A minimally invasive surgery combining temporary percutaneous pedicle screw fixation without fusion and vertebroplasty with transpedicular intracorporeal hydroxyapatite blocks grafting for fresh thoracolumbar burst fractures: prospective study.

BACKGROUND: The conventional surgical treatment for thoracolumbar burst fractures is physically invasive for the patient and also causes problems such as the sacrifice of healthy mobile segments to stabilize the fracture site. We performed a procedure for the treatment of fresh thoracolumbar burst fractures by combining percutaneous short pedicle screw fixation and vertebroplasty with transpedicular intracorporeal hydroxyapatite blocks grafting. METHODS: Patients with type A3 fresh thoracolumbar burst fractures with no or mild neurological symptoms were treated using temporary posterior fixation without fusion. Consecutive 21 patients were studied, with a mean age of 45.4 years (range 23-73) and a mean follow-up period of 21.9 months (range 15-25). We evaluated operative time, estimated blood loss, low back pain on a visual analogue scale, change in the kyphotic angle, correction loss, bone union, and complications. RESULTS: The average operative time was 95.7 min (range 69-143), and the average blood loss was 38.6 mL (range 10-130). The average correction angle was 9.6°. There were slight correction losses of height of the vertebral bodies. Bone union was obtained in all patients, with no instrumentation failures. Our procedure resulted in no surgery-related complications. CONCLUSIONS: For the treatment of type A3 fresh thoracolumbar burst fractures, this method is less invasive and can preserve the adjacent healthy mobile segment. Our treatment is an optional therapeutic strategy for patients with thoracolumbar burst fractures and is a good option particularly for young adult patients.

Usefulness of full spine computed tomography in cases of high-energy trauma: a prospective study.

INTRODUCTION: At this hospital, computed tomography (CT) of the full spine is performed on all patients who have sustained high-energy trauma because spinal fractures can be overlooked by referring only to clinical findings and plain X-rays of the spine. The goal of this study is to prospectively detect the occurrence of spinal fractures in cases of high-energy trauma using full spine CT and to evaluate the usefulness of it. MATERIALS AND METHODS: Subjects were 179 patients (134 male, 45 female) who were deemed to have sustained high-energy trauma in the 21-month period starting in September 2007. Spinal fractures initially revealed by CT were studied in detail. RESULTS: Spinal fractures were found in 54 patients (30.2 %); 19 patients had stable fractures, and 41 had unstable fractures. Forty patients had concomitant injuries to organs in addition to spinal injury; these patients had an average Injury Severity Score of 20.2 (4-70). Of 16 patients with a cervical fracture, 6 (37.5 %) had a fracture that did not appear on plain X-rays of the cervical and that was first identified by CT. Of 43 patients with a thoracolumbar fracture, 6 (14.0 %) had a fracture that would have been difficult to detect if a full spine CT had not been done. CONCLUSION: In patients who have sustained high-energy trauma, spinal fractures may be overlooked during primary care by a diagnosis based only on plain X-rays and clinical manifestations. Therefore, patients who have sustained high-energy trauma should be evaluated with full spine CT during primary care.

Adenosine modulates excitatory synaptic transmission and suppresses neuronal death induced by ischaemia in rat spinal motoneurones.

Although adenosine is an important neuromodulator, its role in modulating motor functions at the level of the spinal cord is poorly understood. In the present study, we investigated the effects of adenosine on excitatory synaptic transmission and neuronal death induced by experimental ischaemia by using whole-cell patch-clamp recordings from lamina IX neurones in spinal cord slices. Adenosine significantly decreased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in almost all neurones examined that could be mimicked by an A(1) receptor agonist, N (6)-cyclopentyladenosine (CPA), and inhibited by an A(1) receptor antagonist, 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX). Interestingly, adenosine increased mEPSC frequency in the presence of DPCPX in a subpopulation of neurones. In these neurones, an A(2A) receptor agonist, 2-[4-(2-carbonylethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS21680), increased mEPSC frequency. Adenosine also induced an outward current that was blocked by the addition of Cs(+) and tetraethylammonium into the patch-pipette solution and inhibited in the presence of Ba(2+). The adenosine-induced outward current was mimicked by CPA, but not CGS21680, and inhibited by DPCPX. Moreover, superfusing with ischaemia simulating medium (ISM) generated an agonal inward current in all of the neurones tested. The latencies of the inward currents induced by ISM were significantly prolonged by adenosine or CPA, but not by CGS21680. These results suggest that adenosine receptors are functionally expressed in both the pre- and postsynaptic sites of lamina IX neurones and that their activation may exert multiple effects on motor function. Moreover, this study has provided a cellular basis for an involvement of A(1) receptors in the neuroprotective actions of adenosine.

Selective vulnerability to ischemia in the rat spinal cord: a comparison between ventral and dorsal horn neurons.

STUDY DESIGN: Whole-cell patch-clamp recordings were performed from ventral horn (VH) and dorsal horn (DH) neurons obtained from the rat spinal cord slices. OBJECTIVE: This study investigated which is more vulnerable to ischemia, spinal VH neurons or DH neurons. SUMMARY OF BACKGROUND DATA: Spinal cord ischemia or injury sometimes causes a greater loss of motor function than of sensory function in patients. However, it is difficult to evaluate whether spinal motor neurons are more vulnerable than sensory neurons because of the anatomic complexity and a variety of physiologic factors in the spinal cord. METHODS: Whole-cell patch-clamp recordings were performed from VH and DH neurons obtained from the spinal cord slices. Ischemia was simulated by superfusing an oxygen- and glucose-deprived medium (ischemia simulating medium [ISM]). RESULTS: Perfusion with ISM generated an agonal depolarization in all VH and DH neurons recorded in current-clamp mode. Following ISM superfusion, an agonal inward current was produced at a holding potential of -70 mV in all VH and DH neurons tested in voltage-clamp mode. The agonal inward current consisted of a slow and subsequent rapid inward current. The average latency of the rapid inward currents after ISM exposures in VH neurons was significantly shorter than that in DH neurons. The average amplitude of the agonal inward currents in VH neurons was significantly bigger than that of DH neurons. Moreover, the recovery ratio by the reintroduction of oxygen and glucose in VH neurons was smaller than that in DH neurons. CONCLUSIONS: These results suggest that VH neurons are more vulnerable to ischemia than DH neurons. This finding may help in achieving a better understanding of the difference between motor and sensory disturbance in spinal cord ischemia or injury patients.