confused behavior, with automatisms and convulsions, 20 years previously (suggestive of complex partial seizures). He was detected to have diabetes mellitus since 1986 and was being treated with glibenclamide 5 mg daily. He also had a squint since birth. Examination revealed normal higher mental functions and cranial nerves (except for congenital concomitant strabismus of the right eye). He had bilateral BS involving the orbital part of the orbicularis oculi with lowering of the eyebrows and Bell’s sign on forcible opening of the eyelids by the examiner (Fig. 1). He also had JCD with trismus, inability to open the mouth, and deviation ofjaw to the right; the masseters and temporalis on both sides were in sustained contraction as ascertained on palpation (Fig. 1). The BS was intermittent but even at times when he did not have overt BS, eye opening was difficult after closure. There was MRC grade 315 distal weakness in the right upper limb and tendon reflexes were exaggerated on the right side. There was no other neurological deficit. The hemogram, blood chemistry, and serum lipids were normal. Tests for syphilis and antinuclear antibodies were negative. The electrocardiogram, chest radiograph, and echocardiogram were normal. Ultrasonogram of the carotids showed mild intimal thickening. The computed tomography (CT) scan of the brain showed small infarcts Discussion This patient had clinical features of repeated left cerebral cortical infarction and CT scan evidence of infarcts in FIG. 1. Closeup of the patient’s face showing corrugator spasm. The jaw is tightly closed and pushed to one side. 794 COMMUNICATIONS 795 Legend to the Videotape Segment 1. The patient has difficulty opening his eyes, which is believed due to orbicularis oculi spasm. Masticatory spasms are also depicted. Segment 2. The patient is free of muscle spasms 5 months later. P. C. Jacob R. Pratap Chand Department of Medicine (Neurology) College of Medicine Sultan Qaboos University Muscat, Sultanate of Oman References FIG. 2. A computed tomography scan shows hypodense nonenhancing lesions (infarcts) in both parietal lobes. both parietal lobes. He had diabetes mellitus and smoking as risk factors and extensive investigations did not reveal any other cause of repeated infarcts in this young man. In the present case the BS and JCD appeared soon after the cerebral infarct and as the patient was improving from the second episode of hemiplegia. This temporal sequence is similar to other movement disorders such as hemichorea or ballism that occur after cerebral infarction ( 3 ) . It is interesting to note that the patient improved spontaneously and completely from the BS and JCD. The BAEP and BR R1 responses do not show evidence of a brainstem lesion. However, a brainstem lesion could not be completely excluded because we could not do a magnetic resonance scan. Such R2 abnormalities as seen in our patient have been described by others in hemispheric strokes; the R2 abnormalities have occurred most consistently with lesions of the inferior postcentral gyms and are postulated to be due to interruption of specific descending facilitatory pathways from the above cortical area (4). A variety of eyelid movement disorders such as ptosis, motor impersistence, apraxia, and reflex BS have been attributed to unilateral and bilateral cerebral hemispheric lesions (5). Possible mechanisms postulated (but not clearly proved) for the focal dystonias in these patients include “denervation supersensitivity” or disinhibition of cranial nerve nuclei due to supranuclear lesions. Such mechanisms may be operative in the present case. However, BS with oromandibular dystonia in association with parietal infarcts has not been reported. The parietal lobe has extensive connections with the putamen. It is possible that just as rostra1 brainstem lesions with damage to substantia nigra can produce BS, rarely cortical lesions can also produce it. Acknowledgment:We thank Mrs. Rose P. Natividad for typing the manuscript. 1 . Keane JR, Young JA. Blepharospasm with bilateral basal ganglia infarction. Arch Neurof 1985;42:1206-1208. 2. Jankovic J, Patel SC. Blepharospasm associated with brainstem lesions. Neurology 1983;33:1237-1240. 3. Burke RE, Fahn S, Gold AP. Delayed onset dystonia in patients with “static” encephalopathy. J Neurol Neurosurg Psychiutry 1980;43:789-797. 4. Kimura J , Wilkinson JT, Damasio H. Blink reflex in patient with hemispheric cerebrovascular accident (CVA). J Neurol Sci 1985;67:15. 5 . Nutt JG. Lid abnormalities secondary to cerebral hemisphere lesions. Ann Neurol 1977;1:149-151. Zotepine in Levodopa-Induced Psychosis To the Editor: Because clozapine exhibits virtually no adverse motor side effects (l), it has become the most important drug in the treatment of levodopa-induced psychosis in Parkinson’s disease (PD) ( 2 , 3 ) . However, clozapine can cause severe agranulocytosis, even with fatal outcome in some cases (4). Consequently, it is of practical importance to develop equivalent drugs not bearing this risk. Zotepine is a new neuroleptic drug with only minor motor side effects. Like clozapine it is a tricyclic compound with a central heptacyclic ring. It binds to Dl-, Dz-, 5-HT,-, 5-HT2-,a,-adrenergic, and cholinergic receptors (9,with relatively high DJD, and 5-HT2/Dzratios (6). In clinical studies (7,8) of acute and chronic schizophrenic patients, zotepine was shown to have an efficacy comparable to that of haloperidol. In contrast to haloperidol, which causes motor side effects in -50% of patients, zotepine leads to motor side effects in only 10%. It might therefore be a promising alternative to clozapine for therapy for levodopa-induced psychosis in PD. We treated five patients with PD who were subsequently admitted to our hospital for levodopa-induced psychosis with this new drug. Case 1 A 59-year-old male patient (disease duration 6 years, Hoehn and Yahr stage 111) was admitted with paranoid hallucinations while taking 550 mg levodopa, 200 mg amantadine, 10 mg selegiline, and 4.5 mg of cabergoline daily. There was a good initial response to 50 mg zotepine Movement Disorders, Vol. 10, No. 6 , 1995