Cases reported "Cerebral Infarction"

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1/41. See-saw nystagmus and brainstem infarction: MRI findings.

    A patient with see-saw nystagmus had a lesion localized by magnetic resonance imaging (MRI) to the paramedian ventral midbrain with involvement of the right interstitial nucleus of Cajal. This the first MRI study of see-saw nystagmus associated with a presumed brainstem vascular event. Our findings support animal and human studies suggesting that dysfunction of the interstitial nucleus of Cajal or its connections is central in this disorder.
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2/41. Convergence retraction nystagmus: a disorder of vergence?

    The pathological mechanism of convergence retraction nystagmus (CRN) is not known. To determine whether CRN is a disorder of vergence or of the saccadic system, the scleral search coil technique was used to record binocularly the three-dimensional components of CRN in a patient with a left mesencephalic infarction involving the nucleus of the posterior commissure and the rostral interstitial nucleus of the medial longitudinal fascicle. CRN had disconjugate horizontal and torsional components. The horizontal amplitude/velocity relationship of CRN aligned with the main sequence of vergence responses of normal control subjects but not with that of saccades. Vergence responses of the right eye and left eye were not asynchronous. The slow phases of CRN showed an exponential decay with a time constant of 70 milliseconds. Thus, CRN is probably a disorder of vergence rather than of opposing adducting saccades.
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3/41. Nodulus infarction mimicking acute peripheral vestibulopathy.

    The authors report two patients with cerebellar infarctions in the territory of the medial branch of the posterior inferior cerebellar artery who had vertigo, spontaneous ipsilesional nystagmus, and contralesional truncal lateropulsion. Although one of the two patients had slight dysmetria, overall signs closely mimicked those of acute peripheral vestibulopathy. The authors suggest that interruption of nodulouvular inhibitory projections to vestibular nuclei may account for the vestibular signs.
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4/41. Conscious visual abilities in a patient with early bilateral occipital damage.

    A 21-year-old male presented with occipital lobes that were extensively damaged by bilateral infarcts present at birth. The absence of the striate cortex was confirmed with anatomic and functional MRI and high-resolution EEG. His cortical visual impairment was severe, but he retained a remarkable ability to see fast-moving stimuli. Horizontal optokinetic nystagmus could be elicited from either eye. Resolution acuity was close to normal providing the patient was allowed to move his head and eyes. The direction of motion in random-dot patterns could be discriminated with perfect accuracy at speeds above 2 deg/s, and the patient reported that he could 'see' the motion at fast but not at slow speeds. This conscious residual vision for motion is known as Riddoch's phenomenon, but it has never been reported in the complete absence of the striate cortex. functional neuroimaging revealed activation that was outside the motion-responsive regions of the extrastriate cortex. This case demonstrates remarkable plasticity in the human visual system and may have implications for understanding the functional organization of the motion pathways.
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5/41. Bowtie and upbeat nystagmus evolving into hemi-seesaw nystagmus in medial medullary infarction: possible anatomic mechanisms.

    A 20-year-old man with bilateral medial medullary infarction showed transition of bowtie and upbeat nystagmus into hemi-seesaw nystagmus. Follow-up MRI revealed near complete resolution of the right medullary lesion. This transition of nystagmus suggests that the upbeat nystagmus was generated by bilateral lesions in the ascending pathways from both anterior semicircular canals (SCC), and that the hemi-seesaw nystagmus was caused by damage to the pathway from the left anterior SCC.
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6/41. A case of isolated nodulus infarction presenting as a vestibular neuritis.

    We reported a patient with cerebellar infarction who presented with purely isolated vertigo, ipsilesional spontaneous nystagmus, and contralesional axial lateropulsion without usual symptoms or signs of cerebellar dysfunction. An MRI of the brain showed a small left cerebellar infarct selectively involving the nodulus. A pure vestibular syndrome in our patient may be explained by ipsilateral involvement of nodulo-vestibular inhibitory projection to vestibular nucleus. Clinicians should be aware of the possibility of a nodulus infarction in patient with acute vestibular syndrome, even if the pattern of nystagmus and lateropulsion is typical of a vestibular neuritis.
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7/41. Gaze deviation from contralateral pseudoperiodic lateralized epileptiform discharges (PLEDs).

    Pseudoperiodic lateralized epileptiform discharges (PLEDs) usually produce "negative" neurologic findings. This contrasts with seizures which typically induce cortical activation with "positive" clinical manifestations. Gaze preference may arise from ipsilateral frontal eye fields (FEFs) damage because of the unopposed action of an intact contralateral FEF. Epileptic nystagmus (EN) and gaze deviation (GD) can also occur with focal temporo-parieto-occipital or hemispheric seizures in awake or obtunded patients. A patient with old right frontal and parieto-temporal cerebral infarctions manifested leftward gaze preference and deviation (without nystagmus) while alert and talking. Digitized EEG demonstrated PLEDs at approximately 1 Hz over the right fronto-central region, without electrographic seizures. This report illustrates that PLEDs without seizures may excite frontal regions proximate to the FEFs to produce contraversive gaze preference in an awake patient, and discusses putative mechanisms. Gaze deviation, in this case, was the principal clinical feature of PLEDs.
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8/41. Rotational vertigo associated with parietal cortical infarction.

    A 65-year-old woman experienced sudden positional vertigo with rightward, horizontal nystagmus that resolved within days. MRI revealed a left parietal lobe infarction involving the supramarginal gyrus. The patient experienced a transient recurrence of vertigo after 7 days but MRI failed to reveal the presence of any new lesions; furthermore, the patient's EEG was normal. We suggest that this patient's vertigo was due to her parietal cortical infarction.
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9/41. Embolic internal auditory artery infarction from vertebral artery dissection.

    A 51-year-old man developed sudden vertigo, right hearing loss and dysphagia. Examination revealed right horner syndrome, spontaneous torsional-horizontal nystagmus, right central type facial palsy, dysarthria, reduced soft palate elevation without gag reflex, left hypesthesia, right dysmetria and imbalance. audiometry and bithermal caloric tests documented right sensorineural hearing loss and canal paresis. brain MRI and cerebral angiography documented right lateral medullary infarction from vertebral artery dissection, without involvement of other parts of the brainstem supplied by the anterior inferior cerebellar artery (AICA). This case suggests artery-to-artery embolism as a possible mechanism of isolated vertigo or hearing loss from labyrinthine infarction.
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10/41. Parietal and bi-occipital lobe infarction confounded by ethanol-induced optic neuropathy.

    A frequent occurrence in geriatric and chronically ill patients is the exhibition of several simultaneously occurring and confounding health problems. This paper reports the case of a 61-year-old-white male who presented with an extensive history of multiple brain infarcts, hemiparesis, personality changes and varied visual complaints. Tests in the neurooptometric work-up for this patient included static automated perimetry, stereoacuity and optokinetic nystagmus evaluation. The results were suggestive of multiple cerebrovascular accidents which included the right and left occipital lobes as well as the right parietal lobe. This clinical picture was complicated by the presence of nutritional or ethanol-induced optic neuropathy. Emphasis was placed on a detailed sequential history of events and a complete neurological and optometric evaluation to ascertain the multiple foci of cortical infarction. Corroboration of clinical findings was obtained by computerized axial tomography (CT scan).
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