Hindawi Case Reports in Neurological Medicine Volume 2019, Article ID 9285460, 5 pages https://doi.org/10.1155/2019/9285460 Case Report A Case of Reverse Takotsubo Cardiomyopathy Incited by a Spinal Subdural Hematoma Kyle Sanchez ,1 Steven Glener,1 Nathan E. Esplin,2 Okorie N. Okorie,3 and Amay Parikh3 1 University of Central Florida College of Medicine, 6850 Lake Nona Boulevard, Orlando, FL 32827, USA 2Department of Neurosurgery, Allegheny General Hospital, 320 E North Ave., Pittsburgh, PA 15212, USA 3Florida Hospital, 601 E Rollins Street, Orlando, FL 32803, USA Correspondence should be addressed to Kyle Sanchez; [email protected] Received 12 March 2019; Accepted 8 July 2019; Published 22 July 2019 Academic Editor: Shahid Nimjee Copyright © 2019 Kyle Sanchez et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Takotsubo cardiomyopathy is a rare syndrome of transient, reversible lef ventricular systolic dysfunction. It mimics myocardial infarction clinically and includes elevated cardiac enzymes, but echocardiography reveals apical ballooning and basal hyperkinesis. Infrequently, midventricular or even reverse Takotsubo patterns have been described, involving ballooning of the basal heart without the characteristic ‘Takotsubo’ appearance. Tere are cases in the literature that support a connection between reverse Takotsubo cardiomyopathy (r-TTC) and neurological insults as inciting factors. We report a case of r-TTC in an otherwise healthy 23-year-old man presenting with back pain, urinary retention, bradycardia, and hypertension. Troponin levels and brain natriuretic peptide (BNP) were elevated, and echocardiogram revealed an ejection fraction (EF) of less than 20%. In addition, MRI demonstrated a spinal subdural hematoma from T1-S1 with no cord compression. Repeated echocardiogram demonstrated an EF of 20-25% with a reverse Takotsubo pattern of cardiomyopathy. With supportive care, his clinical picture improved with normalization of cardiac enzyme and BNP values. Tis case represents a r-TTC presenting as heart failure in a young, apparently healthy male likely incited by a spinal subdural hematoma. To our knowledge, it is the frst of its kind reported. 1. Introduction type, and localized type [2]. In the classical pattern of TTC, the most common type, the base of the ventricle TakotsuboCardiomyopathy(TTC),alsocalledstress- contracts normally or is hyperkinetic while the rest of the induced cardiomyopathy or broken heart syndrome, is a rare ventricle is dyskinetic or akinetic [3], causing the classical syndrome of transient and reversible lef ventricular systolic ballooning of the lef ventricular apex. Reverse, or inverted dysfunction in the absence of coronary stenosis. TTC is type, Takotsubo cardiomyopathy (r-TTC) is a rare variant characterized by ballooning of the lef ventricular apex that is characterizedbyhypokinesisofthebasewithrelativesparing provoked by an emotionally or physically stressful experience of the midventricle and apex [1], causing ballooning to occur [1], although the mechanism is still debated. Te clinical atthebaseoftheheart. presentation of TTC mimics acute coronary syndrome, as it In comparison to other patterns of TCC, r-TCC usu- presents with symptoms ranging from isolated chest pain to ally presents in a younger patient population with higher severe dyspnea and cardiogenic shock, ofen accompanied troponin levels, lower ejection fraction, and a paradoxically by elevation of troponin level and T-wave and ST-segment faster recovery [4]. Te higher troponin levels are believed to abnormalities on echocardiogram (ECG) [2]. Classically, be the result of a larger region of myocardial involvement in echocardiogram shows apical ballooning and basal hyper- r-TTCincomparisontotheapexalone[2].Onthecontrary, kinesis, resembling a ‘crab pot’ or ‘octopus trap’ that, from natriuretic peptides are ofen more elevated in apical and the Japanese word for such, gives this disorder its name. midventricular patterns of TCC and account for the higher Te four known patterns of lef ventricular involvement prevalence of severe symptoms and higher NYHA functional in TTC include classical type, reverse type, midventricular class [2] seen in comparison to r-TTC. Te higher prevalence 2 Case Reports in Neurological Medicine Figure 1: MRI showing thoracic (lef)andlumbar(right) subdural hematomas (arrows). of symptoms despite less damage to cardiomyocytes may be lifing boxes at work. During these hospital visits, the patient explained by the frequent coexistence of mitral regurgitation denied bowel and bladder dysfunction, saddle anesthesia, caused by apical ballooning [2]. Predictors of mortality from fever, and chills. On both occasions, he was discharged home r-TTC include decreased lef ventricular ejection fraction, with the diagnosis of acute lumbar paraspinal muscle strain. development of atrial fbrillation, and neurologic disease.” On this third visit, now with urinary retention, he was Te precise etiology of TCC/r-TCC is unknown, but evi- admitted to the outside facility. Te patient was catheterized, dence indicates that both patterns are associated with strong yielding 1400 mL of urine, which tested positive for THC surges of adrenergic outfow that occur following intense and oxycodone and revealed trace amounts of ketones. Initial emotional or physical stress [5–9], where high circulating laboratory evaluation was signifcant for leukocytosis (14,580 levels of epinephrine may cause coronary spasm, endothelial cells/�L, neutrophil 81.6%) and elevated N-terminal BNP at dysfunction, and indirect myocardial damage [2]. A few case 734 pg/mL (0 – 125 pg/mL). studies have suggested a potential connection between r- Computed tomography (CT) of the head showed no TTC and neurological insults as inciting factors. Reported evidence of signifcant intracranial pathology. CT of the neurological stressors which have induced r-TCC include abdomen and pelvis showed no acute fndings with no cerebellar hemorrhage [2], medulla oblongata hemorrhage evidence of intra-abdominal trauma. Computed tomography [5], subarachnoid hemorrhage [10], inadvertent intrathecal angiogram (CTA) of the chest revealed symmetric infltrates injection [11], and multiple sclerosis [12]. Additionally, the and interlobular septal thickenings of the lungs, presumed presence of neurologic disease may be a good predictor to be pulmonary edema, although difuse multifocal pneu- of mortality in patients with r-TTC [13]. To the best of monia and pneumocystis pneumonia were considered. It ourknowledge,thisisthefrstreportofacaseofr-TTC also revealed dilation of lef ventricle and lef atrium, pneu- presenting afer a spinal subdural hematoma. momediastinum,andfuidintheesophagus.MRIofthe lumbar spine revealed abnormally decreased T2 signal and 2. Case Presentation mildly increased T1 signal involving the ventral central canal spanningfromT5toL2-L3,whichlikelyrefectedasubdural A 23-year-old man presented to an outside Emergency hematoma (Figure 1). It also demonstrated a likely superim- Department (ED) with difculty in voiding both bowel and posed subdural hygroma with fuid signal present that was bladder, and signifcant mid-back pain with associated weak- most prominent beginning at the L2-L3 level and progressing ness, numbness, and tingling in bilateral lower extremities. caudally to the L5-S1 level within the ventral thecal sac. Tere He reported a two-week history of headache, nonproductive was associated dorsal displacement of the nerve roots of cough, nasal congestion, nausea, and vomiting but denied thecaudaequinaandcrowdingofthenerveroots.Tese fank pain and dysuria. On physical exam, he was signifcantly fndingsresultedindifusenarrowingofthelumbarthecal hypertensive (225/119 mmHg) and bradycardic (57 bpm), sac most severely between T7-T8 and the mid-T10 vertebral with paraspinal muscle tenderness, but there was no vertebral body, where the subdural hematoma was largest. Narrowing point tenderness. He was also found to have hypoactive deep of the thecal sac was most severe at the T9-T10 level where tendon refexes at the patella and Achilles tendons. there was moderate to severe narrowing of the thecal sac He had visited the ED twice in the two days prior to present with deformation of the anterior surface of the cord this admission for constant, “achy” back pain in the lumbar that was worse on the lef. Small active Schmorl’s nodes were region, exacerbated by movement, which he attributed to demonstrated along the inferior endplate of L1. Tere was Case Reports in Neurological Medicine 3 Troponin-T 0.11 0.09 0.07 ng/mL 0.05 0.03 0.01 Day 1 Day 2 Day 3 Day 4 Day 5 Day 6Day 7Day 8Day 9 N-Terminal Pro-BNP 6000 5000 4000 3000 pg/mL 2000 1000 Generalized Normal High 0 Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7 Day 8 Day 9 Figure 2: Troponin-T and N-Terminal Pro-BNP levels over the course of hospital stay. also an abnormal signal within the subarachnoid spaces of lung. Tese fndings were believed to have refected severe the lower lumbar spine that was most prominent at the L5-S1 pulmonary edema. CT of the head without contrast was level. Te decreased T2 signal and increased T1 signal present negative for large territorial acute infarction, acute intracra- atthislevellikelyrefectedasubarachnoidhemorrhage.Tere nial hemorrhage, and mass efect. CT angiogram of the was no enhancement on the study to suggest