ABSTRACT
Morita therapy (MT) has been re-evaluated and has attracted much attention internationally to date. However, it is not known what kinds of experiences inpatients with mood disorders undergo during the process of recovery through MT. The purpose of this study was therefore to empirically clarify what subjective experiences influence the recovery from depression when it is treated with MT. Patients with mood disorders who were admitted to the Jikei University Center for Morita Therapy were included. Successive assessments of depression were performed using rating scales. Semi-structured interviews were conducted at the time of discharge regarding factors contributing to improvement, and were analyzed using qualitative data analysis methods to identify factors contributing to the recovery from depression among inpatients treated with MT. There were 24 subjects, 19 of whom completed treatment. The completers had significantly lower severity of depression severity upon discharge. Remarkably, qualitative analysis revealed that nine categories of experiences contributed to recovery from depression. In particular, experiences of "isolation bed-resting of MT", "getting stuck in doing things one's way", "identifying maladaptive behavior patterns", "modifying maladaptive behavior patterns", "restoring self-evaluation", and "change in negative emotions" were considered as the key experiences for recovery.
ABSTRACT
A 75-year-old male showed combined anterior pituitary hormone deficiency (CPHD). Basal and TRH-stimulated PRL levels were undetectable. Basal and GRH-stimulated GH levels were very low, and could barely be measured by means of an ultrasensitive enzyme immunoassay. In addition, basal TSH levels were under the normal limit, and TRH-stimulated TSH secretions were impaired. On the other hand, the secretions of ACTH, LH and FSH remained intact. There was no mutation of Pit-1 gene in this patient, and immunohistochemical studies using human pituitary and the patient's serum showed no positive staining. The HLA types frequently detected in lymphocytic hypophysitis were recognized, supporting the view that the CPHD in this case may be caused by lymphocytic hypophysitis, although magnetic resonance imaging of the pituitary gland showed no specific findings. Interestingly, a high titer of anti-glutamic acid decarboxylase antibody, suggested that the patient suffered from type 1 diabetes mellitus (DM). Five years ago, his thyroid function was normal and the treatment of DM with oral hypoglycemic agent was effective, indicating that the onset of both diseases at least occurred within the last half decade. We report here a rare case of SPIDDM with CPHD which might be caused by lymphocytic hypophysitis.
