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Investigation
Third cranial nerve palsies are most indicative of serious disease when associated with severe headache or altered consciousness. A thorough neurologic examination with CT or MRI is performed. Lumbar puncture is reserved for suspected subarachnoid hemorrhage when CT does not show blood. Cerebral angiography must be performed if aneurysm causing subarachnoid hemorrhage is strongly suspected or when the pupil is clearly affected and no head trauma serious enough to fracture the skull has occurred.
Weakness of the muscle innervated by the 4th (trochlear) nerve (superior oblique muscle).
These palsies are often difficult to detect because they affect vertical eye position predominantly when the eye is turned inward. The patient sees double images, one above and slightly to the side of the other. However, by tilting the head to the side opposite the palsied muscle, the patient may achieve full or almost full ocular motility without double vision.
The eye is turned inward; it moves outward sluggishly, reaching the midline at most.
Idiopathic cases are common, although many occur in elderly or diabetic patients in whom small vessel disease may be suspected. In idiopathic cases, no other cranial nerves are involved, and improvement should occur within 2 mo.
Causes
One identifiable cause is compression of the 6th nerve in the cavernous sinus by a tumor originating in the nasopharynx. Typically, severe pain in the head and anesthesia in the distribution of the first division of the 5th nerve also occur. Anything that causes the brain to shift may stretch the 6th nerve because of the acute angle it makes before entering Dorello's canal. Thus 6th nerve palsies may be due to large brain tumors remote from the nerve, to increased intracranial pressure, or to lumbar puncture.
Causes
Diabetic infarction is one of the more common causes. Other causes include trauma of insufficient force to cause a basilar skull fracture, infections or tumors affecting the meninges, Wernicke's encephalopathy, aneurysm, and multiple sclerosis. In children without evidence of increased intracranial pressure, these palsies can result from respiratory infection and thus may be recurrent.
At surgery or autopsy, intracranial arterial and, less often, venous loops compressing the trigeminal nerve root where it enters the brain stem have been found, suggesting that the tic is a compressive neuropathy. The disorder usually affects adults, especially the elderly. Pain is often set off by touching a trigger point or by activity (eg, chewing or brushing the teeth). Although each bout of intense pain is brief, successive bouts may be incapacitating.
Bell's Palsy
Unilateral facial paralysis of sudden onset and unknown cause.
The mechanism presumably involves swelling of the nerve due to immune or viral disease, with ischemia and compression of the facial nerve in the narrow confines of its course through the temporal bone. Pain behind the ear may precede facial weakness. Weakness develops within hours, sometimes to complete paralysis. The affected side becomes flat and expressionless, but patients may complain instead about the seemingly twisted intact side. In severe cases, the palpebral fissure widens, and the eye does not close. The patient may complain of a numb or heavy feeling in the face, but no sensory loss is demonstrable. A proximal lesion may affect salivation, taste, and lacrimation and may cause hyperacusis.
Diagnosis
Weakness of the entire half of the face distinguishes Bell's palsy from supranuclear lesions (eg, stroke, cerebral tumor), in which the weakness is partial, affecting the frontalis and orbicularis oculi less than the muscles in the lower part of the face. Bell's palsy must be differentiated from unilateral facial weakness due to other disorders of the facial nerve or its nucleus, chiefly geniculate herpes (Ramsay Hunt's syndrome), middle ear or mastoid infections, sarcoidosis, Lyme disease, petrous bone fractures, carcinomatous or leukemic nerve invasion, chronic meningeal infections, and cerebellopontine angle or glomus jugulare tumors. Skull x-rays and CT and MRI scans are obtained when the diagnosis is in doubt. MRI may show contrast enhancement of the facial nerve, but CT and skull x-rays are typically negative. However, they may show a fracture line, bony erosion due to infection or neoplasm, or internal auditory canal expansion due to a cerebellopontine angle tumor. CT and MRI scans may show the contrast-enhancing mass of angle or glomus tumors. Blood tests for Lyme disease help diagnose it. A chest x-ray and serum ACE are used to detect sarcoidosis, a common cause of facial nerve paralysis in blacks.
Corticosteroids
Some studies suggest that corticosteroids (eg, prednisone 60 to 80 mg/day po begun 24 to 48 h after onset and given for 1 wk, then decreased gradually over the 2nd wk) help modestly reduce residual paralysis and expedite recovery. Mild electrical stimulation of the nerve and massage of the facial muscles have no proven benefit. Hypoglossal-facial nerve anastomosis may partially restore facial function if none has returned in 6 to 12 mo but results in difficulty in eating and speaking, so its role is limited.
GLOSSOPHARYNGEAL NEURALGIA
A rare syndrome characterized by recurrent attacks of severe pain in the posterior pharynx, tonsils, back of the tongue, and middle ear. The cause is unknown, and no pathologic change can be found (except rarely, when due to a tumor in the cerebellopontine angle or the neck). Men are more commonly affected, usually after age 40. As in trigeminal neuralgia, intermittent attacks of brief, severe, excruciating pain occur paroxysmally, either spontaneously or precipitated by movement (eg, chewing, swallowing, talking, sneezing). The pain, lasting seconds to a few minutes, usually begins in the tonsillar region or at the base of the tongue and may radiate to the ipsilateral ear. The pain is strictly unilateral. In 1 to 2% of patients, increased vagus nerve activity causes cardiac sinus arrest with syncope. Attacks may be separated by long intervals.