Disease relevance of Psychomotor Agitation

• Parkinsonism, tardive dyskinesia, akathisia, and depression induced by flunarizine [1].
• One woman presented with severe symptoms and 20 months after stopping flunarizine she still had dyskinesia and akathisia [1].
• Treatment-emergent adverse events occurring significantly more frequently during olanzapine treatment were somnolence, dry mouth, increased appetite, weight gain, akathisia, and high alanine aminotransferase levels; those for divalproex were nausea and nervousness [2].
• One patient who suffered from akathisia and drug-induced parkinsonism experienced significant attenuation of both movement disorders in response to treatment with amantadine [3].
• We challenged five patients suffering from tardive akathisia (TA) with intravenous benztropine (2 mg), propranolol (1 mg) and placebo (saline) using a random, double-blind cross-over design to examine the effects of the drugs on the subjective, objective and global manifestations of neuroleptic-induced akathisia [4].

Psychiatry related information on Psychomotor Agitation

• Five patients receiving fluoxetine for the treatment of obsessive compulsive disorder or major depression developed akathisia [5].
• CONCLUSION: Oral quetiapine was as efficacious as intramuscular haloperidol in preventing symptom exacerbation over 48 weeks in patients with schizophrenia or schizoaffective disorder, with fewer extrapyramidal symptoms, especially rigidity and akathisia [6].
• Treatment of psychomotor agitation and self-injurious behavior with estrogen and progesterone in a patient with Sanfilippo syndrome [7].
• Changes in psychopathology correlated significantly with changes in subjective measures of akathisia after benztropine and with subjective and objective measures of akathisia after propranolol [8].
• His medical history included chronic paranoid schizophrenia, obsessive-compulsive disorder, major depressive disorder, obstructive sleep apnea, and akathisia [9].

High impact information on Psychomotor Agitation

• Akathisia from prochlorperazine [10].
• Neuroleptic-induced akathisia and dystonia triggered by alcohol [11].
• Parkinsonism, tardive dyskinesia, akathisia, and depression induced by flunarizine [12].
• Propranolol for akathisia [13].
• Acute akathisia after oral droperidol and metoclopramide preoperative medication [14].

Chemical compound and disease context of Psychomotor Agitation

• Akathisia and metoclopramide [15].
• Akathisia with haloperidol could not be suppressed completely in half of the patients [16].
• Fluoxetine, akathisia, and suicidality: is there a causal connection [17]?
• We studied the incidence of akathisia in two populations of newly admitted schizophrenic patients: one group was treated with haloperidol and the other group was treated with thiothixene hydrochloride [16].
• Diltiazem and akathisia [18].

Biological context of Psychomotor Agitation

• Prevention of metoclopramide-induced akathisia during gastric emptying imaging [19].
• (1987a, 1987b) that haloperidol increases "emotional" defecation in rats in well-habituated environments, but the same model does not replicate the motor component of neuroleptic-induced akathisia seen in human subjects [20].
• Metoclopramide-induced akathisia during the second trimester of a 37-year-old woman's first pregnancy [21].
• It also caused a lower frequency of akathisia than fluoxetine, more stable blood levels over years than sertraline, very low drug interactions, and a low onset of anxiety if using a 5-mg starting dose [22].

Anatomical context of Psychomotor Agitation

• Beta 2-receptor density on mononuclear blood cells in patients suffering from neuroleptic-induced akathisia (NIA) [23].
• The akathisia was transient and occurred only when [11C]SCH 23390 binding in the basal ganglia was at a high level with a central D1-dopamine receptor occupancy of 45-59% [24].

Gene context of Psychomotor Agitation

• In the presented case fluvoxamine-induced akathisia in an OCD patient was partially resistant to the anticholinergic agent biperiden, and was successfully treated with the 5-HT2A/5-HT2C antagonist mianserin [25].
• It seems that the 5-HT1A partial agonist buspirone is of limited value in the treatment of acute neuroleptic-induced akathisia [26].
• Motor restlessness in ADHD has common features with neuroleptic-induced akathisia [27].
• CONCLUSIONS: The lack of difference between propranolol and betaxolol suggests that beta 1-adrenoceptor blockade is sufficient to improve neuroleptic-induced akathisia [28].
• OBJECTIVE: Beta-blocking agents, particularly propranolol, are considered effective in the treatment of neuroleptic-induced akathisia, but considerable controversy exists about the involved receptor subtype(s) [28].

Analytical, diagnostic and therapeutic context of Psychomotor Agitation

• This report suggests that akathisia is frequently unrecognized in chemotherapy patients receiving metoclopramide and prochlorperazine [29].
• Twelve patients with neuroleptic-induced akathisia were treated in a randomised, double-blind, cross-over design with propranolol and matching placebo [30].
• All three patients developed severe akathisia during retreatment with fluoxetine and stated that the development of the akathisia made them feel suicidal and that it had precipitated their prior suicide attempts [31].
• To assess the role of beta-blockade versus membrane stabilization or other shared nonspecific effects in the therapeutic action of propranolol in neuroleptic-induced akathisia (NIA) we treated 11 patients with NIA in a crossover, double-blind study of d-propranolol versus placebo [32].
• Akathisia associated with droperidol during epidural anesthesia [33].

References