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PubMed1989

[Anatomy of the cerebellar arteries].

Origin, course and distribution of the cerebellar arteries and of their branches are described. Anatomical drawings of the territory of these arteries are presented. They are based on a neuropathological study of 64 cases of cerebellar infarctions, the detailed study of which is reported elsewhere. The superior cerebellar artery (SCA) supplies a small brain stem territory, located on the dorsal tegmentum and the tectum of the upper part of the pons. The superior part of the cerebellum supplied by this artery includes the following lobules: lobulus anterior, lobulus simplex, lobulus semilunaris superior, and, in the vermis, lobulus centralis, culmen and clivus. The dentate nucleus belongs to this territory. The anterior inferior cerebellar artery (AICA) irrigates a ponto-cerebellar territory. It usually supplies the lateral territory of the lower part of the pons, the middle cerebellar peduncle, the flocculus and the neighbouring lobules of cerebellum. When the posterior inferior cerebellar artery (PICA) is hypoplastic, AICA takes over the territory usually supplied by the lateral branch of the PICA. The PICA always gives rami to the group of arteries supplying the dorsal medullary territory, but rarely participates to the supply of the lateral medullary territory. It supplies the lobulus semilunaris inferior, the lobulus gracilis, the lobulus biventer, the tonsilla cerebelli, and, in the vermis, the clivus, the tuber, the pyramis, the uvula and the nodulus. PICA never supplies the dentate nucleus. The flocculo-nodular lobe is usually supplied by 2 arteries: the flocculus is supplied by the AICA and the nodulus is supplied by the PICA.

Arteries↗
PubMed1995

[Complications in multiple systems resulting from acute cerebrovascular diseases].

One hundred and eighty five patients died of acute cerebrovascular diseases with complications in multiple systems were studied. Statistical analyses showed that there were no organ and system failure (NOSF) in 47 cases, single organ and system failure (SOSF) in 47 and multiple organ and system failure (MOSF) in 91. Out of 90 (50%) cases who had cerebral herniation, 39 cases were complicated with SOSF and 53 cases with MOSF. Among the patients with acute brain diseases, 25% of them (46) died of SOSF (4%, 8 cases) and MOSF (21%, 38) without herniation. Incidence of failure of organ and system was higher with stomach, metabolism and lung than with heart, kidney and blood. It took on the average 24 and 12.5 hours for the first organ and system to fail and 4 days and 24 hours for the second organ in patients with intracranial hemorrhage and cerebral infarction. Occurrence of organ and system failure was closely related to sex, previous diseases and damage of brain stem, but not to the size and number of the lesion. It is suggested that cerebrogenic organ and system failure (COSF) or cerebrogenic multiple organ and system failure (CMOSF) be referred to functional failure of more than two organs or system not including brain itself as a result of acute brain diseases.

Brain Stem↗
PubMed1994

[A case of bilateral cerebellar peduncle infarction with bilateral hearing impairment of a sudden onset].

We reported a patient with bilateral cerebellar peduncle infarcts who had an abrupt onset of bilateral hearing loss. A hypertensive 56-year-old man suddenly experienced bilateral hearing loss without other accompanying neurological deficits. He was hospitalized and treated for "idiopathic deafness". In addition, dysarthria and ataxic gait appeared two days later and he was transferred to our hospital. On neurological examination, the patient presented with diplopia, neurosensory hearing loss (approximately 70 dB) ataxic dysarthria, bilateral cerebellar ataxia and bilateral Babinski's signs. Auditory brain stem evoked response demonstrated prolonged delay of interpeak latency between waves III-IV. CT and MRI revealed fresh ischemic lesions symmetrically located at the middle cerebellar peduncles and cerebellar medullary body. Cerebral angiography showed total occlusion of the left vertebral artery and a stenotic right vertebral artery at the ostium of the posterior inferior cerebellar artery. We postulated that hearing impairment in this patient resulted from transient ischemia of the bilateral auditory tract in the brain stem or the peripheral cochlear system, but the definitive cause of the transient hearing loss remains undetermined. Concomitant appearance of a symmetrical infarction at the cerebellar peduncles is rare. We suggest that a circulation defect involving a multivascular system, which resulted in "border zone infarction" occurred at these regions.

Arterial Occlusive Diseases↗
PubMed1983

[Vocal cord myoclonus. A case report on the posterior inferior cerebellar artery syndrome].

The present article describes a patient with ischemia in the vascular territory of the posterior inferior cerebellar artery, who developed, in addition to other typical signs of the dorsolateral medulla oblongata, myoclonic movements of the ipsilateral vocal cord. The essential neuropathological lesion is considered to be an impairment of the dentato-olivary system. In this respect there is a close relationship to other types of rhythmical myoclonus due to lesions of the brain-stem and cerebellum.

Cerebellar Ataxia↗
PubMedDate not supplied

[Brain stem involvement in eclampsia and HELLP syndrome].

INTRODUCTION: Nowadays, eclampsia is a rare complication of pregnancy and the puerperium. However, it is still one of the main causes of maternal morbi-mortality. Systemic findings in eclampsia may sometimes include association with microangiopathic hemolytic anaemia, raised liver enzymes and thrombocytopenia. This clinical combination constitutes the HELLP syndrome (Hemolysis Elevated Liver enzymes Low Platelets). The commonest neurological findings in eclampsia are headache, visual alterations, convulsions and stupor or coma. The presence of clinical symptoms and signs due to brainstem disorders is unusual. CLINICAL CASE: We present the case of a thirty year old woman with eclampsia and associated HELLP syndrome, which briefly affected the brain stem. The patient showed progressive general and neurological improvement. Three months afterwards she still had paresia of the sixth right cranial nerve, due to what was presumed to be a right paramedian infarct of the pons. CONCLUSION: We consider it important not to forget this exceptional association so that suitable treatment may be given to such patients since prognosis is not invariably bad.

Adult↗
PubMed2003

Hypertensive brainstem encephalopathy: clinical and radiographic features.

Reversible posterior leukoencephalopathy syndrome associated with hypertension rarely presents with predominant involvement of the brainstem and relative sparing of the supratentorial regions. We describe the clinical and neuroimaging features of three patients with reversible hypertensive brainstem encephalopathy. Headache and confusion in the setting of severe hypertension, with a relative paucity of brainstem signs and symptoms, despite extensive neuroimaging abnormalities in the brainstem support the diagnosis. The clinical findings and neuroimaging abnormalities resolve with treatment of the hypertension, further distinguishing this syndrome from brainstem infarction.

Adult↗
PubMed1981

Cervical vertebral angioplasty for brain stem ischemia.

Fifty-eight patients underwent unilateral vertebral arterial reconstructions over a 16-year period. Thirty-four underwent carotid operations as well. The first 18 patients underwent vertebral arterial reconstructions in conjunction with carotid endarterectomy as mandated in the Joint Study of Extracranial Arterial Occlusion as a Cause of Stoke. The next 40 underwent vertebral procedures for either brain stem symptoms alone, or for combined cerebral cortical and stem symptoms for specific indications after flow-obstructing carotid lesions had been corrected, but symptoms failed to subside. The surgical procedure consisted of subclavian-vertebral angioplasty except in one patient who underwent a subclavian distal-vertebral bypass graft to the level of the second cervical vertebral body. Syncopal episodes occurred as a major symptom in 16 and was controlled by either carotid and vertebral or vertebral artery operation alone except in four who also required cardiac pacemakers and one who needed correction of aortic stenosis. The long-term follow-up reveals that the stroke rate per average year for the first 14 years of follow-up was 1.2% per patient year with only five strokes having occurred in 410 patient years of follow-up and 70% of the patients having sustained no new neurologic episodes at the fourteenth year. Survival, however, was 45% at the fourteenth year with most deaths caused by myocardial infarction. The surgical procedure of vertebral angioplasty is indicated when bilateral vertebral arterial flow-obstructing lesions are found in patients with brain stem ischemia including drop attacks and syncopal episodes if flow-obstructing carotid lesions have been corrected and symptoms persist. The surgical procedure can be performed with a high degree of safety. The differential diagnosis of drop attacks and syncope in this age group should include, in addition to vertebrobasilar arterial insufficiency, transient cardiac arrhythmias, aortic stenosis, and convulsive disorders.

Brain Stem↗
PubMed2006

Neuroprotection in ischemic mouse brain induced by stem cell-derived brain implants.

Protective mechanisms of the brain may reduce the extent of injury after focal cerebral ischemia. Here, we explored in a mouse model of focal cerebral ischemia potential synergistic neuroprotective effects of two mediators of neuroprotection: (i) neuronal or glial precursor cells and (ii) the inhibitory neuromodulator adenosine. Embryonic stem (ES) cells, engineered to release adenosine by biallelic disruption of the adenosine kinase gene, and respective wild-type cells were induced to differentiate into either neural or glial precursor cells and were injected into the striatum of mice 1 week before middle cerebral artery occlusion. All stem cell-derived graft recipients were characterized by a significant reduction in infarct volume, an effect that was augmented by the release of adenosine. Neuroprotection was strongest in adenosine-releasing glial precursor cell recipients, which were characterized by an 85% reduction of the infarct area. Graft-mediated neuroprotection correlated with a significant improvement of general and focal neurologic scores. Histologic analysis before and after ischemia revealed clusters of implanted cells within the striatum of all treated mice. We conclude that ES cell derived adenosine-releasing brain implants provide neuroprotection by synergism of endogenous precursor cell-mediated effects and paracrine adenosine release.

Adenosine↗
PubMed2001

Imaging appearance of the symptomatic perforating artery in patients with lacunar infarction: occlusion or other vascular pathology?

Lacunar infarction is associated with distinct clinical features. It is thought to result from occlusion of a deep perforating artery in the basal ganglia, centrum semiovale, or brain stem. However, occluded perforating arteries have only rarely been observed at postmortem in patients with lacunar stroke and have not been noted previously on imaging despite the increasing sophistication of the techniques. We observed nine patients with lacunar stroke imaged with computed tomography and magnetic resonance imaging in whom we observed a linear structure with density or signal features consistent with an occluded (or at least abnormal) perforating artery associated with the relevant lacunar infarct. The appearance might also have been caused by a leak of blood and fluid into the perivascular space around the artery, as in several patients the width of the tubular vessel-like structure (>1 mm in diameter) was greater than the expected width of a perforating artery (<0.8 mm in diameter). This interpretation is supported by the fact that the area of infarction was usually around the abnormal vessel, not at the end of it. We describe the patients' clinical and imaging features, and discuss alternative explanations for the imaging appearance and the implications for gaining insights into the cause of lacunar infarction.

Aged↗
PubMed2005

Inhibition of brain damage by edaravone, a free radical scavenger, can be monitored by plasma biomarkers that detect oxidative and astrocyte damage in patients with acute cerebral infarction.

We assess the availability of plasma biomarkers to monitor the brain damage and the therapeutic efficacy of edaravone. The study consisted of 51 patients with ischemic cerebral infarcts. They were divided into 2 groups: GI (n = 24) had cortical lesions, and GII (n = 27) had lesions in the basal ganglia or brain stem. Edaravone was administered to 27 randomly selected patients (GIa, n = 13; GIIa, n = 14) and its efficacy was studied by comparing their plasma OxLDL, S-100B, and MnSOD levels to those in patients without edaravone (GIb, n = 11, GIIb, n = 13). Three days after the start of edaravone, plasma OxLDL was significantly lower in GIa than GIb patients (0.177 +/- 0.024 ng/microg apoB vs 0.219 +/- 0.026, P < 0.05). In GIIa patients, pre- and posttreatment plasma OxLDL was not significantly different (0.156 +/- 0.013 vs 0.152 +/- 0.020). In GIa patients, S-100B and MnSOD were significantly lower than in GIb patients (P < 0.05). The neurological condition at the time of discharge had recovered in GIa but not GIb patients. Ours is the first evidence to confirm the efficacy of edaravone by plasma biomarkers. In patients with cortical infarcts, edaravone reduced oxidative damage, thereby limiting the degree of brain damage.

Adult↗
PubMed2002

Blood into brain after stroke.

Using a bone-marrow transplantation chimera-model in mice, we have shown that after a cerebral infarction, bone marrow-derived cells differentiate into cerebral endothelial cells and NeuN-expressing cells

Animals↗
PubMed2005

Mobilization of CD34(+), CD117(+), CXCR4(+), c-met(+) stem cells is correlated with left ventricular ejection fraction and plasma NT-proBNP levels in patients with acute myocardial infarction.

AIMS: The aim of the study was to assess the correlation between the number of CD34(+), CD117(+), c-met(+), CXCR4(+) stem cells mobilized into peripheral blood, left ventricular ejection fraction (LVEF), NT-proBNP levels, and myocardial necrosis markers in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: 43 patients with STEMI were enrolled. Stem cells number was measured using flow-cytometer and concentrations of NT-proBNP, SDF-1, G-CSF, VEGF, IL-6, and HGF were measured using ELISA kits. The number of stem cells mobilized early (<12 h) in AMI was significantly, positively correlated with LVEF: r=0.49 (P=0.0012) for CD34(+) cells, r=0.48 (P=0.0018) for CXCR4(+) cells, r=0.45 (P=0.0043) for CD117(+) cells, and r=0.41 (P=0.01) for c-met(+) cells and negatively correlated with NT-proBNP levels on admission r=-0.35 (P=0.024) for CD34(+) cells, r=-0.42 (P=0.007) for CXCR4(+) cells, r=-0.33 (P=0.04). In patients with LVEF </=40%, the peak number of CD34(+), CXCR4(+), CD117(+), and c-met(+) stem cells was significantly lower when compared patients with LVEF >40%. The number of CXCR4(+) cells on admission and after 24 h was negatively correlated with respective cardiac Troponin I levels (r=-0.37; P=0.029 and r=-0.45, P=0.02) and maximum activity of CK-MB (r=-0.37; P=0.021). No significant correlations between levels of haematopoietic cytokines and LVEF were found. CONCLUSION: The mobilization of CD34(+), CD117(+), CXCR4(+), c-met(+) stem cells into peripheral blood early in STEMI is positively correlated with LVEF and negatively correlated with NT-proBNP levels and myocardial necrosis markers.

Antigens, CD34↗
PubMed1992

[Use of hyperbaric oxygenation in the treatment of acute cerebrovascular disorders in ischemic heart disease].

Altogether 22 patients with concomitant cardio-cerebral acute pathology underwent all-round examinations during and after sessions of hyperbaric oxygenation (HBO). The highest clinical effect was produced by minor, substituting doses of HBO. The revealed phasic nature of the action of HBO in the treatment of patients with acute large-focal myocardial infarction and acute cerebrovascular disorders was found to be due to changes in the function of diencephalic and brain stem formations, determining the decrease of adaptation potentialities in this patients' group. HBO was found to be clinically effective in the treatment of such patients. In order to raise the treatment efficacy, it is necessary that an individual approach be exercised in the choice of therapeutic HBO sessions.

Acute Disease↗
PubMed2006

Administration of hematopoietic cytokines in the subacute phase after cerebral infarction is effective for functional recovery facilitating proliferation of intrinsic neural stem/progenitor cells and transition of bone marrow-derived neuronal cells.

BACKGROUND: Hematopoietic cytokines, granulocyte colony-stimulating factor (G-CSF), and stem cell factor (SCF) were reported to show a neuroprotective effect or to support neurogenesis. These cytokines also mobilize bone marrow (BM) cells into the brain, and the BM-derived cells differentiate into neuronal cells. We administered these hematopoietic cytokines after focal cerebral ischemia and assessed their effects and the therapeutic time window for neuronal regeneration. METHODS AND RESULTS: We induced permanent middle cerebral artery occlusion in mice whose BM had been replaced with BM cells from green fluorescent protein (GFP)-transgenic mice. The occluded mice were treated with G-CSF and SCF in the acute phase (days 1 to 10) or subacute phase (days 11 to 20), and the brain functions and histological changes were evaluated. Separately, we injected bromodeoxyuridine during cytokine treatment to assess cell kinetics in the brain. Six mice were prepared for each experimental group. Administration of G-CSF and SCF in the subacute phase effectively improved not only motor performance but also higher brain function, compared with acute-phase treatment. Acute-phase and subacute-phase treatments identically reduced the infarct volume relative to vehicle treatment. However, subacute-phase treatment significantly induced transition of BM-derived neuronal cells into the peri-infarct area and stimulated proliferation of intrinsic neural stem/progenitor cells in the neuroproliferative zone. CONCLUSIONS: Administration of G-CSF and SCF in the subacute phase after focal cerebral ischemia is effective for functional recovery, enhancing cytokine-induced generation of neuronal cells from both BM-derived cells and intrinsic neural stem/progenitor cells. Because G-CSF and SCF are available for clinical use, these findings suggest a new therapeutic strategy for stroke.

Animals↗
PubMed1982

[Encephalitis with necrosis limited to the brain stem: a case report (author's transl)].

A 38-year-old woman with encephalitis presented no signs of infectious disease or exanthema. After a remission lasting 10 months, she died during a second attack after demonstrating signs of brain stem lesions. Histological examination revealed lesions, mainly in the brain stem and characterized by intense necrosis, moderate degrees of inflammation, and localized foci of gliosis. In spite of the necrotic lesions, the neurones were relatively spared. An old infarct of the left caudate nucleus was present. Taking other demyelinating diseases into account, it is suggested that this is a clinical form of multiple sclerosis, this enabling a relationship to be established between multiple sclerosis and post-infections perivenous encephalitis or acute disseminated encephalomyelitis.

Adult↗
PubMedDate not supplied

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: MR findings.

PURPOSE: To describe the MR appearances of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. METHODS: MR examinations were performed on 15 family members (both symptomatic and asymptomatic). The phenotype was defined by the presence of abnormalities on MR scanning in genetically susceptible individuals. RESULTS: There were 10 abnormal and 5 normal MR scans. Three subjects with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy had moderate or severe neurologic deficits, 4 had transient focal neurologic symptoms, 2 had migraine, and 1 was asymptomatic (all these had abnormal MR scans). Only 1 subject with migraine had a normal MR. Four other asymptomatic family members had normal scans. Two main abnormalities emerged. First, small, linear, and punctate lesions were identified in the periventricular white matter, brain stem, basal ganglia, and thalamus. Second, large confluent patches of abnormal tissue were present in subcortical regions that often were symmetric and had a tendency to occur in the temporal lobes. CONCLUSIONS: The diffuse myelin loss and small infarcts that cause cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy are well demonstrated with MR. Presymptomatic abnormalities can be seen on MR.

Adult↗
PubMed2003

[Role of PPARgamma in the development of the central nervous system].

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that plays a central role in adipocyte differentiation and insulin sensitivity. Recently, a diversity of the action of PPARgamma on many other cell types or organs is indicated. We summarize here the possible role of PPARgamma in the development of the murine central nervous system. Expressions of PPARgamma in newborn or adult mouse brain are extremely low, but high in embryo or fetal mouse brain. Furthermore, we investigated the role of PPARgamma in proliferation or differentiation of neural stem cells (NSCs) isolated from murine embryonic brains, because NSCs are considered to be a major source of neurons in developmental brains. Administrations of PPARgamma-specific ligands on the NSCs from wild-type mice resulted in the stimulation of cell growth. On the other hand, administration of PPARgamma-antagonist showed the cell death and apoptosis of NSCs. These results may indicate that PPARgamma plays an important role during the early stage of the development of the central nervous system.

Animals↗