A neuropathological analysis of neonatal deaths over a 20-year period]

This study is an overview of 2,515 consecutive autopsies on newborn infants who died during the first 28 days of life at the Hospital for Sick Children, Toronto, during the period 1970-1989. The infants were grouped into 2 categories according to their gestational age and then subdivided into the groups of early (0-6 days) and late (7-28 days) neonatal deaths. In this overview trends in the occurrence of neuropathological observation were documented. In each 5-year time period and each gestational group the following diagnoses were recorded; hypoxic-ischemic neuronal changes, periventricular leukomalacia, infarction, kernicterus, meningitis, and hemorrhage (subependymal, parenchymal, choroidal). In these 20 years, the mortality in preterm infants has decreased due to a fall in the incidence of subependymal/intraventricular hemorrhage, kernicterus and meningitis. In contrast, the rate of mortality in term infants has increased due to a higher frequency of hypoxic-ischemic neuronal necrosis and choroid plexus hemorrhage.     

Dynamic neuropathology of tauopathy]

Tauopathy is defined as abnormal accumulation of aberrantly phosphorylated microtubule-associated protein tau in the central nervous system, best demonstrated by immunocytochemistry using anti-tau antibodies. The newly recognized familial tauopathy with mutation in tau gene, that is located on chromosome 17, confirms that the process directly leads to neuronal degeneration. Tau consists of six isoforms translated from alternative splicing of a single gene. They are classified into three repeat (3R) and four repeat (4R) subtypes, by the number of microtubulus-binding domain from the reading or skipping of the exon 10. In sporadic tauopathy, 3R + 4R accumulate in Alzehimer's disease (AD), 3R in Pick's disease, and 4R in progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). In familial tauopathy, the mutations affecting the splicing of the exon 10 accumulate 4R and phenotypically mimick CBD/PSP, while majority of others simulate neurofibrillary tangle-predominant form of dementia (NFTD). Argyrophlic grains (AG) are tau-immunoreactive comma-shaped or filiform structure, and argyrophilic grain dementia (AGD) is a form of senile dementia carrying AG as only morphological substrate explaining dementia. In our consecutive autopsy cases from the oldest old, AGD is the second leading cause of degenerative type of dementia, highlighting the importance of tauopathy in the aging and dementia.     

Cerebromeningeal hemorrhage. Analysis of autopsies performed over a 10-year period

A study was conducted on the medical records of 353 patients who died of a subarachnoid hemorrhage (SAH) and who were submitted to autopsy over the last 10 years. SAH was associated with arterial hypertension in 180 (51%) cases, with ruptured aneurysms in 102 (28.9%), and with other pathologies in 71 (20.1%). The patients with hemorrhage associated with arterial hypertension were mostly males, and those with hemorrhage due to aneurysms were mostly females. Of the patients with aneurysms, 36 (35.3%) had aneurysms in the anterior communicating artery, 30 (29.4%) in the internal carotid artery, and 23 (22.6%) in the middle cerebral artery. Among the patients with aneurysms who suffered rebleeding and vasospasm, 59.1% and 61.5%, respectively, were classified as grade I and II upon admission, and all evolved toward grade IV after these complications. Vasospasm predominated from the 3rd to the 10th day after hemorrhage, and rebleeding from the 9 to 16th day and both were most frequent among patients with aneurysms of the anterior communicant artery. Sixty eight percent of the patients with aneurysms died during the first 9 days after hemorrhage. Because of our conduct was to operate systematically late, a considerable number of patients lost the opportunity to be treated surgically with possible favorable evolution due to vasospasm or rebleeding.     

The neuropathology of autism: a review

Presented is a review of recent progress in the understanding of autism based on investigations of donated human brain tissue. Autism is a pervasive developmental disorder by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria, manifesting by age 3 and characterized by impairments in social interaction and communication, as well as restricted, repetitive, stereotyped patterns of behavior. Based on reported neuropathologic findings, these characteristic behaviors are clinical manifestations of both pre- and postnatal alterations. This review summarizes the current data obtained from postmortem brain studies in the areas of stereology, neurotransmitter systems/synaptic processes, molecular mechanisms, and neuroimmunology. In addition, we discuss current research strategies designed to facilitate translational research and maximize the yield of precious resources (e.g. the Autism Tissue Program), highlight barriers to research, and consider future trends.     

The neuropathology of intracerebroventriculart-butylhydroperoxide

t-Butylhydroperoxide can be used as a model oxidative stress-inducing agent in the brain following intracerebroventricular administration. Mice were treated with saline,t-butanol, ort-butylhydroperoxide.t-Butanol is the major metabolite oft-butylhydroperoxide.t-Butylhydroperoxide had a number of effects, including that it damages dopaminergic, cholinergic, and GABAergic neurons as demonstrated immunohistochemically. Electron microscopic examination demonstrated that astrocytes, oligodendrocytes, endothelial cells, pericytes, and neurons are damaged bytbutylhydroperoxide. Dopamine and its metabolites were affected in a number of brain regions, as were serotonin and its metabolite. Choline acetyl transferase activity was decreased in the striatum. Edema was apparent as assessed by tissue protein levels. There was evidence of lipid peroxidation produced byt-butylhydroperoxide in the midbrain.t-Butylhydroperoxide is a neurotoxin that may be useful in understanding the unexpected ways the brain responds to oxidative stress.     

The neuropathology of schizophrenia

Insofar as schizophrenia is a neuropsychiatric syndrome involving the brain, neuropathology is a promising, if not essential investigative approach. Although traditional neuropathology has yet to yield a pathognomonic lesion in schizophrenia, there have been no shortages of findings. Unfortunately, many of these findings have not only failed to be pathognomonic, but they have not been consistently replicated. Fortunately, newer neuropathological techniques, such as post-mortem neurochemistry, have resulted in findings among the most reproducible in schizophrenia research. Although one of these, increased dopamine receptors in the basal ganglia of schizophrenic patients, has been replicated many times, it suffers from doubts as to its clinical relevance. Are these increases in dopamine receptors primary to the illness or a side effect of the treatment? This article discusses the relevance of this finding, reviews other highlights of post-mortem neurochemistry and traditional neuropathology, and discusses new horizons such as autoradiography, immunocytochemistry, and neuronal morphometrics.     

The neuropathology of sport

The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.     

Anterior type dementia from the viewpoint of neuropathology]

Anterior type dementia is characterized by primary degeneration in the anterior brain region and represents pick symptom. Anterior type dementia includes several pathological disease entities, almost of them usually exhibit variation of atrophic brain regions in greater or lesser degree. This variation of each disease cause confusion, namely, the same clinical manifestations occur even if it is a different disease and diversely, different clinical manifestations can occur even if it is the same disease entity. This is the reason why discrepancy between clinical diagnosis and pathology diagnosis occurs sometimes in anterior type dementia. For reasonable clinical diagnosis, anterior type dementia, separate from neuropathological diseases entity, should be deal with clinical symptom-complex, which consists of frontotemporal dementia (FTD) progressive nonfluent aphasia (PA) and semantic dementia (SD). FTD, PA and SD have, though broadly, corresponding responsible brain lesion respectively.     

The neuropathology of multiple sclerosis

This article reviews the pathology of multiple sclerosis in an attempt to allow the reader to better understand the pathogenesis of the lesions. The elements comprising the lesions are discussed in light of their pathogenic implications. Current ideas of classification are discussed, and wherever possible, correlations with clinical and imaging studies are drawn.     

The neuropathology of benzedrine poisoning

Summary The clinical manifestations and accompanying neuropathology of benzedrine administration in guinea pigs and rats are described.     

The neuropathology of schizophrenia.

This review of brain changes in schizophrenia provides the neuropathologist with a conceptual framework to understand this disease. Numerous conflicting reports describe structural, functional, neurochemical, and neuropathological alterations in brains of schizophrenic patients. A core clinical manifestation of schizophrenia is disruption of thought; a mental process that is poorly localized in the brain and influenced by multiple neural systems. Schizophrenia has variable clinical presentations, natural history, and response to medication that imply a pathologically heterogenous group of diseases. Recent studies suggest that schizophrenia may involve cortical, limbic, and subcortical structures as well as multiple neurotransmitter systems. Schizophrenia may result from a perinatal insult in a genetically predisposed individual that produces neuronal alterations that manifest during final synaptic reorganization and myelination of early adulthood.