• W Muellbacher, C Artner, and B Mamoli.
• Ludwig Boltzmann Institute for Epilepsy and Neuromuscular Disorders, Second Department of Neurology, Neurological Hospital of Vienna, Austria.
• J. Neurol. Neurosurg. Psychiatr. 1998 Nov 1; 65 (5): 755-61.

ObjectivesThe occurrence of a lingual paralysis after unilateral upper motor neuron lesions is an infrequent clinical phenomenon, and the underlying pathophysiological mechanisms are poorly understood. We studied the cortical motor representations of ipsilateral and contralateral lingual muscles in healthy controls and in a selected group of stroke patients, to clarify the variable occurrence of a lingual paralysis after recent monohemispheric ischaemia.MethodsA special bipolar surface electrode was used to record the ipsilateral and contralateral compound muscle action potentials (CMAPs) from the lingual muscles after transcranial magnetic stimulation (TMS) of the human motor cortex and peripheral electrical stimulation (PES) of the hypoglossal nerve medial to the angle of the jaw. Four patients with a lingual paralysis (group 1) and four patients with symmetric lingual movements (group 2) after monohemispheric first ever stroke were studied and compared with 40 healthy controls.ResultsIn controls, TMS of either hemisphere invariably produces CAMPs in the ipsilateral and contralateral lingual muscles, elicited through crossed and uncrossed central motor pathways, respectively. In the 40 healthy controls, TMS of either hemisphere elicited CMAPs of significantly greater amplitudes and shorter onset latencies from the contralateral muscles compared with the ipsilateral responses (p<0.0001). In the patient groups, TMS of the affected hemisphere failed to evoke any CMAP from either lingual side; TMS of the unsevered hemisphere always produced normal ipsilateral and contralateral responses, irrespective of whether the ipsilateral muscles were paralysed or not.ConclusionsBilateral crossed and uncrossed corticonuclear projections are invariably existent in humans. After unilateral interruption of these pathways, some people do exhibit a lingual paralysis whereas others do not. The development of a central lingual paralysis is most likely dependent on the ability of the unsevered hemisphere to utilise the pre-existent uncrossed motor projections. The variable availability of these pathways among individual subjects is in good agreement with the inconstant occurrence of a lingual paralysis after restricted monohemispheric lesions.

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