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Case 34-2022: 57-year-old woman with Covid-19 and delusions

Case 34-2022: 57-year-old woman with Covid-19 and delusions

Dr. Gregory L. Fricchione: In this 57-year-old woman with metabolic syndrome and mixed affective disorder suggestive of bipolar disorder, neuropsychiatric symptoms developed 2 weeks after the onset of Covid-19. The patient had psychomotor agitation, lumpy affect and anxious perseveration that was directed at her father’s care. Three days later, she was noted to become immobile and hypophonic, with staring, speech delay, and verbal persistence. Cognition was intact, but insight and judgment were impaired. In an attempt to explain her neuropsychiatric symptoms, I will consider the potential effects of the medications she received, her underlying psychiatric illness, and her recent infection.

Drug effects

This patient was receiving several medications for the treatment of mixed affective disorder, including bupropion, fluoxetine, and olanzapine. Antidepressants can induce a secondary manic episode, especially in this patient with suspected bipolar disorder. However, her presentation was not typical of drug-related mania, which has the classic symptoms of insomnia, euphoria or irritability, extreme hyperactivity, and strained speech. Although she was receiving psychotropic medications associated with serotonin syndrome, there were no findings suggestive of this diagnosis, such as clonus, tremors, ataxia, hyperreflexia, or fever.1

This patient has recently started taking dexamethasone to treat Covid-19. Glucocorticoids, especially when given in high doses, are potential triggers of the manic reaction commonly referred to as “steroid-induced psychosis.” Glucocorticoid use can cause a myriad of neuropsychiatric affective, cognitive, and behavioral symptoms.2 The persistence of this patient’s psychotic symptoms after discontinuation of dexamethasone argues against a diagnosis of glucocorticoid-related psychosis, although it is possible that the dexamethasone caused the underlying primary psychiatric disorder.

Attacks

The patient was noted to appear withdrawn, and at times would lie motionless and not answer questions. These episodes suggest the possibility of complex partial seizures. Status epilepticus, including non-convulsive status epilepticus, has been reported in patients with Covid-19.3 In addition, the patient was taking bupropion, a drug associated with lowering the seizure threshold. However, if her reduced responsiveness was due to nonconvulsive status epilepticus, I would expect her to have phases of profound unresponsiveness that fluctuate with brief phases of wakefulness with confusion. Because complex partial disorder is often difficult to diagnose, I would perform long-term electroencephalographic (EEG) monitoring while considering alternative diagnoses.

Autoimmune encephalitis

Could this patient have autoimmune limbic encephalitis? Neuropsychiatric symptoms appear to have had a subacute onset followed by rapid progression, suggesting involvement of the limbic system. In addition, white matter changes seen on head CT indicate bilateral brain abnormalities. However, if the patient has autoimmune limbic encephalitis, I would expect the white matter changes to be limited to the medial temporal lobes and the EEG to show focal temporal slowing.4 I would do a magnetic resonance imaging (MRI) of the head and a lumbar puncture for cerebrospinal fluid (CSF) analysis to rule out the diagnosis of autoimmune encephalitis, especially given the potential association of this condition with Covid-19.5,6 Encephalitis associated with anti-N-methyl-dAntibodies to the -aspartate (NMDA) receptor can lead to a neuropsychiatric presentation that often includes catatonic withdrawal and is associated with viral illnesses.7 The link between encephalitis associated with anti-NMDA receptor antibodies and SARS-CoV-2 has not yet been established, but a potential link has been suggested.8

Neuropsychiatric symptoms associated with Covid-19

Could this patient’s neuropsychiatric symptoms be related to her recent diagnosis of Covid-19? Early studies have shown that more than one-third of Covid-19 patients have a neuropsychiatric syndrome.9

Some cases of Covid-19 lead to persistent symptoms or long-term complications that extend beyond the acute illness (a condition sometimes called post-acute Covid-19 syndrome or “long Covid”).10 In such cases, neuropsychiatric symptoms may include fatigue, myalgias, headache, anxiety, depression, dysautonomia, and cognitive impairment (also called “brain fog”).

In one study involving more than 60,000 patients with Covid-19, 18% of patients received a psychiatric diagnosis between 14 and 90 days after infection.11 Neuroinflammation is thought to play a role in the neuropsychiatric disorders associated with Covid-19,12,13 and persistent autoantibodies have been detected in the CSF of patients with these conditions.13-15

New-onset psychosis has been reported in patients with Covid-19. In one report describing 10 patients, psychotic symptoms developed at least 2 weeks after the onset of Covid-19 symptoms, and structured delusions were common.16 A recent systematic review of cases of psychosis associated with Covid-19 confirmed that delusions are the most commonly reported psychotic symptom.17 It should be noted that the majority of patients with Covid-19-related psychosis had only mild acute symptoms of Covid-19.

A head CT scan performed on this patient revealed subcortical white matter disease. The most common neuroimaging abnormalities observed in patients with Covid-19 include white matter changes.18 Covid-19 has been associated with several white matter diseases, including Covid-19-associated disseminated leukoencephalopathy and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).19,20 However, there were no reports of features suggestive of these diagnoses in this patient, such as clinically significant decreased level of consciousness, headaches, cranial nerve signs, sensorimotor deficits, gait defects, or changes in deep tendon reflexes. In addition, there were no other CT findings, such as microhemorrhages or lacunar infarcts. A head MRI would be the next step to help rule out neuropsychiatric complications of Covid-19.

Catatonia

DSM-5 criteria for catatonia associated with major mood disorder and general health.

This patient had several features suggestive of catatonia. Using the Bush-Francis Catatonia Rating Scale, this patient would score for mutism, withdrawal, immobility and stupor, staring, verbal perseveration, and autonomic instability, with a score of approximately 13 (on a scale ranging from 0 to 23, with higher with results indicating more severe catatonia).21 Based on these reported examination findings, the patient would meet the criteria from Diagnostic and Statistical Manual of Mental Disordersfifth edition (DSM-5), for catatonia associated with major mood disturbance and general health (Table 1).22

Catatonia is a disorder of the cingulate cortico-striato-thalamo-cortical circuit that leads to a disconnection between motivation and movement, and has several neuromedical and psychiatric causes.23,24 Catatonia has been reported in several patients with Covid-19.25 In a small study evaluating the results of positron emission tomography and head CT performed in patients with Covid-19 encephalopathy, there was evidence of persistent hypometabolism in the prefrontal cortex, anterior cingulate cortex, insula and caudate cortico-striato-thalamo-cortical network .26

It is possible that this patient had Covid-19-related changes in the blood-brain barrier and choroid plexus that disrupted the cingulate cortico-striato-thalamo-cortical circuit and increased the risk of catatonia. Another possibility is neuroleptic-induced catatonia associated with olanzapine administration. In addition, the patient had a history of hospitalization for probable bipolar affective psychosis and catatonia, and bipolar disorder is the most common cause of psychogenic catatonia. There were no data to indicate catatonia caused by conversion disorder.

The patient’s catatonic symptoms resolved after treatment with a benzodiazepine, which is the first-line treatment for catatonia. However, one of the most striking features of her presentation remains to be explained: her persistent thoughts that she is dead.

Cotard syndrome

This patient expressed self-deprecation and guilt for not being able to care for her father, and had mood-consistent delusions that she and others were dead, along with a delusion that her bladder had disappeared. Her presentation is consistent with Cotard syndrome, a syndrome included in the DSM-5 category of delusional misidentification syndrome.27,28 Patients with Cotard syndrome have nihilistic delusions, such as the belief that they are dead, have lost their souls, or are rotting inside, without functioning organs or limbs. Three subtypes of Cotard syndrome have been described: psychotic depression (a disorder associated with melancholia and nihilistic delusions), type 1 (a nondepressive delusional disorder), and type 2 (a disorder associated with mixed symptoms, including anxiety, depression, and auditory hallucinations).29 Cotard syndrome has been reported in at least one patient with Covid-19,30 and catatonia and Cotard’s syndrome can occur simultaneously.31,32

Support and reassurance are crucial in the treatment of patients with Cotard syndrome, but trying to dissuade patients from delusions is futile. Successful treatment of the underlying condition often helps delusions resolve, although delusions may wax and wane in patients with persistent depression and may become chronic in patients with schizophrenia. Several antipsychotic drugs have been reported to reduce the symptoms of Cotard’s syndrome. If medications fail, electroconvulsive therapy is an important therapeutic option. This patient has received electroconvulsive therapy in the past for the treatment of catatonia, and such therapy has a broad spectrum of action for the treatment of multiple delusions, including Cotard’s syndrome.27 Transcranial magnetic stimulation has shown promising effects in patients with catatonia.33

I suspect that this patient had neuroinflammation associated with Covid-19 that contributed to the depression, catatonia, and Cotard syndrome.



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