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PubMedDate not supplied

Character and origin of rotatory movements evoked by electrical stimulation of the caudate nucleus in cats.

High-frequency stimulation of the caudate nucleus in cats induces three types of rotatory responses: turning the head or stepping movements in a circle toward the side opposite to that of stimulation, psychomotor excitation with contralateral rotation, and ipsilateral turning of the head and trunk. Movements of the last type developed mainly from the ventro-lateral zones of the head of the caudate nucleus, whereas psychomotor excitation, on the other hand, developed from the dorsal zones. Rotatory movements do not depend significantly on a contribution of the internal capsule or cortex. Slow synchronized activity on the EEG at the time of rotation was abolished after curarization of the animals. Caudate rotation is partly due to activation of the globus pallidus, for electrical stimulation of that structure raises the threshold of the responses although it does not block them completely.

Animals↗

PubMedDate not supplied

Participation of emotional structures of the brain in the regulation of gastric secretory function.

The influence of the self-stimulation (SS) positive-reinforcement zones of the brain on the secretion of gastric juice was investigated using eight adult dogs with gastric fistulas. An intracerebral-S3 instrumental response was developed after implanting concentric (bipolar) electrodes into various zones of the reward system (hypothalamus, mammillary bodies, ventral thalamic nucleus, commissura grisea media, internal capsule, nucleus of the stria terminalis, and the crus cerebri). A normal acidity of the stomach contents was found in five dogs after surgery during the interdigestive period and a sharply elevated acidity in three dogs. A large quantity of thick foamy mucus and a turbid juice was secreted 3-5 min after the onset of SS. Self-stimulation did not alter the pH of the stomach contents in dogs with an initially normal pH, while it normalized this parameter in dogs with an initially elevated acidity. Bilateral supradiaphragmatic vagotomy in the animals of the latter group shifted the pH in the alkaline direction; however, the pH was completely normalized only as a result of intracerebral SS. Thus, positive emotional excitation associated with the stimulation of various reward zones normalized the acidity of the stomach contents; moreover, this response was not associated with the efferent systems of the vagus nerves.

Animals↗

PubMed1995

Circumscribed low grade astrocytomas in the dominant opercular and insular region: a pilot study.

Intraoperative mapping techniques allow a reliable identification or exclusion of eloquent brain areas and are well tolerated by the patients. In dominant opercular tumours radical surgery can only be achieved without lasting deficits with intraoperative histological examination of the resection line and mapping. If an early postoperative MRI shows residual opercular tumour in non-eloquent areas re-operation is recommended. In large dominant insular or opercular-insular tumours only biopsy is recommended, because only an incomplete removal can be accomplished, because the trial of radical removal carries a high risk of postoperative deficits due to possible vascular damage of the lenticulo-striate arteries or internal capsule. Because subtotal removal of low grade gliomas does not increase the progression free interval, we would not recommend surgery in these cases, as they carry a significant risk of a further deficit.

Adult↗

PubMed1989

Experimental transplantation gliomas in the adult cat brain. 2. Pathophysiology and magnetic resonance imaging.

In adult cats experimental brain tumours were produced by stereotactical xenotransplantation of the rat glioma clone F 98 into the internal capsule of the left hemisphere. Two to four weeks after transplantation tumours and peritumoural oedema were investigated by magnetic resonance imaging (MRI), electrophysiological recording and analysis of tissue content of water, electrolytes and extravasated serum proteins. Spherical tumours with a diameter of about 10 mm developed at the injection site and were surrounded by massive white matter oedema. Water content in peritumoural white matter increased from 2.63 +/- 0.17 to 3.65 +/- 0.19 ml/g d.w. (means +/- SD), sodium from 187 +/- 11 to 351 +/- 55 mueq/g d.w. and calcium from 7.4 +/- 1.1 to 13.3 +/- 1.3 +/- 1.3 mueq/g d.w. Potassium and magnesium did not change. Oedema development was associated with the extravasation of 18.0 +/- 16.8 mg/g d.w. albumin and 15.8 +/- 12.2 mg/g d.w. immunoglobulin. The calculated electrolyte content of oedema fluid approximated that of plasma but the serum protein content was about 40% lower. The ratio of low (albumin) to high (immunoglobulin) molecular weight proteins was the same in blood and oedema fluid. It is, therefore, concluded that peritumoural oedema consist of two components, a whole plasma extravasate and a protein-free ultrafiltrate. Peritumoural oedema could be clearly detected by MRI but differentiation between tumour and oedema was only possible after contrast enhancement with gadolinium-DTPA. The ratios of the intensities of the MR signal correlated linearly with the water content within white matter. MRI, in consequence, allows quantification of oedema provided a reference area with normal water content is present.

Animals↗

PubMed1989

Diffuse axonal injury after severe head trauma. A clinico-pathological study.

Diffuse Axonal Injury (DAI) is a well known entity that affects many patients with severe head trauma. Classically DAI has been considered the pathological substrate of those cases rendered unconscious at the moment of impact and in which the CT scan does not show mass lesions. Diffuse axonal damage is almost always related to mechanisms of injury in which the rotational acceleration produces shear and tensile strains of high magnitude. In this paper we present a group of 24 patients with a severe head injury in whom the postmortem examination demonstrated unequivocal signs of DAI. Widespread axonal retraction balls, located preferentially in the centrum semiovale and internal capsule were the most constant histological finding. We divided the entire series into two subgroups. One group (15 cases), included all the patients in whom the CT scan did not demonstrate mass lesions. In the second group (9 patients) we considered patients with a diffuse axonal injury in whom the CT scan additionally demonstrated a mass lesion (6 acute subdural haematomas, 2 intracerebral and 1 extradural haematoma). The mean age of the entire group was 26 years. Twenty two patients were injured in a road traffic accident, the remaining two fell from a considerable height. All were rendered immediately unconscious on impact. Diffuse brain damage is a common finding in patients with a severe head injury and immediate coma in whom the CT scan does not show mass lesions. Diffuse axonal injury can also appear in connection with a wide spectrum of focal lesions (acute subdural haematoma, basal ganglia haematoma etc.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1997

Surgical treatment of insular gliomas.

Surgical treatment of glial tumours arising in the insula is specially challenging due to the proximity of the internal capsule. Although small insular gliomas have been removed safely by a transylvian approach, in large dominant insular tumours only biopsy has been recommended to avoid postoperative deficits. Unfortunately that is a suboptimal form of treatment as low grade supratentorial gliomas should be removed radically to prevent tumour progression, malignization and to increase the recurrence-free-interval. Addition of radiotherapy to partial removal is associated with a much higher incidence of recurrences and early malignizations compared to radical removal and no radiotherapy. Between 1st October 1989 and 1st September 1996 we treated twenty-three patients harbouring insular gliomas. To increase the radicality of the resection the surgical procedure was performed under local anaesthesia whenever possible, as general anaesthesia usually leads to more conservative resections. In 20/23 (86.9%) patients complete resection was accomplished, and subtotal in three (13.1%). The removed tumours were: two oligodendrogliomas, five grade I astrocytomas, nine grade II, four grade III and three grade IV. Postoperative neurological deficits occurred in five patients. Four suffered a hemiparesis (that recovered in an average of 6 months) and one a motor dysphasia which took a week to recover. Two of the seventeen patients operated on for low grade insular gliomas underwent malignant change. We conclude that complete surgical removal of insular gliomas should be considered and at least attempted in all cases.

Adult↗

PubMed1997

Transient cerebral ischaemia in Mongolian gerbils pre-exposed to hypoxia.

The objective of this study was to clarify whether pre-exposure to hypoxia influences neuronal death following transient cerebral ischaemia. Twenty gerbils were exposed to 10% oxygen in a chamber for 3 weeks. The other control gerbils (n = 20) were fed in normoxia for 3 weeks. Both carotid arteries in the neck were occluded with aneurysm clips for 5 minutes under halothane anaesthesia in 30 gerbils, recirculated and then fed in normoxia. Five animals in both groups were sacrificed before, and 2, 4, and 7 days after surgery. The animals were fixed with 4% paraformaldehyde and histological study was performed. Immunohistochemical study was also done with antibodies against basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF). The neuronal death in the hippocampus was more severe in the hypoxic group. Expression of both bFGF and VEGF was obvious in the cingulate cortex, corpus callosum and internal capsule before clipping in the hypoxic group, but not observed in the normoxic group before clipping. We observed the expression of both bFGF and VEGF widely in the brain at 2 and 4 days after recirculation in both groups. The expression in the hypoxic group was much more prominent than that in the normoxic group. These expressions were not observed at 7 days in both groups. Pre-exposure to hypoxia followed by transient cerebral ischaemia accelerated neuronal death in the hippocampus, and induced the more obvious expression of both VEGF and bFGF compared with those in the normoxic group.

Animals↗

PubMed1986

Parathyroid hormone secretion by brain and pituitary of sheep.

The secretion of immunoreactive PTH by different brain regions and pituitary of sheep was studied in vitro. Separate tissue samples of gyrus, internal capsule, basal ganglia, cerebellum, and pituitary were incubated in culture medium with low, normal, and high Calcium (Ca)(0.7 mM, 1.2 mM and 2.4 mM) concentrations. PTH release in medium containing low Ca were observed by all samples. The concentrations increased in the fifth and sixth hour from 100% (1st hour basis value) up to 300%. The PTH release showed an inverse relationship to the Ca concentration in the culture medium. To induce any significant decrease in medium concentrations of PTH, 1.25(OH)2D (100 ng/ml) was added to the culture medium. This effect could be reversed by DB-cAMP. Our results indicate that secretion of immunoreactive PTH by brain and pituitary of sheep may occur in vitro. The secretion depends on the content of Ca, 1.25(OH)2D, and DB-cAMP.

Animals↗

PubMed1986

Vascular malformations of the central nervous system: a morphological overview.

Vascular malformations of the central nervous system (C.N.S.) are classified by size, location, and morphologic type, distinguishing capillary telangiectasias, cavernous malformations, venous angiomas, arteriovenous malformations (AVMs) including varix of the great vein of Galen, and other vascular malformations (e.g. Sturge-Weber syndrome). The morphology and predominant location pattern of the different types of vascular malformations in the brain and spinal cord, and their embryology are reviewed. In the brain and its coverings, all types mainly AVMs and venous angiomas do occur, representing 5-9% of all intracranial space-occupying lesions and 20-40% of the sources of surgically treated intracranial hemorrhages. 50-80% of the angiomas are located in the cerebral hemispheres, 10-18% in central brain areas (basal ganglia, internal capsule, choroid plexus), and 10-30% in the posterior fossa. The major types of cerebral vascular malformations are described with reference to their anatomical features, location, chief arterial and venous supply, and prominent complications. Spinal vascular malformations, accounting for 3 to 12% of spinal space-occupying lesions, include vertebral, extradural, dural, subpial and intramedullary angiomas which occur as isolated or complex vascular anomalies and may involve various covering layers at the same level. The preferential occurrence of angiomas on the dorsal surface of the cord and in the caudal regions is related to the embryologic development of spinal vasculature. Frequent association of spinal angiomas (20-25%) with other vascular anomalies and dysplasias emphasizes their hamartomatous nature and developmental origin. Spinal angiomas include capillary telangiectasias with extra- or intradural and, rarely, intramedullary location, cavernomas, mainly arising in vertebral bodies, venous angiomas, mainly located in vertebral bodies and in the extradural space, and AVMs constituting the commonest type, that may affect both the pial and radicular vessels and can penetrate into the cord. They present as simple AV fistulas, cirsoid angiomas with localized vascular plexuses and large complex convolutions ("juvenile" type). The complications of spinal angiomas include subarachnoid hemorrhage, rare epidural hematoma, hematomyelia, compression lesions of the cord and roots, and ischemic changes causing chronic progressive radiculomyelopathy, previously referred to as Foix-Alajouanine syndrome. Chronic damage to the cord and spinal roots results from pressure effects, thrombosis of the abnormal vessels, disorders of venous drainage, and "steal" phenomena related to the vascular anomalies.

Arteriovenous Malformations↗

PubMed1981

Corticosteroid therapy of experimental tumour oedema.

Experimental brain tumours were produced in cats by stereotactic implantation of 4 million suspended cells of a rat glioma clone into the internal capsule. Three weeks after implantation a spherical tumour developed with a diameter of up to 10 mm which was surrounded by vasogenic white matter oedema. In untreated animals water content in the peritumoural white matter increased form 69.1 +/- 0.9 to 80.0 +/0 0.8 ml/100 g w. w., and regional blood flow reciprocally decreased from 32.2 +/- 5.6 to 18.9 +/- 0.05 ml/100 g/min. A single injection of a crystalline suspension of 10 mg/kg dexamethasone given intramuscularly one week before the animals were killed, led to a significant amelioration of brain oedema. Peritumoural white matter water content decreased to 73.0 +/- 0.5 ml/100 g w w. and blood flow rose to 35.7 +/- 2.8 ml/100 g/min. These changes were accompanied by parallel shifts of electrolyte content buy did not correlate with EEG activity, as assessed by Fourier frequency analysis. Corticosteroids did not prevent extravasation of peroxidase or Evans blue across the tumour vessels. The beneficial effect, therefore, is attributed to either an acceleration of resorption or an inhibition of the spread of oedema from tumour into the peritumoural brain tissue.

Animals↗

PubMed1994

Hemolytic uremic syndrome: MR findings of CNS complications.

MR findings of a patient with hemolytic uremic syndrome involving the CNS are described. Abnormal high signal intensity on T2-weighted images combined with swelling in the lentiform nucleus, posterior limb of internal capsule, external capsule bilaterally, and left extreme capsule was shown on initial MR; a small low signal intensity in the left putamen on T1- and T2-weighted images and generalized atrophy in the area of high signal intensity on previous T2-weighted images was shown on follow-up MR. These findings indicate infarct with focal hemorrhage, which is one of the histopathological features of CNS complication in hemolytic uremic syndrome.

Brain Diseases↗

PubMed1991

Imaging considerations of central nervous system manifestations in pediatric patients with neurofibromatosis type 1.

CT and MRI were used in a prospective study of the central nervous system (CNS) manifestations in 41 consecutive children with neurofibromatosis type 1 (NF-1). Gadolinium-DTPA was used in 15 patients. MRI was more effective than CT in delimiting the extension of the optic pathway glioma and in evaluating associated cerebral malformations. MRI visualized lesions generally undetected by CT, in the form of iso- or hyperintense foci with respect to the cerebral cortex in T2-weighted sequences. Well-delimited lesions of high signal intensity were observed in the globus pallidus (22 cases), the internal capsule (6 cases), corpus callosum (2 cases), anterior commissure (1 case) and semioval center (2 cases). Poorly defined hyper- or isointense areas were also observed affecting the cerebellar white matter (21 cases) and brain stem (17 cases). None of these lesions showed Gadolinium-DTPA enhancement, and were of no clinical significance. MRI has displaced CT in the initial diagnosis of patients with NF-1. Periodic annual MRI controls are only justified in patients with MRI changes to evaluate the progression or stabilization of the lesions.

Adolescent↗

PubMed1994

MRI demonstration and CT correlation of the brain in patients with idiopathic intracerebral calcification.

Twenty-two patients aged 36-63 years were diagnosed as having Fahr's syndrome on the basis of the presence on CT of unexpected extensive calcification of the basal ganglia. Even when associated with calcification of other brain areas, the main diagnostic criterion remained basal ganglia calcification larger than 800 mm2. Normal values of parathormone, serum calcium and phosphorus excluded hypercalcaemia and hypoparathyroidism. Mitochondrial CNS disease was excluded clinically. MRI and repeated CT and neurological examination were performed in all of the patients. The patients were divided into two groups: neurologically asymptomatic (group 1) and neurologically symptomatic (group 2). T2-weighted sequences demonstrated hyperintense areas in all of the patients involving the white and the grey matter of the brain. In group 1 the hyperintense lesions were significantly smaller than in group 2. The neurological symptoms correlated better with the hyperintensities on T2-weighted MR images than with the calcification demonstrated on CT. Hyperintensities in T2-weighted MRI and the areas shown by CT to have calcification had different locations. In 15 patients with dementia, the white matter of the entire centrum semiovale was bilaterally hyperintense. In another 3 patients with hemiparesis, hyperintense areas in the internal capsule, contralateral to the side of hemiparesis, were demonstrated in the T2-weighted sequence. The hyperintense T2 signals may reflect a slowly progressive, metabolic or inflammatory process in the brain which subsequently calcifies and are probably responsible for the neurological deficit observed.

Adult↗

PubMed1992

Manganese induced brain lesions in Macaca fascicularis as revealed by positron emission tomography and magnetic resonance imaging.

A series of positron emission tomography scans was made on two monkeys during a 16-month period when they received manganese(IV)oxide by subcutaneous injection. The distribution of [11C]-nomifensine uptake, indicating dopamine terminals, was followed in both monkey brains. The brain distributions of [11C]-raclopride, demonstrating D2 dopamine receptors, and [11C]-L-dopa, as a marker of dopamine turnover, were followed in one monkey each. The monkeys developed signs of poisoning namely unsteady gait and hypoactivity. The [11C]-nomifensine uptake in the striatum was reduced with time and reached a 60% reduction after 16 months exposure. This supports the suggestion that dopaminergic nerve endings degenerate during manganese intoxication. The [11C]-L-dopa decarboxylation was not significantly altered indicating a sparing of [11C]-L-dopa decarboxylation during manganese poisoning. A transient decrease of [11C]-raclopride binding occurred but at the end of the study D2-receptor binding had returned to starting values. The magnetic resonance imaging (MRI) revealed that the manganese accumulated in the globus pallidus, putamen and caudate nucleus. There were also suggestions of gliosis/edema in the posterior limb of the internal capsule. MRI might be useful to follow manganese intoxication in humans as long as the scan is made within a few months of exposure to manganese, i.e. before a reversal of the manganese accumulation.

Animals↗

PubMed1996

Are white matter lesions directly associated with cognitive impairment in patients with lacunar infarcts?

Forty-four patients (mean age 66, SD 8 years) with either clinical evidence of a focal lacunar syndrome (n = 36) or with disorders of memory or gait (n = 8) in the presence of a lacunar infarct on CT were studied for cognitive functioning and for the presence of white matter lesions on MRI. MR images were assessed by a neurologist and a neuroradiologist blinded to the clinical data. Thirty-six patients had one or more lacunar infarcts on CT or MRI (in the thalamus in 5, in the caudate nucleus in 3 and in the internal capsule or corona radiata in the remaining patients). Twelve patients had multiple infarcts. Severe lesions of the white matter were found in 13 patients, mild to moderate lesions in 20 patients. Scores on Digit Span, Digit Symbol and delayed recall of the 15-Words test were significantly lower in group with severe lesions, whilst there was a trend in the same direction for the Cognitive part of the Cambridge Examination of Mental Disorders in the Elderly, the Trailmaking B, Stroop colour interference test and the delayed visual reproduction of the Wechsler Memory Scale. These findings suggest that diffuse lesions of the white matter are an independent factor in the pathogenesis of intellectual dysfunction, also in patients with lacunar infarcts, but a truly independent analysis is difficult because the most severe involvement of the white matter tended to be associated with the largest number of lacunar infarcts.

Aged↗

PubMedDate not supplied

Disorders of higher mental function due to single infarctions in the thalamus and in the area of the thalamofrontal tracts.

Nine patients (five female and four male, mean age 58 years) with small infarcts in the thalamus (TH) or in the region of the thalamofrontal tracts and producing acute mental disturbances which in the acute phase of insult consisted of dementia in seven cases and mild cognitive disturbances in two cases. The complex of mental changes was similar to that seen in "frontal syndrome" and was characterized largely by lack of spontaneity, adynamia, disorientation, loss of attention and memory, slowing of all mental processes, and lack of criticality and adequacy. Accompanying focal neurological symptoms were mild in seven patients and moderate or pronounced in two. In five patients, the severity of mental disturbances decreased with time. Computer tomography demonstrated small infarcts in the anterior or medial parts of the TH in seven patients and in the posteromedial parts of the anterior limb of the internal capsule, i.e., the thalamofrontal tracts, in two cases. In five cases, infarcts were located in the dominant hemisphere, with lesions in the non-dominant hemisphere in three and in both hemispheres in one. The positions of all foci corresponded to structures traversed by pathways connecting the TH and the lower part of the reticular formation to the frontal lobes. It is suggested that disconnection of these pathways leads to cognitive lesions or dementia because of functional inactivation of the frontal cortex.

Adult↗

PubMedDate not supplied

Localization of GTPase-activating protein-(GAP) like immunoreactivity in mouse cerebral regions.

GTPase-activating protein is known to regulate the conversion between ras-GTP and ras-GDP. We studied the basal expression of GTPase-activating protein-like immunoreactivity in mouse cerebral regions using a polyclonal anti-GTPase-activating protein antibody. Cells with GTPase-activating protein-like immunoreactivity were distributed in frontal cortical layers IV and V, and in the parietal cortex, piriform cortex, amygdaloid area, septum, lateral thalamus, and hypothalamus. The GTPase-activating protein-like immunoreactivity was also observed in fiber-like structures in the caudate putamen, stria terminalis, internal capsule, and medial forebrain bundle, and around CA2 pyramidal cells in Ammon's horn. These results imply that GTPase-activating protein is constitutively expressed in mouse brain regions and may have physiological functions in specific neuronal pathways in the brain.

Animals↗

PubMed1998

Neurovirulent simian immunodeficiency virus induces calbindin-D-28K in astrocytes.

Astrocyte activation has been postulated to be a major contributor to functional changes in the brain of AIDS patients. We assessed astrocyte activation in the simian immunodeficiency virus (SIV) model. Four groups of macaque brains were examined: uninoculated controls, animals inoculated with virus that did not cause disease, animals inoculated with virus that caused AIDS but did not cause encephalitis, and animals with SIV encephalitis. We examined expression of calbindin-D-28K, a calcium binding protein that is upregulated in astrocytes during excitotoxic events, as well as glial fibrillary acidic protein (GFAP). The presence of calbindin in astrocytes was confirmed by double-labeling using confocal microscopy. Increases in calbindin staining were most apparent in the white matter, but increases in GFAP staining were most apparent in middle layers of the cerebral cortex. Six of the seven animals with SIV encephalitis had calbindin immunoreactive astrocytes in the subcortical white matter, corpus callosum, internal capsule, cerebral peduncle, pontine white matter, and cerebellar white matter. Very rarely, a few, very lightly calbindin-immunoreactive astrocytes were present in the uninoculated control brains. The increase in calbindin expression by astrocytes in SIV encephalitis suggests that these cells are subject to calcium toxicity. In uninoculated control macaques, and in macaques inoculated with virus that did not cause disease, GFAP-immunoreactive astrocytes were present throughout the subcortical white matter and in layer I, but very few were found in layers III-V of the cerebral cortex. Two animals that died of AIDS without encephalitis had somewhat higher numbers of GFAP immunoreactive astrocytes in middle cortical layers. In seven animals that received passaged neurovirulent virus and developed both AIDS and encephalitis, the number of GFAP-immunoreactive astrocytes in middle cortical layers was high, indicating widespread astrocyte activation.

Animals↗