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Neuropathology
Kinds of Neuropathology Selected AbstractsNeuropathology of Rett syndromeDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 2 2002Dawna Duncan Armstrong Abstract Rett Syndrome is unlike any other pediatric neurologic disease, and its clinical-pathologic correlation can not be defined with standard histology techniques. Based on hypotheses suggested by careful clinical observations, the nervous system of the Rett child has been explored utilizing morphometry, golgi preparations, computerized tomography, magnetic resonance imaging, chemistry, immunocytochemistry, autoradiography, and molecular biologic techniques. From these many perspectives we conclude that Rett syndrome is not a typical degenerative disorder, storage disorder, nor the result of gross malformation, infectious or neoplastic processes. There remain regions of the brain that have not been studied in detail but the available data suggest that the neuropathology of Rett syndrome can be summarized as follows: the Rett brain is small for the age and the height of the patient; it does not become progressively smaller over three to four decades; it has small dendritic trees in pyramidal neurons of layers III and V in selected lobes (frontal, motor, and temporal); it has small neurons with an increased neuronal packing density; it has an immature expression of microtubular protein-2 and cyclooxygenase; it exhibits a changing pattern of neurotransmitter receptors with an apparent reduction in many neurotransmitters, possibly contributing to some symptomatology. A mutation in Mecp2 causes this unique disorder of brain development. Neuronal mosaicism for normal and mutated Mecp2 produces a consistent phenotype in the classic female patient and a small brain with some preserved islands of function, but with an inability to support hand use and speech. This paper summarizes our current observations about neuropathology of Rett syndrome. MRDD Research Reviews 2002;8:72,76. © 2002 Wiley-Liss, Inc. [source] Molecular Neuropathology of Temporal Lobe Epilepsy: Complementary Approaches in Animal Models and Human Disease TissueEPILEPSIA, Issue 2007Michael Majores Summary:, Patients with temporal lobe epilepsies (TLE) frequently develop pharmacoresistance to antiepileptic treatment. In individuals with drug-refractory TLE, neurosurgical removal of the epileptogenic focus provides a therapy option with high potential for seizure control. Biopsy specimens from TLE patients constitute unique tissue resources to gain insights in neuropathological and molecular alterations involved in human TLE. Compared to human tissue specimens in most neurological diseases, where only autopsy material is available, the bioptic tissue samples from pharmacoresistant TLE patients open rather exceptional preconditions for molecular biological, electrophysiological as well as biochemical experimental approaches in human brain tissue, which cannot be carried out in postmortem material. Pathological changes in human TLE tissue are multiple and relate to structural and cellular reorganization of the hippocampal formation, selective neurodegeneration, and acquired changes of expression and distribution of neurotransmitter receptors and ion channels, underlying modified neuronal excitability. Nevertheless, human TLE tissue specimens have some limitations. For obvious reasons, human TLE tissue samples are only available from advanced, drug-resistant stages of the disease. However, in many patients, a transient episode of status epilepticus (SE) or febrile seizures in childhood can induce multiple structural and functional alterations that after a latency period result in a chronic epileptic condition. This latency period, also referred to as epileptogenesis, cannot be studied in human TLE specimens. TLE animal models may be particularly helpful in order to shed characterize new molecular pathomechanisms related to epileptogenesis and open novel therapeutic strategies for TLE. Here, we will discuss experimental approaches to unravel molecular,neuropathological aspects of TLE and highlight characteristics and potential of molecular studies in human and/or experimental TLE. [source] Neuropathology, biochemistry, and biophysics of ,-synuclein aggregationJOURNAL OF NEUROCHEMISTRY, Issue 1 2007Vladimir N. Uversky Abstract Aggregation of ,-synuclein, an abundant and conserved pre-synaptic brain protein, is implicated as a critical factor in several neurodegenerative diseases. These diseases, known as synucleinopathies, include Parkinson's disease, dementia with Lewy bodies (LBs), diffuse LB disease, the LB variant of Alzheimer's disease, multiple system atrophy, and neurodegeneration with brain iron accumulation type I. Although the precise nature of in vivo,-synuclein function remains elusive, considerable knowledge has been accumulated about its structural properties and conformational behavior. ,-Synuclein is a typical natively unfolded protein. It is characterized by the lack of rigid, well-defined, 3-D structure and possesses remarkable conformational plasticity. The structure of this protein depends dramatically on its environment and it accommodates a number of unrelated conformations. This paper provides an overview of the biochemistry, biophysics, and neuropathology of ,-synuclein aggregation. [source] Age-Related Sympathetic Ganglionic Neuropathology: Human Pathology And Animal ModelsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002RE. Schmidt Systematic studies of the autonomic nervous system of human subjects and development of well-defined animal models have begun to substantially improve our understanding of the pathogenesis of autonomic dysfunction in aging and may eventually provide strategies for intervention. Neuropathological studies of the sympathetic ganglia of aged human subjects and rodent models have demonstrated that neuroaxonal dystrophy involving intraganglionic terminal axons and synapses is a robust, unequivocal and consistent neuropathological finding in the aged sympathetic nervous system of man and animals. Quantitative studies have demonstrated that markedly swollen argyrophilic dystrophic axon terminals develop in the prevertebral superior mesenteric (SMG) and coeliac, but to a much lesser degree in the superior cervical ganglia (SCG) as a function of age, sex (males more than females) and diabetes. Dystrophic axons were immunoreactive for neuropeptide Y, tyrosine hydroxylase, dopamine-beta-hydroxylase, trkA and p75(NTR), an immunophenotype consistent with their origin from postganglionic sympathetic neurons, and contained large numbers of highly phosphorylated neurofilaments or tubulovesicular elements. The sympathetic ganglia of aged rodents also showed the hallmark changes of neuroaxonal dystrophy as a function of age and location (many more in the SMG than in the SCG). Plasticity-related synaptic remodeling could represent a highly vulnerable target of the aging process. The fidelity of animal models to the neuropathology of aged humans suggests that similar pathogenetic mechanisms may be involved in both and that therapeutic advances in animal studies may have human application. [source] Neuropathology of Alzheimer's DiseaseMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 1 2010Daniel P. Perl MD Abstract Alois Alzheimer first pointed out that the disease which would later bear his name has a distinct and recognizable neuropathological substrate. Since then, much has been added to our understanding of the pathological lesions associated with the condition. The 2 primary cardinal lesions associated with Alzheimer's disease are the neurofibrillary tangle and the senile plaque. The neurofibrillary tangle consists of abnormal accumulations of abnormally phosphorylated tau within the perikaryal cytoplasm of certain neurons. The senile plaque consists of a central core of beta-amyloid, a 4-kD peptide, surrounded by abnormally configured neuronal processes or neurites. Other neuropathological lesions are encountered in cases of Alzheimer's disease, but the disease is defined and recognized by these 2 cardinal lesions. Other lesions include poorly understood changes such as granulovacuolar degeneration and eosinophilic rodlike bodies (Hirano bodies). The loss of synaptic components is a change that clearly has a significant impact on cognitive function and represents another important morphological alteration. It is important to recognize that distinguishing between Alzheimer's disease, especially in its early stages, and normal aging may be very difficult, particularly if one is examining the brains of patients who died at an advanced old age. It is also noted that instances of pure forms of Alzheimer's disease, in the absence of other coexistent brain disease processes, such as infarctions or Parkinson's disease,related lesions, are relatively uncommon, and this must be taken into account by researchers who employ postmortem brain tissues for research. Mt Sinai J Med 77:32&–42, 2010. © 2010 Mount Sinai School of Medicine [source] Rapidly progressive sporadic dentatorubral pallidoluysian atrophy with intracytoplasmic inclusions and no CAG repeat expansionMOVEMENT DISORDERS, Issue 12 2006Alberto J. Espay MD Abstract A 48-year-old man developed progressive hemidystonia and postural impairment with falls, followed by choreoathetosis, hyporeflexia, ataxia, supranuclear vertical gaze palsy, and dementia, lasting only 3.5 years from symptom onset to death. Family history and genetic testing were unrevealing. Neuropathology showed findings identical to genetic dentatorubral pallidoluysian atrophy (DRPLA), except for the absence of intranuclear inclusions and the presence of intracytoplasmic inclusions in the pons, striatum, thalamus, and subthalamic nucleus. This case expands the clinical and neuropathological spectrum of DRPLA and supports the hypothesis that aggregates may not be intrinsically pathogenic. © 2006 Movement Disorder Society [source] Neuropathology of mild cognitive impairmentNEUROPATHOLOGY, Issue 6 2007Yuko Saito We aim to investigate the pathological background of mild cognitive impairment (MCI). The most recent 545 cases from the Brain Bank for Aging Research (BBAR) were studied, with a mean age of 80.7 years and male : female ratio of 324 : 221. Cases with clinical dementia rating scale (CDR) 0.5 were retrieved as the best substitute of MCI. CDR was retrospectively determined from clinical charts. Pathological examinations followed the BBAR protocol (JNEN 2004). Post mortem assessment of CDR was possible for 486 cases, and was 0 in 201 cases, 0.5 in 57 cases and 1,3 in 228 cases. CDR 0.5 group was clinicopathologically classified into 33 cases with degenerative changes, nine cases with vascular changes, four cases with combined degenerative and vascular changes, two with hippocampal sclerosis, two with trauma, one with metabolic disease and six with unremarkable changes. The degenerative group was further subclassified into groups with pure and combined pathology. The former consisted of six cases each with Alzheimer change (AC), argyrophilic grain change (AGC) and neurofibrillary tangle predominant change (NFTC), three each with Lewy body disease change without parkinsonism (DLBC) or Parkinson's disease (PDMCI) and one case with progressive supranuclear palsy. The latter consisted of three cases with AC plus AGC, two with AGC plus NFTC and one each with AC plus DLBC, DLBC plus amyotrophic lateral sclerosis and AGC plus DLBC. The pathological backgrounds of patients of class CDR 0.5 were varied and not restricted to AC. [source] The 45th Annual Meetings of Japanese Society of NeuropathologyNEUROPATHOLOGY, Issue 2 2004Article first published online: 6 APR 200 First page of article [source] The 45th Annual Meeting of Japanese Society of Neuropathology, Maebashi, Japan 26-28 May, 2004NEUROPATHOLOGY, Issue 1 2004Article first published online: 26 FEB 200 First page of article [source] The 44th Annual Meeting of Japanese Society of NeuropathologyNEUROPATHOLOGY, Issue 2 2003Article first published online: 9 APR 200 First page of article [source] 42nd Annual Meeting of the Japanese Society of NeuropathologyNEUROPATHOLOGY, Issue 2 2001Article first published online: 21 DEC 200 First page of article [source] Section on Cellular Neuropathology, Ninds, National Institutes of Health, Bethesda, MarylandNEUROPATHOLOGY, Issue 2000Henry deF Webster [source] France and Japan in NeuropathologyNEUROPATHOLOGY, Issue 2000Makoto Iwata No abstract is available for this article. [source] Tyrosine phosphorylation of tau accompanies disease progression in transgenic mouse models of tauopathyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2010K. Bhaskar K. Bhaskar, G. A. Hobbs, S-H. Yen and G. Lee (2010) Neuropathology and Applied Neurobiology36, 462,477 Tyrosine phosphorylation of tau accompanies disease progression in transgenic mouse models of tauopathy Aim: Tau protein is a prominent component of paired helical filaments in Alzheimer's disease (AD) and other tauopathies. While the abnormal phosphorylation of tau on serine and threonine has been well established in the disease process, its phosphorylation on tyrosine has only recently been described. We previously showed that the Src family non-receptor tyrosine kinases (SFKs) Fyn and Src phosphorylate tau on Tyr18 and that phospho-Tyr18-tau was present in AD brain. In this study, we have investigated the appearance of phospho-Tyr18-tau, activated SFK and proliferating cell nuclear antigen (PCNA) during disease progression in a mouse model of human tauopathy. Methods: We have used JNPL3, which expresses human tau with P301L mutation, and antibodies specific for phospho-Tyr18-tau (9G3), ser/thr phosphorylated tau (AT8), activated SFK and PCNA. Antibody staining was viewed by either epifluorescence or confocal microscopy. Results: Phospho-Tyr18-tau appeared concurrently with AT8-reactive tau as early as 4 months in JNPL3. Some 9G3-positive cells also contained activated SFKs and PCNA. We also investigated the triple transgenic mouse model of AD and found that unlike the JNPL3 model, the appearance of 9G3 reactivity did not coincide with AT8 in the hippocampus, suggesting that the presence of APP/presenilin influences tau phosphorylation. Also, Thioflavin S-positive plaques were 9G3-negative, suggesting that phospho-Tyr18-tau is absent from the dystrophic neurites of the mouse triple transgenic brain. Conclusions: Our results provide evidence for the association of tyrosine-phosphorylated tau with mechanisms of neuropathogenesis and indicate that SFK activation and cell cycle activation are also involved in JNPL3. [source] Review: The chemokine receptor CXCR3 and its ligands CXCL9, CXCL10 and CXCL11 in neuroimmunity , a tale of conflict and conundrumNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2010M. Müller M. Müller, S. Carter, M. J. Hofer and I. L. Campbell (2010) Neuropathology and Applied Neurobiology36, 368,387 The chemokine receptor CXCR3 and its ligands CXCL9, CXCL10 and CXCL11 in neuroimmunity , a tale of conflict and conundrum The chemokines CXCL9, CXCL10 and CXCL11 (also known as monokine induced by interferon-,, interferon-inducible protein-10 and interferon-inducible T cell ,-chemoattractant, respectively) are structurally and functionally related molecules within the non-ELR CXC chemokine subgroup. These chemokines are generally not detectable in most non-lymphoid tissues under physiological conditions but are strongly induced by cytokines, particularly interferon-,, during infection, injury or immunoinflammatory responses. CXCL9, CXCL10 and CXCL11 each bind to a common primary receptor, CXCR3, and possibly to additional receptors. They are best known for their role in leucocyte trafficking, principally acting on activated CD4+ Th1 cells, CD8+ T cells and NK cells. An abundance of data demonstrates that CXCL9, CXCL10 and CXCL11 are produced in many diverse pathologic conditions of the central nervous system. More recent attention has focussed on the function of these chemokines in the central nervous system inflammation. The results of these studies have proven to be sometimes surprising and other times contradictory. Here we discuss the likely more subtle and perhaps divergent roles for these chemokines in the pathogenesis of neuroinflammatory diseases. [source] Immunohistological intensity measurements as a tool to assess sarcolemma-associated protein expressionNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2010V. Arechavala-Gomeza V. Arechavala-Gomeza, M. Kinali, L. Feng, S. C. Brown, C. Sewry, J. E. Morgan and F. Muntoni (2010) Neuropathology and Applied Neurobiology36, 265,274 Immunohistological intensity measurements as a tool to assess sarcolemma-associated protein expression Aims: The quantification of protein levels in muscle biopsies is of particular relevance in the diagnostic process of neuromuscular diseases, but is difficult to assess in cases of partial protein deficiency, particularly when information on protein localization is required. The combination of immunohistochemistry and Western blotting is often used in these cases, but is not always possible if the sample is scarce. We therefore sought to develop a method to quantify relative levels of sarcolemma-associated proteins using digitally captured images of immunolabelled sections of skeletal muscle. Methods: To validate our relative quantification method, we labelled dystrophin and other sarcolemmal proteins in transverse sections of muscle biopsies taken from Duchenne muscular dystrophy and Becker muscular dystrophy patients, a manifesting carrier of Duchenne muscular dystrophy and normal controls. Results: Using this method to quantify relative sarcolemmal protein abundance, we were able to accurately distinguish between the different patients on the basis of the relative amount of dystrophin present. Conclusions: This comparative method adds value to techniques that are already part of the diagnostic process and can be used with minimal variation of the standardized protocols, without using extra amounts of valuable biopsy samples. Comparative quantification of sarcolemmal proteins on immunostained muscle sections will be of use to establish both the abundance and localization of the protein. Moreover, it can be applied to assess the efficacy of experimental therapies where only partial restoration or upregulation of the protein may occur. [source] Review: On TRAIL for malignant glioma therapy?NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2010J. M. A. Kuijlen J. M. A. Kuijlen, E. Bremer, J. J. A. Mooij, W. F. A. den Dunnen and W. Helfrich (2010) Neuropathology and Applied Neurobiology36, 168,182 On TRAIL for malignant glioma therapy? Glioblastoma (GBM) is a devastating cancer with a median survival of around 15 months. Significant advances in treatment have not been achieved yet, even with a host of new therapeutics under investigation. Therefore, the quest for a cure for GBM remains as intense as ever. Of particular interest for GBM therapy is the selective induction of apoptosis using the pro-apoptotic tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). TRAIL signals apoptosis via its two agonistic receptors TRAIL-R1 and TRAIL-R2. TRAIL is normally present as homotrimeric transmembrane protein, but can also be processed into a soluble trimeric form (sTRAIL). Recombinant sTRAIL has strong tumouricidal activity towards GBM cells, with no or minimal toxicity towards normal human cells. Unfortunately, GBM is a very heterogeneous tumour, with multiple genetically aberrant clones within one tumour. Consequently, any single agent therapy is likely to be not effective enough. However, the anti-GBM activity of TRAIL can be synergistically enhanced by a variety of conventional and novel targeted therapies, making TRAIL an ideal candidate for combinatorial strategies. Here we will, after briefly detailing the biology of TRAIL/TRAIL receptor signalling, focus on the promises and pitfalls of recombinant TRAIL as a therapeutic agent alone and in combinatorial therapeutic approaches for GBM. [source] Review: Recent progress in frontotemporal lobar degenerationNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 1 2010S. M. Pickering-Brown S. M. Pickering-Brown (2010) Neuropathology and Applied Neurobiology36, 4,16 Recent progress in frontotemporal lobar degeneration Frontotemporal lobar degeneration (FTLD) is a highly familial condition and is increasingly being recognized as an important form of dementia. The literature published on this disease is often difficult to collate due to the wide range in nomenclature used. Thankfully, consensus recommendations have now been published to address this issue and hopefully the community will adopt these as intended. Much progress has been made in our understanding of the clinical, pathological and genetic understanding of FTLD in recent years. Progranulin and TDP-43 have recently been identified as new important proteins involved in the pathophysiology of FTLD and this latter protein may have potential as a biomarker of this disease. However, much remains before we have a full picture of the genes that cause FTLD and the biological pathways in which they function. The purpose of this review is to summarize the current concepts and recent advances in our knowledge of this disease. [source] Review: Neuropathology of acute phase encephalitis lethargica: a review of cases from the epidemic periodNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2009L. L. Anderson Introduction: Encephalitis lethargica (EL), an epidemic disease of the early 20th century, has continued to be diagnosed sporadically since that time, including a report of 20 new cases in 2004. Many of the recent case reports state that the primary neuropathology of acute EL consists of inflammatory changes and lesions within the midbrain, basal ganglia and substantia nigra. However, the neuropathology of acute EL cases from the epidemic period was actually much more widespread. Methods: In order to characterize the neuropathology of acute phase EL, we developed a database of EL pathology based on 112 cases from the years 1915 to 1940, of which most died within 2 weeks of EL onset. Results: Our analysis revealed that cortical damage was prevalent in 75% of the 112 cases; damage to the meninges and brainstem occurred in approximately half of the cases; and the substantia nigra was damaged in only 13% of these acute cases. We also found that after 1921, damage to cranial nerve nuclei was not reported. An analysis of the neuropathology and clinical symptoms revealed little correlation. Conclusions: Based on these findings, putative modern cases of acute EL with MRI/CT indicated lesions confined solely to the midbrain, brainstem, and/or basal ganglia should not be considered, consistent with that reported during epidemic period. [source] Greenfield's Neuropathology (8th Edition)NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2008Roy O. Weller No abstract is available for this article. [source] Adams and Graham's Introduction to Neuropathology (3rd edition)NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2007T. S. Jacques No abstract is available for this article. [source] In this month's edition of Neuropathology and Applied NeurobiologyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2004Article first published online: 11 OCT 200 No abstract is available for this article. [source] International Society of Neuropathology XVth International Congress of Neuropathology, Turin 2003NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2004Article first published online: 5 AUG 200 No abstract is available for this article. [source] Principles and Practice of Neuropathology (2nd edition)NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2003Roy O. Weller No abstract is available for this article. [source] Guidelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patientNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 1 2003U. Rüb U. Rüb, E. R. Brunt, D. Del Turco, R. A. I. de Vos, K. Gierga, H. Paulson and H. Braak (2003) Neuropathology and Applied Neurobiology 29, 1,13 Guildelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patient Despite the fact that considerable progress has been made in the last 20 years regarding the three-phase process of ingestion and the lower brain stem nuclei involved in it, no comprehensive descriptions of the ingestion-related lower brain stem nuclei are available for neuropathologists confronted with ingestive malfunctions. Here, we propose guidelines for the pathoanatomical investigation of these nuclei based on current knowledge with respect to ingestion and the nuclei responsible for this process. The application of these guidelines is described by drawing upon the example of the lower brain stem of a male patient with spinocerebellar ataxia type 3, also known as Machado-Joseph disease, who displayed malfunctions during the preparatory phase of ingestion, as well as lingual and pharyngeal phases of swallowing. By way of the representative application of the recommended investigation procedure to 100 µm serial sections through the patient's brain stem stained for lipofuscin pigment and Nissl material, we observed neuronal loss together with astrogliosis in nearly all of the ingestion-related lower brain stem nuclei (motor, principal and spinal trigeminal nuclei; facial nucleus; parvocellular reticular nucleus; ambiguus nucleus, motor nucleus of the dorsal glossopharyngeal and vagal area; gelatinous, medial, parvocellular and pigmented solitary nuclei; hypoglossal nucleus). In view of their known functional role in the three-phase process of ingestion, damage to these nuclei not only offers an explanation of the patient's malfunctions related to the preparatory phase of ingestion and lingual and pharyngeal phases of swallowing, but also suggests that the patient may have suffered from additional esophageal phase swallowing malfunctions not mentioned in his medical records. [source] Dural haemorrhage in non-traumatic infant deaths: does it explain the bleeding in ,shaken baby syndrome'?NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 1 2003J. F. Geddes J. F. Geddes, R. C. Tasker, A. K. Hackshaw, C. D. Nickols, G. G. W. Adams, H. L. Whitwell and I. Scheimberg (2003) Neuropathology and Applied Neurobiology 29, 14,22 Dural haemorrhage in non-traumatic infant deaths: does it explain the bleeding in ,shaken baby syndrome'? A histological review of dura mater taken from a post-mortem series of 50 paediatric cases aged up to 5 months revealed fresh bleeding in the dura in 36/50, the bleeding ranging from small perivascular haemorrhages to extensive haemorrhage which had ruptured onto the surface of the dura. Severe hypoxia had been documented clinically in 27 of the 36 cases (75%). In a similar review of three infants presenting with classical ,shaken baby syndrome', intradural haemorrhage was also found, in addition to subdural bleeding, and we believe that our findings may have relevance to the pathogenesis of some infantile subdural haemorrhage. Recent work has shown that, in a proportion of infants with fatal head injury, there is little traumatic brain damage and that the significant finding is craniocervical injury, which causes respiratory abnormalities, severe global hypoxia and brain swelling, with raised intracranial pressure. We propose that, in such infants, a combination of severe hypoxia, brain swelling and raised central venous pressure causes blood to leak from intracranial veins into the subdural space, and that the cause of the subdural bleeding in some cases of infant head injury is therefore not traumatic rupture of bridging veins, but a phenomenon of immaturity. Hypoxia with brain swelling would also account for retinal haemorrhages, and so provide a unified hypothesis for the clinical and neuropathological findings in cases of infant head injury, without impact or considerable force being necessary. [source] From this month's Neuropathology and Applied NeurobiologyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2002Article first published online: 15 SEP 200 [source] Neuropathology of septic shockNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2002F. Gray Introduction:, Septic shock is the most frequent cause of death in intensive care units. It is often complicated by an encephalopathy and there is increasing evidence that central autonomic nervous system (CANS) dysfunction plays a crucial role in the onset and persistance of the haemodynamic failure. However, only a few neuropathological studies are available; they are always retrospective and often disagree. Material and methods:, Twenty consecutive patient who died from septic shock were examined and compared with eight patients who died from nonseptic shock in the same unit and five ,normal' controls collected from the Forensic Medicine Service. Results and conclusion:, A variety of lesions, including microabscesses, multifocal necrotizing leukoencephalopathy, haemorrhages and disseminated intravascular coagulation, were found, and were most probably related to the biological disturbances associated with sepsis. These lesions may contribute to the ,septic encephalopathy'. Ischaemic changes in ,susceptible' areas were comparable in septic shock and in nonseptic shock. In contrast, ischaemic changes in the nuclei of the CANS were significantly more severe in septic shock than in nonseptic shock. Neuronal apoptosis in these nuclei was significantly more frequent and more severe in septic shock; apoptosis did not correlate exactly with neuronal ischaemia and was associated with only mild microglial activation suggesting that circulating factors may also play a role in its causation. [source] Current Awareness in NMR in BiomedicineNMR IN BIOMEDICINE, Issue 8 2010Article first published online: 27 SEP 2010 In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of NMR in biomedicine. Each bibliography is divided into 12 sections: 1 Reviews; 2 General; 3 Technology; 4 Contrast Agents; 5 Brain and Nerves; 6 Neuropathology; 7 Cancer; 8 Cardiac, Vascular and Respiratory Systems; 9 Liver, Kidney and Other Organs; 10 Muscle and Orthopaedic; 11 Plants, Micro-organisms and Parasites; 12 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted. [source] Current Awareness in NMR in BiomedicineNMR IN BIOMEDICINE, Issue 2 2010Article first published online: 22 FEB 2010 In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of NMR in biomedicine. Each bibliography is divided into 12 sections: 1 Reviews; 2 General; 3 Technology; 4 Contrast Agents; 5 Brain and Nerves; 6 Neuropathology; 7 Cancer; 8 Cardiac, Vascular and Respiratory Systems; 9 Liver, Kidney and Other Organs; 10 Muscle and Orthopaedic; 11 Plants, Micro-organisms and Parasites; 12 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted. [source] | ||||||||||||||||||||||||||||||||||