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PubMed1988

Cerebrovascular lesions in acquired immune deficiency syndrome (AIDS).

Cerebrovascular lesions were seen in 28 of 83 cases (34%) of acquired immune deficiency syndrome (AIDS). Cerebral hemorrhage was noted in 4 cases, cerebral infarct in 23 cases and both in 1 case. Cerebral hemorrhage was in various locations such as intraparenchymal, subarachnoid space, subdural space and epidural space. Large, clinically evident hemorrhage was noted in 2 of 5 cases and bleeding tendency was noted in 2 cases. Most of the 24 cases with cerebral infarcts were not clinically evident; they were multiple, small and mainly involved the striatum, cerebral cortex and brain stem. Mural thickening of occasional small blood vessels was seen in 12 of the cases (50%) with infarcts. Other changes in blood vessels included vasculitis in one case and perivascular lymphocytic infiltration in another. In addition to thrombo-embolism and systemic ischemia/anoxia, these blood vessel changes may have a role in the development of cerebral infarcts in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Wegener granulomatosis: CT and MR findings.

PURPOSE: To demonstrate the spectrum of CT and MR imaging findings in patients with Wegener granulomatosis and to determine how often these findings could be attributed to either direct extension from paranasal or orbital disease sites, remote granulomas, or central nervous system (CNS) vasculitis. METHODS: We retrospectively reviewed the CT or MR studies of 15 patients with Wegener granulomatosis. RESULTS: Abnormal findings were seen in 7 patients (5 examined with MR imaging, 2 with CT). Findings included dural thickening and contrast enhancement (3 patients), infarcts (2 patients), regions of hyperintense signal on T2-weighted MR images (2 patients), and abnormal MR signal in the brain stem (2 patients). Three patients with imaging findings of dural enhancement and thickening were thought to have remote granulomatous lesions involving the dura. No patients had extension from sites external to the CNS or clinical findings suggestive of CNS vasculitis. CONCLUSION: The spectrum of CT and MR findings in Wegener granulomatosis includes dural thickening and enhancements cerebral infarction, and MR signal abnormalities in the brain stem and white matter. Presumed remote granulomatous lesions were the most common causes of CNS findings in this study. Complications related to non-CNS disease (eg, hypertension, endocarditis) also appear to have played a role in some patients.

Adult↗
PubMed1995

Brain stem cheiro-oral syndrome: neurological signs for brain stem lesions.

Cheiro-oral syndrome (COS) is characterized by a sensory disturbance in one hand and the ipsilateral oral corner. It is usually due to a lesion in the parietal cortex, thalamocortical projections or thalamus. Brain stem lesions may rarely produce COS. We present two COS patients with midbrain infarction and pontine hemorrhage, respectively. In our patients, unilateral oculomotor nerve palsy or medial longitudinal fasciculus syndrome concurred with sensory disturbances of cheiro-oral distribution. COS produced by cortical/thalamic lesion is not accompanied with such oculomotor signs. Thus, oculomotor deficits are decisive in differentiating brain stem from cortical or thalamic COS.

Aged↗
PubMed1982

The origins of the subcortical component of the median nerve somatosensory evoked potentials.

Short latency median nerve somatosensory evoked potentials (SEPs) were studied in two patients presenting with well localized unilateral pontine lesions producing hemisensory deficits. Both the early subcortical (N11-N13) and the later cortical component (N19-P22) of the SEP were abnormal in the patient whose lesion involved the medial lemniscus, while they remained unaffected in a second case of lateral inferior pontine infarction in which the medial lemniscus was spread. These results suggest that the N11-N13 component of the scalp recorded SEP emanates from the brain stem medial lemniscal pathway.

Cerebral Hemorrhage↗
PubMed1988

Functional recovery after decompressive craniectomy for cerebral infarction.

There is continuing controversy about the benefits of decompressive craniectomy in the treatment of lesions causing increased intracranial pressure (ICP) and brain edema. Laboratory work has shown a decrease in ICP after craniectomy, but also a paradoxical enhancement in the formation of underlying cerebral edema, which may act to the detriment of the patient. Since Rengachary et al. advocated craniectomy for massive cerebral infarction and reported their group of three patients, we have managed five patients with acute supratentorial cerebral infarction who progressed to uncal herniation and impending death from raised ICP and brain stem compression. All were treated with frontotemporal craniectomy after conventional medical therapy failed to achieve a response. All patients survived and are walking, despite a paresis appropriate to their original stroke. Two have returned to work. Good results with supratentorial craniectomy after infarction show that this procedure is life-saving and can also give acceptable functional recovery.

Adult↗
PubMed2006

Brain stem and cerebellar hyperintense lesions in migraine.

BACKGROUND AND PURPOSE: Migraineurs are at increased risk of cerebellar infarcts and supratentorial white matter lesions. The prevalence, frequency, and distribution of infratentorial hyperintense lesions in migraine are unknown. METHODS: Migraineurs with aura (n=161), without aura (n=134), and controls (n=140) from a population-based sample of adults (30 to 60 years of age) were evaluated with MRI. RESULTS: Infratentorial hyperintensities were identified in 13 of 295 (4.4%) migraineurs and in 1 of 140 (0.7%) controls (P=0.04). Twelve cases had hyperintensities, mostly bilaterally, in the dorsal basis pontis. Those with infratentorial hyperintensities also had supratentorial white matter lesions more often. CONCLUSIONS: We found an increased prevalence of infratentorial (mostly pontine) hyperintensities in migraineurs from the general population. This extends the knowledge about vulnerable brain regions and type of lesions in migraine brains. A hemodynamic ischemic pathogenesis is likely, but further research is needed.

Adult↗
PubMed1980

[Pseudo-tumoral cerebellar infarction. Diagnostic, therapeutic and prognostic aspects in 12 cases (author's transl)].

In those 12 observations, without associated lesion in the brain stem, diagnosis is done 3 times at autopsy, 8 times at surgical time, and once before it, on clinical and radiographic arguments. Diagnosis must be systematically evoked in front of vestibular symptoms, before severe signs, related to intracranial hypertension and brain stem compression, become evident. Iodoventriculography (7 times) and principally computerized tomography (2 times) bring conclusive arguments for diagnosis. Those infarcts are situated 9 times in the territory of the postero-inferior cerebellar artery and 3 times in the area supplied by the antero-superior cerebellar artery. Spontaneous evolution is always lethal, but prognosis after surgery is still severe (4 long term survivals in 9 cases) for the vascular system of those patients remains fragile.

Adult↗
PubMed1994

Acute bilateral cerebellar infarction in the territory of the medial branches of posterior inferior cerebellar arteries.

BACKGROUND: We describe the first clinicoradiological report of acute bilateral cerebellar infarction confined to the territory of the medial branches of the posterior inferior cerebellar arteries. CASE DESCRIPTION: A 65-year-old man with atrial fibrillation and hypertension had sudden onset of vertigo, followed by brief loss of consciousness. Three days later a cranial computed tomographic scan showed acute hydrocephalus and low-density areas in the cerebellar vermis on both sides. On transfer the patient showed mild dysarthria, dysequilibrium with retropulsion, symmetrical bilateral horizontal gaze-evoked nystagmus on lateral gaze, and marked gait ataxia without brain stem signs, followed by marked vertigo that was induced by motion. Cranial magnetic resonance imaging revealed abnormalities consistent with fairly symmetrical bilateral cerebellar hemorrhagic infarction that was confined to the territory of the medial branches of the posterior inferior cerebellar arteries, in addition to minimal high-intensity areas in the pons on T2-weighted images. The patient improved with conservative therapy, including intravenous administration of glycerol. CONCLUSIONS: We speculate that our patient likely had initial transient occlusion of the right vertebral artery at the origin of the right posterior inferior cerebellar artery, which probably gave rise to the bilateral medial branches of posterior inferior cerebellar arteries. This caused infarction in the territory of the medial branches on both sides without remaining brain stem signs. Such an unusual pattern of cerebellar infarction accompanied by acute hydrocephalus posed a diagnostic challenge at the time of transfer to our care, and correct diagnosis was facilitated by cranial magnetic resonance imaging.

Aged↗
PubMed1989

[Clinico-morphologic correlations in cerebral infarction after recurrent hemorrhage].

Clinical-morphological analysis of cases in which, in the course of vasogenic necrotic brain lesion, hemorrhagic foci appeared within the infarcted area, was performed. The material comprised 355 cases with encephalomalacia (223 women and 123 men). The patients died at age between 39 and 96 years. In the clinical picture a sudden onset of the disease prevailed, with hemiparesis or hemiplegia associated in 216 cases with disturbances of consciousness. The course of the disease was in general progressive. Only in 30 patients improvement of clinical state was observed. The time of survival varied from several hours to several weeks. Most patients (140) died in the first week in deep cerebral coma or state of decerebration. In nine cases clinical symptomatology of herniation and secondary hemorrhages into the brain stem was found. A sudden onset and violent course of the disease resulted in a diagnosis of primary hemorrhage with penetration to the subarachnoid space or ventricular system in 32 patients. Only in six cases was a secondary hemorrhage into the primary infarction diagnosed clinically. Hemorrhagic malacia was most frequently (in 255 cases) located in region vascularized by the middle cerebral artery and very seldom, the basilar artery or cerebellar arteries. Malacia was accompanied by considerable brain edema. This was particularly intense in extensive infarctions and persisted even in cases with considerable long survival. In 45 cases secondary hemorrhagic foci were found within brain stem. The morphology of the infarction foci was variable in most cases. Independently to fresh unreactive diffuse necrosis, sometimes areas with various advancement of resorption and organization processes were observed in the same case. Both in areas of fresh reactionless malacia and of advanced macrophage-glial disintegration, or even in areas of advanced gliomesodermal organization, stand-like or spherical hemorrhages could be seen merging sometimes into extensive pools. The morphology of hemorrhagic foci was largely dependent on their size and localization. The hemorrhagic foci located close to the depth of the cortical sulci very often destroyed the cortex and white matter, and penetrated to the subarachnoid space (141 cases). In was usually almost impossible to detect the source of bleeding within the necrotically changed area. The resorption reaction at the edge of extensive hemorrhagic foci was in general minimal. A lesion of the vessel wall, caused by stasis of long duration, resulting from disorders of the vascular function in the course of defficient blood supply and ischemic brain edema are considered the main causes of bleeding into the pale infarction.

Adult↗
PubMed2005

Medial vestibular nucleus lesions in Wallenberg's syndrome cause decreased activity of the contralateral vestibular cortex.

Three patients with the clinical diagnosis of Wallenberg's syndrome caused by acute unilateral ischemic infarctions, which included the vestibular nucleus in the medullary brain stem and afferent vestibular pathways, were examined by positron emission tomography (PET) during caloric vestibular stimulation. They all had typical signs of vestibular dysfunction such as transient rotatory vertigo with vomiting at the onset, ipsiversive body and ocular lateropulsion, and a complete ocular tilt reaction with tilts of the subjective visual vertical. Compared with healthy volunteers, who show activation in a network of temporoparietal vestibular areas within both hemispheres, especially in the posterior insula and retroinsular region that contains the human homologue of the parietoinsular vestibular cortex (PIVC) in monkeys, the activation pattern of the patients with Wallenberg's syndrome was typically changed. During caloric irrigation of the ear ipsilateral to the side of the lesion, they showed no or significantly reduced activation in the contralateral hemisphere, whereas the activation pattern in the ipsilateral hemisphere appeared "normal." These results are compatible with bilateral ascending vestibular pathways from the vestibular nuclei to the vestibular cortex. The novel finding in all three patients was that the activation patterns were compatible with the assumption that only the crossing fibers from the medial vestibular subnucleus to the contralateral medial longitudinal fascicle were affected, but the ipsilateral vestibular thalamocortical projections via the superior vestibular subnucleus were spared. Thus, the activation pattern in the PET study may reflect the vestibular tonic imbalance within the vestibular nuclei circuitry at the cortical level.

Adult↗
PubMed1980

Infarctions of the brainstem and cerebellum: a correlation of computed tomography and angiography.

Forty-nine patients were found to have computed tomographic (CT) and clinical evidence for infarction in the brainstem and cerebellum. Seventeen had correlative angiography, of which 15 had a severe occlusive vascular lesion somewhere in the vertebrobasilar system. The correlation between angiographic and CT localization of the infarcts was not good. Inferiorly located infarcts were probably often missed on CT because of basal artifacts. Combined infarctions of the brainstem and cerebellum were common. Nineteen of the 49 patients had an associated mass effect in the posterior fossa; in eight of these, hydrocephalus developed. Although immediate surgical decompression of the posterior fossa has been recommended for treatment of this complication, most of these patients recovered well with careful medical decompression.

Aged↗
PubMed2005

Transplantation of a novel cell line population of umbilical cord blood stem cells ameliorates neurological deficits associated with ischemic brain injury.

Umbilical cord blood (UCB) is a rich source of hematopoetic stem cells (HSCs). We have isolated a novel cell line population of stem cells from human UCB that exhibit properties of self-renewal, but do not have cell-surface markers that are typically found on HSCs. Analysis of transcripts revealed that these cells express transcription factors Oct-4, Rex-1, and Sox-2 that are typically expressed by stem cells. We refer to these novel cells as nonhematopoietic umbilical cord blood stem cells (nh-UCBSCs). Previous studies have shown that the intravenous infusion of UCBCs can ameliorate neurological deficits arising from ischemic brain injury. The identity of the cells that mediate this restorative effect, however, has yet to be determined. We postulate that nh-UCBSCs may be a source of the UCB cells that can mediate these effects. To test this hypothesis, we intravenously injected one million human nh-UCBSCs into rats 48 h after transient unilateral middle cerebral artery occlusion. Animals in other experimental groups received either saline injections or injections of RN33b neural stem cells. Animals were tested for neurological function before the infusion of nh-UCBSCs and at various time periods afterwards using a battery of behavioral tests. In limb placement tests, animals treated with nh-UCBSCs exhibited mean scores that were significantly better than animals treated with RN33b neural stem cells or saline. Similarly, in stepping tests, nh-UCBSC-treated animals again exhibited significantly better performance than the other experimental groups of animals. Analysis of infarct volume revealed that ischemic animals treated with nh-UCBSCs exhibited a 50% reduction in lesion volume in comparison to saline-treated controls. Histological analysis of brain tissue further revealed the presence of cells that stained for human nuclei. Some human nuclei-positive cells were also co-labeled for NeuN, indicating that the transplanted cells expressed markers of a neuronal phenotype. Cells expressing the human nuclei marker within the brain, however, were rather scant, suggesting that the restorative effects of nh-UCBSCs may be mediated by mechanisms other than cell replacement. To test this hypothesis, nh-UCBSCs were directly transplanted into the brain parenchyma after ischemic brain injury. Sprouting of nerve fibers from the nondamaged hemisphere into the ischemically damaged side of the brain was assessed by anterograde tracing using biotinylated dextran amine (BDA). Animals with nh-UCBSC transplants exhibited significantly greater densities of BDA-positive cells in the damaged side of the brain compared to animals with intraparenchymal saline injections. These results suggest that restorative effects observed with nh-UCBSC treatment following ischemic brain injury may be mediated by trophic actions that result in the reorganization of host nerve fiber connections within the injured brain.

Animals↗
PubMed1979

Regional cerebral blood flow, diaschisis, and steal after stroke.

Regional CBF was measured by 133Xe inhalation in unilateral cerebral infarction, carotid TIAs, and normal volunteers. Regional CBF values were bilaterally and symmetrically reduced in patients measured within 3 weeks after stroke. Later, rCBF values returned toward normal in the contralateral hemisphere of patients with infarction and in both hemispheres with carotid TIAs. In cases with carotid occlusive disease, flow reduction was seen in the contralateral posterior cerebral artery distribution, with hyperemia in ipsilateral occipital lobe caused by interhemispheric steal. Brainstem-cerebellar flow values were increased following acute cerebral infarction if patients were alert but reduced if consciousness was impaired.

Adult↗
PubMed1999

Vertebrobasilar artery territory infarction as an initial manifestation of systemic lupus erythematosus.

Cerebral infarction is a well-documented complication of systemic lupus erythematosus (SLE), that usually occurs several years after the diagnosis of SLE. To our knowledge, however, strokes associated with vertebrobasilar artery involvement were not reported to present as an initial manifestation of SLE. We report two patients, who presented with vertebrobasilar territory infarction as an initial manifestation of SLE. Patient 1 was a 16-year-old girl, who developed dysarthria and ataxia. MRI showed multiple infarcts in the pons, cerebellum and thalamus. Four-vessel cerebral angiography showed multifocal stenoses in the vertebral and basilar arteries with beaded appearance. Patient 2 was a 26-year-old woman, who developed headache associated with dysarthria, dizziness and ataxia. MRI showed multiple infarcts in the cerebellum, medulla, pons, midbrain and thalamus. Cerebral angiography revealed occlusion of both vertebral arteries at the first cervical vertebral level with non-visualization of the basilar artery. Both patients were diagnosed as having SLE supported by laboratory results. Although rare, posterior circulation stroke can present as an initial manifestation of SLE, which may be attributed to vasculitis or dissection in the vertebral/basilar artery.

Adolescent↗