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K A Jellinger

Publications and source records attributed to K A Jellinger.

At least 109 records · Page 6Linked to original sources
PubMed1995

Neurodegenerative disorders with extrapyramidal features--a neuropathological overview.

Although neuropathological examination is the "gold standard" for the diagnosis of neurodegenerative disorders with extrapyramidal features, difficulties may arise in the morphological differentiation of some of these disorders. They are all associated with major structural pathology within or directly affecting the basal ganglia and related neuronal loops. In addition to progressive neuronal loss and gliosis involving specific subcortico-cortical systems or multiple circuits, many of these disorders are characterized by intracellular neuronal and/or glial inclusions indicating cytoskeletal dysmetabolism that may serve as important diagnostic signposts, whereas in other disorders, e.g. Huntington's disease, pallidal or other multisystem degenerations, no such cytopathological hallmarks have been described. The neuropathological diagnostic criteria for the major neurodegenerative disorders with extrapyramidal features based on structural cytoskeletal features and morphological lesion patterns are reviewed, and the difficulties in nosological differentiation between some groups of disorders are discussed. Although current post mortem diagnostic criteria with additional clinical information are useful in the differentiation of these disorders, in view of many clinicopathological overlaps and the lack of in vivo markers, further standardization of criteria is warranted for their exact classification order to provide further insight into their pathophysiology and pathogenesis as a basis for future therapeutic strategies.

Basal Ganglia Diseases↗
PubMed1994

Neurofibrillary tangle predominant form of senile dementia of Alzheimer type: a rare subtype in very old subjects.

In a consecutive autopsy series of 580 demented elderly subjects, 256 with the clinical diagnosis of probable/possible Alzheimer's disease (AD), there were 10 cases aged between 80 and 99 years with moderate to severe dementia or confusional state in which neuropathological studies revealed abundant neurofibrillary tangles with predominant involvement of the allocortex (entorhinal region, subiculum, CA 1 sector of hippocampus, amygdala) but no or only very few senile plaques. Small numbers of diffuse deposits of beta A4 amyloid protein were present in the entorhinal cortex of 3 and in the isocortex of 5 brains, while neuritic plaques were totally absent. Only a few cases of this "senile dementia with tangles only" or, more correctly, "neurofibrillary predominant type of AD" corresponding to the limbic stage of neuritic AD pathology have been described in the literature. This rare subtype occurring in very old (over 80 years of age) subjects that does not fall within the currently used neuropathological criteria for diagnosis of AD warrants further clinico-pathological documentation.

Aged↗
PubMed1993

Neuropathological staging of Alzheimer lesions and intellectual status in Alzheimer's and Parkinson's disease patients.

In both Alzheimer's disease (AD) and Parkinson's disease (PD), neurofibrillary tangles (NFT), in contrast to amyloid deposits, show a hierarchical spreading pattern from the allocortex to isocortical association areas with early involvement of the entorhinal region, a major relay station between hippocampus and isocortex. Based on the distribution pattern of NFT in human brain, a neuropathological staging of neuritic AD pathology has been proposed. Comparative studies of this neuropathological staging of neuritic AD changes with psychometrically assessed intellectual status (mini-mental state) in prospective cohorts of 29 aged individuals and 28 PD patients showed a linear correlation of morphological AD staging with the psychostatus in both disorders. The pattern of neuronal degeneration associated with neuritic AD pathology in both AD and PD may be an important basis of cognitive decline in both disorders.

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PubMed1993

Pathological assessment of movement disorders: requirements for documentation in brain banks.

The general methodological requirements and principal morphologic hallmarks for the post mortem assessment of the major types of movement disorders are critically reviewed. These data may enable Brain Banks to classify movement disorders according to current clinicopathological diagnostic criteria. Comprehensive clinical assessment and accurate neuropathological examination using adequate methods are required for collection of and research on tissues from patients with movement disorders.

Brain Diseases↗
PubMed1992

Primary central nervous system lymphomas--an update.

Primary CNS lymphomas (PCNSL), until recently representing about 1% of all brain tumors, show dramatically increased incidence both in high-risk groups (immunocompromised, AIDS) and in the general population. They are extranodal diffuse non-Hodgkin's lymphomas, the morphology and classification of which are identical to those of systemic lymphomas, although PCNSL show different biological behavior and diagnosis according to the New Working Formulation and updated Kiel classification may be difficult. The majority are large B cell variants of high-grade malignancy; low-grade subtypes and T cell lymphomas are rare. Sixty per cent occur in the supratentorial space (hemispheres, periventricular) and 12% in the posterior fossa; 30% are multiple (50%-70% in AIDS). PCNSL show a male preponderance with a peak incidence in the 5th-7th decade (3rd-4th in AIDS). The duration of diffuse or focal clinical symptoms averages 1-2 months. Computed tomography and magnetic resonance imaging scans show single or multiple or diffuse, often typical lesions. Diagnosis is achieved by evaluation of stereotactic biopsy material or cerebrospinal fluid cytology using immunocytological markers. Current therapy in immunocompetent patients, radiation plus corticosteroids and pre- or postradiation polychemotherapy, shows response rates of 85% with a median survival of 17-44 months, a prognosis similar to that for glioblastoma. Meningeal PCNSL is treated with intrathecal methotrexate or cytosine arabinoside. Transliquoral seeding of PCNSL is frequent, distant metastases occurring in 6%-8%. Therapy of AIDS-related PCNSL makes use of radiation and corticosteroids, and rarely of chemotherapy. The pathogenesis of PCNSL is unknown, but Epstein-Barr virus may be a contributory factor.

Brain Neoplasms↗
PubMed1992

Clinico-pathological correlations in Parkinson's disease.

Based on comparative clinical and morphometric studies in 45 autopsy cases of Parkinson's disease (PD), 27 clinically presenting with akinesia and rigidity (AR-type), 18 with predominant resting tremor (T-type), the neurobiological basis of the major clinical subtypes in PD is discussed. The AR-type showed higher neuronal losses in locus coeruleus (LC) and in medial and lateral parts of substantia nigra (SNM, SNL), suggesting lesion patterns different from the T-type. More severe cell loss in the serotonergic dorsal raphe nucleus was observed in PD patients with depression than in non-depressed ones. Demented PD subjects showed higher cell loss in SNM than non-demented ones indicating dysfunction of the mesocortical dopamine system, and significantly more severe Alzheimer lesions in isocortex and hippocampus. These and other recent data from the literature indicate that some major clinical features of PD are related to lesions of distinct neuronal systems.

Aged↗
PubMed1992

Vascular dementia.

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Dementia, Vascular↗
PubMed1991

Pathology of Parkinson's disease. Changes other than the nigrostriatal pathway.

In Parkinson's disease (PD), in addition to degeneration of the nigrostriatal dopaminergic pathway, a variety of neuronal systems are involved, causing multiple neuromediator dysfunctions that account for the complex patterns of functional deficits. Degeneration affects the dopaminergic mesocorticolimbic system, the noradrenergic locus ceruleus (oral parts) and motor vagal nucleus, the serotonergic raphe nuclei, the cholinergic nucleus basalis of Meynert, pedunculopontine nucleus pars compacta, Westphal-Edinger nucleus, and many peptidergic brainstem nuclei. Cell losses in subcortical projection nuclei range from 30 to 90% of controls; they are more severe in depressed and demented PD patients. Most of the lesions are region-specific, affecting not all neurons containing a specific transmitter or harboring Lewy bodies. In contrast to Alzheimer's disease (AD), subcortical system lesions in Parkinson's disease appear not to be related to cortical pathology, suggesting independent or concomitant degeneration. The pathogenesis of multiple-system changes contributing to chemical pathology and clinical course of Parkinson's disease are unknown.

Acetylcholine↗
PubMedDate not supplied

Proposals for re-evaluation of current autopsy criteria for the diagnosis of Alzheimer's disease.

Defining criteria for the postmortem diagnosis of Alzheimer's disease (AD) has proven difficult due to the phenotypical heterogeneity of the disease, the absence of a specific disease marker and an overlap of AD neuropathology with that observed in a number of nondemented aged individuals. Even though the role of plaques and tangles in the pathogenesis of AD remains undetermined, a host of clinicopathological correlative studies have shown that both lesions, if present in sufficient numbers-particularly in the neocortex-are still to be considered the best morphological signposts for the disease. All currently used criteria for the neuropathologic diagnosis of AD have some weaknesses and need to be reestablished and revalidated. Multivariant analysis in a personal autopsy series of elderly subjects revealed significant correlations between psychostatus and both the CERAD criteria and Braak staging of neuritic Alzheimer-type lesions, and less concordance with the National Institutes of Aging and Tierney criteria. We propose a set of histopathologic diagnostic criteria for both definite and preclinical AD that rely on various constellations of both different types of plaques, except diffuse amyloid deposits, and neurofibrillary tangles, in allocortical and isocortical areas considering their topographic pattern. This set of criteria encompasses phenotypic variations of the pathology and takes into account the chronic, progressive course of AD. It allows the detection of preclinical disease in subjects in whom dementia is not reported and includes those cases in the morphological gray zone between "normal" aging and full-fledged AD that practicing neuropathologists consider the most problematic. The set of criteria includes guidelines concerning tissue sampling and processing, and standardized staining methods that should allow neurologists to minimize interrater and interlaboratory variability in the assessment of morphologic lesions and the diagnosis of AD.

Aged↗