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Published on: April 18, 2011
Acute hypokinetic-rigid syndrome following SARS-CoV-2 infection
Antonio Méndez-Guerrero1, María Isabel Laespada-García2, Adolfo Gómez-Grande2
1From the Departments of Neurology (A.M.-G., M.I.L.-G., M.R.-O., V.A.B.-P., F.J.Z.-D., P.R.-S, C.P.d.F.-F.d.l.H., J.G.d.l.A.), Nuclear Medicine (A.G.-G., D.V.P.), Anesthesiology (E.A.-T., R.R.-M.), Microbiology (A.P.-Z.), Pneumology (J.S.C.), and Neuroradiology (A.R.-G.), Hospital Universitario 12 de Octubre, Madrid, Spain. mendezguerrero.antonio@gmail.com.
Objective:
To report a case of a patient infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) who acutely developed a hypokinetic-rigid syndrome.
Methods:
Patient data were obtained from medical records from the Hospital Universitario 12 de Octubre in Madrid, Spain. [123I]-ioflupane dopamine transporter (DaT) SPECT images were acquired 4 hours after a single dose of 185 MBq of 123I-FP-CIT. Quantitative analysis was performed with DaTQUANT software providing the specific binding ratio and z score values of the striatum.
Results:
We report a previously healthy 58-year-old man who developed hyposmia, generalized myoclonus, fluctuating and transient changes in level of consciousness, opsoclonus, and an asymmetric hypokinetic-rigid syndrome with ocular abnormalities after a severe SARS-CoV-2 infection. DaT-SPECT confirmed a bilateral decrease in presynaptic dopamine uptake asymmetrically involving both putamina. Significant improvement in the parkinsonian symptoms was observed without any specific treatment.
Conclusion:
This case study provides clinical and functional neuroimaging evidence to support that SARS-CoV-2 can gain access to the CNS, affecting midbrain structures and leading to neurologic signs and symptoms.
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