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BMJ Case Reports logoLink to BMJ Case Reports
. 2016 Jun 16;2016:bcr2016215676. doi: 10.1136/bcr-2016-215676

Reversible movement disorders due to toxoplasmosis as initial manifestation of HIV-AIDS, with sequential MR and video imaging

Antonio Jose Reyes 1, Kanterpersad Ramcharan 2,3, Samuel Aboh 4, Nathaniel Duke 4
PMCID: PMC4932380  PMID: 27312857

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

Dosage Period of treatment
Intravenous drug
 Trimethoprim–sulfamethoxazole 160 mg/800 mg 3 times a day 14 days
 Fluconazole 300 mg 2 times a day 5 days
 Aqueous crystalline penicillin 4 million units every 4 hours 10 days
 Acyclovir 800 mg 3 times a day 14
 Haloperidol 5 mg 3 times a day 6 days
Intramuscular drug
 Dexamethasone 16 mg stat followed by 8 mg 3 times a day for 3 days and 4 mg 3 times a day for 3 days 7 days
Oral drug
 Lopinavir–ritonavir 200/50 mg per tablet
2 tablets 2 times a day
4 months
 Tenofovir disoproxil-emtricitabine 245/200 mg per tablet
1 tablet daily
4 months
 Paracetamol 500 mg 3 times a day 6 days
 Pantoprazole 40 mg 2 times a day 6 days
 Azithromycin 500 mg daily for 1 week followed by 1 g weekly 4 months
 Trimethoprim–sulfamethoxazole 80 mg/400 mg per tablet
2 tablets 2 times a day
4 months
 Fluconazole 150 mg daily 4 months
 Carbamazepine 200 mg 2 times a day 6 days
 Phenytoin 100 mg 3 times a day 4 months

Table 2.

Medical investigations

Blood test Result Reference range
White cell count 18.4×109/L 4.5–11.0×109/L
Venereal disease research laboratory on admission Reactive Non-reactive or reactive
Fluorescent Treponema pallidum antibody absorption on admission. Positive Positive or negative
Elisa for HIV Reactive Non-reactive or reactive
Western blot test for HIV Positive Positive or negative
HIV viral load on admission 217 839 RNA copies/mL 20–10 000 000 copies/mL
HIV viral load 1-month after admission 48 477 RNA copies/mL 20–10 000 000 copies/mL
CD4+ T cell count on admission 3 cells/µL 410–1590 cells/µL
CD4+ T cell count 4 months after admission 121 cells/µL 410–1590 cells/µL
Antistreptolysin O titer 26 IU/mL 0–200 IU/mL
T. gondii IgG antibodies on admission 3.63 Positive: >1.09
T. gondii IgM antibodies on admission 0.23 Negative: <0.55
T. gondii IgG antibodies 4 months after admission >250 Positive: >1.09
T. gondii IgM antibodies 4 months after admission 0.0 Negative: <0.55
Herpes virus 1 IgG antibodies 5.00 Index positive: >1.10
Herpes virus 1 IgM antibodies <0.9 Index negative: <0.9
Herpes virus 2 IgG antibodies 1.30 Index positive: >1.10
Herpes virus 2 IgM antibodies <0.9 Index negative: <0.9
Other tests
CSF test (lumbar puncture performed on day 3rd after admission)
 Opening CSF pressure 12 cm of H2O 6–25 cm of water
 Cell count Nil 0–5 cells/mm3
 Protein 28.3 mg/dL 5–40 mg/dL
 Glucose 60 mg/dL 50–80 mg/dL
 Culture No bacterial growth No bacterial growth or bacterial growth
 Cytology Negative for neoplastic cells Negative or positive for neoplastic cells
 India ink for Cryptococcus neoformans Negative Positive of negative
 VDRL No reactive Non-reactive or reactive
 FTA-ABS Negative Positive or negative
 PCR for herpes virus, Cytomegalovirus, Epstein-Barr virus, Enterovirus, Parvovirus, Lymphocytic choriomeningitis virus and T. gondii Tests not obtained Negative or positive
Scalp EEG Normal Normal or abnormal
Brain/leptomeningeal biopsy Consent was declined

CSF, cerebrospinal fluid; FTA-ABS, Fluorescent Treponema pallidum antibody absorption; T. gondii, Toxoplasma gondii; VDRL, Venereal Disease Research Laboratory test.

Figure 1.

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.

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.

Figure 1.

Figure 1

Contined

Video 1.

Download video file (9.7MB, mp4)
DOI: 10.1136/bcr-2016-215676.video01

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.

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.

References

  • 1.Medow MA, Lucey CR. A qualitative approach to Bayes’ theorem. Evid Based Med 2011;16:163–7. 10.1136/ebm-2011-0007 [DOI] [PubMed] [Google Scholar]
  • 2.Tse W, Cersosimo MG, Gracies JM et al. Movement disorders and AIDS: a review. Parkinsonism Relat Disord 2004;10:323–34. 10.1016/j.parkreldis.2004.03.001 [DOI] [PubMed] [Google Scholar]
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