Catatonia in a 16-Year-Old

Chief Complaint and Presenting Problem

K.C. was a 16-year-old African American adolescent girl with no psychiatric history. She was referred from a regional hospital for further evaluation for bizarre behavior and no oral intake.

History of Present Illness

According to mother, the onset of K.C.'s illness occurred ∼7 days before referral. Mother brought her to the hospital for concerns about bizarre behavior, cessation of oral intake, isolative behavior, and inability to care for herself. Mother reported that K.C.'s condition had deteriorated over a period of 7 days; she had been initially isolative and mute, and then gradually stopped eating and drinking. Mother denied any constitutional symptoms such as fever, chills, or cough. Mother also denied any recent travel history or sick contacts.

Psychiatric History

K.C. had no past psychiatric hospitalizations or outpatient psychiatric treatment. She had never been diagnosed with or treated for any substance use disorders. She had no history of suicidal or homicidal ideation or attempts.

Developmental History

Mother reported that there were no complications during the pregnancy or birth, and no in utero exposure to any substances. K.C. was born full term by cesarean section, and birth weight was 7 pounds 5 ounces. She met all of her developmental milestones on time. K.C. did attend speech therapy for frontal lisp, which resolved after 3–4 years of speech therapy in elementary school.

Educational History

K.C. completed ninth grade with B's and C's. She was scheduled to start the 10th grade. She had no history of suspensions, and no history of specialized education.

Social History

K.C. raised by her mother, a single parent, in a nearby city. Mother describes living in an area with limited access to resources, and they did not have transportation due to financial limitations. Birth father was reportedly only intermittently a part of K.C.'s life. Father reportedly died of complications of drug use 1 year before referral. K.C. considered her maternal uncle to be a father figure; he had lived with her until his death 3 years prior. K.C. currently resided with her mother and cousin. There were no siblings.

K.C. was not reported to be in a romantic relationship. Mother was not aware of any specific substance use, but described her daughter as a “follower” and was concerned that she might be using alcohol or drugs with friends. Mother described her as being highly influenced by her peers. Mother denied a history of sexual, physical, or emotional trauma.

Family History

There was no known family history of psychiatric illnesses or suicide. There was a family history of substance use in her biological father (unknown substances), maternal uncle (unknown substances), and mother (cocaine use with 17 years of abstinence). There was a family history of congestive heart failure.

Medical History

Mother denied K.C. had any past medical conditions. K.C. had no history of seizures, loss of consciousness, or traumatic brain injury. She had no past hospitalizations or surgeries, and had no known allergies. She had received all of her vaccinations except the COVID-19 vaccination.

Mental Status Examination on Admission to the ED

Mental status examination revealed an African American adolescent who appeared her stated age and was wrapped in a blanket. She was unable to provide any history upon initial evaluation, and stared blankly into the room with simple nods to yes or no questions. She was disheveled with poor grooming. She was noncooperative and minimally conversational. K.C. was not alert or oriented to time or place. She appeared to have normal posture and did not have repetitive movements or rigidity of hands upon examination. Her affect was flat and mood was constricted throughout the interview. She demonstrated pronounced psychomotor retardation. She also had poverty of speech, and was only able to nod “yes or no” to questions. Thought process was concrete and disorganized. Thought content was not obtainable due to her condition. It appeared that she was not actively responding to internal stimuli; however, she appeared fearful. She appeared to be experiencing dissociation with her environment and was staring into the walls. Insight and judgment were poor and extremely limited due to her condition.

ED Evaluation

After 4–5 hours of observation, K.C. became nervous and started shaking her head rigorously saying, “I want to leave right now.” It was clear that she was not aware of her surroundings and was not able to comprehend the reason for her admission. Urine toxicology was presumptively positive for cannabis use, but not for any other substance.

Bush Francis catatonia rating scale was 2/14 for screening, 5/23 for severity, and negative for catatonia. Urine pregnancy test and noncontrast head computed tomography scan were unremarkable. Laboratories were remarkable for leukocytosis (WBC 16.2). K.C. experienced mild tachycardia with a heart rate of 107 BPM.

K.C. was diagnosed with psychosis not otherwise specified; differential diagnosis included cannabis-induced psychosis. Consent was obtained to treat her with olanzapine 5 mg p.o. for her thought disorder. K.C. was subsequently admitted to the inpatient child and adolescent psychiatry unit for further evaluation and treatment.

Hospital Course

On admission to the unit, K.C. continued to demonstrate poverty of speech. She showed no improvement after the 1st day of treatment with olanzapine 5 mg p.o. nightly. There was concern for dehydration and an underlying organic cause for her presentation, given her leukocytosis on admission and tachycardia of 107. She was transferred to pediatric emergency department (ED) for further medical workup. In the ED, a urinalysis revealed that K.C. had a urinary tract infection (UTI). Repeat CBC showed an improvement in the leukocytosis. No further laboratory work or imaging was obtained. She received a second dose of olanzapine 5 mg p.o. nightly while in the ED before her return to the inpatient child and adolescent psychiatry unit, and was prescribed cephalexin 500 mg p.o. q.i.d. for 5 days.

On admission to the unit, K.C. was observed to be staring with decreased blinking, preserved posturing whereby she would sit still without any movement for sustained periods of time, some facial grimacing, and repetitive nonpurposeful head shaking. Bush Francis catatonia rating scale was performed again and she scored 10 on the screening score, and 20 on the severity score, consistent with catatonia.

A lorazepam challenge was subsequently undertaken with lorazepam 2 mg i.m.. Fifteen minutes later, K.C. showed more reactivity to stimuli in her environment. She began shifting her gaze spontaneously to people addressing her or people walking by her. A second dose of lorazepam 2 mg i.m. was given. At that point she asked for chips, and she drank a cup of water. Lorazepam 2 mg p.o. was scheduled q4h with monitoring of vitals, with parameters to hold the dose for suppression in vitals and/or sedation. K.C. tolerated the medication well without requiring any held doses.

After the 1st day of treatment, she was manifested a staggering gait, and there was concern for too much sedation with a risk of falls. Lorazepam was reduced in frequency to lorazepam 2 mg p.o. q6h. She tolerated this dose for 2 days; however signs, including decreased interactions with others, staring, psychomotor retardation, and posturing, recurred. Frequency of dosing was increased to lorazepam 2 mg p.o. q4h that she tolerated well.

K.C. subsequently began to interact with peers, eat regular meals, and demonstrate improved eye contact. On the 2nd day of treatment, she was more spontaneous in speech, engaging in meaningful conversations, and verbalizing how she felt. Her movements were more fluid.

At this time, K.C. was able to endorse prior daily cannabis use. She reported that she had begun using at age 13 years, with use increasing to one joint per day recently. She also endorsed social alcohol use. By day 3 of lorazepam 2 mg q4h, mother reported that K.C. was back to her baseline. K.C. was then discharged to continue outpatient treatment with a plan to taper lorazepam with close follow-up.

Upon outpatient follow-up within 5 days, K.C.'s condition had resolved and she was tolerating her medication regimen well. She reported adherence and denied any suicidal or homicidal ideation. She continued to deny symptoms of paranoia and psychosis. Per mother, K.C.'s oral intake was improved. After discussion with mother and K.C., the plan was to taper lorazepam 2 mg q4 hours to 2 mg p.o. q5 hours for the next 2 weeks, and to further taper over the next month. Olanzapine was also decreased from 5 mg p.o. qHS to 2.5 mg p.o. qHS with a plan to discontinue it in the next 2 weeks if her condition remained stable. K.C. had not used cannabis since her discharge from the hospital.

Brief Formulation

In summary, K.C. was a 16-year-old African American adolescent girl with no psychiatric history referred for emergency evaluation of bizarre behavior and poor oral intake. She had experienced sudden onset of isolative behavior, poor oral intake, and disorganized thought process that preceded her presentation of mutism and poor hygiene. On initial examination, she exhibited mutism, staring spells, posturing, waxy flexibility, and flat affect. The Bush Francis catatonia rating scale was consistent with catatonia. Toxicology screen was positive for cannabis use, which had increased in quantity over the past few months. She was treated for a UTI and admitted to a child and adolescent psychiatry unit with a presumptive diagnosis of psychosis not otherwise specified, and to rule out cannabis or other substance-induced psychosis. Lorazepam challenge test was successful in demonstrating immediate improvement, and treatment was started with ongoing lorazepam. Treatment was a challenge since K.C. exhibited mixed psychotic features in the context of catatonia, cannabis use, and a UTI.

K.C. was predisposed to her illness by a strong family history of substance use disorder. Her illness was precipitated by escalating cannabis use and a cannabis use disorder, and perpetutated by several important factors, such as loss of male parental figures, peer influences, and lower socioeconomnic status. Protective factors included lack of known family history of psychosis, her gender, lack of comorbid disorders, strong maternal support, involvement in school, and a willingness to engage in and adhere to treatment.

Multiaxial Diagnoses

Discussion

This case presents an interesting diagnostic challenge of progressive catatonia in the setting of leukocytosis and heavy cannabis use. In addition, this presentation raises questions about the nature of substance-induced catatonia and its relationship with psychosis.

When K.C. was discovered to have a UTI, the possibility of delirium secondary to infection was considered; however, K.C.'s age made this diagnosis less likely. In addition, treatment of the UTI did not lead to symptom resolution, suggesting instead that the UTI was a complication of decreased p.o. intake and resulting urinary stasis, as has been noted in the catatonia literature (Funayama et al. 2018).

The most remarkable aspect of K.C.'s history was her significant cannabis use. As urine drug screening was positive for cannabis, cannabis use was considered as a potential etiology for the presenting symptoms. Prior research has indicated that the use of cannabinoids in adolescence increases the risk of psychosis in a dose-dependent manner (Radhakrishnan et al. 2014). However, as the patient's clinical status improved, she continued to deny the presence of perceptual disturbances and delusions. She also denied ever experiencing psychotic symptoms in the past, thus rendering catatonia secondary to a psychotic process less likely.

As K.C.'s symptomatology improved, she was able to clarify her history of daily cannabis use before her admission, which, in the absence of evidence indicating an alternative etiology, led us to strongly consider a catatonic process secondary to heavy cannabis use. Catatonia produced by use of cannabinoids or synthetic cannabinoids has been reported in case reports, and recently summarized in a review article (Palma-Álvarez et al. 2021). The mechanism through which cannabinoids trigger catatonia is hypothesized to be similar to the mechanism through which they trigger psychosis, but this has not been proven (Palma-Álvarez et al. 2021).

Although catatonia was long considered to be a feature of schizophrenic disorders, the DSM-5 includes diagnoses of catatonia secondary to a generalized medical condition, catatonia as a specifier for several psychiatric diagnoses, and catatonic disorder not otherwise specified (Tandon et al. 2013). Of note, some scholars have advocated for catatonia to be an independent diagnostic class, as the understanding of catatonia outside of the schizophrenic spectrum expands (Tandon et al. 2013). As K.C. neither demonstrated nor endorsed psychotic symptoms nor met criteria for a mood disorder, a diagnosis of catatonia secondary to cannabis use disorder seemed most appropriate, although catatonia is not a specifier for substance use disorders in the DSM-5. In the previously cited review of 14 patients with catatonia secondary to cannabis use, 4 patients did not exhibit concomitant psychotic symptoms (Palma-Álvarez et al. 2021). This indicates that the phenomenon of substance-induced catatonia without psychosis may be an area for future study.

In accordance with all other reported cases of cannabis-induced catatonia, we opted to treat K.C. with benzodiazepines. She required high doses of lorazepam for symptom relief; if symptoms had not improved adequately with lorazepam, ECT would have been considered. A challenge for use of high-dose benzodiazepines is the need for the close and frequent follow-up to prevent withdrawal and to manage tapering on an outpatient basis. K.C. was placed on olanzapine at the time of admission due to initial suspicion for psychosis; given that her condition continued to deteriorate until lorazepam was initiated, the exact role of the antipsychotic in this case was less clear. Although antipsychotics may be helpful in treating catatonia secondary to psychosis, they may also potentiate catatonia symptoms in some cases. For K.C., the importance of avoiding cannabis use in the future was emphasized.

In summary, this case illustrates a unique presentation of catatonia in an adolescent without psychosis believed to be secondary to heavy cannabis use. It is possible that the described presentation represents a prodrome of an eventual psychotic illness for which K.C. should be monitored. Clinicians should be aware of and prepared to treat atypical presentations of catatonia, such as those caused by cannabinoids.