[The cognitive point of view in psychodynamic psychotherapy: mentalization-based treatment].

Mentalization, the capacity to understand the mental state of oneself and others which underlies overt behaviour, is a developmental achievement through the context of attachment relationship during infancy and childhood. Mentalization based treatment (MBT) is a psychotherapy that promote the further development of mentalizing. MBT for borderline personality disorder (BPD), developed and manualised by Peter Fonagy and Anthony Bateman, is well-known. According to them, vulnerability to a loss in mentalizing particularly in interpersonal or stressful circumstances is a core feature of BPD. For these patients, traditional psychotherapy would produce iatrogenic harms rather than some improvements. To avoid those iatrogenic effects, MBT therapist takes the stance of "not-knowing". Therapist stimulates the patient's mentalizing, and makes the patient have some inquisitiveness about the mental states of oneself and others. For this purpose, the triad of "event-belief-affect" is explored. At first, the problematic act of the patient is detected. Secondly, rewinding to the time when that problematic act has arisen, the therapist collaborate with the patient to identify the event that provokes the failure of mentalization, and to clarify the affect of patient at the moment. Thirdly, to gain alternative perspectives, that situation is explored through the emotional context. Finally, the specific maladaptive belief which causes a disruption of mentalizing is identified. When the same pattern of mentalizing failure is occurred in the process of the therapy, it was brought up in the "here and now" relationship between the patient and therapist. As seen above, MBT, which explores the relationship between affect and belief, has some technical features similar to cognitive behaviour therapy, which explores the relationship between maladaptive schema and dysfunctional cognition or problematic feeling. However, to the extent of focusing on the "here and now" relationship between patient and therapist, and of placing an emphasis on the context of transference, MBT is still psychodynamic psychotherapy.

A bipotent neural progenitor cell line cloned from a cerebellum of an adult p53-deficient mouse generates both neurons and oligodendrocytes.

Here we report developmental characteristics of a clonal cell line 2Y-3t established from a multifocal neoplasm that arose in a cerebellum of an adult p53-deficient mouse. The tumorigenicity of the line was not observed in soft agar assay or in nude mouse assay. In serum-containing medium, 2Y-3t cells were epithelial-like in morphology and were mitotic. When they were cultured in serum-free medium, the expressions of neural stem and/or progenitor cell markers were decreased. Concomitantly, the expressions of neuronal and oligodendrocyte markers were increased in concert with morphological differentiation, and DNA synthesis ceased. None of astrocyte markers were detected under these culture conditions. Double-labelling studies revealed that two cell populations coexisted, expressing neuronal or oligodendrocyte markers. Triiodothyronine (T3) increased the oligodendrocyte population when 2Y-3t cells were cultured in serum-free medium. Recloning of the line gave rise to three types of subclones. Sixteen subclones were capable of generating both neurons and oligodendrocytes, four subclones were capable of generating only neurons and one subclone was capable of generating only oligodendrocytes. Thus, 2Y-3t cells have characteristics of bipotent neural progenitor cells capable of generating both neurons and oligodendrocytes. In addition, the line expressed mRNA for Pax-2 and had GAD67-positive cells when cultured in serum-free medium. However, none of the mRNAs for Zic-1, Math1, zebrin or Calbindin-D28k were detected, suggesting that the 2Y-3t line might generate the GABAergic interneuron lineage of the mouse cerebellum.

[Does electroencephalogram finding become a predictor of lithium response in bipolar disorder?].

To prescribe lithium appropriately to bipolar patients, detecting clinical predictors of lithium response in bipolar disorder is important. Considering all mood stabilizers except lithium are anticonvulsants, there may be some relationship between lithium response and EEG abnormalities. The present paper reviews the electroencephalogram finding as a possible predictor of lithium response.

Possible relationship between mitochondrial DNA polymorphisms and lithium response in bipolar disorder.

Although many investigators have been searching for genetic markers to predict lithium response in bipolar disorders, no genetic predictor has been established yet. We previously reported the association of mitochondrial DNA (mtDNA) 5178 and 10398 polymorphisms with bipolar disorder. The objective of this study is to clarify whether these mtDNA polymorphisms can predict response to maintenance lithium treatment in bipolar patients. We examined these polymorphisms and some clinical variables in 54 bipolar patients. A logistic regression analysis was performed and revealed that patients carrying the 10398A polymorphism showed a significantly better response to lithium (p=0.03). Some clinical variables such as sex, age at onset, and rapid cycling also showed a significant association with lithium response in univariate analysis (chi2 test, p&0.05). Our findings suggest that the mtDNA 10398 polymorphism might be related to maintenance lithium treatment response.

Biological predictors of lithium response in bipolar disorder.

In order to prescribe lithium appropriately to patients with bipolar disorder, predictors of lithium response are helpful. The present paper reviews the biological predictors of lithium response. As a positive predictor of lithium response, the following have been reported: strong loudness dependence of the auditory-evoked N1/P2-response; higher brain lithium concentration; lower inositol monophosphatase (IMPase) mRNA expression; higher serotonin-induced calcium mobilization; increased N-acetyl-aspartate peak and decreased myo-inositol peak; white matter hyperintensity; decreased intracellular pH; higher frequency of phospholipase C gamma-1 (PLCG1)-5 repeat and PLCG1-8 repeat; and C973A polymorphism in the inositol polyphosphate 1-phosphatase gene. In contrast the following have been reported as a predictor of negative lithium response: epileptiform abnormality of electroencephalography; human leukocyte antigen type A3; decreased phosphocreatine peak area after photic stimulation; and homozygotes for the short variant of the serotonin transporter gene. Most of the possible biological predictors of better lithium response, such as lower IMPase mRNA levels, white matter hyperintensity, lower brain intracellular pH, enhanced calcium response, and PLCG1-5 repeat had been detected as risk factors for bipolar disorder, suggesting that bipolar disorder responding well to maintenance lithium treatment is a distinct category having a certain neurobiological basis, although these findings need further replication. The search for biological predictors of lithium response is still in its infancy. Most of the laboratory or neuroimaging techniques used in these studies are not easily performed in clinical settings, so the development of an easy and useful laboratory test is needed.

Possible relationship between electroencephalogram finding and lithium response in bipolar disorder.

The relationship between electroencephalogram (EEG) finding and lithium response was retrospectively examined in 58 patients with bipolar disorder. All necessary information was obtained from the clinical charts. The patients were categorized into two groups (responder or nonresponder) with regard to the lithium response and into three groups (normal, borderline, or abnormal) concerning the EEG finding. The information both on EEG and lithium response could be obtained from 27 patients. Only five cases were classified as lithium responders. None of these five responders had abnormal EEG finding, while all of five patients with abnormal EEG finding were categorized into nonresponder. No statistically significant interaction was detected between EEG finding and lithium response. This retrospective study suggests that epileptiform EEG abnormality is worth studying further as a possible predictor of lithium resistance in bipolar disorder.