Segmental shrinkage and argentophilia of dendrons after fixation by perfusion with dimethyl sulfoxide (DMSO)-containing solutions.
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Animals↗
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Results for “Brain Stem Infarctions”
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An fMRI study of cortical representation of mechanical allodynia in patients with neuropathic pain.
OBJECTIVE: To investigate cerebral activity associated with allodynia in patients with neuropathic pain. METHODS: The brain responses of 27 patients with peripheral (5), spinal (3), brainstem (4), thalamic (5), lenticular (5), or cortical (5) lesions were studied with fMRI as innocuous mechanical stimuli were addressed to either the allodynic territory or the homologous contralateral region. RESULTS: When applied to the normal side, brush and cold rubbing stimuli did not evoke pain and activated a somatosensory "control" network including contralateral primary (SI) and secondary (SII) somatosensory cortices and insular regions. The same stimuli became severely painful when applied to the allodynic side and activated regions in the contralateral hemisphere that mirrored the "control" network, with, however, lesser activation of the SII and insular cortices. Increased activation volumes were found in contralateral SI and primary motor cortex (MI). Whereas ipsilateral responses appeared very small and restricted after control stimuli, they represented the most salient effect of allodynia and were observed mainly in the ipsilateral parietal operculum (SII), SI, and insula. Allodynic stimuli also recruited additional responses in motor/premotor areas (MI, supplementary motor area), in regions involved in spatial attention (posterior parietal cortices), and in regions linking attention and motor control (mid-anterior cingulate cortex). CONCLUSION: On a background of deafferentation in the hemisphere contralateral to stimuli, enhanced or additional responses to innocuous stimuli in the ipsilateral hemisphere may contribute to the shift of perception from innocuous toward painful and ill-defined sensations.
Basal Ganglia↗
Central deafness associated with a midbrain lesion.
Central deafness has been linked historically to bihemispheric involvement of the temporal lobe, with more recent findings suggesting that compromise of other cortical and subcortical structures can also result in this disorder. The present investigation extends our understanding of the potential anatomical correlates to central deafness by demonstrating that bilateral involvement of an auditory structure within the midbrain can additionally result in this condition. Our subject was a 21-year-old male with a subarachnoid bleed affecting both inferior colliculi. Significant auditory deficits were noted for the middle and late auditory evoked potentials, while electrophysiologic measures of the periphery indicated normal function. The patient was enrolled in a rehabilitation program for approximately 14 weeks. Although initially unresponsive to sounds, the patient regained most of his auditory abilities during the 10 months he was followed. This case documents the range of auditory deficits that may be associated with damage to the inferior colliculi, and it profiles a hierarchical recovery of auditory function consistent with test findings.
Adult↗
MR findings in acute and chronic coccidioidomycosis meningitis.
PURPOSE: To characterize MR findings in acute and chronic coccidioidomycosis meningitis and relate the imaging features to the clinical course. METHODS: We reviewed MR scans and clinical findings of 12 patients with coccidioidal meningitis. RESULTS: Patients with active or untreated disease were found to have hydrocephalus and intense enhancement of the cervical subarachnoid space, basilar, sylvian, and interhemispheric cisterns on postcontrast MR scans. Focal parenchymal signal abnormalities suggesting ischemia or infarction were common. Abnormal MR enhancement decreases during therapy, although patients develop cortical and/or brain stem atrophy. CONCLUSIONS: Widespread cisternal and cervical subarachnoid meningeal involvement is common in coccidioidal meningitis. Serial contrast MR imaging reflects the effects of therapy in patients with coccidioidal meningitis.
Acute Disease↗
[Effects of exercise training on mobilization of BM-CPCs and migratory capacity as well as LVEF after AMI].
BACKGROUND AND PURPOSE: Bone marrow-derived circulating progenitor cells (BM-CPCs) are mobilized in adult peripheral blood (PB) during the acute myocardial infarction (AMI) period and contribute to the regeneration of infarcted myocardium. In this study, the influence of physical training on the mobilization and the migratory activity of the BM-CPCs as well as on the left ventricular function (LVEF) after AMI was examined. PATIENTS AND METHODS: 26 patients with AMI were analyzed in two groups. The first group comprised 17 patients with standardized exercise training for 3 weeks 14 +/- 4 days after AMI, the second group nine control subjects without exercise training. PB concentrations of CD34/45+ and CD133/45+ were measured by FACS. The migratory activity of BM-CPCs was analyzed by migration assay. B-type natriuretic peptide (BNP) in PB and the functional investigations spiroergometry (VO2 and PaO2) and stress echocardiography (LVEF) were determined in both groups. RESULTS: A significant increase in both concentrations, CD34/45+ and CD133/45+, as well as in migratory capacity of BM-CPCs was found after 3 weeks of exercise training, which was significantly decreased 3 months after completion of exercise training. No significant difference was observed in the control group without exercise training. In the functional investigations a significant increase in VO2 as well as PaO2 was shown spiroergometrically after exercise training. There was no difference in stress echocardiographic LVEF at rest in both groups. On the other hand, interestingly, the findings showed that the increase of LVEF at peak stress was significantly higher after exercise training as compared to the control group. Moreover, a significant decrease in BNP values was found after exercise training as well as 3 months after AMI. No difference was found in the control group. CONCLUSION: This study demonstrates that exercise training for 3 weeks after AMI leads to a significant mobilization as well as increase of functional activation of BM-CPCs in humans. Moreover, regular exercise training might contribute to the positive effects on the regenerative potency after AMI.
Aged↗
[Relation between various pathways of collateral circulation and cerebral circulatory disorders resulting from extracranial occlusion of one of the vertebral arteries].
The data obtained during angiographic and clinical examination of 35 patients with extracranial occlusion of one vertebral artery (VA) have been compared. The clinical picture of extracranial occlusion of one VA may vary. Also, the disease may run an asymptomatic course. The clinical symptoms of injuries to the vertebro-basilar vessels are less pronounced during noticeable occlusive alterations within the system of the carotid arteries. The main pathways of collateral circulation in extracranial occlusion of one VA involve intrasystemic anastomoses (within the system of the subclavian arteries). Of the greatest functional importance is the unoccluded VA.
Basilar Artery↗
Brainstem death.
A patient with the clinical picture of brain death resulting from brainstem hemorrhage and subsequent infarction is presented. The EEG showed activity similar to what has been described in the cerveau isolé animal preparations. Cortical evoked potentials were unobtainable from auditory or somatosensory stimulation, but of unusually high amplitude to flash stimuli. The point is made that a diagnosis of brain death cannot be made on clinical grounds alone when a patient is on life support systems, and the differences between cerebral death, brainstem death and brain death are discussed.
Aged↗
A role for G-CSF (granulocyte-colony stimulating factor) in the central nervous system.
G-CSF (Granulocyte-colony stimulating factor) is a hematopoietic growth factor that has been known for 20 years, and has been named for its role in the proliferation and differentiation of cells of the myeloic lineage. We have uncovered a novel spectrum of activities of G-CSF in the central nervous system. G-CSF and its receptor are expressed by neurons in many brain regions, and are upregulated upon experimental stroke. In neurons, G-CSF acts anti-apoptotically by activating several protective pathways. In vivo, G-CSF decreases infarct volumes in acute stroke models in rodents. Moreover, G-CSF stimulates neuronal differentiation of adult neural stem cells in the brain, and improves long-term recovery in more chronic stroke models. Thus, G-CSF is a novel neurotrophic factor, and a highly attractive candidate for the treatment of neurodegenerative conditions. Here we discuss this new property of G-CSF in contrast to its known functions in the hematopoietic system, summarize data from other groups on G-CSF's actions in cerebral ischemia, compare G-CSF to Erythropoietin (EPO) in the CNS, and highlight clinical implications.
Animals↗
Infusion of human umbilical cord blood cells in a rat model of stroke dose-dependently rescues behavioral deficits and reduces infarct volume.
BACKGROUND AND PURPOSE: Intravenously delivered human umbilical cord blood cells (HUCBC) have been previously shown to improve functional recovery of stroked rats. To extend these findings, we examined the behavioral recovery and stroke infarct volume in the presence of increasing doses of HUCBC after permanent middle cerebral artery occlusion (MCAO). METHODS: Rats were subjected to MCAO and allowed to recover for 24 hours before intravenous infusion of 10(4) up to 3 to 5x10(7) HUCBC. Behavioral tests (spontaneous activity, step test, elevated body swing test) were performed 1 week before MCAO and at 2 and 4 weeks after HUCBC infusion. On completion of behavioral testing, animals were euthanized and brain infarct volumes quantified. HUCBC were identified by immunofluorescence for human nuclei and by polymerase chain reaction (PCR) using primers specific for human glycerol 3-phosphate dehydrogenase. RESULTS: At 4 weeks after infusion, there was a significant recovery in behavioral performance when 10(6) or more HUCBC were delivered (p=0.001 to p=0.05). Infarct volume measurements revealed an inverse relationship between HUCBC dose and damage volume, which reached significance at the higher HUCBC doses (10(7) cells, p<0.01; 3 to 5x10(7) cells, p<0.05). Moreover, HUCBC were localized by immunohistochemistry and PCR analysis only in the injured brain hemisphere and spleen. CONCLUSIONS: These results extend previous observations of HUCBC infusion in the MCAO rat stroke model by demonstrating a dose relationship between HUCBC, behavioral improvement, and neuronal sparing.
Animals↗
Management-related morbidity in unselected aneurysms of the upper basilar artery.
A series of 49 consecutively treated patients with 52 aneurysms of the upper basilar artery (BA) is presented. Thirty-nine aneurysms arose at the BA bifurcation, 11 at the origin of the superior cerebellar artery (SCA), and two from the upper BA trunk just below the SCA. The patient population consisted of 36 women and 13 men, with a mean age of 50 years (range 23-74 years). Of the 35 patients presenting with subarachnoid hemorrhage, 10 were Grade I, 10 were Grade II, 11 were Grade III, and four were Grade IV according to the Hunt and Hess scale. Treatment consisted of aneurysm neck clipping in 28, proximal occlusion of the BA in three, and endovascular therapy with coils in four patients. The remaining 14 patients with unruptured aneurysms underwent direct neck clipping. Postoperatively, 38 patients developed diplopia in at least one direction of gaze but this had resolved in 31 of them at the last follow-up evaluation. There were four deaths (8.2%): two as a result of rebleeding following coil compaction at 8 days and 9 months posttreatment, respectively; one as a result of vasospasm; and one as a result of brainstem infarction after proximal occlusion of the BA in a giant bifurcation aneurysm. Of the surviving patients, 33 (67.3%) made an excellent recovery, seven (14.3%) made a good recovery, and five (10.2%) were in poor condition at the last follow-up review. Direct microsurgical clipping of most aneurysms of the BA apex region can be performed with acceptable rates of morbidity. These data from an unselected series of patients in a general hospital provide a basis for comparison with developing alternative techniques.
Adult↗
Degeneration of the corticospinal tract following portosystemic shunt associated with spinal cord infarction.
The clinicopathological aspects of a case of myelopathy that followed the creation of a surgical porto-caval shunt for hepatic cirrhosis and oesophageal varices are presented. Degeneration of the lateral corticospinal tracts associated with diffuse bilateral ischaemic changes of the spinal gray matter and proliferation of Alzheimer type 2 glia in the brain and brain stem were the most prominent findings. The association of corticospinal tract degeneration and ischaemic lesions of spinal gray matter in absence of any anatomical cause of spinal cord infarction suggests that a modification of the spinal blood flow caused by creation of portosystemic shunts might be the basic pathogenetic mechanism of this complication of severe liver disease.
Brain↗
Bilateral medial medullary infarction with oculomotor disorders.
BACKGROUND AND PURPOSE: We describe the first case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging. We discuss the relation between this lesion and the oculomotor signs that were observed clinically. CASE DESCRIPTION: A 71-year-old man initially presented with pure motor hemiparesis, which progressed to complete quadriplegia. He also developed nearly complete vertical and horizontal ophthalmoplegia. Magnetic resonance imaging revealed upper medial medullary infarctions bilaterally that extended to the pontomedullary junction. CONCLUSIONS: We propose that the vertical oculomotor disorders resulted from involvement of the oculomotor system in the caudal brain stem, especially the caudal paramedian pontine reticular formations on both sides.
Aged↗
[ON SOME CASES OF VERTEBRO-BASILAR THROMBOSIS WITHOUT INFARCT LESIONS OF THE ENCEPHALIC TRUNK].
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Basilar Artery↗
Neuropathologic features, including pontine schwannosis, in a four-year survivor of probable Reye's syndrome with secondary Möbius syndrome.
Frequent seizures and loss of motor, language, and intellectual skills necessitated care in an institution for the physically and mentally handicapped for 4 years after diagnosis of presumed Reye's syndrome in a 10-month-old boy. M obius syndrome was diagnosed and bilateral tarsorrhaphy performed for exposure keratitis. Postmortem examination revealed multiple old boundary zone infarcts in the cerebral cortex, small cavitated infarcts in basal ganglia and thalami, diffuse neuronal loss and gliosis, and a focus of old necrosis in the pons; brain stem herniation during the acute phase of Reye's syndrome was responsible for the latter lesion. Irregular congeries of proliferated peripheral nerves, confirmed by ultrastructural study, were ramifying in the gliotic pontine tegmentum. The pathologic substrate for the neurovegetative state in a long-term survivor of probable Reye's syndrome appears to be multifocal cerebral infarction.
Atrophy↗
"Locked-in" syndrome: report of seven cases.
Seven cases of the "locked-in" syndrome are described. This is a disorder in which a conscious, mute patient is completely paralysed apart from some form of eye movement, usually as a result of an infarct in the ventral pons. Such patients are often assumed to be in coma and as a result may be distressed by inappropriate conversation around the bedside.
Adult↗
[Studies on evaluation of brain death].
OBJECTIVE: To investigate the methods of evaluating brain death accurately and objectively. METHODS: Various kinds of clinical examination [including conscious state, Glasgow coma score (GCS), brain stem reflection, cranial nerve dominated actions, spinal reflection, spinal nerve dominated automatic action, respiratory and apnea testing] and laboratory methods [such as electroencephalography (EEG), brainstem auditory evoked potentral (BAEP), brainstem auditory sensery evoked potentral (SLSEP) and transeranial Doppler (TCD)] were used to evaluate 11 cases with brain death. RESULTS: Eleven cases presenting with deep coma were conssedered to have brain death. All of them had GCS score of 3 and disappearance of brain stem reflection and cranial nerve dominated automatic action. Six of them patients showed anisocoria. Nine of them pharyngeal reflex could not be detected because of tracheal cannulization, but this did not influence the evaluation of brain death. None of them showed "flat" EEG and disappearience of BAEP dominant wave. None of the SLSEP show any wave behind N13. TCD showed blood stream characteristic of brain death except in one case blood stream characteristic of increased intracraniai pressure. Apnea test and atropine test provided the final proof brain death. The former had more influence on heart rate, blood pressure and oxygen saturation while the latter were more safe and reliable. CONCLUSION: Combined and continuous observation of clinical and laboratory indices can enhance the accuracy of the evaluation of brain death.
Adult↗
[Isolated nuclear oculomotor nerve palsy due to mesencephalic infarction].
A patient with unilateral nuclear oculomotor palsy due to midbrain infarction is described. A 46-year-old man was admitted because of difficulty in opening right eye and double vision noticed when he awoke in that morning. On admission, neurological examination revealed total right oculomotor palsy with slight impairment of left upward gaze. There were no other neurologic abnormalities at all. Brain CT and cerebral angiograms were also normal. Magnetic resonance imaging (MRI) performed on the ninth day, however, demonstrated high signal intensity in the right tegmentum of the mesencephalon on T2-weighted images, which was shown more clearly after the administration of Gadolinium-DPTA. He was diagnosed as nuclear third nerve palsy caused by midbrain infarction. The majority of isolated oculomotor nerve palsy has been reported to be caused by extraaxial lesion. When the oculomotor palsy is caused by intraaxial ischemic lesion, it is usually accompanied by other brain stem signs, because abundant nuclei and fibers are present adjacent to the oculomotor nucleus and nerve in the mesencephalon. The present case clarified that such a small infarct disclosed only by MRI can cause isolated oculomotor nerve palsy. It is emphasized that the intraaxial ischemic lesion should be ruled out by using the sophisticated diagnostic aid before making diagnosis of peripheral lesion. This is the first report of the isolated third nerve palsy resulting from mesencephalic ischemic lesion in the Japanese.
Cerebral Infarction↗
Central nervous system entry of peripherally injected umbilical cord blood cells is not required for neuroprotection in stroke.
BACKGROUND AND PURPOSE: To date, stem cell graft-mediated neuroprotection is equated with graft survival and secretion of neurotrophic factors in the brain. Here, we examined whether neuroprotection by systemically delivered human umbilical cord blood (HUCB) cells was dependent on their entry into the central nervous system in a rodent model of acute stroke. METHODS: Adult male Sprague-Dawley rats were subjected to right middle cerebral artery occlusion for 60 minutes. During the 1-hour occlusion, animals were randomly assigned to 1 of the following treatments: intravenous injection of HUCB (a subtherapeutic dose of 200,000 cells in 10 microL) with blood-brain barrier (BBB) permeabilizer (1.1 mol/L mannitol at 4 degrees C) or vehicle, intravenous vehicle alone, or intravenous mannitol alone. Behavioral tests, using elevated body swing test and passive avoidance test, were conducted at day 3 poststroke, and thereafter, animals were euthanized for: (1) immunohistochemical examination of HUCB, which were lentivirally labeled with green fluorescent protein; (2) cerebral infarction analysis using 2,3,5-triphenyl-tetrazolium chloride; and (3) enzyme-linked immunosorbent assay of trophic factors within the striatal region. RESULTS: We did not detect intravenously administered low dose of HUCB cells in the brains of animals at day 3 after stroke even when cells were coinfused with a BBB permeabilizer (mannitol). However, HUCB-mannitol treatment significantly increased brain levels of neurotrophic factors, which correlated positively with reduced cerebral infarcts and improved behavioral functions. CONCLUSIONS: Our data show that central nervous system availability of grafted cells is not a prerequisite for acute neuroprotection provided that therapeutic molecules secreted by these cells could cross the BBB.
Animals↗