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Biomedical subjects

N Rizzuto

Publications and source records attributed to N Rizzuto.

At least 163 records · Page 9Linked to original sources
PubMed1977

Toxic polyneuropathies in Italy due to leather cement poisoning in shoe industries. A light- and electron-microscopic study.

The peripheral nerve biopsy specimens of 4 cases of toxic polyneruopathies induced by exposure to leather cement in shoe industries were studied. Analysis of the cements used in the manufacturing process proved them to contain n-hexane as a volatile substance. Light- and electron-microscopic examination of nerve biopsies showed segmental swelling of axons due to the accumulation of packed filaments and thinning of the overlying myelin sheath. Neither active nerve fibre degeneration nor regeneration were frequently seen. It has been suggested that features of so-called giant axonal neuropathy are the most common pattern of peripheral nerve degeneration in chronic n-hexane intoxication.

Adolescent↗
PubMed1977

Decerebrate rigidity in acute head injury.

A comprehensive study of the motor patterns, usually grouped under the heading "decerebrate rigidity," was carried out in a series of 800 patients with severe head injuries. The incidence of these manifestations was 39.6%, and when they were present chances of survival were reduced from 79.4% to 28.1%. Clinical and electromyographic investigations revealed heterogeneous and unstable motor manifestations that did not fit into the classical groups of experimental models of decerebrate rigidity. Combinations of extensor and flexor attitudes and/or responses were frequently found in same patient, but could be separated into homogeneous groups. Each recognized postural pattern had its own distinct neurological signs and prognosis. Age did not significantly affect the outcome, however, intracranial exapnding lesions (73.5%), impairment of the brain-stem oculomotor system (49.8%), and deep coma (88.9%) all contributed to an unfavorable course. Surgical treatment was effective when performed for intracranial hematomas and in patients with incomplete extensor rigidity. Good recovery was achieved in 16% of decerebrate patients, while 12.1% survived in prolonged coma or with severe disabilities. All clinical and neuropathological data suggest that extensor motor abnormalities in the acute phase of cerebral traumatic disease do not always conclusively indicate structural brain-stem damage. A critical analysis of so-called "decerebrate rigidity" (rejecting in some instances its Sherringtonian implications) may allow for a more accurate clinical assessment of the severity of head injury.

Adolescent↗
PubMed1976

Status spongiosus of rat central nervous system induced by actinomycin D.

The effect on central myelin of Actinomycin D, an RNA--and, secondarily, a protein-synthesis inhibitor, has been studied by light and electron microscopy. The intracranial injection of this drug produced an extensive status spongiosus of the white matter in the cerebrum, cerebellum, brain stem and optic nerve within 48 h. The status spongiosus was due to vacuole formation within the myelin sheath and to enlargement of the extracellular space. Three types of vacuoles were observed: (a) the most common varieties formed between the inner tongue and the remainder of the myelin sheath; (b) a second variety formed by enlargement of the periaxonal space with separation of the axon from its myelin sheath, and (c) a less common type of vacuolization was due to splitting of the myelin lamellae at the interperiod line to form large intramyelinic vacuoles. Myelinic vacuoles were preceded by nuclear and cytoplasmic changes in oligodendrocytes, which included nucleolar segregation, disaggregation, and diminution in number of ribosomes. These changes were similar to those previously reported in a variety of cells exposed to Actinomycin D. It is suggested that myelin vacuoles result secondarily from the Actinomycin D inhibitory effect on oligodendroglial RNA--and protein-synthesis, rather than from a direct effect of this drug on the myelin sheath.

Animals↗
PubMed1976

Sudanophilic leucodystrophy: report of a case with tigroid demyelination of the centrum ovale.

A 17-year-old girl with negative familial and personal history developed a progressive neurologic disorder characterized by cortical amaurosis, metal deterioration and spastic tetraparesis. Death occurred one year after the onset of symptoms. Histopathologic examination of the C.N.S. showed the presence of extensive, discontinuous demyelination of the white matter of the centrum ovale, with preservation of perivascular myelin islets, associated with massive fat degradation, loss of axons and severe astroglial proliferation. This case belongs to the group of sudanophilic leucodystrophies, being an atypical case, a transition between pure sudanophilic leucodystrophy and the group of Pelizaeus-Merzbacher's disease.

Adolescent↗
PubMed1975

Striato-nigral degeneration. Report of a case with an unusually short course and multiple system degenerations.

A 50-year-old white woman with an 8-month history of Parkinson's syndrome which did not respond to levodopa therapy was found on pathological examination to have the topographical lesions of striato-nigral degeneration. In addition to those characteristic lesions, an associated degeneration of the optic pathways, from the level of the optic nerve to the geniculo-collicular fibers, of the corticospinal tract and of the olivo-dentate axis, were found. While offering further evidence for the concept of "multiple system degeneration", no pathogenetic relationship either to previous cases of striato-nigral degeneration or to other multiple system degenerations is implied.

Brain↗
PubMed1975

Nuroaxonal degeneration induced by sodium diethyldithiocarbamate in cultures of central nervous tissue.

Well myelinated cultures of newborn mouse cerebellum, exposed to varying concentrations of sodium diethyldithiocarbamate (DDC), a heavy metal chelating agent, were examined by light and electron microscopy. DDC treatment of cultures for 24-48 hours produced swellings of axons and presynaptic endings, the morphological features characteristic of dystrophic axons. The axonal swellings contained an increased amount of endoplasmic reticulum, mitochondria and dense bodies. A continued exposure to DDC induced an extensive degeneration of axons and ensheathing myelin. Glial cells, on the other hand, were structurally intact even after a long-term exposure to DDC. It is suggested that DDC produces in myelinated CNS cultures an initial enlargement of axons and presynaptic endings and then continues to induce Wallerian degeneration in axons.

Animals↗
PubMedDate not supplied

Ponto-cerebellar hypoplasia with dystonia: clinico-pathological findings in a sporadic case.

Microcephaly, absent psychomotor development and dystonic limb movements were the main clinical features of a 3-year-old girl affected by hypoplasia of the pontocerebellar structures. As in the few previously reported cases there are discrepancies between the severity of lesions in the supratentorial and infratentorial compartments. Pathological features such as size reduction of the ventral pons, inferior olive atrophy, dentate nucleus fragmentation, and thinning of the cerebellar cortex suggest an impaired maturation of the involved structures due to a prenatal condition (dated at about 20-28 weeks of gestation). Somatotopic analysis failed to provide conclusive evidence on the primary target of the disease. The affected structures originate from the dorsal rhombencephalic region at about the same gestational age, and their maturation is probably under the control of sets of genes which regulate pattern formation. Early abnormal functioning of such genes might lead to the selected morphogenetical alterations observed in ponto-cerebellar hypoplasia. The normal morphogenetic pattern of the supratentorial structures and the mild lesions observed suggest that their late involvement can be related to a different pathogenetic process.

Atrophy↗