CASE Mute and nonresponsive
Mr. R, a 19-year-old African-American man, is brought to the emergency room (ER) because he has reduced oral intake and mutism, and is not attending to activities of daily living (ADL). His family reports gradual onset of symptoms over the past month after he began using “Spice,” a synthetic cannabinoid (Box1-8).
Mr. R has been using marijuana regularly for a few years. He has no history of psychiatric illness. The family history is positive for schizophrenia (mother).
Mr. R slowly stopped speaking and eating, and no longer responds to verbal stimulation. On examination, he responds only with unintelligible mumbling. Mr. R exhibits blunted affect and fails to maintain eye contact, looking to the side of the interviewer. He exhibits severe psychomotor retardation but without posturing or waxy flexibility. It takes him approximately 3 minutes to transfer between chairs, and he is incontinent of bladder and bowel.
Mr. R has not experienced a similar episode in the past, although he had exhibited brief paranoia while intoxicated with marijuana.
Before this episode, Mr. R had been moving between his grandmother’s and father’s homes and was attending high school classes. Recent stressful events include his brother’s incarceration and his father having re-entered his life after a long absence.
Which treatment would you initiate for Mr. R’s symptoms of catatonia?
a) dantrolene
b) a benzodiazepine
c) an antipsychotic
d) electroconvulsive therapy (ECT)
The authors’ observations
Catatonia is a common complication in a variety of psychiatric and medical contexts. It can be a feature of mood disorders, schizophrenia, metabolic disturbances, drug intoxication, neuroleptic malignant syndrome (NMS), and encephalopathy. The most common psychiatric comorbidity is bipolar disorder; as many as 25% of cases are caused by a medical or neurological condition.9 When accompanied by fever and autonomic instability, so-called malignant catatonia can lead to respiratory failure, coma, and death.
Catatonia is characterized by ≥3 of the elements outlined in Table 1.10
In DSM-5, catatonia is no longer considered a subtype of schizophrenia, but is a specifier in the following disorders: brief psychotic disorder, schizophreniform disorder, schizoaffective disorder, and substance-induced psychotic disorder. In addition, catatonia not otherwise specified is reserved for cases when the cause is not apparent; this diagnosis is intended to lead to greater recognition of catatonia and prompt initiation of treatment. DSM-5 stops short of classifying catatonia as an independent syndrome, however. Changes in clinical status can be charted with instruments such as the Bush-Francis Catatonia Rating Scale.
Workup and treatment
The initial workup of patients with catatonia is extensive. A basic metabolic panel can detect electrolyte disturbances and acute renal failure. Monitoring creatine kinase (CK) allows clinicians to assess for rhabdomyolysis. Patients should also undergo an infectious workup, including complete blood count (CBC) and chest radiography, because patients can develop pneumonia due to atelectasis or aspiration. Additional workup could include EEG, erythrocyte sedimentation rate, D-dimer, urinalysis, urine drug screen, antinuclear antibodies, magnetic resonance imaging, cerebrospinal fluid analysis, anti-N-methyl-D-aspartate receptor antibodies, and serum iron, which could predict development of NMS in patients treated with an antipsychotic.11
Treatment. In addition to supportive measures, the initial treatment of choice for catatonia is a benzodiazepine, lorazepam being the most commonly used agent; dramatic improvement in symptoms can be seen within minutes of IV administration. A high dosage of lorazepam (14 to 16 mg/d) sometimes is required for symptomatic relief. Zolpidem also has been used successfully to treat catatonia, although the supporting literature is less extensive.12
Antipsychotics generally are held during the initial stages of catatonia treatment because they can exacerbate symptoms and increase the likelihood of NMS. Glutamate antagonists, such as amantadine and memantine, also are being investigated for treating catatonia.9
ECT is effective but is reserved for when pharmacotherapy has failed or when a rapid response is required. ECT is associated with cognitive and medical complications, although current techniques have greatly mitigated the risks. Mortality is estimated to be 1 in every 10,000 patients or 1 for every 80,000 treatments, most often due to a cardiac or pulmonary cause.13 Patients receiving ECT could experience temporary anterograde amnesia and confusion as well as retrograde amnesia, particularly memories formed around the time of treatment.
Response to benzodiazepine therapy varies: Some patients experience significant improvement after 1 dose; others require a high dosage for an extended period. More than 70% of cases remit with benzodiazepines; ECT should be considered after several days or earlier if indicated.9 Some patients with catatonia require a slow benzodiazepine taper to prevent symptoms from recurring.
Patients with catatonia are at risk of dehydration and malnutrition, and might require IV fluids or parenteral nutrition. These patients also are at risk of constipation, ileus, decubitus ulcers, deep vein thrombosis, and pulmonary embolism. Encourage early ambulation and consider prescribing an antithrombotic. Some patients might require physical therapy to prevent or treat muscle contractures.