Cerebral. Dysphagia and changes in speech similar to that which is produced by a lesion of the cranial nerves or their nuclei may occur with interruption of the corticobulbar fibers, which provide the brain stem nuclei with innervation from the frontal cerebral cortex. This condition is referred to as pseudobulbar palsy. The brain stem nuclei receive bilateral input; consequently, a unilateral lesion does not result in bulbar symptoms. Speech and swallowing disorders are due to bilateral injury of these pathways. The interruption may occur at any point from the cortex to the brain stem, but most commonly the interruption is due to ischemic injury. y Clinical findings indicative of cerebral lesions producing these pseudobulbar symptoms may include aphasia, sensory changes, or corticospinal tract findings such as limb spasticity, increased tendon and jaw jerk reflexes, and an extensor plantar response. Patients with pseudobulbar palsy also may have impaired emotional control with unprovoked laughter or crying, and emergence of primitive reflexes such as suck and snout.
Cranial Nerves. Lesions of the ninth or tenth cranial nerve nuclei usually affect adjacent brain stem structures, producing ipsilateral sensory disturbance of the face from involvement of the fibers of the descending tract and nucleus of cranial nerve V, vertigo from vestibular nuclei, contralateral limb sensory changes from the lateral spinothalamic, and ipsilateral limb ataxia caused by involvement of the inferior cerebellar peduncle. The ninth and tenth cranial nerves travel closely together between the brain stem and the jugular foramen and consequently are rarely affected independently of one another in their intracranial locations. More peripherally, a lesion at the jugular foramen also affects the spinal accessory nerve, which passes through this opening with the glossopharyngeal and vagus nerves. In addition to disturbance of speech, swallow, and gag, the patient demonstrates weakness of the sternocleidomastoid and trapezius muscles. The twelfth cranial nerve may be involved together with the ninth, tenth, and eleventh nerves by trauma, infection, or neoplasm at the retroparotid space. A lesion of cranial nerve XII produces deviation of the tongue to the side of the lesion when the tongue is protruded.
Motor/Reflexes/Cerebellar/Gait. Changes in muscle tone can be indicative of neurological disease involving cranial nerves IX and X. Cerebral lesions causing pseudobulbar palsy with alteration of speech and dysphagia may be associated with limb spasticity due to corticospinal tract injury. Parkinsonism caused by various etiologies frequently is associated with difficulties in speech and swallowing. No specific lesions exist of the cranial nerves, but rather the subcortical control is affected bilaterally. Patients with progressive supranuclear palsy particularly have prominent difficulty with speech and dysphagia. In patients with suspected cranial nerve IX or X lesions the presence of abnormal reflexes, such as an extensor plantar response, or the emergence of rudimentary reflexes like the suck or snout, are indicators of CNS pathology. Disorders of the neuromuscular junction also produce dysarthria and dysphagia. Repetitive testing of ocular or limb muscle power may produce an inordinate amount of fatigue and weakness pointing to a diagnosis of myasthenia.
A brain stem lesion producing impairment of speech and swallow may also include ataxia of ipsilateral limbs and gait by injury to the inferior cerebellar peduncle that lies adjacent to the nuclei of nerves IX and X.
Sensory. Alteration of pain and temperature sensation of the ipsilateral face with sensory changes of contralateral limbs in association with dysphagia and dysarthric or hoarse speech indicate a brain stem lesion. Sensory changes of the limbs and face on the same side may be produced by a cerebral lesion that contributes to a pseudobulbar state.
Autonomic Nervous System. Disorders of vagal nerve autonomic function may result in symptoms relating to cardiopulmonary and gastrointestinal functions, none of which are testable in the neurological examination. These may be assessed by specialized tests such as the tilt-table cardiac examination or studies of gastrointestinal motility.
Neurovascular. The precise mechanism of neurally mediated syncope (vasovagal vasomotor syncope) remains undetermined. These fainting spells are often provoked by unpleasant sensory stimuli and are accompanied by bradycardia, peripheral vasodilation, and hypotension. Blockage of the vagally mediated bradycardia with atropine does not eliminate the vasodilation and hypotension or the syncope. Vascular function is not a means of assessing glossopharyngeal or vagal status in a setting other than a research environment.
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