Cavernous Malformation

Brain cavernous malformations are relatively common lesions affecting 0.4% to 0.5% of general population.They occur in two distinct forms: a sporadic form characterized with a single lesion and a familial form characterized by multiple lesions and an autosomal dominant mode of inheritence. These lesions can also leave young people disabled for life and cause epilepsy. Their treatment options are still a controversy. Potential benefits must be weighed against the risks of treatment in individual patients [Archives Medical Review Journal 2011; 20(2.000): 107-117

Slitlike arachnoid valve because of post-traumatic symptomatic arachnoid cyst

WOS: 000256162100015Arachnoid cysts are intra-arachnoid collections of cerebrospinal fluid. Arachnoid cysts of the posterior fossa are rare lesions that are considered to be mostly congenital in origin. Arachnoid cysts of the posterior cranial fossa may manifest themselves in several different ways. When they are symptomatic, headache, gait disturbance, nausea, vomiting, focal neurologic signs, dizziness, and seizures are most common in the patients with increased intracranial pressure. Increased intracranial pressure is caused by the ball-valve mechanism of the cyst's membrane that communicates with subarachnoid space or arachnoid cells and contains specialized membranes and enzymes, which have secretory activity. A postsurgical arachnoid cyst in the posterior cranial fossa has doubled and slitlike arachnoid membrane that supports our knowledge about the underlining mechanism is reported

Cerebral Arachnoid Cysts

Arachnoid cysts can occur through inflammatory, traumatic, chemical irritation, skin tumor and postoperative processes. It is diagnosed and differentiated by magnetic resonance imaging and computerized tomography from other lesions. Its differential diagnosis includes colloid cyst , craniopharyngioma, prosencephaly, holoprosencephaly , epidermoid cyst, hydatid cyst, low grade glial tumors, infarcts and subdural hygroma. Most of them are asymptomatic and diagnosed incidentally. Treatment methods such as simple cyst aspiration , total excision of the cyst, basal cysternostomy, ventricular fenestration, cysto or ventriculoperitoneal shunt can be performed by various endoscopic surgery and craniotomy. [Archives Medical Review Journal 2016; 25(3.000): 259-268

Lhermitte-Duclos disease (dysplastic cerebellar gangliocytoma) - Review of the literature

WOS: 000246855900012Objectives: Lhermitte-Duclos disease (LDD), or dysplastic gangliocytoma of the cerebellum is a rare benign unilateral mass of the cerebellar cortex, characterized by a disarrangement of the normal cerebellar laminar cytoarchitecture and circumscribed enlargement of cerebellar folia. LDD was recently considered to be part of a multiple hamartoma-neoplasia syndrome [Cowden disease (CD)]. The debate whether LDD represents a neoplastic or hamartomatous lesion is still in progress. Methods: The aim of the present study is to answer this question with review of the literature emphasize on clinical presentation, radiologic findings, surgical procedures, and histopathologic features of LDD. Results: LDD most frequently presents in the third and fourth decades of life, but the age at clinical manifestation ranges from the neonatal period to the seventh decade. The initial presentation of LDD, similar to other posterior fossa tumors, includes increased intracranial pressure, vomiting, intermittent headache, cerebellar dysfunction, and noncommunicating hydrocephalus. Magnetic resonance imaging is the diagnostic modality and reveals characteristic usually nonenhancing gyriform patterns with enlargement of cerebellar folia. Surgical excision is a therapeutic procedure generally performed. The histopathologic findings of LDD include thickening of the molecular layer, which is occupied by abnormal ganglion cells, absence of the Purkinje cell layer, and hypertrophy of the granule cell layer. Conclusions: LDD is an unusual hamartomatous lesion of the cerebellar cortex, which can be associated with CD. When the diagnosis of either one of these 2 disorders is established, it is imperative to search for the other disease, to detect early malignant lesions that occur in CD

Validity of D-penicillamine in experimental cerebral vasospasm therapy

Background: Cerebral vasospasm is a reversible vessel constriction following subarachnoid hemorrhage. Immunoreactive and inflammatory mechanisms induce long-term vasoconstriction and vessel dilatation inhibition. We hypothesized that D-penicillamine depresses this process given that it reduces the concentration of free oxygen (O2) radicals. We evaluated the effects of D-penicillamine on cerebral vasospasm in rabbits induced with subarachnoid hemorrhage, achieved by autologous blood injection in the basal cistern. Materials and methods: Four experimental groups were studied: Group 1: basilar angiography, Group 2: basilar angiography + D-penicillamine, Group 3: subarachnoid hemorrhage (SAH), and Group 4: SAH + D-penicillamine. Vessel diameter and cerebral vasospasm were evaluated angiographically in each group. Vascular degeneration was studied by electron microscopy of the basilar artery. Free O2 radicals were investigated based on measurements of the levels of vascular superoxide dismutase and malondialdehyde. Myasthenia gravis–like side effects of D-penicillamine application were analyzed by electromyography and electron microscopy of the orbicularis oculi muscle. Results: We detected a 9.03% decrease in basilar artery constriction in Group 4 compared with Group 3. In addition, levels of free O2 radicals were reduced in Groups 2 and 4. Application of D-penicillamine resulted in the prevention of basilar artery wall degeneration, without myasthenia gravis–like side effects. Conclusion: Our study indicated that D-penicillamine application induced vasodilatation and had anti-inflammatory effects

Effects of sodium selenite and amiloride on calvarial calcification in closing small cranial defects

WOS: 000286548500031PubMed ID: 20672896Object. Fresh autogenous bone graft is the most preferred osteoplastic material, whether the purpose is cosmetic, psychological, or for the protection of the brain. These grafts are not rejected and do not react immunologically. The aim of this study was to evaluate the efficacy of autogenous fat rolled with bone dust derived from the bur hole in closing small cranial defects. Additionally, the authors examined the morphological and biochemical effects of Na selenite and amiloride on calvarial calcification. Methods. The study group consisted of 20 domestic pigs. These animals were randomly divided into 4 groups. A bur hole with a diameter of 10 mm was made at the right parietal region in all animals, and then the periosteum around the bur hole was cauterized following exposure of the dura mater. The dura was coagulated with bipolar cautery. Group 1 (controls): only a bur hole was opened, and it was then closed with a mixture of the bone dust that had been created during the opening of the bur hole and fat tissue that was taken from the animal's neck. Group 2 (amiloride): 1 nmol/g body weight of amiloride was applied subcutaneously within 15 minutes after closure of the bur hole with bone dust and fat, and then amiloride was applied once a day for 4 weeks. Group 3 (Na selenite): 30 nmol/g body weight of Na selenite was applied subcutaneously within 30 minutes after closure of the bur hole with bone dust and fat, and then Na selenite was applied once a day for 4 weeks. Group 4 (amiloride and Na selenite): 1 nmol/g body weight of amiloride was applied subcutaneously at 15 minutes, and 30 nmol/g body weight of Na selenite was applied subcutaneously at 30 minutes after closure of the bur hole with bone dust and fat, and these 2 injections were repeated once a day for 4 weeks. At the end of 4 weeks, the animals were anesthetized to evaluate the closure of the bur hole. Tissue samples were obtained for ultrastructural and biochemical examination. Results. The defect was covered with diffuse connective tissue in the control group. Although multiple capillary vessels were present, the authors did not observe osteogenic differentiation. Histological examination of the second group revealed osteogenic changes. Although new matrix was formed, calcification was not detected. The authors observed fibroblast, collagen fibers, and dense connective tissue filled with capillary in the third group of pigs, which had undergone Na selenite application. Calcification was not detected in this group. Both connective and osteogenic tissue were observed in specimens obtained in the fourth group, which had undergone amiloride and Na selenite application. Conclusions. The authors experimentally evaluated the supplementary osteogenic effects of Na selenite and amiloride by using them separately and together. The findings seem promising as a lead-in to new studies in restoring cranial defects. (DOI: 10.3171/2010.6.JNS091767

Ultrastructural and biochemical effects of trauma on normal and dehydrated brain - A research study and review

WOS: 000240335400008Background: In hypertonic dehydration, fluid loss is known to be from the intracellular compartment. Also fluid loss in vascular bed increases the osmotic pressure and results with decrease of fluid flow to these compartments. We applied hypertonic dehydration by fluid restriction to evaluate the effects of dehydration on posttraumatic brain edema and swelling. Methods: Four groups, each including 10 pigs composed the study group. Group 1: we performed craniectomy and followed up for I hour for intracranial pressure (ICP) measurement. Group 2: we performed craniectomy and hypertonic dehydration by fluid restriction for 3 days and followed up for I hour for ICP, measurement. Group. 3: we performed brain trauma with Madsen trauma model. Group 4: we performed brain trauma after dehydration. Findings: ICP was found to be 10 mm Hg at the first, 6.5 mm Hg at the second group but increased gradually after trauma in group 3. At the fourth group ICP was high at the first 30 minutes. After the experiment brain fluid level was 80.9% at the first, 77.9% at the second, 83.5% at the third, and 82.8% at the fourth groups. Ultrastructural examination revealed normal brain tissue at the first, light degeneration at the second, advanced degeneration at the third group. The fourth group was also highly degenerated but was found to be better than the third group. Brain superoxide dismutase and malondialdehyde levels were found to be increased. Interpretation: Even though hypertonic dehydration causes minimal cellular degeneration it increases the resistance of brain to trauma and high ICP especially at the first 30 minutes

Effects of Arginine Vasopressin and V1 Receptor Antagonist on Cerebral Vasospasm Secondary to Subarachnoid Hemorrhage An Experimental Study

AIM: To examine morphological, radiological and biochemical effects of arginine vasopressin (AV) and V1 receptor antagonist on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in rabbits. MATERIAL and METHODS: Forty male New Zealand white rabbits were randomly divided into four groups comprising 10 rabbits each. The groups were; 1) Control group, 2) SAH group, 3) SAH+AV group, 4) SAH+V1 antagonist group. Diameters of the basilar artery in all groups were measured on angiograms. All animals were sacrificed two days following basilar angiography and tissue samples of basilar artery were obtained under microscope immediate after craniectomy for ultrastructural and biochemical examinations. RESULTS: The artery diameters were found to be 50% and 50% at the 30th minute in the groups 2 and 3 respectively. In group 3, CVS was 13% more in comparison with the 2nd group. In group 4, vascular constriction was 34.5% at the 30th minute and about 30.9% at the 300th minute. Despite the increase in regional blood flow, AV did not provide morphological change. Histological appearance was related to vascular stenosis due to CVS. Histological outcome was the best in group 4 because of less CVS. CONCLUSION: Arginine vasopressin plays an important role in CVS. We detected morphological and radiological recovery in basilar artery, besides moderate improvement due to AV receptor antagonist in CVSAIM: To examine morphological, radiological and biochemical effects of arginine vasopressin (AV) and V1 receptor antagonist on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in rabbits. MATERIAL and METHODS: Forty male New Zealand white rabbits were randomly divided into four groups comprising 10 rabbits each. The groups were; 1) Control group, 2) SAH group, 3) SAH+AV group, 4) SAH+V1 antagonist group. Diameters of the basilar artery in all groups were measured on angiograms. All animals were sacrificed two days following basilar angiography and tissue samples of basilar artery were obtained under microscope immediate after craniectomy for ultrastructural and biochemical examinations. RESULTS: The artery diameters were found to be 50% and 50% at the 30th minute in the groups 2 and 3 respectively. In group 3, CVS was 13% more in comparison with the 2nd group. In group 4, vascular constriction was 34.5% at the 30th minute and about 30.9% at the 300th minute. Despite the increase in regional blood flow, AV did not provide morphological change. Histological appearance was related to vascular stenosis due to CVS. Histological outcome was the best in group 4 because of less CVS. CONCLUSION: Arginine vasopressin plays an important role in CVS. We detected morphological and radiological recovery in basilar artery, besides moderate improvement due to AV receptor antagonist in CV