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Cognitive behavioural therapy (CBT) is an effective treatment for improving anxiety symptoms in patients with autism spectrum disorder (ASD). However, some patients with ASD take extra time for learning, and they can find it hard to change their thinking styles and behaviour due to cognitive deficits. The therapist must be creative when implementing CBT in this context. Here, it may be helpful for the patient with ASD to understand CBT’s concepts by using visual aid material. Blended CBT during which the patient is shown visual aid material with his or her therapist has been suggested as effective for adults without ASD to reduce anxiety. Blended CBT combines face-to-face treatment with internet guided support and resource. Blended CBT may facilitate an understanding of essential knowledge and help people with ASD and anxiety acquire skills based on cognitive behavioural science. However, as far as we know, no previous studies have reported on the use of blended CBT for patients with panic disorder co-morbid with ASD. This study, therefore, consecutively performed 16 blended CBT sessions on a biweekly basis to treat panic disorder (PD) in an adolescent Japanese female co-morbid with ASD. The patient exhibited improvements in PD symptoms and agoraphobia after treatment: the Panic Disorder Severity Scale score decreased from 18 to 2. These results indicate that visual aid-assisted treatment may help patients with impaired imagination and social cognition related to ASD. Furthermore, this study’s therapist notes the need for paced treatments and repeated psychoeducation for patients with impairments in central coherence and cognitive flexibility.
Key learning aims
(1) Blended CBT may patients with panic disorder (PD) co-morbid with autism spectrum disorder (ASD) to understand concepts based on cognitive behavioural science and symptoms.
(2) Blended CBT sessions can each be conducted in approximately 20 min (about one-third of the time needed for typical 45- to 90-min CBT sessions); in other words, it is less burdensome for the patient and therapist.
(3) How to adjust blended CBT for those who have low average intelligence quotients (IQ) and/or ASD.
Our recent single-photon emission computed tomography (SPECT) study of patients with late-onset Alzheimer’s disease (AD) revealed that regional cerebral blood flow (rCBF) was reduced in the frontal, temporal, and limbic lobes, and to a lesser degree in the parietal and occipital lobes. Moreover, these patients’ scores on the Alzheimer’s Disease Assessment Scale-cognitive subscale (ADAS-cog) were significantly correlated with rCBF in some gyri of the frontal, parietal, and limbic lobes. Our present study aimed to understand how vascular factors and metabolic disease influenced the relationship between rCBF and ADAS-cog scores.
We divided late-onset AD patients into two groups according to their Hachinski Ischemic Score (HIS), low vascular risk patients had values of ≤4 (n=25) and high vascular risk patients had scores ≥5 (n=15). We examined rCBF using brain perfusion SPECT data.
The degrees and patterns of reduced rCBF were largely similar between late-onset AD patients in both groups, regardless of HIS values. Cognitive function was significantly associated with rCBF among late-onset AD patients with low vascular risk (HIS≤4), but not among those with high vascular risk (HIS≥5). Furthermore, metabolic diseases, such as hypertension and diabetes mellitus, disrupted the relationships between hypoperfusion and cognitive impairments in late-onset AD patients.
Factors other than hypoperfusion, such as hypertension and diabetes mellitus, could be involved in the cognitive dysfunction of late-onset AD patients with high vascular risk.
Treatment-resistant depression is a challenging problem in the clinical setting. Tipepidine has been used as a non-narcotic antitussive in Japan since 1959.
We administered tipepidine to 11 patients with treatment-resistant depression. Tipepidine was given for 8 weeks as an augmentation.
Tipepidine significantly improved depression scores on the Hamilton Rating Scale for depression. Add-on treatment with tipepidine significantly improved scores on the trail making test and Rey auditory verbal learning test. However, no changes were observed in blood concentrations of stress-related hormones (adrenocorticotropic hormone, cortisol, dehydroepiandrosterone sulphate) with tipepidine augmentation.
Tipepidine might be a potential therapeutic drug for treatment-resistant depression.
Accumulating evidences suggest that pro-inflammatory cytokines such as interleukin-6 (IL-6) play a role in the pathophysiology of depression. In the learned helplessness (LH) paradigm, ~35% rats are resilient to inescapable stress.
Levels of IL-6 in the serum and medial prefrontal cortex (mPFC) of LH rats (susceptible) and non-LH rats (resilience) were measured using enzyme-linked immunosorbent assay and western blot analysis, respectively.
Serum levels of IL-6 in the LH rats were significantly higher than those of control and non-LH rats. In contrast, tissue levels of IL-6 in the mPFC were not different among three groups.
The results suggest that peripheral IL-6 may contribute to resilience versus susceptibility to inescapable stress.
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