Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subdural hygromas, which differ from acute and chronic subdural haematomas in clinical features and pathogenetic mechanism, can occur as isolated lesions or in association with ventricular dilatation and/or subarachnoid cysts which are mistaken for atrophy. On the basis of the postulate that these fluid accumulations might be related to a disturbance in CSF circulation, we treated them by ventriculoperitoneal CSF drainage. This was regarded as indicated only for children with symptoms of retardation and a distended ventricular system. Disappearance of the hygroma or the cortical cysts and ventricular dilatation was demonstrated in 9 of 14 children treated by ventriculo-abdominal shunt and in 4 of 7 less seriously affected untreated children. Clinical improvement came later than neuroradiological improvement, and was incomplete in a number of children. Although there are anamnestic factors with an unfavourable effect on development, the hygromas per se can cause cerebral dysfunction which is associated with their bifrontal localization. The principal symptoms are those of retardation in the development of verbal expression, leg motor function and manipulation.
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PMID:Subdural hygroma: results of treatment by ventriculo-abdominal shunt. 722 82

Several studies have demonstrated lowered cerebral blood flow (CBF) in patients with hydrocephalus and symptoms of raised intracranial pressure. Ventricular shunting in such cases permits a sudden increase in CBF. The pathophysiology of functional brain deficit secondary to hydrocephalus is little understood. Improvement of the patient's clinical status after drainage of CSF suggests that cerebral dysfunction is not necessarily due to permanent brain damage. In fact, it improves rapidly after ventricular taps. In view of this it would be helpful to monitor cerebral perfusion. The transcranial Doppler (TCD) ultrasonography technique allows real-time monitoring of the intracranial circulation and makes it possible to evaluate the physiopathological correlation between ventricular dilatation and CBF. Continuous monitoring of the middle cerebral artery (MCA) by TCD was performed in three hydrocephalic children (2 months, 14 months, and 8 years old) during a ventricular-peritoneal shunt operative procedure. A TC-2000S device provided by an IMP-F fixed probe was utilized. In all patients, when the lateral ventricle was shunted and the CSF could flow away, a clear and sudden increase of flow velocity above 30% was detected. The pulsatility index (PI) was also pathologically increased in all patients. A gradual normalization of this index was revealed after the shunting procedure. Our experience has to be considered preliminary, but nonetheless, it suggests a clear correlation between hydrocephalic disease and concomitant CBF alterations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intraoperative monitoring of cerebral blood flow during ventricular shunting in hydrocephalic pediatric patients. 758 87

PKN (protein kinase N; also called protein kinase C-related kinase (PRK-1)), is a serine/threonine protein kinase that is ubiquitously expressed in several organs, including the brain. PKN has a molecular mass of 120 kDa and has two domains, a regulatory and a catalytic domain, in its amino-terminals and carboxyl-terminus, respectively. Although the role of PKN has not been fully elucidated, previous studies have revealed that PKN is cleaved to a constitutively active catalytic fragment of 55 kDa in response to apoptotic signals. Hydrocephalus is a pathological condition caused by insufficient cerebrospinal fluid (CSF) circulation and subsequent excess of CSF in the brain. In this study, in order to elucidate the role of PKN in the pathophysiology of hydrocephalus, we examined PKN fragmentation in hydrocephalic model rats. Hydrocephalus was induced in rats by injecting kaolin into the cisterna magna. Kaolin-induced rats (n=60) were divided into three groups according to the observation period after treatment (group 1: 3-6 weeks, group 2: 7-12 weeks, and group 3: 13-18 weeks). Sham-treated control rats, injected with sterile saline (n=20), were similarly divided into three groups. Spatial learning ability was estimated by a modified water maze test. Thereafter, brains were cut into slices and ventricular dilatation was estimated. Fragmentation of PKN was observed by Western blotting in samples collected from the parietal cortex, striatum, septal nucleus, hippocampus, and periaqueductal gray matter. All kaolin-induced rats showed ventricular dilatation. Most of them showed less spatial learning ability than those of sham-treated controls. In most regions, fragmentation of PKN had occurred in a biphasic manner more frequently than that in controls. The appearance of PKN fragmentation in periaqueductal gray matter was correlated with the extent of ventricular dilation and spatial learning disability. These results revealed that PKN fragmentation was observed in rats with kaolin-induced hydrocephalus, models for chronically-damaged brain dysfunction, suggesting that persistent brain insult, such as apoptosis, had occurred in these models. PKN fragmentation could be a hallmark for evaluating morphological and functional damage of the hydrocephalus.
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PMID:Fragmentation of protein kinase N (PKN) in the hydrocephalic rat brain. 1789 75

Binswanger's disease (BD) is a condition characterized by prominent brain atrophy with ventricular dilatation, diffuse white matter (WM) lesions and a scattering of lacunar infarcts. BD patients have dementia, and have vascular risk factors, focal cerebrovascular deficits and evidence of subcortical cerebral dysfunction. From our clinical studies, the most effective prophylaxis against the development of BD is to manage the hypertension, especially a high nocturnal blood pressure, in the early stage patients showing only a scattering of lacunes and/or mild WM lesions. The pathogenesis of BD is likely to be chronic cerebral ischemia due to hypertensive small artery disease with capillary collagenosis, which causes the multiple lacunes and the alterations in the glia and axons. In addition, arterial hypertension and a subsequent dysfunction of the blood-brain barrier (BBB) may cause the WM lesions. A compromised BBB will permit the entry of serum components, immunoglobulins, complements and fibrinogen into the perivascular neural parenchyma. These substances may subsequently activate both astro- and microglia and thus damage the myelin structures. Experimentally, immunosuppressants, cyclosporin A and FK 506 suppressed both the glial activation and WM changes after chronic cerebral hypoperfusion. The pro-thrombotic state of the microcirculation in BD patients may also contribute to local inflammation and the BBB dysfunction, because thrombin and prostanoids are involved in various tissue reactions including brain edema and glial activation. Therefore, novel therapeutic approaches using the administration of anti-thrombin and cyclo-oxygenase-2 inhibitors as well as immunosuppressants may be useful for preventing the progression of BD.
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PMID:Cytopathological alterations and therapeutic approaches in Binswanger's disease. 1951 55