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Abstract
The violent forces generated by the strong paraspinal muscles during generalised tonic-clonic seizures are known to be associated with numerous musculoskeletal injuries. Vertebral fractures following epileptic seizures are typically compression fractures, occurring in the mid thoracic region, usually without resultant neurological deficit. Despite the relative frequency of vertebral compression fractures complicating tonic-clonic seizures, burst fractures are rare. We report a case of a burst fracture resulting in conus medullaris syndrome following generalised motor seizures. Clinicians managing post-ictal patients should maintain a high degree of suspicion for secondary injury and conduct a detailed clinical examination. If there remains any doubt regarding diagnosis, appropriate imaging should be employed.
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The violent forces generated by the strong paraspinal muscles during generalised tonic-clonic seizures are known to be associated with a number of musculoskeletal injuries. These may range from shoulder dislocations to fractures of facial bones, long bones and vertebrae. Vertebral fractures following epileptic seizures are typically compression fractures, occurring in the mid-thoracic region, usually without neurological deficit.
Case report
A 28-year-old man, with a history of epilepsy, presented following multiple witnessed grand mal seizures, secondary to poor compliance with medication. There was no history of trauma or falls. He was post-ictal on presentation and was commenced on a phenytoin infusion. As his consciousness level improved he complained of severe lower back pain, with altered sensation below his waist and loss of power to his legs.
Clinical examination confirmed a flaccid paralysis in both lower limbs, with altered sensation bilaterally extending to his perineum. Digital rectal examination confirmed altered tone and sensation. Catheterisation revealed 800 ml residual volume.
Imaging identified a burst fracture of the first lumbar vertebra with retropulsion of a bony fragment causing cord compression (figure 1).
Large retropulsed bony fragment lying within spinal canal.
After transfer to a spinal unit he underwent urgent spinal decompression and posterior stabilisation (figure 2). Postoperatively his symptoms improved, with motor function returning. He continued to have altered sensation to his perianal region with faecal and urinary incontinence, and was diagnosed with conus medullaris syndrome.
L1 burst fracture following posterior stabilisation with pediclescrews.
Discussion
Epileptic seizures are relatively common, affecting approximately 0.2–0.5% of the general population.1 Frequency of musculoskeletal injuries resulting from tonic-clonic seizure activity is estimated to be between 1.1% and 16%.2 In the absence of external trauma, the mechanism of vertebral fracture is by the powerful contraction of the paraspinal muscles during a seizure. Lehndorf first suggested this theory in 1907 after observing vertebral fractures in patients following convulsions secondary to tetanus.3 Spinal injuries have been reported to occur more frequently when seizures arise during sleep,4 suggesting external trauma is not necessary.
Studies have shown that anticonvulsive medication can lead to a reduction in the bone mineral density and increased risk of fracture, particularly within the vertebral body.5 Such compression fractures are classically seen in the elderly osteoporotic population. Sheth et al reported a decrease in the bone mineral density of 14% of children prescribed carbamazepine, and 10% in those taking sodium valproate.6
Vertebral compression fractures result in a loss of the anterior height of the vertebral body while the posterior aspect remains intact. In contrast, burst fractures involve both the anterior and posterior aspects of the vertebral body. An axial compression force ‘bursts’ the body into fragments that may retropulse into the canal producing neurological symptoms. Burst fractures are unstable and usually require stabilisation at this level.
Compression fractures have also been reported in patients undergoing electroconvulsive therapy (ECT) for psychiatric conditions. In 1954 Kelly found the total incidence of fractures in patients undergoing ECT was 2.4%, with vertebral fractures occurring in 1% of cases. These were typically compression fractures occurring in the region of T3–T8.7 This work was conducted prior to the use of muscle relaxants and anaesthetic agents for ECT. Vasconcelos reported a 1% incidence of symptomatic vertebral compression fractures in patients following grand mal seizures, with an overall incidence of 15%.3 In both studies a greater frequency of fractures was observed in the male population, suggesting an association between muscle bulk and risk of vertebral fracture.3 7
Our patient had residual neurological deficit despite prompt decompression. The spinal cord tapers at its terminal end at the level of the L1 vertebra, the conus medullaris. The nerve roots continue below this level as the cauda equina. Injury to the conus gives lower back pain, sphincter dysfunction and bilateral paraesthesia in the perianal region.
Despite the relative frequency of vertebral compression fractures complicating tonic-clonic seizures, burst fractures are rare. To our knowledge this is the first reported case in Europe of a burst fracture resulting in conus medullaris syndrome following generalised motor seizures.
Clinicians managing post-ictal patients should maintain a high degree of suspicion and conduct a detailed examination. If there remains any doubt regarding the diagnosis, appropriate imaging may be necessary.
Footnotes
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; not externally peer reviewed.