Isolated brain-stem third nerve palsy.
Midbrain hemorrhage from a presumed vascular anomaly caused a severe third nerve palsy without other ocular motor or neurologic signs or symptoms.
Biomedical subjects
Publications and source records attributed to J R Keane.
Midbrain hemorrhage from a presumed vascular anomaly caused a severe third nerve palsy without other ocular motor or neurologic signs or symptoms.
Of 101 patients with benign intracranial hypertension not related to vasculitis, neck stiffness occurred in 31, tinnitus in 27, distal extremity paresthesias in 22, joint pains in 13, low back pain in 5, and gait "ataxia" in 4. Symptoms resolved promptly upon lowering the intracranial pressure by lumbar puncture, and were probably directly caused by intracranial hypertension. Awareness of these "minor" symptoms of increased intracranial pressure can facilitate diagnosis and management.
A student was diagnosed as having Wilson's disease only after the severe, intermittent inability to open his eyes led him to seek neurologic evaluation. Although lid-opening apraxia is usually a symptom of diffuse extrapyramidal disease, it has not previously been reported in Wilson's disease.
The onset of the Melkersson-Rosenthal syndrome, manifested by bifacial paralysis and severe edema of the upper lip in a 25-year-old man, was followed shortly by signs of secondary syphilis.
Two patients had upward nystagmus on forward gaze before they died with acute caudal brainstem dysfunction. Bilateral dorsal paramedian damage in the rostral medulla, involving the perihypoglossal nuclei, was probably the critical lesion responsible for upbeat nystagmus.
Unilateral and bilateral internuclear ophthalmoplegia can rarely be caused by trauma. This article illustrates a traumatic pontine hemorrhage associated with bilateral internuclear ophthalmoplegia.
Twenty-five patients with upper brain-stem damage after severe transtentorial herniation showed a variety of residual oculomotor signs. Pupillary abnormalities (19 patients), ptosis (15 patients), internuclear ophthalmoparesis (13 patients), vertical gaze paresis (14 patients), and third-nerve dysfunction (11 patients) were the principal findings.
At this point, it is customary for all hands to gather round the old decision tree and whittle on a few algorithms. Because I have been chastened by occasional painful falls from slippery decision branches, however, I must make do with a short reprise. Some nodal points in analyzing vertical diplopia include: (1) evidence of central nervous system involvement; (2) pupillary sparing; and (3) the presence of proptosis of orbital congestion. As endlessly stated, premature closure of the differential diagnosis should be avoided and the tendency to diagnose partial third nerve palsy staunchly resisted. However, all of this will probably be of little comfort to you when you face your next lethargic patient who has small angle diplopia and speaks one of the obscure rural dialects of Freedonia.
Ten patients became locked-in after head and neck trauma. Five had a prompt onset due to either direct trauma or secondary infarction of the brainstem. A delay of 6 to 48 hours in four other patients was probably the interval between vertebral artery damage and vertebrobasilar arterial occlusion. The last patient sustained ischemia and compression of the cerebral peduncles from tentorial herniation.
Seven patients had pendular, vertical, isolated movements of the eyes soon after severe pontine strokes. The movements had a frequency of about 2 Hz and amplitudes of 3 to 40 degrees. Other rhythmic body movements at similar frequencies occurred in four patients after a delay of 6 weeks to 9 months. The character and course of these eye movements identify them as an uncommon form of branchial (palatal) myoclonus.
Strong deviation of the protruded tongue towards the "normal" side is an old sign of hysterical hemiparesis. The following four cases illustrate that hysterical tongue deviation continues to offer a valuable diagnostic clue.
Of 60 patients with acute bilateral ophthalmoparesis, the cause was within the brainstem in 18 (pretectal infarct, phenytoin toxicity, and Wernicke's syndrome), in cranial nerves in 26 (Guillain-Barré or Fisher syndrome, tuberculous meningitis), within the cavernous sinuses in 8 (tumors or infection), and at the myoneural junction in 8 (myasthenia or botulism).
Four patients who attempted suicide by using handguns survived bilateral optic nerve destruction with limited additional neurological damage.
Three cases of radiographic localization of fourth nerve lesions are reported: case 1--bilateral pareses due to traumatic contusion; case 2--left paresis from a collicular gunshot wound; and case 3--bilateral pareses due to a (cysticercal) cyst in the caudal cerebral aqueduct.
Five patients with acute obstructive hydrocephalus experienced arrhythmic, repetitive downward and inward eye movements at a rate ranging from one per three seconds to two per second and an amplitude of one fifth to one half of the full voluntary range. Because of a faster downstroke and appropriate amplitude, these movements were usually diagnosed as ocular bobbing. However, their "V" pattern, the generally faster rate, and pretectal, rather than pontine-associated, signs distinguished them from true ocular bobbing. This pretectal pseudobobbing probably represents a variety of convergence nystagmus, and in contrast with true pontine bobbing, usually indicates a need for prompt surgical attention.
Severe, involuntary, forceful closure of both eyelids, along with dystonia and rigidity, followed hypoxic encephalopathy in a young man whose computed tomographic scan showed symmetric infarcts of the corpus striatum. Symptomatic blepharospasm can result from bilateral damage to the basal ganglia.
A 28-year-old man had a chronic locked-in syndrome following tentorial herniation caused by an epidural hematoma. Postmortem examination revealed bilateral corticospinal tract degeneration caudal to the midbrain, with infarction of the right internal capsule just rostral to the cerebral peduncle and pressure necrosis of the pyramidal portion of the left cerebral peduncle.
Of 408 patients with ocular skew deviation, 47 (12%) had hypertropia that alternated on gaze to either side. Pretectal lesions were responsible for 29 cases, and lower brainstem signs were seen in 5; the site of posterior fossa involvement was uncertain in 13. Acute hydrocephalus, tumors, strokes, and MS were the most frequent causes, followed by spinocerebellar degeneration and tentorial herniation. The mechanism of alternating skew is unknown, but probably involves pathways from both utricles to the vertical-rotatory ocular motor neurons.