Emergence Of Manic Symptoms Research Articles

Glutamatergic Correlates of Bipolar Symptoms in Adolescents.

Objectives: Prior studies demonstrate elevated cortical glutamate (Glu) in patients with bipolar disorder (BD). Studies assessing neurochemistry in early stages of bipolar illness before the emergence of manic symptoms are lacking. This study aimed to examine neurochemical correlates measured by proton magnetic resonance spectroscopy (1H-MRS) and a dimensional measure of bipolarity in a sample of depressed adolescents. Methods: Adolescent participants (aged 13-21 years) underwent a semistructured diagnostic interview and clinical assessment, which included the General Behavior Inventory Parent Version (P-GBI), a 73-item, parent-rated assessment of symptoms and behaviors. 1H-MRS scans of a left dorsolateral prefrontal cortex (L-DLPFC) voxel (8 cm3) were collected using a two-dimensional J-averaged sequence to assess N-acetylaspartate (NAA), Glu, Glx (glutamate + glutamine), and NAA/Glx concentrations. We used generalized linear models to assess the relationships between P-GBI scores and metabolite levels in L-DLPFC. Results: Thirty-six participants (17 healthy controls, 19 depressed) underwent 1H-MRS scans and clinical evaluation with the P-GBI. There was a significant negative relationship between P-GBI score and L-DLPFC NAA/Glx in the whole sample. However, the magnitude of the effect was small and statistical significance was lost after correcting for multiple comparisons. Conclusions: These preliminary results suggest that NAA/Glx may have utility as a marker of bipolar traits in healthy and depressed adolescents. If replicated, 1H-MRS measures of glutamatergic metabolism anomalies might have a role in identifying depressed adolescents at risk for mixed symptom presentations or BD. Identifying bipolarity in the early stages of the disease would have a significant impact on treatment planning and prognosis. Further longitudinal studies should examine neurochemical correlates of mood state during the developmental emergence of BD.

Maintenance Antipsychotic Lowers Risk of Psychotic Depression Relapse

Maintenance Antipsychotic Lowers Risk of Psychotic Depression Relapse

New-Onset Vascular Mania in a Patient With Chronic Depression

New-Onset Vascular Mania in a Patient With Chronic Depression

Aripiprazole-Induced Movement Disorder

Back to table of contents Previous article Next article Letter to the EditorFull AccessAripiprazole-Induced Movement DisorderJENNIFER L. ZACHER, Pharm.D., , and A. DANIEL HATCHETT, M.D., JENNIFER L. ZACHERSearch for more papers by this author, Pharm.D., Bolingbrook, Ill., and A. DANIEL HATCHETTSearch for more papers by this author, M.D., Brecksville, OhioPublished Online:1 Jan 2006https://doi.org/10.1176/appi.ajp.163.1.160-aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Aripiprazole is a dopamine D2 partial receptor agonist (1). Trials have shown rates of extrapyramidal side effects similar to those of placebo administration, as seen with other atypical antipsychotic agents (1). Some case reports have found that atypical antipsychotics may even be helpful in treating tardive dyskinesia (2, 3). Although the occurrence of extrapyramidal symptoms seems to be less frequent with atypical antipsychotics, it is important to note that these effects can still occur. To our knowledge, only one case of aripiprazole-associated dyskinesia has been reported (4). We report a case of pseudoparkinsonism and rabbit syndrome that occurred in an antipsychotic-naive patient during treatment with aripiprazole.Ms. A was a 27-year-old woman diagnosed with bipolar I disorder. Before she received care through our clinic, her condition was maintained with 150 mg/day of extended-release bupropion, 100 mg/day of lamotrigine, and 75 mg/day of extended-release venlafaxine. She had an emergence of manic symptoms and was administered aripiprazole, 10 mg/day. Ms. A had never been treated with an antipsychotic in the past. One month later, her dose of aripiprazole was increased to 20 mg/day. During the course of the next month, she was tapered from lamotrigine and venlafaxine to consolidate her drug regimen. She was seen for follow-up, where she complained of muscle stiffness and tongue movements that had grown increasingly worse over the last 2 months. She was observed by her outpatient psychiatrist to have muscle rigidity, a masked face, a shuffling gait, and orofacial movements consistent with rabbit syndrome.It was decided to taper the aripiprazole and start ziprasidone, 60 mg b.i.d., along with benztropine, 1 mg b.i.d. Ms. A was seen 5 days later with a marked improvement in symptoms. She had no orofacial movements, decreased muscle rigidity, and only a slight tremor. At this visit, aripiprazole was completely stopped, and ziprasidone was increased to 80 mg b.i.d. Two weeks later, Ms. A was seen with no muscle rigidity or orofacial movements. Benztropine was discontinued, and her condition was maintained with ziprasidone without any reemergence of symptoms. When we evaluated these events with the probability scale of Naranjo et al., the case was ranked as a probable adverse drug reaction (5).This case illustrates that the risk of developing extrapyramidal symptoms is still present, even with the newest of atypical antipsychotics. Clinicians should vigilantly monitor all patients for the emergence of symptoms, regardless of which antipsychotic a patient is receiving.

Association between flupenthixol treatment and emergence of manic symptoms

Background. Flupenthixol is an antipsychotic drug with known mood-elevating properties. Its propensity to induce manic symptoms has not been investigated. Methods and results. We describe six patients, four with schizophrenia and two with bipolar disorder, in whom flupenthixol treatment was associated with emergence of manic symptoms. Conclusions. Patients treated with flupenthixol should be carefully monitored for the emergence of manic symptoms.