Biomedical subjects

E Tasdemiroglu

Publications and source records attributed to E Tasdemiroglu.

At least 19 recordsLinked to original sources

PubMed1997

Cerebral metastases in childhood malignancies.

Between January 1982 to June 1994, 154 children with non-CNS malignant tumours excluding leukaemias and lymphomas were admitted and treated at the UKMC. Symptomatic (10 cases; 6.5%) and non-symptomatic (2 cases; 1.2%) cranial metastases (calvarial, dural and/or parenchymal) were seen in 12 (7.8%) cases. Among these 12 cases, 7 had intracranial parenchymal metastases (4.5%). Three cases had multiple intracranial parenchymal metastases. Only one case had infratentorial (cerebellar) metastasis. The patients' ages ranged from 1 to 18 years (mean age was 7.3 years). The male:female ratio was 5:2. While six patients' brain metastases diagnosed during subsequent relapses, one patient first presented with brain metastasis. Time elapsed between the diagnosis of the primary disease and intracranial metastasis ranged from 0 to 755 days (mean 327 days). Histopathological diagnoses were confirmed in 4 cases who had craniotomy and tumour removal. Mean survival following the diagnosis of intracranial lesion was 157 days (ranged from 0 to 412 days). Despite the aggressive treatment, including surgery, chemotherapy and radiotherapy, 6 cases died with progression or relapse of the intracranial disease. In conclusion, the incidence of paediatric intracranial parenchymal metastasis is 4.5%. Prognosis is poor and intracranial disease is the primary cause of death.

Adolescent↗

PubMed1997

Neurologic complications of the primary pediatric extracranial neuroblastomas.

Between January 1982 and June 1994, 32 children with primary extracranial neuroblastomas (n = 24) and ganglioneuroblastomas (n = 8) were admitted and treated at the UKMC. Twenty-two (68.7%) of these patients suffered with 29 neurological complications (up to 3 complications per case) during the course of their disease. Fourteen cases had nervous system metastases or invasion. Nonmetastatic complications, such as nervous system infections (n = 4) and new onset of seizures secondary to brain metastasis, hypertensive and metabolic encephalopathies (n = 3) were seen on 7 cases. Five cases had treatment related complications, one case first presented with opsoclonus-polymyoclonus syndrome. Eight of these 22 patients died, due to relapse or progression of the disease. The mean follow-up period of 14 surviving patients was 44.9 months (range, 12-110 months). Five of these 14 patients suffered with neurologic sequelae. The incidence of neurologic complications was 68.7%. Nervous system metastasis was the most common neurologic complication. Although 5 patients suffered with neurologic sequelae, outcome was not influenced by presence of neurologic complication.

Antineoplastic Agents↗

PubMed1996

MRI of cerebellopontine angle choroid plexus papilloma.

We present a cerebellopontine angle choroid plexus papilloma that originated from the tuft of choroid plexus of the fourth ventricle protruding from the foramen of Luschka. MRI and CT did not establish the diagnosis, but the tumor was shown histopathologically to be a choroid plexus papilloma. Distinct features of the tumor on MRI are described and the differential diagnosis of other cerebellopontine angle tumors is discussed.

Cerebellar Neoplasms↗

PubMed1996

Primary spinal column sarcomas.

Five cases of primary spinal column sarcomas are presented. Sarcomas primarily originating from paravertebral soft tissues were excluded. Patients' age ranged from 1 to 14 years (mean 8.4 years). The male:female ration was 2:3. Two patients had Ewing's sarcoma (ES) originating from L5-S1 and L4-5 pedicles, respectively; two patients had mesenchymal chondrosarcoma (MCS) originating from L1-2 pedicles and L5 body, respectively; and one patient had osteogenic sarcoma (OS) of C4 body. All patients clinically presented with pain and progressive weakness of the extremities. The time that elapsed between the onset of symptoms and diagnoses ranged from one to five months. All cases were treated with chemotherapy, radiotherapy and subtotal tumour resection with spinal canal decompression. Two cases received posterior spinal fusion operations. Three patients were alive 10 to 98 months following diagnosis. Only the case with ES of L5-S1 pedicles was in complete remission and off therapy at the 98th postoperative month. The two MCS cases were in partial remission, and were receiving chemotherapy at the time of analysis. These tumours caused similar clinical findings and prognoses, and required combined treatment, which consisted of surgery, radiotherapy and chemotherapy; histologically three different types of malignant tumours are presented in the same category. We preferred surgical decompression and stabilization procedures especially for neurologically symptomatic patients, even if they had extensive tumours with high grades. By spinal canal decompression and stabilisation, we did not intend to cure the disease; however, we intended to provide neurological improvement, spinal stabilisation, improved quality of life, early mobilisation of the patient, and cytoreduction by means of surgical tumour ablation, which could render the chemotherapy more effective.

Adolescent↗

PubMed1996

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats.

Anaesthetized male rats (n = 86) from both Long-Evans strain (LES) (n = 43) and Wistar strain (WS) (n = 43) were utilized for the experiments. While three animals from each strain were used as control, 40 rats from each strain underwent up to 10 minutes forebrain ischaemia by bilateral common carotid artery (CCA) occlusion combined with systemic hypotension [Mean Arterial Blood Pressure (MABP) = 50 mm/Hg]. The animals from each strain were divided into four (n = 10) groups. In both strains, groups (n = 10) 1 and 2, temporalis muscle (TM) and body temperatures of the animals were kept at 36-37 degrees C during the experiments. The groups 1 and 2 were killed in 3 and 7 days after the ischaemic insult, respectively. The groups 3 and 4 were also killed 3 and 7 days after the ischaemic insult, but the forebrain ischaemia was carried out under mild cerebral hypothermia (TM temperature = 33 degrees C). Pyramidal neurons of the hippocampal CA1 region from each group was evaluated semiquantitatively. In WS, groups 1 and 2 showed moderate and severe neuronal loss in the CA1 region, respectively. However, in LES while the group 1 (3 days survival) did not show any neuronal loss, group 2 showed moderate neuronal loss of the CA1 region. While in group 3 (3 days survival, hypothermia) WS and LES, hypothermia protected the CA1 region, group 4 of LES showed mild neuronal loss. However WS, group 4 (7 days survival, hypothermia) showed severe neuronal loss of the CA1 region. It was concluded that mild hypothermia during ischaemic insults did not prevent the delayed postischaemic neuronal damage of the hippocampal CA1 region of both strains, and following 10 minutes forebrain ischaemia, male LES rats were found more resistant than male WS rats to neuronal loss of the CA1 region.

Animals↗

PubMed1995

Long-term follow-up results of thoracolumbar fractures after posterior instrumentation.

STUDY DESIGN: This retrospective study examined the hospital records of 60 patients with thoracolumbar fractures treated with posterior fusion and spinal instrumentation. The mean follow-up period was 66 months. OBJECTIVES: The goal of this study was to evaluate and analyze the long-term outcome and socioeconomic conditions of patients who had sustained a thoracolumbar fracture. SUMMARY OF BACKGROUND DATA: In four patients, additional spinal injuries were detected. Three of the patients evaluated with magnetic resonance imaging showed cord contusion and edema. In six patients, ruptured disc fragments were detected by preoperative magnetic resonance imaging or during surgery. METHODS: Long-term follow-up results in 60 patients with unstable thoracolumbar fractures treated with posterior fusion and spinal instrumentation were analyzed. Neurologic outcomes and independence in function and daily living activities were reviewed. Age, sex, mechanism of injury, associated injuries to the spinal cord, and associated injuries to the spinal cord and other systems were analyzed. Fractures were classified according to the system of Ferguson and Allen. RESULTS: The patients with incomplete spinal cord injury showed significant functional improvement. During the follow-up period, 28 patients showed neurologic improvement. Postoperative complications occurred in 11 patients. Five patients required late rod removal because of rod dislocation. CONCLUSION: Regardless of neurologic recovery, most patients reported some disability, usually caused by pain. Inability to return to alternative jobs resulted from insufficient educational background rather than neurologic dysfunction. Advanced academic achievement was the single most important predictive factor of ability to return to work.

Adolescent↗

PubMed1995

Reversible hypoperfusion of the cerebral cortex in normal-pressure hydrocephalus on technetium-99m-HMPAO brain SPECT images after shunt operation.

A man with dementia underwent radionuclide cisternography to establish the diagnosis of communicating hydrocephalus. Technetium-99m-HMPAO brain SPECT images showed marked hypoperfusion of both posterior cerebral cortices and three-dimensional displays that demonstrated perfusion defects at both of the posterior parietotemporal regions. A successful ventriculoperitoneal shunt operation was performed. Five and one-half months later, repeat three-dimensional display showed that the perfusion defects had resolved and a repeat brain SPECT image showed marked improvement of the hypoperfusion. This concurred with postoperative clinical improvement. Technetium-99m-HMPAO brain SPECT, which provides objective documentation of clinical recovery after surgery, could be routinely used to evaluate patients with normal-pressure hydrocephalus.

Cerebral Cortex↗

PubMed1994

Effects of antioxidants on the blood-brain barrier and postischemic hyperemia.

The role of free oxygen radicals in blood-brain barrier (BBB) disruption and postischemic hyperemia was evaluated in the rabbit model of focal cerebral ischemia-reperfusion. Six groups of rabbits underwent clipping of the anterior cerebral, middle cerebral, and intracranial internal carotid arteries. Cerebral blood flow (CBF) was measured by using radiolabeled microspheres, before, during, and 15 minutes after 1-hour occlusion of these arteries. After 50 minutes of ischemia, Group 1 animals (control) received a placebo. Animals in Groups 2-4 received one of three drugs: catalase at 10 mg/kg, methimazole at 5 mg/kg, or indomethacin at 10 mg/kg. A fifth group received a tungsten-supplemented diet for 14 days before ischemia was induced, and a sixth group was sham operated. Microvascular integrity within the brain was determined by the presence or absence of Evan's Blue (EB)-albumin dye leakage across the BBB and was measured by microspectrofluorometry. In the control group during ischemia, CBF dropped to 14%, 7%, and 11% of preischemic levels in rostral, middle, and caudal sections of the brain, respectively, as characterized by extensive EB-albumin dye leakage through the BBB into the ischemic hemisphere. During early reperfusion, postischemic hyperemia was associated with an increase in CBF of 128%, 123%, and 129% of control in the rostral, middle, and caudal sections of the brain, respectively. In all treated groups and in the group receiving a tungsten-supplemented diet, BBB integrity was protected during reperfusion without inhibition of postischemic hyperemia. This study suggests that early disruption of the BBB to large molecules is mediated by free oxygen radicals, which inhibit rather than cause postischemic hyperemia.

Animals↗

PubMed1993

Encephalo-myo synangiosis (EMS) in the vertebrobasilar occlusive disease. Case reports.

Two cases of vertebro-basilar insufficiency treated with infratentorial (IT) Encephalo-Myo-Synangiosis (EMS) using the pedicled occipitalis muscle flap, are presented. IT EMS was carried out for revascularization of the vertebro-basilar system. None of these cases has suffered from either carotid or vertebro-basilar insufficiency during seven years follow-up period. As far as we know this is the first report of successful IT EMS for vertebro-basilar insufficiency.

Cerebral Revascularization↗

PubMed1993

Effect of superoxide dismutase on acute reperfusion injury of the rabbit brain.

To study the involvement of free oxygen radicals of the blood-brain barrier (BBB) disruption during early reperfusion, we isolated the distal internal carotid artery, and the middle and anterior cerebral arteries via the transorbital approach in anesthetized rabbits. Using radiolabeled microspheres, regional cerebral blood flow (rCBF) was measured before, during and after 1-hour unilateral occlusion of these vessels. Fifty-five minutes after ischemia, animals received intravenous saline placebo (control), superoxide dismutase (SOD) at 8 mg/kg = 30,000 U/kg, or weakened superoxide dismutase (wSOD) at 8 mg/kg = 30,000 U/kg. Integrity of the BBB was assessed by leakage of Evan's Blue-albumin dye (EB-albumin dye), which was given at 15 minutes of reperfusion and allowed to circulate for an additional hour. In the control and wSOD-treated groups, rCBF decreased (26% and 40% of control, respectively) within the blue-tinted tissue of the occluded hemisphere during ischemia; hyperemia was observed during early reperfusion. In the control and wSOD-treated groups, EB-albumin dye leakage across the BBB increased 49% within the occluded hemisphere. However, within the SOD-treated group, the BBB showed minimal dye leakage even though rCBF of the occluded hemisphere (so-called blue-tinted tissue) decreased by 38% during ischemia. We conclude that 1-hour focal cerebral ischemia and reperfusion produce a vascular endothelial injury at the BBB. Since SOD administration showed significant protection, free-oxygen-radical production during early reperfusion is associated with breakdown of the BBB to large molecules.

Animals↗

PubMed1993

Measurement of cerebrovascular changes in cats after transient ischemia using dynamic magnetic resonance imaging.

BACKGROUND AND PURPOSE: Hemodynamic changes associated with acute ischemia cannot be measured with conventional nuclear magnetic resonance imaging. In this study, we used dynamic susceptibility-contrast magnetic resonance imaging to measure the changes in vascular transit time and relative cerebral blood volume in a feline occlusion-reperfusion model. METHODS: Dynamic susceptibility-contrast measurements were obtained before and during 10 minutes of global cerebral ischemia and for up to 3 hours after the onset of reperfusion. A cerebral blood flow index was calculated from the vascular transit time and relative cerebral blood volume measurements. Functional maps were constructed to demonstrate the regional hemodynamic differences resulting from the induced ischemia. RESULTS: During the early phase after reperfusion, both the relative cerebral blood volume and blood flow index rose sharply, followed by a fall to near-basal levels at 45 minutes (1 x control and 1.3 x control, respectively). Thereafter, the volume rose slowly, whereas the flow index continued to drop. At 3 hours, cerebral blood volume had reached 1.6 times its control value, whereas the flow index had returned to its base value. CONCLUSIONS: The hemodynamic behavior we observed in our model reflects the independent responses of the cerebral blood volume and flow index to ischemic insult. Measurements acquired by our method were consistent with the temporal behavior reported in previous radionuclide studies. Susceptibility-contrast nuclear magnetic resonance tomographic imaging proved to be valuable in detecting and quantifying both immediate and subsequent changes in the hemodynamic state of the ischemic and hyperemic feline brain.

Animals↗

PubMed1992

Pial vessel caliber and cerebral blood flow become dissociated during ischemia-reperfusion in cats.

The relationship between pial arteriolar caliber and cerebral blood flow (CBF) was examined in 11 cats subjected to reperfusion for up to 120 min after 10 min of global cerebral ischemia induced by four-vessel occlusion and systemic hypotension. Thirty minutes after reperfusion CBF, as assessed by radiolabeled microsphere injection, had increased to 588% of control in middle cerebral artery (MSEC) cortical gray matter territory. The caliber of MSEC pial arterioles measured using the closed cranial window technique (greater than 33 to less than 213 microns) increased to 172% of baseline. By 60 min of reperfusion, CBF was 76% of basal levels, but pial arterioles remained 133% of baseline. After 120 min, CBF approximated baseline values, but pial dilatation persisted (115% of control). Intracranial pressure measurements did not differ significantly from resting values. At 45 min and beyond, total cerebrovascular resistance did not differ from resting values. The coexistence of vasodilatation within pial arterioles and normal blood flow in cortical gray matter indicates that pial vessels (greater than 33 microns) cannot be responsible for normal blood flow restoration following postocclusive hyperemia. Resistance during the posthyperemic phase must be increased selectively within parenchymal vessels to account for normal total cerebrovascular resistance, pial vessel dilatation, and normal-low parenchymal blood flow. Whether obstruction rather than vasoconstriction explains the resistance changes within intraparenchymal vessels remains for further study.

Animals↗

PubMed1991

Chronic trigeminal ganglionectomy or topical capsaicin application to pial vessels attenuates postocclusive cortical hyperemia but does not influence postischemic hypoperfusion.

Marked hyperemia accompanies reperfusion after ischemia in the brain, and may account for the propensity of cerebral hemorrhage to follow embolic stroke or carotid endarterectomy, and for the morbidity that follows head injury or the ligation of large arteriovenous malformations. To evaluate the contribution of trigeminal sensory fibers to the hyperemic response, CBF was determined in 12 symmetrical brain regions, using microspheres with up to five different isotopic labels, in four groups of cats. Measurements were made at 15-min intervals for up to 2 h of reperfusion after global cerebral ischemia induced by four-vessel occlusion combined with systemic hypotension of either 10- or 20-min duration. In normal animals, hyperemia in cortical gray matter 30 min after reperfusion was significantly greater after 20 min (n = 10) than after 10 min (n = 7) of ischemia (312 ml/100 g/min versus 245 ml/100 g/min; p less than 0.01). CBF returned to preischemic levels approximately 45 min after reperfusion and was reduced to approximately 65% of basal CBF for the remaining 75 min. In cats subjected to chronic trigeminal ganglionectomy (n = 15), postocclusive hyperemia in cortical gray matter was attenuated by up to 48% on the denervated side (249 versus 150 ml/100 g/min; p less than 0.01) after 10 min of ischemia. This effect was maximal in the middle cerebral artery (MCA) territory, and was confined to regions known to receive a trigeminal innervation. In these animals, substance P (SP) levels in the MCA were reduced by 64% (p less than 0.01), and the density of nerve fibers containing calcitonin gene-related peptide (but not vasoactive intestinal polypeptide or neuropeptide Y) was decreased markedly on the lesioned side. Topical application of capsaicin (100 nM; 50 microliters) to the middle or posterior temporal branch of the MCA 10-14 days before ischemia decreased SP levels by 36%. Postocclusive hyperemia in cortical gray matter was attenuated throughout the ipsilateral hemisphere by up to 58%, but the cerebral vascular response to hypercapnia (PaCO2 = 60 mm Hg) was unimpaired. The duration of hyperemia and the severity of the delayed hypoperfusion were not influenced by trigeminalectomy, capsaicin application, or the intravenous administration of ATP. These data demonstrate the importance of neurogenic mechanisms in the development of postischemic hyperperfusion, and suggest the potential utility of strategies aimed at blocking axon reflex-like mechanisms to reduce severe cortical hyperemia.

Adenosine Triphosphate↗

PubMed1991

Postischemic cerebral blood flow and neuroeffector mechanisms.

The influence of neuroeffector mechanisms in the regulation of postischemic cerebral blood flow was investigated by microsphere determination in 8 cats after chronic unilateral vascular deafferentation by trigeminal ganglionectomy. The animals were subjected to 90 min of reperfusion following 10 min of global ischemia induced by 4-vessel occlusion and systemic hypotension. Cortical hyperemia 30 min after reperfusion was attenuated by up to 48% in cortical gray matter ipsilateral to the side of trigeminal ganglionectomy (p less than 0.01). Axon reflex mechanisms involving the release of neuropeptides from peripheral sensory nerve fibers, such as substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinin A (NKA), mediate this response. SP and NKA cause vasodilation by endothelium-dependent mechanisms (endothelium-dependent relaxing factor), whereas CGRP relaxes vascular smooth muscle by direct receptor interactions. Studies were therefore undertaken to determine the extent to which endothelium-dependent mechanisms mediate the hyperemia following global cerebral ischemia. In 7 intact cats, the postischemic response of pial arterioles to the topical application of acetylcholine (ACh; 10(-7) M), an endothelial-dependent vasodilator, was measured using a closed cranial window technique. Although ACh increased pial arteriolar caliber by 17% under resting conditions, the same dose elicited a vasoconstrictor response (87% of pre-ACh diameter 30 min after reperfusion) for the first 60 min of reperfusion after 10 min of ischemia. ACh-induced vasodilation was restored by 75 min (105%), but was less than control even at 120 min (109 vs. 117%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1991

The role of neuroeffector mechanisms in cerebral hyperperfusion syndromes.

Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides.

Animals↗

PubMed1991

Neuroeffector functions of sensory nerve fibers in the cerebral circulation after global cerebral ischemia.

The importance of trigeminal neuroeffector mechanisms in the regulation of postischemic cerebral blood flow (CBF) was evaluated in cats subjected to chronic unilateral denervation of cortical sensory nerve fibers by trigeminal ganglionectomy or by the topical application of capsaicin to a cortical branch of the middle cerebral artery. CBF was determined using isotopically labeled microspheres before and at intervals after reperfusion following 10 min of global cerebral ischemia induced by four vessel occlusion combined with systemic hypotension. Postocclusive hyperemia 30 min after reperfusion in cortical gray matter ipsilateral to the side of denervation was attenuated by up to 58% (176 vs. 91 ml/100 g per min; p less than 0.05), but resting CBF, the duration of hyperemia, and the cerebrovascular response to hypercapnia were unaffected. These data underline the influence of neurogenic mechanisms in the regulation of postischemic CBF. Blockade of this axon reflex-like mechanism may reduce the morbidity associated with several hyperperfusion syndromes.

Administration, Topical↗

PubMed1990

Neurogenic control of the cerebral circulation during global ischemia.

The influence of the trigeminal nerve on the cerebral circulation was investigated in chronically denervated cats during and after reversible four-vessel occlusion for 10 minutes combined with controlled hypotension (50 mm Hg). Postocclusive hyperemia 30 minutes after reperfusion was attenuated by up to 48% in cortical gray matter of the anterior, middle, and posterior cerebral artery territories on the side of trigeminal ganglionectomy. Similar results were observed for denervation accomplished by direct surgical ablation and by the topical application of capsaicin to a cortical branch of the middle cerebral artery. Denervation did not alter basal cerebral blood flow or the duration of hyperemia, nor did it impair the cerebrovascular response to hypercapnia. These data demonstrate the importance of neurogenic mechanisms in the development of postischemic hyperperfusion and suggest that strategies directed at blocking axon reflex-like mechanisms may be beneficial in reducing the morbidity that follows severe cortical hyperemia.

Animals↗

PubMed1988

Differential sympathetic regulation of automatic, conductile, and contractile tissue in dog heart.

Sympathetic pathways mediating chronotropic, dromotropic, and inotropic responses during ansae subclavia stimulation were determined by sequential dissection around major cardiac vessels. Right sympathetic (RS) projections influencing ventricular contractile force converge at the common pulmonary artery and within the pulmonary artery nerves (PAN). RS projections influencing left atrial contractile force course within the PANs. RS pathways to pacemaker and right atrial contractile tissue were localized between the superior vena cava and ascending aorta. RS projections influencing conductile tissue converge between the common pulmonary artery and proximal right pulmonary artery. Left sympathetic (LS) projections to ventricular contractile tissue were localized at the common pulmonary artery, within the PANs, and in the ventral lateral cardiac nerve (VLCN). LS pathways influencing heart rate and conductile tissue were localized at the left pulmonary artery and coursing between the right pulmonary artery and left superior pulmonary vein. LS projections to atrial contractile tissue were localized within the PANs and coursing between the right pulmonary artery and left superior pulmonary vein. We conclude that there are parallel, yet distinct, projections of sympathetic efferents to automatic, conductile, and contractile tissue of the canine heart.

Animals↗