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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 5  |  Issue : 1  |  Page : 33-35

Spinal cord dysfunction secondary to a sports/exercise event: Two case reports


1 Department of Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico
2 Department of Physical Medicine and Rehabilitation, VA Caribbean Healthcare System, San Juan, Puerto Rico

Date of Submission13-Mar-2021
Date of Decision10-May-2021
Date of Acceptance23-Jul-2021
Date of Web Publication29-Jan-2022

Correspondence Address:
Dr. Edwardo Ramos
Department of Physical Medicine and Rehabilitation, PO Box 365067, San Juan
Puerto Rico
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JISPRM-000132

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  Abstract 


Purpose: The objective of this paper is to present two young patients with SCDys after participation in a sports/exercise event. The authors aim to raise awareness of these unusual causes with potentially fatal results. The authors want to review literature regarding the diagnosis and treatment and particular rehabilitation issues of SCDys. Methods: Two cases of young patients with a history of SCDys consulted the pediatric rehabilitation medicine service. Results: Physical examination revealed incomplete paraparesis and neurogenic bladder. Both final diagnoses were confirmed by magnetic resonance imaging or computerized tomography scan. Treatment was aimed at avoiding further/permanent neurological complications in both cases, taking into consideration their respective etiologies. Conclusion: SCDys is a nontraumatic spinal cord injury that has different etiologies. This paper presents a SCDys due to an unusual etiology.

Keywords: Pediatric, spinal cord dysfunction, spinal cord injury, sports


How to cite this article:
Ramos E, Ortiz-Santiago A, Correa-Mendoza A. Spinal cord dysfunction secondary to a sports/exercise event: Two case reports. J Int Soc Phys Rehabil Med 2022;5:33-5

How to cite this URL:
Ramos E, Ortiz-Santiago A, Correa-Mendoza A. Spinal cord dysfunction secondary to a sports/exercise event: Two case reports. J Int Soc Phys Rehabil Med [serial online] 2022 [cited 2022 May 23];5:33-5. Available from: https://www.jisprm.org/text.asp?2022/5/1/33/336878




  Introduction Top


Atraumatic spinal cord injury, also known as spinal cord dysfunction (SCDys), is rare in the pediatric population. This term was initially described in adults, where the etiology included degenerative spinal conditions, tumors, vascular diseases, infections, and inflammation.[1] Although the literature is scanty, causes of pediatric SCDys include congenital malformations, tumors, viral infections, and inflammation. These injuries have different medical, prognostic, and rehabilitation implications compared with traumatic spinal cord injuries. The authors want to present two rare cases of exercise-related SCDys.

Case 1

A 13-year-old male athlete without medical history presented with sudden onset low back pain. The patient had been visiting on vacation in the Caribbean and had just completed his first 3-h surfing lesson. An hour after finishing his lesson, he developed excruciating pressure-like pain radiating to both legs, 10/10 in intensity requiring emergency room evaluation where analgesics were administered providing symptomatic relief. An hour later, he was unable to walk and presented difficulty voiding, requiring catheterization with a residual of 900 ml. The patient denied headaches, blurry vision, weakness of upper extremities, involuntary movements, or loss of sphincter tone.

He was transferred to the University Pediatric Hospital. Examination showed lower paraparesis 2/5, bilateral foot drop, positive corticospinal signs, and impaired sensation, pinprick, and proprioception; rectal tone was intact. Thoracolumbar magnetic resonance imaging showed central hyperintensities at T7–T8 [Figure 1]. Thoracic level myelopathy due to acute SCDys was suspected, and a diagnosis of Surfer's myelopathy (SM) was done. The patient was admitted to the intensive care unit and started on high-dose methylprednisolone pulse therapy for 3 days with vasopressors (mean arterial pressure [MAP] >85 mmHg). The patient received inpatient rehabilitation, and within a week of presentation, he achieved modified independent ambulation with a standard walker.
Figure 1: (a) Abnormal T2-weighted and (b) Short-tau inversion-recovery images distal to the level of T7–T8 involving the central cord, with mild increase in cord caliber

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Case 2

A 13-year-old male with a history of severe hemophilia A presented to the emergency room with a 6-h onset of excruciating nontraumatic lumbar pain after performing repetitive sit-ups. Oral analgesics were provided with no relief. Twenty-four hours later, he developed progressive paraparesis and urinary retention, requiring transfer to the Pediatric University Hospital. Examination was remarkable for bilateral lower paraplegia, impaired sensation, and proprioception, with absent anocutaneous reflex. Diagnosis of L2 incomplete paraplegia, neurogenic bladder, and bowel was done. Computed tomography scan [Figure 2] revealed an anterior T11–T12 spinal epidural hematoma (SEH) causing cord compression. The patient underwent emergency laminectomy 12 h later and received factor VIII replacement therapy. He completed inpatient rehabilitation with sensory-motor improvements, achieving modified independent locomotion with a manual wheelchair.
Figure 2: (a) Lateral view and (b) Transverse view. Hyperdense lenticular-shaped lesion anterior to the spinal canal at the level of T11– T12, measuring 5 cm3 by 0.7 cm AP by 1.7 cm transverse causing spinal stenosis

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  Discussion Top


General concepts of spinal cord dysfunction in the pediatric population

Two examples of SCDys in the pediatric population secondary to sports/exercise participation were presented. The International Spinal Cord Injury Data Sets for Non-Traumatic Spinal Cord Injury classified these types of injuries based on a two-axis approach.[2] The first axis uses two types: congenital genetic and acquired five-level hierarchy.[3] Based on this classification, our patients fall under acquired abnormalities and vascular disorders.

Pathophysiology

Case 1

The applied anatomy of the myelopathy

SM was first described by Thompson et al.[4] in 2004 in novice surfers, where it was thought that they generated excessive force while using the surfboard creating increased tension on the spinal cord and its vasculature.[4] Recently, some have suggested replacing the term SM with the broader term “acute hyperextension myelopathy.” This allows inclusion of all patients with spinal cord infarction and paraparesis due to acute spinal hyperextension.[5] Proposed causes and mechanisms of the spinal cord infarction have been described given the similarity in acute and atraumatic presentation with spinal cord ischemia associated with surgery or aortic diseases. Other authors propose that inferior vena cava undergoes compression or embolization within the spinal arteries, both secondary to prolonged hyperextension.[6]

Case 2

There was an increased risk of bleeding due to known preexisting severe hemophilia A. The patient had prior episodes of hemarthrosis involving the elbows and knees. Central nervous system hemorrhages occur in 2.2%–7.5% of patients with hemophilia A, with intracranial hemorrhage being the leading cause of death. However, SEH is rare, with a prevalence of 0.24%–1.9%.[7],[8]

The authors were not able to find other cases of SEH in patients with hemophilia A after physical activity involving sit-ups. This exercise may involve Valsalva maneuver during the concentric contractile phase, which is especially accentuated by improper breathing. Systolic and diastolic blood pressure elevations have been shown to reach into a supraphysiologic range up to 370/360 mmHg during heavy resistance exercises, especially when combined with the Valsalva maneuver.[9]

The applied anatomy to the myelopathy

The spinal epidural venous plexus is valveless and has been accused of being a bleeding source during resistance exercises.[10] Sudden increases in pressure due to straining, voiding, crying, and coughing could lead to backflow of blood in the plexus and rupture of the veins.[11]

Management

In both cases, high clinical suspicion and proper imaging studies are essential.

Case 1

There are no treatment guidelines for SM, but prompt minimization of permanent complications is warranted. If a patient presents within 3 h from symptom/sign onset, the National Acute Spinal Cord Injury Society III methylprednisolone protocol may be considered. Whether steroids had a beneficial impact is still unknown, but detrimental effects outweigh the risks of them not being administered. Studies have demonstrated maintaining MAP >85 mmHg for the initial 5–7 days after acute spinal cord injury yielded better neurological recovery.[12] Methylprednisolone was used in this case (24-h dose; 30 mg/kg loading dose; 5.4mg/kg/h infusion x 23h), but other steroid therapies may be considered as well.

Case 2

After diagnosis of SEH, immediate factor VIII replacement therapy is recommended in cases of severe hemophilia.[9] Some patients will require surgical procedures including spinal laminectomy and decompression.[13] Timely intervention after symptom/sign onset is recommended at 48 h for incomplete and 24 h for complete neurologic lesions, as it will increase the chances for a better prognosis.[11]

Rehabilitation issues

SCDys can be progressive, which may challenge establishing neurological and rehabilitation outcomes as well as evaluation for functional prognosis.

In addition, patients with SCDys may require additional medical treatment during their rehabilitation process such as radio/chemotherapy, intravenous immunoglobulin, or immunosuppressant medications, which requires planification to maximize the rehabilitation time in the unit.[3]

It is essential to consider safety equipment, body positioning, maneuvering techniques, and proper breathing during back hyperextension or resistance exercises that involve Valsalva in order to prevent complications such as SCDys.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
New PW, Biering-Sørensen F. Review of the history of non-traumatic spinal cord dysfunction. Top Spinal Cord Inj Rehabil 2017;23:285-98.  Back to cited text no. 1
    
2.
New PW, Marshall R. International spinal cord injury data sets for non-traumatic spinal cord injury. Spinal Cord 2014;52:123-32.  Back to cited text no. 2
    
3.
New PW. A narrative review of pediatric nontraumatic spinal cord dysfunction. Top Spinal Cord Inj Rehabil 2019;25:112-20.  Back to cited text no. 3
    
4.
Thompson TP, Pearce J, Chang G, Madamba J. Surfer's myelopathy. Spine (Phila Pa 1976) 2004;29:E353-6.  Back to cited text no. 4
    
5.
Albuja AC, Qaiser S, Lightner DD, Raslau FD, Zafar MS, Bernard PA, et al. Surfer's myelopathy without surfing: A report of two pediatric patients. Spinal Cord Ser Cases 2017;3:17008.  Back to cited text no. 5
    
6.
Gandhi J, Lee MY, Joshi G, Khan SA. Surfer's myelopathy: A review of etiology, pathogenesis, evaluation, and management. J Spinal Cord Med 2021;44:2-7.  Back to cited text no. 6
    
7.
Antunes SV, Vicari P, Cavalheiro S et al. Intracranial haemorrhage among a population of haemophilic patients in Brazil. Haemophilia 2003;9:573–7.  Back to cited text no. 7
    
8.
de Tezanos Pinto M, Fernandez J, Perez Bianco PR. Update of 156 episodes of central nervous system bleeding in hemophiliacs. Haemostasis 1992;22:259-67.  Back to cited text no. 8
    
9.
Eyster ME, Gill FM, Blatt PM, Hilgartner MW, Ballard JO, Kinney TR. Central nervous system bleeding in hemophiliacs. Blood 1978;51:1179-88.  Back to cited text no. 9
    
10.
Groen RJ, Hans P. Vascular anatomy of the spinal epidural space: Considerations on the etiology of the spontaneous spinal epidural hematoma. Clin Anat 1991;4:413-20.  Back to cited text no. 10
    
11.
Schoonjans AS, De Dooy J, Kenis S, Menovsky T, Verhulst S, Hellinckx J, et al. Spontaneous spinal epidural hematoma in infancy: Review of the literature and the “seventh” case report. Eur J Paediatr Neurol 2013;17:537-42.  Back to cited text no. 11
    
12.
Freedman BA, Malone DG, Rasmussen PA, Cage JM, Benzel EC. Surfer's myelopathy: A rare form of spinal cord infarction in novice surfers: A systematic review. Neurosurgery 2016;78:602-11.  Back to cited text no. 12
    
13.
Bruyn GW, Bosma NJ. Spinal extradural haematoma. In: Bruyn GW, Vinken PJ, editors. Injuries of the Spine and Spinal Cord. Handbook of Clinical Neurology. Vol 26, Part 2. Amsterdam: North-Holland; 1976. p. 130.  Back to cited text no. 13
    


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  [Figure 1], [Figure 2]



 

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