Pharmacopsychiatry 2000; 33(4): 145-146
DOI: 10.1055/s-2000-11226
Case Report
© Georg Thieme Verlag Stuttgart · New York

A Possible Case of Lithium Intoxication Mimicking Creutzfeld-Jakob Syndrome

M. Slama1 , K. Masmoudi2 , N. Blanchard3 , M. Andréjak4
  • 1Unite de Reanimation, Service de Nephrologique
  • 2Service de Neurologie
  • 3Service de Re¿animation Polyvalente
  • 4et Service de Pharmacologie Clinique
  • Centre Hospitalier Universitaire d'Amiens
Further Information

Publication History

13.07.1998

17.02.2000

Publication Date:
31 December 2000 (online)

The development of coma in a patient with clinical and electroencephalographic signs of Creutzfeldt-Jakob disease generally indicates onset of the terminal phase [1]. In such situations, the physician may question the need for intensive care or maintenance of mechanical ventilation in an intubated patient. We observed a case of completely reversible deep coma requiring intubation and ventilation in a context of lithium toxicity.

A 66-year-old woman with a 13-year history of bipolar disorder, treated with lithium carbonate, was admitted to the intensive care unit in a comatose state preceded, over the previous 11 months, by progressive dementia and Parkinsonian syndrome. Neurological examination revealed temporospatial disorientation, resting tremor of the upper limbs, diffuse myoclonus and generalized hyperreflexia. The onset of deep coma (Glasgow score of 4) and respiratory distress secondary to bronchopulmonary congestion required intubation and mechanical ventilation.

The chemical and hemotological values were normal and serum lithium was 1.3 mM. Lumbar punction, cerebral CT, and MRI were performed and were normal. The EEG revealed a slowed background activity and a generalized periodic activity suggestive of Creutzfeldt-Jakob encephalopathy (Fig. [1]). These features remained unchanged for a fortnight, despite the fact that serum lithium levels were undetectable by the 6th day after admission.

On the 15th day, the patient spontaneously opened her eyes and started to respond to pain. Cerebral CT and MRI were unchanged. She was extubated on the 29th day and discharged on the 32nd day with a Glasgow score of 15, resolution of the extrapyramidal signs, marked improvement of cognitive function and disparition of abnormal EEG activity (Fig. [2]). Seventy eight days after admission, clinical examination was mainly normal apart from memory disorders concerning recent events, temporospatial disorientation and a slight speech disorder.

The first case of lithium-induced Creutzfeldt-Jakob like syndrome was reported by Smith and Koeen [5] and other cases have subsequently been reported [2] [4]. Most of the patients had received short-term or long-term lithium therapy and presented with progressive onset of dementia, myoclonus and Parkinsonian syndrome or even prolonged coma, as in our case. Blood lithium levels were either elevated or within the therapeutic range. The EEG was abnormal, with features suggestive of Creutzfeldt-Jakob disease. The clinical course was slowly favorable, usually with return to normal.

The terminal phase of Creutzfeld-Jakob disease and lithium toxicity cannot be distinguished on the basis of these clinical features or EEG signs or by serum lithium assay (which can even be undetectable, as in our case after 6 days), or by MRI which can be normal in the case of authentic Creutzfeldt-Jakob disease as assessed by Demaerel et al. [3].

This case report, therefore, emphasizes the need to continue treatment and symptomatic intensive care (particularly mechanical ventilation) for a long time in patients with coma and clinical and electroencephalographic signs of Creutzfeldt-Jakob disease and presenting a history of lithium treatment, as complete recovery usually may occur only after several weeks.

References

  • 1 Brown P, Cathala F, Castaigne P, Gajdusek D C. Creutzfeldt-Jakob disease: clinical analysis of a consecutive series of neuropathologically verified cases.  Ann. Neurol.. 1986;  20 259-602
  • 2 Casanova B, de Emtrambasaguas M, Perla C, Gomez-Siurana E, Beneto A, Burguera J A. Lithium-induced Creutzfeldt-Jakob syndrome.  Clinical Neuropharmacol.. 1996;  4 256-259
  • 3 Demaerel P, Baert A L, Vanop den Bosch L, Robberecht W, Dom R. Diffusion-weighted magnetic resonance imaging in Creutzfeldt-Jakob disease.  (letter) Lancet. 1997;  349 847-848
  • 4 Masmoudi K, Rosa A, Canaple S, Andréjak M. Pseudo-Creutzfeldt- Jakob par utilisation au long cours de lithium.  The¿rapie. 1996;  51 688-690
  • 5 Smith S JM, Kocen R S. A Creutzfeldt-Jakob like syndrome due to lithium toxicity.  J. Neurol. Neurosurg. Psychiatry. 1988;  51 120-123

Dr. M. Slama

Unite¿ de Re¿animation Service de Ne¿phrologique Centre Hospitalier Universitaire

Ho^pital Sud

80054 Amiens

Cedex 1

France

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