Post-traumatic syringomyelia

Post-traumatic syringomyelia is estimated to develop in more than 20% of individuals with traumatic spinal cord injury (SCI). The development can give rise to clinical symptoms 6 months to 26 years after the injury, and presentation 40 years post-injury has been seen by one of the authors.1234 We present an unusual case for comments and discussion.     

Post-traumatic syringomyelia

Progressive post-traumatic cystic syringomyelia is an uncommon and increasingly recognized cause of morbidity following spinal cord injury. We hereby report a 35-year-old gentleman who sustained wedge compression fracture of L-1 vertebral body 15 years back and had complete paraplegia with bowel/bladder involvement. The neurological deficit recovered with minimal residual motor deficits and erectile dysfunction. He presented now with increasing neurological deficits associated with pain and paresthesia. The MRI spine showed a syrinx extending from the site of injury up to the medulla. He underwent a syringo-peritoneal shunt and at followup his pain and motor functions had improved but erectile dysfunction was persisting.     

Post-traumatic syringomyelia.

Post-traumatic syringomyelia is uncommon. It is seen predominantly after injury to the thoracic or the lumbar spine and rarely after injury to the cervical spine. In this report, three cases of post-traumatic syringomyelia are presented. The injury was limited to the thoracic spine in one case and to the cervical spine in the rest. The symptoms began after two years in two cases and after fifteen years in the third. The diagnosis was suggested by radiographic examination and was confirmed at operation in each case. Following evacuation and drainage of the cyst, significant improvement occurred in two patients.     

Unexpected neurological deficits following recovery from anaesthesia

Two cases of neurological dysfunction are presented. Neurological deficits after recovery from anaesthesia are unusual in young women perioperatively. In the first case, a 39-yr-old woman presented at 36-wk gestation with antepartum haemorrhage and in labour. Pregnancy had been complicated by pre-eclampsia and she underwent emergency Caesarean section under general anaesthesia without complication. The trachea was extubated when she was awake but almost immediately she became hypertensive, obtunded and reintubation was required. Her pupils became fixed and dilated but the Computerised Axial Tomogram (CT) was normal. A coagulopathy was evident. She made a full neurological recovery within 24 hr. On the same day, a previously healthy 4l-yr-old woman who had undergone uneventful surgery for uterine prolapse 24 hr previously developed headache, nausea and over the next four hours signs of progressive brainstem ischaemia. The CT scan showed oedema of the mid- and hindbrain. Brainstem death was confirmed 12 hr later and the post-mortem revealed acute dissection of the vertebral artery secondary to cystic medial necrosis. Such dramatic neurological sequelae are rare but the importance of identifying “at risk” groups is underlined as is early recognition of neurological injury postoperatively.     

Post-traumatic syringomyelia. Report of three cases]

Three cases of post-traumatic syringomyelia are presented and the mechanism of syrinx formation is discussed. Two cases were examined radiologically. Computed tomography and magnetic resonance images (MRI) showed an expansive syrinx with adhesive arachnoiditis in the thoracic levels below the injury site and a localized syrinx on the posterolateral gray matter in the cervical levels above the injury site. These syrinxes existed below the C2 level and had no communication with the fourth ventricle. The other was an autopsy case. Postmortem examination revealed that a syrinx existed from C2 to Th6 and had no communication with the fourth ventricle or the central canal. It is concluded that small traumatic cavities in the gray matter evolve to an extensive syrinx by cerebrospinal fluid (CSF) entering via the posterior root entry zone, and adhesive arachnoiditis is an important factor in increasing the CSF which is entering. MRI was useful for the diagnosis.     

Post-traumatic epilepsy following head injury

The occurrence of post-traumatic epilepsy (PTE) was studied in 164 consecutive closed head injury patients, each of whom had been unconscious and amnestic for at least one hour. The overall incidence of PTE was found to be 25%, significantly higher than previously reported. Analysis of data revealed PTE was not related to the presence or absence of a hematoma, but rather to the duration of the coma. The incidence of PTE was found to be 35% among patients comatose for three weeks or more.     

Neurologic recovery following rapid spinal realignment for complete cervical spinal cord injury

A case of impressive neurologic recovery after a complete cervical spinal cord injury is presented. The importance of prehospital recognition and immobilization and prompt management of cervical spine injuries is emphasized. Full reduction of the fracture-dislocation of C3 on C4 was accomplished 90 minutes postinjury.     

Cesarean delivery in a parturient with syringomyelia and worsening neurological symptoms

A parturient presented at 35 weeks' gestation with worsening neurological symptoms caused by syringomyelia. She underwent urgent cesarean delivery. The etiology and anesthetic considerations for an obstetrical patient with syringomyelia are discussed.     

Post-traumatic growth following spinal cord injury

Context/objective

Examine the relationship of post-traumatic psychological growth (PTG), depression, and personal and injury characteristics in persons with spinal cord injury (SCI).

Design

Cross-sectional survey.

Setting

Community.

Participants

Eight hundred and twenty-four adults with SCI.

Interventions

None.

Outcome measures

Five items from the Post-traumatic Growth Inventory, reflecting positive change after injury in life priorities, closeness to others, new opportunities being available, stronger faith, and personal strength.

Results

Initial structural equation model testing of a conceptual model of personal and injury characteristics, violent etiology, depression, and PTG resulted in a poor fit. Model modifications resulted in an improved fit, but explained only 5% of the variance in PTG. Being female, younger, having less formal education, and less time since injury had significant relationships with PTG, whereas depression, violent etiology, and injury level/severity did not. In each PTG domain, between 54 and 79% of the sample reported at least some positive change after injury.

Conclusions

The results of this study, while promising, explained only a small portion of the variance in PTG. A majority of the sample experienced some positive change after injury, with the greatest change in discovering that they were stronger than they thought they were. Comparing means previously reported in a non-SCI sample of those who experienced trauma, positive change after injury was comparable for each PTG item except for new opportunities being available, which was significantly lower for those with SCI. Future directions of research include the development of theoretical models of PTG after SCI.     

Post-traumatic inflammation following spinal cord injury

Inflammatory reaction following a spinal cord injury (SCI) contributes substantially to secondary effects, with both beneficial and devastating effects. This review summarizes the current knowledge concerning the structural features (vascular, cellular, and biochemical events) of SCI and gives an overview of the regulation of post-traumatic inflammation.     

Myelopathy with syringomyelia following thoracic epidural anaesthesia

Under general anaesthesia and muscle relaxation, a thoracic epidural catheter was inserted at the T8-T9 level in a 7-year-old boy scheduled to have a Nissen fundoplication to provide postoperative analgesia. After 4 ml of lignocaine 1.5% was injected through the catheter, hypotension resulted. Fifty-five minutes later 5 ml of bupivacaine 0.25% produced the same effect. In the recovery room a similar injection resulted in lower blood pressure and temporary apnoea. Sensory and motor deficits were noted the next day and four days later magnetic resonance imaging demonstrated spinal cord syringomyelia extending from T5 to T10. Four years later, dysaesthesia from T6 to T10 weakness of the left lower extremity and bladder and bowel dysfunction persist. The risks of inserting thoracic epidural catheters in patients under general anaesthesia and muscle relaxation are discussed, emphasising the possibility of spinal cord injury with disastrous consequences.     

Administration of MgSO4 failed to improve the neurological recovery after complete global brain ischemia in dogs

The cerebral protective effects of MgSO₄ after complete global brain ischemia were evaluated with EEG, evoked potentials (EP) and the neurological recovery score (NRS) in the dog. Complete global brain ischemia for 15 min was achieved by occluding the ascending aorta and the caval veins. The MgSO₄ group (N=7) were injected with a 10% MgSO₄ solution and the control group (N=7) were administered a normal saline intravenously from the beginning of the resuscitation to 48 h after ischemia. The EEG grades (1=normal, 5=flat) in the control group and the MgSO₄ group were 3.9±0.1 (mean ±SEM) and 3.7±0.3, and the EEG-EP scores (6=normal, 0=serious deterioration) were 2.6±0.4 and 2.7±0.4 4h after ischemia, respectively. The 7-day survival rates for ischemia were equal in both groups (5/7:71%). The NRSs (0=death, 100=normal) in the control group and the MgSO₄ group were 50±3 (n=7) and 43±9 (n=7) on the 3rd day after ischemia, and were 56±5 (n=5) and 42±12 (n=5) on the 7th day. The differences between the two groups were not significant. We conclude that MgSO₄ administered after ischemia has no beneficial effects on the recovery of EEG, EP and the NRS after 15 min of complete global brain ischemia in the dog.