Pseudobulbar Palsy

Magnus reported the first case of pseudobulbar palsy in 1837 in a patient having multiple infarcts. Lepine, in 1877 introduced the term pseudobulbar palsy for differentiation purposes. Pseudobulbar palsy is due to an upper motor lesion caused by bilateral disturbance of the corticobulbar tracts. The corticobulbar tracts exert supranuclear control over brainstem motor nuclei and are involved in the muscular movement of the head and neck. They originate from pyramidal cells in the cortex and terminate at cranial nerve nuclei. These nuclei control mastication, deglutition, and speech. Pseudobulbar palsy is characterized by dysarthria, dysphagia, facial and tongue weakness, and emotional lability.[1][2] Any condition which damages bilateral corticobulbar pathways can cause pseudobulbar palsy.