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A R Mastri

Publications and source records attributed to A R Mastri.

At least 19 recordsLinked to original sources
PubMed1999

HIV infection of choroid plexus in AIDS and asymptomatic HIV-infected patients suggests that the choroid plexus may be a reservoir of productive infection.

The choroid plexus (CPx) may be an important site of viral dissemination since monocytes and dendritic cells in its stroma are infected with HIV in AIDS patients and since the ratio of CPx to brain infection is more than 2 : 1. In order to see if CPx infection also develops in asymptomatic (ASY) HIV-infected patients, we examined archival formalin-fixed brain and CPx from 14 AIDS and seven ASY cases, using routine histology, immunohistochemistry for HIV gp41, and DNA extraction and gene amplification for HIV DNA. Eight of 14 AIDS (57%) had HIV-positive cells in the CPx and four (29%) had HIV encephalitis. Two of seven ASY cases (29%) had HIV-positive cells in the CPx but none had HIV encephalitis. Extracted DNA from brain, CPx and systemic organs of five ASY cases was amplified by nested PCR with or without Southern blotting for HIV env gene. It was positive in systemic organs in five cases; in CPx in four cases; and in brain in one case. This study shows that the CPx is a site of HIV infection in ASY patients and that the frequency of CPx infection is higher than seen in brain in both AIDS and ASY cases. The results are consistent with the hypothesis that the CPx may be a site for hematogeneous spread and a reservoir for HIV infection during the period of clinical latency.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Neuropathology of human immunodeficiency virus infection at different disease stages.

The authors studied the brains of 471 adults infected with human immunodeficiency virus type 1 (HIV-1): 123 asymptomatic carriers, 127 in an early stage of acquired immunodeficiency syndrome (AIDS) with pulmonary tuberculosis or bacterial infections, and 221 in fully developed AIDS with opportunistic infections or neoplasms. Lymphocyte infiltration of the leptomeninges and of perivascular spaces occurred at all stages, but the frequency was significantly higher in asymptomatic carriers. Microglial nodules appeared at all stages of disease; they were not an early indicator of HIV encephalitis (HIVE). The incidence of HIVE was unrelated to the stage of AIDS, suggesting that HIVE occurs before opportunistic infections and neoplasms. Drug abuse, such as cocaine and opiates, may enhance HIV replication and increase the incidence of HIVE in the early stage of AIDS. Opportunistic infections or lymphoma involved only the brain in 31.2% of persons with fully developed AIDS. Conversely, opportunistic infections or neoplasms involved only organs other than the brain in 55.7% of persons with fully developed AIDS. In 13.1% of persons with fully developed AIDS, opportunistic infections or neoplasms involved the brain and other organs. Multiple intracranial opportunistic infections and lymphoma coexisted in 4.1% of persons with fully developed AIDS. The authors identified cerebrovascular disease in 10.6% of asymptomatic carriers, 7.1% of early AIDS, and 5.0% of fully developed AIDS. The observed sequence of abnormalities may be useful in understanding the progression of HIV disease in the brain.

AIDS Dementia Complex↗
PubMed1995

Cocaine induced intracerebral hemorrhage: analysis of predisposing factors and mechanisms causing hemorrhagic strokes.

We analyzed 26 autopsy cases of cocaine induced intracerebral hemorrhage and compared those findings with those of 26 autopsy cases of cocaine induced cerebral aneurysm rupture. The incidence of hypertensive cardiovascular disease (HCVD) was significantly higher in persons with intracerebral hemorrhage than in those with aneurysm rupture. Our findings suggest that HCVD predisposes to cocaine induced intracerebral hemorrhage. We propose that the foregoing relationship results from a cocaine induced alteration of cerebral autoregulation in the context of increased cerebral blood flow.

Adult↗
PubMed1993

Pick's disease versus Alzheimer's disease: a comparison of clinical characteristics.

The clinical recognition of Pick's disease depends on its differentiation from Alzheimer's disease (AD). To identify distinguishing clinical features, we reviewed the clinical records of 21 patients with pathologically confirmed Pick's disease and matched them by sex, age of onset, and duration of dementia with 42 patients having pathologically confirmed AD. In the absence of temporal or frontal lobar atrophy on CTs, all the Pick patients and none of the AD patients had three of five clinical features: presenile onset (before age 65), an initial personality change, hyperorality, disinhibition, and roaming behavior. In addition, the Pick patients had a tendency toward reiterative and other speech disturbances. These findings suggest that Pick patients are potentially distinguishable from AD patients on the basis of clinical manifestations.

Adult↗
PubMed1992

Clinically diagnosed Alzheimer disease: neuropathologic findings in 650 cases.

Despite the introduction of formal clinical criteria for Alzheimer disease (AD), the clinical diagnosis of AD remains one of exclusion of other dementias. To determine the accuracy of a clinical diagnosis of AD as made by practicing physicians, we reviewed the clinicopathologic records of a dementia brain bank and summarized the literature. Of 650 demented patients diagnosed during life as having AD, at autopsy 505 (78%) had AD with or without other neuropathologic conditions; only 390 (60%) of these had AD as the only neuropathologic condition. Of the remaining 145 (22%) patients with no neuropathologic evidence of AD, 39 had the nigrostriatal changes of Parkinson disease (PD), 25 had nonspecific degenerations, 15 had Pick disease, 14 had multiple infarcts, and 11 lacked any neuropathologic abnormality. Although the overall clinical accuracy for AD was lower than that summarized from the literature, clinical accuracy improved significantly between 1986 and 1990. In our broad sample of practitioners, accuracy of clinical diagnosis of AD may be improving, but continues to be hampered by difficulty in distinguishing the dementia of AD from certain dementing conditions and from AD mixed with other neuropathologic conditions.

Aged↗
PubMed1992

A clinicopathological study of CT scans in Alzheimer's disease.

OBJECTIVE: To investigate the accuracy of cranial computerized tomography (CT) scans in distinguishing patients with Alzheimer's disease from those with other dementing conditions. DESIGN: Retrospective clinicopathological correlation with pre-mortem CT scans. SETTING: Urban and rural hospitals and nursing homes in the Upper Midwest. PATIENTS: All 507 patients had clinical dementia diagnosed as Alzheimer's disease during life and the subsequent referral of their brains to a dementia brain bank. Of these, 375 patients had had CT scans as part of the diagnostic work-up for dementia. MAIN OUTCOME MEASURES: The presence of neuropathological evidence of Alzheimer's disease and the specific findings on CT scans. RESULTS: Of the 375 patients evaluated with a CT, 28% were misdiagnosed (lacked neuropathological evidence of Alzheimer's disease); of the 132 patients evaluated without a CT scan, only 18% were misdiagnosed (P less than 0.05). The degree of atrophy and other CT findings were similar in the correctly diagnosed and misdiagnosed groups except for increased ventricular size in the correctly diagnosed patients (P less than 0.05). CONCLUSION: Although CT scans do not usually contribute to the recognition of Alzheimer's disease, the presence of ventricular enlargement may help distinguish Alzheimer's disease from other dementias.

Aged↗
PubMed1992

Risk factors in Alzheimer's disease: a clinicopathologic study.

We investigated potential risk factors for Alzheimer's disease (AD) in a clinicopathologic study of 407 patients with definite AD, 100 non-Alzheimer dementia patients, and 50 normal subjects. The AD patients had more first-degree relatives with dementia than the non-AD dementia group (odds ratio of 1.85, 95% confidence interval of 1.07-3.20) or the normal elderly (odds ratio of 3.60, 95% confidence interval of 1.50-8.64) but did not have significantly more head injuries, medical and psychiatric illnesses, or relatives with Down's syndrome. The AD patients with a family history of dementia had their dementia at a later age than those without an affected relative. These findings indicate a familial risk for AD that is greater than for other dementing illnesses and has age-related penetrance. This study does not support other putative risk factors for AD such as head trauma and familial Down's syndrome.

Aged↗
PubMed1990

Dementia lacking distinctive histologic features: a common non-Alzheimer degenerative dementia.

From a series of 460 dementia patients referred to a regional brain bank, 14 (3%) patients had a pathologic diagnosis of primary degeneration of the brain involving multiple sites (frontoparietal cortex, striatum, medial thalamus, substantia nigra, and hypoglossal nucleus), with cell loss and astrocytosis. There were no neuronal inclusions and essentially no senile plaques. This entity, which we have termed "dementia lacking distinctive histology" (DLDH), presented with memory loss and personality changes, and led to death, usually within 2 to 7 years. Dysarthria and dysphagia were prominent in the later phases of the illness in most patients. The psychometric findings of some of the patients were consistent with a "frontal" lobe dementia. A few patients had prominent caudate atrophy on CT as well as neuropathologically. Eight of our patients had positive family histories for neurologic disease, mainly dementia. DLDH, in addition to Pick's disease, is a major member of the frontal-lobe dementia group. In patients under age 70 years, the frontal lobe dementias represent an important diagnostic consideration.

Aged↗
PubMed1988

The coexistence and differentiation of late onset Huntington's disease and Alzheimer's disease. A case report and review of the literature.

The case report presented is clinically compatible with late onset HD. The diagnosis was initially obscured by a lack of family history due to the early death of both parents and siblings. The presence of symptoms at the age of 59 in one offspring is consistent with the intrafamilial transmission of late onset HD disease. The early neuropsychometric data were consistent with the cognitive changes of HD, particularly with the loss of higher cognitive functions, memory and the relative decline in the performance IQ with the preservation of language skills. The psychiatric symptoms of emotional lability and apathy were also congruent with the diagnosis of HD. The atypical features of this patient's course, including progressively severe dementia, seizures and rigidity, may have provided clinical clues to the coexistence of both AD and HD. The absence of caudate atrophy on serial CT scans in this patient, although inconsistent with the gross findings reported on postmortem exam, perhaps could be explained by the 3 1/2-year interval between the last CT scan and death. Further, it has been noted previously that pathological changes tend to lag behind the clinical manifestations of the disease. The pathologic findings on autopsy were confirmatory for the presence of both AD and HD in this patient. Genetic counseling for this family is now most appropriate.

Age Factors↗
PubMed1987

Pick's disease. Clinical genetics and natural history.

The relatives of 18 probands with neuropathologic evidence of Pick's disease were assessed with the main aim of estimating their risk for dementing illness. Fifteen secondary cases of dementia were discovered among relatives. The risks were significantly greater for probands' first-degree relatives than for second-degree relatives, which suggests an etiologic contribution from genes. Although numbers are small, the distribution of cases and their ages at onset are consistent in suggesting a sex effect, with male subjects more at risk than female subjects.

Adult↗
PubMed1985

Dementia without Alzheimer pathology.

We studied five demented patients who, on neuropathologic examination, had cell loss and Lewy bodies in substantia nigra and locus ceruleus and few Alzheimer-type changes. The nucleus basalis had minimal cell loss in three patients and was not available in two. The lesions in the substantia nigra and locus ceruleus were unlikely to account for the dementia, and other structural or biochemical derangements, probably cortical but possibly subcortical, must also have been present but not visible at the light microscopic level.

Aged↗
PubMed1984

Tuberous sclerosis: a review for the neurosurgeon.

The clinical, radiological, and pathological characteristics of tuberous sclerosis are reviewed. Neurosurgical intervention in the syndrome is discussed in light of two recently treated cases and a literature review.

Adolescent↗
PubMed1984

Brain damage in profound hypothermia. Perfusion versus circulatory arrest.

To investigate brain changes in induced deep core hypothermia (18 degrees C) with or without circulatory arrest, four groups of dogs were subjected to cardiopulmonary bypass (CPB) under the following conditions: (1) differential head perfusion with pulsatile flow and simultaneous circulatory arrest to the rest of the body; (2) differential perfusion to the head with a nonpulsatile flow; (3) total circulatory arrest; and (4) continuous hypothermic perfusion. Parameters analyzed were: (1) blood flow distribution; (2) creatine kinase isoenzyme (CK-BB) elevation in the cerebrospinal fluid (CSF) and in the brain venous return; and (3) microscopy of the brain in animals killed at 30 minutes, 24 and 48 hours, 1 and 2 weeks, and 1 month. Although minor brain tissue flow differences were found at 37 degrees C among the groups, flows equalized at 18 degrees C. A significant seven-fold brain flow increase followed the period of circulatory arrest in Group III. Rise of CK-BB levels occurred in brain venous return but not in CSF in all groups. Microscopic cellular damage appeared in all groups with an equal degree of severity, regardless of the method of hypothermia and perfusion implemented.

Animals↗
PubMed1983

Warburg syndrome: lethal neurodysplasia with autosomal recessive inheritance.

Warburg syndrome is a recently recognized autosomal recessive neurodysplasia characterized by ventricular dilation, agyria, disorganized cortical cytoarchitecture, and dysgenesis of multiple other central nervous system structures. Because the disorder is lethal, with a 25% recurrence risk, it is crucial to distinguish Warburg syndrome from nonheritable phenocopies (caused by infectious agents and other teratogens) as well as from genetic disorders with a better prognosis. The clinical presentation of a markedly depressed newborn infant with hydrocephalus or ocular anomalies should suggest the diagnosis; computed tomography may be useful to demonstrate agyria as well as ventricular dilation. However, the distinctive neuropathologic finding of absent cerebral cortical lamination associated with numerous heterotopias appears to be diagnostic. Thus brain biopsy should be considered, especially at the time of ventricular shunting, whenever the clinical presentation suggests Warburg syndrome.

Abnormalities, Multiple↗
PubMed1983

Aberrant peripheral nerves and microneuromas in otherwise normal medullas.

The occurrence of aberrant peripheral nerve (PN) fibers in otherwise normal medullas was studied in 1,016 consecutively autopsied patients. Fine, myelinated PN fibers occurred as small parallel bundles or microneuromas about arteries and arterioles exclusively in the dorsal half of the medulla. They were more common in male than female patients, but were not related to any specific systemic disease process. The PN lesions were not found in patients under 20 years of age, but were observed in 1.5, 9.6, and 16.4% of those patients 20-49, 50-69, and 70-89 years of age, respectively. We regard these lesions as aberrant nerve fibers regenerated from cranial nerve roots rather than normally developed vascular nerves. We postulate that cranial nerve roots are subject to shearing or compression by strenuous motion of the neck in the course of ordinary activities and that the nerve fibers thus severed regenerate and grow into the pia-arachnoid and perivascular spaces to form the PN lesions. These PN lesions may become exaggerated under various abnormal circumstances such as overt traumatic injury and long-standing diseases affecting the medulla or cranial nerve roots.

Adolescent↗
PubMed1982

Age at onset of Pick's and Alzheimer's dementia: implications for diagnosis and research.

The ages at onset of illness for 39 cases of Pick's and 201 cases of Alzheimer's dementia from two series of unselected cases are presented and analyzed. The frequency of Pick's disease peaks in the sixth decade of life and then decreases, whereas Alzheimer's dementia increases steadily through adult life. At least to age 70 years Pick's and other disorders that cannot reliably be separated from Alzheimer's dementia except by autopsy comprise a significant proportion of dementias. Neuropathological diagnoses are essential for most research in dementing illnesses.

Adult↗