Thalamic Infarct

The patient is a 64 year old man with no major past medical history who, on the day of admission, suddenly developed loss of vision in both eyes and then was unable to open his eyes on his own unless he used his hands. Holding his eyelids open his vision was very blurry. Within minutes he lost consciousness and his wife was unable to arouse him. In the emergency room he was described as unresponsive to pain, with 8 mm sluggish reacting pupils, moving all four extremities with bilateral decorticate posturing and bilateral upgoing toes. A non-contrast Brain CT was read as normal. The patient was admitted to the Intensive Care Unit. Diagnosis: ‘Top of the basilar syndrome'. Neurological examination: Over the next two hours, his level of consciousness fluctuated, ranging from impairment of arousal to occasionally conversing with yes and no to asking questions. When awake he was oriented x3 and then he would drift back to sleep. Repetition, naming and comprehension were intact. He had bilateral ptosis Pupils 6 mm OU, sluggish to light. Eyes straight in primary gaze Normal horizontal and vertical oculocephalic reflex Motor system: Left hemiplegia involving face, arm and leg with normal tone. Reflexes 2+ symmetric with bilateral upgoing toes. Sensory examination: Left hemi-sensory loss. On day 1, the patient was heparinized and placed on pressors to keep the systolic blood pressure greater than 180 as his level of alertness fluctuated markedly with his blood pressure and was dependent on maintaining a systolic blood pressure over 180. On day 3, he was awake and alert and fully oriented. The left sided weakness and hemi-sensory loss had completely resolved and he had no ptosis. On day 5, he tried to get out of bed, which resulted in a drop of systolic blood pressure to 120. Almost immediately he became confused, dysarthric and hemiparetic. As soon as his systolic blood pressure was greater than 180, he was alert and his signs resolved. 2/7/94 CT of the Brain with contrast: 1.Acute right thalamic infarct with the possibility of involvement of the left thalamus not completely excluded. 2.No intracranial hemorrhage or mass 3.Appearance of an old left cerebellar hemispheric infarct. 2/10/90 Brain MRI: Axial T2 WI images show 1.An area of T2 bright signal within the right medial thalamus suggestive of an infarct. 2.Abnormal signal within the left cerebellar hemisphere and punctate areas within the right anterior cerebellar hemisphere, both consistent with infarction. (Figures 1 and 2) Brain MR Angiogram: On MRA the right vertebral artery was segmentally visualized and diminutive in size. probably representing a small hypoplastic vertebral artery with slow flow. However, the possibilities of thrombus and/or dissection could not be excluded. 2/15/94 Cerebral Angiogram: Showed no evidence of vertebral artery dissection or of a basilar tip aneurysm. The basilar artery was normal. A Holter monitor demonstrated some sinus node dysfunction, but cardiology felt that in the absence of syncable symptoms the patient did not require a pacer. On 2/17/94, 13 days post stroke, Neurovisual Consult: The patient was fully alert. He complained that he could not look down and he was unable to read his menu. He had intermittent vertical double vision watching TV, one image being slightly higher than the other, but at the time of the examination this was improving. He mentioned that he was sleeping a lot. He denied headache, vertigo and confusion and he emphasized that his memory "was good". On examination: Visual acuity OD: 20/25 OS: 20/40, pinhole 20/25 Confrontation fields full OU and normal fundus exam. Pupils 4 mm OU reacting normally to light and near Ocular motility: Eyes straight in primary gaze Full horizontal gaze right and left with gaze evoked nystagmus. Full upgaze, no nystagmus Supranuclear paralysis of downgaze Saccades limited to 5 to 10 degrees. Pursuit 20 to 30 degrees down. Intact vertical oculocephalic reflex Absent convergence Intact horizontal optokinetic nystagmus Absent vertical optokinetic nystagmus No skew deviation. Diagnosis: 1.Isolated global supranuclear paralysis of downgaze 2.Right medial thalamic infarct extending into the right mesencephalic reticular formation (MRF) 3.Embolic cerebellar infarcts Etiology: Embolic infarction of the thalamus and MRF supplied by the posterior thalamosubthalamic paramedian artery (Artery of Percherson) Top of the basilar artery syndrome A transthoracic echo cardiogram showed no embolic source from the heart. A transesophageal echo cardiogram showed a small patent foramen ovale. Lower extremity arterial non-invasive study showed no evidence of deep venous thrombosis. Discharge: At the time of discharge the patient was doing very well. The residual neurological findings were: 1.Supranuclear paralysis of downgaze 2.Absent convergence and 3.Increased somnolence. He was discharged home on Coumadin. Follow-Up: The patient's stroke occurred on February 4, 1994. On follow-up on March 23, 1994 he had full vertical gaze down and normal convergence. His wife reported that "he was very sleepy and lethargic in mid-afternoon and generally sleeps a lote and takes frequent naps". See also: http://content.lib.utah.edu/cdm/ref/collection/ehsl-shw/id/114