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Biomedical subjects

J E Pittella

Publications and source records attributed to J E Pittella.

At least 55 records · Page 3Linked to original sources

[Primary intracranial tumors: analysis of a series of consecutive autopsies and biopsies].

A retrospective study of primary intracranial tumors found in 19.760 consecutive autopsies and 72.972 consecutive biopsies during a period of over 41 years was carried out. Two hundred and five neoplasms comprising 69,7% of the primary intracranial tumors were located in the supratentorial compartment whereas 84 tumors (28,6%) were infratentorial in site. Gliomas constituted the largest group of primary tumors comprising 60,9% of the intracranial primary neoplasms. Most of gliomas were found in the cerebral hemispheres, particularly in the frontal lobes. Of the total number of gliomas 40,2% were astrocytomas, 29,6% glioblastomas, 10,6% ependymomas, 10,1% medulloblastomas, 5% oligodendrogliomas and 2,2% choroid plexus papillomas. Meningiomas constituted the second most common primary intracranial tumors being found in 56 cases (19%), most of them in parasagittal region, sphenoid ridge and anterior fossa. In the sella region there were 39 neoplasms including 21 pituitary adenomas, seven meningiomas, five craniopharyngiomas, four epidermoid cysts and two teratomas. Six capillary hemangioblastomas of the cerebellum and two chordomas of the clivus were also found. Sixty-five tumors occurred in patients under 15 years of age, 53,3% of them infratentorial in location--36% in the cerebellum, 9,3% in the brainstem and 8% in the fourth ventricle. The majority of these tumors were astrocytomas, medulloblastomas and ependymomas. The present data are discussed in relation to other pathological series found in the literature.

Adolescent↗

Hypokalemic respiratory muscle paralysis following Strongyloides stercoralis hyperinfection: a case report.

Strongyloides stercoralis hyperinfection in a malnourished 6-year-old boy was characterized by severe diarrhea, dehydration and marked hypokalemia, followed by acute respiratory failure due to respiratory muscle paralysis, and cardiac arrest. He was resuscitated and maintained with positive pressure ventilation and intravenous infusion of potassium and gluco-saline solution. These measures produced recovery from the respiratory muscle paralysis. Stool examination revealed eggs and numerous larvae of S. stercoralis, and thiabendazole was initiated. He continued to have severe diarrhea and again developed marked hypokalemia with respiratory muscle paralysis, abdominal distention, and cardiac arrhythmias with cardiac arrest episodes. In spite of fluid and electrolyte replacement the patient died.

Arrhythmias, Cardiac↗

Optic nerve tuberculoma. A case report.

An intrinsic tuberculoma of the left optic nerve was found at necropsy in a 1 1/2-year-old child with tuberculous meningitis and disseminated miliary tuberculosis.

Humans↗

The contribution of mild thiamine deficiency and ethanol consumption to central cholinergic parameter dysfunction and rats' open-field performance impairment.

We studied at the biochemical, morphological, and behavioral levels the effect of chronic ethanol consumption, associated or not with a mild thiamine deficiency episode. We found that (i) thiamine deficiency induced a significant decrease of the acetylcholinesterase (AChE) activity both in cortex and hippocampus; (ii) chronic ethanol treatment has no effect on cortical AChE activity, but induced a significant decrease of hippocampal enzyme activity; (iii) the reduction in cortical and hippocampal AChE activity induced by chronic ethanol treatment associated with a 1-week thiamine deficiency was also significant and was greater than that induced by ethanol alone. Furthermore, either chronic ethanol or thiamine deficiency induced a significant decrease in the release of acetylcholine (ACh) in the stimulated condition using high potassium concentration; and when both treatments were associated the decrease was even greater. In the unstimulated condition, the reduction in the release of ACh was greater for ethanol treatment than for thiamine deficiency. Open-field tests showed that only in the "sniffing" category were there significant differences among the experimental groups. No morphological change was detected by optical microscopy, suggesting that the injury process was in its initial stages in which only functional and behavioral changes are displayed. In addition, our biochemical results indicate that cortical cholinergic susceptibilities to ethanol and thiamine deficiency are significantly different.

Acetylcholine↗

Progressive formation of neuritic plaques and neurofibrillary tangles is exponentially related to age and neuronal size. A morphometric study of three geographically distinct series of aging people.

Neuronal size and the incidence of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) were morphometrically and quantitatively studied in the entorhinal cortex of 300 autopsied individuals without dementia in three geographically distinct series (Brazil, Germany and Japan), and an additional series including 30 clinically diagnosed Alzheimer's disease patients. The mean ages at onset of NPs and NFTs were similar between the three normal series, and the incidence of NPs and NFTs increased exponentially with age, but at different rates. A correlation was found between larger neuronal size and higher incidence of NPs and NFTs. Neuronal size distribution largely seemed to account for the differences between the series. While the onset of neurodegeneration may be tightly programmed, i.e., in a species-specific manner, our data support the idea that the incidence of NPs and NFTs and the progression from NPs to NFTs may vary remarkably, depending on neuronal size.

Adult↗

Different rates of neuronal degeneration: an exquisite variation of the 'Cascade' hypothesis.

This morphometric, quantitative and correlative multivariate study of the hippocampal formation in human brains from two distinct normal aging populations provides an additional support to the notion that neuritic plaques (NP) are an earlier stage of the pathological process underlying neurofibrillary tangle (NFT) formation. It is shown that the rate of transformation of NP-affected neurons into NFT-bearing neurons may vary remarkably between distinct populations. In addition, it is put forward that different rates of neuronal degeneration may be one of the explanations for the existence of conflicting hypotheses regarding pathogenesis of NP and NFT and the relationships of these important histological markers to psychical deterioration.

Adult↗

Central nervous system involvement in Chagas' disease. An updating.

A review was made of the available literature on central nervous system (CNS) involvement in Chagas' disease. Thirty-one works concerning the acute nervous form and 17 others dealing with the chronic nervous form, all presenting neuropathologic studies, were critically analysed. Based on this analysis, an attempt was made to establish the possible natural history of CNS involvement in Chagas' disease. Among others, the following facts stand out: 1) the initial, acute phase of Trypanosoma cruzi infection is usually asymptomatic and subclinical; 2) only a small percentage of cases develop encephalitis in the acute phase of Chagas' disease; 3) the symptomatic acute forms accompanied by chagasic encephalitis are grave, with death ensuing in virtually all cases as a result of the brain lesions per se or of acute chagasic myocarditis, this being usually intense and always present; 4) individuals with the asymptomatic acute form and with the mild symptomatic acute form probably have no CNS infection or, in some cases, they may have discrete encephalitis in sparse foci. In the latter case, regression of the lesions may be total, or residual inflammatory nodules of relative insignificance may persist. Thus, no anatomical basis exists that might characterize the existence of a chronic nervous form of Chagas' disease; 5) reactivation of the CNS infection in the chronic form of Chagas' disease is uncommon and occurs only in immunosuppressed patients.

Acute Disease↗

Central nervous system involvement in experimental Trypanosomiasis cruzi.

A review of the available literature on central nervous system involvement in experimental trypanosomiasis cruzi is undertaken. From a critical analysis of 26 works on experimental infections with Trypanosoma cruzi (23 on the acute phase, 2 on the chronic phase, and one describing sequentially both phases), all supported by neuropathologic studies, it can be concluded that: 1) central nervous system involvement during the acute phase, in the form of encephalitis in multiple foci, with variable intensity of the parasitism and inflammatory changes, is frequent and well documented; 2) in animals with more severe central nervous system involvement death occurs as a result of the brain lesions or acute chagasic myocarditis, the latter being always present; 3) in animals with more discrete brain involvement death during the acute phase is due to complications not related to the nervous system, among which congestive heart failure secondary to acute chagasic myocarditis, a condition that is always present, regardless of whether or not the central nervous system is infected; 4) it is possible that in surviving animals that had mild encephalitis the inflammatory changes from the acute phase usually regress as the infection progress to the chronic phase.

Animals↗

Pontoneocerebellar hypoplasia: report of a case in a newborn and review of the literature.

A case of pontoneocerebellar hypoplasia (PNCH) in a 9-day-old child--the youngest in the literature--is described. Right after birth the child showed serious respiratory insufficiency and developed frequent episodes of apnea and cardiorespiratory arrests, dying on the 9th day. Postmortem examination showed significant alterations only in the brain. There was intense neuron reduction in the pontine, arcuate, inferior olivary and dentate nuclei, reduction of Purkinje cells and of the granular layer of the cerebellum and the disappearance of the pontocerebellar fibers, together with dense fibrillary astrocytosis, which seems to have first appeared in the pontine nuclei. This case is compared with others in the literature and attention is drawn to the more intense, and probably initial, involvement of the pontine nuclei. The time of appearance of pontoneocerebellar hypoplasia is commented upon, based on data concerning the ontogenesis of the structure and on the presence or absence of gliosis in the pontine nuclei and persistence of the fetal pattern in the inferior olivary and dentate nuclei. It is suggested that the process may start in the 2nd or 3rd month of fetal life, or even later, as probably occurred in the present case, during the second or third trimester of intrauterine life.

Astrocytes↗

Partial hypotrophy of the posterior and lateral columns of the spinal cord, representing a sequela of schistosomiasis mansoni: report of an autopsied case and a review of the literature.

An autopsied case of schistosomiasis mansoni of the spinal cord is reported. The patient had been healthy until about five years before, when he presented with paraparesis, loss of sensibility from the pelvic girdle down and fecal and urinary incontinence which persisted until death. At autopsy there was old necrosis of most of the gray matter in the middle thoracic segment of the spinal cord and severe hypotrophy of the posterior columns in the lumbar spinal cord, of the posterior and anterior spinocerebellar tracts, and of the lateral corticospinal tract, unilaterally, in the entire thoracolumbar spinal cord from the middle thoracic segment on. In correspondence with these lesions, over one hundred Schistosoma mansoni ova were found. No parasitism by S. mansoni in the brain and in the abdominal and thoracic viscera was found. This case is compared to others in the literature and a schistosomal etiology for spinal lesions is proposed. These lesions could represent a sequela of the prolonged destructive action of the granulomatous inflammatory process. The topography of the lesions, the relationship of schistosomiasis of the spinal cord to other anatomo-clinical forms of the disease, and how the spinal cord is reached by S. mansoni are commented upon.

Adult↗

Morphometric study of the neurons in the medial mammillary nucleus in acute and chronic Wernicke's encephalopathy.

A morphometric study was made of the neurons in the medial mammillary nucleus from 25 cases of Wernicke's encephalopathy (WE) and from 15 other cases (control group) in which hepatic or brain disease was excluded and the risk factors associated with WE were not present. The whole area of the mammillary body was also measured in all cases from both groups. The cases of WE were divided into acute and chronic. A highly significant reduction in the area of the mammillary body was noted in the chronic WE group, when compared to the control and acute WE cases. Although no significant differences were detected between the three groups with regard to the total number of neurons of medial mammillary nucleus, cell density was significantly higher in the chronic WE group, when compared to the control and acute WE cases. A significant reduction was noted in the nuclear volume of the neurons in the chronic cases of WE, when compared to the acute WE cases. The positive correlation between the area of the mammillary body and the nuclear volume of the neurons in the medial mammillary nucleus was highly significant for the WE group and significant for the control and chronic WE groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗