Coronary microvascular dysfunction is associated with impaired cognitive function: the Cerebral-Coronary Connection study (C3 study).

BACKGROUND: It remains unknown whether the presence of coronary microcirculatory dysfunction (CMD) correlates with its equivalent condition in the brain, cerebral small vessel disease (CSVD). The cerebral-coronary connection (C3), a prospective blinded study, investigated the prevalence of CMD in patients with coronary artery disease (CAD) and its association with CSVD and cognitive function. METHODS AND RESULTS: Patients with documented CAD fulfilling inclusion criteria underwent physiological assessment of epicardial vessels and the microcirculation using intracoronary pressure and Doppler. Coronary microcirculation-related indices included coronary flow reserve (CFR) and hyperaemic microvascular resistance. Brain magnetic resonance imaging, transcranial Doppler (TCD), and neurocognitive examination were performed. Overall, 67 patients were included in the study (mean age 66 years, 73% female). Patients with abnormal CFR (<2.0) (55.2%) showed higher burden of white-matter hyperintensities: 43.2 vs. 20.0% (P = 0.044). After statistical adjustment, low CFR was associated with lower grey matter volume (P = 0.024) and with parameters of white-matter microstructural damage in diffusion-tensor imaging (lower fractional anisotropy and higher mean diffusivity, P = 0.029 and P = 0.032, respectively). Low CFR was associated with higher resistive (P = 0.027) and pulsatility (P = 0.043) values on TCD, and worse neurocognitive test scores (lower mini mental state examination, P = 0.025, and slower Trail Making Test A, P = 0.034). CONCLUSIONS: Coronary microcirculatory dysfunction is frequent in patients with CAD and correlates with CSVD, abnormal cerebral flow haemodynamics, and significant cognitive impairment. These findings support the hypothesis that microvascular dysfunction in the heart and the brain are part of a single pathological process affecting microcirculation in patients with CAD. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov NCT04131075.

Social cognition deficits in borderline personality disorder: Clinical relevance.

Interpersonal difficulties in borderline personality disorder (BDP) have been suggested to be related to impairments in Social Cognition (SC), mainly due to deficits in Theory of Mind (ToM). However, literature is scarce and ambiguous. This work aims to study the SC impairments in BPD patients, by the specific assessment of ToM deficits, and to investigate the relationship between these SC impairments and clinical variables. 82 BPD patients with BPD and 47 control subjects were assessed with the Movie for the Assessment of Social Cognition (MASC). Clinical variables of severity, chronicity, functionality and anxious-depressive symptomatology were recorded. BPD patients had fewer correct mentalization responses and more overmentalization, undermentalization, and absence of mentalization errors than controls. Chronicity was negatively correlated with overmentalization and positively correlated with undermentalization and absence of mentalization errors. Functionality was indirectly correlated with absence of mentalization. These results confirm previous reports of alterations in SC in BPD patients. Furthermore, this study shows that SC impairments in patients with BPD are dependent on characteristics such as chronicity or degree of functionality. The different ToM profiles in patients with BPD indicate the necessity of developing variants of mentalization therapy depending on the deficits of each patient.

[Analysis of judicial sentences against psychiatrists dictated by appellate courts in Spain between 1992 and 2007]. / Análisis de las sentencias judiciales contra psiquiatras resueltas en segunda instancia en España entre 1992 y 2007.

Sentences against psychiatrists dictated in appellate or higher courts of Spain in the period from 1992 to 2007 were analyzed. Decisions were gathered for 13 of the 17 autonomous communities and statistical analysis yielded the following results: in more than 50% of cases, the decision was unfavorable for the psychiatrist, but the damages never exceeded € 600,000. The most frequent condition in the series was personality disorders (48.9%). The most frequent reasons for seeking legal redress were monitoring errors and negligence; no cases were brought to trial for therapeutic errors. The patient died in 58.3% of cases. It is noteworthy that 10% of the sentences cited defects in patient information or informed consent. The psychiatric health care teams in both the public and private sector should maximize monitoring of institutionalized patients and optimize installations to provide special security measures for the patients.

A ventromedial prefrontal dysrhythmia in obsessive-compulsive disorder is attenuated by nucleus accumbens deep brain stimulation.

BACKGROUND: Obsessive-compulsive disorder (OCD) has consistently been linked to abnormal frontostriatal activity. The electrophysiological disruption in this circuit, however, remains to be characterized. OBJECTIVE/HYPOTHESIS: The primary goal of this study was to investigate the neuronal synchronization in OCD patients. We predicted aberrant oscillatory activity in frontal regions compared to healthy control subjects, which would be alleviated by deep brain stimulation (DBS) of the nucleus accumbens (NAc). METHODS: We compared scalp EEG recordings from nine patients with OCD treated with NAc-DBS with recordings from healthy controls, matched for age and gender. Within the patient group, EEG activity was compared with DBS turned off vs. stimulation at typical clinical settings (3.5 V, frequency of stimulation 130 Hz, pulse width 60 µs). In addition, intracranial EEG was recorded directly from depth macroelectrodes in the NAc in four OCD patients. RESULTS: Cross-frequency coupling between the phase of alpha/low beta oscillations and amplitude of high gamma was significantly increased over midline frontal and parietal electrodes in patients when stimulation was turned off, compared to controls. Critically, in patients, beta (16-25 Hz) -gamma (110-166 Hz) phase amplitude coupling source localized to the ventromedial prefrontal cortex, and was reduced when NAc-DBS was active. In contrast, intracranial EEG recordings showed no beta-gamma phase amplitude coupling. The contribution of non-sinusoidal beta waveforms to this coupling are reported. CONCLUSION: We reveal an increased beta-gamma phase amplitude coupling in fronto-central scalp sensors in patients suffering from OCD, compared to healthy controls, which may derive from ventromedial prefrontal regions implicated in OCD and is normalized by DBS of the nucleus accumbens. This aberrant cross-frequency coupling could represent a biomarker of OCD, as well as a target for novel therapeutic approaches.