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

The objective of this work was to evaluate the most frequent causes of emergency in patients with Chagas disease. Between January 1998-January 1999, individuals with Chagas disease inside the shock-room of Santojanni Hospital in Buenos Aires city, were included in a prospective study. For the statistical analysis, X test with Yates correction has been used. From a total of 1.680 patients entered, there were 95 (6%) with reactive serology for Chagas disease. In 31 individuals the enter cause was syncope, in 28 cardiac insufficiency, in 18 acute coronary events, in 5 stroke, in 3 acute edema of hypertensive lung and in 2 acute encephalitis associated to AIDS. In conclusion, significant association has been observed between: 1) presence of cardiopathy and hospitalization, 2) cardiac insufficiency, syncope, acute encephalitis and mortality, 3) cardiopathy development and mortality and 4) origin place and mortality.
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PMID:[Emergencies in patients with Chagas' disease in Buenos Aires city, Argentina]. 1261 43

The diagnostic approach to the patient with cancer with suspected CNS infection depends on an analysis of the patient's immune defect, the time course of development of manifestations of infection, and the type of clinical syndrome with supportive evidence for a specific diagnosis coming from laboratory and neuroradiographic data. Most patients with CNS infections can be grouped into those with signs of meningitis or meningoencephalitis and those with focal mass lesions. A smaller group presents with stroke-like onset. Except for the group with strokes, those with focal deficits usually present in a more indolent fashion, whereas those with meningitis and encephalitis present more acutely [63]. Patients with B-lymphocyte dysfunction are susceptible to encapsulated bacterial pathogens. Patients with T-lymphocyte impairment develop CNS infections that are caused by intracellular pathogens, particularly viruses (HSV, JC, CMV, HHV-6), Nocardia, Aspergillus, and Toxoplasma. Many noninfectious entities, such as drug treatment complications, radiation effects, recurrent tumor, and paraneoplastic syndromes, can mimic CNS infections. Although cryptococcosis, bacterial meningitis, and some viral infections are easily diagnosed from Gram's stain, culture, or PCR, patients with mass lesions may require tissue biopsy to confirm diagnosis. Patients with cancer differ from normal hosts in the distribution of pathogens, and there is a wider range of differential diagnostic issues, both infectious and noninfectious, for the relatively few clinical syndromes that present as potential CNS infections.
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PMID:Nervous system infections in patients with cancer. 1269 Jun 50

Periodic lateralized epileptiform discharges are special electroencephalographic abnormalities present in adults with stroke, brain tumor, intracranial hemorrhage, or other rare etiologies. Few reports focused on the etiologies in pediatric patients. We retrospectively reviewed 8002 of our pediatric electroencephalographic records for the past 12 years and listed all associated illness and their outcomes. Forty-four children with periodic lateralized epileptiform discharges were collected. We found that there was an obvious difference in etiologies of our pediatric patients from those reported in the literature. Nearly two thirds of our patients (28 children) were associated with central nervous system infections. The other etiologies included head injury, encephalopathy, epilepsy, and others. Herpes simplex virus was responsible for two thirds (12) of the 18 children with identified pathogens causing a central nervous system infection. Ten patients failed to have a defined pathogen. Periodic lateralized epileptiform discharges have a different clinical significance in pediatric patients than in adults. In Taiwan, central nervous system infection is the most common etiology of periodic lateralized epileptiform discharges in pediatric patients. Herpes simplex virus, although the most common pathogen, should not be considered to be the only cause of encephalitis in children with periodic lateralized epileptiform discharges.
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PMID:Periodic lateralized epileptiform discharges of pediatric patients in Taiwan. 1269 59

The integrity of the vasculature and the maintenance of the blood supply to the brain are crucial for the survival of higher vertebrates. However, peripheral mechanisms of sealing the vasculature that rely on the clotting of blood and platelet aggregation around the site of a 'leak' would lead to decreased cerebral perfusion and compromise the viability of terminally differentiated and irreplaceable neurons. Therefore, in higher organisms it is likely that a sealant/anti-coagulant system that maintains vascular supply has evolved as a necessity to life. We propose that one such system involves the amyloid-beta precursor protein (AbetaPP) and its cleavage product Abeta since (1) both AbetaPP/Abeta are known to deposit in the media of the cerebrovasculature wall following localized injury, (2) Abeta is generated from AbetaPP, a known acute phase reactant, (3) Abeta's physiochemical properties allow it to span between the extracellular matrix and the (endothelial) cell membrane and under inflammatory conditions aggregate to form an intracranial 'scab', thereby maintaining structural integrity of the blood brain barrier, (4) AbetaPP/Abeta together act as an anti-coagulant, (5) Abeta promotes vascular/neuronal remodeling, and (6) Abeta deposits resolve after injury. These properties are consistent with the acute phase generation and rapid cortical deposition of AbetaPP/Abeta following injury (either sustained by trauma or stresses associated with aging) that would be an important compensatory response aimed at limiting the loss of terminally differentiated neurons. Such a system would allow the maintenance of blood supply to the brain by sealing vascular lesions, preventing hemorrhagic stroke while at the same time inhibiting the coagulation cascade from blocking capillaries. Obviously, strategies to remove Abeta would have serious consequences for the integrity of the blood-brain barrier. Indeed, recent in vivo evidence demonstrates that the removal of deposited Abeta from the vasculature leads to increased cerebral microhemorrhage and strongly support the above mentioned functions of AbetaPP/Abeta. These insights also explain the root cause of the encephalitis and meningitis suffered by individuals in immunotherapy trials as being directly associated with the removal of Abeta from the vasculature, i.e. immunological responses to Abeta vaccination do not discriminate between physiologically purposive deposits of Abeta (vascular deposits) and pathological deposits of Abeta (senile plaques).
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PMID:Cerebrovascular requirement for sealant, anti-coagulant and remodeling molecules that allow for the maintenance of vascular integrity and blood supply. 1449 67

Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N=11), patients with encephalic injuries associated with impairment of consciousness (ENC, N=7), patients with neurocysticercosis (N=25), and normal subjects (N=8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P=0.01) and albumin quotient (P=0.005), but not sNSE (P=0.14), levels than the other groups (Kruskal-Wallis test). Patients with lower GOS scores had higher cNSE levels (P=0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.
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PMID:Use of neuron-specific enolase for assessing the severity and outcome in patients with neurological disorders. 1468 39

Herpes zoster (HZ) results from recrudescence of varicella zoster virus latent since primary infection (varicella). The overall incidence of HZ is approximately 3/1000 of the population per year rising to 10/1000 per year by 80 years of age. Approximately 50% of individuals reaching 90 years of age will have had HZ. In approximately 6%, a second attack may occur (usually several decades after the first). Patients with HZ can transmit the virus to a non-immune individual causing varicella. HZ is not contracted from individuals with varicella or HZ. Reduced cell-mediated immunity to HZ occurs with ageing, explaining the increased incidence in the elderly and from other causes such as tumours, HIV and immunosuppressant drugs. Diagnosis is usually clinical from typical unilateral dermatomal pain and rash. Prodromal symptoms, pain, itching and malaise, are common. The most common complication of HZ is postherpetic neuralgia (PHN), defined as significant pain or dysaesthesia present >or= 3 months after HZ. PHN results from damage and secondary changes within components of the nervous system subserving pain. Some motor deficit is common; severe and long-lasting paresis may rarely accompany HZ. More than 5% of elderly patients have PHN at 1 year after acute HZ. Predictors of PHN are, greater age, acute pain and rash severity, prodromal pain, the presence of virus in peripheral blood as well as adverse psychosocial factors. Therapy for acute HZ is intended to reduce acute pain, hasten rash healing and reduce the risk of PHN and other complications. Antiviral drugs are close to achieving these aims but do not entirely remove risk of PHN. Oral steroids show no protective effect against PHN. Adequate analgesia during the acute phase may require strong opioid drugs. Nerve blocks and tricyclic antidepressants (TCAs) may reduce the risk of PHN although firm evidence is lacking. PHN requires thorough evaluation and development of a management strategy for each individual patient. Initial therapy is with TCAs (e.g., nortriptyline) or the anticonvulsant gabapentin. Topical lidocaine patches frequently reduce allodynia. Strong opioids are sometimes required. Topical capsaicin cream is beneficial for a small proportion of patients but is poorly tolerated. NMDA antagonists have not proved beneficial with the exception of ketamine. Transcutaneous Electrical Nerve Stimulation (TENS) may be effective in some cases. HZ is a common condition. Severe complications such as stroke, encephalitis and myelitis are relatively rare whereas sight threatening complications of ophthalmic HZ are more common. PHN is common, distressing and often intractable. Good management improves outcome.
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PMID:Management of herpes zoster (shingles) and postherpetic neuralgia. 1501 24

We investigated brain samples of patients with multiple sclerosis (MS) and controls with immunohistochemistry using monoclonal antibodies (MoAbs) against canine distemper virus (CDV) and measles virus (MV) proteins. All stained negative except for MoAb F3-5, which recognises a conserved epitope on the fusion protein of morbilliviruses. F3-5 immunostaining was found in 8/9 MS plaques and 2/5 herpes simplex virus encephalitis brain samples, but not in six controls or four patients with ischaemic stroke. Using RT-PCR we found no evidence for the presence of MV in MS plaques. The F3-5 epitope may represent a protein that is upregulated during inflammation or point to a yet unrecognised morbillivirus in the human central nervous system that might be implicated in MS pathogenesis.
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PMID:Search for morbillivirus proteins in multiple sclerosis brain tissue. 1510 26

In this study we investigated the structural lesions of patients with periodic lateralized epileptiform discharges (PLEDs) to determine the possible relationship of lesions to PLEDs' localization on EEG and to metabolic abnormality. Clinical findings and electroencephalography (EEG), computerized tomography (CT) and magnetic resonance imaging (MRI) of the 71 adult patients with PLEDs were evaluated. Stroke, herpes encephalitis and intracranial tumor or abscess were the most common etiological factors. Cortical gray matter and adjacent subcortical white matter lesions were detected in 64.7%, cortical gray matter lesions in 11.3% and subcortical white matter lesions in 4.2% of the patients. Although it is thought that PLEDs occur mostly with acute lesions, chronic lesions causing PLEDs were found in 35.2% of the patients. Bilateral lesions were detected in 19.7% and 33.8% of the patients had metabolic abnormality. PLEDs localized the region of the lesion in 63.4% of the patients. PLEDs are usually self-limited features, but chronic PLEDs were detected in 5 patients in this study. Acute structural lesions involving cortical gray matter with adjacent subcortical white matter were found in most of the patients with PLEDs, but the lesion localization and age, acute or chronic, varied.
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PMID:Structural lesions in periodic lateralized epileptiform discharges (PLEDs). 1516 16

The finding that patients with amnesia retain the ability to learn certain procedural skills has provided compelling evidence of multiple memory systems in the human brain, but the scope, defining features and ecological significance of the preserved mnemonic abilities have not yet been explored. Here, we tested the hypothesis that subjects with amnesia would be able to learn and retain a broad range of procedural skills, by examining their acquisition and retention performance on five novel experimental tasks. The tasks are based on real-world activities and encompass a broad range of perceptual-motor demands: (i) the weaving task involves weaving pieces of fabric from woollen strings, using a manual weaver's loom; (ii) the geometric figures task consists of tracing geometric figures with a stylus as they move horizontally across a touch screen monitor; (iii) the control stick task involves tracking a sequence of visual target locations using a joystick control; (iv) the pouring task consists of pouring 200 ml of water from a watering can into a series of graduated cylinders, from a point 20 cm above the cylinders; and (v) the spatial sequence task involves learning an ordered sequence of pushing five spatially distributed buttons without visual guidance. Ten chronic and stable amnesic subjects (nine with bilateral medial temporal lobe damage due to herpes simplex encephalitis or anoxia, and one with thalamic stroke) and 25 matching normal comparison subjects were tested on three occasions: initial learning at time 1; retention at time 2 (24 h later); and retention at time 3 (2 months later). Despite impaired declarative memory for the tasks, the amnesic subjects demonstrated acquisition and retention of the five skills; their learning slopes over repeated trials were comparable with those of comparison subjects. These findings indicate that preserved learning of complex perceptual-motor skills in patients with amnesia is a robust phenomenon, and that it can be demonstrated across a variety of conditions and perceptual-motor demands. The comparability of the tasks employed in this study with real-world activities highlights the potential application of this memory dissociation in the rehabilitation of patients with amnesia.
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PMID:The scope of preserved procedural memory in amnesia. 1521 16

Mental fatigue, with decreased concentration capacity, is common in neuroinflammatory and neurodegenerative diseases, often appearing prior to other major mental or physical neurological symptoms. Mental fatigue also makes rehabilitation more difficult after a stroke, brain trauma, meningitis or encephalitis. As increased levels of proinflammatory cytokines are reported in these disorders, we wanted to explore whether or not proinflammatory cytokines could induce mental fatigue, and if so, by what mechanisms.It is well known that proinflammatory cytokines are increased in major depression, "sickness behavior" and sleep deprivation, which are all disorders associated with mental fatigue. Furthermore, an influence by specific proinflammatory cytokines, such as interleukin (IL)-1, on learning and memory capacities has been observed in several experimental systems. As glutamate signaling is crucial for information intake and processing within the brain, and due to the pivotal role for glutamate in brain metabolism, dynamic alterations in glutamate transmission could be of pathophysiological importance in mental fatigue. Based on this literature and observations from our own laboratory and others on the role of astroglial cells in the fine-tuning of glutamate neurotransmission we present the hypothesis that the proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta and IL-6 could be involved in the pathophysiology of mental fatigue through their ability to attenuate the astroglial clearance of extracellular glutamate, their disintegration of the blood brain barrier, and effects on astroglial metabolism and metabolic supply for the neurons, thereby attenuating glutamate transmission. To test whether our hypothesis is valid or not, brain imaging techniques should be applied with the ability to register, over time and with increasing cognitive loading, the extracellular concentrations of glutamate and potassium (K+) in humans suffering from mental fatigue. At present, this is not possible for technical reasons. Therefore, more knowledge of neuronal-glial signaling in in vitro systems and animal experiments is important.In summary, we provide a hypothetic explanation for a general neurobiological mechanism, at the cellular level, behind one of our most common symptoms during neuroinflammation and other long-term disorders of brain function. Understanding pathophysiological mechanisms of mental fatigue could result in better treatment.
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PMID:On the potential role of glutamate transport in mental fatigue. 1552 5


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