Transient Hemiglossal Denervation during Acute Internal Capsule Infarct in the Setting of Dysarthria−Clumsy Hand Syndrome

Abstract

SUMMARY:A case of MR imagingϪdocumented transient unilateral tongue denervation presenting during acute internal capsule infarction is described. Understanding the corticolingual pathway innervation of the hypoglossal nucleus is essential for explaining these findings. Awareness of the findings in this case will facilitate appropriate diagnosis, provide neuroanatomic explanation, and prevent misdiagnosis.ABBREVIATIONS: DCHS ϭ dysarthriaϪclumsy hand syndrome; TMS ϭ transcranial magnetic stimulation W hile permanent hypoglossal denervation is well known to occur subsequent to lower motor neuron injury, 1 hypoglossal palsy due to supranuclear infarction has rarely been reported. [2][3][4][5][6][7] We report a case of transient reversible hemiglossal denervation edema on MR imaging, contralateral to acute internal capsule infarction in the clinical setting of DCHS. A neuroanatomic basis is discussed. Case ReportA 73-year-old man with chronic hypertension presented with acute dysarthria and right arm weakness. Physical examination also revealed right facial droop and right arm incoordination. The tongue and uvula were midline without fasciculations or atrophy. The clinical diagnosis was DCHS. MR imaging performed at 1.5T revealed a focal area of restricted diffusion at the posterior limb of the left internal capsule, indicating acute infarction (Fig 1A). Additionally, the right hemitongue was markedly diffusely swollen and hyperintense on T2-weighted imaging with right-sided posterior prolapse into the oropharynx (Fig 1B). Fatty atrophy was not identified on T1-weighted images. The brain stem was normal.Repeat MR imaging with gadolinium performed 2 days later to assess possible tongue mass revealed persistence of restricted diffusion in the posterior limb of the left internal capsule but with resolved right hemiglossal swelling and T2 hyperintensity and resolved posterior prolapse (Fig 2). There was no abnormal tongue enhancement or brain stem abnormality.After 1 year, the patient had persistent ataxic right hemiparesis with spasticity. The tongue was midline with spasticity.

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