Psychiatric Annals

Case Report 

Catatonia Associated with Clonazepam Withdrawal

Muaid Ithman, MD; Levi Marshall, MD; Geetha Chandrashekar, MD; Meelie Bordoloi, MD; Kimberly Brandt, DO

Abstract

Catatonia is a psychomotor syndrome that can be associated with several psychiatric disorders such as schizophrenia, major depression, bipolar disorder, and non-psychiatric medical conditions such as delirium or substance withdrawal.1,2 Catatonia induced by substance withdrawal itself is rare, but clozapine and benzodiazepine (BZD) have been identified as the principal agents associated with this phenomenon.3 Benzodiazepine withdrawal-induced catatonia (BWIC) tends to occur 2 to 8 days after discontinuation and usually occurs within the first 7 days.4 In this article, we discuss the case of 51-year-old man in an inpatient psychiatry unit who developed catatonic features by day 2 after a taper of his clonazepam.

A 51-year-old man was admitted to the inpatient unit after a suicide attempt by laceration to his left forearm. His history included recurrent major depressive disorder (MDD) and generalized anxiety disorder. At the time of admission, the Patient Health Questionnaire form was completed and revealed a score of 27, indicating severe depression. Hematologic and metabolic indices were unremarkable. The medications he had been taking before admission included 15 mg of escitalopram daily and 2 mg of clonazepam at bedtime. Before taking escitalopram, the patient had been taking venlafaxine extended-release at a dose of 225 mg daily for 18 years, but the venlafaxine had become ineffective so it was stopped and switched to escitalopram by his primary care physician 7 months prior to his admission. The patient had been taking clonazepam for 8 to 12 months prior to admission.

During his first week of treatment, medication modifications were made to better treat his MDD. The dose of escitalopram was 15 mg daily on admission, which we titrated up to 20 mg daily. We added bupropion XL at a dose of 150 mg daily to his regimen. Quetiapine was initiated for augmentation and to help with sleep, and the dose was titrated up to 150 mg at bedtime. Clonazepam was continued during the first week at a dose of 2 mg at bedtime.

During weeks 2 and 3 of the patient's hospital stay, the dose of bupropion XL was optimized. Despite 3 weeks of aggressive treatment, the patient's MDD showed no improvement. Electroconvulsive therapy (ECT) was discussed as an option for refractory MDD.

During weeks 4 and 5, the clonazepam dose was decreased and then stopped after 2 days. Clonazepam was discontinued in preparation for ECT, as BZDs are anticonvulsive and may prevent the desired control seizure activity intentionally produced by ECT. Temazepam at a dose of 30 mg daily was initiated on the same day the clonazepam was stopped. The temazepam was to serve as a sleep aid and to provide a substitute for clonazepam that would not interfere with ECT due to its short half-life, as the ECT was scheduled in the afternoon. The patient developed worsening anxiety and insomnia immediately after the clonazepam taper. By day 2 of discontinuation, he developed catatonic features including fixed posture with posturing and catalepsy, limited facial expression with grimacing, significant speech delay with mutism, and significant motor delays with stupor. Catatonia was suspected and lorazepam at a dose of 2 mg intramuscularly was given. The patient showed rapid improvement. An additional 2 mg of intramuscular lorazepam was given to facilitate further recovery. Temazepam was switched back to clonazepam and the dose titrated up to a total daily dose of 3 mg. The patient ultimately decided he did not want to pursue ECT and was discharged to his family and there was no follow-up.

BZDs are a widely used psychoactive, sedative-hypnotic drug class whose mechanism of action is to increase the frequency of opening of gamma-aminobutyric acid A (GABAA) receptors, thus…

Catatonia is a psychomotor syndrome that can be associated with several psychiatric disorders such as schizophrenia, major depression, bipolar disorder, and non-psychiatric medical conditions such as delirium or substance withdrawal.1,2 Catatonia induced by substance withdrawal itself is rare, but clozapine and benzodiazepine (BZD) have been identified as the principal agents associated with this phenomenon.3 Benzodiazepine withdrawal-induced catatonia (BWIC) tends to occur 2 to 8 days after discontinuation and usually occurs within the first 7 days.4 In this article, we discuss the case of 51-year-old man in an inpatient psychiatry unit who developed catatonic features by day 2 after a taper of his clonazepam.

Case

A 51-year-old man was admitted to the inpatient unit after a suicide attempt by laceration to his left forearm. His history included recurrent major depressive disorder (MDD) and generalized anxiety disorder. At the time of admission, the Patient Health Questionnaire form was completed and revealed a score of 27, indicating severe depression. Hematologic and metabolic indices were unremarkable. The medications he had been taking before admission included 15 mg of escitalopram daily and 2 mg of clonazepam at bedtime. Before taking escitalopram, the patient had been taking venlafaxine extended-release at a dose of 225 mg daily for 18 years, but the venlafaxine had become ineffective so it was stopped and switched to escitalopram by his primary care physician 7 months prior to his admission. The patient had been taking clonazepam for 8 to 12 months prior to admission.

During his first week of treatment, medication modifications were made to better treat his MDD. The dose of escitalopram was 15 mg daily on admission, which we titrated up to 20 mg daily. We added bupropion XL at a dose of 150 mg daily to his regimen. Quetiapine was initiated for augmentation and to help with sleep, and the dose was titrated up to 150 mg at bedtime. Clonazepam was continued during the first week at a dose of 2 mg at bedtime.

During weeks 2 and 3 of the patient's hospital stay, the dose of bupropion XL was optimized. Despite 3 weeks of aggressive treatment, the patient's MDD showed no improvement. Electroconvulsive therapy (ECT) was discussed as an option for refractory MDD.

During weeks 4 and 5, the clonazepam dose was decreased and then stopped after 2 days. Clonazepam was discontinued in preparation for ECT, as BZDs are anticonvulsive and may prevent the desired control seizure activity intentionally produced by ECT. Temazepam at a dose of 30 mg daily was initiated on the same day the clonazepam was stopped. The temazepam was to serve as a sleep aid and to provide a substitute for clonazepam that would not interfere with ECT due to its short half-life, as the ECT was scheduled in the afternoon. The patient developed worsening anxiety and insomnia immediately after the clonazepam taper. By day 2 of discontinuation, he developed catatonic features including fixed posture with posturing and catalepsy, limited facial expression with grimacing, significant speech delay with mutism, and significant motor delays with stupor. Catatonia was suspected and lorazepam at a dose of 2 mg intramuscularly was given. The patient showed rapid improvement. An additional 2 mg of intramuscular lorazepam was given to facilitate further recovery. Temazepam was switched back to clonazepam and the dose titrated up to a total daily dose of 3 mg. The patient ultimately decided he did not want to pursue ECT and was discharged to his family and there was no follow-up.

Discussion

BZDs are a widely used psychoactive, sedative-hypnotic drug class whose mechanism of action is to increase the frequency of opening of gamma-aminobutyric acid A (GABAA) receptors, thus amplifying the effects of GABA at the GABAA receptor.5–7 The GABAA receptor functions as a ligand-gated ion channel for chloride anions, and when open it allows for an influx of these ions. This results in cell membrane hyperpolarization and stabilization,8 which decreases the firing and activity of neurons in the affected areas. The clinical effect on the patient is both sedative and hypnotic (sleep inducing), which is why they are often called “sedative-hypnotic” drugs.9

Withdrawal from BZDs causes a decrease in inhibitory GABAA receptor activity and refractory hyperactivity. Although symptomatic BZD withdrawal is more likely with chronic use, symptoms can vary greatly between patients. A double-blind, placebo-controlled trial in 1981 of people who had been taking BZDs for a mean of 3.6 years found that only between 27% and 45% of patients prescribed diazepam or lorazepam for an average of 3.5 years suffer withdrawal symptoms.10 BZD withdrawal is characterized by anxiety, tachycardia, palpitations, insomnia, and tremors.10–13 Severe symptoms of BZD withdrawal may include seizures, perceptual disturbances, and psychosis.11,12,14 BWIC is another severe symptom but is rare. The existing literature on BWIC primarily includes case studies and case series, with fewer than 30 cases reported in the literature.3,4,15–32

Catatonia is a psychomotor syndrome that may present with a range of up to 12 symptoms. According to the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5),33 catatonia is a clinical picture whose criteria requires 3 (or more) of 12 symptoms listed in Table 1.33

Symptoms of Catatoniaa

Table 1:

Symptoms of Catatonia

Among the possible symptoms, the most classic and pathognomonic features are posturing, waxy flexibility, and verbigeration (obsessive repetition of random words).2,34 Although catatonia was historically classified as a subtype of schizophrenia, over time it began to be recognized with high prevalence in mood disorders and delirium, as well as have comorbidity with nonpsychiatric medical conditions.2 Our patient demonstrated posturing, catalepsy, grimacing, significant speech delays (mutism), and significant motor delays (stupor). Together, these five symptoms meet the DSM-5 criteria for catatonia.

Although the mechanism of catatonia is unclear, it has been associated with hyperactivity within the supplementary motor area (SMA) and presupplementary motor area, especially the left sensorimotor cortex.35–38 The hyperactivity in these areas associated with catatonia seems to be in relation to a deficiency of the inhibitory neurotransmitter GABA or a decreased density of GABA receptors. The SMA may be involved in initiation of the inhibitory processes in other motor areas, including the basal ganglia.36–38

BWIC has been identified as one of the principal causes of substance withdrawal-induced catatonia.3 In this case, to establish a causal relationship between benzodiazepine withdrawal and catatonia, we applied the principles of the Naranjo algorithm for adverse drug reactions39 and concluded that clonazepam withdrawal was, in fact, a possible cause for development of catatonia (score = 4). In our patient the catatonia symptoms followed a temporal sequence after clonazepam was discontinued, catatonia was confirmed by a thorough clinical examination, and the symptoms resolved after reintroducing clonazepam. Another contributing factor to the development of catatonia could have been addition of quetiapine. Although the role of dopamine dysregulation in pathophysiology of development of catatonia is complex, it is well known that antipsychotic medications do contribute to the development of catatonia.40 However, this seems to be the least likely cause in our patient given that he was on a low dose of quetiapine and there was no temporal association between starting the medication and development of catatonia symptoms.

Catatonia tends to occur 3 to 7 days after abrupt discontinuation of BZD.3 Studies suggest that BWIC typically occurs after chronic use and abrupt cessation.3 BZD use in these patients has ranged from 34 days to 40 years.3,16 Older people seem to be more susceptible to this adverse effect. Notably, chronic potentiation of GABA activity at GABAA receptors, from BZD or other GABA-ergic agents, results in down-regulation of GABAA receptors, a phenomenon known as receptor adaptation. When the BZD is abruptly discontinued, a GABAA receptor-deficient state predisposes the patient to develop catatonia.11 Once our patient stopped taking clonazepam and started taking temazepam, the catatonic symptoms began. This suggests the 30 mg of temazepam was not able to prevent refractory BWIC in our patient in a GABAA receptor-deficient state.

Current first-line treatment of catatonia relies on BZDs, specifically lorazepam.41,42 After treating catatonia with lorazepam, it is important to taper the lorazepam (or any other BZD) slowly, so as to avoid recurrence of catatonia.43–45 Once our patient was given lorazepam, the catatonic symptoms rapidly began to resolve.

Furthermore, response to BZDs by catatonic patients varies greatly with several factors, including chronicity, symptomatology, age, and cause.46 A 2018 literature review of withdrawal catatonia found that the average age of patients affected by BWIC was 58 years,3 and our patient was age 51 years. Although older age seems to have a strong association with BWIC, cases of younger patients have been reported. The most noteworthy example is a 2017 case report that described catatonia due to midazolam withdrawal in a boy age 9 years.31

Conclusions

With fewer than 30 cases described in the literature, BWIC is a relatively rare phenomenon. This case report confirms patterns seen in previous literature regarding BWIC. Because BZDs are so widely prescribed, and the catatonia phenomenon is not restricted to older patients, physicians should be aware of the phenomenon of BWIC, and BZD cessation should be done through gradual tapering and close monitoring.

References

  1. Fink M, Shorter E, Taylor MA. Catatonia is not schizophrenia: Kraepelin's error and the need to recognize catatonia as an independent syndrome in medical nomenclature. Schizophr Bull. 2010;36(2):314–320. doi:10.1093/schbul/sbp059 [CrossRef] PMID:19586994
  2. Walther S, Stegmayer K, Wilson JE, Heckers S. Structure and neural mechanisms of catatonia. Lancet Psychiatry.2019;6(7):610–619. doi:10.1016/S2215-0366(18)30474-7 [CrossRef] PMID:31196794
  3. Lander M, Bastiampillai T, Sareen J. Review of withdrawal catatonia: what does this reveal about clozapine?Transl Psychiatry. 2018;8(1):139. doi:10.1038/s41398-018-0192-9 [CrossRef] PMID:30065280
  4. Hauser P, Devinsky O, De Bellis M, Theodore WH, Post RM. Benzodiazepine withdrawal delirium with catatonic features. Occurrence in patients with partial seizure disorders. Arch Neurol.1989;46(6):696–699. doi:10.1001/archneur.1989.00520420118033 [CrossRef] PMID:2730383
  5. Campo-Soria C, Chang Y, Weiss DS. Mechanism of action of benzodiazepines on GABAA receptors. Br J Pharmacol.2006;148(7):984–990. doi:10.1038/sj.bjp.0706796 [CrossRef] PMID:16783415
  6. Costa E, Guidotti A, Mao CC: Involvement of GABA in the action of benzodiazepine: studies on rat cerebellum. Psychopharmacol Bull. 1975;(14):113–130. https://www.ncbi.nlm.nih.gov/pubmed/242198 PMID:242198
  7. Haefely W, Kulcsar A, Mohler H: Possible involvement of GABA in the central actions of benzodiazepines. Adv Biochem Psychopharmacol. 1975;(14):131–151. https://www.ncbi.nlm.nih.gov/pubmed/242199 PMID:242199
  8. Sigel E, Steinmann ME. Structure, function, and modulation of GABA(A) receptors. J Biol Chem. 2012;287(48):40224–40231. doi:10.1074/jbc.R112.386664 [CrossRef] PMID:23038269
  9. Olkkola KT, Ahonen J. Midazolam and other benzodiazepines. Handb Exp Pharmacol. 2008;182:335–360. doi:10.1007/978-3-540-74806-9_16 [CrossRef] PMID:18175099
  10. Tyrer P, Rutherford D, Huggett T. Benzodiazepine withdrawal symptoms and propranolol. Lancet. 1981;1(8219):520–522. doi:10.1016/S0140-6736(81)92861-0 [CrossRef] PMID:6111632
  11. Pétursson H. The benzodiazepine withdrawal syndrome. Addiction. 1994;89(11):1455–1459. doi:10.1111/j.1360-0443.1994.tb03743.x [CrossRef] PMID:7841856
  12. Onyett SR. The benzodiazepine withdrawal syndrome and its management. J R Coll Gen Pract. 1989; 39(321):160–163. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1711840/ PMID:2576073
  13. Onyett SR, Turpin G. Benzodiazepine withdrawal in primary care: a comparison of behavioural group training and individual sessions. Behav Psychother.1988;16(4):297–312. doi:10.1017/S0141347300014154 [CrossRef]
  14. Petursson H, Lader MH: Benzodiazepine dependence, tolerance and withdrawal syndrome. Br J Addict. 1981;76(2):133–145. https://www.ncbi.nlm.nih.gov/pubmed/7023521 PMID:7023521
  15. Rapport DJ, Covington EC. Motor phenomena in benzodiazepine withdrawal. Hosp Community Psychiatry. 1989;40(12):1277–1279. doi:10.1176/ps.40.12.1277 [CrossRef] PMID:2574138
  16. Rosebush PI, Mazurek MF. Catatonia after benzodiazepine withdrawal. J Clin Psychopharmacol. 1996;16(4):315–319. doi:10.1097/00004714-199608000-00007 [CrossRef] PMID:8835707
  17. Glover SG, Escalona R, Bishop J, Saldivia A. Catatonia associated with lorazepam withdrawal. Psychosomatics. 1997;38(2):148–150. doi:10.1016/S0033-3182(97)71484-1 [CrossRef] PMID:9063046
  18. Carroll BT. Catatonia due to mixed sedative withdrawal. J Neuropsychiatry Clin Neurosci. 1997;9(2):303–304. doi:10.1176/jnp.9.2.303 [CrossRef] PMID:9144116
  19. Deuschle M, Lederbogen F. Benzodiazepine withdrawal-induced catatonia. Pharmacopsychiatry.2001;34(1):41–42. doi:10.1055/s-2001-15188 [CrossRef] PMID:11229621
  20. Carroll BT, Thomas C, Tugrul KC, Cononcea C, Goforth HW: GABA A versus GABA B in olanzapine-induced tardive dystonia successfully. J Neuropsychiatry Clin Neurosci. 2007;19(4):484. doi:10.1176/jnp.2007.19.4.484 [CrossRef] PMID:18070869
  21. Brown M, Freeman S. Clonazepam withdrawal-induced catatonia. Psychosomatics. 2009;50(3):289–292. doi:10.1176/appi.psy.50.3.289 [CrossRef] PMID:19567771
  22. Parameswaran R, Moore K, Hannan T, Austin M: Catatonia associated with temazepam withdrawal. Aust N Z J Psychiatry. 2011;45(11):1006–1007. doi:10.3109/00048674.2011.607131 [CrossRef] PMID:21875308
  23. Wang BZ, Gupta A, Bastiampillai T, Sani F. Recurrent clozapine and lorazepam withdrawal psychosis with catatonia. Aust N Z J Psychiatry.2012;46(8):795–796. doi:10.1177/0004867412444992 [CrossRef] PMID:22495953
  24. Amos JJ. Lorazepam withdrawal-induced catatonia. Ann Clin Psychiatry. 2012;24(2):170–171. PMID:22563573
  25. Sivakumar T, Yadav A, Sood M, Khandelwal SK. Lorazepam withdrawal catatonia: a case report. Asian J Psychiatr. 2013;6(6):620–621. doi:10.1016/j.ajp.2013.05.008 [CrossRef] PMID:24309887
  26. Saddawi-Konefka D, Berg SM, Nejad SH, Bittner EA. Catatonia in the ICU: an important and underdiagnosed cause of altered mental status. a case series and review of the literature. Crit Care Med. 2014;42(3):e234–e241. doi:10.1097/CCM.0000000000000053 [CrossRef] PMID:24275514
  27. Holoyda B, Xiong G. Catatonia associated with alprazolam discontinuation in a young man with cardiac cirrhosis. J Clin Psychopharmacol. 2015;35(6):735–736. doi:10.1097/JCP.0000000000000425 [CrossRef] PMID:26444949
  28. Oldham MA, Desan PH. Alcohol and sedative-hypnotic withdrawal catatonia: two case reports, systematic literature review, and suggestion of a potential relationship with alcohol withdrawal delirium. Psychosomatics. 2016;57(3):246–255. doi:10.1016/j.psym.2015.12.007 [CrossRef] PMID:26949118
  29. Peng TJ, Patchett ND, Bernard SA. Takotsubo cardiomyopathy and catatonia in the setting of benzodiazepine withdrawal. Case Rep Cardiol. 2016;2016:8153487. doi:10.1155/2016/8153487 [CrossRef] PMID:27547472
  30. Lebin LG, Cerimele JM. Recurrent benzodiazepine withdrawal catatonia in an older adult. Am J Psychiatry. 2017;174(10):1001–1002. doi:10.1176/appi.ajp.2017.17060637 [CrossRef] PMID:28965464
  31. Duncan-Azadi CR, Johnson PN, Gormley A: Case report of midazolam withdrawal-induced catatonia in a 9-year-old patient. A A Case Rep. 2017; 8(9):242–245. doi:10.1213/XAA.0000000000000482 [CrossRef]. PMID:28181946
  32. Iyengar S, Bornmann C, Abdelmalak F, LaRocca T. Catatonia due to alprazolam withdrawal. BMJ Case Rep. 2018;11(1):e227175. doi:10.1136/bcr-2018-227175 [CrossRef] PMID:30567266
  33. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Publishing; 2013.
  34. Unal A, Bulbul F, Alpak G, Virit O, Copoglu US, Savas HA. Effective treatment of catatonia by combination of benzodiazepine and electroconvulsive therapy. J ECT. 2013;29(3):206–209. doi:10.1097/YCT.0b013e3182887a1a [CrossRef] PMID:23965606
  35. Northoff G, Steinke R, Czcervenka C, et al. Decreased density of GABA-A receptors in the left sensorimotor cortex in akinetic catatonia: investigation of in vivo benzodiazepine receptor binding. J Neurol Neurosurg Psychiatry. 1999;67(4):445–450. doi:10.1136/jnnp.67.4.445 [CrossRef] PMID:10486389
  36. Northoff G, Braus DF, Sartorius A, et al. Reduced activation and altered laterality in two neuroleptic-naive catatonic patients during a motor task in functional MRI. Psychol Med. 1999;29(4):997–1002. doi:10.1017/S0033291798007739 [CrossRef] PMID:10473328
  37. Scheuerecker J, Ufer S, Käpernick M, et al. Cerebral network deficits in post-acute catatonic schizophrenic patients measured by fMRI. J Psychiatr Res.2009;43(6):607–614. doi:10.1016/j.jpsychires.2008.08.005 [CrossRef] PMID:18951556
  38. Payoux P, Boulanouar K, Sarramon C, et al. Cortical motor activation in akinetic schizophrenic patients: a pilot functional MRI study. Mov Disord. 2004;19(1):83–90. doi:10.1002/mds.10598 [CrossRef] PMID:14743365
  39. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239–245. doi:10.1038/clpt.1981.154 [CrossRef] PMID:7249508
  40. Daniels J. Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci. 2009;21(4):371–380. doi:10.1176/jnp.2009.21.4.371 [CrossRef] PMID:19996245
  41. Carroll BT, Lee JWY, Appiani F, Thomas C. The pharmacotherapy of catatonia. Prim Psychiatry. 2010;17(4):41–47.
  42. Rohland BM, Carroll BT, Jacoby RG. ECT in the treatment of the catatonic syndrome. J Affect Disord. 1993;29(4):255–261. doi:10.1016/0165-0327(93)90015-C [CrossRef] PMID:8126312
  43. Dutt A, Grover S, Chakrabarti S, Avasthi A, Kumar S. Phenomenology and treatment of catatonia: a descriptive study from north India. Indian J Psychiatry. 2011;53(1):36–40. doi:10.4103/0019-5545.75559 [CrossRef] PMID:21431006
  44. Sienaert P, Dhossche DM, Vancampfort D, De Hert M, Gazdag G. A clinical review of the treatment of catatonia. Front Psychiatry. 2014;5:181. doi:10.3389/fpsyt.2014.00181 [CrossRef] PMID:25538636
  45. Ali SF, Gowda GS, Jaisoorya TS, Math SB. Resurgence of catatonia following tapering or stoppage of lorazepam—a case series and implications. Asian J Psychiatry. 2017;28:102–105. doi:10.1016/j.ajp.2017.04.002 [CrossRef] PMID:28784360
  46. Ungvari GS, Chiu HFK, Chow LY, Lau BST, Tang WK. Lorazepam for chronic catatonia: a randomized, double-blind, placebo-controlled cross-over study. Psychopharmacology (Berl). 1999;142(4):393–398. doi:10.1007/s002130050904 [CrossRef] PMID:10229064

Symptoms of Catatoniaa

<list-item>

Posturing: spontaneous and active maintenance of a posture against gravity

</list-item><list-item>

Waxy flexibility: resistance to positioning by examiner

</list-item><list-item>

Echolalia: mimicking another's speech by repetition

</list-item><list-item>

Echopraxia: mimicking another's movements

</list-item><list-item>

Catalepsy: fixed posture held against gravity

</list-item><list-item>

Stupor: no psychomotor activity (should not be actively related to environment)

</list-item><list-item>

Mutism: no, or very little, verbal response (exclude symptoms if patient has known aphasia)

</list-item><list-item>

Negativism: opposition of, or no response to, instructions or external stimuli

</list-item><list-item>

Mannerism: odd, circumstantial caricature of normal actions

</list-item><list-item>

Agitation: state of restlessness and tension (should not be influenced by external stimuli)

</list-item><list-item>

Grimacing: an ugly, twisted expression on a person's face, typically expressing disgust or wry amusement

</list-item><list-item>

Stereotypy: repetitive, frequent, non–goal-directed movements (eg, nail biting, hair twirling) or obsessive repetition of random words

</list-item>
Authors

Muaid Ithman, MD, is an Associate Professor of Clinical Psychiatry, University of Missouri School of Medicine. Levi Marshall, MD, is a Year-4 Medical Student, Missouri University Psychiatric Center (MUPC) and University of Missouri School of Medicine. Geetha Chandrashekar, MD, is an Assistant Professor of Clinical Psychiatry, MUPC and University of Missouri School of Medicine. Meelie Bordoloi, MD, is an Assistant Professor of Psychiatry, MUPC and University of Missouri School of Medicine. Kimberly Brandt, DO, is a Assistant Professor of Clinical Psychiatry; the Residency Training Director, General Psychiatry; and the Medical Director, Perinatal Psychiatry Clinic and Consultation Service, MUPC and University of Missouri School of Medicine.

Address correspondence to Muaid Ithman, MD, University of Missouri School of Medicine, 1 Hospital Drive, Columbia, MO 65212; email: ithmanm@health.missouri.edu.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20201006-03

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