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Treatment of a Complex Case of Catatonia and Conversion Features with Electroconvulsive Therapy in a 14-Year-Old Male

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Treatment of a Complex Case of Catatonia and Conversion Features with Electroconvulsive Therapy in a 14-Year-Old Male CASE REPORT Ochsner Journal 20:307–310, 2020 ©2020 by the author(s); Creative Commons Attribution License (CC BY) DOI: 10.31486/toj.19.0026 Treatment of a Complex Case of Catatonia and Conversion Features With Electroconvulsive Therapy in a 14-Year-Old Male Cody Roi, DO, MPH,1 Luke Verret, MD,1 Bradley Peet, MD,1 Erich J. Conrad, MD1,2 1Department of Psychiatry, Louisiana State University Health Sciences Center, New Orleans, LA 2Louisiana State University School of Medicine, New Orleans, LA Background: Pediatric catatonia is a rare and poorly understood phenomenon. The majority of reported cases have a psychiatric etiology. Because of the heterogeneous presentation and treatment issues unique to the pediatric population, identification and management can be challenging. Additionally, few definitive guidelines or practice parameters are available for pediatric patients. The first-line treatment for catatonia is pharmacologic, and when treatment fails or is inadequate, electroconvulsive therapy (ECT) has been shown to be safe and effective. Case Report: A previously healthy, 14-year-old male presented with acute onset of catatonia that resolved at 4 weeks after a short course of ECT with adjunctive lorazepam and risperidone. An interesting feature of this case was the resolution of autonomic symptoms and the emergence of conversion features. The resolution of the catatonia (negativism, mutism, and withdrawal) made it possible for the team to identify a thought disorder and initiate appropriate pharmacologic treatment for the precipitating etiology. Conclusion: ECT was a safe and effective treatment for the resolution of catatonia symptoms in this patient. Conversion andcata- tonia features may exist on a continuum. Keywords: Catatonia, conversion disorder, electroconvulsive therapy, mental disorders Address correspondence to Cody Roi, DO, MPH, Department of Psychiatry, Louisiana State University Health Sciences Center, 2020 Gravier St., New Orleans, LA 70112. Tel: (504) 657-6100. Email: [email protected] INTRODUCTION research on catatonia in the pediatric population is limited, Catatonia is a complex neuropsychiatric syndrome char- some differences vs catatonia in adults have been identified: acterized by a marked psychomotor disturbance that may boys are more affected than girls (2:1 ratio), schizophrenia involve either increased or decreased motor activity.1 Pedi- spectrum disorders are the most frequent cause (compared atric catatonia is associated with many disorders, includ- to mood disorders in adults), and the prevalence of traumatic ing psychiatric, neurologic, and general medical conditions events precipitating the onset is potentially increased.6 (Table 1),2,3 but is associated predominately with mood dis- In addition to the challenges of recognizing and treating orders and schizophrenia.4 the catatonic state, clinicians must also elucidate the pro- The Diagnostic and Statistical Manual of Mental Disor- dromal or primary etiology. Psychiatric diagnoses appear to ders, Fifth Edition (DSM-5) specifies 12 core symptoms of represent the majority of cases in the pediatric population,3 catatonia: stupor, catalepsy, waxy flexibility, mutism, nega- and, regardless of the precipitant etiology, treatment recom- tivism, posturing, mannerisms, stereotypy, agitation, grimac- mendations are similar. However, once medical causes have ing, echolalia, and echopraxia.1 These symptoms are cat- been ruled out, making an accurate diagnosis of underlying egorized as retarded, excited, or malignant. The retarded psychiatric conditions in catatonic patients continues to be form frequently presents with symptoms such as postur- a challenge because of (1) the heterogeneous and more lib- ing, rigidity, mutism, and repetitive movements. The excited eral list of diagnostic criteria for catatonia that now includes form is characterized by restless movements, talkativeness, 3 of 12 potential symptoms in the DSM-5 compared to 3 of and agitation. Fink and Taylor described the malignant form, 5intheDSM-4, (2) the broad differential for catatonia, (3) which is the most severe form and the most likely to be fatal, diagnostic overshadowing for primary precipitating psychi- to be associated with autonomic instability, including hyper- atric diagnosis (eg, schizophrenia vs autism, depression vs tension, tachycardia, tachypnea, and hyperthermia.5 anxiety), and (4) the potentially lengthy course of catatonia, Theories of etiology and treatment recommendations have with variable mental status examination findings throughout. primarily been informed by the adult literature. Although In the pediatric population, an additional confounding factor Volume 20, Number 3, Fall 2020 307 Treatment of Pediatric Catatonia With Electroconvulsive Therapy Table 1. Psychiatric and Nonpsychiatric Etiologies of ior. On presentation to the emergency department, he was Catatonia2,3 mute and unable to walk without assistance. He was ini- tially treated with a course of lorazepam (Ativan) for sus- Nonpsychiatric Medical pected catatonia and appeared to improve. However, upon Psychiatric Etiologies Condition Etiologies his initial transfer to the psychiatric hospital, he became Thought disorders Autoimmune significantly more catatonic with mutism, negativism, and Schizophrenia Autoimmune encephalitis stupor. His initial medical workup was negative and con- Schizoaffective disorder NMDA-receptor sisted of routine laboratory tests, head imaging (computed Brief psychotic disorder encephalitis tomography and magnetic resonance imaging), lumbar Schizophreniform disorder Autoimmune thyroiditis puncture with cerebrospinal fluid cytology, gram stain and Opsoclonus-myoclonus culture, encephalitis panel, enterovirus polymerase chain syndrome reaction, anti-N-methyl-D-aspartate receptor panel, human immunodeficiency virus, rapid plasma reagin, hepatitis Mood disorders Neurologic panel, Lyme serology, antinuclear antibodies, urine toxicol- Bipolar disorder Temporal lobe epilepsy ogy, urinalysis and culture, thyroid panel, acetaminophen Major depressive disorder Status epilepticus level, salicylate level, C-reactive protein, vitamin B12, ammo- Lesion of thalamus or nia, partial thromboplastin time, prothrombin time and inter- parietal or frontal lobe national normalized ratio, and magnesium. Video electroen- Bilateral globus pallidus cephalography showed no evidence of nonconvulsive status disease epilepticus and showed normal awake, drowsy, and sleep Head trauma structure. Because of the patient’s catatonia, a nasogastric Kleine-Levin syndrome tube and intravenous (IV) line were started to maintain nutri- Neurodevelopmental disorders Metabolic tion and hydration as he had stopped taking food and med- Autism spectrum disorder Diabetic ketoacidosis ications orally. Homocystinuria The patient was given lorazepam 2 mg IV and had a rapid Hypercalcemia response, including opening his eyes and following com- Hepatic encephalopathy mands. However, he quickly returned to a catatonic state, Hyponatremia including mutism, negativism, and stupor, as well as eye- Medication induced Genetic lid fasciculations, slowness to constrict pupils, and the for- Neuroleptics Prader-Willi syndrome mation of copious amounts of frothy saliva that he refused Medication induced to expel from his mouth, thought to be associated with Corticosteroids, a psychotic thought process and best described as psy- immunosuppressants chogenic sialorrhea. Idiopathic paroxysmal sialorrhea has been described in the literature but primarily in relation to NMDA, N-methyl-D-aspartate. medical causes.19 Lorazepam was administered to the patient for the next is that children have less developmental history than adults 10 days and titrated up to 2 mg every 4 hours. This treat- for comparison of findings. ment provided some relief initially. The patient was observed Lorazepam is recommended as first-line treatment in conversing briefly with his family, but within 24 hours, he catatonia,7 although successful treatment with other ben- returned to stupor and subsequently responded very little to zodiazepines has been reported.8-10 If the patient shows no the lorazepam. On day 11, amantadine was added to his reg- response to benzodiazepines in 48 to 72 hours, electrocon- imen and titrated up to 100 mg twice daily with no improve- vulsive therapy (ECT) is recommended.11 ment (Figure). Catatonia is thought to be attributable to dysregulation As the patient’s nutritional status deteriorated, ECT was of γ-aminobutyric acid (GABA)–releasing neurons and dys- arranged to be performed at a nearby hospital, and he regulation of dopaminergic and glutaminergic systems, and received his first treatment on day 14. Prior to the first both benzodiazepines and ECT appear to exert their effects treatment, the patient was evaluated by 2 child and ado- through GABA systems.12,13 ECT has been used in chil- lescent psychiatrists: an ECT psychiatrist and a psychia- dren and adolescents primarily for refractory major depres- trist with expertise in religions to ensure that the odd state- sion. ECT is generally considered safe, but an increase in ments the patient made about religious beliefs during lucid the frequency of prolonged seizures is possible.14 ECT has moments were not a culturally appropriate variant. Multiple been shown to be highly effective for the treatment of cata- family meetings took place to obtain informed consent. tonia in adults and adolescents and to lack serious side Utilizing a Thymatron System IV (Somatics, LLC), the effects.15-18 patient
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