American Journal of Emergency Medicine 31 (2013) 1419.e3-1419.e5

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American Journal of Emergency Medicine

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Case Report

Cerebellitis developing after Tricyclic antidepressant poisoning

Abstract

Acute cerebellitis is a rare inflammatory disease involving the cerebellum and is characterized by acute compromise of cerebellar functions. It most frequently originates from infectious causes, although cases of cerebellitis associated with other causes have also been reported. This report discusses a case of cerebellitis developing in a 4-year-old girl who had to be intubated after accidental ingestion of tricyclic antidepressant. There are no previous reports of cerebellitis after tricyclic antidepressant. This case shows that cerebellitis can develop in patients with poisoning of this kind.

Acute cerebellitis is a rare inflammatory disease of the cerebellum diagnosed through clinical and radiological findings. It is one of the primary causes of pediatric acute Cerebellar dysfunction, and infectious causes are generally implicated [1]. It is generally self- limiting and can, rarely, compress the brain stem and fourth ventricle. Findings of fever and meningitis may occur, particularly in infectious cerebellitis. Radiology is very important in diagnosis, in addition to clinical findings. Characteristic magnetic resonance imaging (MRI) findings are diffuse cortical edema and high-density cortical involve- ment in T2-weighted cerebellar sections [1,2]. This report describes a patient receiving high-dose tricyclic antidepressant (TAD) and diagnosed with acute cerebellitis at MRI.

A 4-year-old girl was brought to the emergency department with disequilibrium, impaired speech, and fainting developing suddenly at home. There was no Nuchal rigidity at examination. Glasgow Coma Score was 9, blood O₂ saturation was 96%, arterial blood pressure was 90/50 mm/Hg, pulse rate was 125 beats per minute, and Blood sugar level was 227 mg/dL. Electrocardiography revealed a normal sinus rhythm. Temperature was 36.7?C. The patient had no known disease. Investigation at home revealed that

20 tablets containing amitriptilin used by the mother for major depression were missing. Electrocardiographic changes developed

15 minutes after arrival at the emergency department. Arterial blood pressure then fell to 50/10 mm Hg, and 2 repeated clonic- tonic-type episodes occurred. The patient was intubated and started on rectal diazepam, midazolam, and phenytoin loading treatment. gastric lavage was performed with a diagnosis of TAD poisoning, active charcoal was administered, and bicarbonate therapy was started for blood alkalization. The patient’s laboratory results were glucose 227 mg/dL, blood urea nitrogen/creatinine 10/0.6 mg/dL, alanine transaminase 39 U/L (0-65 U/L), aspartate transaminase 69 U/L (0-35 U/L), Na 140 mmol/L, and K 4.4 mEq/L. The patient was transferred to the university hospital, the regional reference hospital; admitted to the pediatric intensive care unit; and placed under observation. Brain tomography result was normal (Fig. 1A), whereas a second tomography (Fig. 1B) and MRI (Figs. 2, 3, 4) report was compatible with cerebellitis. The patient was started on

antiedema and antiepileptic treatment by the pediatric neurology department. Elevated TAD was determined in the patient’s urine toxicology panel. A hemodialysis catheter was attached, and hypoperfusion was performed. Following hypoperfusion, responses began being given to painful stimuli; and the presence of TAD persisted in the urine toxicology panel. electrocardiographic findings returned to normal. Because Clinical response was obtained, hemoperfusion was repeated the following day. Vital findings improved, and spontaneous respiration was observed; the patient was extubated on the fourth day of observation. No problem was identified at clinical observation, and the patient was discharged on the 13th day.

Acute cerebellitis is mainly seen after Varicella-zoster virus, Epstein-Barr virus, rubella, pertussis, diphtheria, and coxsackie virus infections. It may more rarely be seen after Borrelia burgdorferi, Coxiella burnetii, and Mycoplasma pneumoniae infections. It can also be seen after Cyanide poisoning, lead poisoning, demyelinating processes, vasculitis, and acute demyelinating encephalomyelitis. The agent may not always be identifiable. Cerebellitis generally follows a benign course, and clinical findings usually resolve. It usually affects both cerebral hemispheres and the cortical region [3]. The most common clinical findings are abnormal eye movements, myoclonus, dysarthria, tremor, nausea, vomiting, truncal ataxia, and findings of cerebellar involvement such as altered mental state [4]. However, clinical findings may also be nonspecific in acute cerebellitis. Radiological findings are therefore important in diagnosis. Tomography cannot sufficiently evaluate the posterior fossa. It also assists with the identification of herniation, hydrocephaly, and cerebellar edema. Brain and diffusion MRI in particular is important in the diagnosis of acute cerebellitis. A bilateral signal increase in the cerebellar cortex is generally observed in MRI fluid attenuated inversion recovery (FLAIR) and T2-weighted sequences in cerebellitis. white matter involvement may also sometimes occur [3]. The MRI findings can resolve entirely in the observation of cases of acute cerebellitis. The signal increase may persist for a time in cases with clinical resolution. The most common sequela of cerebellitis is cerebellar atrophy. Parenchymal calcifications may rarely be seen [5]. There is no standard treatment protocol for acute cerebellitis. Symptomatic antiviral and high-dose methyl prednisolone are generally administered [6]. Medical treatment is generally sufficient, whereas External ventricular drainage and Decompression surgery may be performed in the event of brain stem compression and hydrocephaly [6]. Cerebellitis resolved without the need for surgery in this case, and the patient was discharged in a healthy condition (Fig. 4) There are rare cases of cerebellitis developing after drug intoxications. One was a case developing after methadone ingestion [5]. But there are no previous reports of cerebellitis developing following TAD poisoning. This case shows that TAD ingestion may be an atypical cause of cerebellitis in children.

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1419.e4 O. Tatli et al. / American Journal of Emergency Medicine 31 (2013) 1419.e3–1419.e5

Fig. 1. A, Arrival axial brain CT; pons, mesencephalon, fourth ventricle, bilateral thalamuses, basal ganglia, third and lateral ventricles, cortical hemispheric sulci normal. B, Fourth-day axial brain CT; fourth ventricle normal. Areas compatible with hypodense edema in both cerebellar hemispheres.

Fig. 2. Arrival brain MRI; sagittal and axial T1 weighted (A), axial T2 weighted (B). Increased signal and mass effect and accompanying diffusion restrictions in T2A image compatible with cerebellitis (A, yellow narrows). The fourth ventricle was compressed in the same image, and the brain stem was displaced toward the anterior (A, B).

Ozgur Tatli MD

Kanuni Training and Research Hospital Department of Emergency Medicine, Trabzon, Turkey E-mail address: dr.ozgurtatli@gmail.com

Yunus Karaca MD Karadeniz Technical University, Faculty of Medicine Department of Emergency Medicine, Trabzon, Turkey

Mucahit Gunaydin MD Selim Yurtsever MD

Gamze Tuten MD

Kanuni Training and Research Hospital Department of Emergency Medicine, Trabzon, Turkey

http://dx.doi.org/10.1016/j.ajem.2013.05.001

References

1. Montenegro MA, Santos SL, Li LM, et al. Neuroimaging of acute cerebellitis. J Neuroimaging 2002;12:72-4.
2. Bakshi R, Bates VE, kinkel PR, et al. magnetic resonance imaging findings in acute cerebellitis. Clin Imaging 1998;22:79-85.

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   Fig. 3. Diffusion MRI; apparent diffusion coefficient (ADC) image. In diffusion-weighted images, pathological hyperintense signal changes were present.

   Fig. 4. The 12th-day brain MRI; decreased pathological signal change in T2A image.

   De Bruecker Y, Claus F, Demaerel P, et al. MRI findings in acute cerebellitis. Eur Radiol 2004;14:1478-83.

3. Della Nave R, Foresti S, Tessa C. ADC mapping of neurodegeneration in the brainstem and cerebellum of patients with progressive ataxias. Neuroimage 2004;22:698-705.
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