Adjacent Cerebral Cortex Research Articles

A 1 Year Child with Hydrocephalus: A Case Report

Introduction: Hydrocephalus is the accumulation of fluid in the cavities deep within the brain. The extra fluids cause the ventricles to expand, putting pressure on the brain. The brain and spinal column are bathed in cerebrospinal fluid, which usually flows into the ventricles. Excessive cerebrospinal fluid pressure caused by hydrocephalus, on the other hand, can harm brain tissues and result in a variety of cognitive impairments.
 Case Presentation: Here we have selected a case of hydrocephalus. In this case, when the complete history has been taken it found that patient having a history of NICU admission for prematurity and Low Birth Weight for 40 days. During history collection, it found that the child was all right until 4 months of age after which she started to notice that the child's head circumference was increasing at an abnormal rate and has now been brought to AVBRH for further management. After all investigation in MRI brain reveals extensive dilatation of ventricular system including bilateral lateral ventricle and III and IV ventricles associated with wide-open foramen of Luschka and Magendie with thinning of the adjacent cerebral cortex and cerebellar parenchyma. Features suggestive of communicating hydrocephalus. In the EEG record, the background record shows rhythmic synchronous > 13 Hz beta activity in the bilateral hemisphere. Abnormal EEG record. Then, the doctor planned for the Endoscopic Third Ventriculostomy with general anesthesia.
 Conclusion: In this study, we mainly focus on expert surgical management and excellent nursing care which leads to fast recovery of the patient. After a conversation with the patient, her response was positive and after nursing management and treatment, she was discharged without any postoperative complications and satisfaction of recovery.

Massive spontaneous corpus callosal hemorrhage with intraventricular extension

Abstract Spontaneous hemorrhage into the corpus callosum with intraventricular extension is uncommon. In the present article we describe a case 60 year female who had massive hemorrhage along the corpus callosum involving genu, body of corpus callosum and extending on ventral as well as dorsal aspect of the corpus callosum with intraventricular extension and areas of hypodensities in the body of the corpus callosum and adjacent cerebral cortex. In this case the subarachnoid and corpus callosal hemorrhage probably resulted from the ruptured aneurysms of the anterior cerebral artery.

Complications of surgical treatment ofRosai-Dorfman Disease: A case report and review

Background:Rosai–Dorfman disease (RDD) was first described in 1969 as an idiopathic histiocytic proliferative disorder. It commonly presents as a massive and painless adenopathy. Until 1990, extranodal involvement of the central nervous system (CNS) was rare and reported in less than 5% of the total number of patients with extranodal RDD. Complete removal of CNS RDD has been achieved in many cases.Case Description:We report a case of an isolated intracranial RDD in a 53-year-old man. The patient had an episode of generalized seizures. Imaging studies of the brain were compatible with a meningioma en plaque. The mass was exposed by a right frontotemporal craniotomy. The tumor was adhered tightly to the adjacent cerebral cortex and was permeated by pial arteries of the brain surface. The sacrificing of these arteries was inevitable in order to achieve the total removal of the tumor. The patient had incomplete left hemiparesis after the surgery. Brain computed tomography (CT) imaging revealed a postoperative hemorrhage and a low-density lesion in the right frontal lobe. The patient was postoperatively diagnosed with isolated central nervous system RDD.Conclusion:Although the complete removal of dural-based lesions without any neurological deficits has been performed in many cases, the treatment of cases with high risks, such as the present case, indicates conservative excisions and adjuvant radiotherapy with or without chemotherapy.

Agenesia del corpo calloso in feti con ventricolomegalia lieve: ruolo della RM

We evaluated the role of magnetic resonance (MR) imaging in the diagnosis of corpus callosum agenesis - isolated or associated with other anomalies - in fetuses with mild cerebral ventriculomegaly, as depicted at prenatal sonography. Between January 2005 and March 2007, 33 fetuses with a mean gestational age of 28.9 weeks (range 17-37) and mild ventriculomegaly diagnosed at prenatal sonography were included in this prospective study. All fetuses underwent MR imaging according to the following protocol: half-Fourier T2-weighted images along the three orthogonal plane according to the longitudinal axis of the mother, and subsequently three orthogonal planes were acquired according to the fetal brain. Quantitative image analysis included the size of the transverse diameter of the lateral ventricles, in the axial plane, and the thickness of the adjacent cerebral cortex. Qualitative image analysis included morphology of the lateral ventricles (normal, parallel pattern colpocephaly), signal intensity changes of the fetal brain, interruption of the germinative matrix, agenesis of the corpus callosum (complete/partial) and associated malformations. Postnatal physical examination and diagnostic imaging, as well as surgery, were the standard of diagnosis. Mean axial diameter of the lateral ventricle was 11.6 mm (range 10-15 mm), and mean thickness of the adjacent cerebral cortex was 2.1 mm (range 1.8-3 mm); 23/33 fetuses (70%) showed normal morphology of the lateral ventricles, and 8/33 (24%) showed abnormal morphology (parallel pattern, colpocephaly). The entire corpus callosum was visualised in 20/33 fetuses (60%). In 8/33 fetuses (25%), partial agenesis was diagnosed, whereas in 5/33 (15%), there was hypogenesis. In 6/13 fetuses (46%), isolated corpus callosum agenesis was detected, and two cases of hypogenesis of the corpus callosum were misinterpreted - overestimated in one case and underestimated in another. MR imaging may prove to be a useful second-line imaging modality in the prenatal diagnosis of corpus callosum agenesis in fetuses with mild ventriculomegaly.

Cerebral immunoglobulin light chain amyloid angiopathy-related hemorrhages

Introduction Cerebral amyloid angiopathy (CAA) is a common cause of intracerebral hemorrhage (ICH) particularly in elderly patients. In CAA-related hemorrhages, amyloid deposits in the brain vessel walls mainly contain amyloid beta-protein (A-beta). Rarely other forms of amyloid substances have been reported in sporadic CAA-related hemorrhages. Methods We report the case of a 44-year-old patient with recurrent ICH who had surgical evacuation of a large frontal hematoma. Following surgery, samples from the hematoma and adjacent cerebral cortex were obtained for histopathological examination. Results Within the recent hemorrhage, a few arteriolar walls were thickened with an amyloid deposit that was immunostained for immunoglobulin (Ig) M and light chain lambda. In the wall of some vessels, around the amyloid deposits, as well as in the adjacent cerebral cortex, there was an infiltration by monotypic lymphocytes and plasma cells expressing IgM and light chain lambda. No amyloid deposition was found outside the hemorrhage. There was no evidence of multiple myeloma, B-cell malignancy, or systemic amyloidosis. Conclusions Recurrent ICH may be due to amyloid deposition of IgM lambda produced by monotypic proliferation of lymphocytes and plasma cells purely localized to the brain.

Positron emission tomographic findings in a tuberculous brain abscess

Several case reports and studies have described the positron emission tomographic (PET) findings of intracranial tuberculomas and bacterial brain abscesses. However, to our knowledge, the PET pattern of a tuberculous brain abscess has not been previously described. We report the case of a diabetic heavy drinker with a left parietal tuberculous abscess. (18)F-fluoro-2-deoxyglucose (FDG)-PET scans showed intense FDG uptake at the abscess periphery, where contrast enhancement was observed on a magnetic resonance image. FDG uptake was reduced within the abscess cavity and in the adjacent cerebral cortex. The possibility of a tuberculous brain abscess should be considered when FDG accumulates at the periphery of a ring-enhancing lesion in a chronically ill or immunocompromised patient.

Sept4, a Component of Presynaptic Scaffold and Lewy Bodies, Is Required for the Suppression of α-Synuclein Neurotoxicity

In Parkinson disease (PD), alpha-synuclein aggregates called Lewy bodies often involve and sequester Septin4 (Sept4), a polymerizing scaffold protein. However, the pathophysiological significance of this phenomenon is unclear. Here, we show the physiological association of Sept4 with alpha-synuclein, the dopamine transporter, and other presynaptic proteins in dopaminergic neurons; mice lacking Sept4 exhibit diminished dopaminergic neurotransmission due to scarcity of these presynaptic proteins. These data demonstrate an important role for septin scaffolds in the brain. In transgenic mice that express human alpha-synuclein(A53T) (a mutant protein responsible for familial PD), loss of Sept4 significantly enhances neuropathology and locomotor deterioration. In this PD model, insoluble deposits of Ser129-phosphorylated alpha-synuclein(A53T) are negatively correlated with the dosage of Sept4. In vitro, direct association with Sept4 protects alpha-synuclein against self-aggregation and Ser129 phosphorylation. Taken together, these data show that Sept4 may be involved in PD as a dual susceptibility factor, as its insufficiency can diminish dopaminergic neurotransmission and enhance alpha-synuclein neurotoxicity.

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

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

What Constitutes a True Hyperdense Middle Cerebral Artery Sign?

Objectives: The ‘hyperdense MCA sign’ refers to an appearance of increased attenuation of the proximal middle cerebral artery (MCA) that is often associated with thrombosis of the M1 MCA segment and may be the only diagnostic feature on computed tomography early after ischaemic stroke. False positives are recognized, and correct recognition of this sign has, therefore, assumed greater importance with the advent of thrombolytic therapy for stroke. We sought to define objective criteria for hyperdensity of the MCA. Methods: Brain computed tomographs obtained by a standard protocol in a neuroradiology department were analyzed by a single observer. All consecutive scans reported as exhibiting a hyperdense MCA were compared to controls reported as having normal scans. Ovoid regions of interest were placed over the vessels and cerebral cortices, and the attenuation in Hounsfield units (HU) measured. Absolute attenuation and ratios of one side to the other were compared. Results: MCA attenuation was unrelated to age in cases (n = 18) and controls (n = 80). The mean MCA attenuation was greater in the affected MCA of cases as compared with controls [54.0 HU (99% confidence interval CI 46.7–61.2) vs. 41.3 HU (99% CI 39.7–43.0); p < 0.00001]. Cases were subdivided into true and false positives by the ratio of denser:less dense MCA (within or without the 95% prediction interval for controls). In all true positives, the MCA ratio was > 1.2. 9 of 10 true positives had acute ischaemic stroke; 1 patient had herpes simplex encephalitis, but had MCA attenuation within the 95% CI for controls. False positives had mature cerebral infarction or non-ischaemic pathologies. The ratio of MCA attenuation to adjacent cerebral cortex was significantly higher in both true and false positives than in controls. Conclusions: Hyperdense MCAs associated with acute ischaemic stroke can be distinguished from normal vessels and false positives by measurement of absolute attenuation of affected and normal vessels: an absolute density of >43 HU and a MCA ratio of >1.2 defined hyperdensity and excluded all other pathologies. Confirmation in other centres is required.

Kappa opioid receptor immunoreactivity in the nucleus accumbens and caudate–putamen is primarily associated with synaptic vesicles in axons

A rabbit polyclonal antiserum, raised against a C-terminal oligopeptide of the mouse kappa opioid receptor, was used to localize the cellular distribution of kappa receptors in the dorsal and ventral striatum of rats with light and electron microscopic immunocytochemistry. Prominent, diffuse kappa receptor immunoreactivity was present in the nucleus accumbens, particularly in the shell, ventral caudate–putamen and olfactory tubercle. The density of receptor immunoreactivity decreased in more dorsal areas of the caudate–putamen. In contrast, neuronal cell bodies stained clearly in the dorsal endopiriform nucleus, claustrum and layer VI of the adjacent cerebral cortex. Observations at the electron microscopic level in the dorsomedial shell of the nucleus accumbens and caudate–putamen revealed that the kappa receptor immunoreactivity was predominantly located in axons, often associated with synaptic vesicles, remote from the terminal or preterminal area. The few terminals which were labeled made slightly more asymmetrical than symmetrical contacts and the percentage of asymmetrical contacts observed was greater in the caudate than in the accumbens. A small number of postsynaptic spines was labeled; most of them were contacted by asymmetrical terminals. No labeling was observed in dendritic shafts. Thus, the predominant localization of kappa receptor immunoreactivity in axons is consistent with its role as a major inhibitor of glutamate and dopamine release in the dorsal and ventral striatum.

Immunoblot and immunohistochemical comparison of murine monoclonal antibodies specific for the rat D1a and D1b dopamine receptor subtypes

The two D1-like dopamine receptor subtypes, D1a and D1b, are structurally similar and pharmacologically indistinguishable using currently available ligands. To differentiate between the D1-like dopamine receptor subtypes, murine monoclonal antibodies to the rat D1a and the rat D1b dopamine receptor have been prepared. Rat D1-like and D2-like dopamine receptors expressed in Sf9 cells were used to verify the immunospecificity of the monoclonal anti-(D1a dopamine receptor) and anti-(D1b dopamine receptor) antibodies using immunoblot and immunohistochemical techniques. These two antibodies were used to compare the temporal dynamics of D1-like dopamine receptors expressed in Sf9 cells following infection with recombinant baculovirus and to monitor the partial purification of detergent solubilized receptors following ion exchange chromatography. Immunoreactivity of the anti-(D1a receptor) antibody was observed in the striatum and cortical regions of the rat brain using immunoblot techniques. No reactivity on immunoblots was observed for the anti-(D1b receptor) antibody using rat brain tissue, probably due to the low levels of receptor expression. For immunohistochemical studies using rat brain slices, the anti-(D1a receptor) antibody heterogeneously labeled cells and punctate processes within the striatal neuropil while labeling in the adjacent cerebral cortex was weak. Anti-(D1b receptor) antibody immunoreactivity was weak in the striatum and generally limited to sparse perikarya in the dorsal region. However, immunoreactivity was observed in numerous cells within the vertical and horizontal limbs of the diagonal band and in the ventral pallidum. Immunoreactivity of the anti-(D1b receptor) antibody was also observed in layer V pyramidal neurons of the frontal sensorimotor cortex.

Retinoids are produced by glia in the lateral ganglionic eminence and regulate striatal neuron differentiation.

In order to identify molecular mechanisms involved in striatal development, we employed a subtraction cloning strategy to enrich for genes expressed in the lateral versus the medial ganglionic eminence. Using this approach, the homeobox gene Meis2 was found highly expressed in the lateral ganglionic eminence and developing striatum. Since Meis2 has recently been shown to be upregulated by retinoic acid in P19 EC cells (Oulad-Abdelghani, M., Chazaud, C., Bouillet, P., Sapin, V., Chambon, P. and Dollé, P. (1997) Dev. Dyn. 210, 173-183), we examined a potential role for retinoids in striatal development. Our results demonstrate that the lateral ganglionic eminence, unlike its medial counterpart or the adjacent cerebral cortex, is a localized source of retinoids. Interestingly, glia (likely radial glia) in the lateral ganglionic eminence appear to be a major source of retinoids. Thus, as lateral ganglionic eminence cells migrate along radial glial fibers into the developing striatum, retinoids from these glial cells could exert an effect on striatal neuron differentiation. Indeed, the treatment of lateral ganglionic eminence cells with retinoic acid or agonists for the retinoic acid receptors or retinoid X receptors, specifically enhances their striatal neuron characteristics. These findings, therefore, strongly support the notion that local retinoid signalling within the lateral ganglionic eminence regulates striatal neuron differentiation.

Striatal glutamate antagonism induces contralateral neglect

To assess the role of striatal glutamatergic synapses in mediating sensorimotor orientation behavior, glutamate receptor antagonists were infused into the left striatum of awake rats and behavioral orientation to contralateral and ipsilateral stimuli were quantified. The AMPA–kainate antagonist, DNQX, and the NMDA antagonist, CPP, both induced a large asymmetry in responding, such that the rats oriented much less to stimuli presented contralateral to the antagonist infusions. Furthermore, intrastriatal glutamate antagonist infusions increased the occurrence of incorrect responses, or turning away from a contralaterally-presented stimulus. In a separate experiment, intrastriatal DNQX was shown to block kainic acid (KA)-induced Fos expression in the striatum, but not in adjacent cerebral cortex, suggesting that the diffusion of this drug is restricted to the striatum.

Dynamic changes of focal hypometabolism in relation to epileptic activity

The interictal hypometabolism in patients with focal epilepsy is usually regarded as stationary. In this study we investigated to which extent the hypometabolism may depend on the activity of the epileptic focus. In focal penicillin-induced epilepsy in rats the epileptic focus is hypermetabolic. This focus is accompanied by hypometabolism in widespread areas of adjacent cerebral cortex. The experiments revealed that these metabolic alterations are transient. Data from a patient experiencing a focal seizure during PET scanning gave similar results. They showed that the transition from interictal to ictal activity was accompanied by the development of a hypermetabolic epileptic focus and the dynamic enlargement of the surrounding hypometabolism. Both, the experimental and clinical data provide evidence that the cerebral hypometabolism may vary in size depending on the activity of the epileptic focus. It is hypothesized that in human PET studies the large interictal hypometabolism may prevent the identification of hyperactive interictal epileptic foci due to the partial volume effects resulting from the limited spatial resolution of PET cameras.

Vasoconstriction in telencephalic microvessels: a response to one model for intraventricular hemorrhage in beagle pups.

Telencephalic microvessels were morphologically and morphometrically evaluated in beagle pups at 24, 48, and 72 hours of age following an experimental insult consisting of exposure to acute hypovolemic hypotension followed by rapid corrective blood reinfusion. Animals were anesthetized throughout the procedure and maintained for 75 minutes prior to sacrifice. Microvessels from the germinal matrix, where intraventricular hemorrhage (IVH) most commonly occurs, were compared to those of the adjacent cerebral cortex and choroid plexus. Perfusion, fixation and processing of the tissue followed our previously published protocol (Leuschen et al.: Anatomical Record 208:435-443, 1984). Both germinal matrix and cortical microvessels had collapsed lumens and normal endothelial cell morphology; mitochondria contained distinct cristae, junctional complexes were present and a basement lamina completely surrounded most vessels. Morphometric data on matrical and cortical microvessels supported vasoconstriction. Microvessels from choroid plexus were not vasoconstricted; tight junctions were infrequently seen and microvesicular elements were present. An increased cerebral blood flow to the germinal matrix and the adjacent cerebral cortex has been reported during and immediately following hypovolemic hypotensive insult. By 75 minutes following insult, our ultrastructural studies support a rebound phenomena including vasoconstriction of microvessels. The resulting vasoconstriction and associated cerebral ischemia may play an important role in subsequent tissue damage to the matrical area and ultimately to the etiology of IVH.

B16 melanoma spontaneous brain metastasis: occurrence and development within leptomeninges blood vessels.

Subcutaneous tumors initiated with mouse B16 melanoma clones G3.5 and G3.12 disseminated visible spontaneous brain metastases in 67 per cent and 32 per cent, respectively, of mice with extensive lung metastasis. Most brain metastases appeared as pigmented emboli within blood vessels of the leptomeninges overlying the cerebral cortex. Intravascular metastases consisted of tumor cell aggregates surrounded by fibrous material and generally contained viable cells that proliferated in culture. Some metastatic emboli apparently proliferated intravascularly to such an extent as to cause vessel disruption, permitting tumor invasion into the adjacent cerebral cortex. Cultured cells from G3.12 leptomenings metastases produced tumors that metastasized to a much greater extent than unselected G3.12 tumors, but brain metastasis still occurred only secondarily, after initial dissemination to the lungs. In contrast, G3.5 brain metastasis-derived populations formed tumors that ultimately metastasized to the brain to lesser extents than did unselected G3.5 tumors. One selected variant, G3.12/BM2, reproducibly formed visible and viable brain metastases in more than 80 per cent of tumor-bearing mice, and lethal or potentially lethal brain metastases in 10-15 per cent of mice. This variant may serve as a model for clinical brain metastasis.

Subdural empyema: CT findings.

CT scans in 49 patients with surgically proven subdural empyema were evaluated. The empyemas were crescentic or lentiform extra-axial hypodense collections (density approximating that of cerebrospinal fluid) with prominent, sharply etched medial rim enhancement. Enhancement of the adjacent cerebral cortex was identified in many cases. Mass effect was always present and in 10 cases so extensive that it overshadowed a small extra-axial collection. CT allowed for precise localization of the lesion, including contiguous or isolated involvement of the interhemispheric subdural space. Mortality was 12% (6/49 cases), a marked improvement when compared with mortality figures obtained prior to the advent of CT (40%). CT findings indicative of involvement of the adjacent parenchyma via retrograde thrombophlebitis with resultant infarction and/or abscess formation were associated with poor prognosis. Improvement in prognosis since the advent of CT is the direct result of early accurate diagnosis and timely intervention.

Analytical Electron Microscopy (AEM) of Meningeal Cells Exposed to Particulate Cobalt During Studies of Experimental Epilepsy

Metallic cobalt acts as an epileptogenic agent when placed on the brain surface of some experimental animals. The mechanism by which this substance produces abnormal neuronal discharge is unknown. One potentially useful approach to this problem is to study the cellular and extracellular distribution of elemental cobalt in the meninges and adjacent cerebral cortex. Since it is possible to demonstrate the morphological localization and distribution of heavy metals, such as cobalt, by correlative x-ray analysis and electron microscopy (i.e., by AEM), we are using AEM to locate and identify elemental cobalt in phagocytic meningeal cells of young 80-day postnatal opossums following a subdural injection of cobalt particles.

Reacting ultrastructure of the human oligodendrocyte

Electron microscopical examination of adjacent human cerebral cortex from patients with brain tumour revealed the following morphological distinctive features of the oligodendrocyte: the presence of a diffuse electron dense material, large quantities of free ribosomes or ribosomal rosettes, eccentric nucleus with irregular clumps of chromatin, swollen perinuclear cisterna, extensive cytoplasmic microtubules, well-developed Golgi apparatus opposite the eccentric nuclei, dilated endoplasmic reticulum and mitochondria. The majority of oligodendrocytes contain large indefinable heterogeneous electron-dense structures within their perikaryon or processes. Oligodendrocytes with similar inclusion bodies are seen in the vicinity of capillaries. For these reasons a possible phagocytic activity of the human oligodendrocyte seems likely.

An intracellular study of neuronal organization in the visual cortex.

Neuronal connections in the visual cortex of cat (areas 17 and 18) were studied with intracellular recording and electrical stimulation techniques under Nembutal anaesthesia. Four types of axonal projection were seen; 1. association efferent cells projecting to adjacent cerebral cortex on the ipsilateral side, 2. commissural efferent cells to visual cortex on the contralateral side, 3. corticofugal efferent cells to the ipsilateral lateral geniculate body and superior colliculus, and 4. non-efferent cells whose projection is confined within the visual cortex. Both association and commissural efferent cells were located in layer III, corticofugal efferent cells in layer V and non-efferent cells in layers II–VI. Upon these cells two types of synaptic actions were exerted by the specific visual afferents that originate from the lateral geniculate body; 1. type I, monosynaptic excitation plus disynaptic inhibition and 2. type II, disynaptic excitation plus trisynaptic inhibition. Type I effects were found in layers III–V, and type II in layers II and VI. In the border region between areas 17 and 18 monosynaptic excitation and disynaptic inhibition were produced also by the commissural efferents originating from the contralateral visual cortex. On the basis of these results, a possible neuronal circuitry in the visual cortex is postulated.