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. 2016 May 9;2(2):89-92.
doi: 10.1515/jccm-2016-0009. eCollection 2016 Apr.

Parkinsonian Syndrome and Toxoplasmic Encephalitis

Anca-Adriana Arbune  1 , Manuela Arbune  2 , Victorita Stefanescu  2
Affiliations

Parkinsonian Syndrome and Toxoplasmic Encephalitis

Anca-Adriana Arbune et al. J Crit Care Med (Targu Mures). .

Abstract

Toxoplasmosis encephalitis in patients with human immunodeficiency virus may progress rapidly with a potentially fatal outcome. Less common neurological symptoms associated with this are Parkinsonism, focal dystonia, rubral tremor and hemichorea-hemiballismus syndrome. A 58 year old woman suddenly lost consciousness and was admitted to the emergency service. Her medical history was unremarkable, except for frequent headaches in the last year, recurrent herpes simplex skin lesions and an episode of urticaria. A computer tomography scan showed supra and infra-tentorial lesions on suggestive of cerebral toxoplasmosis. Both Toxoplasma gondii and HIV tests were positive. In the intensive care unit, antiparasitic and antiretroviral drugs were administered, and she recovered from the coma after six weeks but presented with tetraparesis, diplopia, and depression. The LCD4 count increased from 7 to 128/mm3. The neurological lesions slowly resolved over the next two months, although postural instability, rigidity, bradykinesia and predominantly left side tremor persisted. Mild improvement was achieved after the administration of levodopa. Associated Parkinsonian syndrome in HIV patients is a rare condition, explained by the location of the brain and basal ganglia lesions, and by the observed effect of Toxoplasma gondii which increases dopamine metabolism in neural cells. Early HIV diagnostic and treatment are necessary to prevent neurological disability.

Keywords: AIDS; dopamine; parkinsonism; toxoplasmosis.

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Conflict of interest statement

Conflict of interest: Nothing to declare

Figures

Fig. 1
Fig. 1
Native cerebral MRI axial T2 section (A, C, E), FLAIR (B, D, F) at the same comparison level. There are identified multiple small round lesions hyper dense in T2 (liquid), inhomogeneous FLAIR signal (determined by haemorrhages or calcifications), situated supra and infra-tentorial, cortical, sub-cortical and in the basal ganglia, predominantly on the left side.
Fig. 2
Fig. 2
Native sagittal T1 section (A), post contrast T1 (B), exhibit small lesions in the frontal region, with discrete peripheral contrast enhancement (“bullseye” images) and homogeneous cerebellar enhancement.
Fig. 3
Fig. 3
Axial FLAIR section (A), post-contrast T1 (B), with reduced lesions after enhancement.
See this image and copyright information in PMC

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