Transient Unilateral Catalepsy and Right Parietal Damage

The Japanese Journal of Psychiatry and Neurology, Vol. 47, No. 3, 1993

Transient Unilateral Catalepsy and Right Parietal Damage Toshio Fukutake, M.D., Keizo Hirayama, M.D. and Takayuki Komatsu, M.D. Department of Neurology, Chiba University School of Medicine, Chiba

Abstract: We describe the appearance of transient catalepsy of the left upper extremity in a patient without previous psychiatric illness after a right parietal subcortical hemorrhage. This case, and five other available cases in the relevant literature, demonstrates that catalepsy can be produced by right parietal damage. Key Words: catalepsy, catatonia, parietal lobe, neglect Jpn J Psychiatr Neurol47: 647-650, 1993

INTRODUCTION Catatonia is generally considered to be a subtype of schizophrenia and yet many other neurological, as well as psychiatric, diseases can give rise to symptoms of catatonia, which have been called the catatonic syndrome.2 Catalepsy, a tendency to maintain postures induced by the examiner, is well known as the most specific and dramatic motor manifestation of the catatonic syndrome. Current research on the mechanisms of catalepsy has been limited, primarily, to pharmacological studies in animal preparations, and little is known about the cerebral localization of the responsible lesion in humans. The reasons for such uncertainty include the fact that the anatomical localization of idiopathic psychiatric disorders in general has remained problematical and, in patients with the secondary catatonic syndrome, the organic lesion is often found to be bilateral or diffuse. NeverReceived for publication on Nov. 25, 1992. Mailing address: Toshio Fukutake, M.D., Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260, Japan.

theless, various authors have argued that the catatonic syndrome or catalepsy may appear with focal lesions.' We describe a patient without previous psychiatric illness who developed the catatonic syndrome, notably cataleptic posturing conlined to the left upper extremity, after a right parietal subcortical hemorrhage. CASE REPORT

A 67-year-old, right-handed man was admitted to our hospital because of mild left hemiparesis. Three days prior to admission, he experienced difficulty in grasping a cup with his left hand and, on going to the toilet on the following morning, fell and struck his forehead on the left side. He had no history of psychiatric disease or exposure to neuroleptic agents. A general physical examination on admission was unremarkable. A neurological examination revealed mild confusion, disorientation to time, left lower homonymous quadrant hemianopia, and mild left hemiparesis (4/5). Tendon reflexes were within the normal range but a right plantar response

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was extensor. Left-sided proprioceptive sensations were impaired; abnormalities were seen in the “thumb localizing tesP3, one of the examination techniques of proprioception, whereas superficial sensations were intact all over the body. There was tactile extinction on the left side of the body. Slight muscle rigidity of all the four extremities and mild bradykinesia were noted. Coordination was intact. No grasp or avoiding reaction was noted. Neuropsychological testing disclosed left hemispatial neglect, constructional impairment, difficulty in dressing, dyscalculia and optic ataxia. No abnormalities were seen

in tests for aphasia, agraphia, alexia, hypergraphia, unilateral anosognosia and hemisomatognosia. Cataleptic posturing was noted in the left upper extremity (Fig. 1). After completing the thumb localizing test or other examiners’ positioning, the patient maintained the last posture produced by the examiner for up to 10 minutes. Neither his right arm nor either leg showed such abnormality. Catalepsy persisted for about 12 hours and, the following morning, could not be elicited. Psychiatrically, he was notably agitated on admission and after several days had psychotic hallucinations, somatosensory or visual, disturbance of the diurnal cycle, and jealous delusions. Thereafter he gradually became less agitated. An acute computed tomographic scan revealed a fresh hemorrhage in the superior parietal subcortical region, and bilateral linear low attenuation areas, indicating old vascular lesions4, in the putamen (Fig. 2). DISCUSSION

Fig. 1: Cataleptic posturing of the left upper extremity on admission. After completing the “thumb localizing test,” the patient maintained the last posture produced by the examiner for up to 10 minutes.

Our patient’s catalepsy, confusion, agitation, hallucinations, and delusions seem sufficient for the diagnosis of the catatonic syndrome.’ Two aspects of his presentation are unique: (1) the unilaterality of cataleptic posturing and ( 2 ) the direct association with a well-documented unilateral parietal lesion, although the old putaminal lesions might be involved in the emergence of part of his manifestations. The catatonic syndrome or catalepsy is not characteristic of parietal lobe disease, probably because these are not generally localized symptoms, or because these may occur in the acute stage and be easily overlooked. We have found five other reported cases of the catatonic syndrome caused by lesions involving parietal lobes.6 lo Details of these cases, along with our own, are shown in Table 1. Cerebral lesions of these cases were unilateral in three patients and bilateral in the other

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Catalepsy and Right Parietal Damage

Fig. 2 : Computed tomographic scans obtained on the day of admission, showing fresh subcortical hemorrhage in the right superior parietal region and bilateral linear low attenuation areas in the putamen.

Table 1 : Clinical Data from Six Patients No. of Patients Ref. 1

2 3

Age/

Lesion

sex Location

Type

[ l l ] 58/M Rt P-T Subdural ? and Lt hematoma 0 [lo] 45/M Rt & Infarction Body Lt P [6] 47/F Rt P - 0 HemorLimbs rhage

4

[6] 58/F Rt P - 0 Hemorrhage

5

[81

6

75/M Rt P-0-T

psychotic Lt Impaired Muscle spatial PropriSymptom Neglect oception Tone

ConsciousSite

Course transient

Relatively unclouded

persist

Confusion

transient

Lt arm transient

Infarction L t > R t arm > 1% present 67/M Rt P HemorLt arm case and Blt rhage Old Put CVA

neSS

transient

transient

+

Hallucination

Mutism Negativism Lethargic Agitation, Delusion Hallucination Obey simple Agitation, command Delusion Hallucination Difficulty Inappropriwith com- ate cheerprehensions fulness Confusion Excitation, Delusion Hallucination ~

rigid

hypertone

+

+

+

+

+

+

~

hypertone rigid

~~

P: parietal lobe, 0:occipital lobe, T: temporal lobe, Put: putamen, Rt: right, Lt: left, Blt: bilateral, CVA: cerebrovascular accident

three; all six had a lesion in the right parietal lobe in common, with variable lesions in the temporal and/or occipital lobe on the same side, in the parietal or occipital lobe on the

other side, or in the bilateral putamens. The precise location of the lesion in patient No. 1 was somewhat uncertain, but was a subdural hematoma. In the other five patients, the

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lesion was hemorrhage or infarction in the parietal lobe. Catalepsy was found transiently for a short period following the strokes or convulsions in all except patient No. 2, in whom maintaining an unusual body posture persisted for a longer period at the chronic stage. In patients Nos. 4 and 6, the cataleptic posturing was seen only in the left upper extremity and patient No. 5 had an asymmetric feature, with perseveration of posture more prominent in the left-sided extremities contralateral to the cerebral lesion. Associated clinical manifestations included deficits of consciousness or comprehension, and mental state changes in all, constructional apraxia in four (patients Nos. 3-6), left hemispatial neglect in three (patients Nos. 4-6), and proprioceptive impairment in four (patients Nos. 1 and 4-6). Muscle rigidity was found in two (patients Nos. l and 6) and increased muscle tone was noted in two (patients Nos. 3 and

5). These cases demonstrate that catalepsy, usually asymmetric, can be produced by right parietal damage. Patient No. 3, with damage in the right hemisphere, had bilateral catalepsy, and patients Nos. 4-6 had left hemispatial neglect and left or left-dominant catalepsy. These facts support the view that left hemispatial neglect is produced by a lesion of the right hemisphere since it dominates the process of spatial perception and sensory attention.’ Catalepsy could be similarly explained. REFERENCES 1. Fisher, C.M.: “Catatonia” due to disulfiram toxicity. Arch Neurol 46:798-804, 1989.

2. Gelenberg, A.G.: The catatonic syndrome. Lancet 1: 1339-1341, 1976. 3. Hirayama, K., Fukutake, T. and Kawamura, M.: Thumb localizing test; examination for disturbance of articular localization. Clin Neurol (Tokyo) 26: 448-454, 1986 (in Japanese). 4. Jellinger, K.: (Exogenous) strial necrosis. In: Vinken, P.J., Bruyn, G.W., Klawans, H.L. (Eds.), Handbook of Clinical Neurology, Volume 49. North Holland, Amsterdam, pp 499-518, 1986. 5. Joseph, A.B.: Catatonia. In: Joseph, A.B., Young, R.R. (Ms.), Movement Disorders in Neurology and Neuropsychiatry. Blackwell Scientific Publications, Boston, pp 335-342, 1992. 6. Levine, N. and Finklestein, S.: Delayed psychosis after right temporoparietal stroke or trauma: relation to epilepsy. Neurology (Ny) 32: 267-273, 1982. 7. Mesulam, M.-M.: Attention, confusional states, and neglect. In: Mesulam, M.-M. (Ed.), Principle of Behavioral Neurology. F.A. Davis Co. Publishers, Philadelphia, pp 125-168, 1985. 8. Saver, J.L., Greenstein, P., Ronthal, M. and Mesulam, M.-M.: Asymmetric catalepsy after right hemisphere stroke. Mov Disord 8: 6973, 1993. 9. Strub, R.L.: Mental disorders in brain disease. In: Vinken, P.J., Bruyn, G.W. and Klawans, H.L. (Eds.), Handbook of Clinical Neurology, Volume 46. North-Holland, Amsterdam, pp 413-441, 1985. 10. Tippin, J. and Dunner, F.J.: Biparietal infarction in a patient with catatonia. Am J Psychiatry 138: 13861387, 1981. 11. Woods, S.W.: Catatonia in a patient with subdural hematomas. Am J Psychiatry 137: 983-984, 1990.