Biomedical subjects

L Chimelli

Publications and source records attributed to L Chimelli.

At least 55 records · Page 3Linked to original sources

PubMed1991

Prominent cortical atrophy with neuronal loss as correlate of human immunodeficiency virus encephalopathy.

A 25-year-old homosexual AIDS patient presented with progressive cognitive, motor and behavioral disturbances consistent with HIV encephalopathy. CT scans demonstrated progressive diffuse brain atrophy. Neuropathology showed predominant cortical changes including severe neuronal loss corroborated by morphometry. Only minimal changes were found in the white matter and basal ganglia. Immunocytochemistry for HIV stained occasional microglial cells more markedly in the cerebral cortex. This suggests that HIV infection of the brain may cause predominant cortical nerve cell loss, and that HIV encephalopathy is not necessarily due to white matter lesions.

AIDS Dementia Complex↗

PubMed1991

Macrophages in human sensory ganglia: an immunohistochemical and ultrastructural study.

The paper describes the immunohistochemical and ultrastructural features of normal posterior root ganglia in a group of humans aged 1 day to 80 years and compares the findings with those seen in the ganglia of normal rats of various ages, some of which underwent permanent traumatic lesions of the sciatic nerve. In humans, cells with the immunohistochemical reactions of macrophages are present in small number at birth, most of them having an endoneurial position. Subsequently, their number increases and more of them are seen around neurons, where their processes intermingle with those of satellite cells. Ultrastructural studies confirm that, in addition to interstitial cells, a small number of cells in satellite position have features of mesenchymal cells. In this respect, human sensory ganglia differ from those of rodents and this difference may explain why no nodules of Nageotte can be found either in ageing animals or after a permanent damage to the nerve has produced considerable cell loss. Other features observed in human ganglia, but absent in rats, are multiple layers of satellite cells surrounding each neuron and desmosome-like structures between satellite cell processes. Previous studies describing maturation of the satellite-nerve cell complex in animals are confirmed. In addition, the present investigation shows that, in human ganglia, satellite cells acquire a more elaborate structure than in rodents. It is also suggested that mesenchymal cells may play a role in the trophism of nerve cells and their removal after irreversible damage.

Adolescent↗

PubMed1991

Tapia's syndrome caused by Paracoccidioidis brasiliensis.

Tapia's syndrome is due to extracranial involvement of the XIIth nerve and the recurrent laryngeal branch of the Xth nerve. There is ipsilateral paralysis of vocal cords, soft palate and tongue. The main causes are parotid and other tumors or injuries to the high neck. We describe here a Brazilian female patient who presented with a lesion in the nasal mucosa, and soon after had dysphagia and dysphonia. Examination revealed paralysis of the soft palate, vocal cords and tongue ipsilaterally. Microscopic examination of the lesion in the nasal mucosa revealed the presence of the fungus. The patient was treated with sulfonamide and ketoconasol.

Adult↗

PubMed1991

Fulminating multiple sclerosis-like leukoencephalopathy revealing human immunodeficiency virus infection.

A 66-year-old French homosexual man and a 42-year-old Brazilian man with no known risk factors for HIV infection developed headaches, asthenia, and neurologic episodes of abrupt onset. CT showed multiple hypodense, nonenhancing lesions. Serology for HIV was positive. They died respectively 2 months and 1 month after onset of the illnesses. Autopsy in both cases showed multiple, well-demarcated, demyelinating foci in the white matter of the cerebral hemispheres, brainstem, and cerebellum with histologic features characteristic of recent plaques of multiple sclerosis. There were no multinucleated giant cells or microglial nodules. Immunostaining for HIV was negative. Although a random coincidence of MS and HIV infection cannot be ruled out, the close temporal relationship between the 2 disorders suggests a possible etiologic association.

Adult↗

PubMed1991

Peripheral neuropathy in hypereosinophilic syndrome with vasculitis.

A 53-year-old woman with non-productive cough of unexplained aetiology for two years, developed a sub-acute symmetrical polyneuropathy involving all four limbs, accompanied by fever, cutaneous rash and myalgia in lower limbs. Laboratory studies revealed a leukocytosis with 70% eosinophils and excluded any cause for the hypereosinophilia. An echocardiogram showed increase in thickness of the atrial septum. Motor and sensory conduction velocity were reduced in ulnar and median nerve and unrecordable in peroneal and tibial nerves. A sural nerve biopsy showed an axonal degeneration involving myelinated and unmyelinated fibers as well as a vasculitis with fibrinoid necrosis and perivascular infiltration of eosinophils. There was considerable clinical and laboratory improvement with the use of steroids. The differential diagnosis between idiopathic hypereosinophilic syndrome and other disorders known to course with vasculitis and hypereosinophilia is discussed.

Biopsy↗

PubMed1991

[Polyneuropathy caused by ethylene oxide. Report of a case with clinical, electrophysiological and histopathological studies].

A man who worked as an operator in a factory of sterilization of heat-sensitive materials has been exposed to ethylene oxide for seven years. He developed a mild sensori-motor polyneuropathy. The electromyography and nerve condition studies showed an axonal degenerative type of neuropathy. The sural nerve biopsy revealed mild loss of myelinated fibers, some fibers with axonal degeneration, some clusters of regeneration and few rows of myelin ovoids in the teased nerve fiber preparation. This is the first report of ethylene-oxide polyneuropathy in Brazil.

Adult↗

PubMed1991

[Axonal polyneuropathy in Chagas disease].

We report the case of a 44-year-old woman presenting with chronic symmetrical, sensitive polyneuropathy on the lower limbs in the course of Chagas' disease. The electrophysiological findings were in keeping with axonal degeneration. The histological data displayed axonal degeneration with perivascular inflammatory mononuclear cells in the epineurium, with some neutrophils and eosinophils. Mononuclear cells surrounding endoneurial vessels were observed. Laboratory data did not suggest neither a mixed connective tissue disease nor a collagen vascular disorder. Hematological disease, malignancies, drug-or medicine-induced neuropathy were ruled out. The polyneuropathy in this case was probably related to Trypanosoma cruzi infection on account of the presence of high levels of anti-T. cruzi antibodies, and an immune mechanism might play a role in the vasculitic process.

Adult↗

PubMed1990

Monoclonal antibodies against sensory neuron specific antigens define the extent of neuronal abnormality in the mf mutant rat.

The mutant rat mutilated foot (mf) is affected by a sensory neuropathy which does not involve the parts of the body innervated by the thoracic cord. The possibility that sensory cells subserving clinically normal regions may be functionally spared by the mutation has been investigated by studying the expression of cell surface oligosaccharides by dorsal root ganglia (DRG) and their central processes in the spinal cord. The study included 3 lactoseries epitopes (TC6, LD2 and LA4) and the globoseries epitope SSEA3. The results show that at cervical and lumbar levels in mf rats there are reduced numbers of DRG cells reacting with the various antibodies and less immunostaining in the dorsal horns. The unexpected finding that thoracic ganglia and cord share similar appearances suggests that, in spite of being normal in number and able to produce normal amounts of substance P, thoracic DRG cells in mf rats take part in the mutation as shown by their inability to produce normal amounts of oligosaccharides and to transport them to the axon terminals.

Animals↗

PubMed1990

[Polyneuropathy caused by trichlorfon: report of a case with electrophysiologic and histopathologic study of the sural nerve].

The authors observed a patient who worked in a farm and suffered an organophosphate intoxication (trichlorfon). The immediate effect was manifested by vomiting and abdominal cramps. Three months later he presented a distal symmetric sensorimotor (predominantly motor) neuropathy with distal muscle atrophy. Electromyography has revealed denervation changes in every muscle studied and the sensory and motor nerve conduction was slowed in arms and legs. The sural nerve biopsy specimen studied by light microscopy with semi-thin section and teased fiber preparation showed axonal degeneration. The ultrastructural studies of the axonal alterations consisted of degeneration of the neurofilaments and the neurotubules with granular appearance of the axoplasm.

Aged↗

PubMed1990

[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↗

PubMed1989

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↗

PubMed1989

[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↗

PubMed1989

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↗

PubMed1989

[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↗

PubMed1987

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↗

PubMed1986

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↗

PubMed1986

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↗

PubMed1985

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↗