Ibn Sina (often known by his last name in Latin, Avicenna; 980–1037 A.D.) was the most famous physician and philosopher of his time. His Canon of Medicine, one of the most famous books in the history of medicine, surveyed the entire medical knowledge available from ancient and Muslim sources and provided his own contributions. In this article the authors present a unique picture of the neurosurgical technique of Ibn Sina and briefly summarize his life and work.
Asita S. Sarrafzadeh, Nuri Sarafian, Almut von Gladiss, Andreas W. Unterberg and Wolfgang R. Lanksch
Andreas W. Unterberg, Oliver W. Sakowitz, Asita S. Sarrafzadeh, Götz Benndorf and Wolfgang R. Lanksch
Object. Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH.
Methods. In 60 patients a microdialysis catheter was inserted into the brain parenchyma that is most likely to be affected by vasospasm directly after aneurysm clipping. Hourly analyses of glucose, pyruvate, lactate, and glutamate levels were performed using a bedside device. Blood-flow velocities were obtained using serial TCD measurements. Cerebral angiography was routinely performed on Day 7 after aneurysm clipping or earlier in cases of clinical deterioration (30 patients). In all patients the results of microdialysis monitoring, TCD ultrasonography, and angiography were correlated.
The mean duration of monitoring was 7.3 ± 2.5 days. In patients with acute ischemic neurological deficits (18 patients) immediate microdialysis-recorded alterations were observed if the probe was placed close to the malperfused region. In 13 of 15 patients with symptomatic vasospasm (delayed ischemic neurological deficit [DIND]), the microdialysis-recorded values revealed secondary deterioration. In terms of confirming DIND, microdialysis had the highest specificity (0.89, 95% confidence interval [CI] 0.78–1) compared with TCD ultrasonography (0.63, 95% CI 0.46–0.8) and angiography (0.53, 95% CI 0.35–0.7). For microdialysis, the positive likelihood ratio was 7.8, whereas this was significantly lower for TCD ultrasonography (1.7) and angiography (2.1).
Conclusions. Although angiography also demonstrates vessel narrowing in asymptomatic patients, online microdialysis reveals characteristic metabolic changes that occur during vasospasm. Thus, online microdialysis may be used to confirm the diagnosis of vasospasm.
Asita S. Sarrafzadeh, Oliver W. Sakowitz, Tim A. Callsen, Wolfgang R. Lanksch and Andreas W. Unterberg
The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury.
Thirty-five severely head injured patients (with Glasgow Coma Scale scores ≤ 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring. The PtiO2 catheter was placed into the unaffected frontal white matter within 32.2 hours postinjury (range 7–48 hours). The microdialysis catheter was placed close to the PtiO2 probe via a 2- or 3-way skull screw that was connected to a pump and perfused with Ringer's solution at 0.3 μl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate–pyruvate 5-minute ratio, and glutamate. Data were analyzed for identification of episodes of impending (PtiO2 10–15 mm, Hg > 5-minute duration) and present cerebral hypoxia (PtiO2 10 mm, Hg, > 5-minute duration). In 62% of the patients hypoxic episodes occurred and were most frequently associated with hyperventilation (p < 0.001). During impending hypox-ia, extracellular glutamate concentrations were increased (p = 0.006) whereas energy metabolites remained stable. During cerebral hypoxia, the extracellular glutamate (p < 0.001) and lactate (p = 0.001) concentrations were significantly higher than during normal oxygenation, whereas the lactate–pyruvate ratio was only slightly increased (p = 0.088, not significant).
The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.