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Limbic encephalitis manifesting as a psychotic disorder

Encefalite límbica expressa como transtorno psicótico

LETTERS TO THE EDITORS

Limbic encephalitis manifesting as a psychotic disorder

Encefalite límbica expressa como transtorno psicótico

Dear Editor,

Several neurological diseases become apparent as a behavioral disorder that may be misunderstood as a primary psychiatric disorder. For instance, a series of degenerative (Huntington's disease), inflammatory (systemic lupus erythematosus), infectious (viral encephalitis, neurosyphilis), and metabolic disorders (porphyria, leukodystrophies) might have psychosis as their initial manifestation.1-3 Herein we report on a case of limbic encephalitis that has been misdiagnosed as a schizophreniform disorder with catatonic features.

A 40-year-old man with a history of psychotic symptoms and behavioral abnormalities for 6 months was referred to our department. According to his relatives, he was completely asymptomatic until the development of progressive behavioral changes. At onset he alternated periods of agitation and aggressiveness with periods of apathy. He also reported auditory and visual hallucinations as well as intense feelings of fear. He had been evaluated by a psychiatrist in the countryside and medicated with haloperidol 5 mg/day. Despite treatment, he evolved with puerility and became very dependent for personal care. He had no previous history of substance abuse, psychiatric or neurological diseases.

His examination revealed a patient with obvious cognitive deficits (Mini-Mental Score Examination: 9/30 - the expected for 4 years of formal education is 25/304), including memory and naming. No psychotic symptom was evident. He presented gegenhalten, generalized hyperreflexia and bilateral Babinski's sign. Abnormal involuntary movements such as grimacing and bruxism were also noticed. Based on his clinical history (one of progressive behavioral and cognitive decline) and physical findings, it was hypothesized that an organic mental disorder was presenting as a psychotic syndrome.

Laboratory work-up, including complete blood count, creatine kinase level, electrolytes, renal, liver and thyroid function tests, serology for syphilis and HIV were unremarkable. Magnetic Resonance (MR) imaging revealed T2-weighted and FLAIR hyperintense lesions in medial temporal lobes and cingulate gyrus, compatible with limbic encephalitis (Figure 1). CSF analysis showed only mild increase in protein level (65 mg/dl; normal value < 45 mg/dl). As the etiological diagnosis was not available and the images on MR could reflect active lesions, he was submitted to guided brain biopsy. The pathological analysis demonstrated gliosis throughout the brain specimen, but no active inflammatory foci or cellular inclusions. These findings were compatible with previous viral encephalitis. On follow-up the patient maintained dependence for personal care, but no recurrence of psychotic symptoms.


This case highlights the relevance of a high level of suspicion and a careful investigation of secondary causes of psychotic disorders. This is particularly relevant in psychosis initiating after the third decade of life. Of note, psychotic symptoms were present while there was an active inflammatory process related to viral infection in limbic structures. Moreover, this may reinforce the current view that the limbic system, especially temporal lobes, may play a role in psychotic phenomena.3,5 It is possible that an early detection by CSF PCR (polymerase chain reaction) analysis and treatment of the viral encephalitis (especially if caused by herpes simplex virus) could prevent the behavioral and cognitive decline of the reported patient.

Antonio Lucio Teixeira, José Augusto Malheiros, José Teotônio de Oliveira

Department of General Medicine, Medical School, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte (MG), Brazil

Rodrigo Nicolato, Humberto Corrêa

Department of Mental Health, Medical School, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte (MG), Brazil

References

1. Cummings JL, Mega MS, eds. Neuropsychiatry and behavioral neuroscience. New York: Oxford University Press; 2003.

2. Teixeira AL, Alvarenga-Silva H. Clínica e terapêutica do primeiro episódio de esquizofrenia. Psiquiatr Biol. 2003;11:91-7.

3. Costa-Silva M, Salgado JV, Teixeira AL. Ideação paranóide após traumatismo crânio-encefálico grave: relato de caso e implicações na fisiopatologia da esquizofrenia. Psiquiatr Biol. 2004;12:45-9.

4. Brucki SM, Nitrini R, Caramelli P, Bertolucci PH, Okamoto IH. Sugestões para o uso do mini-exame do estado mental no Brasil. Arq Neuropsiquiatr. 2003;61(3B):777-81.

5. Freedman R. Schizophrenia. N Engl J Med. 2003;349(18):1738-9.

Financing: None

Conflict of interests: None

Publication Dates

  • Publication in this collection
    26 June 2006
  • Date of issue
    June 2006
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