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)

This paper reviews the main neurological complications of psychiatric drugs, in particular antipsychotics and antidepressants. Extrapyramidal syndromes include acute dystonia, parkinsonism, akathisia, tardive dyskinesia and tardive dystonia. Extrapyramidal symptoms (EPS) are less frequent with atypical than with conventional antipsychotics but remain common in clinical practice partly due to lack of screening by health professionals. Neuroleptic malignant syndrome (NMS) consists of severe muscle rigidity, pyrexia, change in conscious level and autonomic disturbance but partial forms also occur. NMS is particularly associated with the initiation and rapid increase in dose of high-potency antipsychotics but it has been reported with all the atypical antipsychotics and rarely with other drugs including antidepressants. Serotonin toxicity comprises altered mental state (agitation, excitement, confusion), neuromuscular hyperactivity (tremor, clonus, myoclonus, hyper-reflexia) and autonomic hyperactivity and occurs on a spectrum. Severe cases, termed serotonin syndrome, usually follow the co-prescription of drugs that increase serotonergic transmission by different pathways, for example a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI). Most antipsychotics and antidepressants lower the seizure threshold and can cause seizures; the risk is greater with clozapine than with other atypical antipsychotics and greater with tricyclic antidepressants (TCAs) than with SSRIs. In randomised controlled trials in elderly patients with dementia atypical antipsychotics are associated with a higher risk of stroke and death than placebo. Cohort studies suggest that conventional drugs carry at least the same risk. Cessation of treatment with antipsychotics and antidepressants can lead to a wide range of discontinuation symptoms which include movement disorders and other neurological symptoms. Clinicians need to be familiar with strategies to reduce the risk of these adverse events and to manage them when they arise. Their occurrence needs to be balanced against the benefits of psychiatric drugs in terms of efficacy and improved quality of life in a range of disorders.
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PMID:Neurological complications of psychiatric drugs: clinical features and management. 1809 17

A previous study in subjects with focal dystonia suggested that the greater and longer-lasting effect induced by botulinum toxin type A (BoNT-A) on the tonic vibration reflex (TVR) than on the maximal M-wave (M-max) might be the physiological marker of the toxin's action at the level of intrafusal muscle fibres. With this approach, we investigated the possible effect of BoNT-A on fusimotor synapses in eight patients with post-stroke spasticity (four with no residual motor capacity before treatment and four with partially spared muscle strength and residual motor capacity). TVR and M-max were recorded from the wrist and finger flexor muscles before treatment and at 1, 4 and 7 months afterwards. The TVR reduction was greater than the M-max reduction and remained fairly constant over time only in the subjects with a residual motor capacity before the treatment. This pilot study suggests that some degree of strength and active movement is necessary for the action of BoNT-A on intrafusal fibres.
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PMID:Intrafusal effects of botulinum toxin in post-stroke upper limb spasticity. 1826 70

Acute or sub-acute movement disorders represent a small percentage of neurological emergencies but it is necessary to be aware of their existence because a failure in their diagnosis or treatment can result in significant morbidity and mortality. Clinical presentation of acute movement disorders can be diverse. In some cases acinesia or rigidity predominates, while others are characterized by dystonia, chorea o balism. The type of movement disorder suggest a specific aetiology. Drugs represent the most frequent etiologic factor and are the cause of neuroleptic malignant syndrome and serotoninergic syndrome. Emergencies secondary to Parkinson's disease are reviewed, including parkinsonism-hyperpirexia syndrome, acute psychosis and the emergencies derived from deep brain stimulators. Different aetiologies of acute dystonia and chorea are also covered and, finally, acute movement disorders due to stroke are reviewed.
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PMID:[Movement disorders in the emergency department]. 1852 49

Botulinum toxin type A (BTX-A) has been used to treat several neurological conditions such as sialorrhea, hyperhydrosis, dystonia, hemifacial spasm, spasticity and pain. Although spasticity has been successfully treated with BTX-A, few are the authors studying the use of BTX-A to treat shoulder pain secondary to stroke. In order to study if BTX-A is effective to treat post-stroke shoulder pain, we followed up during 4 months 16 patients with sustained shoulder pain. Patients received BTX-A according to previous discussion with the rehabilitation group to determine the muscles and dose to be injected and were evaluated by the join range of motion and analogic pain scale. There was decrease of pain during shoulder motion, mainly during the movements of extension and rotation. We conclude that BTX-A is a safe and efficacious therapy.
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PMID:Botulinum toxin type A for refractory post-stroke shoulder pain. 1854 85

Extradural motor cortex stimulation has been employed in cases of Parkinson's disease (PD), fixed dystonia (FD) and spastic hemiparesis (SH) following cerebral stroke. Symptoms of PD are improved by EMCS: results were evaluated on the basis of the UPDRS and statistically analysed. In PD EMCS is less efficacious than bilateral subthalamic nucleus (STN) stimulation, but it may be safely employed in patients not eligible for deep brain stimulation (DBS). The most rewarding effect is the improvement, in severely affected patients, of posture and gait. FD, unresponsive to bilateral pallidal stimulation, has been relieved by EDMS. In SH reduction of spasticiy by EMCS allows improvement of the motor function.
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PMID:Results by motor cortex stimulation in treatment of focal dystonia, Parkinson's disease and post-ictal spasticity. The experience of the Italian Study Group of the Italian Neurosurgical Society. 1864 28

There have been few reports on the surgical treatment of secondary hemidystonias, most of which are due to basal ganglia stroke or trauma. We present 2 patients with hemidystonia secondary to thalamic hemorrhage whom we successfully treated with unilateral globus pallidus internus (GPi) stimulation. Case 1 is a 56-year-old man with abnormal posturing and intolerable muscle contraction pain in the left arm. Case 2 is a 73-year-old woman who developed severe abnormal posturing in the right arm and gait disturbance due to hyperextension of the right leg. The dystonic symptoms of both patients were refractory to medication. Three months after the inception of high frequency GPi stimulation, the motor scores on the Burke-Fahn-Marsden Dystonia Rating Scale were improved by 49.2% and 34.3% in Cases 1 and 2, respectively. We suggest GPi stimulation as a possible alternative to treat secondary hemidystonia.
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PMID:Hemidystonia secondary to thalamic hemorrhage treated with GPi stimulation. 1866 63

Hypertonia, which is characterized by stiff gait, abnormal posture, jerky movements, and tremor, is associated with a number of neurological disorders, including cerebral palsy, dystonia, Parkinson's disease, stroke, and spinal cord injury. Recently, a spontaneous mutation in the gene encoding trafficking protein, kinesin-binding 1 (Trak1), was identified as the genetic defect that causes hypertonia in mice. The subcellular localization and biological function of Trak1 remain unclear. Here we report that Trak1 interacts with hepatocyte-growth-factor-regulated tyrosine kinase substrate (Hrs), an essential component of the endosomal sorting and trafficking machinery. Double-label immunofluorescence confocal studies show that the endogenous Trak1 protein partially colocalizes with Hrs on early endosomes. Like Hrs, both overexpression and small-interfering-RNA-mediated knockdown of Trak1 inhibit degradation of internalized epidermal growth factor receptors through a block in endosome-to-lysosome trafficking. Our findings support a role for Trak1 in the regulation of Hrs-mediated endosomal sorting and have important implications for understanding hypertonia associated with neurological disorders.
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PMID:Hypertonia-associated protein Trak1 is a novel regulator of endosome-to-lysosome trafficking. 1867 23

The aim of the study--to estimate the effect of therapy with Magne 6 on the indices of cardiac hemodynamics, tolerance to physical load, activity of antioxidant protection enzymes and grade of hypoxia in youths with 1 grade mitral valve prolapse (MVP) without regurgitation. In 73 cases with impaired compensatory adaptive possibilities the extent of main syndromes of autonomic dystonia and state of cardiac hemodynamic indices were evaluated. The activity of catalase (C), glutathione reductase (GR), superoxide dismutase (SOD), lactate (L) and pyruvate (P) level were detected in red blood cells, the coefficient lactate/pyruvate (L/P) was been calculated according to the standard method. In the study the high-grade of autonomic dystonia (36.6 +/- 2.1 scores) was been revealed. The number of scores in the control group is 10.8 +/- 1.8. There was found the confident increase of stroke by 37.18%, cardiac output by 24%, stroke index--by 38.45% and cardiac index--by 43.06% in comparison with healthy persons (a < 0.05). The time of cycle ergometer load was significantly lower than in reference group 20.22% (a < 0.05). The red blood cells levels of PVK and L were correspondingly 95.4% and 51.4% higher than in control (p < 0.05). The L/P ratio was 22.5% in excess of the value in reference group (p < 0.05). C activity was 4.59 times less, SOD and GR activity were correspondingly 6.23 and 1.85 times (p < 0.05) as mush, than in healthy persons. Associated with Magne 6 therapy for a month the improvement in indices of cardiac hemodynamics, rising of tolerance to physical load, the fall in GR activity and decrease of hypoxia were been noted. Magne 6 may be used for magnifying of compensatory--adaptive possibilities in youths with 6 MVP.
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PMID:[The use of Magne B6 in order to increase compensatory-adaptive possibilities in youths with primary mitral valve prolapse]. 1875 51

The brain-derived neurotrophic factor gene (BDNF) is one of many genes thought to influence synaptic plasticity in the adult brain and shows a common single nucleotide polymorphism (BDNF Val66Met) in the normal population that is associated with differences in hippocampal volume and episodic memory. It is also thought to influence possible synaptic changes in motor cortex following a simple motor learning task. Here we extend these studies by using new non-invasive transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (TDCS) techniques that directly test the excitability and plasticity of neuronal circuits in human motor cortex in subjects at rest. We investigated whether the susceptibility to TMS probes of plasticity is significantly influenced by the BDNF polymorphism. Val66Met carriers were matched with Val66Val individuals and tested on the following protocols: continuous and intermittent theta burst TMS; median nerve paired associative stimulation; and homeostatic plasticity in the TDCS/1 Hz rTMS model. The response of Met allele carriers differed significantly in all protocols compared with the response of Val66Val individuals. We suggest that this is due to the effect of BNDF on the susceptibility of synapses to undergo LTP/LTD. The circuits tested here are implicated in the pathophysiology of movement disorders such as dystonia and are being assessed as potential new targets in the treatment of stroke. Thus the polymorphism may be one factor that influences the natural response of the brain to injury and disease.
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PMID:A common polymorphism in the brain-derived neurotrophic factor gene (BDNF) modulates human cortical plasticity and the response to rTMS. 1904 18

Transcranial magnetic stimulation (TMS) was introduced nearly 20 years ago and has since been developed as a sophisticated tool for neuroscience research. It is an excellent technique that complements other non-invasive methods for studying human brain physiology. The aim of the present study was to review the basic concepts and principles of the repetitive TMS (rTMS) technique, gathering evidence of its applications in neurorehabilitation. Several clinical studies have reported that sessions of rTMS can improve some or all of the motor symptoms associated with Parkinson's disease, dystonia and stroke. However, since these changes are transient, it is premature to propose these applications as realistic therapeutic options, even though the rTMS technique has shown itself to be, potentially, a modulator of sensorimotor integration and neurogenesis. Future work in this area promises to advance our understanding of the pathophysiology of a wide range of neurological conditions, generate widely applicable diagnostic tools for clinical neurophysiology, and perhaps establish neuromodulation as a viable therapeutic option in neurorehabilitation.
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PMID:Therapeutic applications of repetitive transcranial magnetic stimulation in clinical neurorehabilitation. 1915 30


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