Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The history of vascular dementia can be traced back to cases of dementia postapoplexy described by Thomas Willis in 1672. During most of the 18th and early 19th century, "brain congestion" (due in all likelihood to the effects of untreated hypertension) was the most frequent diagnosis for conditions ranging from stroke to anxiety and to cognitive decline, and bloodletting became the commonplace therapy. The modern history of vascular dementia began in 1894 with the contributions of Otto Binswanger and Alois Alzheimer, who separated vascular dementia from dementia paralytica caused by neurosyphilis. In the 1960s, the seminal neuropathological and clinical studies of the New Castle school in England inaugurated the modern era of vascular dementia.
 ...
PMID:Vascular dementia: a historical background. 1619 Dec 11

Secondary parkinsonism has comprised about 20 to 40 percent of all parkinsonism patients in movement disorders clinic. Most of them are induced by certain medications. About 5 to 10 percent of these patients are caused by sudden vascular events, who suffer from their parkinsonism abruptly, and usually of aged people with quite apparent stroke risk factors. Hemosiderosis was only occasionally reported as a causative factor in patients with parkinsonism, who presented with an insidious onset parkinsonism and a progressive supranuclear palsy-like clinical picture. We encountered two patients with stroke-related parkinsonism, whose high resolution MRI image showed apparent cortical or intraparenchymal hemosiderosis, although Binswanger type white matter change was also noted. Intracerebral hemosiderosis that manifests clinically as vascular parkinsonism might be much more frequent than we thought.
 ...
PMID:Cerebral hemosiderosis as a causative factor of vascular parkinsonism. 1642 48

Two hundred and twenty-one Saudi patients admitted for stroke in King Khalid University Hospital between 1982 and 1987 were evaluated clinically and by laboratory and radiological investigations. Twelve patients were found to have leukoraiosis on brain CT and a clinical picture compatible with Binswanger disease (subcortical arteriosclerotic encephalopathy). Arterial hypertension was present in all cases, seizure disorders in 25%, and dementia in 83%. The features of these cases are compared with similar cases reported from other places. The importance of control of hypertension in prevention of Binswanger disease is emphasized.
 ...
PMID:Binswanger disease: The King Khalid University Hospital experience. 1759 Jul 23

Increasing evidence suggests the presence of apoptotic cell death in many neurodegenerative diseases. However, in Binswanger's disease (BD), no information is available concerning the apoptosis-related pathologic changes that may occur in the white matter. To investigate whether apoptotic cell death is included in the pathophysiology of the white matter changes in BD, autopsied brains from patients with BD (n = 5) were compared with those of non-neurologic controls (n = 5). Terminal deoxynucleotidyl transferase-mediated dUTP in situ nick end labeling (TUNEL) was used as a marker for cell damage with DNA fragmentation. A proteolipid protein (PLP) messenger RNA (mRNA) hybridization signal was also used as a sensitive and specific marker of oligodendrocytes as well as glial fibrillary acidic protein (GFAP) immunoreactivity as a marker of astrocytes. There were frequent TUNEL-positive cells in the rarefied white matter of patients with BD. TUNEL-positive cells were found 15-fold more numerously in BD than in controls (P < .01). TUNEL-positive cells were presumably oligodendrocytes because of their coexpression with PLP mRNA. The numbers of GFAP-positive astrocytes were significantly decreased in BD compared with those in control subjects. The reduction in numbers of PLP mRNA-positive oligodendrocytes were also seen in BD, but these changes did not reach the level of significance. The pathologic alterations in BD brains include increased TUNEL-positive oligodendrocytes, associated with degradation of myelin. Although TUNEL-positive glial cells did not show typical apoptotic morphologic features, these findings suggest that increase in in situ nick end labeling of oligodendrocytes in white matter may play an important role in the pathophysiology of BD.
J Stroke Cerebrovasc Dis
PMID:Increasing in situ nick end labeling of oligodendrocytes in white matter of patients with Binswanger's disease. 1790 1

Vascular cognitive impairment is a term used to describe a heterogeneous group of diseases, including large vessel disease with strategic single and multiple strokes and small vessel disease with progressive damage to the deep white matter. Identification of patients with the progressive form of vascular cognitive impairment, referred to by some investigators as Binswanger disease, is important for treatment trials. Pathologically, Binswanger disease is associated with small vessel disease, extensive regions of demyelination, inflammatory cells around damaged blood vessels, and lacunar infarcts. Clinically, patients with Binswanger disease have impairments of gait and balance, focal neurological findings, and executive dysfunction on neuropsychological tests. White matter changes on MRI are thought to be due to hypoxic episodes related to hypoperfusion of the vulnerable deep white matter secondary to hypertension, diabetes, and other vessel diseases. Disruption of the blood-brain barrier suggests an inflammatory response. Matrix metalloproteinases are present in the brain of patients with vascular cognitive impairment and can be measured in the cerebrospinal fluid of some patients. Preliminary studies with quantification of the blood-brain barrier, using the multiple time graphical method (Patlak plots), supports disruption of the blood-brain barrier. Because no single clinical feature or diagnostic test is sufficient to identify patients with the small vessel form of vascular cognitive impairment, we propose that a multimodal approach will be needed to select patients for treatment trials.
Stroke 2009 Mar
PMID:Inflammation and white matter damage in vascular cognitive impairment. 1906 97

Susceptibility weighted imaging (SWI) is a magnetic resonance (MR) technique that is exquisitely sensitive to paramagnetic substances, such as deoxygenated blood, blood products, iron, and calcium. This sequence allows detection of haemorrhage as early as 6h and can reliably detect acute intracerebral parenchymal, as well as subarachnoid haemorrhage. It detects early haemorrhagic transformation within an infarct and provides insight into the cerebral haemodynamics following stroke. It helps in the diagnosis of cerebral venous thrombosis. It also has applications in the work-up of stroke patients. The sequence helps in detecting microbleeds in various conditions, such as vasculitis, cerebral autosomal dominant arteriopathy, subacute infarcts and leucoencephalopathy (CADASIL), amyloid angiopathy, and Binswanger's disease. The sequence also aids in the diagnosis of vascular malformations and perinatal cerebrovascular injuries. This review briefly illustrates the utility of this MR technique in various aspects of stroke diagnosis and management.
 ...
PMID:Susceptibility weighted imaging: a new tool in magnetic resonance imaging of stroke. 1907 Jul 1

Small vessel disease (SVD) is responsible for brain chronic circular disorder, and accounts for 20%-30% cases of ischemic stroke as well as cerebral hemorrhage, and to a great extent, encephalopathy. Binswanger's disease and multiple small strokes, which are common in older people, are also closely associated with SVD. These disorders often cause decline in cognition, vascular dementia, impairment in gait and balance, mood depression, and urinary incontinence, and often brings great social and economic burdens. SVD-related encephalopathy increases the incidences of fall, disability and death in elderly people. With the aging of the society, more attention should be paid to the importance of early diagnosis and prophylactic treatment of SVD. Here the clinical manifestations and pathophysiology of SVD are reviewed.
 ...
PMID:The clinical manifestations and pathophysiology of cerebral small vessel disease. 2050 5

An accumulating amount of evidence suggests that the white matter hyperintensities on T2 weighted brain magnetic resonance imaging predict an increased risk of dementia and gait disturbance. This state has been proposed as cerebral small vessel disease, including leukoaraiosis, Binswanger's disease, lacunar stroke and cerebral microbleeds. However, the concept of cerebral small vessel disease is still obscure. To understand the cerebral small vessel disease, the precise structure and function of cerebral small vessels must be clarified. Cerebral small vessels include several different arteries which have different anatomical structures and functions. Important functions of the cerebral small vessels are blood-brain barrier and perivasucular drainage of interstitial fluid from the brain parenchyma. Cerebral capillaries and glial endfeet, take an important role for these functions. However, the previous pathological investigations on cerebral small vessels have focused on larger arteries than capillaries. Therefore little is known about the pathology of capillaries in small vessel disease. The recent discoveries of genes which cause the cerebral small vessel disease indicate that the cerebral small vessel diseases are caused by a distinct molecular mechanism. One of the pathological findings in hereditary cerebral small vessel disease is the loss of smooth muscle cells, which is an also well-recognized finding in sporadic cerebral small vessel disease. Since pericytes have similar character with the smooth muscle cells, the pericytes should be investigated in these disorders. In addition, the loss of smooth muscle cells may result in dysfunction of drainage of interstitial fluid from capillaries. The precise correlation between the loss of smooth muscle cells and white matter disease is still unknown. However, the function that is specific to cerebral small vessel may be associated with the pathogenesis of cerebral small vessel disease.
 ...
PMID:[What is cerebral small vessel disease?]. 2173 31

Cerebral small vessel disease (CSVD) is a group of pathological processes with multifarious etiology and pathogenesis that are involved into the small arteries, arterioles, venules, and capillaries of the brain. CSVD mainly contains lacunar infarct or lacunar stroke, leukoaraiosis, Binswanger's disease, and cerebral microbleeds. CSVD is an important cerebral microvascular pathogenesis as it is the cause of 20% of strokes worldwide and the most common cause of cognitive impairment and dementia, including vascular dementia and Alzheimer's disease (AD). It has been well identified that CSVD contributes to the occurrence of AD. It seems that the treatment and prevention for cerebrovascular diseases with statins have such a role in the same function for AD. So far, there is no strong evidence-based medicine to support the idea, although increasing basic studies supported the fact that the treatment and prevention for cerebrovascular diseases will benefit AD. Furthermore, there is still lack of evidence in clinical application involved in specific drugs to benefit both AD and CSVD.
...
PMID:Cerebral small vessel disease and Alzheimer's disease. 2660 17

In the normal central nervous system, endothelin-1 (ET-1) is found in some types of neurons, epithelial cells of the choroid plexus, and endothelial cells of microvessels, but it is usually not detectable in glial cells. However, in different pathological conditions, astrocytes adapting a reactive phenotype express high levels of ET-1 and its receptors, mainly the ETB receptor. ET-1 released by reactive astrocytes appears mainly to have neurodeleterious effects by mechanisms that include constriction of cerebral arterioles leading to impairment of the cerebral microcirculation, increase of blood brain barrier permeability, inflammation, excitotoxicity, impairment of fast axonal transport, and astrogliosis. A few studies in rodents found that ET-1 increased the astrocytic expression of brain-derived neurotrophic factor, glial cell-line derived neurotrophic factor and neurotropin-3, and the production of endocannabinoids. However, whether this occurs in physiological or pathological conditions is unclear. This review summarizes current knowledge about the role of the astrocytic ET-1 system in acute and chronic neurological conditions, including multiple sclerosis, ischemic stroke and hypoxic/ischemic brain injury, traumatic brain injury, subarachnoid hemorrhage, Alzheimer's disease, Binswanger's disease and post-stroke dementia, amyotrophic lateral sclerosis, and CNS infections. Counteracting the harmful effects of astrocytic ET-1 may represent a promising therapeutic target for mitigating secondary brain damage in a variety of neurological diseases. We also briefly address the role of astrocytic ET-1 in astrocytic tumors and pain.
 ...
PMID:The pathophysiological role of astrocytic endothelin-1. 2713 21


<< Previous 1 2 3 4 5 6 7 Next >>