Clinical features of predominantly sensory stroke due to brainstem infarction

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Abstract

We report 13 patients presenting with predominantly sensory strokes due to brainstem infarction, without any other brainstem symptoms such as hemiparesis, dysarthria or vertigo. All of them had lacunar infarctions localized at the medial lemniscus and/or spinothalamic tract, at the pontine (12 patients) or midbrain (1 patient) tegmentum. The presenting symptom was dysesthesia with a variety of distributions for all cases, and a thalamic-pain-like unpleasant dysesthesia persisted in 4 patients. The lesion on brain MRI was usually very small, and was sometimes overlooked by radiological evaluation, which led to a long delay in the correct diagnosis of a stroke in two cases. Median nerve somatosensory evoked potentials showed a depressed N20 amplitude or a loss of the P15 potential unilaterally with preserved P13/14 potential in 7 out of 10 cases examined, and was useful in localizing the lesion intracranially. During the 4-year study period, 10 patients with brainstem infarctions were admitted to our department as acute sensory stroke cases (2.1% of all acute strokes), whereas 11 patients with thalamic infarctions (2.3%) were admitted due to similar symptoms. Cases with brainstem infarctions had sensory symptoms localized below the neck more frequently (5/10) than cases with thalamic infarctions (1/11), thus would be more likely to be confused with cervical or peripheral nerve disorders. The relative frequency of brainstem infarction as compared to thalamic infarction was higher than that in previous reports, implying that some cases with brain-stem infarction might have been overlooked due to difficulty in obtaining the correct diagnosis. One should always keep this syndrome in mind when assessing patients with acute-onset sensory symptoms.

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APA

Hokkoku, K., Sonoo, M., Murashima, H., Iwanami, T., Nishiyama, K., Kawamura, Y., … Shimizu, T. (2011). Clinical features of predominantly sensory stroke due to brainstem infarction. Clinical Neurology, 51(4), 248–254. https://doi.org/10.5692/clinicalneurol.51.248

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