APIK Journal of Internal Medicine (Jan 2020)

A rare case of movement disorder disease

  • R Madhumathi,
  • G N Devamsh

DOI
https://doi.org/10.4103/AJIM.AJIM_48_19
Journal volume & issue
Vol. 8, no. 2
pp. 85 – 87

Abstract

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Hemifacial spasm (HFS) is a neuromuscular disorder characterized by brief or persistent involuntary tonic or clonic contractions of the muscles innervated by the ipsilateral seventh cranial nerve. It may be idiopathic or secondary to an identifiable cause. It is most frequently attributed to vascular loop compression at the root exit zone of the facial nerve. However, there are several other causes of HFS. Here, we report a case in whom HFS was a presenting feature of central nervous system (CNS) toxoplasmosis. A 53-year-old, known diabetic with retroviral disease on highly active antiretroviral therapy presented with a 6-day history of involuntary, episodic twitching of the left side of his face. There were no associated symptoms. The patient was afebrile, and there was no lymphadenopathy. Examination revealed left HFS. The rest of the neurological examination was normal. Hemogram, liver function test, renal function test, and serum electrolytes were normal. Hepatitis B, C and syphilis serology were negative. CSF showed three lymphocytes, normal protein, and low glucose. Chronic meningitis workup was negative. Magnetic resonance imaging with contrast showed multiple focal ill-defined T2/fluid-attenuated inversion recovery hyperintensities with rim-like enhancement, likely infective. There was no evidence of bony/vascular abnormalities. Toxoplasma serology was positive. The patient recovered with treatment for CNS toxoplasmosis. The prevalence and pathophysiology of HFS have not been widely researched upon. Our patient's HFS was due to CNS toxoplasmosis. Many patients go undiagnosed. Infections such as otitis media, neurocysticercosis, and CNS tuberculosis have been reported to cause HFS. Ours is the first case report attributing CNS toxoplasmosis as the etiology for HFS. The most probable explanation in our case would be irritation/compression of the facial nerve root along its intracranial course due to a focal inflammatory process.

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