Only binge drinking days were significantly lower in the post-CCA sample, and the groups did not differ on anxiety symptoms, with evidence of greater sleep interference in the post-CCA sample when participants with data that straddled the CCA were excluded. All of these pre-to post-CCA differences were relatively modest with small to moderate effect sizes for the substance use outcomes and small effect sizes for psychopathology. Given the large size of the U.S. college population, though, these modest effects can have large overall impacts. Universities should continue to consider innovative ways to screen for substance use and mental health symptoms and to initiate treatment, and those with pre-existing problems might have the greatest treatment needs. As more states have legalized both recreational and medical marijuana use, the number of first-time users has risen dramatically. The perception that marijuana is an innocuous drug has led to significant increases in cannabis consumption both for its recreational properties and for its alleged medicinal properties.As a result, emergency departments and psychiatrists are treating a growing number of patients with medical and psychiatric complications of cannabis use.Cannabis users are being exposed to higher concentrations of delta 9-tetrahydrocannabinol  than in previous years. In the 1960s and 1970s, confifiscated marijuana samples contained anywhere from 1% to 3% THC. However, the average concentration of THC found in illicit samples has grown to approximately 12% in 2014.3 On the other hand, the content of cannabidiol  has shown a general decline over the last decade, going from approximately 0.5% in 2004 to less than 0.2% in 2014.3 THC is the primary compound implicated in the psychoactive effects of marijuana. The effects of THC are primarily mediated through two G protein-coupled receptors, cannabidiol receptor 1 , and cannabidiol receptor 2 .

CB1 receptors in the brain are primarily expressed in the neocortex, basal ganglia, and hippocampus. CB2 receptors are primarily in the immune system but also in the central nervous system at lower concentrations than CB1. CBD is a compound produced by the grow cannabis in containers plant that is believed to block or reduce many side effects of THC. CBD lacks significant affifinity for the CB1 receptor but has been shown to displace THC at low concentrations. It is postulated that CBD may act antagonistically against THC at CB1 via a nonorthosteric binding site. When CBD is coadministered with THC, it significantly reduces tachycardia and anxiety associated with THC.Cannabis containing high CBD content has also been associated with fewer symptoms of psychosis in recreational cannabis users.Furthermore, synthesis of high-potency resin/hash oils through solvent extraction has resulted in THC concentrations reaching as high as 80%. Resin oil is commonly created using butane and aptly named “butane hash oil,” “oil,” “dabs,” “honeycomb,” and “wax.” “Dabbing” is a common term to describe the inhalation of vaporized resin oil or wax. Marketing of resin oil has focused on superior pain relief, better utilization of the cannabis plant, and less product needed for the same effect. Resin oils can be used with a classic “oil rig” water pipe or e-cigarette  device.6 Vaping devices, or “e-cigarettes,” are used as a delivery system for nicotine, THC, and other chemicals. Advertisements focus on flflavoring, being “safer” than traditional cigarettes, not leaving behind a stench, and being easier to hide.7 There is growing concern for the use of vaping products especially among teenagers. For the first time, the National Institute on Drug Abuse’s Monitoring the Future Survey of 2019 included reports on daily cannabis vaping, with 0.8% of eighth graders, 3.0% of tenth graders, and 3.5% of twelfth gradersreporting daily use.

National Institute on Drug Abuse data also indicate that 14% of twelfth graders had engaged in THC vaping in the past month. Moreover, the number of students answering “Yes” to the question of “ever vaping” more than doubled from 2018 to 2019: 7% of eighth graders, 19.4% of tenth graders, and 20.8% of twelfth graders. This is the second largest 1- year jump ever tracked for any substance in the history of the 45-year-old survey. Of additional interest, the largest jump in the survey’s history was from 2017 to 2018 regarding nicotine vaping among twelfth graders.8 We present a case report of a patient who presented with symptoms of catatonia, mania, and psychosis in the setting of recent cannabis vaping and are concerned this severe presentation could be related to increased psychiatric toxicity associated with the high concentration of THC present in cannabis oils.Mr. R was a 20-year-old man with previous diagnoses of mania, cannabis use, and generalized anxiety disorder who originally presented to our psychiatric triage department with a chief complaint of “severe anxiety” and was admitted to our free-standing psychiatric hospital for evaluation and management. On the initial mental status examination after arrival on the unit, he exhibited severe poverty of thought content and appeared to be responding to internal stimuli. Most of his limited speech was repetitive and nonsensical with repeating phrases such as “shoes and socks.” He was also seen making bizarre postures in the hall, standing on one foot, holding his hands above his head, or standing with his head between his knees without moving for extended periods of time. He also avoided eating or drinking.

A Bush-Francis catatonia rating scale was administered at that time and was positive with a score of 19 for symptoms of mutism, posturing, stupor, staring, grimacing, verbigeration, stereotypy, and withdrawal. He exhibited paranoia in not wanting to take medications and fearfulness of being outside of his room. He was given a 2 mg intramuscular lorazepam challenge with some improvement of his symptoms, with a lowered Bush-Francis score of 10. At that time, the diagnoses of catatonia and psychosis were made. Owing to communication difficulties related to profound thought blocking and internal preoccupation, history taking from him was difficult. Laboratory studies were ordered including a complete blood count, complete metabolic panel, thyroid stimulating hormone, HIV, and urine drug screen. These were unremarkable aside from a urine drug screen immunoassay that was positive for cannabinoids and negative for cocaine, opiates, benzodiazepines, amphetamines, and barbiturates. We were unable to characterize the amount or pattern of cannabis use at that time because of his inability to provide information himself. From this, we learned he had one other admission six months before the first admission, with no reported manic or psychotic symptoms before this. He had also been diagnosed with generalized anxiety disorder and prescribed paroxetine by his primary care provider for several years before presenting to our hospital for the first time. He had taken a prescription stimulant brieflfly a year before admission to help with poor attention during college courses but was not taking this before either admission. During the first admission, he was found to have mania and psychosis with symptoms of grandiosity, decreased need for sleep, and psychomotor agitation. The psychiatrist postulated his symptoms were due to either his new onset use of vaping cannabis  or underlying bipolar disorder . A urine drug screen immunoassay during this admission was also positive only for cannabinoids. He suggested that his pot for cannabis use had preceded the onset of the symptoms of mania and psychosis. At that time, he was started on olanzapine and lithium, and his acute psychiatric symptoms resolved before discharge. His outpatient psychiatrist later questioned the diagnosis of BPD and favored a substance-induced etiology for his symptoms. He was tapered off of lithium and olanzapine and then started on sertraline for generalized anxiety disorder. He continued on this regimen for 6 months and according to notes by his outpatient therapist was functioning well without recurrence of psychosis or manic symptoms. His parents were heavily involved in his care and acted as surrogate decision makers when needed owing to his lack of capacity.

They corroborated the history from his past hospitalization but were unaware of his substance use before the current admission.During his most recent hospitalization, he was started on 2 mg of lorazepam  every four hours. Owing to the diagnosis of catatonia, further laboratory studies were performed, including creatine phosphokinase , which was elevated to a peak of more than 700 U/L. He also continued to refuse to eat or drink. For these reasons, he was sent by an ambulance to an associated medical hospital owing to the need for intravenous hydration that could not be provided at our free-standing psychiatric facility. He was seen by the medical hospital’s consultation-liaison psychiatry service and continued on lorazepam given intravenously and titrated to a total daily dose of 5 mg. He was restarted on lithium at this time as he had responded well to this medication during his prior hospitalization, and there was concern that his symptoms could be related to an underlying BPD. He was not started back on olanzapine as in his prior admission owing to concerns this could exacerbate his catatonic state. After three days, he had stabilized enough to transfer him back to our psychiatric facility. From there, we continued treatment with lorazepam, and his symptoms of catatonia continued to improve: his speech became more flfluid and he was able to engage in meaningful clinical discussions, was active on the unit, behaved appropriately with staff, and was able to meet his physical needs by eating and drinking. Lithium was titrated to a dose of 900 mg daily, and he was continued on sertraline 100 mg daily owing to history of generalized anxiety disorder. At the time of his discharge, his CK level had returned to within the normal limits, his lithium level was 0.4, and his Bush Francis score was 0. After the catatonic symptoms resolved, he was more capable of providing a detailed history of the events leading up to his admission. The history surrounding this episode was similar to his prior hospitalization: he once again reported symptoms of grandiosity, increased activity, decreased need for sleep, hallucinations, and paranoia in the days leading up to admission and again reported daily cannabis oil vaping for 14–21 days before his presentation. He felt that his symptoms were again related to heavy use of vaping cannabis just before onset of symptoms of mania and psychosis. Although he did report a long history of anxiety, the symptoms of mania, psychosis, and catatonia were only present during periods of cannabis use. He denied a history of major depressive episodes and did not believe he had BPD. He reported first use of cannabis one year prior to his first admission, with use increased in the month before his first admission after he obtained a vaping device. He also reported experimentation once with alkyl nitrate “poppers,” but use of these were not associated with his admissions. He reported a family history of anxiety symptoms in his mother and obsessive compulsive disorder in his brother. After a total hospitalization of eleven days, he was discharged home on lorazepam, sertraline, and lithium with close outpatient follow-up with our residency clinic.

Over a period of 4 months, he was slowly tapered off of lorazepam, decreasing by 1 mg per month. He was continued on lithium 900 mg daily and sertraline 100 mg daily. After eight months of no significant mood symptoms, he was tapered off of lithium. No further mood symptoms have been noted since that time. He reported no further use of cannabis since hospital discharge.Catatonia is a neuropsychiatric condition commonly characterized by striking behavioral abnormalities and can progress to life-threatening symptoms in severe cases. Common symptoms include immobility, mutism, refusal to eat or drink, staring, and negativism. A typical laboratory evaluation includes tests to rule out underlying medical conditions and substance use. In addition, serum creatine phosphokinase, white blood cell count, and serum transaminases can be elevated in patients with catatonia. Because catatonia impairs the ability to care for oneself, hospitalization is usually required. Fluid and nutrient intake must be maintained, often with intravenous lines or feeding tubes as patients with this syndrome often do not eat or drink. Benzodiazepines such as lorazepam are considered the firstline treatment for catatonia.9 Before 1970, catatonia was primarily linked with schizophrenia. Literature since the 1970s indicates catatonia is common among psychiatric inpatients and occurs most often in mood disorders such as bipolar disorder  with mixed or manic symptoms .