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Abstract

Catatonia is a severe motor syndrome found in approximately 10% of all acute psychiatric hospital admissions. It can occur in various psychiatric diseases. We report the first case report of catatonia during cannabis withdrawal. Mr. A, a 32-year-old man, reported to have daily smoked approximately 20 grams of cannabis since aged 11 years. Mr. A was incarcerated and was reported three weeks later to the medical department for having completely ceased talking and eating. At admission in our department, the patient presented with classical catatonia symptoms (Bush-Francis Catatonia Rating Scale (BFCRS) score = 39/69). All laboratory results and brain MRI were normal. Six weeks after his admission and treatments by lorazepam and memantine, his BFCRS score was 0/69. This single-case study highlights the previously under-reported emergence of physical and motor symptoms following cannabis withdrawal. Pathophysiological aspects of abrupt cannabis cessation contributing to GABA/glutamate balance dysregulation and to catatonia are discussed.
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Catatonia and Cannabis Withdrawal: a case report
Mathieu Caudron M.D.
a
, Benjamin Rolland M.D. PhD
bc
, Sylvie Deheul M.D.
d
, Pierre Alexis
Geoffroy M.D.
efg
, Pierre Thomas M.D. PhD
a
& Ali Amad M.D. PhD
a
a
Pôle de psychiatrie, Univ Lille Nord de France, CHRU de Lille, F-59000 Lille, France
b
Addiction Consultation-Liaison Service, Department of Addiction Medicine, University
Hospital of Lille, France
c
Department of Pharmacology, INSERM U1171, University of Lille, France
d
Department of Addictovigilance, University Hospital of Lille, France
e
Inserm, U1144, Paris, F-75006, France
f
Université Paris Descartes, UMR-S 1144, Paris, F-75006, France & Université Paris Diderot,
UMR-S 1144, Paris, F-75013, France
g
AP-HP, GH Saint-Louis - Lariboisière - Fernand Widal, Pôle Neurosciences, 75475 Paris
Cedex 10, France
Accepted author version posted online: 06 Aug 2015.
To cite this article: Mathieu Caudron M.D., Benjamin Rolland M.D. PhD, Sylvie Deheul M.D., Pierre Alexis Geoffroy M.D.,
Pierre Thomas M.D. PhD & Ali Amad M.D. PhD (2015): Catatonia and Cannabis Withdrawal: a case report, Substance Abuse,
DOI: 10.1080/08897077.2015.1052869
To link to this article: http://dx.doi.org/10.1080/08897077.2015.1052869
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1
Catatonia and Cannabis Withdrawal: a case report
Mathieu CAUDRON
1
M.D., Benjamin ROLLAND
2,3
M.D. PhD, Sylvie DEHEUL
4
M.D.,
Pierre Alexis GEOFFROY
5,6,7
M.D., Pierre THOMAS
1
M.D. PhD, Ali AMAD
1
M.D. PhD
1) Pôle de psychiatrie, Univ Lille Nord de France, CHRU de Lille, F-59000 Lille, France
2) Addiction Consultation-Liaison Service, Department of Addiction Medicine, University
Hospital of Lille, France
3) Department of Pharmacology, INSERM U1171, University of Lille, France
4) Department of Addictovigilance, University Hospital of Lille, France
5) Inserm, U1144, Paris, F-75006, France
6) Université Paris Descartes, UMR-S 1144, Paris, F-75006, France & Université Paris Diderot,
UMR-S 1144, Paris, F-75013, France
7) AP-HP, GH Saint-Louis - Lariboisière - Fernand Widal, Pôle Neurosciences, 75475 Paris
Cedex 10, France.
Correspondence should be addressed to Ali Amad, MD, PhD, Unité d'Hospitalisation,
Spécialement Aménagée (UHSA) Lille-Seclin, Chemin du bois de l'hôpital, 59113 SECLIN,
France. Email : ali.amad@outlook.com
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ABSTRACT. Background: Catatonia is a severe motor syndrome found in approximately 10%
of all acute psychiatric hospital admissions. It can occur in various psychiatric diseases. We
report the first case report of catatonia during cannabis withdrawal. Case presentation: Mr. A, a
32-year-old man, reported to have daily smoked approximately 20 grams of cannabis since aged
11 years. Mr. A was incarcerated and was reported three weeks later to the medical department
for having completely ceased talking and eating. At admission in our department, the patient
presented with classical catatonia symptoms (Bush-Francis Catatonia Rating Scale (BFCRS)
score = 39/69). All laboratory results and brain MRI were normal. Six weeks after his admission
and treatments by lorazepam and memantine, his BFCRS score was 0/69. Discussion: This
single-case study highlights the previously under-reported emergence of physical and motor
symptoms following cannabis withdrawal. Pathophysiological aspects of abrupt cannabis
cessation contributing to GABA/glutamate balance dysregulation and to catatonia are discussed.
Keywords: Cannabis withdrawal, catatonia, gaba/glutamate balance
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INTRODUCTION
Catatonia is a severe motor syndrome found in approximately 10% of all acute psychiatric
hospital admissions
1
. It can occur in various psychiatric diseases, including mood disorders and
schizophrenia, as well as substance intoxication/withdrawals and other medical conditions
1,2
.
This is the first published case report of catatonia during cannabis withdrawal.
CASE DESCRIPTION
Mr. A was a 32-year-old man incarcerated for interrupting a chase related to a drug
trafficking. His medical history showed evidence of mild intellectual disability (IQ = 67) and a
polyneuropathy at the age of sixteen, which affected his cranial nerves. Full recovery was
obtained with corticosteroid therapy. Family and general practitioner (GP) reports showed no
personal or family psychiatric history, nor notable personal medical history.
Mr. A. reported to have daily smoked approximately 20 grams of cannabis (resin and
marijuana), since aged 11 years. During three previous incarcerations for drug trafficking, he
reported using far lower amounts, without any complications. Due to religious and cultural
beliefs, Mr. A never consumed alcohol or other illicit drugs, confirmed by his GP and family.
Mr. A's family described his behavior as normal on the day before his imprisonment. Both the
GP and the psychiatrist who examined him on his arrival in jail did not report any medical
symptoms. During his current incarceration the patient was unable to obtain cannabis due to a
lack of money. Three weeks later the patient was reported to the medical department, having
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completely ceased talking and eating for several days, as well as having set his coat on fire,
without any skin damage thanks to intervention of the prison staff. The patient was then
transferred from jail to the emergency medical department due to confusion and mutism. Blood
tests were normal and after examination, the psychiatrist decided on compulsory admission to
our forensic psychiatry department.
At admission the patient presented with classical catatonia symptoms, including apathy,
mutism, disorientation in time and space, psychomotor agitation, catalepsy, waxy flexibility,
impulsivity, ‘mitgehen’ (movement in any direction in response to a very light finger pressure),
plastic hypertonia and cogwheel. On the Bush-Francis Catatonia Rating Scale
3
(BFCRS) the
patient scored 39/69, suggesting a diagnosis of catatonia. No psychotic symptoms, including
delusions or disorganization were evident.
Due to catatonic symptomatology, we attempted a zolpidem test
4
, but the patient refused
any oral treatment. We then decided to administer 1 mg of clonazepam by intramuscular
injection, which allowed for treatment with oral lorazepam, starting at 10mg per day
5
. By
gradually increasing the lorazepam dose, his symptomatology improved. At 25 mg per day, the
improvement in his catatonic symptoms stagnated. We then added oral memantine
5
, starting at 5
mg per day, which further decreased his catatonic symptomatology.
During this hospitalization, and given the patient’s history, many examinations were performed.
All laboratory results were normal, including: toxicological analyses (cannabis, amphetamines,
cocaine, opiates/opioids), full blood count, electrolyte panel, liver function panel, coagulation
panel, serum protein electrophoresis, C reactive protein, fibrinogen, blood glucose, thyroid
function tests, B9 vitamin, albumin, hepatitis panel, angiotensin converting enzyme, salivary
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gland biopsy, HIV and syphilis. The involvement of autoimmune and paraneoplastic processes
were also excluded by the analysis of a variety of factors, including: homocystein, anti-nuclear
antibodies, anti-transglutaminase antibodies, antineutrophil cytoplasmic antibodies and onco-
neural antibodies, which were all negative. The tuberculin skin test and quantiferon level were
also negative. Vitamin B12 and iron levels were normal. Brain MRI showed two minor non-
specific lesions in the white matter of the left periventricular and insular areas.
Six weeks after his admission, his BFCRS score was 0/69. After a period of consolidation,
his medication was decreased to lorazepam 1.5 mg/week, with no symptom re-emergence. Mr.
A left the hospital on his release from jail, with treatment continued in a psychiatry outpatient
department.
DISCUSSION
To our knowledge, this is the first reported case of cannabis withdrawal-induced catatonia.
Laboratory and imagery investigations were within normal limits and excluded delirium,
toxicological, neurological, systemic and paraneoplastic causes of his catatonic symptoms. We
hypothesize that the patient experienced catatonia following sudden heavy cannabis use
cessation. According to the WHO-UMC Causality Assessment
6
, derived from clinical-
pharmacological aspects of the case history, the causality between cannabis cessation and
catatonia was "probable", given that the event appeared with reasonable temporal relationship to
drug withdrawal and being unlikely to be attributable to disease or other drugs.
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Physical and motor symptoms are generally lower, compared with other symptoms, after
cannabis cessation
7
and the relation between cannabis dose and the magnitude of abstinence
effects is still being debated
8
. However, these symptoms are included in the DSM-5 cannabis
withdrawal syndrome
9
. Such physical symptoms occur more frequently from day 5 following
cannabis cessation
7
. However, given Mr. A's initial incarceration, there is no certainty as to the
sequence of symptom emergence, being only reported when clearly visible after at least two
weeks incarceration.
Pathophysiologically, abrupt cannabis cessation can dysregulate the GABA/glutamate
balance, contributing to catatonia. Indeed, chronic consumption of cannabinoids, like Δ9
tetrahydrocannabinol, decreases extracellular glutamate and increases extracellular GABA, as
well as enhancing dopamine release in both the striatum and mesolimbic system
10
. This pattern is
reversed by abrupt cannabis cessation, leading to a typical catatonia pattern of GABA-A and
dopamine D2 receptor hypoactivity and glutamate NMDA receptor hyperactivity
5
. Interestingly,
GABA-ergic regulating drugs, such as the selective GABA-B agonist, baclofen, show promise in
the management of cannabis dependence
11
.
In conclusion, the single-case study detailed here highlights the previously under-reported
emergence of physical and motor symptoms following cannabis withdrawal. This case report
further highlights how sudden cessation due to incarceration can be extremely dangerous,
without appropriate management. This common clinical situation requires careful monitoring
and more research on abrupt heavy cannabis cessation is needed in order to improve patient care
and management.
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FUNDING
The authors received no funds for this research. The authors declare no conflicts of
interest.
AUTHOR CONTRIBUTIONS
MC and AA managed the case, MC, BR and AA wrote the first draft, SD, PAG and PT
were responsible for critical revision of the manuscript. All authors have read and approved the
final version of the manuscript.
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... Abrupt cannabis cessation can dysregulate GABA/glutamate balance contributing to catatonia [10]. Interestingly, GABAergic regulating drugs such as selective GABA-B agonist Baclofen is postulated in the management of cannabis dependence [10]. ...
... Abrupt cannabis cessation can dysregulate GABA/glutamate balance contributing to catatonia [10]. Interestingly, GABAergic regulating drugs such as selective GABA-B agonist Baclofen is postulated in the management of cannabis dependence [10]. Our patient was unable to recall if he suddenly stopped using cannabis in the days leading to his admission. ...
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An association between cannabis and psychosis is well established. Cannabis use is known to precipitate schizophrenia in vulnerable individuals and it can exacerbate existing psychosis. However, there is a paucity of knowledge about the emergence of catatonia and abnormal gait associated with cannabis use. History of cannabis use is associated with long-lasting changes in open-chain elements of walking gait. Cannabinoid receptors are located in movement-related brain regions and cannabis use is suggested to affect gait. This report is a unique case of a 16-year-old male with no known past medical history, no past psychiatric history, with family history significant for psychosis who presented to the hospital for bizarre, disorganized behavior, and decreased oral intake following heavy cannabis use over the past three months in the context of a break-up. Upon arrival, he was found to be in a catatonic state with an impaired gait. As catatonia resolved with treatment, he was able to speak and the psychosis surfaced which was addressed with antipsychotics. This case report highlights an atypical but serious clinical picture observed to be precipitated by chronic, heavy cannabis use.
... This is in line with previous studies reporting a positive correlation between consumption of THC concentrations and risk for psychosis (Di Forti et al., 2009). Nonetheless, it should be mentioned that one case report on catatonia-like symptoms reported that catatonic symptoms were precipitated by cannabis cessation (Caudron et al., 2016). Hence, further studies are needed on how cannabis/SC concentrations are related to catatonic symptoms. ...
... Although the current review was focused on the relationship between cannabis or SC use and catatonia-like symptoms from a clinical perspective, several neurobiological factors that go beyond the scope of this review are also worth highlighting. Important factors to take into account are the gamma-aminobutyric acid (GABA) and the glutamate because both neurotransmitters are related to catatonia, cannabis use disorder and substance-induced disorders (Caudron et al., 2016;Deng et al., 2018;Duggal & Singh, 2005;Manseau & Goff, 2015;Walther et al., 2019). This could be related to the fact that THC may alter the physiological control that the endogenous cannabinoid system has on glutamate and GABA liberation (Deng et al., 2018). ...
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Objective: Cannabis and synthetic cannabinoids (SC) are related to several neuropsychiatric symptoms and disorders, especially psychotic symptoms and disorders. Interestingly, catatonia-like symptoms associated with cannabis and SC have been generally neglected in research and scarcely described despite the clinical repercussions. Hence, this review aims to analyze current clinical publications on catatonia induced by cannabis or SC in a systematized way. Methods: A search using PRISMA guidelines was performed on three databases based on a specific inclusion and exclusion criteria. Results: 11 publications describing 14 patients (10 males; mean age 22.50 ± 6.67 years old) with catatonia apparently precipitated by the use of cannabis (n = 6) or SC (n = 8) were found. Clinical features and treatment are described and discussed. Conclusion: From a clinical perspective, cannabis and SC use may be related to catatonia-like symptoms and catatonia syndrome in the same way these substances (cannabis and SC) are related to induced-psychotic episodes. However, further research will be required to understand the exact nature of that relationship. Additionally, investigations focused on the clinical significance (i.e., prognosis, evolution, and outcomes) of catatonia-like symptoms induced by cannabis and SC use in patients are also needed.
... 3 Such an overview was thus required as Addictovigilance signals have been identified, notably through the descriptions of young, apparently healthy, cannabis users suffering from unexpected cardiovascular disorders. 4 These findings, which corroborated those from other studies conducted in different contexts, [5][6][7][8][9][10][11][12][13] raise concerns as to whether cannabis use could also affect other systems. ...
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Aims: To describe the adverse events (AEs) of recreational cannabis use in France between 2012 and 2017. Methods: AEs related to recreational cannabis use, alone or in combination with alcohol and/or tobacco reported to the French Addictovigilance Network were analysed (excluding cannabidiol and synthetic cannabinoids). Results: Reporting of AEs tripled between 2012 (n = 179, 6.3%, 95% confidence interval [CI] = 5.4-7.2) and 2017 (n = 562, 10.1%, 95% CI = 9.3-10.9), reaching 2217 cases. They concerned mainly men (76.4%) and users aged between 18 and 34 years (18-25: 30.9%; 26-34: 26.3%, range: 12-84 years). Cannabis was mainly inhaled (71.6%) and exposure was most often chronic (64.2%). Many types of AEs were reported: psychiatric (51.2%), neurological (15.6%), cardiac (7.8%) and gastrointestinal (7.7%), including unexpected AEs (n = 34, 1.1%). The most common effect was dependence, ranging from 10.1% (95% CI = 7.9-12.3) to 20.3% (95% CI = 17.3-23.2) over the study period. Cannabinoid hyperemesis syndrome (n = 87, 2.8%) emerged from 2015. Deaths accounted for 0.2% of all AEs (4 men and 3 women aged on average 35 years). A chronic pattern of cannabis use was reported in 4 of them (intracranial hypertension in the context of lung cancer, suicide, cerebral haematoma, neonatal death with concomitant chronic alcohol use), while in the other cases the toxicological analysis identified cannabis use (ruptured aneurysm and unknown aetiology). Conclusion: This study showed a multitude of AEs related to recreational cannabis use, including unexpected AEs and deaths. It highlights the problem of dependence and the emergence of cannabinoid hyperemesis syndrome.
... substance-related catatonia has previously been described in a patient with acute amphetamine intoxication (Chern & Tsai, 1993) and in an individual with cannabinoid withdrawal (Caudron et al., 2016). More recently, Palma-Alvarez et al. (2021) conducted a systematic review of catatonia associated with cannabis or synthetic cannabinoid use and identified 11 case series or reports with a total of only 14 patients (Palma-Alvarez et al., 2021). ...
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Objective: Substance use has increasingly been linked to the onset of catatonic episodes; however, no large observational studies have examined this association. This study aimed to identify catatonic episodes temporally associated with acute intoxication, withdrawal or chronic substance use, investigate which substances were involved, and compare clinical characteristics of substance-related and non-substance-related catatonic episodes. Methods: This study retrospectively identified all catatonic episodes recorded in an electronic case register hosted at a large secondary mental health trust in London, UK. Episodes were categorized as substance-related if the clinical record reported either a positive urine drug screen, an ICD-10 diagnosis of a mental or behavioral disorder due to substance use, or documented substance use between two weeks prior to the catatonic episode and the date of the catatonic episode. Results: 108 of 2130 catatonic episodes (5.1%) were deemed substance-related. The number of contemporaneously reported substance-related episodes increased between 2007 and 2016 [r = 0.72, p = 0.02]. Episodes in the context of acute intoxication (n = 54) were most frequently related to cannabis (n = 31) or cocaine (n = 5) use, whilst those in the context of drug withdrawal (n = 8) were most commonly related to alcohol, opioids and benzodiazepines. There were 50 episodes of catatonia associated with chronic substance use without intoxication or withdrawal, of which the majority were related to cannabis use (n = 37). 21 episodes had overlapping intoxication, withdrawal and chronic use of different substances within an episode. Compared to catatonic episodes not related to substance use, episodes of substance-related catatonia occurred in individuals who were younger (mean age 31.3 years [SD 12.2] vs 35.7 years [SD 16.3], p = 0.01) and more likely to be men (74.0% vs 54.3%, p < 0.001). The clinical features of catatonia were similar between the two groups. Conclusions: A relatively small proportion of catatonic episodes were temporally associated with reported substance use within their electronic records. Substance-related catatonic episodes were mostly related to cannabis use, but other substances including cocaine, alcohol, opioids and benzodiazepines were sometimes implicated. This is likely an underestimate of substance-related catatonia use due to issues with documentation and appropriate investigation.
... [14][15][16][17]. ...
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Chapter
The catatonic syndrome is an example of a multifactorial neurobehavioral disorder that causes much morbidity and mortality but also has the potential to unlock the mystery of how motivation and movement interact to produce behavior. In this chapter, an attempt is made to understand better the catatonic syndrome through the lens of neurobiology and neuropathophysiology updated by recent studies in molecular biology, genomics, inflammasomics, neuroimaging, neural network theory, and neuropsychopathology. This will result in a neurostructural model for the catatonic syndrome that centers on paralimbic regions including the anterior and midcingulate cortices, as they interface with striatal and thalamic nodes in the salience decision-making network. Examination of neurologic disorders like the abulic syndrome, which includes in its extreme catatonic form, akinetic mutism, will identify the cingulate cortex and paralimbic neighbors as regions of interest. This exploration has the potential to unlock mysteries of the brain cascade from motivation to movement and to clarify catatonia therapeutics. Such a synthesis may also help us discern meaning inherent in this complex neurobehavioral syndrome.
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