Video reconstruction of vasospastic transient monocular blindness.
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Adult↗
Biomedical subjects
Axel Petzold
Publications and source records attributed to Axel Petzold.
Decreased cerebrospinal fluid apolipoprotein E after subarachnoid hemorrhage: correlation with injury severity and clinical outcome.
BACKGROUND AND PURPOSE: The apolipoprotein E (APOE) epsilon4 allele has been associated with unfavorable outcome after subarachnoid hemorrhage (SAH), suggesting that apoE plays an important role in the response of the brain to SAH. We determined the concentration of apoE in the cerebrospinal fluid (CSF) of patients with SAH and a control group to test the hypothesis that alterations in CSF apoE reflect the response of the brain to SAH and are correlated with the severity of injury and outcome. METHODS: ApoE and S100B (a marker of brain injury) were measured by ELISA in CSF from a non-brain-injured control group and patients with SAH. The severity of SAH was determined from the Glasgow Coma Scale, and the clinical outcome was determined from the Glasgow Outcome Scale. RESULTS: In contrast to increased CSF concentration of S100B, CSF apoE concentration was significantly lower in patients after SAH than in control subjects (Mann-Whitney test, P<0.0001). SAH patients with more severe injury and less favorable outcome had lower CSF apoE concentration than did patients with milder injury and better clinical outcome (Fisher exact test, P=0.02). CONCLUSIONS: The concentration of apoE in the CSF decreases after SAH, despite the likely leakage of plasma apoE into the CSF. We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury, where, in view of previous data, it may have a protective role.
Adult↗
Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage.
Cerebral vasospasm is a recognised but poorly understood complication for many patients who have aneurysmal subarachnoid haemorrhage and can lead to delayed ischaemic neurological deficit (stroke). Morbidity and mortality rates for vasospasm are high despite improvements in management. Since the middle of the 1970s, much has been written about the treatment of cerebral vasospasm. Hypervolaemia, hypertension, and haemodilution (triple-H) therapy in an intensive-care setting has been shown in some studies to improve outcome and is an accepted means of treatment, although a randomised controlled trial has never been undertaken. In this review, the rationale for this approach will be discussed, alongside new thoughts and future prospects for the management of this complex disorder.
Calcium Channel Blockers↗
Cerebrospinal fluid apolipoprotein E concentration decreases after traumatic brain injury.
The APOE epsilon4 allele has been associated with unfavorable outcome after several types of acute brain injury, yet the biological mechanisms underlying this observation are poorly understood. Postmortem and experimental brain injury studies suggest the presence of increased amounts of apolipoprotein E (apoE) within the neuropil after acute brain injury. We assayed the concentration of apolipoprotein E in the cerebrospinal fluid (CSF) of non-injured controls and patients with traumatic brain injury (TBI) to determine whether differences exist, and if these differences correlate with injury severity and clinical outcome. CSF apoE and S100B, a marker of injury severity, were measured by enzyme linked immunosorbant assay. CSF was sampled from 27 traumatic brain injury patients (mean age 32, median 25, range 16-65 years) within 3 days of injury, and 28 controls (mean age 40, median 37, range 19-73 years). The TBI patients all had a Glasgow Coma Score (GCS) of less than eight (i.e., severe head injury). Clinical outcome was determined using the Glasgow Outcome Score (GOS). The average concentration of apoE in the CSF of controls was 12.4 mg/L (95% CI: 10.5-14.3 mg/L) and in TBI patients was 3.7 mg/L (95% CI: 2.1-4.1 mg/L; Mann-Whitney: p < 0.0001). In contrast, the concentration of S100B in the CSF of TBI patients was significantly higher than that of controls (Mann-Whitney: p < 0.0001). We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury where in view of previous data, it may have a protective role.
Adolescent↗
Alterations in cerebrospinal fluid apolipoprotein E and amyloid beta-protein after traumatic brain injury.
There is evidence that apolipoprotein E (apoE) and amyloid beta-protein (Abeta), which are implicated in the pathology of chronic neurodegenerative disorders, are involved in the response of the brain to acute injury; however, human in vivo evidence is sparse. We conducted a prospective observational study to determine the magnitude and time-course of alterations in cerebrospinal fluid (CSF) apoE and Abeta concentrations after traumatic brain injury (TBI), and the relationship of these changes to severity of injury and clinical outcome. Enzyme linked immunosorbant assay (ELISA) was used to assay apoE, Abeta(1-40) and Abeta(1-42) in serial CSF samples from 13 patients with TBI and 13 controls. CSF S100B and tau were assayed as surrogate markers of brain injury. There was a significant decrease in CSF apoE (p < 0.001) and Abeta (p< 0.001) after TBI contrasting the observed elevation in CSF S100B (p < 0.001) and tau (p < 0.001) concentration. There was significant correlation (r = 0.67, p = 0.01) between injury severity and the decrease in Abeta(1-40) concentration after TBI. In vivo, changes in apoE and Abeta concentration occur after TBI and may be important in the response of the human brain to injury.
Adolescent↗
Role of serum S100B as an early predictor of high intracranial pressure and mortality in brain injury: a pilot study.
OBJECTIVE: To investigate whether serum S100B is suitable as a sensitive biomarker for early prediction of increased intracranial pressure and mortality rates after brain injury. DESIGN: A prospective, longitudinal study. SETTING: Neurosurgical intensive care unit. PATIENTS: Twenty-one patients with acute brain injury and 13 healthy controls. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We assessed Glasgow Coma Scale score and pupil reaction on admission and quantified serum S100B (in-house enzyme-linked immunosorbent assay) and intracranial pressure on admission and the subsequent 6 days. Serum S100B concentrations on admission and day 1 were significantly higher in patients with fatal outcome (p <.05, p<.01, respectively), with a sensitivity of 100% and a specificity of 75-83%. Patients with high serum S100B on admission had an eight-fold and on day 1 a 12-fold increased relative risk of a fatal outcome. Subsequent serum S100B values predicted the development of high intracranial pressure in patients with traumatic brain injury (p <.01). Patients with high intracranial pressure on day 5 had an 11-fold and on day 6 a nine-fold increased risk of fatal outcome. CONCLUSIONS: Serum S100B is a sensitive biomarker for early prediction of the development of high intracranial pressure and fatal outcome following acute brain injury. Monitoring S100B concentrations could contribute to early detection of patients at risk of secondary increases in intracranial pressure and subsequent mortality. This would allow earlier targeting of therapy in selected patients.
Adult↗