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Ketamine for Acute Catatonia: a Case Report

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Ketamine for Acute Catatonia: a Case Report Med/Psych Update KETAMINE FOR CATATONIA Ketamine for acute catatonia: A case report Our patient’s experience suggests this agent might reduce mutism and immobility s. C, age 44, who has major depressive disorder (MDD), anxiety, obsessive-compulsive disorder (OCD) (religious Msubtype), and has experienced multiple episodes of treat- ment-resistant catatonia, is brought to the emergency depart- ment (ED) by her parents. She has immobility, mutism, rigidity, and decreased oral intake that she has experienced for 1 day. The night before, Ms. C had been stressed about an upcom- ing job interview. She cancelled the interview and went to her bedroom. Later that night her parents found her lying on the floor, immobile. Before the onset of her psychiatric symptoms, Ms. C had been high functioning. She had been an athlete in college and had a career as a school psychologist. The Sidebar (page 26) summa- KATERYNA KOVARZH/GETTY IMAGES KOVARZH/GETTY KATERYNA rizes Ms. C’s psychiatric history, which includes similar complex Brian Kobayashi, BS Michael Burns, MD episodes and multiple hospitalizations. She also has a history of Medical Student Emergency Medicine Physician hypothyroidism. UC Irvine School of Medicine Department of Emergency In the ED, the psychiatry team evaluates Ms. C. She displays Irvine, California Medicine UC Irvine School of Medicine a similar pattern of mutism, immobility, and rigidity as she did Chela Wright, MD Irvine, California upon her initial presentation. Her father reports that she had PGY-3 Psychiatry Resident Department of Psychiatry Rimal Bera, MD been compliant with her medications but had not taken them UC Irvine School of Medicine Clinical Professor of Psychiatry the previous night. Ms. C screens positive for catatonia on the Irvine, California Department of Psychiatry Bush-Francis Catatonia Rating Scale (BFCRS). Her severity score of UC Irvine School of Medicine Irvine, California 10/69 indicates a mild presentation. She is diagnosed with cata- tonia and is administered IV lorazepam, 2 mg, with no response. Because Ms. C has been hospitalized many times for similar presentations, the treatment team decides to initiate a trial of IV ketamine. Disclosures The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products. Current Psychiatry 24 June 2021 doi: 10.12788/cp.0132 Catatonia can manifest in many differ- supported by a neurophysiologic model of ent ways in patients with psychiatric ill- catatonia that suggested the condition was ness. If left untreated, it is associated with caused in part by glutamate hypoactivity a high rate of mortality.1 Catatonia often at the NMDA receptor.9 However, recent MDedge.com/psychiatry is described along a continuum from studies have shown that the NMDA recep- retarded/stuporous to excited, and presen- tor antagonists amantadine and memantine tations can vary substantially. The physi- may be useful for treatment-refractory cases ologic and psychological mechanisms of of catatonia, which suggests that a broader catatonia are poorly understood. model of glutamatergic dysfunction, and not Traditionally, most patients respond simply glutamate hypoactivity, may be more well to low-dose benzodiazepines, with accurate.10,11 Denysenko et al12 proposed electroconvulsive therapy as a second-line that the efficacy of memantine for patients intervention for refractory and malignant with lorazepam-resistant catatonia could be cases. However, these interventions are not explained by increases in dopamine levels always successful or readily available. in the frontal cortex and striatum. While this Research into the anesthetic ketamine effect could explain why amantadine has is gradually expanding, and the use of this anticatatonic effects, it does not explain why Clinical Point agent for treating various psychiatric ill- other NMDA antagonists such as ketamine Empiric evidence nesses, including both unipolar and bipolar are potentially pro-catatonic. Other pro- depression, has been increasing.2 Empiric posed physiologic mechanisms explaining suggests ketamine is evidence suggests ketamine is effective for this difference include the fact that meman- effective for certain certain psychiatric disorders, but the mecha- tine and ketamine have differing effects on psychiatric disorders, nism of action remains unclear. Although the brain-derived neurotrophic factor (BDNF) but the mechanism evidence base is small, additional cases dem- expression and certain glutamatergic post- of action remains onstrating the effectiveness of ketamine in synaptic density proteins.13,14 the treatment of acute catatonia might make Ketamine originally was used for seda- unclear it a therapeutic option for use by psychia- tion, and much of its safety and risk pro- trists and emergency medicine clinicians. file has been developed from decades of In this article, we discuss ketamine’s administration as an anesthetic. Studies possible role in the treatment of catatonia, have found that ketamine has a large thera- possible adverse effects, dosing strategies, peutic window in children and adults.15,16 and theories about ketamine’s mechanism Moreover, it does not depress the respira- of action. tory system. As an anesthetic, ketamine has a rapid onset and a quick resolution, with its sedative and disorienting effects resolving Ketamine’s utility in psychiatry within 30 to 120 minutes.17 Ketamine’s rapid Ketamine is a rapid-acting anesthetic that onset of action extends beyond its sedating acts primarily by antagonizing N-methyl-d- effects. Trials with the intranasal spray esket- aspartate (NMDA) receptors in the CNS. It is amine for treatment-resistant depression characterized by dissociative anesthesia as it have demonstrated an onset antidepressant disrupts association pathways in the brain.3 effects within 2 days.18 This is much faster Ketamine has been shown to be efficacious than that of traditional antidepressants, such in treating MDD and posttraumatic stress as selective serotonin reuptake inhibitors.18 disorder, and for the long-term manage- Based on these features, ketamine has the ment of chronic pain disorders, including potential to be a useful medication in the Discuss this article at fibromyalgia and many neuro pathic condi- emergency psychiatric setting, particularly www.facebook.com/ 4-7 tions. Esketamine is an intranasal formu- for acute presentations such as catatonia. MDedgePsychiatry lation of ketamine that is FDA-approved for treatment-resistant depression.8 There is scant literature describing using ketamine Beware of the potential risks for treating catatonia. Although ketamine may be clinically use- Previously, ketamine had been thought ful, it also carries some risks. Adverse effects Current Psychiatry to induce a catatonic state, which was associated with ketamine include sedation, Vol. 20, No. 6 25 dissociation, hallucinations, elevated blood studies have demonstrated addiction and pressure, nausea, increased heart rate, vom- cognitive deficits with repeated use of ket- iting, dizziness, fatigue, blurred vision, amine in rodents.21 This research has led to itching, and emesis. Clinicians also should concerns that chronic use of ketamine to be aware that some patients may use illicit treat illnesses such as depression might lead ketamine, either as self-treatment to control to similar long-term adverse outcomes. depressive symptoms or for recreational Ketamine purposes. When misused/abused, long- for catatonia term use of ketamine can cause neurologic Dosing damage.19 Studies also have reported rare As a sedative, IV ketamine dosing is gener- occurrences of recurrent hallucinations even ally 1 to 2 mg/kg, and IM ketamine dosing is after discontinuation of ketamine.20 Animal 3 to 5 mg/kg.16 As an antidepressant, small SIDEBAR Ms. C’s psychiatric history In 2013, Ms. C experienced severe social During this time, the highest dose of IM olanzapine, and risperidone. In June 2019, stress from both her work as a psycholo- lorazepam was 20 mg/d in divided doses. her symptoms returned. She was hospi- gist and a divorce. She sold all of her pos- talized and required a nasogastric tube sessions and was living in motels and Some improvement with ECT to address malnutrition. She was eventu- hotels searching for the “truth of God.” Four months into her hospitalization, ally stabilized on a regimen of risperidone In February 2016, she was hospitalized Ms. C’s lorazepam was titrated down and lorazepam, which she continued after refusing to eat and self-discontinu- to 4 mg 4 times a day, and she under- as an outpatient until she was hospital- ing all medications, including her thyroid went a trial of electroconvulsive therapy ized again in August 2019. During this medications. She was then placed under (ECT). Following the fourth ECT session, hospitalization, Ms. C failed to respond the conservatorship of her parents. she displayed significant improvement. to risperidone or lorazepam, up to 2 mg In July 2017, Ms. C was hospital- Ms. C engaged with her clinicians, dis- 3 times a day. After several changes to her ized again for refusing to eat or take played bright mood and affect, began regimen, she began to respond to olan- her medications; this time she also eating again, and was able to recount zapine, 30 mg/d; mirtazapine, 15 mg/d; exhibited selective mutism. Catatonia her depressive symptoms following and lorazepam, 2 mg 3 times a day. was suspected and she was started her divorce. At this time, she received
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