1/17. buspirone as an antidote to SSRI-induced bruxism in 4 cases.BACKGROUND: One hypothesis to explain selective serotonin reuptake inhibitor (SSRI)-induced bruxism states that SSRIs increase extrapyramidal serotonin levels, thereby inhibiting dopaminergic pathways controlling movement. Previous reports have emphasized buspirone's postsynaptic dopaminergic effect as a partial antidote to the suppressed dopamine levels. case reports: Four patients, recently started on treatment with the SSRI sertraline, presented with new-onset complaints attributable to SSRI-induced bruxism. All 4 responded to adjunctive buspirone, a serotonin-1A (5-HT1A) receptor agonist, with relief of bruxism and associated symptoms. DISCUSSION: We expand the hypothesis put forth in previous reports by proposing that buspirone is not only acting postsynaptically in the extrapyramidal system, but also presynaptically on serotonergic neurons that influence masticatory modulation in the mesocortical tract. Our 4 cases support the concept of buspirone acting as a full agonist at the presynaptic 5-HT1A somatodendritic receptors located on the cell bodies of raphe serotonergic neurons that project to the ventral tegmental area (VTA) of the midbrain. These serotonergic neurons modulate the firing of the mesocortical tract, which itself projects from the VTA to the prefrontal cortex and acts on masticatory muscle activity through inhibiting spontaneous movements such as bruxism. While the literature is confusing and contradictory on definitions of bruxism and etiologies of incompletely understood movement disorders, we believe SSRI-induced bruxism is best conceptualized as a form of akathisia.- - - - - - - - - - ranking = 1keywords = state (Clic here for more details about this article) |
2/17. Paradoxical lithium neurotoxicity: a report of five cases and a hypothesis about risk for neurotoxicity.There have been many reports of probable lithium-induced organic brain syndromes occurring when serum lithium levels are within or close to the therapeutic range. The authors report on five patients who developed clinical syndromes suggestive of severe neurotoxicity during lithium treatment. In all cases lithium levels were between .75 and 1.7 mEq/liter. The patients who developed neurotoxicity had markedly higher global ratings of psychotic symptomatology and anxiety in the pretoxic period than did patients who never deveoped neurotoxicity. When the acute manic state is characterized by marked psychotic symptoms and intense anxiety, it may be associated with increased vulnerability to the development of severe lithium neurotoxicity.- - - - - - - - - - ranking = 15854.688304046keywords = anxiety, state (Clic here for more details about this article) |
3/17. Extrapyramidal side effects of antiemetics presenting as psychiatric illness.Although extrapyramidal side effects of two commonly used antiemetics, metoclopramide and prochlorperazine, are well known, it may be difficult for even the experienced practitioner to distinguish some of these extrapyramidal reactions from such psychiatric symptoms as anxiety, depression, or catatonia. Certain patient groups have increased susceptibility to these extrapyramidal reactions, including patients under 30, those with AIDS, those with renal disease, oncology patients, and possibly women. physicians should maintain a high index of suspicion for depression, anxiety, or catatonia if their patients are taking antiemetics. These symptoms may be extrapyramidal side effects of the antiemetic rather than indications of a primary mental disorder.- - - - - - - - - - ranking = 15853.688304046keywords = anxiety (Clic here for more details about this article) |
4/17. Persistent tardive rebound panic disorder, rebound anxiety and insomnia following paroxetine withdrawal: a review of rebound-withdrawal phenomena.OBJECTIVE: To describe tardive rebound anxiety phenomena (panic, anxiety and insomnia) following abrupt paroxetine discontinuation. METHOD: Case report, with comprehensive literature review on rebound and withdrawal phenomena associated with psychotropic medications. RESULTS: Three different discontinuation syndromes with psychotropics are described: (1) new-onset CNS-depressant type withdrawal symptoms (minor and major); (2) rebound syndromes; and (3) supersensitivity symptoms. Abrupt paroxetine discontinuation has been well described and fits the first category. Tardive rebound panic disorder-phenomena with paroxetine has some features of the supersensitivity category. CONCLUSION: Chronic paroxetine treatment may lead to 5-HT2-receptor down regulation, with desensitization of 5-HT1A and 5-HT2 receptors, which may contribute to tardive rebound symptoms upon abrupt withdrawal. Early reports suggest that genetic factors may also contribute to withdrawal symptoms in susceptible individuals. Cholinergic rebound may also occur and could explain tardive insomnia and anxiety in paroxetine withdrawal.- - - - - - - - - - ranking = 55487.909064161keywords = anxiety (Clic here for more details about this article) |
5/17. Reexposure to fluoxetine after serious suicide attempts by three patients: the role of akathisia.Considerable controversy exists regarding the relationship between fluoxetine and the emergence of suicidal ideation. Three cases are presented of patients who were reexposed to fluoxetine after having previously made a serious suicide attempt during fluoxetine treatment. 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. The akathisia and suicidal thinking abated upon the discontinuation of the fluoxetine or the addition of propranolol. The emergence of suicidal ideation during treatment with fluoxetine may be secondary to the development of akathisia. Gradual increments of fluoxetine dose and the prompt recognition and treatment of akathisia may reduce further the rare occurrence of suicidal ideation during fluoxetine treatment.- - - - - - - - - - ranking = 1keywords = state (Clic here for more details about this article) |
6/17. Adrenocortical suppression presenting with agitated depression, morbid jealousy, and a dementia-like state.A 66-year-old woman showed profound neuropsychiatric disturbance after withdrawal from prolonged corticosteroid treatment. Reintroduction of an alternative corticosteroid, at low dose, produced a return to premorbid mental state.- - - - - - - - - - ranking = 5keywords = state (Clic here for more details about this article) |
7/17. Treatment of tardive akathisia with clonidine.Two cases of tardive akathisia, which were misdiagnosed as anxiety originating from a schizophrenic disorder, had been treated with anxiolytics in addition to neuroleptics and anticholinergics. The diagnoses were changed to tardive akathisia, the anticholinergics were discontinued, and the patients were treated with clonidine successfully. In view of the similar effects of clonidine and anticholinergics, the pathophysiology of tardive akathisia must be very similar to that of tardive dyskinesia.- - - - - - - - - - ranking = 7926.844152023keywords = anxiety (Clic here for more details about this article) |
8/17. Akathisia. When treatment creates a problem.1. Akathisia is a state of restlessness and motor agitation, which includes subjective feelings of inner tension, emotional unease, anxiety, a constant need to move, restless motor activity, and an inability to tolerate inactivity or rest. 2. Akathisia is often unrecognized or misdiagnosed as agitation or anxiety of psychiatric origin; this often leads to inappropriate increases in the antipsychotic dosage, which then potentiates its severity, or to the misuse of antianxiety agents, which masks symptoms. 3. Akathisia can be easy to recognize by simple clinical observation of the patient's behaviors, especially if the symptoms worsen after increases in antipsychotic dosages or the frequent use of as needed medications. Assessment must also include the patient's own report.- - - - - - - - - - ranking = 23781.532456069keywords = anxiety, state (Clic here for more details about this article) |
9/17. midazolam-induced benzodiazepine withdrawal syndrome.A case history of a patient who developed severe anxiety and agitation on two occasions after discontinuation of a midazolam infusion is presented. The withdrawal symptoms interfered with effective mechanical ventilation and the patient required the reintroduction of a long-acting benzodiazepine to treat the withdrawal state and to facilitate weaning from mechanical ventilation.- - - - - - - - - - ranking = 7927.844152023keywords = anxiety, state (Clic here for more details about this article) |
10/17. fluoxetine-induced akathisia: clinical and theoretical implications.Five patients receiving fluoxetine for the treatment of obsessive compulsive disorder or major depression developed akathisia. The typical fluoxetine-induced symptoms of restlessness, constant pacing, purposeless movements of the feet and legs, and marked anxiety were indistinguishable from those of neuroleptic-induced akathisia. Three patients who had experienced neuroleptic-induced akathisia in the past reported that the symptoms of fluoxetine-induced akathisia were identical, although somewhat milder. Akathisia appeared to be a common side effect of fluoxetine and generally responded well to treatment with the beta-adrenergic antagonist propranolol, dose reduction, or both. The authors suggest that fluoxetine-induced akathisia may be caused by serotonergically mediated inhibition of dopaminergic neurotransmission and that the pathophysiology of fluoxetine-induced akathisia and tricyclic antidepressant-induced "jitteriness" may be identical.- - - - - - - - - - ranking = 7926.844152023keywords = anxiety (Clic here for more details about this article) |
| | Next -> |