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F Scaravilli

Publications and source records attributed to F Scaravilli.

At least 145 records · Page 8Linked to original sources
PubMed1990

The involvement of the cerebral cortex in human immunodeficiency virus encephalopathy: a morphological and immunohistochemical study.

The encephalopathy resulting from direct infection of the brain by human immunodeficiency virus (HIV), which correlates clinically with the AIDS dementia complex, has been reported as being localized to the white matter where it induces myelin loss, gliosis and perivascular infiltration by mononuclear macrophages and multinucleated giant cells. Damage to the cortical grey matter in HIV encephalopathy was investigated in nine randomly selected HIV-positive cases with or without clinical or morphological evidence of encephalopathy and in five age-matched controls, using routine histology and immunohistochemical methods [glial fibrillary acidic protein (GFAP), microglia and HIV antibodies]. Increased numbers of GFAP-expressing astrocytes and Ricinus communis agglutinin 1-120-expressing microglial cells were found in all the HIV-positive cases (including asymptomatic) and their severity could be correlated with the severity of the encephalopathy in the white matter; the increase in number of cells expressing GFAP was diffuse and the intensity of the staining higher than that of microglial cells. The subpial region was the most severely involved. It is suggested that involvement of the cortical grey matter is more common in HIV infection than previously suspected and that clinical evidence of a dementing process in AIDS is not necessarily due only to white matter lesions.

AIDS Dementia Complex↗
PubMed1990

Cytomegalovirus (CMV) encephalomyeloradiculitis and human immunodeficiency virus (HIV) encephalitis: presence of HIV and CMV co-infected multinucleated giant cells.

A 25-year-old homosexual male with AIDS presented with a cauda equina syndrome clinically suggestive of cytomegalovirus (CMV) myeloradiculitis. He was treated with ganciclovir with transient improvement of neurological signs and died 4 months after onset of neurological signs. Neuropathological examination revealed human immunodeficiency virus (HIV) encephalitis, CMV subependymal encephalitis and CMV myeloradiculitis. The latter was characterised by myelin loss, Schwann cell proliferation and presence of CMV early antigens in the nuclei of S-100 protein-positive cells in the spinal roots. In the subependymal regions, morphologically characteristic multinucleated giant cells, positive for CD68, contained early CMV antigens (E13) in their nuclei and HIV antigens (gp41 and p24) in their cytoplasm. The observation that HIV and CMV can co-infect the same cell in vivo raises the possibility of a direct synergistic interaction of both viruses at cell level. This suggests that CMV may play a role as a co-factor in the pathogenesis of HIV encephalopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Cytomegalovirus encephalopathy in an infant with congenital acquired immuno-deficiency syndrome.

A female infant born pre-term to a HIV seropositive mother presented at birth with seropositivity for HIV and CMV viruria. At five months of age she developed an AIDS-related complex. Six months later she died from rapidly progressive diffuse encephalopathy. Post mortem examination revealed generalized CMV infection. Neuropathological examination showed a nodular encephalitis with occasional cytomegalic cells containing characteristic CMV inclusion bodies. There was no evidence of HIV encephalitis; immunostaining for HIV antigen (gp 41) was negative. Opportunistic infections in infants with congenital AIDS are the exception. To our knowledge, only one case of CMV encephalitis in an infant with congenital AIDS has been reported previously. In that case, as in the present one, a reactivation of a congenital CMV infection is likely.

AIDS-Related Complex↗
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

[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

Neuropathology of HIV infection in haemophiliacs: comparative necropsy study.

OBJECTIVE: To discover whether pathological and neuropathological findings at necropsy are different in haemophiliacs and other subjects positive for HIV. DESIGN: Pathological and neuropathological findings at necropsy were compared in haemophiliacs and non-haemophiliacs, most of them homosexual men. SETTING: Necropsies performed in the south of England. SUBJECTS: 11 Haemophiliacs (mean age 41, range 15-69) and 31 non-haemophiliacs, 29 of whom were homosexual men (mean age 40, range 21-60). AIDS was diagnosed before death in four haemophiliacs and all but one of the non-haemophiliacs. MAIN OUTCOME MEASURES: Prevalence of various forms of neuropathology and systemic pathology in the haemophiliacs and non-haemophiliacs, compared with Fisher's exact test. RESULTS: The prevalences of opportunistic infections of the central nervous system were significantly higher in the non-haemophiliacs (cerebral toxoplasmosis 23% (7), progressive multifocal leucoencephalopathy 10% (3), and cerebral cytomegalovirus infection 19% (6) in the non-haemophiliacs v no cases in the haemophiliacs). The prevalences of fresh and old intracranial haemorrhages and cirrhosis of the liver were significantly higher in the haemophiliacs (fresh intracranial haemorrhage 45% (5), old intracranial haemorrhage 36% (4), and cirrhosis of the liver 27% (3) in the haemophiliacs v no cases in the non-haemophiliacs). The prevalence of neuropathological changes in the non-haemophiliacs was similar to that found in other necropsy series. CONCLUSIONS: The main causes of death in haemophiliacs positive for HIV included intracranial haemorrhage and cirrhosis of the liver. The haemophiliacs died when the characteristic neuropathological changes associated with HIV infection were at a fairly early stage in their development.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Orbital optic nerve glioma in adult life.

In seven cases, optic nerve glioma presented as an expanding orbital mass in previously asymptomatic adults. Clinically and histologically, these tumors were similar to the orbital optic nerve gliomas of childhood; in contrast to the rapidly progressive malignant gliomas of the chiasm well described in adults, the patients with these tumors had a more benign clinical course. Management of optic nerve glioma in adulthood should be conservative in the presence of useful vision.

Adolescent↗
PubMed1989

Reduced numbers of calcitonin gene-related peptide-(CGRP-) and tachykinin-immunoreactive sensory neurones associated with greater enkephalin immunoreactivity in the dorsal horn of a mutant rat with hereditary sensory neuropathy.

The mutilated foot rat is a mutant with autosomal recessive sensory neuropathy and frequent mutilation of the hindlimbs. Decreased numbers of dorsal root ganglion cells and diminished sensitivity to painful stimuli are characteristics of these animals. By use of immunocytochemistry, changes in the distributions of peptides involved in sensory and/or autonomic regulation, i.e., calcitonin gene-related peptide (CGRP), tachykinins, enkephalin and neuropeptide Y in spinal cord, dorsal root ganglia and skin of these animals, were studied. In comparison with normal litter-mate controls, the dorsal horn of mutilated foot rats contained substantially fewer CGRP- and tachykinin-immunoreactive fibres but more fibres immunoreactive for enkephalin. Many enkephalin-immunoreactive cell bodies were also found in the dorsal horn of the mutants, by contrast none were visible in control animals. Neuropeptide Y immunoreactivity was, however, unchanged in the spinal cord of the mutants. In the dorsal root ganglia of the mutants, the number of CGRP- or tachykinin-immunoreactive cells and their proportion to total neuronal numbers were significantly less in comparison with normal controls. The diameter range of CGRP- and tachykinin-immunoreactive cells shifted from small (15-25 microns) to medium size (25-45 microns) as revealed by frequency distribution histograms. The skin from the affected fore- and hindlimbs of the mutant rats, in keeping with fewer CGRP- and tachykinin-immunoreactive cells in the dorsal root ganglia, contained substantially less fibres immunoreactive for CGRP and tachykinins; a difference that was not seen in skin of unaffected areas (whiskers and snout). By contrast, neuropeptide Y-immunoreactive fibres showed a normal distribution around blood vessels and sweat glands of mutilated foot rats. The data suggest that diminished pain perception in the mutilated foot rat is related to loss of peptide-containing sensory neurones. Furthermore, the intraspinal increase of enkephalinergic neurons in the dorsal horn, concomitant with the decreased number of primary sensory neurones, may also play a contributory rôle in reducing pain thresholds.

Animals↗
PubMed1989

Combined HIV-CMV encephalitis presenting with brainstem signs.

Two cases of combined HIV-CMV encephalitis are described. One presented with a sixth nerve palsy and a tetraparesis, the other with an internuclear ophthalmoplegia. Pathologically brain stem involvement was predominantly due to CMV.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Current role of radical surgery in the treatment of breast tumors].

Though currently conservative surgical procedures have an ever-growing importance in breast cancer treatment, there is still place for radical surgery. The Authors describe radical techniques and their indications. The surgeon must know how to choose the proper radical technique, when it is not possible to perform a conservative surgical procedure.

Breast Neoplasms↗
PubMed1989

Chronic basal meningitis and vasculitis in acquired immunodeficiency syndrome. A possible role for human immunodeficiency virus.

We describe the clinical and postmortem findings in a 57-year-old man with human immunodeficiency virus who presented with neurologic symptoms attributed to stroke. In addition to multiple foci of ischemic necrosis, pathologic examination of the brain showed chronic basal meningitis and vasculitis. No microorganisms were found. The association of meningitis and vasculitis in patients with acquired immunodeficiency syndrome is unusual and the possibility that these conditions may be due to primary human immunodeficiency virus infection is raised.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Familial multiple sclerosis.

Siblings of patients with multiple sclerosis have an increased risk of developing the disease. In this report we describe 3 families with multiple affected members, representing the largest published aggregation of cases in first degree relatives. In the 2 families in which HLA tissue-typing was performed the affected individuals shared part of the haplotype HLA-DR2 (+ HLA-DQW1), BfS (+ C2C), C4A3, C4B1. The implications of these findings for the aetiology of multiple sclerosis are discussed.

Adolescent↗
PubMed1988

The neuropathology of the acquired immune deficiency syndrome (AIDS). A review.

The nervous system has been involved in the majority (at least 75%), of cases of acquired immune deficiency syndrome (AIDS) examined postmortem, but the pathogenetic mechanisms involved are not well understood. The predominant pathological process is opportunistic infection secondary to the decrease of T-helper (T4) cells and includes toxoplasmosis, encephalitis due to cytomegalovirus and progressive multifocal leucoencephalopathy. On the other hand, mycoses (mainly cryptococcosis) are relatively uncommon. Primary lymphomas are three times more common than secondary lymphoma spreading from other sites. Cerebral involvement by Kaposi sarcoma is metastatic, probably from primary foci in the lungs. Lesions due to the direct involvement of the nervous system by the human immune deficiency virus (HIV) include subacute encephalitis and vacuolar myelopathy. The former is reported with increasing frequency and is localized predominantly to the white matter in which multinucleated giant cells can be found. These are considered typical of AIDS and have been shown to contain HIV particles in their cytoplasm. AIDS lesions due to infectious agents do not always conform to the typical pattern of the uncomplicated disease and not uncommonly there is evidence of more than one infectious agent in the same area. Peripheral nervous system lesions in HIV infections, responsible for a variety of clinical symptoms, usually appear, in biopsy material, as nonspecific inflammatory in type. CMV inclusions and lymphomatous infiltrations of peripheral nerve have been reported in autopsy cases.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Nature, incidence and prognosis of neurological involvement in the acquired immunodeficiency syndrome in central London.

Clinical neurological involvement at various times throughout the illness was recorded in 52% of 122 patients seen in central London who died from acquired immunodeficiency syndrome (AIDS). Various metabolic encephalopathies, dementias, focal encephalopathies, retinopathies and peripheral nerve pathology were the most frequent manifestations. Seven of 9 patients with a neurological presentation had no other major systemic illness. The median time from diagnosis of AIDS to death was 9 months and from onset of neurological symptoms to death 4 months. Human immunodeficiency virus dementia, central nervous system opportunistic infections, presence of Kaposi sarcoma, neurological presentations and minor symptoms were not associated with major change in survival time.

Acquired Immunodeficiency Syndrome↗
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↗