Biomedical subjects

I M Germano

Publications and source records attributed to I M Germano.

31 records · Page 2Linked to original sources

PubMed1995

Cortical blood flow and cerebral perfusion pressure in a new noncraniotomy model of subarachnoid hemorrhage in the rat.

BACKGROUND AND PURPOSE: Acute cerebral ischemia after subarachnoid hemorrhage (SAH) is a major cause of morbidity whose precise etiology is unclear. The purpose of this study was to examine the relationships between cerebral perfusion pressure (CPP) and cortical blood flow during SAH using a new experimental model in the rat. METHODS: CPP (mean arterial pressure minus intracranial pressure), cortical laser-Doppler flowmetry (LDF), and electroencephalogram were continuously recorded during and after SAH in 16 ventilated rats. SAH was produced by advancing an intraluminal suture from the external carotid artery through the internal carotid artery to perforate the vessel near its intracranial bifurcation. RESULTS: Eight rats (50%) died within 24 hours of SAH. In all rats, blood was widely distributed throughout the basal, convexity, and interhemispheric subarachnoid spaces and throughout the ventricular system. CPP decreased after SAH at an initial rate of 1.1 +/- 0.2 mm Hg/s, reaching its nadir 59 +/- 9 seconds after the onset of SAH. During the same period, LDF fell at a rate of 1.4 +/- 0.3%/s (P = NS vs CPP). After reaching its nadir, CPP rose at a rate of 0.4 +/- 0.01 mm Hg/s, but LDF continued to fall at 0.2 +/- 0.03%/s (P < .05 vs CPP) reaching a nadir of 21.7 +/- 2.5% significantly later than CPP (189.5 +/- 39 s after SAH, P < .05). No correlation was found between peak changes in CPP and LDF. Electroencephalogram activity followed the changes in LDF, reaching nadir values 289 +/- 55 seconds after SAH. CONCLUSIONS: These findings demonstrate that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction. This noncraniotomy model of SAH in the rat has several advantages over existing models.

Animals↗

PubMed1994

Intracranial meningiomas of the first two decades of life.

Meningiomas arising in the first two decades of life are uncommon and their characteristics are controversial. Some authors believe meningiomas in younger patients occur in different locations, have more malignant histological features, and have a worse prognosis than those in adults. To address this controversy, the authors retrospectively reviewed 23 cases of meningiomas in patients under 21 years of age at diagnosis who were operated on at the University of Turin (1948 to 1990) or at the University of California, San Francisco (1970 to 1989). These tumors represented 2.9% of all tumors in this age group and 1.8% of all meningiomas during the study period at the two institutions. There were 14 males and nine females. The mean age at surgery was 13.3 +/- 5.6 years; nine cases occurred in the first decade and 14 in the second. The most common neurological symptoms were a focal neurological deficit (33%) and seizures (25%). Seventy percent of the tumors were supratentorial. A gross total resection was performed in 60% of the cases. Histologically, the majority (74%) of the tumors were meningothelial or mixed. An increased number of mitoses was observed in 33% of the tumors, focal necrosis in 29%, and invasion of adjacent brain in 14%; however, none of the tumors was classified as a Grade III (anaplastic) meningioma. All patients are alive without evidence of recurrent disease 3 to 22 years (mean +/- standard deviation: 10 +/- 7.3 years) after surgery. This study confirms the rarity of meningiomas of the first two decades of life and the absence of the female predominance associated with meningiomas in adults. The location and histological features of these tumors are similar to those in adults; they have a low recurrence rate, and the outcome and survival rate are excellent.

Adolescent↗

PubMed1994

Reoperation for recurrent temporal lobe epilepsy.

The indications for the risks and outcome of reoperation for medically refractory temporal lobe epilepsy have not been well documented. A retrospective review is presented of 40 patients who underwent reoperation on the temporal lobe for recurrent seizures. The mean patient age at the first operation was 22 +/- 7 years (+/- standard deviation). Electrocorticography during the first operation showed interictal epileptic abnormalities from surface electrodes in 97% of the cases and from depth electrodes in the mesiotemporal structures in 38%. The seizures recurred with the same pattern within 6 months after the first operation in 60% of patients and within 2 years in 90%. Postoperative neuroimaging studies showed residual mesiotemporal structures in all cases. The mean time between the two operations was 5.5 +/- 5 years and the mean patient age at the second operation was 28 +/- 8 years. The second operation involved focal resection of the mesiotemporal structures in 30 cases. The mean postoperative follow-up period was 4.8 +/- 2.7 years (range 2 to 11 years). After the second operation, 63% of the patients were seizure-free or had rare seizures (one or two per year). There were no permanent neurological complications. Patients who did not benefit from reoperation had electroencephalographic abnormalities in multiple brain areas. Reoperation for temporal lobe epilepsy effectively controls seizures in the majority of patients, and the procedure is safe if rigorous technical rules are observed. More complete resection of mesiotemporal structures during the first operation, even in the absence of intraoperative electrographic abnormalities, could prevent the need for reoperation in defined cases.

Adolescent↗

PubMed1994

Frameless stereotaxy for surgery of the epilepsies: preliminary experience. Technical note.

Frameless stereotactic techniques used in conjunction with three-dimensional images allow accurate planning and performance of a variety of neurosurgical procedures. The authors have used the frameless stereotactic Allegro Viewing Wand system to provide real-time correlation of the operating field and computerized images in 42 neurosurgical operations, including 31 epilepsy procedures. The system consists of an image-processing computer that creates three-dimensional and triplanar images; a mobile computer to display reformatted magnetic resonance images; and a hand-guided, articulated, position-sensing arm with a probe. At the start of the operation, the probe identifies the patient's facial and scalp features and correlates these with the computerized images. The position-sensing arm can then guide the operation and locate anatomical structures and lesions of interest. This system can be used to advantage in performing smaller craniotomies and intraoperatively locating anatomical structures and lesions to be removed. Postoperative magnetic resonance images demonstrate that this technique was accurate to within 3 mm in measuring the anteroposterior resection of fixed structures, such as hippocampus and corpus callosum. Disadvantages include longer preoperative preparation for data analysis and lack of both real-time computer analysis of tissue removal and angiographic data display. Preliminary experience suggests that the viewing wand system's advantages outweigh the disadvantages, and it is most helpful as an adjunctive navigational device in the microsurgical treatment of epilepsy.

Adolescent↗

PubMed1993

Direct endarterectomy of the middle cerebral artery for treatment of symptomatic stenosis: case report.

The authors report the clinical course and surgical technique used to treat a patient with a high-grade stenosis of the proximal middle cerebral artery that had caused a previous infarction and threatened the remaining dominant hemisphere. Trapping of the involved middle cerebral artery segment allowed direct exposure for excision of the atheromatous plaque and subsequent closure of the arteriotomy. Intraoperative angiography confirmed the reestablishment of flow. The patient made an uneventful postoperative recovery. Direct middle cerebral artery endarterectomy has the advantage of potentially reestablishing flow to lenticulostriate branches. The technique may also avoid the problem of occlusion at the site of maximum stenosis that can be caused by the use of an extra/intracranial bypass graft. Middle cerebral artery endarterectomy is a potentially valuable technique that deserves further investigation.

Cerebral Angiography↗

PubMed1992

Histopathological follow-up study of 66 cerebral arteriovenous malformations after therapeutic embolization with polyvinyl alcohol.

Embolization with polyvinyl alcohol (PVA) is an accepted method of rendering complex arteriovenous malformations (AVM's) more amenable to surgery, but its effects on human vascular tissues have not been adequately documented. The authors reviewed the histopathology of 66 intracranial AVM's resected 1 to 76 days after embolization with PVA. The mean age of the patients was 36 years, and their AVM's were located in the cerebral hemispheres (92%), the cerebellum (6%), or the corpus callosum (2%). In 79% of cases, at least one vessel contained PVA particles; in most cases, the vessel was filled with sharp, angular PVA particles in a serpiginous pattern. Polyvinyl alcohol particles indented the endothelium in 69% of cases but were rarely found subendothelially. Clotted blood and fibroblasts were present among the particles, and abundant intraluminal mononuclear and polymorphonuclear inflammatory cells were found in all vessels containing PVA particles. Foreign-body giant cells appeared 2 to 14 days after embolization in the majority of cases. Patchy mural angionecrosis and necrotizing vasculitis were found in 39% of the cases. Recanalized lumina were seen in 18% of PVA-embolized vessels. Foreign materials resembling cotton fibers and other particulate substances, which were probably contaminants of the contrast solution or the embolic material, were found in 65% of the cases. These findings suggest a specific chain of events in the interaction between PVA and vessel wall components and may explain some important sequelae of embolization therapy.

Adolescent↗

PubMed1989

Magnetic resonance imaging and 31P magnetic resonance spectroscopy for evaluating focal cerebral ischemia.

Recent advances in magnetic resonance (MR) imaging and MR spectroscopy (MRS) allow the noninvasive in vivo study of a variety of anatomical, physiological, and biochemical alterations that may occur in different cerebral pathologies. The authors have investigated the use of MR imaging and MRS to monitor the evolution of experimental focal cerebral ischemia in rats. Permanent focal cerebral ischemia was induced in 36 rats, and 12 normal rats were used as a control group. Changes in high-energy phosphate metabolites were followed in vivo using MRS during the 1st hour and at 3 and 6 hours after ischemic insult. Changes in vivo MR images were evaluated at 1, 3, 6, 12, and 24 hours after ischemic insult. Significant decreases (p less than 0.05) in phosphocreatine/inorganic phosphate ratios and intracellular pH values occurred immediately after the induction of ischemia. The presence of an infarcted area seen on MR images was a constant finding at 3 hours after ischemic insult, and was well defined and localized at 12 and 24 hours. The location of areas of infarction seen on MR images correlated well with areas identified histopathologically. The T1 and T2 MR relaxation times were significantly increased 3 hours after ischemic insult and remained prolonged for at least 24 hours. The results show that MR imaging is a sensitive method to measure cerebral infarction, and that MRS is a sensitive measure of changes that occur in the early phases of ischemia, perhaps when cellular changes may still be reversible. At 3 and 6 hours after the ischemic insult, however, 31P-MRS spectra may appear to be "normal" despite the presence of well-documented areas of infarction.

Animals↗

PubMed1989

Correlation of histopathological features and proliferative potential of gliomas.

One hundred fifty-two intracranial gliomas of various types were reviewed in order to correlate the histopathological features with the proliferative potential of each tumor as reflected by the bromodeoxyuridine (BUdR) labeling index (LI). Patients undergoing surgical removal of gliomas were given a 30-minute intravenous infusion of BUdR (150 to 200 mg/sq m) to label S-phase tumor cells. The tumor specimens were stained immunohistochemically for BUdR and processed for routine histopathological diagnosis. The BUdR LI was calculated as the percentage of labeled cells among cells analyzed. Twenty-seven histological features in three categories (degenerative, vascular, and cellular changes) were considered. A significantly higher BUdR LI (p less than 0.05) was found in tumors with necrosis than in those without this feature; tumors with both coagulative and liquefactive necrosis had the highest BUdR LI (p less than 0.05). Increased vascularity was also associated with a higher BUdR LI (p less than 0.05). Although tumors with abnormal mitotic figures had a significantly higher BUdR LI than those without, the number of mitoses did not correlate with a higher BUdR LI. These results suggest that the number of mitoses is not a good indicator of tumor growth rate. Necrosis and increased vascularity should be heavily weighted in predicting the proliferative potential of individual gliomas.

Adult↗

PubMed1988

High energy phosphate metabolism in experimental permanent focal cerebral ischemia: an in vivo 31P magnetic resonance spectroscopy study.

Relative levels of phosphate metabolites in the brain were examined in vivo by 31P magnetic resonance spectroscopy (MRS) in 50 Sprague-Dawley rats before, during, and after induction of focal permanent cerebral ischemia. After acquisition of baseline spectra, rats were subjected to injury within the core of the MR spectrometer, and 31P spectra were collected for 60 min after injury: in 7 rats, permanent, acute focal cerebral ischemia was induced (ischemia group); in 6 rats, mild hypoxia (FiO2 14%) was induced at the time of the ischemic insult and was maintained for 20 min (ischemia-hypoxia group); in 6 rats, mild hypoxia (FiO2 14%) only was induced for 20 min (hypoxia group). Control studies were performed in 25 rats. Cerebral intracellular pH, calculated from the chemical shift of inorganic phosphate (Pi), decreased immediately after injury in the ischemia and ischemia-hypoxia groups. The first 31P spectrum obtained after injury was characterized by an increase in Pi and a decrease in phosphocreatine (PCr) in the ischemia and ischemia-hypoxia groups; these changes in spectra were significantly greater in the ischemia-hypoxia group. No significant changes in adenosine triphosphate (ATP) were found in either group. Within 60 min of occlusion, 31P spectra returned toward baseline spectra in both ischemia-hypoxia and ischemia groups. No significant changes were seen in spectra of rats subjected to hypoxia alone. These results confirm that 31P MRS is a sensitive measure of early changes of high energy metabolites in focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Kynurenate inhibition of cell excitation decreases stroke size and deficits.

Pharmacological inhibition of excitatory neurotransmission attenuates cell death in models of global ischemia/reperfusion and hypoglycemia. The current investigations extend these observations to a model of focal ischemia. Kynurenic acid, a broad-spectrum antagonist at excitatory amino acid receptors, was used as treatment (300 mg/kg; 3 doses at 4-hour intervals) before and after focal cerebral ischemia in rats (n = 54). Preischemia but not 1 hour postischemia treatment with kynurenate attenuated infarction size (p less than 0.001) and improved neurological outcome (p less than 0.001) studied at 24 hours after injury. These data support the role of excitatory neurotransmission in acute neuronal injury and support pharmacological inhibition of cell excitation as a potential therapy for stroke.

Animals↗

PubMed1987

The therapeutic value of nimodipine in experimental focal cerebral ischemia. Neurological outcome and histopathological findings.

Recent studies suggest that nimodipine, a potent calcium-channel antagonist that causes significant cerebrovascular dilatation, may improve neurological outcome after acute experimental permanent focal cerebral ischemia when given before or immediately after occlusion of the middle cerebral artery (MCA) in various animals. The authors describe the effect of nimodipine on cerebral ischemia in a rat model. At 1, 4, or 6 hours after occlusion of the MCA, rats were treated in a double-blind technique with either nimodipine, placebo, or saline. Neurological and neuropathological evaluation was performed at 24 hours. Neurological outcome was better in rats treated with nimodipine 1, 4, or 6 hours after occlusion (p less than 0.001, p less than 0.01, p less than 0.05 respectively), and the size of areas of infarction was statistically smaller in nimodipine-treated groups (p less than 0.01, p less than 0.01, p less than 0.05, respectively) when compared with control rats treated with saline or placebo. The best neurological outcome and the smallest area of infarction were found in nimodipine-treated rats 1 hour after occlusion. Compared with controls, the size of the periphery of the infarcted area was smaller in nimodipine-treated rats. The results show that nimodipine improves neurological outcome and decreases the size of infarction when administered up to 6 hours after ischemic insult. These results suggest a possible mechanism of action of nimodipine on the "penumbra" of the ischemic area.

Animals↗

PubMed1986

Combined magnetic resonance imaging and spectroscopy in experimental regional injury of the brain. Ischemia and impact trauma.

Combined magnetic resonance imaging (MRI) and spectroscopy (MRS) allows unique experimental insights into the central nervous system (CNS) disorders. Clinical applications are forthcoming. In order to address the potential clinical uses of MRI/MRS, experimentally induced focal brain lesions were evaluated with this modality. Focal lesions more closely mirror clinical situations than do global insults, but have rarely been the focus of MRS studies. Fluid-percussion trauma in 48 rats, focal ischemia in 18 rats and in 16 mongrel dogs were produced, with various degrees of severity. A discrepancy between temporal evolution data of MRI and MRS was found: MRI always showed an increase in lesion extension over time while 31P and 1H MRS almost always showed improvement. The severity and evolution of these MRS findings was surprising, and differed from the results reported for global brain injuries. Besides possibly reflecting real improvement in the metabolic state, other explanations for the phenomena exist. Diffusion of inorganic phosphate out of the regional site of injury and its reincorporation for more prominent lactate build-up in regional injury are possible. Therefore the use of MRS to predict metabolic and clinical outcomes of regional brain injury requires methodologic caution, but its combination to MRI offers an unprecedented tool for studies of focal CNS pathology.

Animals↗

PubMed1986

Magnetic resonance imaging in the evaluation of nimodipine-treated acute experimental focal cerebral ischemia.

We evaluated the sensitivity of magnetic resonance (MR) imaging in documenting effects of nimodipine in experimental focal cerebral ischemia. Twenty-five Sprague Dawley rats underwent unilateral occlusion of the middle cerebral artery and were imaged at different intervals thereafter. Neuropathologic and neurologic data were correlated with MR imaging results. Compared with controls, nimodipine-treated rats showed a significantly smaller infarct size (p less than 0.001), as documented by MR imaging and confirmed by neuropathologic evaluations. A less intense signal on the T2 weighted sequence was found in nimodipine-treated rats in basal ganglia (p less than 0.001) and cortex (p less than 0.05). MR imaging may afford unprecedented diagnostic sensitivity in assessing pharmacologic efficacy in cerebral ischemia.

Animals↗