The validity of administrative data to classify patients with spinal column and cord injuries.

International Classification of Diseases (ICD) codes are used to document patient morbidity in administrative databases. Although administrative data are used for research purposes, the validity of the data to accurately describe clinical diagnostic information is uncertain. We compared the clinical diagnoses for spinal cord and column injuries from a longitudinal patient registry, the Rick Hansen Spinal Cord Injury Registry (RHSCIR), to the ICD-10 spinal injury codes from the Discharge Abstract Database (DAD) at one institution. There were 603 RHSCIR participants with data describing the spinal cord injury, and 341 had data on the spinal column injury. The validity of DAD data to describe spinal injuries was evaluated using the sensitivity and positive predictive values of specific ICD-10 codes; 5.3% of the spinal column injuries and 10.9% of the spinal cord injuries documented in RHSCIR were missed in data from the DAD using ICD-10 codes. The most problematic spinal column ICD-10 code was the dislocation of the cervical vertebra (S13.1); only 14.0% of the dislocations of the cervical vertebrae in RHSCIR were correctly coded in the DAD. The most problematic spinal cord injury ICD-10 code was the incomplete lesion of the lumbar spinal cord (S34.1X); 66.7% of incomplete lesions of the lumbar spinal cord in RHSCIR were correctly coded in the DAD. The validity of DAD data to code spinal injuries is variable, and cannot be reliably used to classify all types of spinal injuries. Patient registries, such as RHSCIR, should be used if accurate detailed diagnostic data are required.

Incidence and prevalence of spinal cord injury in Canada: a national perspective.

BACKGROUND: Despite decades of research, there are no national estimates of the incidence or prevalence of spinal cord injury (SCI) in Canada. Our objective was to utilize the best available data to estimate the incidence and prevalence of traumatic SCI (TSCI) and non-traumatic SCI (NTSCI) in Canada for 2010. METHODS: Initial incidence (number of TSCIs at injury scene) and discharge incidence (number discharged into the community) were calculated using published TSCI rates from Alberta and NTSCI rates from Australia. Prevalence was estimated by applying TSCI and NTSCI discharge incidence rates to historical Canadian population demographics using a cohort survival model and age-specific mortality rates for tetraplegia and paraplegia. RESULTS: The estimated 2010 initial incidence of TSCI is 1,785 cases per year, and the discharge incidence is 1,389 (41 per million). The estimated discharge incidence for NTSCI is 2,286 cases (68 per million). The prevalence of SCI in Canada is estimated to be 85,556 persons (51% TSCI and 49% NTSCI). CONCLUSIONS: This study provides the first estimates of the incidence and prevalence of SCI in Canada. More population-based studies are needed, particularly for NTSCI, as an increasing number of Canadians are expected to be affected by SCI.

Mirrored bilateral slow-wave cortical activity within local circuits revealed by fast bihemispheric voltage-sensitive dye imaging in anesthetized and awake mice.

Spontaneous slow-wave oscillations of neuronal membrane potential occur about once every second in the rodent cortex and may serve to shape the efficacy of evoked neuronal responses and consolidate memory during sleep. However, whether these oscillations reflect the entrainment of all cortical regions via propagating waves or whether they exhibit regional and temporal heterogeneity that reflects processing in local cortical circuits is unknown. Using voltage-sensitive dye (VSD) imaging within an adult C57BL/6J mouse cross-midline large craniotomy preparation, we recorded this depolarizing activity across most of both cortical hemispheres simultaneously in both anesthetized and quiet awake animals. Spontaneous oscillations in the VSD signal were highly synchronized between hemispheres, and acallosal I/LnJ mice indicated that synchrony depended on the corpus callosum. In both anesthetized and awake mice (recovered from anesthesia), the oscillations were not necessarily global changes in activity state but were made up of complex local patterns characterized by multiple discrete peaks that were unevenly distributed across cortex. Although the local patterns of depolarizing activity were complex and changed over tens of milliseconds, they were faithfully mirrored in both hemispheres in mice with an intact corpus callosum, to perhaps ensure parallel modification of related circuits in both hemispheres. We conclude that within global rhythms of spontaneous activity are complex events that reflect orchestrated processing within local cortical circuits.

Treatment of intracerebral hemorrhage in rats with 12 h, 3 days and 6 days of selective brain hypothermia.

Intracerebral hemorrhage (ICH) is a devastating stroke with no proven treatment to reduce brain injury. In this study we modeled ICH by injecting 100 microL of autologous blood into the striatum of rats. We then tested whether hypothermia would reduce brain injury and improve recovery as has been repeatedly observed for ischemic and traumatic brain damage. Aside from reducing blood-brain barrier disruption, inflammation and edema, hypothermia has not consistently improved behavioral or histological outcome after ICH in animal studies. As this might relate to the choice of cooling method and the duration of hypothermia, we used a system that selectively cooled the injured hemisphere to approximately 32 degrees C (striatum) while the body remained normothermic. Cooling (vs. normothermia) started 1 h after ICH and lasted for 12 h, 3 days or 6 days followed by slow re-warming (approximately 1 degrees C/h). Functional impairment was evaluated from 2 to 3 weeks post-ICH at which time brain injury was determined. The ICH caused significant impairment on a neurological deficit scale and in tests of walking (horizontal ladder), skilled reaching (tray task) and spontaneous limb usage (cylinder test). Only the limb use asymmetry deficit was significantly mitigated by hypothermia, and then only by the longest treatment. Lesion volume, which averaged 16.9 mm3, was not affected. These results, in conjunction with earlier studies, suggest that prolonged mild hypothermia will not be a profound neuroprotectant for patients with striatal ICH, but it may nonetheless improve functional recovery in addition to its use for treating cerebral edema.

The effects of selective brain hypothermia on intracerebral hemorrhage in rats.

Prolonged hypothermia effectively treats global cerebral ischemic injury in animal models as well as in cardiac arrest victims. Furthermore, clinical trials, based upon encouraging animal findings, are underway to assess efficacy in ischemic stroke. Intracerebral hemorrhage (ICH) is a more devastating stroke, but one that shares mechanisms of injury with ischemia. Accordingly, ICH may be amenable to hypothermia treatment. In this study we tested whether selective brain hypothermia improves outcome after an ICH in rats created by infusing 100 microL of autologous whole blood into the striatum. Striatal hypothermia ( approximately 32 degrees C) was induced with a novel method (implanted cooling coil) that does not cause systemic cooling, thereby providing a safer and potentially more effective treatment for stroke than systemic hypothermia. Edema occurred for 4 days after ICH, but it peaked at 3 days ( approximately 5%). At this time it was significantly reduced (to approximately 2%) by cooling starting 1 h after ICH (3 day duration). Next, we determined whether 1 and 12 h delayed cooling treatments (4 day duration) would lessen functional impairment and lesion size. Untreated (normothermic) ICH resulted in significant forelimb use asymmetry, as well as deficits in walking and skilled reaching. These deficits were unaffected by hypothermia, as was the volume of tissue lost ( approximately 20 mm(3)) at 1 month. Thus, attenuated edema did not result in behavioral or histological benefit. In conclusion, while additional research with alternative cooling protocols and ICH models are required, these findings suggest that while hypothermia lessens edema, it will not be directly neuroprotective after ICH.

The influence of hypothermia on outcome after intracerebral hemorrhage in rats.

BACKGROUND AND PURPOSE: Late hypothermia (HYPO) reduces injury after collagenase-induced intracerebral hemorrhage (ICH), whereas early HYPO does not because it exacerbates the protracted bleeding that occurs in this model. We hypothesized that early HYPO would not increase bleeding after whole blood infusion and thus expected early HYPO to improve outcome through reducing secondary consequences of ICH (eg, inflammation). METHODS: Autologous blood (100 microL) was infused into the striatum. Rats were maintained at normothermia or subjected to mild (33 degrees C to 35 degrees C) HYPO for 2 days starting 1 (HYPO-1) or 4 hours (HYPO-4) after ICH. Hematoma volume was measured at 12 hours to determine whether HYPO-1 aggravated bleeding. We measured blood-brain barrier (BBB) disruption and edema 2 days after ICH in all groups. At 4 days, we counted degenerating neurons, neutrophils, and iron-positive cells (eg, macrophages) in the lesioned hemisphere. Recovery was assessed using several behavioral tests (ie, staircase reaching task, ladder walking task, limb use cylinder test) over 7 or 30 days, at which time we quantified lesion volume. RESULTS: HYPO did not increase bleeding. Both HYPO treatments reduced BBB disruption and infiltration of inflammatory cells. HYPO-1 treatment modestly reduced edema and provided limited to no functional benefit in the behavioral tests. HYPO did not affect lesion volume. CONCLUSIONS: HYPO reduced edema, BBB disruption, and inflammation. Although encouraging, HYPO treatment must be improved so that histological and functional benefit are obtained before clinical investigation. Otherwise clinical failure is anticipated.