Unresponsive and mute after he smoked ‘Spice’
Mr. R, age 19, who has no psychiatric history, experiences new-onset catatonia after ingesting a synthetic cannabinoid with the street name ‘Spice.’ How would you care for him?
TREATMENT Benzodiazepines, ECT
Mr. R is admitted for stabilization of catatonic symptoms. A basic metabolic panel, CBC with differential, urine drug screen, urinalysis, folate level, thyroid-stimulating hormone level, vitamin B12, EEG, and a stool culture are unremarkable. Ammonia level is slightly elevated at 40 µmol/L.
Mr. R is started on IM lorazepam, 1 mg every 8 hours. Antipsychotics are held in part because of an elevated CK level (614 U/L). CK is rechecked daily and increases to 5,681 U/L by the second week. Internal medicine is consulted because Mr. R could develop NMS. However, the treatment team thinks that CK elevation is caused by immobility, because Mr. R remains afebrile, normotensive, and without leukocytosis.
After 4 days of treatment, Mr. R can follow simple commands. He nods or shakes his head when questioned. IV fluids are started because of limited oral intake. As the month progresses, Mr. R’s CK levels slowly trend downward, toward 500 U/L.
Mr. R progresses slowly with benzodiazepine therapy. He begins to ambulate, make eye contact, and look at interviewers. Lorazepam is slowly titrated to 4 mg IM every 8 hours. On hospital Day 20, his functioning reaches a plateau; Mr. R’s cognition continues to fluctuate with periods of unresponsiveness, immobility, and incontinence.
The treatment team obtains consent from the family to begin ECT. On hospital Day 24, bilateral transtemporal ECT is initiated and continued 3 times a week. Mr. R tolerates the procedure without complications. After the first treatment, he demonstrates spontaneous speech for the first time since admission. He continues to improve overall but has a variable clinical course.
By Day 30, Mr. R can state the day, month, year, and that he is in the “psych” unit. He remembers being on the unit for a long time and says that he had been attempting to talk but “it wasn’t coming out.” When further questioned about substance use, he admits to using Spice for the month before admission and marijuana regularly over several years. He denies using other illicit drugs or alcohol.
Mr. R is started on olanzapine, 2.5 mg/d, titrated to 15 mg/d. He becomes increasingly interactive, although with occasional bouts of confusion, and regains bladder and bowel control. He receives a total of 12 ECT treatments. The family is adamant that Mr. R should not receive more ECT treatments, and is not interested in maintenance therapy. Mr. R’s father and grandmother visit and believe that he is back to baseline functioning. After 51 days of inpatient treatment, Mr. R is discharged on olanzapine, 15 mg/d, and oral lorazepam, 1 mg/d.
Nine days later, Mr. R is brought to the ER because of unresponsiveness, poor oral intake, refusal of medication, bowel and bladder incontinence, and inability to perform ADL. His father reports that he administered olanzapine but, because he only recognized the brand name of lorazepam, he did not get that prescription filled. Mr. R slowly decompensates and, by the time of readmission, refuses all medications.
Over the next few months, Mr. R is readmitted several times for similar symptoms. Again, the family states they do not want further ECT; the father believes that these treatments have caused his son’s condition. Complicating the matter is that the father had been out of his son’s life for an extended period and is unaccustomed to his son’s display of psychiatric symptoms.
The authors’ observations
The use of ECT for drug-induced psychosis is not well described in the literature because substance abuse is exclusionary in many trials. The safety and efficacy of ECT has been established for adolescents with first-episode psychosis14 and with catatonia.15,16
The use of ECT in Spice-induced catatonia has been reported in 2 case studies.17,18
Case 1. A 36-year-old man with schizophrenia and Cannabis dependence was admitted for auditory hallucinations, disorganization, paranoia, and manic symptoms, which progressed to catatonia.17 His symptoms were profound, including psychomotor retardation, rigidity, posturing, waxy flexibility, and inability to perform ADL.
The patient later reported that, 3 weeks prior, he had stopped taking his psychotropic medications and started smoking “K2,” a synthetic cannabinoid, because it was cheaper and easier to obtain than Cannabis. He had never experienced disturbances in motor function or speech in the past, even during episodes of Cannabis use and medication non-adherence.
After clozapine and benzodiazepine treatment (as high as 12 mg/d of lorazepam) did not resolve his symptoms, the patient received 6 bilateral ECT treatments over 16 days, with complete resolution of catatonic symptoms. He showed marked improvement, including resumption of speech after the first treatment, although he required an additional 20 days of inpatient care. As in our case, exposure to synthetic cannabinoids was self-reported; no confirmatory tests were performed.
