A survey of prehospital and acute hospital care in three low and middle income countries.

A prospective survey of neurotrauma admitted to neurosurgical units in three low and middle income countries (LMIC) indicated a frequent lack of organised prehospital care. On site care was usually provided by a member of the public. The accident victim was rarely accompanied within an equipped ambulance by trained personnel. Intensive care management and intracranial pressure monitoring was rare. There appeared to be limited rehabilitation in all regions.

Apoptosis in human compressive myelopathy due to metastatic neoplasia.

STUDY DESIGN: Immunohistochemical assessment of apoptotic markers in human cases of compressive myelopathy due to neoplastic compression. OBJECTIVE: To characterize the role of apoptosis in neoplastic compressive myelopathy in human postmortem tissue with extramedullary tumor involvement. SUMMARY OF BACKGROUND DATA: Neoplasms, whether primary or metastatic, may lead to compression of the spinal cord and development of a compressive myelopathy syndrome. Apoptotic processes of cell death are thought to contribute to cell death in chronic compressive myelopathy because of degenerative spondylosis, but this has not previously been described in neoplastic compression. METHODS: Six postmortem cases of human neoplastic compressive myelopathy were assessed for apoptosis using a panel of immunohistochemical markers including Fas, B-cell lymphoma 2 (Bcl-2), caspase-3 and 9, DNA-dependent protein kinase catalytic subunit (DNA-PKcs), poly (ADP-ribose) polymerase (PARP), apoptosis-inducing factor (AIF), and terminal deoxynucleotide transferase dUTP Nick End Labeling (TUNEL). RESULTS: Apoptosis was maximal at the site of tumor compression. Glial cells, predominantly oligodendrocytes, were immunopositive for DNA-PKcs, PARP, AIF, and TUNEL. Axons were immunopositive for caspase 3, DNA-PKcs, and AIF. Neurons were immunopositive for DNA-PKcs, PARP, AIF, and TUNEL. CONCLUSION: The current study demonstrates that apoptosis plays a role in human neoplastic compressive myelopathy. Necrosis dominates the severe end of the spectrum of compression. The prominent oligodendroglial involvement is suggestive that apoptosis may be important in the ongoing remodeling of white matter due to sustained compression. LEVEL OF EVIDENCE: 4.

How rapidly does cerebral swelling follow trauma? Observations using an animal model and possible implications in infancy.

To study the speed of development of cerebral edema in an animal model, five 2-year-old male anesthetized Merino sheep were impacted in the left temporal region by a humane stunner. Following the induction of blunt craniocerebral trauma a highly significant increase in intracranial pressure (ICP) values occurred relative to control animals (ANOVA, p<0.001). An immediate increase in ICP to values over 20 mmHg occurred within the first 30 min, and by 60 min, mean ICP was over 25 mmHg (p<0.05 versus controls). ICP continued to increase with time such that by 4h after injury, values were consistently greater than 30 mmHg (p<0.001 versus controls). The mean brain tissue oxygenation (P(bt)O(2)) in control animals over the 4h monitoring period was 52+/-8 mmHg with a highly significant (ANOVA, p<0.001) and early decrease in P(bt)O(2) recorded in impacted animals following craniocerebral trauma. By 30 min after injury, P(bt)O(2) was approximately 35 mmHg, while by 60 min, it had decreased to 20+/-2 mmHg (p<0.001 versus controls). The P(bt)O(2) continued to decline with time such that by 4h, the value was 14+/-2 mmHg (p<0.01 versus controls), or 27% of the mean control values. These data demonstrate that vasoreactive changes with increased blood volume and interstitial transfer of fluid may occur rapidly within brain tissue after blunt trauma. Detection of cerebral swelling at autopsy may not, therefore, imply prolonged survival.

The relationship between intracranial pressure and brain oxygenation following traumatic brain injury in sheep.

BACKGROUND: While it is understood that raised intracranial pressure (ICP) after traumatic brain injury (TBI) may negatively impact on brain tissue oxygenation (PbtO2), few studies have characterized the inter-relationship between these two variables, particularly in a large animal model that replicates the human gyrencephalic brain. The current study uses an ovine model to examine the dynamics of ICP and PbtO2 after TBI. MATERIALS AND METHODS: Five 2-year-old male Merino sheep were anesthetized with isoflurane and impacted in the left temporal region using a humane stunner. ICP and PbtO2 were then monitored over the following 4 h using a Codman ICP Express monitoring system and a LICOX brain tissue oxygen monitoring system, respectively. Two additional sheep were anesthetized and monitored as sham (uninjured) controls. FINDINGS: Mean ICP 60 min following TBI was over 25 mmHg (p < 0.05 versus controls) and by 4 h, values were consistently greater than 30 mmHg (p < 0.001). With respect to PbtO2, values fell from mean control values of 52 +/- 11 to 20 +/- 4 mmHg by 60 min (p < 0.001) and by 4 h to 14 +/- 3 mmHg (p < 0.01). The sigmoidal relationship between the two variables included a negative linear correlation when ICP was between 13 to 27 mmHg. CONCLUSIONS: Our results suggest that TBI results in early changes in ICP that are associated with profound declines in PbtO2, and may indicate the need for earlier management of ICP after TBI.

Downregulation of amyloid precursor protein (APP) expression following post-traumatic cyclosporin-A administration.

The aim of these studies was to assess and quantitate the effects of cyclosporin-A (CyA) on brain APP messenger RNA and neuronal perikaryal APP antigen expression following controlled focal head impact in sheep. Impact results in a significant increase in both APP mRNA and neuronal perikaryal APP antigen expression. Post-traumatic administration of CyA (intrathecal 10 mg/kg) resulted in a reduction in APP mRNA and neuronal perikaryal antigen expression. At 2 h postinjury, CyA treatment caused a statistically significant (p < 0.05) 1.3 +/- 0.1-fold decrease in APP mRNA in the central gray matter of impacted sheep compared to untreated impacted sheep. A more profound reduction in APP mRNA synthesis (1.6 +/- 0.2 fold) was evident at 6 h (p < 0.05). The mean percentage brain area with APP immunoreactive neuronal perikarya at 6 h post-injury was 94.5% in untreated impacted animals, 10.0% in CyA-treated impacted animals, 5.5% in untreated nonimpacted animals, and 6% in CyA-treated non-impacted controls. These results demonstrate that CyA has a downregulatory effect on increased APP expression caused by TBI.

Surgical treatment of nocardial brain abscesses.

OBJECTIVE: Nocardial brain abscesses are associated with significant morbidity and mortality rates. The optimal management remains unclear. We reviewed the surgical outcomes of patients treated with a relatively uniform policy at a single institution. METHODS: Eleven patients were treated at the Royal Adelaide Hospital between 1970 and 2001. Their clinical presentations, surgical treatment, and outcomes were reviewed. RESULTS: Clinical presentations most frequently involved focal neurological deficits (91%). Predisposing factors were identified for 63% of the patients. Nine patients were treated only with aspiration and long-term chemotherapy. Two patients underwent craniotomy and lesion excision. The majority of patients required either one or two procedures. There were no deaths in this series. Management complications were observed for three patients. Abscess aspiration was complicated by parenchymal hemorrhage and ventriculitis for one patient and temporary worsening of hemiparesis for two patients. CONCLUSION: Our results suggest that aspiration alone (repeated as clinically indicated) is a safe, efficacious treatment for the majority of patients with nocardial brain abscesses.