Subdural haematoma as a rare complication of cochlear implantation: case report and literature review.

OBJECTIVE: To report a case of subdural haematoma occurring as an extremely rare and life-threatening complication of cochlear implantation, and to explore the causative association between intracranial haemorrhage and cochlear implantation surgical techniques. This association has not previously been reviewed in depth. CASE REPORT: A three-year-old boy was diagnosed with a large subdural haematoma, one week after cochlear implantation. After emergency evacuation of the haematoma, the patient made an excellent recovery and was discharged from hospital without any neurological deficit. RESULTS: Mechanisms of injury are discussed and the literature reviewed, focusing on the possible causes of intracranial haemorrhage identified after cochlear implantation. Notably, bone drilling had been used in all reported cases, and the probable causative injury had always occurred after such drilling. CONCLUSION: The issue of bone drilling during cochlear implantation is raised, and alternative methods of implant housing suggested, in order to avoid intracranial haemorrhage.

Bacterial brain abscesses: prognostic value of an imaging severity index.

AIM: To assess the correlation between imaging findings [computed tomography (CT) or magnetic resonance imaging (MRI)] and neurological status before and after the treatment of bacterial brain abscesses. MATERIALS AND METHODS: CT and MRI images of 96 patients with brain abscesses were retrospectively evaluated in terms of the number, location and size of lesions, and the presence and extent of perilesional oedema and midline shift. An imaging severity index (ISI) based on these different radiological parameters was calculated. Initial Glasgow Coma Scale (GCS) scores and ISI were assessed and the prognostic value of these two indices was calculated. The Pearson correlation test, Mann-Whitney test, Chi-square test, receiver-operating characteristic (ROC) analysis, together with comparison of ROC analyses and Fisher's exact test were used. RESULTS: There was a negative correlation between ISI and the initial GCS values: ISI increased as the GCS score decreased, indicating an inverse relationship (r=-0.51, p<0.0001). There was a significant difference between the ISI and GCS scores of patients with an adverse event compared with patients with good recovery. Outcome was significantly worse in patients with initial ISI over the calculated cut-off values of 8 points or GCS scores under the cut-off value of 13 points. CONCLUSION: ISI is a useful prognostic indicator for bacterial brain abscess patients and correlates strongly with the patient outcome for all parameters studied. ISI score had a better prognostic value than GCS.

Phenytoin penetration into chronic subdural haematomas.

The pathophysiology of chronic subdural haematomas (CSH) is still unclear. In the light of recent ultrastructural examination, exudation from the macrocapillaries in the outer membrane of CSH may play an important role in the enlargement of CSH. In this study, exudation from the macrocapillaries was assessed by the measurement of phenytoin, a protein-bound antiepileptic agent used in cases of CSH. In 22 patients, 1 h after the administration of 250 mg of phenytoin intravenously, blood and subdural haematoma samples were taken and phenytoin levels were measured. The ratio of subdural haematoma level to the blood phenytoin level was determined and defined as the phenytoin penetration ratio (PPR). The correlation between the phenytoin penetration ratio and clinical neurological grades (Markwalder and Glasgow Coma Scale), age of the patients and the CT appearance of CSH were investigated. The mean phenytoin penetration ratio was 19.5%. As the neurological grades of patients increased, average PPR also increased. The average PPR values were 17.64 and 20.84% in the patients younger than 60 years (nine patients) and older patients (13 patients), respectively. Mean PPRs in the groups according to the CT appearance were as follows: low density 11.21% (seven patients), isodensity in 15.88% (10 patients), high density in 38.5% (five patients). A subdural reaccumulation was detected in nine patients with a mean PPR of 27.72%, while mean PPR was 14.56% in the others. Exudation from macrocapillaries in the outer membrane of chronic subdural haematomas probably plays an important role in the enlargement of chronic subdural haematoma, and measuring phenytoin levels in the chronic subdural haematoma is a simple method for the quantitative estimation of the exudation in CSH.

An iridoid glucoside from Euphrasia pectinata.

A new iridoid glucoside, 5beta,6beta-dihydroxyboschnaloside (1), was isolated from the aerial parts of Euphrasia pectinata. Five known iridoid glucosides, 6beta-hydroxyboschnaloside (2), aucubin, euphroside, plantarenaloside, and geniposidic acid, and two known phenylethanoid glycosides, verbascoside (= acteoside) and leucosceptoside A, were also obtained and characterized. The structure of compound 1 was established by spectroscopic evidence.

The effect of tizanidine on chronic vasospasm in rats.

BACKGROUND: Cerebral vasospasm after subarachnoid hemorrhage (SAH) has remained a major cause of morbidity and mortality in patients with SAH. Excitatory neurotransmitters are gathered in the extracellular space during ischemia due to cerebral vasospasm and initiate or stimulate a series of pathophysiological biochemical processes which consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103-282, 5-chloro-4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a centrally-acting muscle relaxant and a selective alpha 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic alpha 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on vasospasm was evaluated. METHODS: We used a femoral artery vasospasm model in rats which has been described by Okada et al. 60 rats were examined in three groups. The first group was used as control group (Control) (n = 20), in the second group subarachnoid hemorrhage was performed (SAH) (n = 20), in the third group Tizanidine was administered in addition to SAH (SAH + Tizanidine administration) (n = 20). Animals in SAH + Tizanidine administration group received 0.3 mg/kg/day intraperitoneally for 7 days. Seven days after the experiment, after perfusion-fixation, 10 mm segments of both femoral arteries were removed and the femoral artery was prepared for light microscope examination, scanning and transmission electron microscopy and for morphometric analysis. RESULTS: There was a statistically significant difference between the electron, scanning and light microscopic observations and morphometric analysis of SAH + Tizanidine administration group and SAH group, and no statistically significant difference between SAH + Tizanidine administration group and control group. CONCLUSION: This study has disclosed that Tizanidine administration before the vasospasm reduces ultrastructural and morphometric vasospastic insult significantly. However, the clinical application of Tizanidine as a protective and therapeutic agent in cerebral vasospasm needs further studies including the employment of clinically more relevant SAH models.

Tizanidine is an effective agent in the prevention of focal cerebral ischemia in rats: an experimental study.

BACKGROUND: Focal cerebral ischemia secondary to cerebral vessel occlusion is still an important cause of mortality and morbidity. Excitatory neurotransmitters are gathered in the extracellular space during ischemia and initiate or stimulate a series of pathophysiological biochemical processes and consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103-282, 5-chloro4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a selective alpha 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic alpha 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on reversible focal cerebral ischemia was evaluated. METHODS: Cerebral blood flow to the left hemisphere of adult Sprague-Dawley rats (n=48) was temporarily interrupted by middle cerebral artery and bilateral common carotid artery occlusion for 3 hours in eight rats of each group. Tizanidine was given to each group of rats intraperitoneally before the ischemic insult, 2 hours after ischemia, right after the reperfusion, 2 h after reperfusion, and 4 hours after reperfusion; the animals survived for 24 hours after the reperfusion. After killing and triphenyltetrasoliumchloride staining of brain slices, infarction volumes and ratios of the brains were calculated and the results were compared with those of the control group. RESULTS: Infarction volumes and infarction ratios of the Tizanidine group 1/2 hours before ischemia (143.7+/-6.34 mm3 and 10.1+/-0.43%) and the Tizanidine group 2 hours after ischemia (145.6+/-6.32 mm3 and 10.3+/-0.43%) were found to be significantly lower in favor of the Tizanidine groups when compared with those of the control group (173.9+/-6.38 mm3 and 12,4+/-0.41%). Tizanidine is not effective if used just after reperfusion or later. CONCLUSION: This study shows that Tizanidine pretreatment before the ischemic insult and the administration of the drug within the 2 hours after ischemia reduces ischemic damage significantly. Therefore, this drug can be used as a protective and therapeutic agent in ischemic diseases.

Neurotransmitter and amino acid analysis and ultrastructural observations of fetal brain cortex transplantation to adult rat brain under the effect of dexamethasone.

OBJECTIVE: To conduct an investigation of fetal cortical tissue graft survival using transmission electron microscopy and analyzing neurotransmitters and amino acids and their function, with special reference to the effect of dexamethasone. METHODS: Transplantation of fetal cortical brain tissue to 100 adult Wistar albino rats weighing 170 to 220 g was performed. The rats were divided into three groups. Only transplantation of fetal cortical brain tissue was performed in the first group (n=36). In the second group (n=48), dexamethasone was administered in addition to fetal cortical tissue transplantation. The third group (n=16) was used as the surgical control group. The rats were allowed to live for 6 weeks and were then decapitated. The grafts were examined by electron microscopy. Additionally, quantitative analyses of the neurotransmitters and amino acids of the grafts were conducted using high-pressure liquid chromatography. RESULTS: Electron microscopic observations revealed that the grafts were still surviving at the end of the 6th week in both groups. However, in the group that received dexamethasone, neurons and their organelles were better developed than in the group that did not receive dexamethasone. Concommitantly, results of quantitative analysis in the dexamethasone group revealed statistically extremely significant higher amino acid values for glutamic acid, aspartic acid, beta-alanine, and lysine and significantly higher values for gamma-aminobutyric acid, glutamine, glycine, and serine when compared to the nondexamethasone group. CONCLUSION: Dexamethasone is effective in increasing the survival and in developing the ultrastructural and functional outcome of transplanted neurons in fetal grafts.