Neurologic safety event rates in the SENTIS trial control population.

BACKGROUND: Adverse event (AE) rates for interventional stroke trials are not well established. AIMS: We prospectively evaluated control arm AEs from a randomized stroke trial to establish expected rates of neurologic AEs. METHODS: Control data from the Safety and Efficacy of NeuroFlo Technology in Ischemic Stroke (SENTIS) Trial were evaluated. Patients were ≥ 18 years with National Institutes of Health Stroke Scale (NIHSS) scores 5-18 within 14 h of stroke onset. Follow-up was 90 days. Neurological AEs and serious AEs (SAEs) were adjudicated and the following defined times used to determine treatment relatedness: 24-h imaging for intracranial hemorrhage (ICnH) including hemorrhagic transformation, 7 days each for cerebral edema and neurologic worsening/stroke progression, and 30 days for new ischemic strokes. RESULTS: The control group included 257 patients, 49.4% female, mean age of 68.3 years, and median NIHSS of 10. Neurologic AEs occurred at the following rates: ICnH 27.6%, cerebral edema 6.6%, neurologic worsening 18.3%, and new stroke 4.7%. Most of these events occurred within the defined times: ICnH 74.6%, cerebral edema 94.1%, neurologic worsening 87.2%, and new stroke 83.3%. CONCLUSIONS: SENTIS Trial control arm neurologic events provide estimates of expected AE rates and defined times that can be used for future stroke trial's safety assessments.

The crossed paralyses. The original brain-stem syndromes of Millard-Gubler, Foville, Weber, and Raymond-Cestan.

In this article, the crossed syndromes of Millard-Gubler (facial palsy and contralateral hemiparesis), Foville (facial palsy, conjugate gaze paralysis, and contralateral hemiparesis), Weber (oculomotor palsy and contralateral hemiparesis), and Raymond-Cestan (internuclear ophthalmoplegia and contralateral hemiparesis) are detailed from the original reports. These and other related syndromes were instrumental in establishing important principles in brain-stem localization: the occurrence of cranial nerve palsies contralateral to hemibody motor or sensory disturbances, the concepts of the medial longitudinal fasciculus and conjugate gaze, and the corticobulbar innervation of the facial nerve nucleus.

SPECT in patients with cortical visual loss.

Single-photon emission computed tomography (SPECT) with 99mTc-hexamethylpropyleneamine oxime (HMPAO) was used to investigate changes in cerebral blood flow in seven patients with cortical visual impairment. Traumatic brain injury (TBI) was the cause of cortical damage in two patients, cerebral ischemia in two patients and carbon monoxide (CO) poisoning, status epilepticus and Alzheimer's Disease (AD) each in three separate patients. The SPECT scans of the seven patients were compared to T2-weighted magnetic resonance image (MRI) scans of the brain to determine the correlation between functional and anatomical findings. In six of the seven patients, the qualitative interpretation of the SPECT studies supported the clinical findings (i.e., the visual field defect) by revealing altered regional cerebral blood flow (rCBF) in the appropriate regions of the visual pathway. MR scans in all of the patients, on the other hand, were either normal or disclosed smaller lesions than those detected by SPECT. We conclude that SPECT may reveal altered rCBF in patients with cortical visual impairment of various etiologies, even when MRI studies are normal or nondiagnostic.

Tuberculous meningitis with blindness and perichiasmal involvement on MRI.

An 11-year-old boy with tuberculous meningitis developed blindness, a rare complication of this disease in the United States. Magnetic resonance imaging demonstrated perichiasmal enhancement, suggesting that arachnoiditis caused the visual loss. Serial neuroimaging over 7 months revealed a persistent inflammatory process in the chiasmatic cistern, hydrocephalus, and progressive cerebral infarctions.

Transient migraine-like symptoms with internal carotid artery dissection.

We report three patients with angiographically confirmed internal carotid artery (ICA) dissection who presented with transient symptoms resembling migraine with aura. Marching impairments from one modality to another preceded recognition of the diagnosis of dissection and were not associated with clinical or radiologic evidence of cerebral infarction. We review the clinical patterns in which ICA dissection may be identified in the setting of migrainous symptoms, given the different therapeutic approaches to migraine and dissection and the non-invasive means to diagnose dissection with magnetic resonance imaging (MRI). We offer mechanisms for recurrent neurologic symptoms in patients with ICA dissection.

Cerebellar top-of-the-basilar syndrome.

We present a patient with unusual cerebrovasculature due to the absence of anastomosis between anterior and posterior circulations and bilateral fetal posterior cerebral arteries. This resulted in an atypical 'cerebellar' top-of-the-basilar syndrome, with bilateral superior cerebellar artery infarctions. We review the clinical presentation and radiologic findings and explain the embryologic origin of this vascular anatomy.

Practice parameter: recurrent stroke with patent foramen ovale and atrial septal aneurysm: report of the Quality Standards Subcommittee of the American Academy of Neurology.

OBJECTIVES: 1) To evaluate the risk of subsequent stroke or death in patients with a cryptogenic stroke and a patent foramen ovale (PFO), atrial septal aneurysm (ASA), or both. 2) To establish the optimal method of stroke prevention in this population of patients. METHODS: MEDLINE, the Cochrane database of systematic reviews, key meeting abstracts from 1997 to 2002, and relevant reference lists were searched to select studies that prospectively collected outcome data in cryptogenic stroke patients with and without interatrial septal abnormalities. Studies were also selected that prospectively compared at least two treatment options. The quality of each study was graded (class I to IV) using a standard classification-of-evidence scheme for each question. Risk analyses were performed and data were pooled when appropriate. RESULTS: The literature search generated 129 articles of which only four fulfilled the inclusion and exclusion criteria. Two studies were graded class I, one study was graded class II, and one study was graded class IV for prognosis. Pooled results of the two class I and one class II studies demonstrated no increased risk of subsequent stroke or death in patients with PFO compared to those without (RR = 0.95, 95% CI 0.62 to 1.44). One class I study found increased risk of recurrent stroke in patients with PFO and ASA (annual rate = 3.8% versus 1.05%, RR = 2.98, 95% CI 1.17 to 7.58) but not increased risk of a composite of stroke and death (annual rate = 3.8% versus 1.8%, RR = 2.10, 95% CI 0.86 to 5.06). Regarding therapy, one study was graded class II, one study class III, and two studies class IV. Among patients with cryptogenic stroke and PFO or ASA, there was no significant difference in stroke or death rate in warfarin-treated patients relative to aspirin-treated patients and the confidence intervals were unable to rule out a benefit of one drug over the other (annual rate = 4.7% versus 8.9%, RR = 0.53, 95% CI 0.18 to 1.58). Minor bleeding rates were higher in the cohort of patients who received warfarin (22.9/100 patient-years versus 8.66/100 patient-years, rate ratio = 2.64, p < 0.001). No studies compared medical therapy with surgical or endovascular closure. CONCLUSION: PFO is not associated with increased risk of subsequent stroke or death among medically treated patients with cryptogenic stroke. However, both PFO and ASA possibly increase the risk of subsequent stroke (but not death) in medically treated patients younger than 55 years. In patients with a cryptogenic stroke and an atrial septal abnormality the evidence is insufficient to determine if warfarin or aspirin is superior in preventing recurrent stroke or death, but minor bleeding is more frequent with warfarin. There is insufficient evidence to evaluate the efficacy of surgical or endovascular closure.

Vertebrobasilar dolichoectasia associated with Marfan syndrome.

We report a 37-year-old woman with Marfan syndrome (MFS) who presented with acute myelopathy secondary to a subdural spinal hematoma. The patient died of a subarachnoid hemorrhage 4 days later. Autopsy showed a markedly ectatic vertebrobasilar system with fragmentation of the internal elastic lamina. Microscopic examination of the aorta similarly showed a fragmented internal elastic lamina. We discuss the implications of our patient's early onset vertebrobasilar dolichoectasia; this intracranial disease represents a rare cause of subarachnoid hemorrhage in MFS.