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Two papers in this issue of Practical Neurology provide important insights that inform clinical assessment of the tongue.
The first describes lateral deviation on protrusion,1 apparently without any other motor or sensory signs, as a result of a localised cortical infarct. This suggests that although corticobulbar neurones may project bilaterally, there is clinically relevant asymmetry of cortical control, and that a discrete region of the motor cortex projects to the hypoglossal nuclei. These observations confirm earlier work on tongue movement in patients with dysphagia after hemisphere stroke.2
The second case3 is a patient with a low medullary infarction in whom the protruded tongue deviated to the contralateral side, suggesting that the corticolingual fibres can decussate in the lower medulla—almost at the level of the hypoglossal nuclei—rather than higher up in the pons. Therefore, tongue deviation in diseases involving the medulla, usually attributed to involvement of the hypoglossal nucleus or fascicle, could indicate involvement of uncrossed corticobulbar fibres.
Even though tongue deviation seems to be poorly lateralising, and a poor guide to upper or lower motor neurone involvement, these observations are welcome additions to the relatively small knowledge base that helps us interpret signs of lower cranial nerve dysfunction. In common with other bulbar structures, the repertoire of signs in the tongue is limited. In the limbs, we have large areas to inspect, lots of movements to observe, easy purchase for the testing of tone, strength and reflexes, and ready access to two sensory systems, before we even think about function and behavioural …
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