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Biomedical subjects

D Spagnoli

Publications and source records attributed to D Spagnoli.

At least 19 recordsLinked to original sources

Postoperative pain in neurosurgery: a pilot study in brain surgery.

The incidence, magnitude, and duration of acute pain experienced by neurosurgical patients after various brain operations are not precisely known, because of a lack of well-designed clinical and epidemiological studies. We assessed these important pain variables in 37 consecutive patients who underwent various brain neurosurgical procedures. Postoperative pain was more common than generally assumed (60%). In two-thirds of the patients with postoperative pain, the intensity was moderate to severe. Pain most frequently occurred within the first 48 hours after surgery, but a significant number of patients endured pain for longer periods. Pain was predominantly superficial (86%), suggesting somatic rather than visceral origin and possibly involving pericranial muscles and soft tissues. Subtemporal and suboccipital surgical routes yielded the highest incidence of postoperative pain. Age and sex were significantly associated with the onset of pain, with female and younger patients reporting higher percentages of postoperative pain. Psychological Minnesota Multiphasic Personality Inventory profiles of patients with and without pain significantly differed on the Hypochondriasis scale, with patients without pain scoring unexpectedly higher than patients with pain. It is possible that hypochondriasis serves as a defense mechanism against pain, at least in some patients. Results of this pilot study indicate that postoperative pain after brain surgery is an important, although neglected, clinical problem, that deserves greater attention by surgical teams, to provide better and more appropriate treatment.

Adult

Central nervous system trans-synaptic effects of acute axonal injury: a 1H magnetic resonance spectroscopy study.

N-acetylaspartate (NAA) has previously been proposed as a neuronal marker. 1H magnetic resonance spectroscopy (MRS) is able to detect NAA in brain, and decreases of NAA have been documented after brain injury. The reason for this decrease is not fully understood and neuron loss damage and "dysfunction" have all been proposed. It is hypothesized that acute central nervous system (CNS) deafferentation causes a trans-synaptic NAA decrease and that high resolution 1H MRS is able to detect such a decrease. To test this hypothesis, an experimental model was used in which axonal lesions were obtained by stretch injury in guinea pig right optic nerve (95-99% crossed fibers). The trans-synaptic concentration of NAA, total creatine (Cr), and the NAA/Cr ratio in lateral geniculate bodies (LGB) and superior colliculi (SC) sample extracts were measured 72 h later by high resolution 1H MRS. In the left LGB/SC, which is where right optic nerve fibers project, reductions of NAA and NAA/Cr were found whereas Cr levels were normal. NAA, NAA/Cr, and Cr values were all normal in the right LGB/SC. Histology and EM findings revealed no abnormalities. At 7 days, left LGB/SC NAA and NAA/Cr values were in the normal range. It was concluded that 1) acute deafferentation in the CNS causes a trans-synaptic decrease of NAA levels that can be detected by 1H MRS and 2) NAA decrease may be due to changes of NAA metabolism caused by functional neuronal inactivity rather than neuronal loss, injury or "dysfunction." 1H MRS is a potential tool for the study of functional effect of CNS lesions in vivo.

Animals

Long-term outcome in aqueductal stenosis.

In this study, 78 patients with aqueductal stenosis were submitted to detailed neurodevelopmental assessment with a follow-up of 5-25 years. Sixty-eight percent of patients were categorized as normal; they either attended normal school courses or had regular jobs. Among these, 34% had some motor abnormalities (ataxia, mild hemiparesis, visual disturbances). Twenty-four percent (19 cases) were moderately disabled (trainable retardation) and 8% (6 cases) were severely handicapped. Epilepsy was observed in 13% of the cases. Incidence of recurrent and generalized seizures paralleled neurodevelopmental outcome (5% in normal, 16% in moderately disabled and 50% in severely disabled patients). Endocrine dysfunctions were evident in 28% of the cases and were characterized by precocious or delayed puberty, amenorrhea and somatic underdevelopment. No patient with ventricular enlargement and a cortical mantle width below 20 mm showed a good outcome. Large ventricles were compatible with normal mental development when compensated with a corresponding cranial vault enlargement. In patients with normal mental status and motor abnormalities, long-term CT scan findings revealed the presence of focal brain abnormalities (poroencephaly, brain atrophy, calcifications, extracerebral collections).

Adolescent

Risk factors for late posttraumatic epilepsy.

The usually accepted risk factors for late post-traumatic seizures (LPTS) are those identified years ago by Jennet: early post-traumatic seizure (EPTS), depressed fracture, intracranial haematoma. Prolonged unconsciousness (PTA greater than 24 hrs) is another factor usually added. More recently, personal experience of the Authors and the data of the literature, compel us to question the validity of known risk factors based on clinical data. Authors believe that the identification of patients at risk for LPTS depends mainly on the precise definition of trauma severity and on CT or surgically documented lesions of brain substance. Three groups of patients, characterized by the presence of one or more of the accepted risk factors of LPTS, have been studied. In our experience, while in adults the presence of documented cortico-subcortical lesions represents the main risk factor of LPTS, in children the appearance of EPTS per se increases the risk of LPTS, irrespective of the presence of documented brain lesions. Alteration of consciousness without a focal lesion, even if prolonged and severe, is not a risk factor for LPTS.

Adolescent

Multicenter evaluation of temporomandibular joint Proplast-Teflon disk implant.

Seven oral and maxillofacial surgeons from all U.S. American Association of Oral and Maxillofacial Surgeons districts participated in a retrospective study of Proplast II Teflon interpositional implants that were placed after meniscectomy in 680 TMJs (465 patients) and followed from 6 to 76 months. At longest follow-up a relatively high number (85.9%) 584 of 680 implants were in place with an average weighted follow-up of nearly 32 months. Of these 584 joints, a very high number, 540, (92.4%) were asymptomatic, however, 224 asymptomatic and 25 symptomatic joints with the implants in place exhibited some degree of condyle resorption that included 45 with malocclusion. In the worst case scenario, if condylar resorption is indicative of a worn Proplast II Teflon interpositional implant, then 364 (54%) of the 680 implants may fail. Failure rates per year range from Vitek's reported 3% to an average 18% clinician report in the literature. Higher rates are reported by individual clinicians, and our recent in vitro wear tests of Proplast II Teflon interpositional implants suggest an in vivo service life of only 3 years. Because no one has reported follow-up beyond 5 years, the long term performance and survival of any of these implants is doubtful. Asymptomatic patients should be evaluated yearly with tomography, CT, or MRI. Symptomatic patients should be evaluated every 4 to 6 months. Implant removal should be recommended if occlusal changes or condyle/fossa articular bone changes are active past the time of expected remodeling from surgery. This report summarizes the success/failure incidence from the literature and makes recommendations on follow-up, removal, and repair surgery.

Aluminum Oxide

Morphology and neurophysiology of focal axonal injury experimentally induced in the guinea pig optic nerve.

A new model of focal axonal injury was reproduced by rapid and controlled elongation (uniaxial stretch) of the guinea pig optic nerve. Light microscopy study of optic nerve specimens after horseradish peroxidase injection into the vitreous of the animal's eye showed that axonal lesions were identical to those seen in human and primate post-traumatic diffuse axonal injury (DAI). The lesions were characterized by the formation of terminal clubs in severed axons and focal axonal enlargements in those axons that were lesioned-in-continuity. Visual-evoked potentials upon flash stimulation were recorded before and after injury. Mean amplitude and mean latency of occipital peaks were significantly elongated in the acute post-traumatic phase. Electron microscopy examination showed that the main axonal changes observed in this model were cytoskeleton disorganization, accumulation of axoplasm membrane-bound bodies at the site of terminal balls and dilatations-in-continuity and detachment of the axolemma from the myelin sheath. Such axonal alterations were similar to those found in many other biological models of central and peripheral axonal injuries in which the lesion was produced by invasive methods. This model is unique since it reproduces the same mechanism of injury and the identical lesions that have been demonstrated in humans and primates with post-traumatic (DAI).

Animals

Neuropsychological follow-up of patients operated for aneurysms of anterior communicating artery.

The neuropsychological outcome of 43 patients operated for ACoA aneurysms was assessed with a battery of 15 tests, tapping a wide spectrum of cognitive abilities. As a group ACoA aneurysms patients were impaired on 8 tests, including the three assessing memory. When however, patients falling below the cut-off point determined in normal controls were considered, 42% of the sample was unimpaired and only 35% fell on two or more tests. The analysis of single cases showed that memory was often affected, but short-term memory even more than long-term memory. In addition to the well known memory disorder, the patients showed a wide range of neuropsychological defects, including language and space functions. The hypotheses that could account for this broad-based neuropsychological impairment are discussed.

Follow-Up Studies

Neuropsychological follow-up of patients operated for aneurysms of the middle cerebral artery and posterior communicating artery.

This study assessed with a neuropsychological battery the outcome of 27 patients operated on for an aneurysm of the Middle Cerebral Artery a mean of 35 months before, and of 27 patients operated for aneurysms of the Posterior Communicating Artery, a mean of 47 months before. Both groups showed a defective pattern of performance that was related to the hemispheric side of the aneurysm with left-sided patients impaired on naming, verbal fluency and verbal short-term memory and right sided patients on both short-term and long-term spatial memory and discrimination of line orientation. In single cases, the scope of neuropsychological impairment was sometimes wider than that expected only on the basis of the competence of the affected hemisphere.

Follow-Up Studies

Neuropsychological outcome of patients operated upon for an intracranial aneurysm: analysis of general prognostic factors and of the effects of the location of the aneurysm.

One hundred and fourteen patients operated on for an intracranial aneurysm were followed up in order to investigate their neuropsychological outcome and to detect if there were any clinical features assessed around the time of operation that had prognostic significance. The neuropsychological examination evaluated language, apraxia, memory, intelligence and spatial ability. In the statistical analysis the overall severity of neuropsychological disorder was studied. "Late surgery timing" had a negative influence upon the neuropsychological outcome. There was not a difference between different aneurysm sites. Several patients with an apparently good clinical outcome showed neuropsychological deficits. Neuropsychological assessment is important in the evaluation of outcome after subarachnoid haemorrhage.

Adolescent

alpha-Bungarotoxin and P15 toxin binding site in mammalian sympathetic ganglia.

alpha-Bungarotoxin (alpha-Bgtx) demonstrates a specific and saturable binding to rat superior cervical ganglion, yet it does not block ganglionic response mediated by nicotinic receptors in the guinea pig vas deferens-hypogastric nerve preparation. P15 toxin, a probe for ganglionic nicotinic receptor, prevents the binding of alpha-Bgtx to rat ganglia, and alpha-Bgtx prevents the ganglioplegic action of hexamethonium. Hexamethonium does not block the binding of alpha-Bgtx and P15 to rat ganglia. It is concluded that alpha-Bgtx and P15 bind to ganglionic nicotinic receptor at a common site which is different from that of cholinergic agonists and antagonists.

Animals

Effects of hormones on the activity of glucose-6-phosphatase in primary cultures of rat hepatocytes.

Although the activity of glucose-6-phosphatase in rat liver is altered markedly following the administration of a variety of hormones in vivo, it is not certain whether the hormones act directly on the hepatocyte. To study this problem hepatocytes were isolated by a collagenase-perfusion technique and cultured on collagen gel/nylon mesh membranes. The activity of glucose 6-phosphatase in cells cultured with fetal calf serum and with Dulbecco's modified Eagle's medium or Leibovitz L-15 medium decreased to less than 10-30% of the activity in freshly isolated cells by 96 h. However, when L-15 plus newborn or fetal calf serum was supplemented with glucagon (10(-6)M), epinephrine (10(-6)M), triiodothyronine (10(-6)M), and dexamethasone (10(-5)M) (L-15-GETD), the activity of glucose-6-phosphatase was maintained so that, after 144 h, the activity was at least 80% of that detected in freshly isolated cells. In cells cultured in L-15 plus serum for 72 or 96 h and then in L-15-GETD, glucose-6-phosphatase increased 30-50% over that in control cultures after 24 h. Insulin, which decreases glucose-6-phosphatase activity when administered to intact animals, also decreased the glucose-6-phosphatase activity in cultured hepatocytes to 20-50% of that in controls.

Animals

Functional MRI: primary motor cortex localization in patients with brain tumors.

PURPOSE: Our goal was (a) to test the ability of functional MRI (fMRI) to localize the hand primary motor cortex in patients with brain neoplasms using a conventional scanner and (b) to compare within the same subject the location and morphology of the activated motor areas in the affected hemisphere with the contralateral ones. METHOD: Seventeen right-handed patients with frontoparietal intra- and extraaxial tumors were studied. Hand motor performance ranged from normal to slight impairment of finger dexterity. The fMRI study was based on a series of FLASH images. Two or three contiguous slices parallel to the bicommissural plane were acquired through the level of frontoparietal cortex. Each patient was requested to perform with each hand a finger-tapping task or a simpler repetitive flexion-extension of the last four fingers. Pseudo-color activation maps were then calculated by a Z-score method and superimposed on high resolution images. RESULTS: Five patients were excluded because of gross motion artifacts. In all other patients, areas of significant signal increase were detected on the precentral gyrus. They had a spot-like appearance, and no substantial side-to-side differences in shape or extension could be observed. In the presence of severe compression of the gyri, a displacement of the activated areas in the affected hemisphere with respect to the contralateral ones was noticeable. CONCLUSION: fMRI localization of the primary motor area using a conventional scanner can be obtained also in patients with brain tumors, although with a lower success rate than in normal volunteer studies, mainly because of subject compliance problems. Areas of significantly increased signal are detectable even in cortex where normal anatomical patterns are lost.

Adolescent

Posttraumatic diffuse cerebral lesions. Relationship between clinical course, CT findings and ICP.

One hundred and fifty patients with posttraumatic diffuse cerebral lesions were reviewed. Criteria of inclusion were immediate coma and CT appearance of diffuse lesions, that were classified as follows: (a) Diffuse axonal injury (70 cases): patients with normal CT scan (50 cases) and patients with shearing injury (focal hemorrhages in corpus callosum, basal ganglia and brain stem; gliding contusions) (20 cases); (b) Diffuse brain swelling (80 cases): reduced or absent lateral ventricles, absence of 3rd ventricle and basal cisterns. Many of these patients had either subarachnoid haemorrhage or subdural blood effusion. Clinical course and mortality rate were in a ranking order in the considered groups. Patients with normal CT had a less severe coma and a better outcome than patients with shearing injury and diffuse brain swelling. There was evidence of high intracranial pressure in 75% of the patients with brain swelling, whereas no patient with normal CT had ICP elevation. Diffuse axonal injury represents a primary posttraumatic diffuse lesion. Secondary vascular involvement, due to hypoxia, shock and other unknown causes, is responsible for the appearance of vasoparesis, hyperemia and diffuse brain swelling.

Adult