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Reversible movement disorders due to toxoplasmosis as initial manifestation of HIV-AIDS, with sequential MR and video imaging
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  1. Antonio Jose Reyes1,
  2. Kanterpersad Ramcharan2,3,
  3. Samuel Aboh4,
  4. Nathaniel Duke4
  1. 1Neurology Unit, Department of Medicine, San Fernando Teaching Hospital, San Fernando, Trinidad and Tobago
  2. 2Department of Medicine, San Fernando Teaching Hospital, San Fernando, Trinidad and Tobago
  3. 3Department of Medicine, Surgi-Med Clinic, San Fernando, Trinidad and Tobago
  4. 4Infectious Disease Unit/Medicine, San Fernando Teaching Hospital, San Fernando, Trinidad and Tobago
  1. Correspondence to Dr Kanterpersad Ramcharan, kramcharan79{at}yahoo.com

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Description

A previously well 22-year-old African man had cognitive decline for 1 month and involuntary movements for 10 days. Video in segment 1 showed right-sided choreoathetosis. Segment 2, day 6, after 5 days of treatment (table 1) demonstrated less choreoathetosis and brief dystonia of the right foot. Segment 3, on day 10 exhibited normality. The patient scored 5/30 on the Mini Mental State Examination (MMSE). Investigations showed HIV-AIDS associated with secondary syphilis and also a third condition, central nervous system (CNS) toxoplasmosis (table 2). MRI scan of the brain showed cystic and solid areas with hyperintensities and perilesional oedema in some areas on T2-weighted and fluid-attenuated inversion recovery sequences and low signal on T1-weighted imaging in the right parietal-temporal lobes and in the frontal regions, basal ganglia and thalamus bilaterally. The cystic lesions also demonstrated restricted diffusion on diffusion-weighted imaging/apparent diffusion coefficient-weighted images (figure 1A–D). Empirical antibiotic and antiretroviral treatment was, by the use of qualitative Bayesian probability, a necessity since consent for brain biopsy was declined.1 On highly active antiretroviral therapy, intravenous penicillin for the spirochate syphilis and the antiprotozoal drug, oral trimethoprim–sulfamethoxazole for cerebral toxoplasmosis, the patient gradually improved over the next 4 months, when the MMSE improved to 30/30 and the patient became fully ambulant. Repeat MRI (figure 2A–D), HIV viral load and CD4+ T cell count performed 12 weeks after treatment showed improvement. A significant fourfold rise in serum toxoplasmosis IgG confirmed cerebral toxoplasmosis (table 2).

Table 1

Medical treatment

Table 2

Medical investigations

Figure 1

(A) Axial T2-weighted fluid-attenuated inversion recovery MRI view with multiple abnormal hyperintense signals in basal ganglia and thalamus bilaterally, frontal regions and right parietal and temporal lobes suggestive of central nervous system (CNS) toxoplasmosis, but HIV encephalopathy and/or CNS lymphoma could not be ruled out. Some lesions showed mild perilesional oedema. (B) Axial diffusion-weighted imaging with restricted diffusion of the cystic lesions involving both cerebral hemispheres. (C) Axial T1-weighted MRI view with low signals located in basal ganglia and thalamus bilaterally, and in frontal regions and right parietal-temporal lobes. (D) Axial MRI apparent diffusion coefficient (ADC) map with reduced ADC values, which confirms restricted diffusion in the cystic lesions.

Figure 2

(A) Axial T2-weighted fluid-attenuated inversion recovery MRI view with significant improvement of abnormal hyperintense signals and oedema throughout. Small abnormal hyperintense signals remain in basal ganglia bilaterally, and in frontal regions and right parietal-temporal lobes. (B) Axial diffusion-weighted imaging with restricted diffusion of the cystic lesions involving both cerebral hemispheres with significant improvement. (C) Axial T1-weighted MRI view with low signals located in basal ganglia and thalamus bilaterally, and in frontal regions, and right parietal and temporal lobes, with significant improvement. (D) Axial MRI apparent diffusion coefficient (ADC) map with reduced ADC values, which confirms restricted diffusion in the significantly decreased number of cystic lesions.

Video 1

Segment 1 showed right-sided choreoathetosis;Segment 2, day 6, after 5 days of treatment (table 1) demonstrated less choreoathetosis and brief dystonia of the right foot; Segment 3, on day 10 exhibited normality.

Damage to the thalamus, subthalamic areas, caudate and/or putamen nucleus and globus pallidus has been postulated as the pathogenic mechanism in movement disorders associated with HIV-AIDS.

To the best of our knowledge, serial imaging demonstrating movement disorders in a patient with HIV-AIDS of new onset, with positive serology for syphilis and confirmed CNS toxoplasmosis, has not been reported previously.2 ,3

Learning points

  • HIV-AIDS related multiple neuropathology is a documented cause of abnormal movement disorders.

  • Damage to the thalamus, subthalamic areas, caudate and/or putamen nucleus, and globus pallidus has been postulated as the pathogenic mechanism in movement disorders associated with HIV-AIDS.

  • Constrained by the demand of patients for non-invasiveness, or due to unavailability of tests, aggressive empirical antibiotic and antiretroviral therapy is, by the use of Bayesian probability, a practical necessity that can prevent death and disability among patients with HIV-AIDS-related multiple neuropathology.

Acknowledgments

The authors would like to thank Dr Fidel Rampersad for assistance with the radiological aspects, Dr Shane Karim for preparation of the video and Ms Sharon Sealy for preparation of the images.

References

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Footnotes

  • Contributors AJR conceived the idea of this case report. All the authors contributed equally to preparation of the manuscript and approved the final contents.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.