Posttraumatic Cervical Syringomyelia

Study design: Case report of a patient with subacute delayed myelopathy after an acute low thoracic spine injury. Objectives: To draw awareness to a rarely described complication with potential to add devastating neurological insult to the original spinal cord injury, and to discuss evidence supporting a vascular mechanism. Setting: Health Science Centre, Winnipeg, Manitoba, Canada. Case report: A 35-year-old woman developed clinical and MRI evidence of ascending myelopathy, extending up to C5, 16 days after a T11/12 fracture dislocation. The distribution of MRI signal abnormality, MRI evidence of prominent venous markings, and association with upright mobilization and the wearing of a thoraco-lumbo-sacral orthosis, suggest that elevated spinal venous pressure in conjunction with low arterial pressure may have induced impaired spinal cord vascular perfusion. Conclusion: After recent spinal cord injury, factors exacerbating spinal venous hypertension and/or arterial hypotension may in some patients lead to impaired spinal cord perfusion. These factors should be considered and corrected if symptoms or signs of progressive myelopathy emerge in the first few days or weeks after injury.

Section: Introductionmentioning

confidence: 99%

Subacute delayed ascending myelopathy after low spine injury: case report and evidence of a vascular mechanism

Schmidt

2005

“…3 The incidence of PTS is increasing and is evaluated di erently in the recent literature depending on whether it was diagnosed by clinical means (3.2%, 4 4.45%, 5 3.43% 6 ) or by neuroradiological examinations. 7 The unforseeable nature, and the seriousness of this complication, raise the problem of pathogenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Post-traumatic syringomyelia and post-traumatic spinal canal stenosis: A direct relationship: Review of 75 patients with a spinal cord injury

Perrouin-Verbe¹,

Lenne-Aurier²,

Robert³

et al. 1998

This study aims to demonstrate predictive factors for post traumatic syringomyelia (PTS), and in particular to correlate the role of insu ciency of reduction of a spinal fracture with the occurrence of syringomyelia. One hundred and twenty-eight spinal cord injured patients (SCI) were studied during the years 1992 and 1993. Among them, 75 underwent a complete and reliable evaluation including: review of the initial vertebral lesion, and of the surgery report, and a radiological study of the lesion site with standard X-rays, a CT scan, and an MRI. The CT Scan included slices in sagittal reconstructions and in the axial plane at the site of injury with the calculation of a percentage of canal stenosis in the two planes of the space. An MRI was carried out with T1 and T2 weighted images, including sagittal entire cord images in addition to sagittal and axial slices centred on the site of injury. A syrinx was diagnosed in 28% of the patients. The occurrence of a syrinx is signi®cantly correlated with spinal canal stenosis in the sagittal plane (DD) with a P50.001 and in the axial plane (DS) (P50.05). This present study demonstrates the major role of the insu ciency of reduction of the vertebral lesion in the genesis of a syrinx. The quality of the initial treatment of the vertebral injury is the ®rst step in the prevention of a syrinx. The treatment of a syrinx, besides techniques of drainage, must also take into account the spinal realignment.

“…In the same sense, the patient reports of symptoms worsening with time was not anticipated. Conceivable explanations are neuronal dropout in the damaged intermediolateral columns as in the Shy Drager syndrome, 13 post traumatic syringomyelia, 14 destabilization of blood pressure associated with bowel or bladder distention, and overtreatment with drugs which can produce hypotension ± eg antispastics, inhibitors of angiotensin I converting enzyme, calcium channel blockers and diuretics. 4,15 The failure of the sympathetic nervous system to protect the circulation against gravity in these patients is evidenced by reduced levels of catecholamines and loss of vasomotor adjustments.…”

Section: Discussionmentioning

confidence: 99%

Postural hypotension and abnormalities of salt and water metabolism in myelopathy patients

Frisbie

Steele

1997

To describe the clinical manifestations of postural hypotension (PH) in myelopathy patients a standardized interview and chart review were carried out. Of 232 myelopathy patients with more than 2 years of paralysis seen during a 2 year period, 30 had been treated for PH. All PH patients were paralysed at levels higher than thoracic 7. The highest risk patients were tetraplegic, motor complete, 24 of 73 (33%). The common symptoms of PH were those of reduced consciousness (100%), strength (75%), vision (56%) and breath (53%). Precipitating factors were hot weather (77%) bowel care (33%) and meals (30%). Symptoms worsened with the duration of paralysis in 12 patients. Chronic hyponatremia was found in 54% of the PH patients and 16% of those without, P50.001. Of ®ve PH-hyponatremic patients with urine sodium and osmolality determinations, ®ve continued to retain water (4150 mOsm/kg) while four failed to conserve salt (419 mmol Na/L). PH is common among myelopathy patients with higher levels of paralysis, symptoms are variable, and abnormal salt and water metabolism often coexist.