CASE REPORT
Surfer's Myelopathy with Magnetic Resonance Imaging Evidence Suggestive of Venous Congestion: A Case Report
2026 年 13 巻 p. 131-134
詳細
2026 年 13 巻 p. 131-134
Surfer's myelopathy is a rare, nontraumatic spinal cord injury affecting novice surfers. Although spinal ischemia is considered the primary mechanism, whether the initial insult is arterial or venous remains controversial. We report a case of surfer's myelopathy with magnetic resonance imaging findings suggestive of venous congestion-radiological features that, to our knowledge, have not been previously described.
A previously healthy 23-year-old man developed acute low back pain, progressive lower limb weakness, and bladder and bowel dysfunction after his first surfing experience. Magnetic resonance imaging on admission showed longitudinal T2 hyperintensity from T8/9 to the conus medullaris without abnormalities on diffusion-weighted imaging. On day 2, repeat magnetic resonance imaging again demonstrated no diffusion-weighted imaging changes, whereas the apparent diffusion coefficient map revealed hyperintensity, indicating vasogenic edema. These findings were more consistent with venous rather than arterial ischemia. The patient was treated with antiplatelet and anticoagulation therapy along with rehabilitation and ultimately achieved complete neurological recovery.
This case may represent the first description of magnetic resonance imaging findings suggestive of venous congestion in surfer's myelopathy. Apparent diffusion coefficient hyperintensity in the absence of diffusion restriction may reflect reversible venous ischemia. Incorporating diffusion-weighted imaging and apparent diffusion coefficient maps into routine magnetic resonance imaging protocols for suspected surfer's myelopathy could provide valuable insight into pathophysiology and prognosis.
Surfer's myelopathy (SM) was first described by Thompson et al.1) in 2004. It predominantly occurs in novice surfers; however, the number of reported cases remains small, and many aspects of its pathophysiology and standard management remain unclear. We report a case of SM in a person who developed paraparesis with bladder and bowel dysfunction and subsequently achieved complete recovery. Importantly, this case demonstrated distinct radiological findings compatible with venous congestion-findings that, to our knowledge, have not been previously described in SM-and may provide new insight into the underlying pathophysiology.
A healthy 23-year-old man experienced mild low back pain while surfing for approximately 4 hours during his first surfing experience. He remained ambulatory; however, after returning home, he developed worsening back pain, progressive lower extremity weakness, and bladder and bowel dysfunction. He initially visited a local orthopedic clinic, where he received a lumbar block injection without symptom improvement and was subsequently referred to our hospital. On arrival, he was awake and alert. Cranial nerve function was intact, and upper extremity strength was normal. Manual muscle testing (right/left) of the lower extremities revealed the following: iliopsoas 3/3, quadriceps 3/3, hamstrings 3/4, tibialis anterior 3/3, and gastrocnemius 4/4, consistent with incomplete paraparesis. Deep tendon reflexes (right/left) were patellar 2+/2+ and Achilles +/+. Pathological reflexes, including Babinski and Chaddock signs, were absent. Touch and proprioception were intact, whereas pain and temperature sensation were decreased below the L2 dermatome. Based on the neurological examination, the American Spinal Injury Association Impairment Scale (AIS) grade was D on admission. Urinary retention and reduced anal sphincter contraction were noted, although perineal sensation was preserved. Spinal magnetic resonance imaging (MRI) on admission (approximately 30 hours after symptom onset) revealed intramedullary hyperintensity on T2-weighted imaging extending from T8/9 to the conus medullaris, without diffusion-weighted imaging (DWI) abnormality (Figure 1). Axial T2-weighted images demonstrated mild spinal cord swelling without focal anterior horn predominance. Because of paraparesis, bladder and bowel dysfunction, and impaired ambulation, he was admitted for further evaluation. On day 2, repeat MRI (approximately 50 hours after onset) again showed no DWI abnormality; however, the apparent diffusion coefficient (ADC) map demonstrated hyperintensity (Figure 2). The ADC map demonstrated diffuse intramedullary hyperintensity involving the central portion of the cord. By day 8, T2 hyperintensity had improved. No spinal canal stenosis was present, and computed tomography angiography revealed no vascular abnormalities. Given the acute onset of back pain in a novice surfer, the rapid development of myelopathy within several hours, and longitudinal intramedullary signal changes extending from the lower thoracic cord to the conus, a diagnosis of SM was made. He was treated with aspirin, heparin, and alprostadil alfadex, along with rehabilitation therapy. Antiplatelet and anticoagulation therapy were selected to address a possible ischemic mechanism, given the acute onset and imaging findings at admission, while carefully monitoring for hemorrhagic complications. For urinary dysfunction, urological consultation was obtained. Urodynamic studies were performed, and clean intermittent catheterization was initiated; spontaneous voiding was ultimately restored. Muscle strength began to improve from approximately day 2, independent ambulation was achieved by day 14, and spontaneous voiding stabilized by day 90. He was transferred to a rehabilitation ward on day 17 and discharged home on day 38. Outpatient rehabilitation continued, and he ultimately achieved complete neurological recovery at 6 months of follow-up, with improvement of the AIS grade from D on admission to E at final follow-up. Informed consent was obtained from the patient and the patient's family for publication of this case report and accompanying images.
(A) A sagittal T2-weighted image on admission (approximately 30 hours after symptom onset) shows intramedullary hyperintensity from T8/9 to the conus medullaris (arrowheads).
An axial T2-weighted image obtained on admission demonstrates mild spinal cord swelling without focal anterior horn predominance.
(B, C) DWI and the ADC map show no abnormalities.
ADC: apparent diffusion coefficient; DWI: diffusion-weighted imaging
(A) A sagittal T2-weighted image obtained on day 2 (approximately 50 hours after symptom onset) shows more extensive and distinct intramedullary hyperintensity compared with Figure 1 (arrowheads).
(B) DWI shows no abnormality.
(C) The ADC map shows intramedullary hyperintensity from T8/9 to the conus medullaris (arrowheads), consistent with vasogenic edema.
ADC: apparent diffusion coefficient; DWI: diffusion-weighted imaging
SM is believed to represent spinal cord ischemia triggered by hyperextension of the back while paddling in the prone surfing position. However, whether the mechanism is primarily arterial or venous remains controversial. Three main hypotheses have been proposed:
Arterial ischemiaHyperextension may stretch or cause spasm in spinal arteries, resulting in transient ischemia in watershed areas.1) Several studies have reported absent radicular arteries or absence of the artery of Adamkiewicz on angiography, supporting this mechanism.2,3)
Venous congestionProlonged prone positioning may elevate intra-abdominal pressure and impair inferior vena cava outflow. Valsalva maneuvers during paddling may cause retrograde pressure transmission into the epidural venous plexus, leading to venous congestion and infarction.4)
Fibrocartilaginous embolismNucleus pulposus material may embolize the sulcal arteries, typically following exertion and acute back pain.5)
In the present case, arterial infarction was considered less likely because DWI showed no restricted diffusion and the ADC map demonstrated hyperintensity, findings that are generally inconsistent with cytotoxic edema typically seen in acute arterial ischemia. In addition, axial MRI did not show anterior horn-predominant involvement, which is characteristic of anterior spinal artery infarction. Fibrocartilaginous embolism was also considered unlikely, as there was no history of significant axial loading or trauma, cerebrospinal fluid examination showed no inflammatory changes, and the clinical course was characterized by gradual improvement rather than sudden irreversible deterioration. Tashiro, who personally experienced SM, reported that individuals with limited spinal flexibility might not develop sufficient arterial traction during hyperextension to induce arterial ischemia.6) Instead, marked increases in intrathoracic and intra-abdominal pressure during paddling may obstruct venous outflow, leading to venous ischemia or congestion.
Imaging findingsA review of 23 SM cases reported typical MRI findings of fusiform swelling of the conus and longitudinal T2 hyperintensity extending from the mid-thoracic cord to the conus.7) DWI findings in SM have been inconsistent: although some reports describe DWI hyperintensity and restricted diffusion in most cases,2) others have found no consistent DWI or ADC abnormalities.8) Positive DWI with low ADC values has generally been interpreted as cytotoxic edema, consistent with an arterial mechanism. In contrast, our case demonstrated isointensity on DWI combined with ADC hyperintensity, indicating vasogenic edema rather than cytotoxic edema. Vasogenic edema is characteristic of venous ischemia or venous congestion, including spinal venous congestive disorders.9) Although similar DWI/ADC patterns have been reported in spinal venous congestion, such as spinal dural arteriovenous fistula, these imaging findings have not been previously documented in SM.10) Although venous involvement in the pathogenesis of SM has been clinically suggested, radiologic evidence directly supporting this hypothesis has been limited. To our knowledge, this is the first reported case demonstrating MRI findings compatible with venous congestion in SM. Although these findings are not definitive and other mechanisms cannot be completely excluded, they support venous involvement as a plausible mechanism in at least some patients. The reversible nature of vasogenic edema is consistent with the patient's complete neurological recovery. These observations suggest that incorporating DWI and ADC map into MRI protocols for suspected SM may be valuable in elucidating pathophysiology and predicting prognosis.
TreatmentNo standardized acute treatment has been established. Therapeutic approaches described in the literature2) include:
・intra-arterial or intravenous tissue plasminogen activator
・intra-arterial nimodipine
・lumbar drainage
・reduction of cerebrospinal fluid pressure
・anticoagulation or antiplatelet therapy
・maintaining mean arterial pressure above 85 mmHg
・corticosteroid administration
However, strong evidence supporting these treatments is lacking.11) At admission, because the underlying pathophysiology was unclear and both arterial and venous ischemic mechanisms were considered, antiplatelet and anticoagulation therapies were initiated concurrently, with careful monitoring for hemorrhagic complications. After follow-up MRI findings suggested venous involvement as a more plausible mechanism, antiplatelet therapy was discontinued, anticoagulation therapy alone was continued, and it was discontinued after several days without adverse events. Steroid pulse therapy was not administered in this case because inflammatory myelopathy was considered unlikely based on clinical and imaging findings, and the potential benefit in SM remains unproven. In this patient, antiplatelet and anticoagulation therapies were administered, although spontaneous recovery cannot be excluded. Urinary dysfunction required urological evaluation and was managed with intermittent catheterization until spontaneous voiding returned. Further case accumulation is needed to determine effective treatments.
PrognosisThe prognosis of SM is generally favorable, with many cases achieving substantial recovery.12) However, severe cases with persistent paraplegia have been reported.6) The initial AIS grade correlates strongly with outcome.7) In this patient, the AIS grade improved from D on admission to E at follow-up.
ConclusionWe report a case of SM with MRI findings compatible with venous congestion. To our knowledge, no previous reports have demonstrated radiological findings supporting venous involvement in SM, making this case particularly valuable. Although the pathophysiology of SM remains incompletely understood and alternative mechanisms cannot be entirely excluded, further case accumulation is essential. Given that poor outcomes may occur even in otherwise healthy young individuals, it is important to raise awareness of SM, particularly among surfing instructors and novice surfers.
All authors have no conflict of interest.
