Pseudobulbar palsy is characterized by dysarthria, dysphagia, facial and tongue weakness, and emotional lability. Any condition which damages bilateral corticobulbar pathways can cause pseudobulbar palsy. Magnus reported the first case of pseudobulbar palsy in 1837 in a patient having multiple infarcts.
Pseudobulbar palsy Describes bilateral supranuclear (UMN) lesions of lower cranial nerves producing weakness of the tongue and pharyngeal muscles. This resembles, superficially, a bulbar palsy: hence pseudobulbar. Findings are a stiff, slow, spastic tongue (not wasted), dysarthria and dysphagia.
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.
Bulbar palsy is the result of diseases affecting the lower cranial nerves (VII-XII). A speech deficit occurs due to paralysis or weakness of the muscles of articulation which are supplied by these cranial nerves. The causes of this are broadly divided into: Muscle disorders. Diseases of the motor nuclei in the medulla and lower pons.
Pseudobulbar palsy is a syndrome of upper motor neuron paralysis that affects the corticobulbar system above the brain stem bilaterally. Although it presents with most of the signs and symptoms of bulbar palsy, the causative lesion is not in the brain stem. This condition causes dysphagia, dysarthria, and paresis of the tongue (without atrophy.
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