Thromboprophylaxis in patients with acute spinal injuries: an evidence-based analysis.

BACKGROUND: The increased risk for venous thromboembolic events following spinal trauma is well established. The purpose of the present study was to examine the literature in order to determine the optimum thromboprophylaxis regimen for patients with acute spinal injuries with or without spinal cord injury. METHODS: EMBASE, MEDLINE, and Cochrane databases were searched from the earliest available date to April 2008 for clinical trials comparing different methods of thromboprophylaxis in adult patients following acute spinal injuries (with or without spinal cord injury). Outcome measures included the prevalences of deep-vein thrombosis and pulmonary embolism and treatment-related adverse events. RESULTS: The search yielded 489 studies, but only twenty-one of them fulfilled the inclusion criteria. The prevalence of deep-vein thrombosis was significantly lower in patients without spinal cord injury as compared with patients with spinal cord injury (odds ratio = 6.0; 95% confidence interval = 2.9 to 12.7). Patients with an acute spinal cord injury who were receiving oral anticoagulants had significantly fewer episodes of pulmonary embolism (odds ratio = 0.1; 95% confidence interval = 0.01 to 0.63) than those who were not receiving oral anticoagulants (either untreated controls or patients managed with low-molecular-weight heparin). The start of thromboprophylaxis within the first two weeks after the injury resulted in significantly fewer deep-vein-thrombosis events than delayed initiation did (odds ratio = 0.2; 95% confidence interval = 0.1 to 0.4). With regard to heparin-based pharmacoprophylaxis in patients with spinal trauma, low-molecular-weight heparin significantly reduced the rates of deep-vein thrombosis and bleeding episodes in comparison with the findings in patients who received unfractionated heparin, with odds ratios of 2.6 (95% confidence interval = 1.2 to 5.6) and 7.5 (95% confidence interval = 1.0 to 58.4) for deep-vein thrombosis and bleeding, respectively. CONCLUSIONS: The prevalence of deep-vein thrombosis following a spine injury is higher among patients who have a spinal cord injury than among those who do not have a spinal cord injury. Therefore, thromboprophylaxis in these patients should start as early as possible once it is deemed safe in terms of potential bleeding complications. Within this population, low-molecular-weight heparin is more effective for the prevention of deep-vein thrombosis, with fewer bleeding complications, than unfractionated heparin is. The use of vitamin K antagonists appeared to be effective for the prevention of pulmonary embolism.

Decorrelating actions of Renshaw interneurons on the firing of spinal motoneurons within a motor nucleus: a simulation study.

A simulation of spinal motoneurons and Renshaw cells was constructed to examine possible functions of recurrent inhibition. Recurrent inhibitory feedback via Renshaw cells is known to be weak. In our model, consistent with this, motoneuron firing was only reduced by a few pulses per second. Our initial hypothesis was that Renshaw cells would suppress synchronous firings of motoneurons caused by shared, dynamic inputs. Each motoneuron received an identical pattern of noise in its input. Synchrony coefficients were defined as the average motoneuron population firing relative to the activity of selected reference motoneurons; positive coefficients resulted if the motoneuron population was particularly active at the same time the reference motoneuron was active. With or without recurrent inhibition, the motoneuron pools tended to show little if any synchronization. Recurrent inhibition was expected to reduce the synchrony even further. Instead, it reduced the variance of the synchrony coefficients, without a comparable effect on the average. This suggests-surprisingly-that both positive and negative correlations between motoneurons are suppressed by recurrent inhibition. In short, recurrent inhibition may operate as a negative feedback mechanism to decorrelate motoneurons linked by common inputs. A consequence of this decorrelation is the suppression of spectral activity that apparently arises from correlated motoneuron firings due to common excitatory drive. Without recurrent inhibition, the power spectrum of the total motoneuron pool firings showed a peak at a frequency corresponding to the largest measured firing rates of motoneurons in the pool. Recurrent inhibition either reduced or abolished this peak, presumably by minimizing the likelihood of correlated firing among pool elements. Renshaw cells may act to diminish physiological tremor, by removing oscillatory components from aggregate motoneuron activity. Recurrent inhibition also improved coherence between the aggregate motoneuron output and the common drive, at frequencies above the frequency of the "synchronous" peak. Sensitivity analyses demonstrated that the spectral effect became stronger as the duration of inhibitory synaptic conductance was shortened with either the magnitude or the spatial extent of the inhibitory conductances increased to maintain constant net inhibition. Overall, Renshaw inhibition appears to be a powerful way to adjust the dynamic behavior of a neuron population with minimal impact on its static gain.