Abnormal corneal nerve morphology and brain volume in patients with schizophrenia.

Neurodevelopmental and neurodegenerative pathology occur in Schizophrenia. This study compared the utility of corneal confocal microscopy (CCM), an ophthalmic imaging technique with MRI brain volumetry in quantifying neuronal pathology and its relationship to cognitive dysfunction and symptom severity in schizophrenia. Thirty-six subjects with schizophrenia and 26 controls underwent assessment of cognitive function, symptom severity, CCM and MRI brain volumetry. Subjects with schizophrenia had lower cognitive function (P ≤ 0.01), corneal nerve fiber density (CNFD), length (CNFL), branch density (CNBD), CNBD:CNFD ratio (P < 0.0001) and cingulate gyrus volume (P < 0.05) but comparable volume of whole brain (P = 0.61), cortical gray matter (P = 0.99), ventricle (P = 0.47), hippocampus (P = 0.10) and amygdala (P = 0.68). Corneal nerve measures and cingulate gyrus volume showed no association with symptom severity (P = 0.35-0.86 and P = 0.50) or cognitive function (P = 0.35-0.86 and P = 0.49). Corneal nerve measures were not associated with metabolic syndrome (P = 0.61-0.64) or diabetes (P = 0.057-0.54). The area under the ROC curve distinguishing subjects with schizophrenia from controls was 88% for CNFL, 84% for CNBD and CNBD:CNFD ratio, 79% for CNFD and 73% for the cingulate gyrus volume. This study has identified a reduction in corneal nerve fibers and cingulate gyrus volume in schizophrenia, but no association with symptom severity or cognitive dysfunction. Corneal nerve loss identified using CCM may act as a rapid non-invasive surrogate marker of neurodegeneration in patients with schizophrenia.

Mania and hypomania associated with COVID-19: a series of 15 cases seen by the consultation-liaison psychiatry service in Qatar.

BACKGROUND: A range of neuropsychiatric diagnoses have been reported in association with coronavirus disease 2019 (COVID-19). However, only sporadic cases of mania or hypomania have been reported in patients with COVID-19. This study aimed to report clinical characteristics of 15 consecutive cases of COVID-19-associated mania or hypomania seen in three general hospitals in Qatar in the early months of the pandemic in 2020. METHODS: This study is a retrospective case-note review of 15 cases of COVID-19-associated mania or hypomania (confirmed by polymerase chain reaction test), seen as inpatient consultations out of the first 100 consecutive patients managed by consultation-liaison psychiatric teams in Qatar between 2 March 2020 and 7 July 2020. RESULTS: The mean age of the 15 patients was 40 years. Twelve patients had mania, and three had hypomania. Regarding the physical severity of COVID-19, 10 patients were asymptomatic, two had upper respiratory tract symptoms alone and three had pneumonia. None of the patients were intubated. Potential risk factors for mania/hypomania included pandemic-related psychosocial stress before admission (n = 9), past history of mania/bipolar disorder (n = 6) or psychosis (n = 2), raised inflammatory markers (n = 7) and steroid use (n = 3). None had a history of recent substance misuse. Other than one patient with advanced cancer, none had comorbidity regarded as likely to have caused mania or hypomania. Three patients had mild white matter ischaemic changes on brain imaging. Standard pharmacological treatment for mania (i.e. antipsychotic medication supplemented by prn benzodiazepines) was effective. Ten patients were discharged home from the COVID-19 facility where they presented, but five required transfer to Qatar's psychiatric hospital for further treatment of mania. CONCLUSION: The association of mania or hypomania with COVID-19 may be spurious (e.g. representing an initial presentation of bipolar disorder) or causal. The reported cases illustrate a range of potential aetiological mechanisms by which COVID-19 could cause mania or hypomania. Cohort studies are necessary to determine the incidence, aetiology and prognosis of COVID-19-associated mania/hypomania.