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P Cervera

Publications and source records attributed to P Cervera.

At least 19 recordsLinked to original sources
PubMed1992

Alzheimer's disease: is the decrease of the cholinergic innervation of the hippocampus related to intrinsic hippocampal pathology?

Consistent findings in the hippocampi of patients with Alzheimer's disease are the presence of neurofibrillary tangles in pyramidal neurons and the loss of choline acetyltransferase activity due to degeneration of hippocampal cholinergic terminals. The present study sought to clarify, in the brains of five patients with Alzheimer's disease and four controls, whether the loss of cholinergic terminals in the hippocampal stratum pyramidale in Alzheimer's disease is related to degenerative changes in hippocampal pyramidal cells. A polyclonal antibody to human choline acetyltransferase was employed to visualize immunohistochemically cholinergic terminals. Hippocampal neurons were stained with Cresyl Violet, neurofibrillary tangles with thioflavin S and a monoclonal antibody against phosphorylated neurofilament (RT97). Quantification of the stained structures was performed in CA4, CA1 and the subiculum, on five sections selected from the entire anteroposterior extent of each hippocampus. In the group of Alzheimer patients, the densities of cholinergic terminals were homogeneously diminished in the three hippocampal subregions in comparison with the controls (32-33%). In contrast, a significant loss of pyramidal neurons was found only in CA1, and the density of neurofibrillary tangles was markedly increased only in CA1 and the subiculum in Alzheimer's disease. These findings suggest that there is no relationship between the loss of cholinergic terminals and the degeneration of pyramidal cells in the hippocampus of patients with Alzheimer's disease.

Aged↗
PubMed1992

Cerebral palsy in twins.

Eighty-six children with cerebral palsy (CP) born as a product of twin pregnancies were studied. Data regarding their co-twins were also gathered. The authors' findings suggest that (1) monozygotic twins have a higher risk of CP than dizygotic twins, (2) twin order at birth does not seem to be a relevant factor in the etiology of CP, (3) mothers less than 24 or more than 34 years of age had the highest incidence of children with CP as a product of a twin pregnancy, and (4) the data do not support a genetic basis for the disease.

Birth Order↗
PubMed1992

[Oligodendroglial inclusions, a marker of multisystemic atrophies].

Nine cases of multiple system atrophy and 1 case of autosomal dominant olivopontocerebellar atrophy (neuropathological diagnosis) were retrospectively examined for the presence of oligodendroglial inclusions. Clinical diagnosis in the first 9 cases had been: olivopontocerebellar atrophy (3 cases), atypical Parkinson's disease (2 cases), Shy-Drager syndrome (2 cases) and multiple system atrophy (1 case); one of the patients could not be included in any of the above mentioned groups. The oligodendroglial inclusions were argyrophilic and located in the cytoplasm around the nucleus. They were revealed by Bodian's method in all cases of multiple system atrophy. They were not found in the case of autosomal dominant olivopontocerebellar atrophy. They were labelled by anti-ubiquitin antibodies, and were negative with anti-tau antibodies. At electron microscopy, they consisted of rectilinear profiles coated with a fuzzy material (diameter: 20-33 nm); this aspect was compatible with microtubules. Oligodendroglial inclusions were prominent in regions selectively vulnerable in multiple system atrophy (tegmentum pontis, putamen, inferior olives, substantia nigra and cerebellar white matter), even in those areas where neuronal loss or fascicular atrophy were minimal or absent. They were also observed in regions considered to be spared in multiple system atrophy, such as the motor cortex and the corpus callosum. Argyrophilic oligodendroglial inclusions are an early and specific marker of multiple system atrophy. It is suggested that autosomal dominant olivopontocerebellar atrophy lacking oligodendroglial inclusions does not belong to multiple system atrophy.

Adult↗
PubMed1991

Differential vulnerability of cholinergic projections to the mediodorsal nucleus of the thalamus in senile dementia of Alzheimer type and progressive supranuclear palsy.

The cholinergic innervation of the mediodorsal nucleus of the thalamus, which is thought to originate primarily in the laterodorsal tegmental nucleus and the substantia innominata, was studied by acetylcholinesterase histochemistry and immunohistochemistry with a polyclonal antiserum against human choline acetyltransferase on autopsy tissue from eight control subjects, five patients with progressive supranuclear palsy and four patients with senile dementia of Alzheimer type. In controls, cholinergic innervation of the mediodorsal nucleus of the thalamus was distributed heterogeneously in densely labelled patches surrounded by less heavily stained matrix. In patients with progressive supranuclear palsy, the density of choline acetyltransferase-positive varicosities decreased by 75% in the matrix and 60% in the patches. The number of choline acetyltransferase-positive cell bodies decreased by 84% in the laterodorsal tegmental nucleus, but more moderately (-33%) in the substantia innominata. In patients with senile dementia of Alzheimer type, choline acetyltransferase-positive varicosities decreased by 34% in the matrix, but 46% in the patches. Choline acetyltransferase-labelled cell bodies were spared in the laterodorsal tegmental nucleus, whereas severe loss (-80%) was observed in the substantia innominata. These results suggest that cholinergic innervation of mediodorsal nucleus matrix derives mainly from the laterodorsal tegmental nucleus and mediodorsal nucleus patches from the substantia innominata. Differential loss of innervation to the matrix and patches in progressive supranuclear palsy and senile dementia of Alzheimer type may in turn differentially affect mediodorsal nucleus innervation of the frontal cortex, resulting in dissimilar symptomatologies.

Acetylcholinesterase↗
PubMed1991

Progressive supranuclear palsy: loss of choline-acetyltransferase-like immunoreactive neurons in the pontine reticular formation.

We performed a quantitative immunocytochemical study using a polyclonal antibody directed against choline acetyltransferase (ChAT) in the lower pontine reticular formation in four control subjects and three patients with progressive supranuclear palsy (PSP). In the normal brains, there was detectable ChAT-like immunoreactivity in the nucleus papillioformis, a precerebellar reticular nucleus, and in the nucleus pontis centralis caudalis. In PSP patients, the mean estimated total number of ChAT-like immunoreactive cells was 54% of controls in nucleus papillioformis and 40% of controls in nucleus pontis centralis caudalis. The demonstration of ChAT-like immunoreactivity in nucleus papillioformis is consistent with studies suggesting an extrinsic cholinergic innervation of the cerebellar cortex. Loss of cholinergic cells in nucleus pontis centralis caudalis that corresponds largely to the paramedian pontine reticular formation may be related to disturbances of horizontal saccades in PSP patients.

Aged↗
PubMed1990

Constant neurofibrillary changes in the neocortex in progressive supranuclear palsy. Basic differences with Alzheimer's disease and aging.

Neocortical neurofibrillary tangles (NFT) revealed by Bodian technique and anti-tau immunolabelling were seen in 5/5 cases of progressive supranuclear palsy (PSP) aged 58-76 years. These lesions differed from Alzheimer's disease or age-related changes: (1) they were most frequent in the precentral gyrus (Brodmann's area 4) whereas associative areas are predominantly lesioned in Alzheimer's disease; (2) they affected mainly large pyramidal neurons and small cells, relatively sparing the cell population selectively involved in Alzheimer's disease; (3) they predominated in layers V and VI of area 4, whereas NFT are most dense in layers III and V in Alzheimer's disease; (4) mature senile plaques (1/5 cases) and beta-amyloid diffuse deposits (3/5 cases), which usually precede or go together with NFT in Alzheimer's disease were rare or absent (2/5) in PSP. Neuropil threads and tufts of abnormal fibres were also seen. In addition, NFT and neuropil threads were found in the hippocampus. PSP is thus another example of abnormal storage of tau developing in the neocortex in the absence of beta-amyloid deposits. It might prove a useful model for the understanding of the mechanisms of localization and spreading of tau storage in the brain.

Aged↗
PubMed1990

Tyrosine hydroxylase-like immunoreactivity in senile plaques is not related to the density of tyrosine hydroxylase-positive fibers in patients with Alzheimer's disease.

The numbers of silver-stained senile plaques and plaques containing tyrosine hydroxylase (TH)-like immunoreactivity were counted in the neocortex, amygdala and hippocampus of control subjects and patients with Alzheimer's disease, and compared with the density of TH-positive nerve fibers. The number of silver-stained senile plaques was lowest in the hippocampus and highest in the amygdala, and increased in all three structures in relation to the degree of dementia in the patients. A small proportion of plaques in the hippocampus of the most demented subjects and a large proportion of plaques in the amygdala were TH-positive. No TH-like immunoreactivity was found in plaques in the neocortex, although this structure contained almost as many silver-stained senile plaques and was as densely innervated by TH-positive fibers as the amygdala. The number of plaques containing TH-like immunoreactivity was, therefore, not proportional to the innervation of the structures by TH-positive fibers, nor to the total number of plaques in the structure, suggesting that the dissociation between the proportion of TH-positive plaques in the amygdala and neocortex may be due to differences in the populations of TH-positive fibers innervating the structures.

Aged↗
PubMed1990

Piroxicam-induced photosensitivity and contact sensitivity to thiosalicylic acid.

A photocontact dermatitis developed in three patients after the application of gel containing 0.5% piroxicam. Patch tests were positive to thiomersal and thiosalicylic acid. Photopatch tests with piroxicam at several concentrations were positive in the three patients but negative in 62 normal volunteer subjects. Patch tests performed on 14 patients with proved systemic photosensitivity to piroxicam were positive for thiomersal and thiosalicylic acid. Nine of 12 patients previously sensitized to thiosalicylic acid and with no history of exposure to piroxicam showed positive photopatch test reactions to this chemical. These results support a relation between piroxicam-induced photosensitivity and contact sensitivity to thiosalicylic acid. Contact allergic sensitivity to the latter is a marker for patients with a high risk of developing photosensitivity reactions to piroxicam. These reactions may be due to photoproducts of the drug rather than metabolites.

Adult↗
PubMed1990

Catecholaminergic systems in the medulla oblongata in parkinsonian syndromes: a quantitative immunohistochemical study in Parkinson's disease, progressive supranuclear palsy, and striatonigral degeneration.

We investigated tyrosine-hydroxylase (TH)-immunoreactive neurons in the medulla oblongata corresponding to the A1 and A2 cell groups in autopsy tissue of patients with Parkinson's disease (PD) (n = 3), progressive supranuclear palsy (PSP) (n = 3), striatonigral degeneration (SND) (n = 2), and in controls (n = 4). The estimated total number of TH-positive neurons in the A1 and the A2 regions was normal in PD and PSP patients. The sparing of medullary catecholaminergic cells in PD and PSP may be related to their minor degree of melanization and the possibility that intermediate compounds associated with the oxidative catabolism of norepinephrine and epinephrine may be less cytotoxic than those generated by degradation of dopamine. Patients with SND showed a marked loss of TH-immunoreactive cells in the A1 and the A2 groups, which may contribute to the impairment of vasomotor control characteristic of the disease.

Aged↗
PubMed1989

Distribution of monoaminergic, cholinergic, and GABAergic markers in the human cerebral cortex.

Mapping of a number of biochemical markers for noradrenergic, dopaminergic, serotoninergic, cholinergic and GABAergic systems was undertaken in 93 samples removed from the human cerebral cortex. The right hemisphere of brains from two subjects with no known history of neurological and psychiatric diseases was examined. Neurotransmitter markers were present in all cortical samples analysed, suggesting a widespread distribution of the corresponding neurons throughout the cerebral cortex. Each marker distributed heterogeneously in a distinct pattern. Noradrenaline concentrations were highest in the frontoparietal region and lowest in prefrontal and occipital areas. Markers for dopaminergic neurons (dopamine levels, dopamine/noradrenaline ratio and homovanillic acid levels) seemed denser in the prefrontal and temporal regions. 5-Hydroxyindolacetic acid levels were particularly high in the occipital area and decreased along the caudorostral axis. Choline acetyltransferase activity was highest in temporal and frontal lobes, at variance with muscarinic receptor distribution, which was highest in occipital cortex. Glutamate decarboxylase activity, an index of GABAergic innervation, did not vary markedly among the different areas of the cerebral cortex. The different biochemical markers investigated were detected in all cerebral cortical regions; their distribution was not homogeneous. A mismatch was observed between the distribution of cholinergic neuronal systems and receptors.

Aged↗
PubMed1989

Choline acetyltransferase-like immunoreactivity in the hippocampal formation of control subjects and patients with Alzheimer's disease.

A qualitative and quantitative immunohistochemical study of cholinergic systems in the human hippocampal formation was performed with an antibody against choline acetyltransferase. Four control subjects and six patients with Alzheimer's disease, matched for age and post-mortem delay, were examined. Immunoreactive nerve fibres and terminals were visualized, but no cholinergic cell bodies were seen. The distribution of the fibres and terminals suggests that a major afferent cholinergic pathway enters the hippocampus dorsally via the fimbria-fornix, a minor input entering from the temporal lobe along the alvear path. The cholinergic innervation suffers some degenerative change in normal aged subjects, but decreases considerably in density in patients with Alzheimer's disease. The extent of the decrease differs somewhat among the subregions of the hippocampus, but is homogeneously distributed within each subregion, and throughout the rostrocaudal extent of the structure. Compensatory sprouting in reaction to denervation was not detected.

Aged↗
PubMed1989

Selective loss of cholinergic neurons in the ventral striatum of patients with Alzheimer disease.

Cholinergic neurons were studied by immunohistochemistry with an antiserum against human choline acetyltransferase in the caudate nucleus, putamen, and ventral striatum (including the nucleus accumbens) of three patients with Alzheimer disease and three control subjects. Immunoreactive cell bodies were mapped and counted. In the ventral striatum of patients with Alzheimer disease, a 60% decrease in the number of cholinergic neurons was observed, whereas in the caudate nucleus and putamen values for control subjects and patients were similar. To determine whether all neurons in the ventral striatum were affected, neuropeptide Y-containing neurons were also immunostained, mapped, and counted. The number of these neurons was the same in control subjects and patients with Alzheimer disease, indicating that neuronal loss is not generalized in the ventral striatum and may be specific to the cholinergic population.

Acetylcholinesterase↗
PubMed1988

[Cerebral cysticercosis: imaging, serology, treatment and evolution. Apropos of 2 cases].

The authors present two cases of neurocysticercosis diagnosed both by serology and medical imaging (computed tomographic scan and magnetic resonance imaging). The first patient had a mixed form with localization of the parasites in the different anatomic parts. He developed suddenly a severe encephalitis which growth has been quickly fatal in spite of a prompt praziquantel and corticosteroids treatment. The second patient had a parenchymal form, and the same treatment was very effective.

Adolescent↗