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PubMed1984

The distribution of hypoglycemic brain damage.

Rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose, they were allowed to wake up and survive for 1 week. Control rats were recovered at the stage of EEG slowing. After sub-serial sectioning, the number and distribution of dying neurons was assessed in each brain region. Acid fuchsin was found to stain moribund neurons a brilliant red. Brains from control rats showed no dying neurons. From 10 to 60 min of cerebral isoelectricity, the number of dying neurons per brain correlated positively with the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min. Neuronal necrosis was found in the major brain regions vulnerable to several different insults. However, within each region the damage was not distributed as observed in ischemia. A superficial to deep gradient in the density of neuronal necrosis was seen in the cerebral cortex. More severe damage revealed a gradient in relation to the subjacent white matter as well. The caudatoputamen was involved more heavily near the white matter, and in more severely affected animals near the angle of the lateral ventricle. The hippocampus showed dense neuronal necrosis at the crest of the dentate gyrus and a gradient of increasing selective neuronal necrosis medially in CA1. The CA3 zone, while relatively resistant, showed neuronal necrosis in relation to the lateral ventricle in animals with hydrocephalus. Sharp demarcations between normal and damaged neuropil were found in the hippocampus. The periventricular amygdaloid nuclei showed damage closest to the lateral ventricles. The cerebellum was affected first near the foramina of Luschka, with damage occurring over the hemispheres in more severely affected animals. Purkinje cells were affected first, but basket cells were damaged as well. Rare necrotic neurons were seen in brain stem nuclei. The spinal cord showed necrosis of neurons in all areas of the gray matter. Infarction was not seen in this study. The possibility is discussed that a neurotoxic substance borne in the tissue fluid and cerebrospinal fluid (CSF) contributes to the pathogenesis of neuronal necrosis in hypoglycemic brain damage.

Animals↗
PubMed2001

[Brain infarction related to hepatic arterial infusion chemotherapy].

We examined the occurrence of brain infarction with hepatic arterial infusion chemotherapy for liver cancer. One hundred and eighty-one cases of hepatic arterial infusion chemotherapy were carried out for liver cancer patients in 4 hospitals associated with Osaka University 2nd Dept. of Surgery. These included metastatic (n = 103) and primary (n = 78) liver tumors. The medication was mainly 5-FU with/without CDDP and IFN. Catheters were inserted via the left subclavian artery in 106 cases and via the femoral artery in 75 cases. Among these patients, brain infarctions occurred in seven patients. Occlusions were found in the cerebellum (n = 3), thalamus (n = 1), brain stem (n = 1) and TIA (n = 2). All these patients had catheterization from the left subclavian artery. Furthermore, 64 patients of Ikeda Municipal Hospital were examined and analyzed for brain infarction, in order to eliminate the difference between facilities (all patients in Ikeda Municipal Hospital were catheterized via the left subclavian artery). Many more brain infarctions occurred in metastatic liver cancer patients than in primary liver cancer patients. The hemostasis function deteriorated in primary liver cancer patients, and is thought to be involved in the brain infarction. Six of seven cases of brain infarction occurred in vertebral artery supply area. It may be that the occurrence of brain infarction was related to the flow of the blood vessels.

Aged↗
PubMed2000

Gene polymorphism of the renin-angiotensin system associates with risk for lacunar infarction. The Ohasama study.

The polymorphism of the angiotensin-converting enzyme gene is considered to be associated with increased risk for stroke, but there is a diversity in the results obtained. The genetic involvement of the renin-angiotensin system in stroke also remains unclear. To predict the genetic risk of lacunar infarction, we conducted an association study in an Ohasama population, which is the cohort in a rural region of northern Japan. A total of 134 subjects without major neurological, cardiovascular, or metabolic disorders were recruited. Using brain magnetic resonance imaging, the number of lacunae in each of four brain regions were calculated, and periventricular hyperintensity was classified into five grades. We used the following four candidate gene polymorphisms: angiotensin converting enzyme (ACE)/Insertion(I)-Deletion(D), angiotensinogen (AGT)/M235T, angiotensin II type 1 receptor (AT1)/ A1166C, type 2 receptor (AT2)/C3123A, to examine the association between polymorphisms and the severity of lacunar infarction. AGT/M235T was significantly associated with the number of lacunae in the brain stem, the basal ganglia (P < .05), and whole brain (P < .005) regions. The AT1 polymorphism was also significantly associated with the number of lacunae in the basal ganglia and whole brain regions (P < .05), and with periventricular hyperintensity grade (P < .005) in the younger population. However, ACE and AT2 polymorphisms failed to show an association with either the number of lacunae or the PVH grade. We concluded that AGT and AT1 polymorphisms are independent genetic risk factors for lacunar infarction.

Aged↗
PubMed2000

Amyotrophic lateral sclerosis with a 'pseudo-infarction' pattern on the electrocardiograph. A case report.

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease involving both the upper and lower motor neurons in the brain stem and spinal cord. Although it is well known that various central nervous system disorders can produce a 'pseudo-infarction' pattern on the electrocardiogram, there have been no reports of this particular pattern in ALS patients. This report concerns an ALS patient who presented with an ECG pattern of S-T elevation followed by biphasic T and inverted T without any detectable myocardial abnormality. Data from the present case suggest that this pattern may be an inherent characteristic of ALS.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

[Lacunar cerebral infarcts].

Lacunes are small infarcts in the deep structures of the cerebral hemispheres and in the brain stem. They account for approximately 20 percent of all ischemic strokes, and usually occur in patients with chronic hypertension. The well-defined vascular changes and clinical pictures are described, as well as the principles of diagnosis and therapeutical management.

Aged↗
PubMed2002

Fatal subarachnoid hemorrhage, with brainstem and cerebellar infarction, caused by Aspergillus infection after cerebral aneurysm surgery: case report.

OBJECTIVE AND IMPORTANCE: Intracranial aspergillosis has been reported to cause subarachnoid hemorrhage (SAH) attributable to ruptured mycotic aneurysms. We describe a case of Aspergillus arteritis that caused SAH without aneurysm formation, followed by successive brainstem and cerebellar infarction. CLINICAL PRESENTATION: A 50-year-old woman experienced a sudden onset of headache. Computed tomography demonstrated SAH. After angiography revealed an aneurysm of the anterior communicating artery, a complete neck-clipping operation was performed, without neurological deterioration. However, the patient experienced another episode of SAH on the 26th postoperative day. INTERVENTION: We repeated the craniotomy and confirmed that the clip was still intact. A second angiographic evaluation did not reveal an aneurysm or any other cause of hemorrhage. On the 30th postoperative day, magnetic resonance imaging demonstrated cerebellar infarction in the territory of the anteroinferior cerebellar artery. The patient died on the 40th postoperative day, after another episode of SAH and progressive cerebellar and brainstem infarction. The postmortem examination revealed destruction of the basilar artery and occlusion of the basilar and vertebral arteries attributable to Aspergillus arteritis. CONCLUSION: When a patient presents with SAH of unknown origin followed by cerebral infarction, Aspergillus arteritis should be included in the differential diagnosis. Earlier recognition of this fungal infection improves the prognosis.

Arteritis↗
PubMed1981

A case of cortical deafness.

The presentation of cortical deafness, associated with mild dysphasia due to bilateral temporo-parietal infarction in a 70-year-old man, is described. Partial return of hearing occurred and associated with this a more complex cortical hearing disorder was seen with elements of both decreased auditory acuity and auditory agnosia. After 1 year a mild hearing loss persisted with difficulty in speech discrimination and an inability to recognise music. Bilateral temporo-parietal infarction was confirmed by CT scan. The cortical auditory evoked responses were initially absent despite intact brain stem auditory evoked responses. After a year, the cortical evoked responses had returned.

Aged↗
PubMed1987

[Magnetic resonance tomography of non-tumorous lesions of the pons].

The paper gives details of the diagnostic value of MRI in 20 cases of non-tumorous lesions of the pons. MR findings in haematoma (3), vascular malformations (2), infarctions (6), encephalitis (1), demyelinations (6) and atrophies (2) resulted in signal changes typical of the kind of disease. A pontine volume increase or decrease was proved comparing the data of the normal and affected brain stem. The topography of lesions was clearly documented by MRI. Subacute haematomas were better outlined than by CT, while acute infarctions, foci of demyelination and one case of ponsencephalitis were proved only by MRI. Small calcifications and vessels of an arteriovenous malformation, however, caused the same MR signal patterns.

Adult↗
PubMed2004

The effects of isolated brainstem lesions on human REM sleep.

BACKGROUND: Clinical and electrophysiologic data support the role of multiple brainstem structures responsible for sleep architecture. To determine if patients with isolated brainstem lesions have detectable abnormalities of sleep architecture with polysomnography (PSG). METHOD: The objective of this study is to determine if patients with isolated brainstem lesions defined by magnetic resonance imaging (MRI), and without sleep complaints, underwent PSG. The data was compared to age-matched controls. Eight patients met inclusion criteria. Of the eight locations, one was midbrain, two were pontomesencephalic, four were pontine and one was pontomedullary. RESULTS: Four of the eight patients had a decreased percentage of Rapid Eye Movement (REM) sleep. The abnormal studies occurred in patients with a right paramedian pontine infarct, a left pontomedullary cavernous hemangioma (CH), a left pontine CH, and a right pontomesencephalic CH. REM sleep, as a percentage of total bed time, was 8.7, 12.3, 14.8, and 16.7%, respectively. CONCLUSION: These findings concur with non-human data that depict pontine structures as the major generators of REM sleep.

Adult↗
PubMed1987

Acute direct and indirect lesions of the brain stem--CT findings and their clinical evaluation.

Since the introduction of computer tomography (CT) (Ambrose 1973, Hounsfield 1973) it has become an essential instrument in the diagnosis of acute intracranial lesions. The precise analysis of the CT and in particular the evaluation of the basal cisterns, yields results which are already wellknown, basically, from post-mortem investigations and clinical findings. However, while these were retrospective analyses and results, serial CT examinations which are free of risk for the patient and can be used in correlation with the clinical neurological findings, allow important assertions intra vitam, as well as a definitely better assessment of the prognosis. In addition to acute supratentorial lesions, acute and subacute infratentorial lesions are analysed and their clinical significance described. In this way, for the first time, the dynamics of the mechanical factors in raised intracranial pressure can be analysed. Important conclusions are drawn for the clinical management of the patients, and even some new indications for operation. Analysis of the acute hyperdense brain stem lesions--pathognomonic for haemorrhages--allows for the first time the diagnosis and continuous observation of traumatic and secondary haemorrhages caused by raised pressure, as well as spontaneous ones. As regards the mortality and morbidity, the results in this large series of traumatic and secondary haemorrhages are in striking contrast to previous analyses based on post mortem findings. Acute hypodense brain stem lesions are not amenable to any definite pathogenetic classification--softening, inflammatory lesions, tumours and oedema must all be considered. With acute lesions we are only dealing with infarcts, which are only incompletely assessable in the computer tomogram, and their diagnosis must still depend on the clinical findings. Secondary ischaemic lesions in acute raised intracranial pressure are identifiable in over 18% as infarcts which involve the entire territory of an artery. These additional space-occupying lesions are only survived by 11% of the patients. Hence the correlation which has been established between the basal cisterns and intracranial pressure is of great clinical significance. From our own research group several reports on different aspects of raised intracranial pressure and lesions of the brain stem have appeared since 1979. Similar analyses of partial aspects of the basal cisterns, have been published only recently, and came essentially to the same conclusions.

Acute Disease↗
PubMed1986

[Nuclear magnetic resonance imaging of the brainstem: evaluation of the normal structures and small lesions].

Nuclear magnetic resonance (NMR) imaging of the brainstem region from 12 asymptomatic individuals were reviewed in addition to these of 12 patients with various symptoms of small brainstem lesions. Abnormalities consisted of 3 cases of multiple sclerosis, 1 case of neuro-Behçet disease, 5 cases of infarction and hematoma and 3 cases of degenerative disease. NMR transverse imaging using inversion recovery sequence was able to locate many of the normal intra-axial brainstem nuclei, such as the periaqueductal gray matter, the red nucleus, the substantia nigra, the pontine nuclei, the pontine reticular nuclei, the facial nerve nucleus and so on in an about half of 12 asymptomatic individuals. The remarkable gray-white matter differentiation was obtained on NMR imaging using inversion recovery sequence and enabled the internal structures to be visualized within the brainstem. In addition, the midsagittal imaging provided an excellent demonstration of anatomical relationships of the brainstem and surrounding structures. In the diencephalic region, the mamillary body, the anterior commissure and the optic chiasma were also demonstrated on the midsagittal imaging. The lesions within the brainstem were vaguely shown on X-ray computed tomography in 6 of 12 patients but NMR imaging using inversion recovery or spin echo sequence provided more detailed data and revealed clear small lesions, such as the demyelinated plaques of multiple sclerosis and lacunar infarcts in 9 of 12 patients. Especially, in 2 of 3 multiple sclerosis patients, the plaques of the brainstem were definitely identified on NMR imaging only and the accurate localized lesion which was responsible for the facial myokymia or the Foville syndrome was identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Neurochemical changes following occlusion of the middle cerebral artery in rats.

We have developed a stroke model involving middle cerebral artery occlusion in the rat which elicits changes in cardiac and autonomic variables that are similar to those observed clinically. It is likely that these neurogenic autonomic responses are mediated by changes in neurotransmitter systems subsequent to the stroke. This possibility was investigated by examining changes in immunohistochemical staining for tyrosine hydroxylase, neuropeptide Y, leu-enkephalin, neurotoxins and dynorphin following middle cerebral artery occlusion in the rat. Computerized image analysis was used to provide semi-quantitative measurements of the changes. The ischemic region was centered primarily in the insular cortex. The results indicate that there are significant increases in immunostaining for tyrosine hydroxylase and neuropeptide Y in the insular cortex within the peri-infarct region. Neuropeptide Y staining was also significantly increased in the basolateral nucleus of the amygdala, ipsilateral to the middle cerebral artery occlusion, which did not appear to be included in the infarct. Leu-enkephalin, neurotensin and dynorphin staining was significantly elevated in the central nucleus of the amygdala ipsilateral to the occlusion of the middle cerebral artery. These neurochemical changes are discussed as possible mechanisms mediating the cardiac and autonomic consequences of stroke or as part of a process to provide neuro-protection following focal cerebral ischemia.

Amygdala↗
PubMed1978

Brainstem lesion with coma for five years following manipulation of the cervical spine.

A woman, aged 38, lost consciousness immediately after manipulation of the cervical spine and remained in coma for nearly 5 years in a combined decorticate and decerebrate state. Cerebral angiography revealed impaired circulation in the vertebrobasilar system. The EEG initially showed generalized cerebral dysrhythmia but tended, over the years, to become more normal with desynchronized fast activity of low voltage. Neuropathological examination postmortem revealed a large cystic lesion in the pressure equalization area of the carotid and basilar circulation in the upper pons, mesencephalon, posterior hypothalamus and basal thalamus. No definite stenosis or occlusion was seen in the cerebral vessels on angiography or at the postmortem examination. The mechanism of the lesion is considered to have been temporary interference with the blood flow in the vertebrobasilar system during manipulation of the cervical spine sufficient to cause ischemia and subsequent infarction of the brainstem. The pathogenesis of vascular lesions of the brain stem following manipulation of the cervical spine is discussed briefly.

Adult↗
PubMed1987

Artery-to-artery embolism causing stroke in the posterior circulation.

The features of strokes caused by embolism from the vertebral artery (VA) to the posterior cerebral artery (PCA) are reported in 12 patients ("local" or "artery-to-artery embolism"). Occipital infarction occurred with prominent, fluctuating brainstem ischemic symptoms in six; with minor, transient brainstem symptoms in five; and with basilar artery occlusion in one. Visual field abnormalities were found on initial examination in eight and several days after the onset of brainstem symptoms in four. Radiographic studies in 11 identified extracranial (5 patients) or intracranial (3 patients) VA disease, or occlusion of both segments (3 patients) as sources of emboli to the PCA. Mural thrombus in the VA or embolic occlusion of distal branches of the PCA was visualized in five.

Adult↗
PubMed2004

Topodiagnostic investigations on the sympathoexcitatory brain stem pathway using a new method of three dimensional brain stem mapping.

OBJECTIVES: To study the incompletely understood sympathoexcitatory pathway through the human brain stem, using a new method of three dimensional brain stem mapping on the basis of digitally postprocessed magnetic resonance imaging (MRI). METHODS: 258 consecutive patients presenting with acute signs of brain stem ischaemia underwent biplane T2 and EPI diffusion weighted MRI, with slice orientation parallel and perpendicular to a transversal slice selection of the stereotactic anatomical atlas of Schaltenbrand and Wahren, 1977. The individual slices were digitally normalised and projected onto the appropriate slices of the anatomical atlas. For correlation analysis lesions were imported into a three dimensional model of the human brain stem. RESULTS: 31 of the 258 patients had Horner's syndrome caused by acute brain stem ischaemia. Only four of the patients with Horner's syndrome had pontine infarctions, 12 had pontomedullary lesions, and 15 had medullary lesions. Correlation analysis showed significantly affected voxels in the dorsolateral medulla but not in the pons. A statistical comparison with infarct topology in patients with medullary lesions but without Horner's syndrome indicated that involvement of the medial and ventral part of affected voxels located in the ventrolateral medullary tegmentum was specific for Horner's syndrome. CONCLUSIONS: Based on this first in vivo topodiagnostic study, the central sympathoexcitatory pathway probably descends through the dorsal pons before converging on specific generators in the ventrolateral medullary tegmentum at a level below the IX and X nerve exits.

Aged↗
PubMed2004

Functional recovery of stroke rats induced by granulocyte colony-stimulating factor-stimulated stem cells.

BACKGROUND: Stroke is a leading cause of death and disability worldwide; however, no effective treatment currently exists. METHODS AND RESULTS: Rats receiving subcutaneous granulocyte colony-stimulating factor (G-CSF) showed less cerebral infarction, as evaluated by MRI, and improved motor performance after right middle cerebral artery ligation than vehicle-treated control rats. Subcutaneous administration of G-CSF enhanced the availability of circulating hematopoietic stem cells to the brain and their capacity for neurogenesis and angiogenesis in rats with cerebral ischemia. CONCLUSIONS: G-CSF induced increases in bone marrow cell mobilization and targeting to the brain, reducing the volume of cerebral infarction and improving neural plasticity and vascularization.

Animals↗
PubMed1988

Magnetic resonance imaging in young adults with cerebral infarction due to moyamoya.

The number, size, and location of cerebral infarctions, and blood flow in the middle cerebral artery as seen on proton magnetic resonance imaging were assessed in six white adults with angiographically documented moyamoya. Findings were correlated with clinical presentation, computed tomography, and angiography. Large hemispheric infarctions were found in five hemispheres, predominantly in watershed regions. Subcortical infarctions (n = 56) were found in all hemispheres. They were predominantly located in the centrum semiovale, in the distal beds of supply of the penetrating branches of the anterior and middle cerebral arteries. Infarction of the putamen was found in three hemispheres, caudate nucleus in four, globus pallidus in two, and anterior limb of the internal capsule in two. There were none in the posterior limb of the internal capsule, thalamus, brain stem, or cerebellum. Middle cerebral artery flow was visualized as a signal-void flow sign in only three hemispheres. Cerebral infarctions due to moyamoya are bilateral, multiple, often small, and asymptomatic, affecting predominantly the carotid circulation in watershed regions. Subcortical infarctions in the centrum semiovale and large hemispheric infarctions in hemodynamically compromised areas are the predominant findings.

Adolescent↗
PubMedDate not supplied

Magnetic resonance imaging findings and correlations in spasmodic dysphonia patients.

A sample of 19 spasmodic dysphonia (SD) patients was selected from a larger population of such patients to undergo magnetic resonance imaging (MRI), auditory brain stem response (ABR) testing, speech analysis, and extensive physical examination. Six patients had abnormal spin-echo MRI findings, ranging from infarcts within the basal ganglia to demyelinating lesions within the supralateral angles of the lateral ventricles. A weakly positive correlation was noted between the abnormal MRI findings and an abnormal ABR. The lack of a significant correlation between the MRI findings and other predictors of brain stem and midbrain disease, and the current spatial resolution limitations of MRI, suggest that we are visualizing the associated lesions rather than the actual foci of SD. The range of MRI findings is consistent with the concept that SD is a voice disorder in a heterogeneous patient population.

Adult↗