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BACKGROUND: Delirium is common in the setting of infection with severe acute respiratory syndrome coronavirus 2. Anecdotal evidence and case reports suggest that patients with delirium in the setting of Coronavirus 2019 (COVID-19) may exhibit specific features, including increased tone, abulia, and alogia. OBJECTIVE: To determine whether differences exist in sociodemographic and medical characteristics, physical examination findings, and medication use in delirious patients with and without COVID-19 infection referred for psychiatric consultation. METHODS: We undertook an exploratory, retrospective chart review of 486 patients seen by the psychiatry consultation service at a tertiary care hospital from March 10 to May 15, 2020. Delirious patients were diagnosed via clinical examination by a psychiatric consultant, and these patients were stratified by COVID-19 infection status. The strata were described and compared using bivariate analyses across sociodemographic, historical, objective, and treatment-related variables. RESULTS: A total of 109 patients were diagnosed with delirium during the study period. Thirty-six were COVID-19+. Median age was 63 years and did not differ between groups. COVID-19+ patients with delirium were more likely to present from nursing facilities (39% vs 11%; Fisher's exact test; P = 0.001) and have a history of schizophrenia (11% vs 0%; Fisher's exact test; P = 0.011). Myoclonus (28% vs 4%; P = 0.002), hypertonia (36% vs 10%; P = 0.003), withdrawal (36% vs 15%; P = 0.011), akinesia (19% vs 6%; P = 0.034), abulia (19% vs 3%; P = 0.004), and alogia (25% vs 8%; P = 0.012) were more common in COVID-19+ patients. COVID-19+ delirious patients were significantly more likely to have received ketamine (28% vs 7%; P = 0.006), alpha-adrenergic agents besides dexmedetomidine (36% vs 14%; P = 0.014), and enteral antipsychotics (92% vs 66%; P = 0.007) at some point. CONCLUSIONS: Patients with COVID-19 delirium referred for psychiatric consultation are more likely to reside in nursing facilities and have a history of schizophrenia than delirious patients without COVID-19. Patients with delirium in the setting of COVID-19 may exhibit features consistent with akinetic mutism. Psychiatrists must assess for such features, as they may influence management choices and the risk of side effects with agents commonly used in the setting of delirium.
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Purpose: Infection with COVID-19 has presented diversely in patients, including neuropsychiatric symptoms such as akinetic mutism. Most of these cases involve patients of middle-to-late age or with other health comorbidities. This is a unique case of a long hospitalization for severe catatonic symptoms in a patient with covid-19 infection in which ultimately, ECT helped produce rapid improvements in catatonia. Access to prompt ECT has been limited during the ongoing pandemic, and this case illustrates the importance of managing contamination risk and maintaining access to psychiatric treatment resources. Copyright © 2022
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CASE: A 64-year-old woman was brought in by husband for inability to care for patient. Previously active, she developed gait instability, slurred speech, and memory lapse to the point of selective mutism and being bed-bound within three months. Her medical history was notable for hypertension and Covid four months prior. She had had mild upper respiratory symptoms and recovered in ten days. Examination revealed general encephalopathy, dysarthria, limited ability to follow commands. She had decreased strength but increased tone and rigidity in all extremities. She had rhythmic jaw movement and bradykinesia with scatter myoclonic movements. Cerebellar exam was notable for ataxia, but she had normal cranial nerve and sensory exams and normal reflexes. MRI of the brain revealed restricted diffusion and T2/Flair signal abnormality involving bilateral basal ganglia, ventral medial thalami, hippocampi, and cerebral cortices. Toxic metabolic workup was unrevealing. CSF was positive for 14-3-3 protein and elevated total tau protein, confirming Creutzfeldt-Jakob disease. IMPACT/DISCUSSION: Creutzfeldt-Jakob Disease (CJD) is a prion disease with one in a million prevalence. Patients present with rapidly progressing dementia, myoclonus, and signs of cerebellar, corticospinal and extrapyramidal involvement including nystagmus, ataxia, hyperreflexia, spasticity, hypokinesia, bradykinesia, dystonia, and rigidity. CJD is fatal within months to two years. Patients with end stage disease may have akinetic mutism. Magnetic resonance imaging (MRI), electroencephalogram (EEG), and cerebrospinal fluid (CSF) analysis are important for evaluation of CJD. Most sensitive in early stages, MRI Brain commonly shows hyperintense signal involving the cerebral cortex, corpus striatum, caudate, and putamen. EEG may capture pattern of periodic bi-or triphasic period sharp wave complexes. CSF might detect 14-3-3 protein with elevation of tau protein but real-time quaking-induced conversion (RT-QuIC) has the highest specificity for diagnosis for CJD. Though brain biopsy is the sole method of definitive diagnosis, results of MRI, EEG, and CSF analysis along with presenting signs and symptoms are sufficient for clinical diagnosis of CJD. Our patient's dementia, myoclonus, ataxia, hypokinesia, bradykinesia, dystonia, and rigidity all progressing to akinetic mutism within three months are classic presentation of CJD. EEG was normal, but MRI with hyperintensity of basal ganglia and cerebral cortices and CSF analysis with positive 14-3-3 and elevated tau proteins are all lead to diagnosis of CJD. CONCLUSION: This case illustrates a classic case of a Creutzfeldt-Jakob Disease, a rare prion disease marked by rapidly progressive dementia with neuropsychiatric features.
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CASE: A 44 year old female with history of depression and recent suicide attempt presents with one week of cognitive and functional decline. One month prior to presentation, patient attempted suicide with opioids requiring intubation for respiratory depression and stroke sequelae. She was discharged from this stay after 12 days having returned to mental and functional baseline. Two weeks later, she demonstrated decreased focus and concentration, progressing to decreased mobility and akinesis, eventually presenting to our hospital. Admission metabolic and toxic workup was negative. CT head redemonstrated findings of previously known stroke. MRI demonstrated new increased T2 Flair of the parietal lobes and the cerebral white matter. LP was without evidence of infection or inflammation. Encephalitis panel and autoimmune workup were negative. Neurology consult suggested delayed post-hypoxic leukoencephalopathy as a possible diagnosis, given clinical course of improvement and subsequent decline, along with akinetic mutism and deep cortical white matter flair abnormalities. After failed trial of lorazepam, she was started on amantadine and her cognitive and functional status improved slowly. IMPACT/DISCUSSION: Delayed post-hypoxic leukoencephalopathy (DPHL) is a rare syndrome characterized by biphasic time course with initial recovery and subsequent cognitive and functional decline. DPHL can follow any event of prolonged cerebral hypoxia most frequently CO poisoning. It can occur with more common causes of hypoxia including overdose, cardiac arrest, and seizures;recent case reports have reported DPHL following severe covid infection. The clinical course involves a hypoxic event followed by a return to functional baseline typically lasting 7-21 days, after which progressive physical and mental decline occur. Signs include neuropsychiatric symptoms like amnesia and disorientation, as well as parkinsonism or akinetic mutism (1). The mechanism of DPHL is unclear. One possible mechanisms involves diffuse demyelination. The half life of myelin basic proteins is approximately 20 days, the length of the lucid interval. Hypoxia may abruptly halt the myelination process but symptoms may not emerge until a critical threshold of loss was achieved. Evaluation of DPHL involves considering other causes of encephalopathy, such as infection, substance use, stroke, catatonia, and toxins. In the absence of other causes, diagnosis of DPHL is based on characteristic time course following hypoxic event, symptoms, and MRI findings of diffuse T2 hyperintensity of cerebral white matter are pathognomonic (1). Treatment of DPHL is generally supportive. Limited evidence suggests amantadine may be of benefit. CONCLUSION: Physicians should consider DPHL in patients who have experienced cerebral hypoxia and present with the characteristic time course and imaging findings.
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AIMS AND METHOD: Catatonia has been increasingly described in cases of COVID-19; we therefore aimed to investigate the evidence for catatonia in patients with COVID-19. We searched PubMed, EMBASE, PsycINFO, BIN and CINAHL databases for articles published in English, from the initial descriptions of the COVID-19 pandemic to January 2022. RESULTS: A total 204 studies were identified, 27 (13%) of which met the inclusion criteria. The evidence available was based on case reports. The articles included in this review identified a total of 42 patients, ranging from the ages of 12 to ≥70 years, with confirmed or possible catatonia during or after a COVID-19 infection. CLINICAL IMPLICATIONS: This review provides valuable information to clinicians in medical practice for treating patients with COVID-19, and a foundation for further research for this uncommon syndrome of COVID-19.
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Objectives: Acute necrotizing encephalopathy (ANE) is a rare neurological disorder arising from a para- or post-infectious "cytokine storm. "It has recently been reported in association with coronavirus disease 2019 (COVID-19) infection. Methods: A 56-year-old male with a diagnosis of ANE 48 h following the first dose of ChAdOx1 nCoV-19 vaccination was investigated. Cytokine analyses on serum and cerebrospinal fluid (CSF) were performed. The patient was treated with high-dose corticosteroids and followed clinically and radiologically. Results: Favorable clinical and radiological outcomes were noted. There was an upregulation in serum levels of CXCL5, CXCL1, Il-8, IL-15, CCL2, TGF-B, and EGF, and up-regulation in CSF levels of CXCL5, IL-2, IL-3, and IL-8. Discussion: As COVID-19 infection has been previously reported as a possible rare cause of ANE, we speculate on an aberrant immune response mechanism that was brought about by the vaccine. To increase our understanding of the pathogenesis of ANE in the context of COVID-19 vaccination and to better define its clinical features and outcomes, clinicians and scientists should continue reporting convincing cases of such entities.
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BACKGROUND: Coronavirus disease 2019 (COVID-19) has been associated with neuropsychiatric complications ranging from new-onset psychosis to delirium, dysexecutive syndromes, catatonia, and akinetic mutism (AM). AM can be conceptualized as a disorder of motivation wherein patients exhibit a loss of speech and spontaneous movement, owing to disruption of underlying frontal-subcortical circuits. OBJECTIVES: The objectives of this study were to review the concept and differential diagnosis of AM, as well as the clinical literature on AM in COVID-19 and discuss potential implications for underlying functional neuroanatomy and mechanistic pathways, as well as clinical management. METHODS: A narrative literature review was performed using PubMed querying published articles for topics associated with AM and its occurrence in COVID-19. RESULTS: AM has been described in case reports and a prospective cohort study of patients with COVID with neurological complaints. Three COVID-19 AM subgroups can be distinguished, including individuals with severe respiratory illness, those with meningoencephalitis, and those with delirium and pre-existing neuropsychiatric illness. Electrophysiology and functional imaging suggest COVID-19 AM may result from underlying frontal lobe dysfunction and disruption of associated distributed circuits subserving goal-directed behavior. Distinctive combinations of pathophysiological mechanisms may be at play in the different subgroups of COVID-19 AM cases. CONCLUSION: AM has been described in association with COVID-19 and may manifest in clinically heterogenous subgroups with distinct underlying mechanisms. The diagnosis of AM and evaluation of potential etiologies can be complex. The occurrence of AM contributes evidence to the hypothesis of frontal lobe dysfunction in COVID-19.
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Mutismo Acinético , COVID-19 , Humanos , Motivación , Estudios Prospectivos , SARS-CoV-2RESUMEN
INTRODUCTION: Neuropsychiatric manifestations of the coronavirus disease 2019 (COVID-19) have been described, including anosmia, ageusia, headache, paresthesia, encephalitis and encephalopathy. Little is known about the mechanisms by which the virus causes central nervous system (CNS) symptoms, and therefore little guidance is available regarding potential workup or management options. CASES: We present a series of four consecutive cases, seen by our psychiatry consultation service over a one-week period, each of which manifested delirium as a result of infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). DISCUSSION: The four cases highlighted here all occurred in older patients with premorbid evidence of cognitive decline. Unique features seen in multiple cases included rigidity, alogia, abulia, and elevated inflammatory markers. In all four cases, a change in mental status was the presenting symptom, and three of the four cases lacked significant respiratory symptoms. In addition to discussing unique features of the cases, we discuss possible pathophysiologic explanations for COVID-19 delirium. CONCLUSIONS: Delirium should be recognized as a potential feature of infection with SARS-CoV-2 and may be the only presenting symptom. Based on the high rates of delirium demonstrated in prior studies, hospitals should consider adding mental status changes to the list of testing criteria. Further research is needed to determine if delirium in COVID-19 represents a primary encephalopathy heralding invasion of the CNS by the virus, or a secondary encephalopathy related to systemic inflammatory response or other factors.