Cerebral Palsy

Patients with parieto-occipital brain damage may show simultanagnosia, a selective impairment in the simultaneous perception and integration of multiple objects (global perception) with normal recognition of individual objects. Recent findings in patients with simultanagnosia indicate improved global perception at smaller spatial distances between local elements of hierarchical organized complex visual arrays. Global perception thus does not appear to be an all-or-nothing phenomenon but can be modified by the spatial relationship between local elements. The present study aimed to define characteristics of a general principle that accounts for improved global perception of hierarchically organized complex visual arrays in patients with simultanagnosia with respect to the spatial properties of local elements. In detail, we investigated the role of the number and size of the local elements as well as their relationship with each other for the global perception. The findings indicate that global perception increases independently of the size of the global object and depends on the spatial relationship between the local elements and the global object. The results further argue against the possibility of a restriction in the attended or perceived area in simultanagnosia, in the sense that the integration of local elements into a global scene is impaired if a certain spatial “field of view” is exceeded. A possible explanation for these observations might be a shift from global to local saliency in simultanagnosia.

The term amyloidosis refers to the extracellular deposition of fibrils composed of different types of plasma proteins. Various clinical symptoms are caused by the tissue damage related to the deposited fibrillary material. Except of the brain, all organs can be affected: kidney, liver, spleen, lung, gastrointestinal tract, endocrine organs, skin, heart and autonomous nervous system. Diagnosis is confirmed by specific histological methods (congo red stain, polarized and electron microscopy, immunohistochemistry) and genetic testing. Scintigraphy with radioisotope labeled serum amyloid P-component is helpful in the localization of the process and in the assessment of therapeutic effect. In the majority of cases the underlying disease is a plasma cell disorder, light chains aggregate to amyloid fibrils. Therefore chemotherapy and – in selected patients – stem cell transplantation is the choice of treatment. Another common type of amyloidosis is caused by chronic inflammatory diseases (amyloid fibrils are composed of elevated serum amyloid A being related to C reactive protein), or by some hereditary fever syndromes. Treatment of the underlying disorder may bring resolution of the amyloid burden. In 10% of the cases, amyloid fibrils are composed of genetically modified proteins. Depending on the source of the mutant protein liver transplantation, hepatorenal or cardiorenal transplantation may cure the disease.

Astrocytic tumors are the most frequent primary brain neoplasms. They are clinically characterized by wide variations in histology. Analysis of chromosome DNA imbalance may help to advance diagnosis, grading, and classification, and to determine appropriate therapeutic approaches for tumors of astrocytic lineages. Comparative genomic hybridization (CGH) provides comprehensive information about chromosome DNA aberrations, and is an important technique for evaluating the differences at genomic levels among the same or different grade tumors. In this study, 63 astrocytic tumors of Chinese patients were screened by CGH, and the relationship between their chromosome DNA imbalances and the histopathological classification, grading, and clinical features was analyzed. Most tumors showed genomic copy aberrations detected by CGH. The most frequent abnormalities were regional gains in chromosome 1q and 7p; regional losses in chromosome 1p, 2q, 4q, 6p, 10q, 12q, 15q, 19q, and 22q were also frequently observed. The gain of 1q and the loss of 15q were relevant to the histological types and grades of WHO classification. The losses of 4q and 10q correlated with age in the group of anaplastic astrocytoma, which was unreported in the literature. This study confirmed that chromosomal aberrations, such as +1q, -4q, -10q, +7p, and -15q possibly contributed to the pathogenesis of these tumors. Our data was the first report on the chromosomal aberrations of astrocytic tumors of Chinese patients. Copyright © 2010 Elsevier GmbH. All rights reserved.

Chronic hypertension and cerebral amyloid angiopathy (CAA) are the main pathologies which can induce the rupture of cerebral vessels and intracerebral hemorrhagies, as a result of degenerative changes in the vascular wall. A lot of progress has been made in this direction since the successful creation of the first mouse model for the study of Alzheimer’s disease (AD), as the spectrum of AD pathology includes a plethora of changes found in pure cerebrovascular diseases. We describe here some of these mouse models having important vascular changes that parallel human AD pathology, and more importantly, we show how these models have helped us understand more about the mechanisms that lead to CAA formation. An important cellular event associated with reduced structural and functional recovery after stroke in aged animals is the early formation of a scar in the infarcted region that impairs subsequent neural recovery and repair. We review recent evidence showing that the rapid formation of the glial scar following stroke in aged rats is associated with premature cellular proliferation that originates primarily from the walls of capillaries in the corpus callosum adjacent to the infarcted region. After stroke several vascular mechanisms are turned-on immediately to protect the brain from further damage and help subsequent neuroregeration and functional recovery. Although does occur after stroke, vasculogenesis is overshadowed in its protective/restorative role by the angiogenesis and arteriogenesis. Understanding the basic mechanisms underlying functional recovery after cerebral stroke in aging subjects is likely to yield new insights into the treatment of brain injury in the clinic.

Of the 23.8 million military veterans living in the United States, approximately 3 million have served in Operation Enduring Freedom or Operation Iraqi Freedom. The injuries and illnesses that affect veterans returning from combat are predictable. Blast injuries are common and most often present as mild traumatic brain injury, which is synonymous with concussion. Family physicians caring for returning veterans will also encounter conditions such as posttraumatic stress disorder at rates higher than those in the general population. The symptoms associated with posttraumatic stress disorder and mild traumatic brain injury often overlap and can present concurrently. Treatment of traumatic brain injury should be based on symptoms and guided by clinical practice guidelines from the U.S. Department of Veterans Affairs and Department of Defense. Family physicians should understand the range of post-war health concerns and screen returning service members for posttraumatic stress disorder, substance abuse, suicidality, and clinical depression. Family physicians are well positioned to offer continuity of care for issues affecting returning service members and to coordinate the delivery of specialized care when needed. (Am Fam Physician. 2010;82(1):43-49. Copyright (c) 2010 American Academy of Family Physicians.).

OBJECTIVE: Damage to the developing brain may be caused by maternal environment, nutritional deficiencies, failure of protective mechanisms, etc. Further, the developing brain may be damaged by intrauterine ischemia or by ischemia in newborns complicated by perinatal asphyxia. There is an effort to find agents with neuroprotective effect on the developing brain. The aim was to study the effect of the new pyridoindole antioxidant SMe1EC2 on the resistance of offspring hippocampus exposed to ischemia in vitro after treatment of mothers. MATERIALS AND METHODS: The electrically evoked responses were determined by extracellular recording from offspring hippocampal slices. The effect of oral treatment of rats with SMe1EC2 over 18 consecutive days, from day 15 of gestation to day 10 post partum (PP) was analyzed in the model of ischemia in vitro measured on the hippocampus of 21-day-old pups, with focus on neuronal function recovery in reoxygenation. RESULTS: Increased recovery of neuronal response was found at the end of 20-min reoxygenation in offspring hippocampal slices exposed to 10-min hypoxia/hypoglycemia from rats whose mothers were treated with the dose of 50 and 250 mg/kg of SMe1EC2, compared to control offspring slices (mothers received vehicle over the same time). CONCLUSIONS: The increased offspring hippocampus resistance to hypoxia/hypoglycemia due to 18-day maternal treatment with SMe1EC2 might have been obtained via the transplacental way as well as in the neonatal period via breast milk, skin and saliva. The manifested neuroprotective effect of SMe1EC2 on the developing brain might find exploitation during risk pregnancy and delivery.

ABSTRACT: Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer’s disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer’s disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases.

The development of potential neuroprotective therapies for neurodegenerative diseases (Parkinson's and Alzheimer's Disease) must be based on understanding their molecular and biochemical pathogenesis. Many potential pathways of neuronal cell death have been implicated in a mouse model of neurodegenerative disease, including excitotoxicity, toxicity from reactive oxygen species (superoxide anion, nitric oxide, hydroxyl radical), apoptosis (caspase-dependent and -independent pathways), necrosis and glial injury. Some agents that act on these pathways may be available for protecting the brain against chronic neurodegenerative conditions like Parkinson's and Alzheimer's disease. Drugs currently used to treat neurological disease and injuries provide temporary relief of symptoms but do not stop or slow the underlying neurodegenerative process. Restorative therapies for Parkinson's Disease are currently focused on cell replacement and administration of growth factors and small-molecule neurotrophic agents. The new experimental drugs, by contrast, target the common, underlying cause of destructive process of brain cell death. For example, p53 inhibitors attack a key protein involved in nerve cell death and represent a new strategy for preserving brain function following sudden injury or chronic disease. Analogues of pifithrin-alpha (PFT), which was shown in previous studies to inhibit p53, were designed, synthesized and tested to see whether they would work against cultured brain cells and animal models of neurodegenerative disease. Moreover, several agents based on the predominant anti-amyloid strategy, targeting amyloid-beta (Aβ) peptide, which aggregates in the plaques that are a hallmark of Alzheimer's disease, would affect disease progression. Researchers are already making great strides in developing a vaccine for this progressive brain disorder. Immunization could offer a way to blunt or even prevent the deadly, memory-robbing disease. Here we review many of potential neuroprotective therapies, and strategies that might be suited to the development of innovative approaches that prevent degeneration and restore function in Parkinson's disease.

We aimed to determine the effect NAC (N-acetylcysteine) and melatonin on the histopathological and biochemical paramethers in the rats poisoned with CO (Carbon monoxide) experimentally. Winster albino female rats were placed in a plexiglass chamber and they were poisoned with CO. After the poisoning, rats were randomly divided into 3 groups. The group given only normal saline, was used as a control group (n = 9). The second group was given 30 mg/kg intraperitonally NAC (n = 10). And the third group was treated with 10 mg/kg of melatonin intramuscularly (n = 9). It is determined that some biochemical values affected by NAC but not by melatonin. CK, ALT, Lactate, MDA levels were significantly higher in NAC group than control and Melatonin group (p < 0.01 for all comparisons). Thiol level was lower in NAC group than control group and Melatonin group (p < 0.01 and p < 0.001, respectively). There were no statistical significant differences between the melatonin and control group. There were statistically significant difference between control, NAC and Melatonin groups according to brain and lung tissue damage. It is shown that both NAC and Melatonin are reducing the brain and lung tissue damage of CO poisoning but due to biochemical results worsened by NAC, Melatonin may recommend for CO poisoning (Tab. 3, Ref. 21).

Steroid therapy is considered to improve clinical symptoms in hypertrophic pachymeningitis. We present a 70-year-old man with idiopathic hypertrophic pachymeningitis, whose clinical signs progressively worsened despite steroid therapy. He died of subarachnoid hemorrhage (SAH) with pituitary apoplexy 2 months after the admission regardless of improvement of laboratory data and magnetic resonance imaging appearance by one-and-half-month steroid therapy. Autopsy revealed thickened dura mater supporting the diagnosis of hypertrophic pachymeningitis. Brain parenchyma is generally not affected by the disease; however, histological investigation suggested that inflammation of the dura caused damage to superior hypophyseal artery resulting in SAH and apoplexy in the anterior lobe of the pituitary gland. The higher dose and the longer duration of steroid therapy should have achieved in our case although most laboratory data recovered within the normal range. The aggressiveness of hypertrophic pachymeningitis must be evaluated by clinical signs rather than by laboratory data or imaging examinations.