No abstract

Cortical vein thrombosis without sinus involvement is rarely diagnosed, although it may commonly be overlooked. We report four cases of cerebral venous thrombosis limited to the cortical veins. The diagnosis was made on surgical intervention in one patient and by angiography in three patients. Together with a survey of the published cases, the clinical and neuroimaging patterns of our patients allow delineation of several features suggestive of cortical venous stroke. Focal or generalized seizures followed by hemiparesis, aphasia, hemianopia, or other focal neurologic dysfunction in the absence of signs of increased intracranial pressure should suggest this possibility. Neuroimaging (CT, MRI) shows an ischemic lesion that does not follow the boundary of arterial territories and often has a hemorrhagic component, without signs of venous sinus thrombosis. Conventional angiography demonstrates no arterial occlusion but may show cortical vein thrombosis corresponding to the infarct, although these may also be nonspecific findings. The role of MR angiography, which is well-established in sinus thrombosis, remains to be assessed in patients with brain ischemia due to isolated cortical vein occlusion.

Objectives-To review the clinical features, electronystagmography findings, the possible mechanism, and a possible therapeutic approach to benign paroxysmal positional vertigo (BPPV).

See-saw nystagmus is an uncommon but highly characteristic eye movement disorder comprising intorsion and elevation of one eye, with synchronous extorsion and depression of the other. It generally has a pendular waveform and is due to a midline, extrinsic, suprasellar mass lesion compressing or invading the brainstem bilaterally at the meso-diencephalic junction. This report deals with the clinical and MRI findings in three patients (and binocular three-dimensional quantitative oculographic findings in one patient) with a jerk waveform see-saw nystagmus due in each case to a unilateral meso-diencephalic lesion. In each patient the torsional component of the nystagmus fast phases rotated the upper poles of the eyes toward the side of the lesion. Jerk see-saw nystagmus can be clinically indistinguishable from pendular see-saw nystagmus and from the torsional-vertical nystagmus which occurs with medullary lesions. We propose that jerk see-saw nystagmus is due to unilateral inactivation of the torsional eye-velocity integrator, thought to be in the interstitial nucleus of Cajal, with sparing of the torsional fast-phase generator, thought to be in the adjacent rostral interstitial nucleus of the medial longitudinal fasciculus.

An overview of possible treatment options for oculomotor disorders that prevent clear vision is given. Downbeat nystagmus, upbeat nystagmus, seesaw nystagmus, periodic alternating nystagmus, acquired pendular nystagmus, and saccadic oscillations such as opsoclonus/ocular flutter are discussed. In addition, superior oblique myokymia and vestibular paroxysmia are reviewed. All treatment recommendations available in the literature are classified as class C only. In general, only some of the patients benefit from the treatment.