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Biomedical subjects

F Iannotti

Publications and source records attributed to F Iannotti.

At least 37 records · Page 2Linked to original sources
PubMed1997

EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium.

Guidelines for the management of severe head injury in adults as evolved by the European Brain Injury Consortium are presented and discussed. The importance of preventing and treating secondary insults is emphasized and the principles on which treatment is based are reviewed. Guidelines presented are of a pragmatic nature, based on consensus and expert opinion, covering the treatment from accident site to intensive care unit. Specific aspects pertaining to the conduct of clinical trials in head injury are highlighted. The adopted approach is further discussed in relation to other approaches to the development of guidelines, such as evidence based analysis.

Adult↗
PubMed1997

Differential vulnerability of the CA1 and CA3 subfields of the hippocampus to superoxide and hydroxyl radicals in vitro.

The relative roles of the superoxide and hydroxyl radicals in oxidative stress-induced neuronal damage were investigated using organotypic hippocampal slice cultures. Cultures exposed to 100 microM duroquinone, a superoxide-generating compound, for 3 h developed CA1-selective lesions over a period of 24 h. The damage accounted for approximately 64% of the CA1 subfield, whereas CA3 showed just 6% damage, a pattern of damage comparable to that observed following hypoxia/ischaemia. Duroquinone-induced damage was attenuated by a spin-trap agent. In contrast, hydroxyl radical-mediated damage, generated by exposure to 30 microM ferrous sulphate for 1 h, resulted in a CA3-dominant lesion. The damage developed over 24 h, similar to that observed with duroquinone, but with approximately 45% damage in CA3 compared with only 7% in CA1. These data demonstrate a selective vulnerability of the CA1 pyramidal neurones to superoxide-induced damage and suggest that of the free radicals generated following hypoxia/ischaemia, superoxide, rather than hydroxyl radical, is instrumental in producing neuronal damage.

Animals↗
PubMed1997

Induction of 72 kDa heat-shock protein following sub-lethal oxygen deprivation in organotypic hippocampal slice cultures.

The phenomenon of induced tolerance to a normally lethal episode of ischaemia by preconditioning with sub-lethal ischaemia has been linked to induction of the 72 kDa heat-shock protein (HSP72). However, a direct correlation between HSP72 expression and ischaemic preconditioning in vivo has not been proven. Using an in vitro model of ischaemia-related neuronal damage we have investigated whether HSP72 protein expression is temporally correlated with subsequent tolerance to a normally lethal ischaemic episode. Organotypic hippocampal slice cultures were maintained in vitro for 14 days before being exposed to hypoxia for 15-180 min. Periods of hypoxia shorter than 60 min did not produce neuronal damage. No HSP72 immunoreactivity was observed in either untreated cultures or in those exposed to hypoxia for 15 min. Following 30 and 45 min hypoxia a significant induction of HSP72 occurred in neurons of both the CA1 and CA3/4 regions of the pyramidal cell layer. A significant number of microglia were positively stained with HSP72. The peak of HSP72 expression occurred 18 h after the induction of hypoxia but remained significantly elevated for 48 h post-hypoxia. Prolonged hypoxia (60 or 180 min) produced a selective lesion of the CA1 pyramidal cell layer which was not associated with an induction of HSP72. Pre-conditioning with 45 min hypoxia 18 h prior to 180 min hypoxia did not reduce the neuronal damage associated with 180 min hypoxia alone. These data strongly suggest that HSP72 does not directly confer tolerance in this in vitro model of ischaemia-related neuronal death.

Animals↗
PubMed1996

Brain-derived neurotrophic factor, but not neurotrophin-3, prevents ischaemia-induced neuronal cell death in organotypic rat hippocampal slice cultures.

We have investigated the neuroprotective actions of neurotrophins in a model of ischaemia using slice cultures. Ischaemia was induced in organotypic hippocampal cultures by simultaneous oxygen and glucose deprivation. Cell death was assessed 24 h later by propidium iodide fluorescence. Pre- but not post-ischaemic addition of brain-derived neurotrophic factor (BDNF) produced a concentration-dependent reduction in neuronal damage. Neurotrophin-3 was not neuroprotective. These data suggest that BDNF may form part of an endogenous neuroprotective mechanism.

Animals↗
PubMed1996

A clinical study of parenchymal and subdural miniature strain-gauge transducers for monitoring intracranial pressure.

OBJECTIVE: Previous studies have shown that a new strain-gauge MicroSensor (Codman/Johnson & Johnson Professional, Inc., Randolph, MA) for measuring intracranial pressure (ICP) performs well in the intraventricular space. We hoped to evaluate the MicroSensor in the subdural space and the brain parenchyma, because ICP is often measured in these compartments when the ventricles are difficult to cannulate. METHODS: Fifteen patients had simultaneous recordings of ICP from an externally transduced fluid-filled subdural catheter, a MicroSensor placed within the subdural catheter, and a nearby MicroSensor placed intraparenchymally in the right frontal lobe. RESULTS: The total number of valid simultaneous recordings of ICP was 95,946. A highly significant correlation was found between the tissue MicroSensor ICP (TMICP) and the subdural MicroSensor ICP (SMICP) (n = 95,946; r = 0.89; P < 0.00005), the TMICP and the fluid-transduced subdural catheter ICP (r = 0.86, P < 0.00005), and the fluid-transduced subdural catheter ICP and SMICP (r = 0.88, P < 0.00005). The mean simultaneous difference between the TMICP and the SMICP was 0.1 +/- 3.8 mm Hg with no obvious bias. The fluid-transduced subdural catheter ICP was 2.8 +/- 3.9 mm Hg lower than the TMICP and 2.7 +/- 3.9 mm Hg lower than the SMICP (P < 0.0005). The mean zero drifts of the tissue and subdural MicroSensors were 0.312 and 0.475 mm Hg/d, respectively. The tissue MicroSensor recordings showed the best quality wave form with the least damping. CONCLUSION: The strain-gauge MicroSensor is highly accurate and stable in the tissue and subdural spaces.

Brain↗
PubMed1996

Selective N-type calcium channel antagonist omega conotoxin MVIIA is neuroprotective against hypoxic neurodegeneration in organotypic hippocampal-slice cultures.

BACKGROUND AND PURPOSE: Neuroprotection by antagonists of both L-type and N-type calcium channels occurs in in vivo models of ischemia. The site of action of calcium channel antagonists is unclear, however, and it is likely that a combination of vascular and direct neuronal actions occurs. We have investigated the effects of blocking neuronal calcium channels using an organotypic hippocampal-slice model of ischemia. METHODS: Organotypic hippocampal-slice cultures prepared from 10-day-old rats were maintained in vitro for 14 days. Cultures were exposed to either 3 hours of oxygen deprivation (hypoxia) or 1 hour of combined oxygen and glucose deprivation (ischemia). Neuronal damage was quantified after 24 hours by propidium iodide fluorescence. RESULTS: Three hours of anoxia produced damage exclusively in CAT pyramidal cells. This damage was prevented by preincubation with omega conotoxin MVIIA, a selective N-type calcium channel blocker, and omega conotoxin MVIIC, which blocks N-type and other presynaptic neuronal calcium channels. The dihydropyridine nifedipine and the mixed calcium channel blocker SB201823-A were not protective. Furthermore, if addition of conotoxin MVIIA was delayed until after the hypoxic episode, a dose-dependent neuroprotective effect was observed, with an IC50 of 50 nmol/L. In contrast to hypoxia, none of the compounds was neuroprotective in the model of oxygen-glucose deprivation, although it was determined that extracellular calcium was essential for the generation of ischemic damage. CONCLUSIONS: These studies present clear evidence that neuroprotection by selective N-type calcium channel antagonists is mediated directly through neuronal calcium channels. In contrast, the neuroprotective effects of dihydropyridines may be mediated through vascular calcium channels or indirectly through actions in other brain regions.

Animals↗
PubMed1995

Craniofacial osteotomies for skull base access.

During a five year period 150 craniofacial access osteotomies for skull base access have been performed allowing direct exposure of pathology in difficult anatomical acreas with minimal complications. These approaches have been developed by considering the craniofacial skeleton as a single osteoplastic structure. Bone segments are mobilised and replaced using rigid fixation. In this way osteotomies can be planned which significantly improve access and preserve form and function in the complex region of the skull base.

Adult↗
PubMed1995

Focal brain damage enhances experimental allergic encephalomyelitis in brain and spinal cord.

The immunological basis of multiple sclerosis (MS) is well recognized but the factors inducing MS lesions are unclear. In this study, we test the hypothesis that focal brain injury, inflicted during the pre-clinical stages of experimental allergic encephalomyelitis (EAE), will enhance the severity of immunological damage in the cerebral hemispheres and spinal cord. Acute EAE was induced in 30 Lewis rats by the injection of guinea pig spinal cord homogenate in complete Freund's adjuvant. A cryolesion to the surface of the left cerebral hemisphere was induced at 3 days (n = 6) or 8 days (n = 10) postinoculation (p.i.) and animals were killed at 15 days p.i. Control animals were EAE only (n = 9), cryolesion only (n = 4), EAE and sham cryolesion (n = 5) and normal animals (n = 3). Brain and spinal cord were stained by immunocytochemistry using W3/13 (T-lymphocytes) OX6 (MHC Class II) and GFAP (astrocytes) antibodies. The results showed a 2-fold increase in the number of EAE lesions in the brain with significant and widespread increase of MHC Class II antigen expression by microglia, in the cryolesion EAE 8 days p.i. when compared with EAE only animals. The pattern of enhancement suggests that it is due to (i) local spread of tissue or serum factors from the cryolesion; (ii) neural factors affecting remote regions of the CNS; (iii) stimulation of the immune system which may occur due to products of brain injury draining to regional cervical lymph nodes. Investigation of the mechanisms involved may prove fruitful in establishing factors which initiate, aggravate or ameliorate brain damage in multiple sclerosis.

Animals↗
PubMed1995

Hyperfibrinolysis during intracranial surgery: effect of high dose aprotinin.

A patient undergoing intracranial surgery developed disseminated intravascular coagulation with life threatening peroperative bleeding. Thromboelastography established the diagnosis of hyperfibrinolysis, usually a fatal complication of a neurosurgical operation. With the administration of a high dose regimen of aprotinin (Trasylol) the haemorrhage was controlled and the hyperfibrinolytic state reversed. Evaluation of blood samples from the jugular bulb suggested that there was a pronounced local release of tissue plasminogen activator into the circulation.

Aged↗
PubMed1995

Assessment of autoregulation by means of periodic changes in blood pressure.

BACKGROUND AND PURPOSE: The aim of this study was to test the hypothesis that the phase difference that occurs between an induced oscillation in blood pressure and the resultant oscillation in middle cerebral artery (MCA) flow velocity could reflect the competence of cerebral autoregulation. METHODS: Fourteen volunteers performed 19 cycles of 10 seconds of squatting followed by 10 seconds of standing. Peak MCA velocity was measured with transcranial Doppler ultrasound, and blood pressure was measured with a servo-controlled finger plethysmograph held level with the head. Waveforms from each cycle were added to obtain averaged waveforms of arterial blood pressure and MCA velocity. These results were processed by Fourier analysis to extract the phase difference between the fundamental components of velocity and pressure. Each volunteer performed the exercise three times: first breathing normally, secondly hyperventilating (hypocapnia), and finally while breathing air containing 5% carbon dioxide (hypercapnia). Under these conditions the volunteers were expected to have normal, enhanced, and impaired auto-regulation, respectively. RESULTS: The measurements made with normal breathing showed a phase lead of velocity ahead of pressure of 46 +/- 14 degrees (mean +/- SD). We noted a highly significant reduction in phase lead with hypercapnia (P < .00015) (Wilcoxon signed rank test, two-tailed) and a highly significant increase in phase lead with hypocapnia (P < .002). CONCLUSIONS: The results support our hypothesis and may lead to a technique for assessing the competence of cerebral autoregulation.

Adolescent↗
PubMed1994

Propidium iodide in vivo: an early marker of neuronal damage in rat hippocampus.

We have investigated the use of the fluorescent exclusion dye propidium iodide as a marker for acutely degenerating cells in vivo, and report here that combined injection of kainic acid and propidium iodide into the lateral cerebral ventricle results in labelling of CA3 pyramidal cells 1 and 6 h after injection. Alternate sections stained with thionin at these early times revealed little evidence of histologically detectable cell damage.

Animals↗
PubMed1994

Perivascular edema fluid pathway in astrocytic tumors.

Perivascular spaces are anatomical routes for the bulk flow drainage of fluid from the gray matter to the subarachnoid space in normal rat brain. Perivascular cells are the resident scavengers in perivascular spaces. Following focal brain damage, perivascular cells upregulate MHC Class II antigens associated with uptake of edema fluid. Similar cells can be defined in damaged human brain. In the present investigation, the distribution of MHC Class II upregulated perivascular cells was measured in 30 astrocytic tumors and adjacent edematous tissues by immunocytochemistry using the following antibodies: HLA-DR (MHC Class II), PGM1 and MAC387 (macrophages). Perivascular cells were PGM1+/MAC387- and were located in perivascular spaces along blood vessels of all sizes. MHC Class II+ perivascular cells were distributed mainly in the tumors but in some cases (4 of 10 in astrocytomas, 4 of 10 in anaplastic astrocytomas, and 7 of 10 in glioblastomas) they were also found in adjacent edematous brain. The extensive MHC Class II expression on perivascular cells suggests that perivascular cells play a scavenging role in the perivascular spaces in human brain. The results of the present study indicate the similarity between perivascular spaces in human and rat brains and emphasize the significance of perivascular spaces as anatomical routes for edema fluid drainage from human brain tissue.

Animals↗
PubMed1994

Postoperative hematoma: a 5-year survey and identification of avoidable risk factors.

This study examines the surgical practice at the Wessex Neurological Centre over the 5-year period from 1989 to 1993 to determine the incidence of postoperative hematoma and to identify risk factors for a perioperative bleeding disorder. The study includes only those postoperative hematomas (at any site) that followed and were related to a neurosurgical operation and were surgically evacuated. The study is prospective for the year 1993 and retrospective for the preceding years. Over the 5 years, 6668 operations were performed and 71 postoperative hematomas were surgically evacuated, accounting for an overall rate of 1.1% of operations. The records were available for 69 cases. The most frequent diagnosis leading to postoperative hematoma was meningioma surgery with a rate of 6.2% of cases (13 of 211); followed by craniotomy for trauma, 3.7% (7 of 192); aneurysm surgery, 2.6% (11 of 428); and intrinsic supratentorial tumors, 2.2% (10 of 451). Postoperative hematomas were intraparenchymal in 43% of cases, subdural in 5%, extradural in 33%, mixed in 8%, and confined to the superficial wound in 11%. The overall mortality was 32% (37% for intraparenchymal and 12% for extradural). Risk factors for a perioperative bleeding disorder were present in two-thirds of the patients. Administration of antiplatelet agents (aspirin and nonsteroidal anti-inflammatory drugs) was the most commonly associated risk factor. At least 75% of these identified risk factors could potentially have been avoided or corrected.

Anticoagulants↗
PubMed1993

The suboccipital transcondylar approach to the clivus and cranio-cervical junction for ventrally placed pathology at and above the foramen magnum.

The dorsolateral suboccipital transcondylar approach for pathology anterolateral or ventral to the neuraxis around the lower clivus and brainstem was used in 10 patients with a variety of different pathological problems: Key features of the approach include exposure and mobilisation of the vertebral artery and resection of the postero-medial portion of the atlanto-occipital joint. Despite the excellent access achieved additional exposure may be required in some patients with strictly anterior pathology or a lesion above the mid-clivus.

Adult↗