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Biomedical subjects

L Chimelli

Publications and source records attributed to L Chimelli.

50 records · Page 3Linked to original sources

[Cytomegalovirus encephalo-myelo-radiculitis in acquired immunodeficiency syndrome].

A 30 year-old male, with the acquired immune deficiency syndrome (AIDS) presented with rapidly progressive flaccid paraplegia and sphincter incontinence. Cerebrospinal fluid examination showed elevated protein and pleocytosis. Death occurred 2 months after the onset of neurological signs. Post-mortem examination showed inflammatory necrotic lesions, relatively sparing the axons and predominantly involving the roots of the cord. Numerous cytomegalovirus (CMV) inclusion bodies were found in the necrotic lesions, in the subarachnoid spaces and in Schwann cells. CMV encephalitis and involvement of the 3rd cranial nerves were also observed. Only 8 well-documented clinico-pathological cases of acute CMV myeloradiculitis, which all presented as progressive cauda equina syndrome, have been reported until now in AIDS patients.

Acquired Immunodeficiency Syndrome↗

Chronic recurrent Guillain-Barré syndrome: report of 3 cases.

The classical Guillain-Barré syndrome is an acute or subacute polyradiculo-neuropathy whose main clinical features are progressive weakness of the limbs, decrease or absence of tendon reflexes, and sensory changes. Although in most of the cases there is complete recovery in weeks or months, some patients have a slow and progressive relapsing course and present thickening of the peripheral nerves. In this paper we describe three cases of the chronic and relapsing variety of Guillain-Barré syndrome, two of which had prominent hypertrophic changes in the peripheral nerves with onion bulb formations. The clinical and pathological features of this disease are reviewed. The three patients improved with the use of steroids.

Aged↗

[Hypoglycemic polyneuropathy: report of a case with insulinoma].

A case of a young man who presented symptoms and clinical signs of polyneuropathy that occurred in connection with recurrent hypoglycemic episodes is reported. The hypoglycemia was probably caused by a pancreatic islet tumor. There were symmetric weakness and wasting of hands and feet, absent tendon reflexes and 'glove and stocking' loss of sensation. Electromyographic studies showed denervation potentials with slight reduction of nerve conduction velocities. Sural nerve biopsy studied by optic and electronic microscopy showed axonal degeneration without signs of demyelination or remyelination. There are only 30 similar cases reported in the literature. According to experimental findings, the authors believe that glucopenia is the mechanism responsible for the development of the neuropathy, and that at present time there is no evidence for a direct insulin effect.

Adenoma, Islet Cell↗

Lipoma of the midbrain. Post-mortem finding in a patient with breast cancer.

Intracranial lipomas are rare, usually do not have clinical expression and are located more frequently in the corpus callosum. Other locations include the spinal cord, midbrain tectum, superior vermis, tuber cinereum, infundibulum and more rarely cerebellopontine angle, hypothalamus, superior medullary velum and insula. We report the case of a lipoma of the left inferior colliculus which was a post-mortem finding in a woman who died of breast cancer. Although there are reports of intracranial lipomas in patients with malignant tumors there is no explanation for the co-existence of the two tumors. The present tumor also includes a segment of a nerve which is not uncommon, but a less common finding was the presence of nests of Schwann cells within it, shown by immunohistochemistry.

Bone Neoplasms↗

[Clinico-pathologic correlations in 78 biopsies of the sural nerve].

Peripheral nerve biopsies when processed with conventional techniques for paraffin embedding usually do not provide sufficient data for the diagnostic conclusion. However, if the nerve is processed for resin embedding for semi and ultra-thin sections and teasing of fibres, several aspects can be analysed including quantitative and morphometric data. We studied the sural nerve biopsy of 78 patients examined at the Antonio Pedro University Hospital, Niterói RJ, applying those techniques and we found that in 55 cases (70.5%) the pathologic diagnosis was conclusive, in 11 (14.1%) although the nerve had abnormalities it was not possible to establish a diagnosis, and in 12 (15.4%) the nerve was normal. In 68 cases there was a clinical diagnosis which was confirmed in 49 but not in the remaining 19, since 8 had non-specific changes and 11 were normal. From the 10 cases which did not have a clinical diagnosis the biopsy was conclusive in 6, showed non-specific changes in 4, and was normal in 1 case. The pathologic conclusion in most of our cases was possible because not only we had the clinical data but all the nerves were processed for resin embedding.

Axons↗

The development of the gracile nucleus in the rat: the time of ingrowth of ascending primary sensory fibres and effect of early deafferentation.

An investigation was carried out of the time of ingrowth of primary sensory fibres in the medulla and of their penetration into the gracile nucleus, and of the effect of an early loss of these fibres upon the development of the nucleus in rats. After injection of the conjugate horseradish peroxidase-wheat germ agglutinin in the hind limbs of fetuses, a bundle of labelled fibres was seen in close proximity of the gracile nucleus at embryonic day 17. However, fibres did not appear to leave the bundle until embryonic day 19, when they were seen to project ventrally and penetrate the nucleus which, on embryonic day 20 and thereafter, contained an increasing number of labelled fibres. Synaptic contacts within the gracile nucleus were found at all stages of the observation; the presynaptic processes consisted of an electron-lucent matrix which contained round vesicles. Although no mature glomeruli were observed, an occasional terminal appeared to be presynaptic to more than one process. After transection of the primary sensory afferents at embryonic day 18 and 19, no degeneration was seen within the gracile nucleus; degenerated boutons were occasionally seen after deafferentation at embryonic day 20 and became more numerous thereafter; nerve cells in various stages of degeneration could also be seen. Removal of primary afferents to the gracile nucleus at the time they reach the nucleus or soon after was followed by a severe loss of nerve cells and a reduced increment in size of the remaining ones. Moreover, the results of the present investigation show that penetration of primary sensory fibres into the gracile nucleus takes place approximately 2 days after they have been seen in the medulla and are in keeping with observations made in other pathways of the nervous system of the rat as well as in other animals. The findings that mature glomeruli, previously described in 1-day-old rats, are not present shortly before birth, suggest a fast rate of maturation of these synapses.

Afferent Pathways↗

The abnormal development of the gracile nucleus in the neurological mutant rat mf.

A morphological and quantitative study was carried out of the prenatal and early postnatal development of the gracile nucleus in the mutant rat 'mutilated foot' (mf), which is affected by a sensory neuropathy inherited by autosomal recessive transmission. Microscopic examination showed that the nucleus of both normal and mf rats become morphologically identifiable at embryonic day 19 and that its appearance was comparable in the two groups of rats up to postnatal day 2. Subsequently the nucleus in the mutants appeared smaller than in control rats and the number of nerve cells in it decreased dramatically. Glomeruli, the type of synapses known to be formed between primary sensory ascending fibres and dendrites of gracile nerve cells, were observed in the mf rat, but were greatly reduced in number and in size compared with those in normal littermates. Reconstruction of nerve cell volumes showed that, in mf rats, volumes increased considerably less than in controls. These results suggest that the abnormalities observed in the gracile nucleus of mf rats are secondary to the decreased number of afferent fibres originating from the dorsal root ganglia and represent a form of 'anterograde transneuronal degeneration'. In the mutant this is particularly severe and occurs at a rapid pace since it takes place in immature organisms, known to be particularly vulnerable to this type of lesions.

Afferent Pathways↗

The development and pathogenesis of the sensory neuropathy in the mutant rat mf.

A study was made of the development of sensory pathways in the mutant rat mutilated foot (mf) which is affected by a sensory neuropathy with autosomal recessive inheritance. Microscopic abnormalities are well recognizable at the fifteenth embryonic day. By day 16, dorsal root ganglia are smaller than normal and show more numerous foci of cell necrosis which continue throughout the remainder of gestation and during the first and second postnatal days. During this period the number of ganglion cells decreases sharply. Reconstruction of cell volumes shows that the larger cells are more severely affected. The secondary sensory nuclei (gracile nuclei) are normal at birth but during the first two postnatal weeks become progressively smaller than in normal rats. The results suggest that the mutant gene acts primarily on the dorsal root ganglia causing excessive neuronal cell death. Qualitatively, the events in this mutant are closely similar to 'programmed cell death' in the normal. It is likely that neurons of second order nuclei, which are not contacted by afferent fibres, undergo a process of transneuronal degeneration as a secondary effect of excessive ganglion cell loss.

Animals↗

Secondary transneuronal degeneration: cortical changes induced by peripheral nerve section in neonatal rats.

Secondary transneuronal degeneration of the cortico-spinal tract (CST) has been induced after sciatic nerve section in newborn rats. Observations made 21-60 days after the lesion showed a considerable decrease in number of myelinated and unmyelinated fibres of the CST ipsilateral to the lesion and of horseradish peroxidase-labelled nerve cells in the somato-sensorimotor cortex of the contralateral cerebral hemisphere. This phenomenon which has never been observed in spite of the frequent studies of experimental peripheral nerve lesions, may be significant in normal and pathological development.

Animals↗

Granular cell tumor of the fifth cranial nerve: further evidence for Schwann cell origin.

Granular cell tumors arising from the cranial nerves are rare. We describe a granular cell neoplasm of the fifth cranial nerve in a 66-year-old male. Light microscopic appearances included rows and clusters of cells with small peripheral nuclei and abundant eosinophilic cytoplasm. Ultrastructurally the cytoplasm of these cells contained numerous dense bodies, multivesicular bodies and vacuoles. In some areas tumor cells were intermingled with myelinated and unmyelinated nerve fibers showing the same relationships as do Schwann cells and nerve fibers. The association between tumor cells and axon seen in this case lends further support to the putative Schwann cell origin of this neoplasm.

Aged↗

Autonomic dysfunction in Chagas disease: lack of participation of the vagus nerve.

To evaluate the possible role of the vagus nerve in the development of the dysautonomia in Chagas disease, we examined 18 nerves from chagasic patients and 8 from non-chagasic patients, autopsied at the Department of Pathology, Ribeirão Preto School of Medicine, Brazil. Histological analysis showed mild inflammatory infiltrate composed predominantly of T lymphocytes, in epi-, peri- and endoneurium. No parasites were observed. Semithin sections showed swollen unmyelinated fibres, occasional thinly myelinated fibres, degenerated and atrophic axons, related to myelinated fibres. These findings were confirmed by electron microscopy, and in teased fibres. The changes were observed both in chagasic and in non-chagasic patients. Statistical analysis of the morphometric findings (myelinated fibre density, axonal and fibre diameters) failed to show significant differences between the 2 groups. The frequency of myelinated fibres of various diameters was also similar in the 2 groups. The morphological and morphometrical findings in chagasic patients are mild, non-specific, and could be related to the age of the patients, or with artefacts, since they have also been observed in non-chagasic patients. Retrograde changes due to the ganglionic lesions in the innervated organs cannot be completely ruled out. Our results do not allow us to implicate the vagus nerve in the dysautonomia in Chagas disease.

Age Distribution↗

[The neuropathology of the acquired immunodeficiency syndrome (AIDS)].

The nervous system is frequently involved in patients with AIDS. The lesions can be due to the human immunodeficiency virus (HIV), to opportunistic agents, to the development of tumours, and to occasional nonspecific factors, such as circulatory, metabolic and degenerative changes. The changes directly related to the presence of the HIV include the HIV encephalitis and leucoencephalopathy, the diffuse polydystrophy and the vacuolar myelopathy. The pathogenesis of these lesions is not yet completely clear. Macrophages are the main cells infected by the HIV, and it seems that the cytotoxic effects on the nervous tissue are indirect, may be due to the release of substances by infected macrophages. Among the opportunistic infections, the most frequent is toxoplasmosis followed by cryptococcosis and cytomegalovirus infection, with some differences in series from various countries. Many other agents have been observed in the brain of patients with AIDS. B-cell lymphoma is the most frequent tumour found in the brain and it is not uncommon the association of infections and/or tumours.

AIDS Dementia Complex↗

Dengue: neuropathological findings in 5 fatal cases from Brazil.

Neuropathological examination of 5 patients with dengue who died of shock in Rio de Janeiro during an outbreak in summer 1987, showed nonspecific lesions (edema, vascular congestion, hemorrhagic foci and perivascular lymphocytic infiltrates). In one case with delayed marked neurological symptoms, several foci of perivenous demyelination were observed. Neurological manifestations are various and not uncommon in dengue, but their anatomical substratum is not known. An immunopathological mechanism has been postulated in some cases but has never been demonstrated morphologically. The perivenous leukoencephalitis observed in one of our cases could represent the morphological substratum of such an immunological mechanism.

Adolescent↗