COVID-19 and catatonia: Prevalence, challenges, pathophysiology, and treatment.

BACKGROUND: Emerging literature supports the association between acute COVID-19 infection and neuropsychiatric complications. This article reviews the evidence for catatonia as a potential neuropsychiatric sequela of COVID-19 infection. METHODS: PubMed was searched using the terms catatonia, severe acute respiratory syndrome coronavirus 2, and COVID-19. Articles were limited to those published in the English language between 2020 and 2022. Forty-five articles that specifically studied catatonia associated with acute COVID-19 infection were screened. RESULTS: Overall, 30% of patients with severe COVID-19 infection developed psychiatric symptoms. We found 41 cases of COVID-19 and catatonia, with clinical presentations that varied in onset, duration, and severity. One death was reported in a case of catatonia. Cases were reported in patients with and without a known psychiatric history. Lorazepam was successfully used, along with electroconvulsive therapy, antipsychotics, and other treatments. CONCLUSIONS: Greater recognition and treatment of catatonia in individuals with COVID-19 infection is warranted. Clinicians should be familiar with recognizing catatonia as a potential outcome of COVID-19 infection. Early detection and appropriate treatment are likely to lead to better outcomes.

Hereditary pseudocholinesterase deficiency discovery after electroconvulsive therapy.

Inherited pseudocholinesterase deficiency refers to an uncommon defect in the butyrylcholinesterase enzyme which can result in prolonged muscle paralysis due to delayed breakdown of choline ester paralytic anaesthetic agents. We describe a 25-year-old woman receiving electroconvulsive therapy (ECT) for treatment of depression in whom motor function did not recover adequately after administration of succinylcholine. Investigated post-ECT, she was found to have severe pseudocholinesterase deficiency. Implications of pseudocholinesterase deficiency for ECT treatment and anaesthetic strategies are discussed.

Common neurofunctional dysregulations characterize obsessive-compulsive, substance use, and gaming disorders-An activation likelihood meta-analysis of functional imaging studies.

Compulsivity and loss of behavioral control represent core symptoms in obsessive-compulsive disorder (OCD), substance use disorder (SUD), and internet gaming disorder (IGD). Despite elaborated animal models suggesting that compulsivity is mediated by cortico-striatal circuits and a growing number of neuroimaging case-control studies, common neurofunctional alterations in these disorders have not been systematically examined. The present activation likelihood estimation (ALE) meta-analysis capitalized on previous functional magnetic resonance imaging (fMRI) studies to determine shared neurofunctional alterations among the three disorders. Task-based fMRI studies of individuals with SUD, OCD, or IGD were obtained. ALE was performed within each disorder. Next, contrast and conjunction meta-analyses were performed to determine differential and common alterations. Task-paradigm classes were group according to Research Domain Criteria (RDoC) domains to determine contributions of underlying behavioral domains. One hundred forty-four articles were included representing data from n = 6897 individuals (SUD = 2418, controls = 2332; IGD = 361, controls = 360; OCD = 715, controls = 711) from case-control studies. Conjunction meta-analyses revealed shared alterations in the anterior insular cortex between OCD and SUDs. SUD exhibited additionally pronounced dorsal-striatal alterations compared with both, OCD and IGD. IGD shared frontal, particularly cingulate alterations with all SUDs, while IGD demonstrated pronounced temporal alterations compared with both, SUD and OCD. No robust overlap between IGD and OCD was observed. Across the disorders, neurofunctional alterations were mainly contributed by cognitive systems and positive valence RDoC domains. The present findings indicate that neurofunctional dysregulations in prefrontal regions engaged in regulatory-control represent shared neurofunctional alterations across substance and behavioral addictions, while shared neurofunctional dysregulations in the anterior insula may mediate compulsivity in substance addiction and OCD.

Limiting progressive hippocampal metabolic abnormalities after smoke inhalation injury.

A 46-year-old man had a smoke inhalation injury. Within 1 month, he developed neuropsychiatric problems including toxic encephalopathy, cognitive disorder, depression symptoms and personality change. From 3 to 14 years after the toxic inhalation injury, the patient received treatment with sertraline and methylphenidate. The (18)F-fluorodeoxyglucose positron emission tomography scan at 3 years after injury showed deterioration of glucose metabolism in the hippocampus and orbital frontal region; at 14 years after injury, the hippocampus had no significant change but the orbital frontal region had deterioration of glucose metabolism. It was hypothesised that sertraline may have provided selective hippocampal neuroprotection. Further study is justified to evaluate sertraline as a possible neuroprotective agent after smoke inhalation injury.

Distress due to lithium-induced polyuria: exploratory study.

Lithium-induced polyuria, although common, often goes unrecognized. The purpose of the present study was therefore to investigate the complaints of polyuria, and distress and functional impairment associated with polyuria, in 56 patients with bipolar disorder on long-term lithium treatment. All participants underwent 24-h urine collection, and renal function tests. Polyuria (24-h urine volume > 3 L) was found in 70% of subjects. Unless directly enquired about, polyuria was underreported. Impairment in work and daily routine due to increased urine output/frequency was associated with 24-h urine volumes. Polyuria is a highly prevalent, distressing and impairing side-effect of long-term lithium treatment, requiring due attention.

Cognitive functions in bipolar affective disorder and schizophrenia: comparison.

AIMS: Earlier comparisons of cognitive impairment among patients with bipolar disorder and schizophrenia have found a largely similar profile of deficits, but results have varied between studies. This prompted the current attempt at another such comparison. METHODS: Executive functions, memory, IQ, attention-concentration and perceptuomotor function were assessed in 48 bipolar disorder patients with operationally defined euthymia, and compared with 32 schizophrenia patients in remission, and 23 normal controls. Comparisons were re-attempted after controlling for years of schooling and residual affective symptoms. RESULTS: Uncontrolled comparisons indicated that, compared to controls, both bipolar disorder and schizophrenia patients were significantly impaired on different tests of executive function, memory, IQ and perceptuomotor functions. Controlling for years of schooling and residual affective symptoms, however, served to remove most of the differences between patients and controls, apart from some aspects of executive function in schizophrenia and memory impairment in both schizophrenia and bipolar disorder. Patients with schizophrenia consistently performed worse than patients with bipolar disorder, but none of the differences between schizophrenia and bipolar disorder were significant. CONCLUSIONS: Patients with bipolar disorder exhibit cognitive difficulties that are very similar to schizophrenia in terms of their profile, although patients with schizophrenia may have more severe and widespread impairments. The resemblance in cognitive profiles has important implications for the etiology and treatment of both disorders.

Comparison of cognitive functions between first- and multi-episode bipolar affective disorders.

BACKGROUND: Cognitive impairment has been commonly found in euthymic patients with bipolar affective disorder (BPAD). Information about onset and course of cognitive deficits is, however, scarce. This study examined the cognitive profile of patients following their first episode of BPAD to determine whether cognitive problems are present at such an early stage. METHODS: Executive functions, memory, IQ, attention-concentration and perceptuomotor function were assessed in 16 euthymic patients with BPAD following their first episodes, and compared with a group of 30 euthymic patients with multiple episodes of BPAD and 20 normal controls. Comparisons were controlled for educational status, current IQ and residual symptoms. RESULTS: First-episode patients were significantly impaired, compared to normal controls, on tests of executive function, sustained attention, perceptuomotor function and IQ. Additionally, their performance was significantly worse than patients with multi-episode BPAD on tests of executive functions, sustained attention and perceptuomotor function. Multi-episode patients had impaired memory, compared to normal controls, and performed poorly on a subtest of executive functions compared to first-episode patients. LIMITATIONS: Sample sizes were small, assessments cross-sectional; all confounds could not be controlled for. CONCLUSIONS: Widespread cognitive disturbances following the first episode of BPAD were found in this study. Whether these disturbances progress following repeated episodes was not entirely clear. Since cognitive impairment can have several adverse consequences for patients of BPAD in terms of disability, quality of life, outcome etc., this must remain a priority area for future research.