Gag reflex cranial nerve 9 and 1011/10/2023 Facial expressions: absent (expressionless face).Dysphagia, drooling, nasal regurgitation.Upper motor neuron palsy of the respective muscles.Bilateral damage or injury of corticobulbar tracts to nerve nuclei of cranial nerves V, VII, IX, X, XI, and XII.Lower motor neuron palsy of the respective muscles.Bilateral damage or injury of the nerve nuclei of cranial nerves IX, X, XI, and XII.Injury or malignancy of the high brainstem.Neurodegenerative disease: amyotrophic lateral sclerosis, progressive supranuclear palsy, multiple sclerosis.Infectious neuropathies: poliomyelitis, diphtheria, neurosyphilis.Autoimmune neuropathies: Guillain-Barré syndrome, myasthenia gravis.Neurodegenerative diseases: amyotrophic lateral sclerosi s, s yringobulbia.CSF analysis and MRI of the brain help identify the etiology. Lower motor neuron signs ( atrophy and fasciculations of the tongue, absent gag reflex) differentiate bulbar palsy from pseudobulbar palsy, which presents with upper motor neuron signs ( spastic tongue, exaggerated gag, and jaw jerk reflexes). In addition, patients with pseudobulbar palsy present with a lack of facial expression, difficulty chewing, and emotional lability. Both bulbar and pseudobulbar palsy are seen mainly in men over 75 years old and present with dysarthria and dysphagia. Any condition which disrupts or damages the cranial nerve nuclei or corticobulbar tracts can cause bulbar or pseudobulbar palsy (e.g., stroke, multiple sclerosis, infections, brain stem tumors). Pseudobulbar palsy is an upper motor neuron palsy that affects the corticobulbar tracts of the V th, VII th, IX th, X th, XI th, and XII th cranial nerves. Use of the neurological exam subtests for the vestibulocochlear nerve illuminates the changes a patient may go through.Bulbar palsy is a lower motor neuron palsy that affects the nuclei of the IX th, X th, XI th, and XII th cranial nerves. Additionally, within a single patient, the symptoms and signs may change as the disease progresses. From patient to patient, the exact presentation of the disease can be different. The patient can suffer from vertigo, a low-frequency ringing in the ears, or a loss of hearing. Ménière's disease is a disorder that can affect both equilibrium and audition in a variety of ways. Damage to structures near the two nuclei can result in deficits to one or both systems.īalance or hearing deficits may be the result of damage to the middle or inner ear structures. Deficits in one or both systems could occur from damage that encompasses structures close to both. Though they are part of distinct sensory systems, the vestibular nuclei and the cochlear nuclei are close neighbors with adjacent inputs. They both emerge from the inner ear, pass through the internal auditory meatus, and synapse in nuclei of the superior medulla. The sensory nerves from these two structures travel side-by-side as the vestibulocochlear nerve, though they are really separate divisions. The cochlea is responsible for transducing sound waves into a neural signal. The vestibule is the portion for equilibrium, composed of the utricle, saccule, and the three semicircular canals. Within the petrous region of the temporal bone is the bony labyrinth of the inner ear. Problems with balance, such as vertigo, and deficits in hearing may both point to problems with the inner ear. Though the two senses are not directly related, anatomy is mirrored in the two systems. The vestibulocochlear nerve (CN VIII) carries both equilibrium and auditory sensations from the inner ear to the medulla. Those fibers are conveying peripheral visual information to the opposite side of the brain, so the patient will experience “tunnel vision”-meaning that only the central visual field will be perceived. If the pituitary gland develops a tumor, it can press against the fibers crossing in the chiasm. The pituitary gland is located in the sella turcica of the sphenoid bone within the cranial floor, placing it immediately inferior to the optic chiasm.
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