CASE: New-onset psychosis
Ms. T, age 26, presents to the psychiatric emergency room after a 1-week change in behavior. According to her family, Ms. T began to experience hyperactivity, increased rate of speech, and decreased sleep after her mother passed away 1 week ago. On the day of presentation, Ms. T had returned to work after a week’s hiatus. Coworkers brought her to the hospital when Ms. T threw herself on the floor and flailed about. Family members report that Ms. T had been complaining of headache that day and during the preceding week. In the emergency room, the patient is intrusive and easily distractible, although able to give a history.
Ms. T has no psychiatric history. Her family history is positive for bipolar spectrum illness. Our initial consideration is that Ms. T is experiencing mania or psychotic symptoms triggered by the recent loss of her mother. Ms. T is evaluated in the medical emergency room to rule out a primary medical illness. Standard labs and head CT are normal, so she is returned to the psychiatric emergency room. She becomes severely agitated and requires multiple IM antipsychotics—2 courses of haloperidol, 10 mg; 2 courses of ziprasidone, 20 mg; and olanzapine, 10 mg. She is admitted to the inpatient psychiatric service with a diagnosis of psychosis not otherwise specified.
Soon after admission, Ms. T suffers a witnessed generalized tonic-clonic seizure and is transferred to the internal medicine service. After the seizure she is awake but minimally responsive. She does not display purposeful movements, opens her eyes but can follow the examiner only on occasion, and displays periodic facial grimacing. In addition, Ms. T is intermittently hypoxic—requiring supplemental oxygen via nasal cannula—and febrile, with persistent tachycardia. Electroencephalography (EEG) shows nonconvulsive status epilepticus involving the bilateral temporal regions.
Ms. T is transferred to the neurosurgical intensive care unit for monitoring and IV anticonvulsants. Subsequent EEGs demonstrate generalized slowing but no epileptiform activity. An infectious workup is negative. Head MRI shows bilateral cerebellar T2/FLAIR increased signal, which is a nonspecific finding. Cerebrospinal fluid (CSF) studies show lymphocytic pleocytosis and oligoclonal bands. These findings suggest a CSF humoral immune response; an extensive laboratory workup is otherwise largely unremarkable ( Table 1 ).
The authors’ observations
We consider that Ms. T may have schizophrenia. Schizophrenia onset is insidious, often with prodromal symptoms occurring months to years before diagnosis.1,2 In Ms. T, the onset of the disturbance was brief; her family noted a change in behavior for only 1 week before presentation. Given this history, brief psychotic disorder remains high on the differential diagnosis because Ms. T’s disorganized speech and behavior occurred seeming in relation to her mother’s death.
Bipolar disorder is characterized by strong heritability, with risks increasing if there is a first-degree relative with the illness. The hallmark of bipolar I disorder is a manic episode, which presents as:
- decreased need for sleep
- grandiosity
- flight of ideas
- reckless or thoughtless behaviors
- increased energy
- increased productivity
- expansive or irritable mood.
Psychiatric symptoms secondary to seizure disorder are well documented. Cognitive, mood, anxiety, and psychotic phenomena may occur in up to 50% of patients with seizures.3 Typically, these symptoms are categorized as occurring during a seizure, after a seizure (post-ictal), or between seizures (interictal).
Manic syndromes secondary to seizure disorders present in an atypical manner with irritability and hyperactivity. Psychotic syndromes, on the other hand, appear with more classic schizophrenia-type symptoms:
- paranoia and persecutory delusions
- auditory and visual hallucinations
- amotivation
- apathy
- flattened affect
- disorganization.3
Paraneoplastic syndromes may be associated with mood changes and other psychiatric symptoms.4-6 Diagnosis is contingent on discovering the primary neoplasm, with or without specific paraneoplastic antibodies. Treatment is tailored to the oncologic process.
Table 1
Ms. T’s laboratory workup*
Test | Result |
---|---|
C-reactive protein | 0.7 |
Erythrocyte sedimentation rate | 5 |
Cryptococcal antigen (serum) | Negative |
Antinuclear antibody | Negative |
CSF lymphocytes | 88 |
CSF nucleated cells | 200 |
CSF RBC | 33 |
CSF glucose | 44 |
CSF protein | 45 |
CSF igG index | 1.2 |
CSF oligoclonal bands | Present |
CSF: cerebrospinal fluid; igG: immunoglobulin G; RBC: red blood cell | |
*Results were negative for gonorrhea, chlamydia, lupus, human immunodeficiency virus, syphilis, Lyme disease, varicella zoster virus, West Nile virus, herpes simplex virus, Epstein-Barr virus, cytomegalovirus, tuberculosis, and California, St. Louis, eastern equine, and western equine encephalitis |