Cerebral malaria: A diagnostic dilemma

Cerebral Malaria: A Diagnostic Dilemma A Case Report Richard A. Oberfield,

M.D.

AssistantProfessorof Psychiatry,

New York University School of Medicine, New York, New York

Lynn Burkes, M.D. Assistant Professor of Psychiatry, New York University School of Medicine, New York, New York

Simeon S. Feinberg,

M.D.

Resident in Psychiatry, Albert Einstein School of Medicine, New York, New York

Abstract: The following report describes an adolescent patient with falciparum malaria, who was initially seen in a florid psychotic state. Formulation of a diagnosis necessitated differentiation among three diagnostic possibilities: a coincidental functional psychosis, cerebral malaria, or cerebral malaria acting as the precipitating factor for a functional psychosis in a predisposed personality.

has shown a marked resurgence in recent years owing to increased travel to and from areas where malaria continues to be endemic (1). Cerebral malaria, a potentially fatal complication of Plasmodium fulciparum infection, occurs in approximately 2% of such cases (2,3). It is a diffuse encephalopathy for which diagnosis can be fairly well established in a patient with confirmed parasitemia, who displays signs of cerebral dysfunction not explained by hyperpyrexia, anemia, or metabolic abnormalities (4). This cerebral dysfunction can manifest as a wide variety of neurologic and psychiatric signs and symptoms. Differentiation between an acute organic psychosis and a functional psychosis may become problematic. If the psychiatric symptomatology of cerebral malaria is the major presentation of this syndrome, then a mistaken admission to a psychiatric unit may have disastrous results (2). Malaria

Case Report A 16-year-old black female from Uganda was admitted to the pediatric ward of University Hospital, New York, for evaluation of persistent fevers of up to 104°F. General Hospital Psychiatry 3, 227-229, 1981 0 Elsevier North Holland, Inc., 1981 52 Vanderbilt Avenue, New York, NY 10017

The medical diagnosis was malaria, falciparum type. A psychiatric evaluation was requested because the patient demonstrated unusual behavior, including agitation, aggression toward staff, and speaking nonsense. The patient‘s father reported that 18 months prior to admission, she had developed three days of spiking temperatures, malaise, poor appetite, shaking chills, and bizarre behavior. She was taken to a hospital and was given medication-believed to be quinine--for one week. The fever disappeared, but the unusual behavior lasted for two months. The diagnosis was cerebral malaria. Nine months prior to admission, the patient visited the United States and had a medical evaluation at University Hospital. At that time, her physical examination was negative; a thick blood smear was, however, positive for Plasmodium falciparum. An EEG showed intermittent dysfunction involving both cerebral hemispheres, right more than left; and a CAT scan was negative. She was treated in the hospital with chloroquine, 0.5 g daily for three days. Upon discharge to her home in Uganda, the family was instructed to wait three weeks, then to give the patient chloroquine, 0.5 g per week indefinitely, because malaria was endemic there. The patient’s father reported that chloroquine had been unobtainable in Uganda, and seven months prior to the most recent hospital admission, the patient again exhibited bizarre behavior. Although afebrile, she had auditory and visual hallucinations. The family was unable to send her back to the United States for medical attention. Thus, she was untreated, and her symptoms persisted until the time of this report. Past medical history is significant for two episodes of malaria. On both occasions, she received antimalaria drugs. The patient’s father reported that she did not

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display unusual behavior during these episodes. No previous psychiatric history was obtained. On admission to the hospital, the patient had a fever of 104”F, and again demonstrated bizarre behavior. The physical examination was negative and without focal neurological signs. Thick blood smear was positive for Plasmodium falciparum. Electroencephalogram (EEG) and CAT scan were normal. She was treated with chloroquine, 1.5 g during the first 12 hours, then 0.5 g daily for two days; quinine sulfate, 600 mg q.i.d. for two days; and pyrimethamine, 75 mg initially and 25 mg b.i.d. for two days. The medications eradicated the fever, but the bizarre behavior continued. Psychiatric consultation was obtained on the third day of hospitalization. Mental status examination revealed a female adolescent lying in bed who was only intermittently cooperative. The patient called all doctors by the same name and often shut her eyes or stared away in response to questions. Looseness of association was present. Her mood was subdued, with inappropriate affect. She was oriented to place, person, and approximate date, her ability to perform calculations was fair. Her recent memory was poor, and visual hallucinations were present. A Bender Gestalt was administered, which revealed mild organic impairment. The patient responded positively to 100 mg per day of chlorpromazine, which was initiated on the fifth day of hospitalization. This dosage was continued for approximately four weeks, when she was well enough to be transferred to an open psychiatric unit. She continued to receive the chlorpromazine, which was increased to 200 mg per day, and was noted to be quiet, rather asocial, but without unusual behavior. She was referred for neurometric EEG, which was interpreted as consistent with an organic psychosis. By the fifth week of hospitalization, chlorpromazine was discontinued, and the patient was subsequently discharged. Three months after discharge, she was reported to be in stable condition, and returned to Uganda.

Discussion The association between malaria and psychosis has known since the time of Hippocrates (4). Cerebral malaria often manifests as an acute organic psychosis characterized by confusion, disorientation, and intellectual deterioration (2,4,-7). Less frequently, an association between functional psychosis and cerebral malaria has been reported (415,819)* Arieti (4) saw cerebral malaria acting as the precipitating factor in psychosis, for Ihe predisposed individual. Arbuse (8), noted cerebral malaria pabeen

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tients with thought disorders, bizarre behavior “simulating schizophrenia.” Blocker et al. (5) reported on cerebral malarial patients with “apparent” functional psychosis with subtle signs of organic impairment. He emphasized the need for a thorough mental status exam and psychological testing, both of which revealed in his patients an organic basis to the psychiatric symptomatology. Recurrence of the psychosis, as seen in our patient, in association with what was subsequently diagnosed as a recrudescence of the malarial infection-probably due to inadequate previous treatment-has been reported by Arbuse (8). He noted a group of patients with frequent malarial attacks characterized by various combinations of intellectual, attentive, memoq, and emotional disorders. However, the onset of a second psychotic episode significantly prior to obvious malarial symptoms, as in the patient described here, has not been reported. Despite adequate antimalarial and antipsychotic therapy, our patient continued to demonstrate psychotic symptoms. Blocker et al. (5) reported that after antipsychotic therapy, psychotic symptoms resolved within 48 hours. Durrant (10) saw catatonic symptoms in African teenagers with cerebral malaria which also only slowly responded to adequate antimalarial and antipsychotic therapy over approximately two weeks with no further relapses following treatment. To attempt to differentiate the etiology of the psychosis based on the clinical manifestations would seem difficult in light of the various symptomatology reported with cerebral malaria. Blocker reported subtle signs of organic impairment in his patients who, while oriented to person, place, and approximate date, could not recall the names of their physicians, displayed decreased attention span, and a waxing and waning of concentrationall quite similar to the case presented. The continued stable post-hospital course of this patient is more indicative of an acute organic etiology, with a better prognosis than that associated with a functional etiology. The psychological performance of our patient, while actively psychotic, was consistent with an organic basis for the psychosis. We firmly agree with Blocker et al. (5) on the importance of psychological testing as a helpful tool in the diagnostic process. In conclusion, the diagnosis of cerebral malaria should be considered in a psychotic patient with a relevant travel history. If one does entertain this diagnosis, a complete history, physical exam, men-

Cerebral Malaria

tal status, psychological battery, and appropriate laboratory tests should be undertaken.

Acknowledgments We would like to thank Drs..Shirley Stone and Sidney Q. Cohlan of the N.Y.U. Department of Pediatrics for referring this patient for psychiatric consultation.

References Lopez CE, Ruebush TK II, Schultz MC: Occurrence of malaria acquired during travel abroad among American civilians, 1970-1976. J Infect Dis 139:255260, 1979 Marsden I’D, Bruce-Chwatt LJ: Cerebral Malaria. In Hornabrook RW (ed): Topics on Tropical Neurology, Contemporary Neurology Series. Philadelphia, FA Davis Co, 1975, pp 2944 Daroff RB, Deiler J], Kastl AJ, et ai: Cerebrai malaria. JAMA 202:679-682, 1967 Arieti S: Histopathologic changes in cerebral malaria and their relation to psychotic sequels. Arch Neurol Psychiatry 56:79-1&l, 1946

5. Blocker WW, Kastl AJ, Daroff RB: The psychiatric manifestations of cerebral malaria. Am J Psychiatry 12588-92, 1968 Simpson WM, Sagebiel JL: Cerebral malaria. US Naval Med Bull 41:1596-1602, 1943 Fitzhugh T Jr, Pepper DS, Hopkins HU: The cerebral form of malaria. US Army Med 83:3948, 1944 Arbuse DI: Neuropsychiatric Manifestations in Malaria. US Naval Med Bull 45:304-309, 1945 Koranyi EK: Two cases of malaria presenting with psychiatric symptoms. Biol Psychiatry 11445449, 1976 10. Durrant W: Catatonia after malaria. Br Med J 2:893, 1977

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Richard A. Oberfield, M.D. Department of Psychiatry New York University Medical Center 550 First Avenue New York, NY 10016

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