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Results for “Brain Stem Infarctions”

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PubMed1988

Wallerian degeneration of the descending tracts. CT and MRI features of the brain stem.

The authors have studied by CT brain infarcts of different ages in 16 patients, two of whom were also examined by MRI. The early and CT signs of wallerian degeneration of the descending tracts within the brain stem are described. Three cases of crossed cerebellar atrophy are reported; in one of them, the cerebral lesion had been present for less than 8 years. The physiopathology of pontine hemiatrophy and crossed cerebellar atrophy is discussed.

Adolescent↗
PubMed1997

Usefulness of magnetic resonance imaging in diagnosing vertebro-basilar insufficiency.

To estimate the usefulness of magnetic resonance imaging (MRI) in diagnosing vertebro-basilar insufficiency (VBI), 41 VBI patients with vertigo or dizziness and 26 subjects without vertigo or dizziness (as control) were examined by MRI. Sixty-eight percent of the VBI group and 12% of the control group showed a large difference between the right and the left vertebral artery diameter, the incidence being significantly higher in the VBI group. Thirty-nine percent of the VBI group and 12% of the control group had lacunar infarction in the brain stem, of which the incidence was significantly higher in the VBI group, MRI can be recommended to diagnose VBI providing information on both blood vessel disorder and ischemic changes in the brain.

Aged↗
PubMed2005

Overexpression of eNOS in brain stem reduces enhanced sympathetic drive in mice with myocardial infarction.

Reduced nitric oxide (NO) in the brain might contribute to enhanced sympathetic drive in heart failure (HF). The aim of this study was to determine whether increased NO production induced by local overexpression of endothelial NO synthase (eNOS) in the nucleus tractus solitarius (NTS) of the brain stem reduces the enhanced sympathetic drive in mice with HF. Myocardial infarction (MI) was induced in mice by ligating the left coronary artery. MI mice exhibited left ventricular dilatation and a reduced left ventricular ejection fraction. Urinary norepinephrine excretion in MI mice was greater than that in sham-operated mice, indicating that sympathetic drive was enhanced in this model. Thus this model has features that are typical of HF. Western blot analysis and immunohistochemical staining for neuronal NOS (nNOS) indicated that nNOS protein expression was significantly reduced in the brain stem of MI mice. MI mice had a significantly smaller increase in blood pressure evoked by intracisternal injection of N(G)-monomethyl-L-arginine than sham-operated mice. Adenoviral vectors encoding either eNOS (AdeNOS) or beta-galactosidase (Adbeta gal) were transfected into the NTS to examine the effect of increased NO production in the NTS on the enhanced sympathetic drive in HF. After the gene transfer, urinary norepinephrine excretion was reduced in AdeNOS-transfected MI mice but not in Adbeta gal-transfected MI mice. These results indicate that nNOS expression in the brain stem, especially in the NTS, is reduced in the MI mouse model of HF, and increased NO production induced by overexpression of eNOS in the NTS attenuates the enhanced sympathetic drive in this model.

Adenoviridae↗
PubMed1995

Posterior circulation infarction: anatomy, pathophysiology, and clinical correlation.

Posterior circulation cerebrovascular disease may be responsible for clinical syndromes that are determined by the vascular territory affected. An anatomic/topographic approach to the brain stem and cerebellum, relating the cross-sectional and functional anatomy to the vascular supply territories, is useful in the analysis of imaging studies of patients with posterior circulation cerebrovascular disease. Knowledge of the typical vascular distributions may be particularly useful for cases that do not show the classical clinical brain stem and cerebellar infarction syndromes. This approach may serve to improve our understanding of cerebrovascular disease in the posterior fossa.

Brain Stem↗
PubMed1978

[Circulatory disorders in the area of supply of the vertebrobasilar arteries in clinical and morphological picture].

The material comprised 40 autopsied cases in which vasogenic lesions in the brain stem were the only area of central nervous system damage or preceded the involvement of the cerebral hemispheres. Only 3 of them had been diagnosed correctly during the life of the patients. The material was divided into three groups: I. 22 cases with very dramatic onset suggesting in neurological appearance injury to the hemispheres, leading in most cases (15 out of 22) to death within 1 week. II. 18 cases in which the survival was from 2 months to 6 years. The vasogenic damage to the brain stem preceded considerably the development of brain softening or supratentorial haemorrhage 12 cases, in 7 cases the brain stem lesion was clinically silent in neurological examination. Fresh infarctions (group I) in the brain stem were located usually in the region of vascularization of the short circumferential and paramedian arteries, mainly in the basal part of the pons and midbrain. In group II single or multiple cavities were situated unilaterally or bilaterally mainly in the pons, at the watershed of the vascularization areas of paramedial and short or long circumflex arteries. The foci in the brain stem were associated in most cases (32 out of 40) with vascular lesions in the remaining areas of the same vascularization region. In the discussion on the pathogenesis the significance of degenerative changes in the walls of the vessels in this region and presence of thrombi in them for the development of necrotic changes has been stressed.

Adult↗
PubMed1996

[Sleep and breathing disorders in patients with brain stem lesions].

Most information about the structures within the brain stem that modulate respiration and sleep are gathered from animal experiments. Therefore we examined 10 patients several weeks after an infarction of the brain stem by means of polysomnography and tested the chemosensitive drives of respiration. None of these patients complained about symptoms of sleep disordered breathing. In each case polysomnographic measurements and ventilatory response curves revealed pathologic findings. The respiratory response to CO2 was diminished or completely abolished in each patient. In some cases hypoventilation or disturbances of the respiratory rhythmicity could be seen. In several cases missing REM sleep, sleep fragmentation or the reduction of slow wave sleep were observed. The study indicates that on the base of results from animal research the comparison of morphological and pathophysiological data is helpful to gain a better understanding on the coupling of the respiratory system with sleep at the brain stem level as well as on the pathomechanism of sleep related breathing disorder.

Adult↗
PubMed1988

Serious complications of microvascular decompression operations for trigeminal neuralgia and hemifacial spasm.

Serious complications of microvascular decompression operations for trigeminal neuralgia or hemifacial spasm are reported. Among 278 patients who underwent microvascular decompression, 9 serious complications were observed: 1 intracerebellar hematoma with acute hydrocephalus, 1 cerebellar swelling with acute hydrocephalus, 1 supratentorial acute subdural hematoma, 2 status epilepticus, 1 infarction of the brain stem, 1 subarachnoid hemorrhage due to traumatic aneurysm, and 1 infarction in the territory of the posterior cerebral artery. Of the 9 patients with such complications, 2 died. The possible causes of such serious complications are discussed.

Adult↗
PubMed1996

[Cerebral infarct in chronic acetylsalicylic acid poisoning].

Salicylates increase the risk of hemorrhage. An ischemic brain infarct has not previously been described following intoxication with salicylates. Case report. A 58-year-old comatose patient was admitted with symptoms of a basilar artery thrombosis. A diagnostic angiography was impossible because laboratory results showed a prothrombin time (Quick) of 9% and a toxic salicylate level of 528 mg/l. During the next few days CCT and MRI scans revealed ischemic infarctions within the brain stem. Discussion. Salicylates can induce hemorrhage both by inhibiting platelet aggregation and - especially in higher doses - by vitamin K antagonism, leading to severe coagulopathy. The occurrence of an ischemic infarction, as presented in this case report, can be explained by a reduction of the vitamin K-dependent protein C level.

Aspirin↗
PubMed2004

Effects of blood hyperviscosity on functional integrity in the brain stem: a brain stem evoked auditory potential study.

Clinical hemorheological and brain stem auditory evoked potential (BAEP) investigations were performed in patients with ischaemic brain stem stroke. Lesions were verified by MRI. 55 healthy persons with negative rheological and BAEP findings were used as controls (group A/1). 33 stroke patients with negative rheological parameters (group A/2) and 34 patients with hyperviscosity (group A/3) were also enrolled. In group A/3 bilateral pathological BAEP patterns were found, that could be explained by microcirculatory disturbances. 36 persons with verified blood hyperviscosity, but without neurological signs were also examined (group A/4). In this group, as in group A/3, either total lack of any waveforms, or a bilateral prolongation of wave III was observed. In 31 cases of group A/4, control BAEP was performed after effective haemodilution therapy, and 6-12 months later (group B/1). Here, normalization of rheological profile had a temporary beneficial effect on BAEP in 14 of 18 cases with former wave III prolongation, but had no effect on BAEP patterns in 13 cases, where lack of waves had been verified by the first investigation. These data suggest that hyperviscosity can result in subclinical pathological symmetric BAEP patterns, both in ischaemic stroke patients and in hyperviscosity patients without neurological symptoms.

Adult↗
PubMed1991

[Lateralization of secondary lesions of the brain stem in stroke by the method of short-latency auditory evoked potentials].

Twenty-seven patients with acute cerebral circulation disorders (ACCD) in large hemispheres and 4 patients with ACCD in the cerebellum were examined by means of short-latent acoustic evoked potentials (SAEP). The signs of the secondary stem syndrome were recorded in the neurological status of all the patients. Computer-aided tomography discovered displacement of the median structures of varying degree and deformation of cisternal spaces of the stem. The data obtained allowed a conclusion about a possibility of lateralization of the side of a greater injury to the stem by means of SAEP. As a rule, it was made ipsilaterally to the supratentorial focus. Provided the focus is seated subtentorially, a special pattern of SAEP may occur, namely primary changes in 1-3 components till complete disappearance of the evoked response.

Acute Disease↗
PubMed1993

Suppressed sympathetic skin response in brain infarction.

BACKGROUND AND PURPOSE: Autonomic failure is known to manifest commonly in stroke, but very little attention has been given to various features of sympathetic dysfunction such as sudomotor dysregulation in cerebrovascular diseases. In the present study, our purpose was to assess quantitatively sympathetic reflex activity in brain infarction by measuring the sympathetic skin response. METHODS: We recorded the sympathetic skin response to electric and auditory stimulations simultaneously on both hands in 58 patients with brain infarction and in 36 healthy control subjects. RESULTS: The response amplitudes were significantly decreased and the latencies prolonged in both hemispheral (n = 49) and brain stem (n = 9) infarctions compared with the control subjects. The amplitudes were diminished in both the acute and late phases of infarction, but the latencies were prolonged only in the acute phase. CONCLUSIONS: Sympathetic dysfunction in brain infarction seems to be much more extensive than has previously been thought. In the present study, we have demonstrated impaired sympathetic skin responses, reflecting definite suppression of the reflex activity of the sympathetic nervous system.

Acoustic Stimulation↗
PubMed1997

MRI and MR angiography of vertebral artery dissection.

A review of 4,500 angiograms yielded 11 patients with dissection of the vertebral arteries who had MRI and (in 4 patients) MR angiography (MRA) in the acute phase of stroke. One patient with incidental discovery at arteriography of asymptomatic vertebral artery dissection and two patients with acute strokes with MRI and MRA findings consistent with vertebral artery dissection were included. Dissection occurred after neck trauma or chiropractic manipulation in 4 patients and was spontaneous in 10. Dissection involved the extracranial vertebral artery in 9 patients, the extra-intracranial junction in 1, and the intracranial artery in 4. MRI demonstrated infarcts in the brain stem, cerebellum, thalamus or temporo-occipital regions in 7 patients with extra- or extra-intracranial dissections and a solitary lateral medullary infarct in 4 patients (3 with intracranial and 1 with extra-intracranial dissection). In 2 patients no brain abnormality related to vertebral artery dissection was found and in one MRI did not show subarachnoid haemorrhage revealed by CT. Intramural dissecting haematoma appeared as crescentic or rounded high signal on T1-weighted images in 10 patients examined 3-20 days after the onset of symptoms. The abnormal vessel stood out in the low signal cerebrospinal fluid in intracranial dissections, whereas it was more difficult to detect in extracranial dissections because of the intermediate-to-high signal of the normal perivascular structures and slow flow proximal and distal to the dissection. In two patients examined within 36 h of the onset, mural thickening was of intermediate signal intensity on T1-weighted images and high signal on spin-density and T2-weighted images. MRA showed abrupt stenosis in 2 patients and disappearance of flow signal at and distal to the dissection in 5. Follow-up arteriography, MRI or MRA showed findings consistent with occlusion of the dissected vessel in 6 of 8 patients.

Adult↗
PubMed1998

Diffusion-weighted echo-planar MRI of lacunar infarcts.

We studied 35 patients with lacunar infarcts, using diffusion-weighted echo-planar imaging (DW-EPI) at 1.5 T. The relative apparent diffusion coefficient ratio (ADCR) of each lesion was calculated and lesion conspicuity on DW-EPI was compared to that on images acquired with fast fluid-attenuated inversion recovery and T2-weighted fast spin-echo sequences. Acute small infarcts (within 3 days) were identified with DW-EPI as an area of decreased ADCR (range 0.33-0.87; mean 0.67) and high signal, subacute small infarcts (4-30 days) as a high-signal or isointense areas of decreased or nearly normal ADCR (0.54-0.98; 0.73), and chronic small infarcts (> 30 days) as low- or high-signal areas of nearly normal or increased ADCR (0.97-1.92; 1.32). In three patients, small infarcts of the brain stem in the hyperacute phase (within 6 h) were seen only with DW-EPI. In five patients, fresh small infarcts adjacent to multiple old infarcts could be distinguished only with DW-EPI.

Aged↗
PubMed2003

Functional recovery after simultaneous transplantation with neuro-epithelial stem cells and adjacent mesenchymal tissues into infarcted rat brain.

BACKGROUND: Cerebral infarction results in impairment of motor and cognitive functions. We performed intracranial transplantation of multipotential neuro-epithelial stem cells with mesenchyme into experimentally large ischemic lesions to study their potential to relieve deficits. METHODS: Wistar albino rats were subjected to transient middle cerebral artery occlusion for 60 minutes, producing an extensive ischemic lesion in the ipsilateral striatum and adjacent cerebral cortex. The rat mesencephalic neural plate at the early somite stage (embryonic day 10.5) together with adjacent ventral mesenchyme was used as donor material. We performed histological and immunohistochemical studies, with antibodies against tyrosine hydroxylase, and dopamine- and adenosine 3': 5'-monophosphate-regulated phosphoprotein 32 (DARPP-32; a striatal marker). Micro-angiograms were made by using Microfil silicone rubber. Morris Water-maze learning and treadmill task were employed to evaluate motor and cognitive functions. FINDINGS: A viable non-tumoral mass was recognized in the rat striatum, up to as long as 156 days after transplantation. There were many cells positive for tyrosine hydroxylase or DARPP-32 in the graft. Some of the DARPP-32 positive cells within the graft had extended their dendrites into host tissues. In the micro-angiograms, many fine vessels were observed within the graft and dilated vessels meandered around the graft. Transplanted animals recovered significantly better in motor and cognitive functions than animals injected with only culture medium. INTERPRETATION: Neuro-epithelial stem cells may follow several lines of differentiation; along the naturally genetically programmed line of differentiation, or along other cell lines depending on different environments. Grafting of neuro-epithelial stem cells with mesenchyme may merit a further study as a treatment for cerebral infarction.

Animals↗
PubMed1976

[Intracranial cerebral herniations and secondary lesions in the brain stem].

Intracranial cerebral herniations with secondary lesions in the brain stem are reported. The secondary lesions founded on the upper brain stem of 23 encephala with cerebral herniations are described. Hemorrhages in arteries were seen in all the brains. The lesions points to a mechanical etiology, the caudal displacement of the brain stem being the most important factor. Areas of ischemic infarction were found in the brain stem in all the cases; it is suggested that they were produced by factors other than the causative of the hemorrhagic lesions.

Brain Stem↗