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Biomedical subjects

G Cavaletti

Publications and source records attributed to G Cavaletti.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effects of repeated administration of low doses of cisplatin on the rat nervous system.

Cisplatin is a very effective antineoplastic drug. To date its major toxic dose-limiting effect is peripheral neuropathy. Whereas the clinical and neurophysiological features of cisplatin-induced neuropathy are fairly well known, its pathogenesis is still unclear. We treated a group of Wistar rats with low doses of cisplatin for 70 days in order to evaluate the light-microscopic and ultrastructural changes induced by chronic cisplatin administration in the spinal cord, spinal ganglia and peripheral nerves. Although the most striking pathological alterations were observed in the spinal ganglia neurons, initial axonal neuropathy was also demonstrated, whereas the spinal cord neurons were completely normal. Our findings further support the hypotheses that spinal ganglion neurons are the primary target of cisplatin peripheral neurotoxicity and that peripheral nerve damage is secondary to this neuronopathy.

Animals↗
PubMed1990

Persistent memory impairment after high altitude climbing.

High altitude climbing without supplementary oxygen is a common sporting practice and athletes have been extensively evaluated with respect to possible brain functional impairment during its performance. Little is known on the contrary about long-term effects of hypoxia on the central nervous system. We evaluated, at sea level, a group of 10 high-altitude climbers with a battery of neuropsychological tests before and 75 days after the ascent. Our results suggest the occurrence of an impairment of memory performance after return to sea-level at least in some subjects, while speech and certain practical abilities were unchanged.

Adolescent↗
PubMed1990

A clinico-pathological and follow up study of 10 cases of essential type II cryoglobulinaemic neuropathy.

Ten patients with essential cryoglobulinaemia type II were examined for peripheral nerve damage. In six cases distal symmetrical nerve involvement was present, while in three other cases abnormalities restricted to single nerves were found. Electrophysiological and morphological data were consistent with axonal damage, the larger myelinated fibres being most affected. Although active signs of vasculitis and immunoperoxidase staining for immunoglobulins were not present, endoneurial vessels were widely damaged, with abnormally thick endothelial cells and redundant basal membranes. These findings, together with a patchy distribution of myelinated fibre loss, suggest ischaemia as a cause of peripheral neuropathy during essential cryoglobulinaemia type II. A follow up examination, performed one year after haematologial remission, revealed that no further peripheral nerve damage had occurred.

Aged↗
PubMed1990

Neuropathological and enzymatic studies in a case of adult form of metachromatic leukodystrophy with very late onset of clinical symptoms.

Metachromatic leukodystrophy is a genetical disorder due to a deficiency of arylsulphatase A activity. According to the age of onset of symptoms three different forms of the disease are described: late infantile, juvenile and adult types. We report the clinical, neuroimaging, biochemical and morphological features in a man in which the first symptoms ensued at the age of 39. In this patient, whose clinical manifestations were represented by "psychiatric" symptoms, the onset was particularly late in comparison with the large majority of the previously reported cases.

Adult↗
PubMed1990

Adrenoleukodystrophy. Report of a case with extremely slow progression of symptoms.

Adrenoleukodystrophy (ALD) is a sex-linked disorder characterized by very long chain fatty acid accumulation in different tissues, but mainly in the adrenal cortex, gonads and nervous system. The typical symptoms are hypoadrenalism, hypogonadism and central and peripheral nervous system impairment due to demyelination. On neurological grounds visual and hearing loss associated with quadriparesis are the most common symptoms, onset in childhood and a rapidly progressive course leading to a vegetative state and death. We report the case of a 31-year-old man affected by ALD, whose neurological symptoms started at the age of 12 and showed a markedly slow progression during the following years.

Adrenoleukodystrophy↗
PubMed1989

Hemorrhagic infarction: risk factors, clinical and tomographic features, and outcome. A case-control study.

A radiological diagnosis of hemorrhagic infarction (HI) was made in 41 of 2726 cases with cerebrovascular lesions (1.9%). The clinical records of the cases and those of 82 age- and gender-matched subjects with ischemic infarction were examined, and notes of the principal risk factors of cerebrovascular disorders, the clinico-radiologic features and the outcome of the disease were taken for comparison. Cardiac sources of emboli (atrial fibrillation, native or prosthetic valve disorders, recent myocardial infarction) were present in 44% of cases and in 24% of controls. Diabetes mellitus was recorded in 31% and 18% respectively. Thirteen percent of cases and 35% of controls gave a history of transient ischemic attacks. Stupor or coma during the acute phase and a more severe course were more common among cases. In general, HIs were significantly larger than ischemic infarcts, with mass-effect, although the size of the lesion did not seem to be related to the presence of cardiogenic embolism.

Adolescent↗
PubMed1989

Blood-nerve barrier of endoneural vessels in experimentally-induced hypothyroidism in rats.

Hypothyroidism may cause peripheral nerve damage, even if the pathophysiology of these changes is still unclear. It has been suggested by some that an increased vascular permeability is involved in hypothyroidism, while others have suggested a "compressive" mechanism caused by mucinous material deposited in the endoneurium. We have studied histologically the endoneurium and evaluated endoneural-vessel permeability in sciatic nerve by means of the leakage of horseradish peroxidase (HRP) in pharmacologically-induced hypothyroidism in rats. We did not find any substantial differences between the hypothyroid group of animals and the controls with respect to endoneural-vessel permeability. In particular, no macromolecular deposits were present in the extracellular space of the endoneurium in either the treated or the control rats. We therefore believe that a "vascular" hypothesis is unlikely for nerve involvement during hypothyroidism, nor was the "compressive" hypothesis supported by our histological findings.

Animals↗
PubMed1988

Histological features of nerve fibers and endoneural vessels in a case of Wegener's granulomatosis.

A sural nerve biopsy obtained from a patient with Wegener's granulomatosis and overt clinical signs of polyneuropathy showed degenerative changes of both myelinated and unmyelinated fibers. The pathological aspects were those of an axonopathy. Endoneural vessels were also involved, showing changes either in the endothelial cells, which were thickened and enriched with organelles, or in the basal membrane, which was reduplicated and thicker than in the controls. There were no cellular infiltrates nor was there clear evidence of fibrosis in the vascular wall. We suggest that peripheral neuropathy in Wegener's granulomatosis could be secondary to endoneural vessel changes on the basis of a possible immune complex action.

Blood Vessels↗
PubMed1987

Endoneural vessel involvement in hypothyroidism.

Light-microscope findings and pathological ultrastructural changes in sural nerve biopsies from two patients affected by hypothyroidism, one with overt signs of peripheral neuropathy, the other asymptomatic, were studied. In both patients the endoneural vessels showed clear pathological changes similar to those of other metabolic neuropathies, but more marked in the symptomatic patient. It is proposed that the changes observed in the nerve fibers in hypothyroid neuropathy are secondary to changes in the endothelial cells and in the vessel wall.

Biopsy↗
PubMed1984

The ultrastructural organization of lamina VI of the spinal cord of the cat. Morphological characterization of the synaptic population.

The synaptic population of lamina VI of the cervical enlargement of the cat spinal cord has been studied analysing 9 different morphological features and determining the incidence of possible combinations. The most important factors to characterize the synaptic boutons were the shape and size of pre-synaptic vesicles and the size of the synaptic boutons. The incidence of features like the density of the synaptic vesicles, the characteristics of the synaptic junction, the occurrence of post-synaptic specializations, the fibrillar or glycogen content of the pre-synaptic bag and the presence of dense-core vesicles, was unimportant. Most of the boutons (69%) contain pleomorphic vesicles (P boutons), 22% round vesicles (R boutons) and 9% flattened vesicles (F boutons). These synaptic types were further subdivided on the basis of the size of their synaptic vesicles. Most of the synapses (84%) were symmetrical, without relation to the shape of the pre-synaptic vesicles. Dense-core vesicles were found in 15% of the synaptic boutons and occurred most frequently in R boutons. On the basis of the analysis performed, we propose to classify synaptic boutons of lamina VI in 13 different types.

Animals↗
PubMedDate not supplied

Antiepileptic drugs and peripheral nerve function: a multicenter screening investigation of 141 patients with chronic treatment. Collaborative Group for the Study of Epilepsy.

One hundred forty-one adult patients treated for no less than 6 months with standard daily doses of the commonest antiepileptic drugs (AEDs) were recruited in five Italian centers and submitted to intensive clinical and electrophysiologic investigation to assess the effects of AEDs on peripheral nerves. Eighty percent of the patients were receiving monotherapy. Carbamazepine (CBZ) was the most common AED (51 cases), followed by phenytoin (PHT) (46), phenobarbital (PB) (42), and valproate (VPA) (25). Fifty-three percent of the patients had one or more symptoms of polyneuropathy (paresthesias being the most common complaint). The neurologic examination was abnormal in 32%. Electrophysiologic findings in two or more separate nerves were abnormal in 77 patients (54.6%); of these, 27 (19.1%) had abnormal neurologic findings and 21 (14.9%) also had symptoms of polyneuropathy. Sensory functions were most frequently impaired. Sural nerve biopsy was performed in 4 patients receiving monotherapy with CBZ, PHT, PB, and VPA. Except in patients receiving VPA (in whom no morphologic abnormalities were detected), mild predominantly axonal damage with secondary myelin changes was noted. A correlation was noted between polyneuropathy, age of the patient and, to a lesser extent, receipt of two or more AEDs.

Adult↗
PubMedDate not supplied

Circulating nerve growth factor level changes during oxaliplatin treatment-induced neurotoxicity in the rat.

BACKGROUND: Oxaliplatin neurotoxicity represents a clinically-relevant problem and its etio-pathogenesis is still unknown. We explored the possible role of some neuronal growth factors ("neurotrophins") during the course of oxaliplatin sensory neuronopathy. MATERIALS AND METHODS: In our rat model two different doses of oxaliplatin were used (2 and 3 mg/kg i.v. twice weekly for 9 times). The neurotoxicity of the treatment was assessed with neurophysiological and pathological methods and serum neurotrophin levels were measured by ELISA. RESULTS: Both oxaliplatin-treated groups showed the neurophysiological and neuropathological changes which mimic the chronic effects of oxaliplatin administration in humans, e.g. reversible sensory impairment due to dorsal root ganglia neuron damage. These changes were associated with a significant and dose-dependent reduction only in the circulating level of nerve growth factor (NGF), which returned to normal values after neurophysiological and pathological recovery. CONCLUSION: This specific association between neurological impairment and NGF modulation indicates that NGF impairment has a role in the neurotoxicity of oxaliplatin.

Animals↗