Abnormal movements, including HYPERKINESIS; HYPOKINESIA; TREMOR; and DYSTONIA, associated with the use of certain medications or drugs. Muscles of the face, trunk, neck, and extremities are most commonly affected. Tardive dyskinesia refers to abnormal hyperkinetic movements of the muscles of the face, tongue, and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (Adams et al., Principles of Neurology, 6th ed, p1199)
An autosomal recessive disorder characterized by a triad of DEXTROCARDIA; INFERTILITY; and SINUSITIS. The syndrome is caused by mutations of DYNEIN genes encoding motility proteins which are components of sperm tails, and CILIA in the respiratory and the reproductive tracts.
Abnormal involuntary movements which primarily affect the extremities, trunk, or jaw that occur as a manifestation of an underlying disease process. Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES.
A motility disorder characterized by biliary COLIC, absence of GALLSTONES, and an abnormal GALLBLADDER ejection fraction. It is caused by gallbladder dyskinesia and/or SPHINCTER OF ODDI DYSFUNCTION.
The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.
Conditions caused by abnormal CILIA movement in the body, usually causing KARTAGENER SYNDROME, chronic respiratory disorders, chronic SINUSITIS, and chronic OTITIS. Abnormal ciliary beating is likely due to defects in any of the 200 plus ciliary proteins, such as missing motor enzyme DYNEIN arms.
Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists.
Dyneins that are responsible for ciliary and flagellar beating.
Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as CHOREATIC DISORDERS. Chorea is also a frequent manifestation of BASAL GANGLIA DISEASES.
An inhibitor of DOPA DECARBOXYLASE that does not enter the central nervous system. It is often given with LEVODOPA in the treatment of parkinsonism to prevent the conversion of levodopa to dopamine in the periphery, thereby increasing the amount that reaches the central nervous system and reducing the required dose. It has no antiparkinson actions when given alone.
Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Populations of thin, motile processes found covering the surface of ciliates (CILIOPHORA) or the free surface of the cells making up ciliated EPITHELIUM. Each cilium arises from a basic granule in the superficial layer of CYTOPLASM. The movement of cilia propels ciliates through the liquid in which they live. The movement of cilia on a ciliated epithelium serves to propel a surface layer of mucus or fluid. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.
A congenital abnormality in which organs in the THORAX and the ABDOMEN are opposite to their normal positions (situs solitus) due to lateral transposition. Normally the STOMACH and SPLEEN are on the left, LIVER on the right, the three-lobed right lung is on the right, and the two-lobed left lung on the left. Situs inversus has a familial pattern and has been associated with a number of genes related to microtubule-associated proteins.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
A condition associated with the use of certain medications and characterized by an internal sense of motor restlessness often described as an inability to resist the urge to move.
A bundle of MICROTUBULES and MICROTUBULE-ASSOCIATED PROTEINS forming the core of each CILIUM or FLAGELLUM. In most eukaryotic cilia or flagella, an axoneme shaft has 20 microtubules arranged in nine doublets and two singlets.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
An inhibitor of DOPA DECARBOXYLASE, preventing conversion of LEVODOPA to dopamine. It is used in PARKINSON DISEASE to reduce peripheral adverse effects of LEVODOPA. It has no antiparkinson actions by itself.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
A condition marked by recurrent seizures that occur during the first 4-6 weeks of life despite an otherwise benign neonatal course. Autosomal dominant familial and sporadic forms have been identified. Seizures generally consist of brief episodes of tonic posturing and other movements, apnea, eye deviations, and blood pressure fluctuations. These tend to remit after the 6th week of life. The risk of developing epilepsy at an older age is moderately increased in the familial form of this disorder. (Neurologia 1996 Feb;11(2):51-5)
A family of multisubunit cytoskeletal motor proteins that use the energy of ATP hydrolysis to power a variety of cellular functions. Dyneins fall into two major classes based upon structural and functional criteria.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
Drugs that bind to and activate dopamine receptors.
A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.
A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.
Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
An attitude or posture due to the co-contraction of agonists and antagonist muscles in one region of the body. It most often affects the large axial muscles of the trunk and limb girdles. Conditions which feature persistent or recurrent episodes of dystonia as a primary manifestation of disease are referred to as DYSTONIC DISORDERS. (Adams et al., Principles of Neurology, 6th ed, p77)
Diseases of the BASAL GANGLIA including the PUTAMEN; GLOBUS PALLIDUS; claustrum; AMYGDALA; and CAUDATE NUCLEUS. DYSKINESIAS (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include CEREBROVASCULAR DISORDERS; NEURODEGENERATIVE DISEASES; and CRANIOCEREBRAL TRAUMA.
Endogenous compounds and drugs that specifically stimulate SEROTONIN 5-HT1 RECEPTORS. Included under this heading are agonists for one or more of the specific 5-HT1 receptor subtypes.
A non-specific host defense mechanism that removes MUCUS and other material from the LUNGS by ciliary and secretory activity of the tracheobronchial submucosal glands. It is measured in vivo as mucus transfer, ciliary beat frequency, and clearance of radioactive tracers.
Compounds containing dibenzo-1,4-thiazine. Some of them are neuroactive.
The representation of the phylogenetically oldest part of the corpus striatum called the paleostriatum. It forms the smaller, more medial part of the lentiform nucleus.
A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279)
Persistent abnormal dilatation of the bronchi.
An antiviral that is used in the prophylactic or symptomatic treatment of influenza A. It is also used as an antiparkinsonian agent, to treat extrapyramidal reactions, and for postherpetic neuralgia. The mechanisms of its effects in movement disorders are not well understood but probably reflect an increase in synthesis and release of dopamine, with perhaps some inhibition of dopamine uptake.
Lens-shaped structure on the inner aspect of the INTERNAL CAPSULE. The SUBTHALAMIC NUCLEUS and pathways traversing this region are concerned with the integration of somatic motor function.
A class of opioid peptides including dynorphin A, dynorphin B, and smaller fragments of these peptides. Dynorphins prefer kappa-opioid receptors (RECEPTORS, OPIOID, KAPPA) and have been shown to play a role as central nervous system transmitters.
The proximal portion of the respiratory passages on either side of the NASAL SEPTUM. Nasal cavities, extending from the nares to the NASOPHARYNX, are lined with ciliated NASAL MUCOSA.
A serotonin receptor subtype found distributed through the CENTRAL NERVOUS SYSTEM where they are involved in neuroendocrine regulation of ACTH secretion. The fact that this serotonin receptor subtype is particularly sensitive to SEROTONIN RECEPTOR AGONISTS such as BUSPIRONE suggests its role in the modulation of ANXIETY and DEPRESSION.
Compounds with a benzene ring fused to a thiazole ring.
A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.
A genus of the subfamily CALLITRICHINAE occurring in forests of Brazil and Bolivia and containing seventeen species.
A subtype of dopamine D2 receptors that are highly expressed in the LIMBIC SYSTEM of the brain.
The phylogenetically newer part of the CORPUS STRIATUM consisting of the CAUDATE NUCLEUS and PUTAMEN. It is often called simply the striatum.
A plant family of the order Geraniales, subclass Rosidae, class Magnoliopsida.
A serotonin 1A-receptor agonist that is used experimentally to test the effects of serotonin.
Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells.
A phenylethylamine derivative that acts as a calcium antagonist showing hemodynamic effects in patients with acute myocardial infarction.
Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres.
A dopamine D2 antagonist that is used as an antiemetic.
The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.
Drugs used for their effects on serotonergic systems. Among these are drugs that affect serotonin receptors, the life cycle of serotonin, and the survival of serotonergic neurons.
An ethnic group with shared religious beliefs. Originating in Switzerland in the late 1600s, and first migrating to the mid-Atlantic, they now live throughout Eastern and Mid-Western United States and elsewhere. Communities are usually close-knit and marriage is within the community.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
A complex group of fibers arising from the basal olfactory regions, the periamygdaloid region, and the septal nuclei, and passing to the lateral hypothalamus. Some fibers continue into the tegmentum.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
The sphincter of the hepatopancreatic ampulla within the duodenal papilla. The COMMON BILE DUCT and main pancreatic duct pass through this sphincter.
The physical activity of a human or an animal as a behavioral phenomenon.
That part of the genome that corresponds to the complete complement of EXONS of an organism or cell.
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
A drug formerly used as an antipsychotic and treatment of various movement disorders. Tetrabenazine blocks neurotransmitter uptake into adrenergic storage vesicles and has been used as a high affinity label for the vesicle transport system.
A dopamine D2 agonist. It is used in the treatment of parkinson disease, particularly for alleviation of tremor. It has also been used for circulatory disorders and in other applications as a D2 agonist.
A phosphoprotein that was initially identified as a major target of DOPAMINE activated ADENYLYL CYCLASE in the CORPUS STRIATUM. It regulates the activities of PROTEIN PHOSPHATASE-1 and PROTEIN KINASE A, and it is a key mediator of the biochemical, electrophysiological, transcriptional, and behavioral effects of DOPAMINE.
Relatively invariant mode of behavior elicited or determined by a particular situation; may be verbal, postural, or expressive.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.
Abnormal thoracoabdominal VISCERA arrangement (visceral heterotaxy) or malformation that involves additional CONGENITAL HEART DEFECTS (e.g., heart isomerism; DEXTROCARDIA) and/or abnormal SPLEEN (e.g., asplenia and polysplenia). Irregularities with the central nervous system, the skeleton and urinary tract are often associated with the syndrome.
Absence of crystalline lens totally or partially from field of vision, from any cause except after cataract extraction. Aphakia is mainly congenital or as result of LENS DISLOCATION AND SUBLUXATION.
Diseases of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.
Therapy for MOVEMENT DISORDERS, especially PARKINSON DISEASE, that applies electricity via stereotactic implantation of ELECTRODES in specific areas of the BRAIN such as the THALAMUS. The electrodes are attached to a neurostimulator placed subcutaneously.
A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.
A family of serine-threonine kinases that are specific for G-PROTEIN-COUPLED RECEPTORS. They are regulatory proteins that play a role in G-protein-coupled receptor densensitization.
The posterior filiform portion of the spermatozoon (SPERMATOZOA) that provides sperm motility.
Organic or functional motility disorder involving the SPHINCTER OF ODDI and associated with biliary COLIC. Pathological changes are most often seen in the COMMON BILE DUCT sphincter, and less commonly the PANCREATIC DUCT sphincter.
Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about.
Tryptamine substituted with two hydroxyl groups in positions 5 and 7. It is a neurotoxic serotonin analog that destroys serotonergic neurons preferentially and is used in neuropharmacology as a tool.
The spatial arrangement of the atoms of a nucleic acid or polynucleotide that results in its characteristic 3-dimensional shape.
Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.
A species of the genus MACACA which typically lives near the coast in tidal creeks and mangrove swamps primarily on the islands of the Malay peninsula.
Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The observable response an animal makes to any situation.
A portion of the nucleus of ansa lenticularis located medial to the posterior limb of the internal capsule, along the course of the ansa lenticularis and the inferior thalamic peduncle or as a separate nucleus within the internal capsule adjacent to the medial GLOBUS PALLIDUS (NeuroNames, http://rprcsgi.rprc. washington.edu/neuronames/ (September 28, 1998)). In non-primates, the entopeduncular nucleus is analogous to both the medial globus pallidus and the entopeduncular nucleus of human.
Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)
The characteristic three-dimensional shape of a molecule.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
Elements of limited time intervals, contributing to particular results or situations.
Facilities which administer the delivery of psychologic and psychiatric services to people living in a neighborhood or community.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
The mucous lining of the NASAL CAVITY, including lining of the nostril (vestibule) and the OLFACTORY MUCOSA. Nasal mucosa consists of ciliated cells, GOBLET CELLS, brush cells, small granule cells, basal cells (STEM CELLS) and glands containing both mucous and serous cells.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.
Any tests done on exhaled air.
Drugs used in the treatment of movement disorders. Most of these act centrally on dopaminergic or cholinergic systems. Among the most important clinically are those used for the treatment of Parkinson disease (ANTIPARKINSON AGENTS) and those for the tardive dyskinesias.

Early retreatment of infantile esotropia: comparison of reoperation and botulinum toxin. (1/98)

AIM: To compare the efficacy of reoperation and botulinum toxin injection in treating infantile esotropes early after unsatisfactory surgical alignment. METHODS: 55 strabismic children who had been unsuccessfully operated for infantile esotropia were randomised to reoperation (28 patients) or botulinum toxin injection (27 patients). The motor outcomes (percentage of successful motor outcome and percentage change in deviation) were compared at 6 months, 1 year, and 3 years after retreatment, and the sensory outcomes (percentage with fusion ability and stereo perception) at the 3 year follow up visit. RESULTS: The motor and sensory outcomes and the stability of motor results were similar in patients reoperated and treated with botulinum injection. At the 3 year visit 67.8% and 59.2% of children were, respectively, within 8 prism dioptres of orthotropia (p=0.72). The frequency of fusion ability was, respectively, 60.7% and 51.8% (p=0.71), and the frequency of stereo perception (+info)

Early experience with intrasphincteric botulinum toxin in the treatment of achalasia. (2/98)

BACKGROUND: Recent reports have suggested that intrasphincteric injection of botulinum toxin is effective and long-lasting in the treatment of achalasia. AIM: To report our experience of botulinum toxin injection in a prospective series of consecutive patients with achalasia. METHODS: Eleven consecutive patients with achalasia (eight male, mean age 55 years, range 20-87) were treated with 60 units of botulinum toxin (Dysport; Speywood Pharmaceuticals Ltd, UK) into each of four quadrants at the lower oesophageal sphincter. Patients were assessed pre-treatment and 1 month after treatment using a symptom score and oesophageal manometry. Median follow-up was 12 months (range 6-28). RESULTS: The injection procedure was simple to perform and free of adverse effects. Although treatment had a beneficial effect on dysphagia (median pre-treatment score 3 [interquartile range 3-3]; post-treatment score 2 [0-3]: P=0.03) 1 month following therapy, there was no significant improvement in chest pain or regurgitation scores. Similarly, no significant reduction in median lower oesophageal sphincter pressure was observed (29.5 mmHg [21-42] pre-treatment, 28.5 [17.5-55.5] post-treatment P=0.67). Four patients (36%) required further therapy within 3 months and the overall relapse rate was 73% (eight of 11) within 2 years. CONCLUSION: Although botulinum toxin injection was well tolerated, these results using Dysport at a dose of 240 mouse units question its efficacy as a treatment for achalasia.  (+info)

Tardive and idiopathic oromandibular dystonia: a clinical comparison. (3/98)

OBJECTIVE: Most patients with tardive dystonia have a focal onset involving the cranial-cervical region. Because of its resemblance to idiopathic cranial dystonia, a common form of dystonia, it often poses a diagnostic problem. To compare clinical features and response to botulinum toxin (BTX) injections between patients with tardive and idiopathic oromandibular dystonia (OMD). METHODS: Patients seen in a movement disorder clinic who satisfied the inclusion criteria for tardive or idiopathic OMD were studied. The clinical variables and responses to BTX between the two groups of patients were compared. In the tardive group, we also compared the clinical variables between those with oro-facial-lingual stereotypies, and those without. RESULTS: Twenty four patients with tardive OMD and 92 with idiopathic OMD were studied. There were no differences in the demographic characteristics. Most were women, with duration of symptoms longer than 8 years. The mean duration of neuroleptic exposure was 7.1 (SD 7.9) years. Jaw closure was the most frequent subtype of OMD (tardive=41.7%, idiopathic=51.1%). Idiopathic patients were more likely to have coexistent cervical dystonia (p<0.05), whereas isolated OMD was significantly higher in tardive patients (p<0.05). Limb stereotypies, akathisia, and respiratory dyskinesia were seen only in the tardive OMD. Frequency of oro-facial-lingual stereotypy was significantly higher in the tardive than the idiopathic group (75.0% v 31.5%, p<0.0001). The peak effect of BTX was similar in both groups. CONCLUSIONS: Oro-facial-lingual stereotypies were significantly more frequent in the tardive than the idiopathic group. Presence of stereotypic movements in the limbs, akathisia, and respiratory dyskinesias in patients with OMD strongly suggests prior neuroleptic exposure. Dystonia in tardive OMD is more likely to be restricted to the oromandibular region, whereas in patients with idiopathic OMD, there is often coexistent cervical dystonia. BTX is equally effective in both groups of patients.  (+info)

Tardive dystonia. (4/98)

This paper provides an overview of the phenomenology, epidemiology, and treatment of tardive dystonia. Tardive dystonia is one of the extrapyramidal syndromes that starts after long-term use of dopamine receptor antagonists. The diagnosis is based on the presence of chronic dystonia, defined as a syndrome of sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures. Furthermore, dystonia must develop either during or within 3 months of a course of antipsychotic treatment, and other causes such as Wilson's disease, acute dystonia, or a conversion reaction must be ruled out. Tardive dystonia occurs in about 3 percent of patients on long-term antipsychotic treatment. Some probable risk factors for tardive dystonia are younger age, male, and the presence of tardive dyskinesia. The treatment of tardive dystonia starts with an evaluation of the need for using the causative drug. If antipsychotics must be continued, a switch to an atypical antipsychotic, particularly clozapine, may be helpful. If the dystonia is relatively localized, botulinum toxin is an effective but not well-known treatment possibility. If tardive dystonia is more extensive, either dopamine-depleting drugs or high dosages of anticholinergics can be tried.  (+info)

A multicentre randomised study of intrasphincteric botulinum toxin in patients with oesophageal achalasia. GISMAD Achalasia Study Group. (5/98)

BACKGROUND: Intrasphincteric injection of botulinum toxin (Botx) has been proposed as treatment for oesophageal achalasia. However, the predictors of response and optimal dose remain unclear. AIMS: To compare the effect of different doses of Botx and to identify predictors of response. PATIENTS/METHODS: A total of 118 achalasic patients were randomised to receive one of three doses of Botx in a single injection: 50 U (n=40), 100 U (n=38), and 200 U (n=40). Of those who received 100 U, responsive patients were reinjected with an identical dose after 30 days. Clinical and manometric assessments were performed at baseline, 30 days after the initial injection of botulinum toxin, and at the end of follow up (mean 12 months; range 7-24 months). RESULTS: Thirty days after the initial injection, 82% of patients were considered responders without a clear dose related effect. At the end of follow up however, relapse of symptoms was evident in 19% of patients who received two injections of 100 U compared with 47% and 43% in the 50 U and 200 U groups, respectively. Using Kaplan-Meier analysis, patients in the 100x2 U group were more likely to remain in remission at any time (p<0.04), with 68% (95% CI 59-83) still in remission at 24 months. In a multiple adjusted model, response to Botx was independently predicted by the occurrence of vigorous achalasia (odds ratio 3.3) and the 100x2 U regimen (odds ratio 3.2). CONCLUSIONS: Two injections of 100 U of Botx 30 days apart appeared to be the most effective therapeutic schedule. The presence of vigorous achalasia was the principal determinant of the response to Botx.  (+info)

Botulinum toxin injected in the gastric wall reduces body weight and food intake in rats. (6/98)

BACKGROUND: Botulinum toxin is a powerful, long-acting inhibitor of muscular contractions in both voluntary and smooth muscle. It acts by blocking the release of the neurotransmitter acetylcholine. In the stomach, propulsive contractions of the antrum are necessary for the gastric contents to pass into the duodenum. AIMS: To investigate whether intramuscular injections of botulinum toxin type A into the gastric antrum of rats would cause a reduction in food intake and hence body weight, by inhibition of gastric emptying. MATERIALS AND METHODS: This was a prospective, randomized, 3-way parallel group study in rats. The first group was anaesthetized, laparotomized and given 20 U of botulinum toxin type A by intramuscular injection into the gastric antrum (botulinum toxin type A group, n=14). The second group was anaesthetized, laparotomized and injected with saline (sham group, n=14) and the third group did not have any intervention (control group, n=5). Food intake was measured daily for 7 weeks and body weight was measured daily for 10 weeks. RESULTS: There was a significant difference in loss of body weight between the two treated groups (14.0 +/- 8.2% botulinum toxin type A group, 4.4 +/- 2.7% sham group; P < 0.001). Further, the time to reach the weight nadir was significantly longer in the botulinum toxin type A group (8.7 +/- 3.9 days) compared with the sham group (5.3 +/- 3.8 days; P < 0.04). There were no significant differences between the sham and control groups for any of the body weight parameters. The minimum dietary intake was significantly lower in the botulinum toxin type A group than in the sham group (37.8 +/- 21.8% of the basal value in the botulinum toxin type A group, vs. 65.5 +/- 32.0 in the sham group, P < 0.05). In addition, the time to reach the nadir was significantly prolonged (8.2 +/- 3.5 days, botulinum toxin type A group vs. 4.9 +/- 1.7 days, sham group, P < 0.001). CONCLUSIONS: The parallel reduction of body weight and food intake in botulinum toxin type A treated animals is consistent with a long lasting inhibition of the antral pump. This is probably due to slowed gastric emptying leading to early satiety. Patients with morbid obesity might benefit from endoscopic injections of botulinum toxin type A into the stomach wall.  (+info)

Two cases of severe non-specific oesophageal dysmotility showing different response to botulinum injection therapy. (7/98)

We report 2 cases where treatment of achalasia type symptoms due to severe non-specific oesophageal dysmotility have shown symptom resolution and manometric improvement to intrasphincteric botulinum injections either by itself or in combination with oesophageal dilatation.  (+info)

Serotonin facilitates AMPA-type responses in isolated siphon motor neurons of Aplysia in culture. (8/98)

1. Serotonin (5-HT) facilitates the connections between sensory and motor neurons in Aplysia during behavioural sensitization. The effect of 5-HT on sensorimotor synapses is believed to be primarily presynaptic. Here we tested whether 5-HT can have an exclusively postsynaptic facilitatory effect. 2. Siphon motor neurons were individually dissociated from the abdominal ganglion of Aplysia and placed into cell culture. Brief pulses of glutamate, the putative sensory neuron transmitter, were focally applied (0.1 Hz) to solitary motor neurons in culture, and the glutamate-evoked postsynaptic potentials (Glu-PSPs) were recorded. 3. When 5-HT was perfused over the motor neuron for 10 min, the amplitude of the Glu-PSPs was significantly increased. The 5-HT-induced enhancement of the Glu-PSPs persisted for at least 40 min after washout. 4. Prior injection into the motor neuron of the calcium chelator BAPTA, GDP-beta-S or GTP-gamma-S blocked the 5-HT-induced facilitation of the Glu-PSPs. However, the facilitation was not blocked when APV, an NMDA receptor antagonist, was applied together with the 5-HT. 5. The enhancement of the Glu-PSPs by 5-HT was reversed by the AMPA receptor antagonist DNQX, indicating that 5-HT increased the functional expression of AMPA-type receptors in the motor neuron. 6. The presence of botulinum toxin in the motor neuron blocked the 5-HT-induced enhancement of the Glu-PSPs. As botulinum toxin prevents exocytosis we hypothesize that during sensitization 5-HT causes the insertion of additional AMPA-type receptors into the postsynaptic membrane of sensorimotor synapses via exocytosis. This postsynaptic mechanism may contribute to facilitation of the synapses.  (+info)

Background: Upper limb function is essential for activities of daily living impacting on quality of life in children with cerebral palsy (CP). In preschool children, dysfunctional upper extremity manipulation not only leads to disability but may further delay global development and substantially increase career burden. Even modest functional improvement could have tremendous long-term benefit in activities of daily living and significantly reduce career burden. Hypertonia is the main symptom causing motor dysfunction in CP. Intramuscular Botulinum toxin injection is one way of treatment. In spite of anecdotal evidence suggesting that early intervention can lead to better outcomes, Israeli physicians are unable to prescribe this treatment for the upper extremities due to limited health insurance coverage. A paucity research evidence is often cited as the reason for limiting the insurance coverage, in particular to the upper limb. We therefore propose to study the effects of Botox® in treating ...
Intrasphincteric botulinum toxin injection may be appropriate in those achalasia patients who are elderly or have concomitant medical problems but concern persists regarding the length of the response and untoward side effects.
Meige Syndrome is a rare neurological movement disorder (dyskinesia) characterized by spasms of the muscles of the eyelids and associated loss of tone in these eyelid muscles.
Neuromuscular Agents: Drugs used for their actions on skeletal muscle. Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS.
Dystonia is a movement disorder in which your muscles contract involuntarily, causing repetitive or twisting movements. This dystonia can affect one muscle, a muscle group or even your entire body. When your masticatory, lower facial and the tongue muscles are affected, it is oromandibular dystonia.. Symptoms:. Dystonia of the neck muscles, larynx, and eyelids are often related to oromandibular dystonia. Symptoms sometimes only occur when you perform specific actions, such as chewing or speaking. In addition, some people may have difficulty in swallowing and chewing.. Causes:. Oromandibular dystonia can be divided into primary one and secondary one. Primary oromandibular dystonia occurs with or without a family history of the disorder, while the secondary one occurs because of secondary causes, such as certain disorders or exposure to drugs.. Diagnosis:. After asking patients about his or her medical information, doctors may perform the following tests to help diagnose this condition:. ...
INTRODUCTION AND HYPOTHESIS Botulinum toxin has become a widely adopted treatment for patients with recalcitrant overactive bladder (OAB) symptoms. Some recommend clean intermittent self-catheterisation (CISC) if a postvoid residual (PVR) ,200 ml posttreatment, but there is no evidence for this recommendation. The aim of this study was to identify whether abstinence from CISC as a routine strategy for patients with a PVR following intradetrusor botulinum toxin injections is associated with any measurable adversity. METHODS This was a cohort observation study. Patients with lower urinary tract symptoms (LUTS) attending a medical urology centre were observed before and after botulinum toxin treatment. Intradetrusal botulinum toxin injections were administered in the day-treatment centre at a medical urology centre in London, UK. Patients were reviewed at follow-up consultations to measure PVR. RESULTS Of the 240 patients studied, 215 were women and 25 were men, of whom, 196 (82%) received ...
Botulinum toxin injections price online from Europe online store, trusted supplier. Steroids price list. We Offers new injectable steroids, botulinum toxin injections price. Cortisone can help to quickly soothe disease, higher BMI, and size, and sex drive gains. Term anabolic refers to promoting.
Primary cervical dystonia (CD) affects about 20-40/100.000 population. The disease is chronic and life-long. The therapy of choice are local intramuscular Botulinum Toxin injections given every three months. Oral medication such as anticholinergics or dopamine depleting drugs are usually of limited efficacy or their use is limited by intolerable side-effects. About 5-10% of CD patients develop neutralizing antibodies against Botulinum Toxin. Two previous controlled multicenter trials have shown the efficacy and safety of bilateral pallidal stimulation in patients with primary segmental and generalized dystonia (one study was performed by our group).. Following surgery, patients will be randomized 1:1 to verum or placebo stimulation for a period of three months. Primary outcome measure is the TWSTRS (Toronto Western Spasmodic Torticollis Rating Scale) - a validated and widely accepted physician-based outcome measure for cervical dystonia. The independent TWSTRS raters are movement disorders ...
Repeated botulinum toxin injection for idiopathic overactive bladder: will chemodenervation become a long-term solution?: Botulinum toxin A (BTX-A) has emerged
Dysphagia was suspected in 36% of patients with cervical dystonia on the basis of clinical assessment. The incidence of dysphagia increased to 72% on electrophysiological evaluation of oropharyngeal swallowing.. Clinical and videofluoroscopic evaluations have also indicated a high incidence of swallowing disorders in patients with cervical dystonia3,4,8,9 before any treatment such as botulinum toxin injection or rhizotomy. The incidence of dysphagia varied between 22 and 100% of patients (mostly over 50%). The incidence of dysphagia increased more significantly after botulinum toxin injection4,10,17-19 and after selective rhizotomy.8,9 Similarly, dysphagia in patients with spasmodic dysphonia has been reported before and after treatment of this condition.1,2,6,7. In our patient groups 11 had pure spasmodic torticollis and 7 had torticollis with generalised dystonia. However, in our 7 patients with oromandibular and laryngeal dystonia there were no abnormal neck movements except in one patient. ...
Botulinum toxin injections may significantly improve lower limb kinematics in gait of children with spastic forms of cerebral palsy. Here we aimed to analyze the effect of lower limb botulinum toxin injections on trunk postural control and lower limb intralimb (intersegmental) coordination in children with spastic diplegia or spastic hemiplegia (GMFCS I or II). We recorded tridimensional trunk kinematics and thigh, shank and foot elevation angles in fourteen 3-12 year-old children with spastic diplegia and 14 with spastic hemiplegia while walking either barefoot or with ankle-foot orthoses (AFO) before and after botulinum toxin infiltration according to a management protocol. We found significantly greater trunk excursions in the transverse plane (barefoot condition) and in the frontal plane (AFO condition). Intralimb coordination showed significant differences only in the barefoot condition, suggesting that reducing the degrees of freedom may limit the emergence of selective coordination. Minimal
Botulinum toxin injections may significantly improve lower limb kinematics in gait of children with spastic forms of cerebral palsy. Here we aimed to analyze the effect of lower limb botulinum toxin injections on trunk postural control and lower limb intralimb (intersegmental) coordination in children with spastic diplegia or spastic hemiplegia (GMFCS I or II). We recorded tridimensional trunk kinematics and thigh, shank and foot elevation angles in fourteen 3-12 year-old children with spastic diplegia and 14 with spastic hemiplegia while walking either barefoot or with ankle-foot orthoses (AFO) before and after botulinum toxin infiltration according to a management protocol. We found significantly greater trunk excursions in the transverse plane (barefoot condition) and in the frontal plane (AFO condition). Intralimb coordination showed significant differences only in the barefoot condition, suggesting that reducing the degrees of freedom may limit the emergence of selective coordination. Minimal
Botulinum toxin injections in surgical wound closure immediately after surgery improve facial surgery scars, according to a small study published in the March i
Learn more about Botulinum Toxin Injections -- Medical at Largo Medical Center DefinitionReasons for ProcedurePossible ComplicationsWhat to ExpectCall Your Doctorrevision ...
Learn more about Botulinum Toxin Injections -- Medical at Regional Medical Center of San Jose DefinitionReasons for ProcedurePossible ComplicationsWhat to ExpectCall...
Learn more about Botulinum Toxin Injections -- Medical at Medical City Dallas DefinitionReasons for ProcedurePossible ComplicationsWhat to ExpectCall Your Doctorrevision ...
Learn more about Botulinum Toxin Injections -- Medical at Medical City Dallas DefinitionReasons for ProcedurePossible ComplicationsWhat to ExpectCall Your Doctorrevision ...
TY - JOUR. T1 - Discussion. Oromandibular dystonia treated with botulinum toxin. T2 - Report of case. AU - Brin, Mitchell F.. AU - Blitzer, Andrew. AU - Stewart, Celia F.. PY - 1995/3. Y1 - 1995/3. UR - http://www.scopus.com/inward/record.url?scp=0007581921&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0007581921&partnerID=8YFLogxK. U2 - 10.1016/0278-2391(95)90236-8. DO - 10.1016/0278-2391(95)90236-8. M3 - Comment/debate. AN - SCOPUS:0007581921. VL - 53. SP - 335. EP - 337. JO - Journal of Oral and Maxillofacial Surgery. JF - Journal of Oral and Maxillofacial Surgery. SN - 0278-2391. IS - 3. ER - ...
Drug induced movement disorders have been described with an increasing frequency since the introduction of chlorpromazine (thorazine) in 1952.1 This and other dopamine receptor blocking drugs, also referred to as neuroleptic drugs, can cause a wide variety of movement disorders.1 20-22 In 1982, Burkeet al,2 comprehensively characterised tardive dystonia as a variant of tardive dyskinesia in 42 patients exposed to neuroleptic drugs. Since then, tardive dystonia has been widely recognised as a separate entity from tardive dyskinesia, and both can manifest at the same time.1-4 7 10 Studies on tardive dystonia have focused on the prevalence of the anatomical areas involved, and its clinical progression.2 3 7 The craniocervical region has been demonstrated as the most common region initially affected in patients with tardive dystonia.1-4 7 As it is relatively common for patients and their family members to be unaware of an exposure to neuroleptic drugs, the presence of suggestive clinical signs that ...
In 2012 one of the first symptoms I developed was severe Oromandibular Dystonia. This meant that my jaw, mouth and tongue go into painful, and often extreme spasms. On these occasions I struggle to speak; this can be due to several factors such as: my tongue spasming and making it impossible to talk, the…
Results show that: 1) one or two intrasphincteric injections of botulinum toxin result in clinical and objective improvement in about 84% of achalasia patients and are not associated with serious side-effects; 2) patients over 50 years showed better benefit than younger patients; 3) no correlation w …
Surgical treatments for dystonia may be an option for individuals whose symptoms do not respond to oral medications or botulinum toxin injections. Researchers are actively refining current techniques and collecting information about which patients may benefit the most from surgical treatments.. There is no single surgical procedure that can be applied to all forms of dystonia. Surgical procedures for dystonia can be divided into two broad categories: brain surgery and peripheral surgery. Peripheral surgery includes procedures that target parts of the body other than the brain.. In both brain and peripheral procedures, the goal of surgery is to interrupt the faulty communication between the brain and muscles that causes involuntary muscle movements. Surgery intends to treat symptoms and improve function but does not cure the underlying condition.. Because dystonia is a chronic disorder, the management of symptoms is an ongoing, lifelong process. Just as medications and botulinum toxin injections ...
DISTONIA OROMANDIBULAR PDF - Abstract. OBJECTIVES Oromandibular dystonia (OMD) is a focal dystonia manifested by involuntary muscle contractions producing repetitive, patterned mouth.
Authors noted that while the difference was statistically significant, it had uncertain clinical importance, and patients who received injections were more likely to develop urinary tract infections and to need transient self-catheterization.
C.L.I.M.B.®, an injection training program for Dysport® (abobotulinumtoxinA). Read Important Safety Information & Boxed Warning.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나 그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며, 이를 위반시 정보통신망법에 의해 형사처벌됨을 유념하시기 바랍니다. [게시일 2003년 4월 2일 ...
Information on Middlesex University's Research Repository: a online collection of Middlesex University's research outputs
This chapter explains the mechanism by which botulinum neurotoxin (BoNT) causes its neuromuscular paralytic effects, and reviews the developments that led these effects to be harnessed therapeutically. It specifically focuses upon the conditions of dystonia and spasticity. Within the spectrum of these diseases, it discusses those situations where BoNT injections are the treatment of choice. The very accurate targeting of BoNT into specific muscles in many situations is both desirable and crucial in some situations BoNTs therapeutic neuroparalytic effect may need to be restricted to a single muscle fascicle.. In some cases, an inaccurately placed injection may be associated with unacceptable side effects. In order to achieve accuracy of BoNT injection delivery, intramuscular injections of BoNT aided by electromyography (EMG) guidance allows the very accurate targeting of specific muscles. The practical aspects related to the preparation of BoNT for injection and the methodology and techniques for
Cervical Dystonia Global Clinical Trials Review, H1, 2017 Cervical Dystonia Global Clinical Trials Review, H1, 2017 Summary GlobalDatas clinical trial report,
Rush movement disorder experts tailor dystonia treatments (e.g., botulinum toxin injections or deep brain stimulation) to address your dystonia symptoms.
Keywords: Clinical Practice Special Interests: Management of Parkinson disease and parkinsonism, dystonia, tremor, chorea, tics, myoclonus, gait disorders, tardive dyskinesia, dementia, memory disorders and Botulinum toxin injections for movement disorders, the effects of movement and memory disorders on daily function and quality of life, exercise interventions, gait problems, self-management, self-efficacy, caregiver strain, outcomes research, data visualization and health disparities,Parkinsons Research - Biomarkers, Informatics and Outcomes ...
Botulinum toxin injections,or Botox, are one of the most popular cosmetic treatments in the world, and Snowberrry Lane is proud to offer this service.
Cervical dystonia is a movement disorder affecting your neck. Also known as spasmodic torticollis, this painful condition is most common in women.
Cervical dystonia is a movement disorder affecting your neck. Also known as spasmodic torticollis, this painful condition is most common in women.
Cervical dystonia, known as spasmodic torticollis, is a neurological disorder which causes the neck and shoulder muscles to involuntarily contract and...
XEOMIN® is approved for treating adults with cervical dystonia, which causes twitching, spasms, and contractions. Learn more about possible muscles involved, types of head movements, and symptoms.
Surgical treatment of cervical dystonia (costs for program #205821) ✔ University Hospital Bonn ✔ Department of Neurosurgery ✔ BookingHealth.com
Worldwide Cervical Dystonia Therapeutics Market 2021-2028 Industry Research Report contains thorough analysis of market and numerous related factors that range. Read more ...
Read clinical results of Dysport® (abobotulinumtoxinA), FDA-approved botulinum toxin therapy for children (2 & older) w/ LLS. Read Safety Info & Boxed Warning.
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
We have a ton of updates to cover today. Lets get praying! First of all, Larry Stefano has had a wonderful report! He had several biopsies recently, and the results were, miraculously, completely clear. There is still one spot on his hip that the doctors dont want to biopsy, so he is still being treated like he has recurring bone … ...
Botulinum Toxin Therapy for Chronic Migraine What is botulinum toxin? Botulinum toxin (Onabotulinum Toxin A) is made from a toxin produced by the bacterium Clostridium botulinum. In high doses it can produce muscle paralysis. In low doses, it is used to treat many conditions. Botulinum toxin is a medicine approved by the FDA to prevent chronic migraines. How does it work? It is unclear how botulinum toxin treats chronic migraine. Botulinum toxin injections can cause relaxation of muscles and can block nerve signal transmission. The effects last about 12 weeks. It works best if treatment is done every 12 weeks. It may take more than one treatment to feel the full effect of botulinum toxin therapy. How do I know it will help me? Botulinum toxin treatments are expensive and come with some risk. Both your provider and insurance consider this treatment when less invasive treatments have not worked for you. Botulinum toxin has been found to work well for chronic migraine. Most people (up to 70%) feel ...
Treatment for oromandibular dystonia must be highly customized to the individual. A multitude of oral medications has been studied to determine benefit for people with oromandibular dystonia. About one-third of peoples symptoms improve when treated with oral medications such as Klonapin® (clonazepam), Artane® (trihexyphenidyl), diazepam (Valium®), tetrabenezine, and Lioresal® (baclofen).. Although the symptoms may vary from person to person, approximately 70% of people with oromandibular dystonia experience some reduction of spasm and improvement of chewing and speech after injection of botulinum toxin into the masseter, temporalis, and lateral pterygoid muscles. Botulinum toxin injections are most effective in jaw-closure dystonia, while treating jaw-opening dystonia may be more challenging. Botulinum toxin injections may also be an option for lingual dystonia. Side effects such as swallowing difficulties, slurred speech, and excess weakness in injected muscles may occur, but these side ...
Botulinum toxin injection bilateral rectus femoris, medial hamstrings, and gastrocnemius soleus muscles, phenol neurolysis of bilateral obturator nerves, application of bilateral short leg fiberglass casts.
Botulinum Toxin Botox.The advantage of botulinum toxin over oral medication is that the toxin can be targeted only at the muscles causing the problem.
Long lauded for its ability to reduce the appearance of wrinkles, botulinum toxin is now being considered for reducing scarring.. By using botulinum toxin to denervate underlying muscle and immobilize tension?which increases inflammation, fibrosis, erythema and scar size?scarring can potentially be reduced, say researchers writing in a review published in the Journal of Drugs in Dermatology. ...
Acknowledging its growing popularity and the market growth, Market Research Future, recently published a study report - The Global Cervical Dystonia Market. Which indicates that the Market is booming and estimated to gain further prominence over the forecast period. Further MRFR asserts that the Market will demonstrate a massive growth by 2023, phenomenally superseding its previous growth records in terms of value with a whooping CAGR during the anticipated period (2017 - 2023). The Global cervical dystonia market research report is expected to grow at a CAGR of 5% during forecasted period 2017-2023.. Market Research Future published new report, titled Cervical Dystonia Market -Research Report: Global Forecast till 2023.. The study report worldwide Cervical Dystonia Market covers the market analysis for the regions - North America, Europe, Asia Pacific/ Southeast Asia and Row and country analysis of China, Japan, and India focusing on top manufacturers in world market and the market share they ...
Cervical dystonia is characterized by involuntary, abnormal movements and postures of the head and neck. Current views on its pathophysiology, such as faulty sensorimotor integration and impaired motor planning, are largely based on studies of focal hand dystonia. Using resting state fMRI, we explored whether cervical dystonia patients have altered functional brain connectivity compared to healthy controls, by investigating 10 resting state networks.
TY - JOUR. T1 - Long-Term Abobotulinumtoxin A Treatment of Cervical Dystonia. AU - Bentivoglio, Anna Rita. AU - Di Stasio, Enrico. AU - Mulas, Delia. AU - Ialongo, Tamara. AU - Petracca, Martina. PY - 2017. Y1 - 2017. N2 - Botulinum toxin is considered as first-line therapy for cervical dystonia, but few papers have addressed these issues in the long term. Aim of this study was to investigate the long-term efficacy and safety of abobotulinumtoxin A (A/Abo) in patients with primary cervical dystonia. Consecutive patients who received at least six injections with A/Abo were included. Safety was assessed on patients self-reports. Efficacy was assessed by recording the total duration of benefit, duration of maximum efficacy, disease severity measured by means of the Tsui score, and pain intensity evaluated by means of the visual analog scale (VAS). Thirty-nine patients with PCD were included. The mean dose injected was 701.5 ± 280.6 U. The mean duration of the clinical improvement was 93.0 ± 30.7 ...
Abstracts of scientific studies on the use of PEMF with Whiplash:. Evaluation of electromagnetic fields in the treatment of pain in patients with lumbar radiculopathy or the whiplash syndromeBack pain and the whiplash syndrome are very common diseases involving tremendous costs and extensive medical effort. A quick and effective reduction of symptoms, especially pain, is required. In two prospective randomized studies, patients with either lumbar radiculopathy in the segments L5/S1 or the whiplash syndrome were investigated. Inclusion criteria were as follows: either clinically verified painful lumbar radiculopathy in the segments L5/S1 and a Laségues sign of 30 degrees (or more), or typical signs of the whiplash syndrome such as painful restriction of rotation and flexion/extension. Exclusion criteria were prolapsed intervertebral discs, systemic neurological diseases, epilepsy, and pregnancy.. A total of 100 patients with lumbar radiculopathy and 92 with the whiplash syndrome were selected ...
TY - THES. T1 - Motor and non-motor symptoms in cervical dystonia. T2 - a serotonergic perspective. AU - Smit, Marenka. PY - 2017. Y1 - 2017. N2 - In this thesis, we detected a high frequency of non motor symptoms (NMS) in patients with cervical dystonia (CD) , with a high impact on quality of life (HR-QoL). Psychiatric co-morbidity and fatigue are most likely primary symptoms and part of the phenotype of CD, while excessive daytime sleepiness and impaired sleep quality were highly related to psychiatric co-morbidity and pain. To improve the recognition and treatment of NMS, we proposed and explored a NMS questionnaire as a first step towards a dystonia specific NMS questionnaire. Future studies are warranted to explore the effect of NMS treatment on HR-QoL. Secondly, we explored the role of serotonin in the pathophysiology of dystonia, using PET imaging. It appeared that serotonergic perturbations in the raphe nuclei and in basal ganglia output regions are related to both motor- and NMS in CD. ...
Tweet While secondary lymphedema is caused by blockage or damage to a normally functioning lymphatic system resulting from surgery, radiation, trauma and other known insults, the formation of primary lymphedema is caused by pathology affecting the lymphatic system directly in form of a developmental abnormality, most commonly hypoplasia or hyperplasia involving lymph vessels and/or . . . → Read More: Primary Lymphedema. ...
A disabling form of tardive dystonia and dyskinesia in a young schizophrenic patient is reported. Severe forms of dystonia plus dyskinesia associated with long term neuroleptic exposition are not rare. Although tomographic scans were normal, blood perfusion examination through single photon computed tomography (SPECT) showed basal ganglia hypoperfusion, indicating striatum involvement in this late neuroleptic side effect. The patient was treated with relative success by the association of high doses of propranolol, diazepan and biperiden. A critical discussion about some clinical, neurobiological and treatment issues related to severe forms of tardive dystonia is presented. The association of beta-adrenergic antagonists, gaba agonists and anticholinergic drugs are suggested as a possible alternative for the treatment of this condition ...
Runners dystonia (RD) is a task-specific focal dystonia of the lower limbs that occurs when running. In this retrospective case series, we present surface electromyography (EMG) and joint kinematic data from thirteen patients with RD who underwent instrumented gait analysis (IGA) at the Functional and Biomechanics Laboratory at the National Institutes of Health. Four cases of RD are described in greater detail to demonstrate the potential utility of EMG with kinematic studies to identify dystonic muscle groups in RD. In these cases, the methodology for muscle selection for botulinum toxin therapy and the therapeutic response is discussed. Lateral heel whip, a proposed novel presentation of lower-limb dystonia, is also described.
Cervical dystonia patients get help with coverage and reimbursement for Dysport® (abobotulinumtoxinA) from IPSEN CARES®. Read Safety Info & Boxed Warning.
Background: Cervical dystonia (CD), the most common form of adult-onset focal dystonia, has a heterogeneous clinical presentation with variable clinical features, leading to difficulties and delays in diagnosis. Owing to the lack of reviews specifically focusing on the frequency of primary CD in the general population, we performed a systematic literature search to examine its prevalence/incidence and analyze methodological differences among studies.
Dysphagia, or swallowing disorder, is a term used to describe the inability to move food from the mouth to the stomach. This condition can accompany a neurological disorder such as stroke, Parkinsons disease, cerebral palsy, Lou Gehrigs Disease, etc., as well as bacterial, viral, or fungal infections. Dysphagia can occur at any of the 3 stages of swallowing: oral, pharyngeal, and esophageal.. Depending on the type of swallowing disorder, changing a persons diet by adding thickeners and physical therapy may help alleviate the problem in noninvasive ways. Sometimes drug therapy helps relieve symptoms of the underlying neurological cause and thus relieves the swallowing problems. Less commonly, botulinum toxin injections can be used when food or liquid cannot enter the esophagus. Severely affected individuals may require surgery or feeding tubes.. Next >>. ...
2) Even small amounts of participation is appreciated: This works better for first year students who often have little clinical experience, but I think it does help even with more experienced learners. In the botulinum toxin injection clinic, I will have the students only observe for the first day or so. After that I have them clean the injection area with alcohol swabs, and hook up the EMG ground and reference leads. Although that doesnt sound like much, for a student, it makes them understand that they are being helpful and are a valued part of your team. In truth, it does make things go faster as it takes about the same amount of time to wash my hands as it does to prep the patient for the injections. As possible, I also try to let the students do one injection in a relatively straight forward site by the end of the ten weeks. It doesnt always work out that a good patient/ injection works out on the last day of the rotation. But, even doing one injection for a student is potentially a big ...
Drooping of the eyelid, or ptosis, is a side effect of botulinum toxin injections, which can be caused by poor injection technique. Dr Zahida Butt describes the side effects and contraindications using apraclonidine, or Iopidine, to treat Botox-induced ptosis. ...
The following tests and treatments are some of the most common tests and treatments offered by specialists in this area. These specialists offer many other advanced tests and treatments for a wide range of medical problems. Please call (888) 352-RUSH (7874) if you have questions about specific tests or treatments not listed here. Bone Scan Botulinum Toxin Injections
Researchers have identified a gene that causes adult-onset primary cervical dystonia, an often-painful condition in which patients necks twist involuntarily. The discovery by a team from the Jacksonville, Fla., campus of ...
TY - JOUR. T1 - Reply. T2 - Contributions of visual and motor signals in cervical dystonia. AU - Shaikh, Aasef G.. AU - Zee, David S.. AU - Crawford, J. Douglas. AU - Jinnah, Hyder A.. N1 - Copyright: Copyright 2021 Elsevier B.V., All rights reserved.. PY - 2017/1. Y1 - 2017/1. UR - http://www.scopus.com/inward/record.url?scp=85048324974&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=85048324974&partnerID=8YFLogxK. U2 - 10.1093/brain/aww292. DO - 10.1093/brain/aww292. M3 - Letter. C2 - 27993889. AN - SCOPUS:85048324974. VL - 140. JO - Brain. JF - Brain. SN - 0006-8950. IS - 1. M1 - e5. ER - ...
This rare movement disorder causes neck muscles to contract involuntarily. This can make your head twist or turn into often painful positions.
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It is also an anti-asthmatic agent and a demethylized metabolite of caffeine. Small open-label trials suggest that theophylline ... Istradefylline is a A2A receptor antagonist which increases motor activity and decreases dyskinesia caused by a prolonged ... Several xanthines and non-xanthines are under development as potential anti-parkinsonism agents, which are selective for A2A ... Some effects were found to be due to enhanced activity of natural killer cells and also due to enhanced efficacy of anti-PD-1 ...
The most common types of these agents are antipsychotics and anti-nausea agents. The classic form of TD refers to stereotypic ... Tardive dyskinesia or tardive dystonia, both referred to as "TD", refers to a wide variety of involuntary stereotypical ... Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and ... Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine ...
... the Veterans Administration Cooperative Study Group in Anti-hypertensive Agents, and the Systolic Hypertension in the Elderly ... It was previously used to treat symptoms of dyskinesia in patients suffering from Huntington's disease, but alternative ... ISBN 978-1-59541-101-3. Thanvi B, Lo N, Robinson T (2007). "Levodopa‐induced dyskinesia in Parkinson's disease: clinical ...
These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia. Studies have ... From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, ... If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal ... The term "tardive dyskinesia" first came into use in 1964. Tardive dyskinesia is characterized by repetitive, involuntary ...
... are receptor subtype-specific drugs and other specific agents. An example is the push for better anti-anxiety agents ( ... but cause a variety of dyskinesias by their action on motor cortex. Modern studies are revealing details of mechanisms of ... producing more desirable results than a more selective agent would. An example of this is Vortioxetine, a drug which is not ... and in vitro studies using selective binding agents on live tissue cultures. These allow neural activity to be monitored and ...
Prokinetic agents (e.g. domperidone) Anti-cholinergic agents (e.g. orphenadrine) Evidence suggests that opioid-inclusive ... Due to severe side effects such as tardive dyskinesia, haloperidol is now rarely used. A related drug, prochlorperazine is more ... Amongst analgesics there are a small number of agents which act on the central nervous system but not on the opioid receptor ... Paracetamol and nonsteroidal anti-inflammatory drugs including ibuprofen and naproxen are considered safer alternatives. They ...
A case report of adrafinil-induced orofacial dyskinesia exists. Reports of this side effect also exist for modafinil. In ... Additionally, "adrafinil is known to a larger nonscientific audience, where it is considered to be a nootropic agent." ... active metabolite modafinil were added to the list of substances prohibited for athletic competition according to World Anti- ... 20-. ISBN 978-3-88763-075-1. Milgram, Norton (1999). "Adrafinil: A Novel Vigilance Promoting Agent". CNS Drug Reviews. 5 (3): ...
In the inter-war period, the first anti-bacterial agents such as the sulpha antibiotics were developed. The Second World War ... due to serious adverse effects such as tardive dyskinesia. Patients often opposed psychiatry and refused or stopped taking the ... These were drugs that worked chiefly as anti-anxiety agents and muscle relaxants. The first benzodiazepine was Librium. Three ... Anti-allergy: mast cell inhibitors. *Anti-glaucoma: adrenergic agonists, beta-blockers, carbonic anhydrase inhibitors/ ...
Bromocriptine is less effective than L-Dopa in reducing symptoms, but provides less dyskinesia. Often, the two drugs are used ... Although aNMDA receptor antagonists and anti-inflammatory drugs were tested in a clinical environment, more promising clinical ... cholinergic agents such as choline and lecithin were hypothesized to augment the progression. However, these attempts were ... can be initiated by inflammatory prostaglandins or leukotrienes and are therefore the targets of nonsteroidal anti-inflammatory ...
It is not possible to truly know the risks of tardive dyskinesia when taking atypicals, because tardive dyskinesia can take ... but clinical experience with these newer agents is not as developed as that with the older agents. The mechanism of these ... The atypical anti-psychotic paliperidone was approved by the FDA in late 2006.[citation needed] The atypical antipsychotics ... However, tardive dyskinesia typically develops after long-term (possibly decades) use of antipsychotics. It is not clear if ...
Tardive dyskinesia may be persistent and irreversible in some people. The majority of reports of tardive dyskinesia occur in ... As a perioperative anti-emetic, the effective dose is usually 25 to 50 mg (compared to the usual 10 mg dose). It is also used ... Agents in the benzodiazepine class of drugs may be helpful, but benefits are usually modest and side effects of sedation and ... The FDA required a warning about tardive dyskinesia to be added to the drug label in 1985 stating that: "tardive dyskinesia ...
Each anti-convulsant agent has a unique side-effect profile. Valproic acid can frequently cause sedation or gastrointestinal ... Taking antipsychotics for long periods or at high doses can also cause tardive dyskinesia - a sometimes incurable neurological ... It is generally considered a second-line agent due to its side effect profile. Lamotrigine is considered a first-line agent for ... as in 2003 the American Psychiatric Press noted that atypical anti-psychotics should be used as adjuncts to other anti-manic ...
In the inter-war period, the first anti-bacterial agents such as the sulpha antibiotics were developed. The Second World War ... due to serious adverse effects such as tardive dyskinesia. Patients often opposed psychiatry and refused or stopped taking the ... Anti-fungal: imidazoles, polyenes. Anti-inflammatory: NSAIDs, corticosteroids. Anti-allergy: mast cell inhibitors. Anti- ... These were drugs that worked chiefly as anti-anxiety agents and muscle relaxants. The first benzodiazepine was Librium. Three ...
Tardive dyskinesia: involuntary muscle movements in the lower face and distal extremities; this can be a chronic condition ... Other anti-dopaminergic drugs, like the antiemetic metoclopramide, can also result in extrapyramidal side effects. Short and ... The treatment varies by the type of the EPS, but may involve anticholinergic agents such as procyclidine, benztropine, ... When other measures fail or are not feasible, medications are used to treat tardive dyskinesia. These include the vesicular ...
... anti-nausea and anti-vertigo drugs. Symptoms of akathisia are often described in vague terms such as feeling nervous, uneasy, ... tardive dyskinesia, or other neurological and medical conditions. The controversial diagnosis of "pseudoakathisia" is sometimes ... and descriptions of akathisia predate the existence of pharmacologic agents. Akathisia can be miscoded in side effect reports ... but was more properly classed as dyskinesia.[medical citation needed] The presence and severity of akathisia can be measured ...
... finding is in agreement with the pharmaceutical development of chlorpromazine and other antipsychotics as anti-histamine agents ... Rarely tardive dyskinesia can occur when the medication is stopped. Chlorpromazine is a very effective antagonist of D2 ... Posner, Lysa A.; Burns, Patrick (2009). "Chapter 13: Sedative agents: tranquilizers, alpha-2 agonists, and related agents". In ... It is commonly used to decrease nausea in animals that are too young for other common anti-emetics.[citation needed] It is also ...
It has serious potential side-effects, e.g., tardive dyskinesia. In a study conducted at the RFC,[clarification needed] 25 out ... Haloperidol is frequently used because of its anti-dopaminergic effect. ... and side effects of certain anticonvulsants or psychotropic agents.[citation needed] ... familial dyskinesia-facial myokymia (Bird-Raskind syndrome) due to an ADCY5 gene mutation, glutaric aciduria, Lesch-Nyhan ...
This was followed in the inter-war period by the development of the first anti-bacterial agents such as the sulpha antibiotics ... due to serious adverse effects such as tardive dyskinesia. Patients often opposed psychiatry and refused or stopped taking the ... This was denounced by the anti-psychiatric movement in the 1960s and later. The ABO blood group system was discovered in 1901, ... the use of plants as healing agents, as well as clays and soils is ancient. Over time, through emulation of the behavior of ...
To confirm recent streptococcal infection: Throat culture Anti-DNAse B titre (peaks at 8-12 weeks after infection) Anti- ... Haloperidol used previously but probably more side effects e.g. tardive dyskinesia. Case reports to support carbamazepine and ... phenytoin or psychotropic agents. Although some of these can similarly present in an acute way, there will typically be other ... familial dyskinesia-facial myokymia (Bird-Raskind syndrome) due to an ADCY5 gene mutation, glutaric aciduria, Lesch-Nyhan ...
"Metoclopramide & Tardive Dyskinesia". Tardive Dyskinesia Center. Archived from the original on March 23, 2013. Retrieved March ... "Can anti-depressants cause sexual dysfunction?". WebMD. May 15, 2011. Archived from the original on March 21, 2013. Retrieved ... from vaccines a decade ago the rate of autism has not decreased as would be expected if it had been the causative agent.[40][41 ... Tardive dyskinesia associated with use of metoclopramide and many antipsychotic medications[39] ...
In addition, anti-dopaminergic drugs such as metoclopramide and typical anti-psychotics should be avoided. These interactions ... Amantadine was approved by the U.S. Food and Drug Administration in October 1968, as a prophylactic agent against Asian (H2N2) ... In 2017, the extended release formulation was approved for use in the treatment of levodopa-induced dyskinesia. Off-label uses ... Amantadine, sold under the brand name Gocovri among others, is a medication used to treat dyskinesia associated with ...
Elliott was also the project leader of an anti-stroke agent, PS-519, that completed Phase IIa clinical trials. Support for the ... their ability to modulate the tardive dyskinesias elicited by certain neuroleptics. Subsequently, Dr. Elliott took a post- ... Julian Adams, he co-developed a novel, anti-cancer agent, Velcade (PS-341), currently used to treat multiple myeloma. The ... as head of Pharmacology (1993-1996) where he focused on novel drugs to treat stroke, and also on a permeabilizing agent, RMP-7 ...
... , by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation ( ... tardive dyskinesia, and depression. However, this is not the case with domperidone, because, unlike other D2 receptor ... Furthermore, anti-nausea drugs, such as metoclopramide, which do cross the blood-brain barrier may worsen the extra-pyramidal ... This led to the discovery of domperidone as a strong anti-emetic with minimal central effects. 1978 - On 3 January 1978 ...
Agents. 35 (6): 524-6. doi:10.1016/j.ijantimicag.2009.12.019. PMID 20188526. Amaral, L; Viveiros, M (May 2012). "Why ... As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia (an often permanent neurological ... but chronic use of thioridazine and other anti-psychotics in people with dementia is not recommended. For further information ... Thanacoody, HKR (November 2007). "Thioridazine: resurrection as an antimicrobial agent?". British Journal of Clinical ...
... another drug that has anti-Parkinson effects. DHEC differs in that it is hydrogenated in C9-C10 and lacks bromine in C2. In ... is a dopamine agonist of the ergoline group that is used as an antiparkinson agent in the treatment of Parkinson's disease. It ... a standardized rating scale of Parkinson's Disease symptoms such as gait parameters and dyskinesia. Another clinical study has ... Peripheral oedema Several in vitro and in vivo studies have demonstrated that dihydroergocriptine is an effective anti- ...
Galanolactone, a diterpenoid found in ginger, is a 5-HT3 antagonist and is believed to at least partially mediate the anti- ... Zullino DF, Eap CB, Voirol P (2001). "Ondansetron for tardive dyskinesia". Am J Psychiatry. 158 (4): 657-8. doi:10.1176/appi. ... Pasricha, Pankaj J. (2006). "Treatment of Disorders of Bowel Motility and Water Flux; Antiemetics; Agents Used in Biliary and ... 1991). "Anti-5-hydroxytryptamine3 effect of galanolactone, diterpenoid isolated from ginger". Chem Pharm Bull. 39 (2): 397-9. ...
Several anti-tumor agents such as mitosenes, indolequinones, aziridinylbenzoquinones and β-lapachone have been designed be ... Mutations in this gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to ... rats and humans indicates their importance in detoxifying agent, since their location facilitates exposure to compounds ...
Manufacture and Marketing of the Anti-Epileptic Agent Zonisamide in Asia". Dainippon Pharmaceutical News Releases for 2005. ... In an open-label trial zonisamide attenuated the symptoms of tardive dyskinesia. It has also been studied for obesity with ... Zonisamide is an antiseizure drug chemically classified as a sulfonamide and unrelated to other antiseizure agents. The precise ... Stiff DD, Robicheau JT, Zemaitis MA (January 1992). "Reductive metabolism of the anticonvulsant agent zonisamide, a 1,2- ...
... other xenobiotic DNA damaging agents (such as drugs or chemotherapy) or other DNA damaging agents including reactive oxygen ... Infertility associated with viable, but immotile sperm may be caused by primary ciliary dyskinesia. The sperm must provide the ... adrenal disease Hypothalamic-pituitary factors Hyperprolactinemia Hypopituitarism The presence of anti-thyroid antibodies is ... Environmental factors Toxins such as glues, volatile organic solvents or silicones, physical agents, chemical dusts, and ...
Anti-Parkinsons Agents. Parkinsons patients are especially prone to develop tardive dyskinesia and should use caution when ... Anti-cholinergics. Anti-cholinergics (anti-spasmodics) are class of medications prescribed for respiratory problems such as ... Other medications not included here can also cause tardive dyskinesia.. Neuroleptics. Neuroleptics (anti-psychotics) are ... The anti-malarial drug Chlorquine (brand name: Aralen) can cause tardive dyskinesia. ...
Antiparkinson Agents. Anti-Dyskinesia Agents. Dopamine Agents. Neurotransmitter Agents. Molecular Mechanisms of Pharmacological ... diphasic dyskinesias or end of dose dyskinesias could be included if peak dose dyskinesias were also present. ... The UDysRS is administered to assess dyskinesia. The scoring range is 0-104, where higher score means more dyskinesia. ... A Clinical Study of IRL790 in Patients With Parkinsons Disease Experiencing Levodopa Induced Dyskinesia. The safety and ...
Antiparkinson Agents. Anti-Dyskinesia Agents. Dopamine Agents. Neurotransmitter Agents. Molecular Mechanisms of Pharmacological ... Anti-Infective Agents. Analgesics, Non-Narcotic. Analgesics. Sensory System Agents. Peripheral Nervous System Agents. ... without dyskinesia, ON with non-troublesome dyskinesia, and ON with troublesome dyskinesia. The results were based on 2 ... Dyskinesia Levodopa-Induced Dyskinesia (LID) Parkinsons Disease (PD) Drug: ADS-5102 Other: Placebo Phase 3 ...
Anti-dyskinesia Agents. Drugs used in the treatment of movement disorders. Most of these act centrally on dopaminergic or ... and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (Adams et al., Principles of Neurology, 6th ... If you are a legal copyright holder or a designated agent for such and you believe a post on this website falls outside the ... Tardive Dyskinesia. Drug-related movement disorder characterized by uncontrollable movements in certain muscles. It is ...
Drug reaction to anti-platelet / anticoagulation agents / contrast media; Dyskinesia; Dyspnea; Edema; Emboli (air, thrombus, ... Do not expose instruments to cleaning or rinse agents that are not compatible with polysulfone or polyphenylsulfone. ... Patients who cannot tolerate procedural anticoagulation or post procedural anti-platelet regimen ...
Antiparkinson Agents. Anti-Dyskinesia Agents. Dopamine Agents. Neurotransmitter Agents. Molecular Mechanisms of Pharmacological ...
Antiparkinson Agents. Anti-Dyskinesia Agents. Dopamine Agents. Neurotransmitter Agents. Molecular Mechanisms of Pharmacological ... Their parkinsonian symptoms and dyskinesias are evaluated and videotaped every 30 minutes for about 6 hours. Blood is drawn and ... Patients between 21 and 80 years of age with Parkinsons disease and dyskinesias may be eligible for this study. ... This study will evaluate the effects of the experimental drug talampanel on dyskinesias (involuntary movements) that develop in ...
antidyskinesia agent Any compound which can be used to treat or alleviate the symptoms of dyskinesia. ... procyclidine (CHEBI:8448) has role antidyskinesia agent (CHEBI:66956) procyclidine (CHEBI:8448) has role antiparkinson drug ( ...
antidyskinesia agent Any compound which can be used to treat or alleviate the symptoms of dyskinesia. ... L-dopa (CHEBI:15765) has role antidyskinesia agent (CHEBI:66956) L-dopa (CHEBI:15765) has role antiparkinson drug (CHEBI:48407 ... L-dopa (CHEBI:15765) has role dopaminergic agent (CHEBI:48560) L-dopa (CHEBI:15765) has role hapten (CHEBI:59174) L-dopa (CHEBI ... dopaminergic agent A drug used for its effects on dopamine receptors, on the life cycle of dopamine, or on the survival of ...
There is no known effective treatment for tardive dyskinesia; anti-parkinsonism agents do not alleviate the symptoms of this ... these symptoms are readily controlled when an anti-parkinsonism agent is administered concomitantly. Anti-parkinsonism agents ... Tardive Dyskinesia. As with all antipsychotic agents, tardive dyskinesia may appear in some patients on long-term therapy or ... Tardive Dyskinesia. Tardive dyskinesia, a syndrome consisting of potentially irreversible, involuntary, dyskinetic movements, ...
Anti-Dyskinesia Agents / administration & dosage * Anti-Dyskinesia Agents / pharmacology* * Botulinum Toxins / administration ...
Anti-Dyskinesia Agents / administration & dosage * Anti-Dyskinesia Agents / therapeutic use* * Botulinum Toxins / ...
There is no known effective treatment for tardive dyskinesia; anti-parkinsonism agents do not alleviate the symptoms of this ... Tardive Dyskinesia: As with all antipsychotic agents, tardive dyskinesia may appear in some patients on long-term therapy or ... these symptoms are readily controlled when an anti-parkinsonism agent is administered concomitantly. Anti-parkinsonism agents ... Treatment with anti-parkinsonian agents, benzodiazepines or propranolol may be helpful.. Pseudo-parkinsonism: Symptoms may ...
There is no known effective treatment for tardive dyskinesia; anti-parkinsonism agents do not alleviate the symptoms of this ... Tardive Dyskinesia: As with all antipsychotic agents, tardive dyskinesia may appear in some patients on long-term therapy or ... In most cases these symptoms are readily controlled when an anti-parkinsonism agent is administered concomitantly. Anti- ... Treatment with anti-parkinsonian agents, benzodiazepines or propranolol may be helpful.. Pseudo-Parkinsonism: Symptoms may ...
Theoretically, anti-apoptotic agents would slow this process in neurons. Currently, these types of therapies are being used in ... Amantadine may help reduce Parkinsons-triggered dyskinesia, or involuntary movements.. Apoptosis (programmed cell death) ... Anti-inflammatory agents. These have painkilling properties, but can they also affect the inflammatory processes involved in ... Anti-excitotoxic agents. In theory, blocking the glutamate receptors will prevent excitotoxicity and degeneration. However, ...
0 (Adrenergic Uptake Inhibitors); 0 (Anti-Dyskinesia Agents); 0 (Antipsychotic Agents); 0 (Dopamine Antagonists); 56LH93261Y ( ... Anti-Hipertensivos/farmacologia. Celiprolol/farmacologia. Citocinas/sangue. [Mh] Termos MeSH secund rio:. Animais. Press o ... Anti-Hipertensivos/uso terap utico. Barorreflexo/efeitos dos f rmacos. Bisoprolol/uso terap utico. Press o Sangu nea/efeitos ... Anti-Hipertensivos/farmacologia. Celiprolol/farmacologia. S ndrome de Ehlers-Danlos/tratamento farmacol gico. S ndrome de ...
PD patients develop daily fluctuations in mobility and troublesome involuntary movements known as levodopa-induced dyskinesias ... Future Scenarios for Levodopa-Induced Dyskinesias in Parkinsons Disease ... MPTP-lesioned primates are very useful to test potential antidyskinetic and/or anti-parkinsonian pharmacological agents. ... Maladaptive plasticity in levodopa-induced dyskinesias and tardive dyskinesias: old and new insights on the effects of dopamine ...
These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia. Studies have ... From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, ... If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal ... The term "tardive dyskinesia" first came into use in 1964. Tardive dyskinesia is characterized by repetitive, involuntary ...
Central Nervous System Agents [D27.505.954.427]. *Anti-Dyskinesia Agents [D27.505.954.427.090] ... Agents used in the treatment of Parkinsons disease. The most commonly used drugs act on the dopaminergic system in the ... "Antiparkinson Agents" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "Antiparkinson Agents" by people in Harvard Catalyst Profiles ...
Compare risks and benefits of common medications used for Tardive Dyskinesia. Find the most popular drugs, view ratings, user ... On occasion, if the anti-psychotics are stopped after the tardive dyskinesia has been present for a long period, the condition ... The condition may be reversible, if recognized in the earliest stages, by stopping the causative agent, but may be permanent. ... About Tardive Dyskinesia: Tardive dyskinesia are involuntary movements, especially of the lower face, that develop after ...
Study Anti-Psychotics -- Segars flashcards from Andrew Herrmann ... Typical agent(s) -- dystonia, akathisia, dyskinesia, parkinson- ... Which agents are more likely to block D1 and D4 receptors also?. Which agents are more likely to block 5-HT receptors also? ... Long-acting injectable agents. Typicals = Haloperidol, Fluphenazine. Atypicals = Risperidone, Olanzapine, Aripiprazole, ...
... useful as therapeutic agents in conjunction with classic anti-psychotic agents to prevent the formation of tardive dyskinesia. ... Indeed, it is likely that these compounds will be useful in treating the tardive dyskinesia that classic anti-psychotics may ... they are unlikely to produce the up-regulation of dopamine receptors that is produced by classical anti-psychotic agents. ... tardive dyskinesia, certain forms of schizophrenia and other dystonias and dyskinesias. Dysfunctions of the dopamine-responsive ...
Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS. ... Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING ... AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). ... Neuromuscular Agents: Drugs used for their actions on skeletal muscle. ...
Anticholinergic agents have been used with mixed results in patients with essential tremor, dystonias and certain dyskinesias. ... Either of these anti-cholinergic drugs may be helpful in managing significant tremor early in the course of Parkinsons disease ... dyskinesias have not been observed in patients who have never been exposed to levodopa. The association of dyskinesias with ... This agent is meant to be used as an adjunct to levodopa therapy. Theoretically, it allows levodopa to be administered less ...
Tardive dyskinesia can be precipitated or aggravated by anti-parkinsonian drugs. Short lived dyskinesias may occur after abrupt ... The concomitant use of chlorpromazine with lithium, other QT prolonging agents, and dopaminergic anti-parkinsonism agents is ... The serum concentration of chlorpromazine is increased by anti-malarial agents.. Cimetidine has been reported to both increase ... with fairly marked anti-cholinergic and anti-emetic activity and a moderate tendency to cause extrapyramidal reactions. ...
... and so people using this agent must take an antiemetic agent. In addition, apomorphine can provoke dyskinesias and other side ... Consult a doctor before taking any of the following to avoid possible interactions: alcohol, anti-psychotics, medications that ... With training provided by the PD specialist, people with PD, spouses and family members can be taught to administer the agent, ... In general, dopamine agonists are not as potent as carbidopa/levodopa and may be less likely to cause dyskinesias. ...
It took over fifteen years to recognize the problem of tardive dyskinesia following the introduction of long-term anti- ... Hypnotic agents are administered to many different types of patients, under widely different co~ditio~s, and for varying ... No hypnotic agent has yet been comprehensively studied according to the criteria suggested earlier in this Appendix, which is ... 21/ This may have been related to an anti-anxiety effect upon the untrained subjects. In the same study, however, the diazepam ...
Dopa Induced Dyskinesia. Investigator: Andreas H. Kottmann, PhD Dr. Kottmann is an Associate Professor at the CUNY School of ... Results from the proposed project might possibly open the door for testing Smoothened agonists as anti-dyskinetic agents in ... Interestingly, this mouse line exhibits dyskinesia upon chronic L-Dopa dosing. Conversely, we found that compounds that act as ... Validation of the G-Protein Coupled Receptor Smoothened as a Target for Ameliorating L- Dopa Induced Dyskinesia. ...
This new anti-psychotic agent appears to cause fewer side effects (most importantly with respect to tardive dyskinesia) ... Appendix I: Common Anti-Psychotic Medications. Five different chemical families of anti-psychotic drugs are used in most ... Anti-psychotic drugs stay in the system for six weeks to three months. This "grace" period gives you some time to deal with the ... Tardive dyskinesia is a side effect that may appear after a long period of medication. It consists of involuntary facial ...
... dopamine depleting agents such as tetrabenazine, anti-seizure medications such as valproic acid, or benzodiazepines may help. ... side effects such as tardive dyskinesia are extremely unlikely. As is the case for any neurological medications, however, a ... These medications, also known as anti-psychotics or neuroleptics, are prescribed for conditions such as bipolar disorder, ... When chorea symptoms are disabling, low doses of potent dopamine receptor blocking agents such as haloperidol, ...
  • Anti-cholinergics (anti-spasmodics) are class of medications prescribed for respiratory problems such as COPD, bladder control problems, Parkinson's disease, and other reasons. (brainandspinalcord.org)
  • A Randomised, Double-blind, Placebo-controlled, Phase Ib Study Evaluating the Safety and Tolerability of IRL790 in Patients With Parkinson's Disease (PD) Experiencing Levodopa (L-Dopa) Induced Dyskinesia (LID). (clinicaltrials.gov)
  • This is a multi-center, randomized, double-blind, placebo-controlled, 2-arm, parallel group study to evaluate the efficacy and safety of ADS-5102 extended release (ER) capsules, an investigational formulation of amantadine, dosed once nightly at bedtime for the treatment of levodopa-induced dyskinesia (LID) in subjects with Parkinson's disease (PD). (clinicaltrials.gov)
  • This study will evaluate the effects of the experimental drug talampanel on dyskinesias (involuntary movements) that develop in patients with Parkinson's disease as a result of long-term treatment with levodopa (Sinemet). (clinicaltrials.gov)
  • Patients between 21 and 80 years of age with Parkinson's disease and dyskinesias may be eligible for this study. (clinicaltrials.gov)
  • People with Parkinson's have difficulty moving, whereas people with tardive dyskinesia have difficulty not moving. (wikipedia.org)
  • Agents used in the treatment of Parkinson's disease. (harvard.edu)
  • Despite the therapies targeting dopamine being effective on Parkinson's-related motor disturbances, they produce undesirable side effects, such as dyskinesia and hallucinations. (wikipedia.org)
  • Dopamine replacement therapy in the form of levodopa results in a significant proportion of patients with Parkinson's disease developing debilitating dyskinesia. (frontiersin.org)
  • Long term treatment of Parkinson's disease with levodopa may result in the emergence of motor fluctuations and dyskinesia. (bmj.com)
  • Cheshire, PA & Williams, D 2012, ' Serotonergic involvement in levodopa-induced dyskinesias in Parkinson's disease ', Journal of Clinical Neuroscience , vol. 19, no. 3, pp. 343 - 348. (monash.edu)
  • Preliminary results indicate that it may hold even more promise than the drugs currently used for this disorder, many of which (ironically) have serious neurotoxic side effects, including dyskinesia - a movement disorder identical to the symptoms of Parkinson's disease. (mercola.com)
  • Scanning changes in functional brain activity associated with dyskinesia in parkinsonian rats, Parkinson's Disease Society Innovations grant. (cardiff.ac.uk)
  • The duration of improvement after each dose of drug shortens (" wearing off ")and patients can experience swings from intense akinesia as the symptoms of Parkinson's return to dyskinesia, an involuntary movement that can accompany peak doses of levodopa. (pharmiweb.com)
  • Anti-inflammatory agents may offer a novel approach to the treatment of Parkinson's disease. (pharmiweb.com)
  • A PD home diary was used to score 5 different conditions in 30-minute intervals: ASLEEP, OFF, ON (ie, had adequate control of PD symptoms) without dyskinesia, ON with non-troublesome dyskinesia, and ON with troublesome dyskinesia. (clinicaltrials.gov)
  • Their parkinsonian symptoms and dyskinesias are evaluated and videotaped every 30 minutes for about 6 hours. (clinicaltrials.gov)
  • Any compound which can be used to treat or alleviate the symptoms of dyskinesia. (ebi.ac.uk)
  • The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). (wikipedia.org)
  • While anti-cholinergic agents do not cause or control this syndrome, when given in combination with neuroleptics they may exacerbate the symptoms of tardive dyskinesia or reduce the threshold at which dyskinesias appear in patients predisposed to this abnormality. (medicines.ie)
  • Valdecoxib is a non-steroidal anti-inflammatory drug (NSAID), prescribed for osteoarthritis, rheumatoid arthritis, and painful menstruation and menstrual symptoms. (medindia.net)
  • The presence of these symptoms, which are clinical manifestation of dyskinesia and mucositis respectively [ 3 ], suggests that radiation-induced acute oesophagitis might be associated with altered organ motility. (biomedcentral.com)
  • also went on wellbutrin, to reduce depressive symptoms and to quit smoking, managed to quit smoking but have been having some involuntary tics and I'm worried that it may be permanent or tardive dyskinesia from sero. (medhelp.org)
  • Tardive dyskinesia, a syndrome consisting of potentially irreversible, involuntary, dyskinetic movements, may develop in patients treated with neuroleptic (antipsychotic) drugs. (nih.gov)
  • Although the vast majority respond positively to treatment, a significant proportion of PD patients develop daily fluctuations in mobility and troublesome involuntary movements known as levodopa-induced dyskinesias (LIDs). (frontiersin.org)
  • Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements, which may include grimacing, sticking out the tongue, or smacking the lips. (wikipedia.org)
  • Tardive dyskinesia is characterized by repetitive, involuntary movements. (wikipedia.org)
  • Tardive dyskinesia are involuntary movements, especially of the lower face, that develop after exposure to a group of medications known as neuroleptics. (drugs.com)
  • This phenomenon, termed levodopa-induced dyskinesia (LID), is characterized by involuntary dystonic and/or choreic movements of the trunk, limbs, and face, most commonly when the plasma concentration of DA is high ("peak dose" dyskinesia) ( 5 ). (frontiersin.org)
  • Beyond the multiple phenomenology of LIDs in PD patients, further insights on the pathophysiology of hyperkinetic movement disorders derive from studies conducted in patients with idiopathic dystonia, tardive dyskinesia (TD), and Gilles de la Tourette syndrome (GTS). (frontiersin.org)
  • After advocating for treatment for them, a variety of helpful treatments were found and so far the anti-convulsant Vimpat (remember this is its first usage on tardive dystonia alone outside of the animal model so the question as to whether it wil help others is still tentative but quite promising) has shown the best results. (medhelp.org)
  • 14. (+)-a-dihydrotetrabenazine for use according to any one of claim 7 to 13 wherein the movement disorder is a hyperkinetic movement disorder such as Huntington's disease, hemiballismus, senile chorea, tic disorders, tardive dyskinesia, dystonia, myoclonus and Tourette's syndrome. (sumobrain.com)
  • The following overview of drugs which can cause tardive dyskinesia is by no means exhaustive. (brainandspinalcord.org)
  • Other medications not included here can also cause tardive dyskinesia. (brainandspinalcord.org)
  • they can cause tardive dyskinesia. (brainandspinalcord.org)
  • This may be published in a case study and I have conducted testimony in person and through letter writing and email (which I have recieved correspondence back from many noted provider agencies in support) that new schizophrenia research be prioritized into new classes of antipsychotics such as the NMDA receptor modulates of which glycine is one(which will not cause tardive dyskinesia) be prioritized. (medhelp.org)
  • Are caused by potent dopamine-blocking drugs, which are used for their anti-emetic side effects (Metoclopramide, lesser degree promethazine) and for their antipsychotic properties (typicals like haloperidol, thorazine but also atypicals like risperidone, olanzapine - the only antipsychotics that are not described to cause tardive dyskinesia are quetiapine and clozapine). (clinicaladvisor.com)
  • The longer a person is on a tardive dyskinesia inducing-drug the more likely he or she is to develop tardive dyskinesia. (brainandspinalcord.org)
  • people age sixty and older are especially vulnerable and may develop tardive dyskinesia after only a month on metoclopramide. (brainandspinalcord.org)
  • AIMS Examination": This test is used when psychotropic medications have been prescribed because people sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. (wikipedia.org)
  • Approximately 20 per cent of the patients treated with neuroleptics for long periods develop tardive dyskinesia, a syndrome of choreoathetoid movements of the tongue, mouth, face, neck, limbs, and trunk, which may continue after the drug is stopped. (thefreedictionary.com)
  • Tardive dyskinesia refers to abnormal hyperkinetic movements of the muscles of the face, tongue, and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (bioportfolio.com)
  • The term TD referred to abnormal movements produced by the chronic exposure to dopamine receptor blocking agents. (frontiersin.org)
  • Alternate approaches to dopamine replacement in parkinsonism generally (and to wearing-off and dyskinesia, specifically) are therefore urgently needed. (aspetjournals.org)
  • Several xanthines and non-xanthines are under development as potential anti-parkinsonism agents, which are selective for A2A receptors. (wikipedia.org)
  • Duvoisin, R. C.: The mutual antagonism of cholinergic and anticholinergic agents in Parkinsonism. (springer.com)
  • Drug-induced parkinsonism may result from the use of anti-dopaminergic agents. (capriles-urgencias.com)
  • The term 'tardive' differentiates these dyskinesias from acute dyskinesia, parkinsonism, and akathisia, which appear very soon after exposure to antipsychotic drugs. (uptodate.com)
  • Trihexyphenidyl is an anticholinergic used in the symptomatic treatment of all etiologic groups of parkinsonism and drug induced extrapyramidal reactions (except tardive dyskinesia). (drugbank.ca)
  • Approximately 15% of parkinsonian patients have atypical parkinsonism and do not respond to this agent. (pharmiweb.com)
  • Akathisia is a common and potentially debilitating adverse effect of many psychotropic agents. (healio.com)
  • Antiparkinson Agents" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • Parkinsonian monkeys with prior levodopa-induced dyskinesias followed by fetal dopamine precursor grafts do not display graft-induced dyskinesias. (harvard.edu)
  • The aim of this review is to enumerate and highlight developments that occurred in last few decades and also review the advantages and disadvantages of those anti-parkinsonian therapies in the years to come. (mdpi.com)
  • 2) do not interfere with the anti-parkinsonian activity of levodopa nor produce general motor-suppression, making them particularly for clinical studies in PD patients. (parkinsonalliance.net)
  • In rodent and primate models, KW6002 provides symptomatic relief from parkinsonian motor deficits without provoking dyskinesia or exacerbating existing dyskinesias. (neurology.org)
  • I had a BBSRC CASE award studentship with Prof Peter Jenner and Dr Sharon Cheetham (then Knoll Pharmaceuticals) on the potential of BTS 74398, a monoamine uptake inhibitor, as a possible anti-parkinsonian medication. (cardiff.ac.uk)
  • Among the most important clinically are those used for the treatment of Parkinson disease (ANTIPARKINSON AGENTS) and those for the tardive dyskinesias. (bioportfolio.com)
  • Tardive dyskinesias. (medicines.ie)
  • In a proportion of patients undergoing neuroleptic treatment, tardive dyskinesias will occur. (medicines.ie)
  • This graph shows the total number of publications written about "Antiparkinson Agents" by people in Harvard Catalyst Profiles by year, and whether "Antiparkinson Agents" was a major or minor topic of these publication. (harvard.edu)
  • Below are the most recent publications written about "Antiparkinson Agents" by people in Profiles. (harvard.edu)
  • BACKGROUND: Tardive dyskinesia (TD) is a disabling movement disorder associated with the prolonged use of antipsychotic medication. (bireme.br)
  • Tardive dyskinesia was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs. (wikipedia.org)
  • Since then a large number of agents similar to chlorpromazine have been developed and were used until the mid-1990s, when the 'atypical' antipsychotic agents were introduced. (ddw-online.com)
  • There are other causes such as exposure to heavy metals, such as prolonged exposure to copper and manganese or exposure to pesticides and exposure to antipsychotic drugs like phenothiazines, prochlorperazine, thioridazine, chlorpromazine, haloperidol and anti-vomiting agent metoclopramide. (news-medical.net)
  • 2. Denoting the actions of such an agent (for example, chlorpromazine). (thefreedictionary.com)
  • While tardive dyskinesia has been associated primarily with neuroleptic drugs, other medications can cause this condition, including some medications given for digestive troubles and nasal allergies. (brainandspinalcord.org)
  • Non-antipsychotic catecholaminergic drugs for antipsychotic-induced tardive dyskinesia. (bireme.br)
  • Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder, and as a result, people are prescribed neuroleptic drugs, which increase the probability that the person will develop a severe and disabling case, and shortening the typical survival period. (wikipedia.org)
  • Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). (curehunter.com)
  • Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS. (curehunter.com)
  • In addition, apomorphine can provoke dyskinesias and other side effects associated with dopamine drugs. (parkinson.org)
  • Tardive dyskinesia occurs due to downregulations of dopamine (D2) receptors after long-term exposure to D2-blocking agents such as antipsychotic drugs and metoclopramide. (prsync.com)
  • New approaches to enhance and restore the activity of glutamatergic neurotransmission may lead to the next generation of anti-psychotic drugs. (ddw-online.com)
  • Anti-epileptic drugs (AEDs) are the main form of treatment for people with epilepsy. (psychiatricdrugs.net)
  • Tardive dyskinesia (TD) is a hyperkinetic movement disorder that appears with a delayed onset after prolonged use of dopamine receptor blocking agents, mainly the antipsychotic drugs (also called neuroleptics) and the antiemetic drug, metoclopramide [ 1,2 ]. (uptodate.com)
  • these drugs are administered orally as anti-emetics and appetite stimulants for patients with AIDS or on chemotherapy. (bmj.com)
  • Depakote belongs to a group of drugs called anticonvulsants or anti-epileptic drugs. (faintpower.tk)
  • The value in 2004 of the world market for anti-cholesterol drugs was worth over $25 billion, making this drug class the most successful therapeutic area in the world. (pharmiweb.com)
  • medications made the news, when the FDA announced that metoclopramide would be required to carry a "black box" label warning of the risk of tardive dyskinesia with long term use. (brainandspinalcord.org)
  • Tardive dyskinesia occurs in some people as a result of long-term use of dopamine-receptor-blocking medications such as antipsychotics and metoclopramide. (wikipedia.org)
  • Antipsychotic medications taken for psychiatric conditions like Schizophrenia or anti-nausea agents like Metoclopramide may lead to these movement disorders. (news-medical.net)
  • In some cases, people taking atypical neuroleptics have developed tardive dyskinesia. (brainandspinalcord.org)
  • Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia. (wikipedia.org)
  • L-DOPA and graft-induced dyskinesia : different treatment, same story? (lu.se)
  • On the basis of the results from the NIMH-funded Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE), this article reviews the principles of antipsychotic therapy selection based on individual patient profiles as it pertains to perphenazine (the representative typical anti-psychotic in the CATIE study), olanzapine, risperidone, quetiapine, ziprasidone, and clozapine. (psychiatrictimes.com)
  • In general, typical antipsychotics have a greater propensity to cause extrapyramidal side effects, tardive dyskinesia, and prolactin elevations than do atypical anti-psychotics. (psychiatrictimes.com)
  • The atypical agents led to a breakthrough in managing patients as they have significantly improved efficacy and side-effect profiles. (ddw-online.com)
  • Schizophrenia is currently the second largest CNS market behind depression and has surpassed epilepsy during the late 1990s based on the success of the atypical type agents. (ddw-online.com)
  • Therefore, these findings suggest that the DAT is an important pharmacological target in the study and treatment of L-dopa induced dyskinesia. (ubc.ca)
  • A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. (drugcentral.org)
  • Effect of active tannoid principles of E. officinalis, comprising of emblicanin A (37%), emblicanin B (33%), punigluconin (12%) and pedunculagin (14%), was investigated on a rat model of tardive dyskinesia (TD) induced by once daily administration of haloperidol (1.5 mg/kg, ip) for 28 days. (bvsalud.org)
  • Pimozide also has less potential for inducing sedation and hypotension as it has more specific dopamine receptor blocking activity than other neuroleptic agents (and is therefore a suitable alternative to haloperidol). (drugbank.ca)
  • The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. (wikipedia.org)
  • The severity of dyskinesias is inversely correlated to the glutamate levels in the denervated striatum. (parkinsonalliance.net)
  • The drug will be tested alone and in combination with amantadine-a drug commonly used to alleviate dyskinesias. (clinicaltrials.gov)
  • Catechol- O -methyltransferase and monoamine oxidase inhibitors are currently used to alleviate wearing-off, but they do not increase "on-time" without exacerbating dyskinesia. (aspetjournals.org)
  • Delusions and hallucinations are often modified and may be eliminated by such an agent, but once the drug is discontinued, the delusions and hallucinations often return within a short while. (thefreedictionary.com)
  • Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). (fpnotebook.com)
  • Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. (bioportfolio.com)
  • The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from tardive dyskinesia in preference to tricyclic antidepressants, which aggravate this condition. (bioportfolio.com)
  • They found that PD patients with dyskinesias display an immediate hypersensitivity of the SMA and putamen to levodopa. (frontiersin.org)
  • Moreover, abnormal resting-state functional connectivity between the IFC and the putamen was demonstrated in PD patients with LID at 60 min after levodopa intake, consistent with the expected time peaks of dyskinesia ( 7 ). (frontiersin.org)
  • Although most patients respond positively to l -DOPA treatment, after ~4-6 years of l -DOPA therapy, a significant proportion of patients (~40%) exhibit a decline in the therapeutic efficacy of l -DOPA and develop debilitating dyskinesias ( 5 ). (frontiersin.org)
  • Kemadrin may be combined with levodopa or amantadine in patients who are inadequately controlled on a single agent. (medicines.ie)
  • Valbenazine is a vesicular monoamine transporter 2 inhibitor, prescribed to treat a nervous system disorder symptom called tardive dyskinesia in adult patients. (medindia.net)
  • receptors) for the treatment of levodopa-induced dyskinesias, which are complications experienced by the majority of PD patients as consequence of their long-term use of levodopa. (parkinsonalliance.net)
  • Irving Kirsch, PhD - Careful analysis of the role of the "active placebo" in available clinical trials (38 trials including 3,000 patients) on antidepressants reveals that the placebo effect is the driving force behind these agents (75% of the treatment effect). (madinamerica.com)
  • The most successful agent to date, Zyprexa™ (Olanzapine) developed and marketed by Lilly, rapidly became a blockbuster in the management of schizophrenia and has created a global market that reached $4.8 billion annually in the past year. (ddw-online.com)
  • Prochlorperazine Maleate is classified as an anti-emetic and antipsychotic agent. (nih.gov)
  • I can say for myself that after having made a full recovery from schizoaffective disorder with glycine a novel antipsychotic agent in Phase II FDA study (the antipsychotic agent was tried because I have advanced tardive dyskinesia and could not tolerate Clozaril) it was found that I had a secondary series of psychosis and dysmentia that were neurological. (medhelp.org)
  • Specialising in neuropharmacology options and spending an industrial year at Knoll Pharmaceuticals working on the pharmacology of the anti-obesity agent sibutramine. (cardiff.ac.uk)
  • In general, dopamine agonists are not as potent as carbidopa/levodopa and may be less likely to cause dyskinesias. (parkinson.org)
  • Conversely, we found that compounds that act as agonists of the Shh co- receptor Smoothened can ameliorate the formation and display of L-Dopa induced dyskinesia (LID) in mice. (apdaparkinson.org)
  • Results from the proposed project might possibly open the door for testing Smoothened agonists as anti-dyskinetic agents in clinical trials. (apdaparkinson.org)
  • To identify the PPAR receptor subtypes responsible for the anti-dyskinetic effects of FAAH inhibitors and evaluate the efficacy of selective PPAR agonists as anti-dyskinetic agents. (parkinsonalliance.net)
  • Here, we review the evidence for serotonergic involvement in dyskinesias from animal and human data, and highlight some of the translational gaps which may explain why the success of serotonin autoreceptor agonists as anti-dyskinetic agents in experimental models has failed to be replicated in clinical trials. (monash.edu)
  • or = 14 days, and, aside from the prescribed study medications, discontinued treatment with all analgesics, anti-inflammatory agents, and skeletal muscle relaxants during the study period. (curehunter.com)
  • Vildagliptin is an oral antidiabetic agent, prescribed for type 2 diabetes mellitus along with other medications. (medindia.net)
  • convincing cases have not occurred after the chronic use of antidepressants or anti-anxiety medications [ 1,2 ]. (uptodate.com)
  • We compared the use of catecholaminergic interventions versus placebo, no intervention, or any other intervention for the treatment of antipsychotic-induced tardive dyskinesia. (bireme.br)
  • And the effect of anti-depressants, which was the basis for proposing the chemical-imbalance theory in the first place, turns out to be largely a placebo effect. (madinamerica.com)
  • The change from baseline to day 28 of treatment (Visit 4) in the sum of the items comprising the Unified Dyskinesia Rating Scale (UDysRS). (clinicaltrials.gov)
  • The UDysRS is administered to assess dyskinesia. (clinicaltrials.gov)
  • People over age sixty-five are more likely to develop drug-induced tardive dyskinesia than younger people are. (brainandspinalcord.org)
  • the wide-spread use of this medication means that more people are now at risk for drug-induced tardive dyskinesia. (brainandspinalcord.org)
  • Selective A2A receptor antagonists have shown to be beneficial for enhancing the therapeutic effects of L-DOPA and reducing dyskinesia from long-term L-DOPA treatment. (wikipedia.org)
  • The global tardive dyskinesia treatment market 2019-2023 is expected to post a CAGR of more than 4% during the forecast period, according to the latest market research report by Technavio. (prsync.com)
  • Botulinum toxin (BoNT) is an acetylcholine release inhibitor and a neuromuscular blocking agent used for the treatment of a variety of neurologic and medical conditions. (nih.gov)
  • Levodopa-induced dyskinesias (LID) represent a substantial barrier to effective symptomatic management of Parkinson s disease, but current treatment options for this debilitating side effect are limited, despite an increasing understanding of their pathophysiology from animal models. (monash.edu)
  • See 'Tardive dyskinesia: Clinical features and diagnosis' and 'Tardive dyskinesia: Prevention and treatment' . (uptodate.com)
  • However, following long-term chronic treatment, the therapeutic effects of L-dopa are often accompanied by debilitating peak-dose dyskinesia. (ubc.ca)
  • The results from these experiments lend support to our hypothesis that reversal of the DAT through chronic L-dopa treatment contributes to the pathogenesis of L-dopa induced dyskinesia. (ubc.ca)
  • Vincristine is a chemotherapy agent, prescribed for certain types of cancer such as leukemia, Hodgkin disease, and non-Hodgkin lymphomas. (medindia.net)
  • Nasal MCC was measured in 50 children (CF, primary ciliary dyskinesia (PCD) and no respiratory disease). (ersjournals.com)
  • The development of neuroprotective agents that slow the gradual loss of dopamine neurons represents an alternate approach that is attracting much attention (for a general insight into neurodegenerative disease treatments and markets see World Neurodegeneratives Disease Markets, 2005-2009 ). (pharmiweb.com)
  • Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES. (fpnotebook.com)
  • 6-Thioguanosine shows potential as an anti-anthrax therapeutic agent. (faintpower.tk)
  • In this article, we review the literature on selective and nonselective DAT inhibitors, their antiparkinsonian effect as monotherapy, and their effects on on-time and dyskinesia as adjunct therapy. (aspetjournals.org)
  • Which agents are more likely to block D1 and D4 receptors also? (brainscape.com)
  • Broad reviews from 2006 have been focusing on adenosine receptors as therapeutic targets, adenosine receptor antagonists as potential therapeutics, antagonist for A2A-receptors, adenosine receptor ligands as anti-inflammatories and many more. (wikipedia.org)
  • WIN exerts its anti-dyskinetic effects not only via activation of CB1 receptors, but also by desensitizing TRPV1 receptors and reversing levodopa-induced PKA over-activity in the striatum of dyskinetic rats. (parkinsonalliance.net)
  • Experiments with dopamine D 2 receptor knockout mice showed that A 2A receptors can function and anti-PD activities of A 2A antagonists can occur independent of the dopaminergic system. (neurology.org)
  • 6 ) investigated brain functional activity of LIDs during a motor task, continuously for 45 min after levodopa intake before the beginning of peak-dose dyskinesias. (frontiersin.org)
  • Scientists hope to find neuroprotective agents that will protect against nerve damage. (medicalnewstoday.com)
  • SELECTION CRITERIA: We selected studies if they were randomised controlled trials focusing on people with schizophrenia or other chronic mental illnesses and antipsychotic-induced tardive dyskinesia. (bireme.br)
  • Interestingly, this mouse line exhibits dyskinesia upon chronic L-Dopa dosing. (apdaparkinson.org)
  • Unfortunately, chronic l -DOPA administration is marred by the emergence of dyskinesia and wearing-off. (aspetjournals.org)
  • Levodopa-induced dyskinesias (LID) can be modeled via chronic administration of levodopa to rats with unilateral denervation of the nigrostriatal pathway produced by the neurotoxin 6-OHDA. (parkinsonalliance.net)
  • He highlights risks such as tardive dyskinesia, akathesia, and more subtle risk factors that accumulate over time that he terms: "medication spellbinding", affective volatility, and chronic brain impairment. (madinamerica.com)
  • Apomorphine may cause severe nausea, and so people using this agent must take an antiemetic agent. (parkinson.org)
  • Blockade of dopaminergic transmission in various areas is thought to be responsible for the major antipsychotic, antiemetic effects of these agents as well as neurologic side effects. (thefreedictionary.com)
  • Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. (wikipedia.org)
  • Curcumin is capable of crossing the blood-brain barrier, which is one reason why it holds promise as a neuroprotective agent in a wide range of neurological disorders. (mercola.com)