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Biomedical subjects

C Duyckaerts

Publications and source records attributed to C Duyckaerts.

At least 109 records · Page 6Linked to original sources
PubMed1994

Dementia in two histologically confirmed cases of multiple sclerosis: one case with isolated dementia and one case associated with psychiatric symptoms.

During the past 10 years, considerable attention has been devoted to cognitive impairment in multiple sclerosis. Occasionally this impairment may be so severe that multiple sclerosis presents as a dementia associated with only minor neurological signs and symptoms. The cases of two women affected by multiple sclerosis who presented with a pure dementia are reported. In the first patient, a progressive apragmatic behavioural disturbance with reduced short term memory and learning abilities were the main clinical features. Neuropathological examination of the brain disclosed numerous plaques in the periventricular white matter, with severe atrophy of the corpus callosum. Plaques were also seen in the white matter of both hippocampus and in the columns of the fornix. The impairment of short term memory could be linked to these lesions. Behavioural changes were probably related to the bilateral lesions of the long associative bundles that disconnected the frontal lobes from other parts of the cerebral hemispheres. In the second patient, visual hallucinations were associated with cognitive dysfunction. MRI showed large plaques in the white matter of both left frontal and temporal lobes. Smaller plaques were also present in the periventricular white matter of the occipital lobes, the nature of which were confirmed by a stereotactic biopsy.

Adult↗
PubMed1994

Role of pontine nuclei damage in smooth pursuit impairment of progressive supranuclear palsy: a clinical-pathologic study.

We performed a quantitative study of the pontine nuclei in the basis pontis and a semiquantitative study of extrapontine structures involved in smooth pursuit in four patients with severe impairment of horizontal smooth pursuit and histopathologically confirmed diagnosis of progressive supranuclear palsy (PSP). There were only slight changes in the extrapontine structures involved in smooth pursuit, but there was a significant neuronal loss--massive in three patients and mild in one patient--in all nuclei of the basis pontis. Our results suggest that degenerative lesions affecting the pontine nuclei are largely responsible for the horizontal smooth pursuit impairment in PSP.

Aged↗
PubMed1994

[Neuropathology of 20 centenarians. I. Clinical data].

We report a clinical study of 20 patients aged more than 100 years, and deceased in Charles Foix Hospital, Ivry/Seine, France, where they had stayed for 10 days to 16 years (mean: 3.3 years, median: 4 years). Each of them was studied neuropathologically (the results of this study will be published later on). The case selection excluded only those patients whose neuropathological study could not be complete. The prevalence of sensorial deficits was high: 15/20 patients had deterioration of hearing, 8 of them were deaf; 14/20 patients had deterioration of sight, 4 of them were blind. Motor deficits were numerous: 15 patients were not ambulatory. The patients were classified as demented or not, according to the criteria of the DSMIII R (American Psychiatric Association 1987), on the basis of a retrospective evaluation of clinical records, and of an inquiry among the caring staff. Their mental status was also evaluated by the Global Deterioration Scale of Reisberg et al (1985). Five patients had been demented, four had been intellectually normal, and 11 had suffered from mild disturbances of memory or cognitive functions. This series was not representative of the general population of centenarians, but probably of those institutionalized in France. We observed a low proportion of demented patients despite the prevalence expected from epidemiological studies. This is difficult to interpret. The low proportion of dementia in this small sample is not due to the short duration of the course of diseases responsible for dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Low affinity nerve growth factor receptor, adrenal transplant and Parkinson's disease.

Immunohistochemistry of low-affinity nerve growth factor receptor (LNGFR) was performed postmortem in the striatum and the adrenal gland of a parkinsonian patient with an adrenal to brain transplantation. Few LNGFR-positive fibers were observed in the necrotic graft. By contrast numerous immunostained fibers were detected in a restricted zone of the host striatum adjacent to the graft, corresponding to a selective zone of sprouting of tyrosine hydroxylase-positive fibers. This suggests that nerve growth factor or related growth factors may promote sprouting of catecholaminergic fibers in the host striatum.

Adrenal Medulla↗
PubMed1993

Heterogeneity and selectivity of the degeneration of cholinergic neurons in the basal forebrain of patients with Alzheimer's disease.

Cholinergic neurons were studied by immunohistochemistry, with an antiserum against choline acetyltransferase (ChAT), in the basal forebrain (Ch1 to Ch4) of four patients with Alzheimer's disease (AD) and four control subjects. ChAT-positive cell bodies were mapped and counted in Ch1 (medial septal nucleus), Ch2 (vertical nucleus of the diagonal band), Ch3 (horizontal nucleus of the diagonal band) and Ch4 (nucleus basalis of Meynert). Compared to controls, the number of cholinergic neurons in AD patients was reduced by 50% on average. The interindividual variations in cholinergic cell loss were high, neuronal loss ranging from moderate (27%) to severe (63%). Despite the small number of brains studied, a significant correlation was found between the cholinergic cell loss and the degree of intellectual impairment. To determine the selectivity of cholinergic neuronal loss in the basal forebrain of AD patients, NPY-immunoreactive neurons were also investigated. The number of NPY-positive cell bodies was the same in controls and AD patients. The results (1) confirm cholinergic neuron degeneration in the basal forebrain in AD and the relative sparing of these neurons in some patients, (2) indicate that degeneration of cholinergic neurons in the basal forebrain contributes to intellectual decline, and (3) show that, in AD, such cholinergic cell loss is selective, since NPY-positive neurons are preserved in the basal forebrain.

Aged↗
PubMed1993

Alterations of glial fibrillary acidic protein mRNA level in the aging brain and in senile dementia of the Alzheimer type.

The GFAP mRNA levels were compared to the density of the senile plaques (SP) in postmortem brain samples of 8 cases, either non-demented or affected by senile dementia of the Alzheimer type. In the frontal neocortex, the GFAP mRNA level is not affected, even if SP are present. In the temporal neocortex, a positive correlation between GFAP mRNA level and SP density was highly significant. This shows that in this area, astrocytes are altered at transcriptional or post-transcriptional levels, or both. The different responses of this astrogliosis marker in each area may be related to the loss of specific neurotransmitter system.

Aged↗
PubMed1993

Two distinct ubiquitin immunoreactive senile plaques in Alzheimer's disease: relationship with the intellectual status in 29 cases.

The aim of this study was the analysis of the development of neurofibrillary tangles (NFT) and senile plaques (SP) during aging and senile dementia of the Alzheimer type. The lesions stained by ubiquitin, tau and beta A4 antibodies were studied in Brodmann's area 22 (superior temporal gyrus) in 29 cases. Samples were from a group of women over 75 years of age, psychometrically assessed and either normal or affected by Alzheimer's disease at various degrees of severity. NFT were less numerous when revealed by ubiquitin than by tau antibodies, suggesting that ubiquitin immunoreactivity appeared later in the course of the disease. Ubiquitin immunoreactive (IR) SP were made of clusters of IR neurites usually organized around a central amyloid core. Two types of ubiquitin-IR SP were designated. "Globular neurite SP" contained weakly immunostained globular neurites. They were densest in the least affected cases. However, they were not seen in every normal or lightly affected case, and were always present in the most affected ones. The density of these globular neurite SP was not significantly correlated with the severity of dementia, nor with the density of the lesions stained by tau antibodies (neuritic component of SP, NFT and neuropil threads) or by beta A4 antibodies (diffuse or dense deposits). The "curly neurite" type of SP contained curly neurites strongly immunostained by ubiquitin antibodies. They exhibited the highest density in the most affected cases, where they were always present. They were lacking in the least affected cases. They were always found together with the globular neurite SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Diffuse primary leptomeningeal gliomatosis.

A 38 year old patient developed multiple cranial nerve palsy, seizures and progressive alteration in consciousness. CSF examination revealed tumor cells and a tentative diagnosis of leptomeningeal carcinomatosis from an unknown primary tumor was made. Treatment with intrathecal methotrexate and cranial radiation therapy was started without effect. At autopsy widespread leptomeningeal gliomatosis originating from a previously unknown astrocytoma of the hippocampus was found.

Adult↗
PubMed1993

Oligodendroglial and neuronal inclusions in multiple system atrophy.

Argyrophilic cytoplasmic inclusions of oligodendrocytes have been described in cases of multiple system atrophy (olivopontocerebellar atrophy, striatonigral degeneration, and Shy-Drager syndrome). The oligodendroglial cytoplasmic inclusions are immunolabeled with antiubiquitin antibodies. Ultrastructurally, they appear as granule-associated filaments. They have not been found in other neurological diseases or in normal brains, and are now considered to be early and specific markers of multiple system atrophy. More recently, similar argyrophilic inclusion bodies have been reported in the cytoplasm of neurons and in both oligodendroglial and neuronal nuclei of multiple system atrophy brains. Neuronal and oligodendroglial cytoplasmic inclusions have identical ultrastructural characteristics, but different antigenic properties. The chemical nature of the inclusions is presently unknown and their significance remains controversial: they could be a primary event in the course of the degenerative process or merely an epiphenomenon of some disordered cytoskeletal metabolism.

Corpus Striatum↗
PubMed1993

Alzheimer's lesions labelled by anti-ubiquitin antibodies: comparison with other staining techniques. A study of 15 cases with graded intellectual status in ageing and Alzheimer's disease.

We compared the densities of lesions immunolabeled with ubiquitin, tau and beta A4 antibodies and stained by various silver impregnations, with the intellectual status. The densities of senile plaques and neurofibrillary tangles labelled by anti-ubiquitin antibody were correlated with the Blessed test score. Ubiquitin-positive neurofibrillary tangles were less numerous than those labelled by Gallyas, anti-tau, Bodian's and Bielschowsky's methods. There were five times more beta A4 deposits than ubiquitin positive plaques. beta A4 deposits could be numerous in cases in which ubiquitin immunolabelling was entirely negative. Bielschowsky's method, silver methenamine and thioflavin S revealed more senile plaques than anti-ubiquitin, whereas anti-tau, Gallyas', Bodian's and Cross' techniques revealed similar numbers. Anti-ubiquitin positive lesions were correlated with the severity of dementia. Compared with other staining methods, sensitivity of anti-ubiquitin was weaker for neurofibrillary tangles than for senile plaques. These findings suggest that ubiquitin epitopes are linked to the neurofibrillary changes (in the perikaryon or within the senile plaques), and are absent from beta A4 deposits, either diffuse or compact.

Aged↗
PubMed1993

Infarcts in the middle cerebral artery territory. Pathological study of the mechanisms of death.

Correlates of the size of infarcts, the time from stroke to death, and the mechanisms of death were studied in 77 consecutive patients who died from infarction in the middle cerebral artery territory. The area of infarcts was assessed by planimetry on schemas of representative brain levels and the results were expressed as a ratio of infarcted area on the whole MCA territory. No clear relationship was found between the size of infarcts in the MCA territory, and any of the characteristics of the patients, but extensive infarcts were more frequent when the internal carotid artery was occluded. No evidence was found of an adverse effect of age, diabetes or initial hyperglycemia on the size of infarcts. The mechanisms of death were not linked to sex, age, high blood pressure, diabetes, blood glucose level at admission, presence and location of an arterial occlusion, or etiology of the infarct. On the contrary, they varied as a function of interval from stroke to death. Transtentorial herniation, the main cerebral cause of death, occurred mainly in the first week and was related to the large size of infarcts. Rare recurrences of stroke and frequent extracerebral mechanisms of death (mainly pneumonia, pulmonary embolism and cardiopathy) occurred later on.

Aged↗
PubMed1993

HIV-1-associated cognitive/motor complex: absence of neuronal loss in the cerebral neocortex.

We performed a postmortem morphometric study in six AIDS patients and six controls to determine if a neocortical neuronal loss occurs in HIV-1-associated cognitive/motor complex. Patients were selected during a prospective study including psychometric evaluation and neuroimaging, and none had focal lesions. Two had HIV-1-associated myelopathy with mild cognitive impairment, and four had HIV-1-associated dementia complex. Planimetry did not show any cerebral atrophy. Cortical thickness, mean neuronal size, and mean neuronal densities in Brodmann's areas 4, 9, and 40 were not statistically different in patients and controls. There were no significant changes in neuronal densities of columnar and laminar samples, indicating that there was neither global nor selective neuronal loss. HIV-1-associated cognitive/motor complex is not necessarily related to neocortical neuronal loss, but could be due to subcortical lesions or metabolic dysfunction.

Adult↗
PubMed1993

A brain bank in a neuropathology laboratory (with some emphasis on diagnostic criteria).

The Brain Bank of La Salpêtrière Hospital (Paris) is implanted in a neuropathology laboratory. It is multipurpose, prospective, and "free of charge" for the users. Protocols are prospectively established, in collaboration with the neuroscientists. One of our major difficulties in the collection of cases concerns presently the controls: the neurological status of patients coming from Neurology departments has usually been correctly assessed but those patients are bad controls. The normality of the neurological status of patients dying in other departments is difficult to assess retrospectively. A general autopsy is performed in each case. Several systematic sampling and fixation procedures are currently in use; their pros and cons are discussed. The main safety problem we are confronted with is the risk of HIV and Jakob-Creutzfeldt transmission. We try to standardize our diagnostic procedures; criteria used in Alzheimer's disease, Parkinson's disease, Huntington's chorea are briefly reviewed. We plan, in the future, to standardize our procedures for control cases. The Brain Bank has had a very positive impact on the way this neuropathology laboratory works: it introduced new techniques; on the other hand, the adequate processing and diagnosis of the samples was, in many aspects, simplified by the collaboration with the neuropathology department. The demand for human brain samples is steadily increasing in Neuroscience, for at least 2 reasons: 1. some diseases are specifically human and lack adequate animal models (Alzheimer's disease, multisystem atrophy), or animal models may appear irrelevant in some aspects (multiple sclerosis) or finally, results obtained in animal models may have to be confronted with human pathology (AIDS ...) 2. many aspects of human neuroanatomy can not be extrapolated from animal data There are many ways of organizing a brain bank and no golden standard (Swaab et al., 1989): the neuroscientist himself may collect the samples in a given pathology or the neuropathologists may modify their practice to provide adequate samples to the neuroscientists. When the neuroscientist himself collects his own samples, he obviously proceeds more rapidly. However, he is confronted with the difficult problem of the controls, which require both a clinical follow-up and a pathological check up of the tissues, both of which may be difficult to obtain in a research unit. In our opinion, the neuropathologists are the natural "brain bankers": they are indeed naturally "rich", their job being precisely to collect human samples, in connection with the clinicians.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain↗