Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Plasma aromatic amino acid (AAA) and branched-chain amino acid (BCAA) concentrations were determined in 197 alcoholics. The BCAA/AAA molar ratio in patients with alcohol withdrawal symptoms was compared with the ratio in patients without such symptoms. The BCAA/AAA molar ratio in patients with emotional disturbance or with transient hallucination was significantly lower than that in patients without these symptoms. The BCAA/AAA molar ratio tended to be lower in patients with alcohol withdrawal convulsion or with delirium tremens as compared to patients without such symptoms. The BCAA/AAA molar ratio had a negative correlation with plasma total bilirubin and LDH and had a positive correlation with plasma choline esterase and albumin. Oral administration of amino acid preparations (Aminoleban EN) to the patients elevated the BCAA/AAA molar ratio and normalized liver function. These results indicate that abnormalities of amino acid metabolism caused by liver damage in alcohol dependence may have an important role in the pathogenesis of alcohol withdrawal syndrome.
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PMID:[Plasma amino acid levels in alcoholics]. 834 3

Recent neuropathologic autopsy studies found that 15 to 25% of elderly demented patients have Lewy bodies (LB) in their brainstem and cortex, and in hospital series this may constitute the most common pathologic subgroup after pure Alzheimer's disease (AD). The Consortium on Dementia with Lewy bodies met to establish consensus guidelines for the clinical diagnosis of dementia with Lewy bodies (DLB) and to establish a common framework for the assessment and characterization of pathologic lesions at autopsy. The importance of accurate antemortem diagnosis of DLB includes a characteristic and often rapidly progressive clinical syndrome, a need for particular caution with neuroleptic medication, and the possibility that DLB patients may be particularly responsive to cholinesterase inhibitors. We identified progressive disabling mental impairment progressing to dementia as the central feature of DLB. Attentional impairments and disproportionate problem solving and visuospatial difficulties are often early and prominent. Fluctuation in cognitive function, persistent well-formed visual hallucinations, and spontaneous motor features of parkinsonism are core features with diagnostic significance in discriminating DLB from AD and other dementias. Appropriate clinical methods for eliciting these key symptoms are described. Brainstem or cortical LB are the only features considered essential for a pathologic diagnosis of DLB, although Lewy-related neurites, Alzheimer pathology, and spongiform change may also be seen. We identified optimal staining methods for each of these and devised a protocol for the evaluation of cortical LB frequency based on a brain sampling procedure consistent with CERAD. This allows cases to be classified into brainstem predominant, limbic (transitional), and neocortical subtypes, using a simple scoring system based on the relative distribution of semiquantitative LB counts. Alzheimer pathology is also frequently present in DLB, usually as diffuse or neuritic plaques, neocortical neurofibrillary tangles being much less common. The precise nosological relationship between DLB and AD remains uncertain, as does that between DLB and patients with Parkinson's disease who subsequently develop neuropsychiatric features. Finally, we recommend procedures for the selective sampling and storage of frozen tissue for a variety of neurochemical assays, which together with developments in molecular genetics, should assist future refinements of diagnosis and classification.
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PMID:Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. 890 16

Plasma aromatic amino acid (AAA) and branched-chain amino acid (BCAA) concentrations were determined in 292 alcoholics. The BCAA/AAA molar ratio in patients with alcohol withdrawal symptoms was compared with the ratio in patients without such symptoms. The BCAA/AAA molar ratio in patients with transient hallucinations or with delirium tremens was significantly lower than that in patients without these symptoms. The BCAA/AAA molar ratio tended to be lower in patients with alcohol withdrawal seizures than in patients without such symptoms. The BCAA/AAA molar ratio had a negative correlation with plasma total bilirubin and LDH, and a positive correlation with plasma cholinesterase and albumin. These results indicate that abnormalities of amino acid metabolism caused by liver damage in alcohol dependence may have an important role in the pathogenesis of the alcohol withdrawal syndrome.
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PMID:Aromatic and branched-chain amino acid levels in alcoholics. 906 12

Neuropsychiatric abnormalities, as well as the commonly associated neuropsychological symptoms, are clinical characteristics of Alzheimer's disease (AD), the most common form of dementia. Thus, in addition to a general cognitive and functional decline, neuropsychiatric manifestations, such as agitation, apathy, anxiety, psychoses and disinhibition, are frequently evident in AD patients. Such neuropsychiatric symptoms of AD are the source of considerable patient and caregiver distress, resulting in the prescription of neuroleptics, benzodiazepines or other psychotropic agents, and are a major factor in the decision to transfer the care of patients into nursing homes. Recent evidence suggests that some neuropsychiatric changes associated with AD are related to the cholinergic deficits in the brains of AD patients and that such abnormalities may be responsive to cholinergic therapy. Cholinergic drug therapies indicated for the symptomatic treatment of AD, for example tacrine and the newer cholinesterase (ChE) inhibitors such as donepezil, have been demonstrated to improve memory, language and praxis. Furthermore, although less is known about the effect of ChE inhibitors on the neuropsychiatric symptoms of AD, preliminary evidence suggests that they reduce apathy, anxiety, hallucinations, disinhibition and aberrant motor behaviour. Thus, the newer-generation ChE inhibitors that are well tolerated, easy to administer and show promise in reducing the cognitive, as well as neuropsychiatric disturbances of AD, may emerge as important treatments for some neuropsychiatric symptoms in patients with central cholinergic deficits, including AD.
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PMID:Neuropsychiatric symptoms and cholinergic therapy for Alzheimer's disease. 987 14

Delirium is a common complication of dementia and may produce considerable morbidity. In addition to psychotic symptoms such as hallucinations and delusions, delirium may produce considerable agitation, which may be refractory to conventional medications such as antipsychotics and benzodiazepines. The main approach to delirium is to treat any underlying medical problem that could cause the delirium. However, delirium is not always reversible, and there is no specific treatment for persistent delirium. The authors present a case of delirium complicating a preexisting dementia that resolved rapidly following initiation of the cholinesterase inhibitor donepezil, suggesting that cholinergic dysfunction may have played a role in the etiology of this patient's delirium. Future research needs to be directed at the issue of cholinergic activity in delirium through monitoring of serum anticholinergic activity and its response to procholinergic therapy.
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PMID:Donepezil improves symptoms of delirium in dementia: implications for future research. 989 35

Alzheimer's disease accounts for 50-60% of dementia cases in older people. Dementia with Lewy bodies is now recognized as the second most common type of dementia. It is different from Alzheimer's disease and has important pharmacotherapeutic implications. Key features include early-onset, persistent, well-formed, visual hallucinations and motor features of parkinsonism. Pharmacologic management of neurobehavioral symptoms is complicated by an exaggerated response to neuroleptics, which causes excessive morbidity and mortality. Patients with dementia with Lewy bodies may be particularly responsive to cholinesterase inhibitors. When neurobehavioral symptoms are severe enough to require pharmacologic intervention, it is recommended that agents such as trazodone or cholinesterase inhibitors be considered first-line therapy. If these fail, neuroleptics may be prescribed with caution.
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PMID:Dementia with Lewy bodies: review and pharmacotherapeutic implications. 1041 27

Dementia with Lewy bodies (DLB) is the second most frequent cause of primary degenerative dementias, following Alzheimer's disease (AD). The nosologic situation of this disease has fragile limits. There is controversy as to whether Parkinson's disease (PD) and DLB are two different entities or whether they make up part of the same spectrum. The terms diffuse Lewy bodies disease and the variant of Lewy bodies in senile dementia or AD have been used to describe pathologic changes with clinical manifestations of dementia and parkinsonism. At present, DLB should be understood as an entity with the essential feature being the presence of Lewy bodies in the brain stem and cerebral cortex. From the point of view of clinical examination, DLB is characterized by the presence of subcortical or progressive cortical dementia, at times without severe memory disorders, with great fluctuations and well detailed recurrent visual hallucinations. These cognitive alterations are associated with parkinsonism. Other frequent disorders are falls, syncopes, transitory alterations in consciousness, great sensitivity to neuroleptic drugs and visual illusions with pseudoperception. The correct diagnosis of this entity is important to administer adequate treatment, to avoid classical neuroleptic drugs and to establish precise prognosis. From a therapeutic point of view, cholinesterase inhibitors show some efficacy in the treatment of cognitive alterations.
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PMID:[Dementia with Lewy bodies]. 1073 62

The objective of this study was to assess the tolerability and efficacy of rivastigmine in a group of patients with probable dementia with Lewy bodies (DLB), using an open label study. Open label treatment was with rivastigmine up to maximum tolerated dose (mean 9.6 mg daily, range 3-12 mg). Eleven patients with DLB, mean age 78.5 years, were treated with this cholinesterase inhibitor. After 12 weeks of treatment, mean Neuropsychiatric Inventory scores fell by 73% for delusions, 63% for apathy, 45% for agitation and 27% for hallucinations. Five of the patients (45%) experienced very significant clinical improvements that had not been achieved with other treatments, including low dose neuroleptics. Medication was well tolerated and parkinsonian symptoms tended to improve. Cholinesterase inhibition may be a safe and effective alternative to neuroleptic treatment in DLB. Such effects may also prove to be applicable to the management of neuropsychiatric symptoms in Parkinson's disease and Alzheimer's disease.
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PMID:Rivastigmine in the treatment of dementia with Lewy bodies: preliminary findings from an open trial. 1082 36

In Alzheimer disease, therapies to improve the core symptoms and perhaps even slow disease progression include cholinesterase inhibitors, receptor agonists, antiinflammatory drugs, and antioxidants. Neuroleptics, antiepileptics, and nondrug approaches are used to control and relieve complications such as delusions, hallucinations, paranoia, and agitated behavior. We outline a practical approach to the use of these therapies.
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PMID:Effective treatment of Alzheimer disease and its complications. 1086 Feb 27


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