Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperkineses are a clinical and pathogenetic counter-part of parkinsonism (MP). Their underlying cause is increased activity of the dopaminergic system or insufficiency of the cholinergic system. Treatment inhibiting the dopaminergic system, similarly as anticholinergic treatment is of little effectiveness in MP. A trial of substitutive treatment was undertaken activating the cholinergic system with a precursor of acetylcholine (dimethyl-amino-ethanol-deanol--Bimanol) with simultaneous inhibition of cholinesterase with prostigmin. The results of this treatment were compared with previously applied antidopaminergic treatment (Haloperidol) and with the effects of L-dopa. This treatment was given to 11 patients with Huntington's chorea (ChH), 4 with faciolingual dyskinesis (DFL), 3 with torticollis spasmodicus (TS), 3 with maladie des tics (MT) and 8 with dyskinesia following treatment with L-dopa (MP). Cholinergizing treatment gave better results than antidopaminergic treatment in TS and ChH, and worse in MT. In dyskinesia following L-dopa cholinergizing treatment gave also no effects reported by others. Differences in the results of cholinergizing and antidopaminergic treatment may indicate non-homogenous pathological mechanism of these hyperkineses. Cholinergizing treatment in hyperkineses is based on a similar principle as L-dopa treatment in MP and this approach seems to be proper but more effective preparations should be sought for.
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PMID:[Cholinergizing treatment in hyperkinesis]. 15 May 48

Chemodenervation of cervical muscles with botulinum A toxin, although useful in treating spasmodic torticollis, has been associated with dysphagia. Retrospective analysis of dose and injection site (sternomastoid vs. posterior cervical muscle groups) in 26 patients (49 injections) suggested that dysphagia was related to the quantity of toxin injected into the sternomastoid muscle: dysphagia, median 150 IU (7 injections); and no dysphagia, median 100 IU (42 injections; p = 0.026 Wilcoxon test). In a prospective study (31 injections to 24 patients), limiting the dose administered to the sternomastoid to 100 IU, substantially reduced the incidence of dysphagia (0 of 31, p = 0.27, Fisher's exact test). Denervation of human orbicularis muscle fibers, 5 weeks to 4 months after injection of botulinum A toxin for the treatment of blepharospasm, was successfully demonstrated by intense, diffuse acetylcholinesterase staining. A weight-adjusted dose similar to that given for torticollis was injected into longissimus dorsi muscle in 6 albino rabbits. Using the acetylcholinesterase stain as a marker, a diffusion gradient was noted over a distance of 30 to 45 mm from the point of injection and in contralateral muscle 15 to 25 mm from this point. Thus, denervation was demonstrated to occur within a definable area which crossed anatomic barriers, such as fascia and bone. These clinical and laboratory data suggest that dysphagia following botulinum toxin therapy results from toxin spread to pharyngeal musculature from the sternocleidomastoid injection site. Limiting of the injection dose to 100 IU or less to the sternomastoid substantially decreases the incidence of this complication.
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PMID:Botulinum A toxin for the treatment of spasmodic torticollis: dysphagia and regional toxin spread. 221 Oct 99

There is a growing body of evidence that the central nervous system (CNS), even in the adult animal, is capable of adaptation and reorganization not only as a result of partial damage to the CNS but also in response to stimulation. Environmental stimulation produces changes including expansion of visual cortex, increases in dendritic branching, glia and cholinesterase. Environmental stimulation also produces behavioural changes. Experimental electrical stimulation produces changes in synapse size, synaptic vesicle change, dendritic branching and changes in synaptic transmission. In man, repetitive electrical stimulation via epidural electrodes increases plasma levels of norepinephrine, epinephrine, and dopamine, and CSF levels of norepinephrine. Repetitive electrical stimulation in man dates back to 1967 and has been used for the control of pain, to improve spasticity, bladder control, motor deficit and the autonomic hyperreflexia of spinal cord injury. In addition, improvement has been reported in epilepsy, cerebral palsy, torticollis and peripheral vascular diseases. The best controlled studies are in multiple sclerosis and peripheral vascular disease, and these results will be presented in more detail.
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PMID:Rehabilitation following brain damage: some neurophysiological mechanisms. The effects of repetitive stimulation in recovery from damage to the central nervous system. 718 88