PubMed Health⌕ Search

Biomedical subjects

J Plas

Publications and source records attributed to J Plas.

35 records · Page 2Linked to original sources
PubMed1985

[Neuropathology of amnesic syndromes in man].

Controversies exist about the type of lesions observed in Korsakoff's syndrome or amnestic syndromes. A review of clinicopathologic data in the literature and findings in a personal series of 31 patients with amnestic syndromes (14 with alcoholism and nutritional deficiency, 8 with tumors including 2 with craniopharyngiomas, 5 with Pick's disease and presbyophrenic manifestations, 2 with vascular affections and one each with anoxia and herpetic encephalitis) were used to determine most frequently responsible lesions. Although it is generally accepted that there must be bilateral lesions divergent opinions are found with regard to the significance of limbic-hippocampomammillary circuit lesions. Some authors refute any specific role for the limbic circuit, and particularly any part played by Ammon's horn, in favor of a role for the temporal isthmus while others reject the possible role of the mammillary bodies and implicate the dorsomedian nucleus of the thalamus. The present study confirmed the importance of the limbic-hippocampomammillocingulus circuit in the maintenance of long-term memory. Involvement of the hippocampus appears obvious, particularly in disorders due to lesions of the subiculum and sommer's field. Mammillary body lesions are a constant finding in amnestic syndromes due to alcoholic nutritional deficiency and may also be present in Korsakoff's syndromes of tumoral origin e.g. a compression due to a craniopharyngioma. The rarely mentioned lesions of the cingular convolution are a further possible cause. The role of a thalamic lesion has not been totally confirmed, findings indicating equally frequent involvement of laterodorsal and dorsomedian nuclei. Clinical evidence, however, points to correlations between fabulation, false recognition and a thalamic lesion. The role of the fornix is debatable, although it is difficult to understand how destruction of the hippocampic formation or of the mammillary bodies can provoke memory disorders while an interruption in the structure that links them would have no consequences, unless it is admitted that as in animals other pathways exist that pass little or not at all through the fornix. Clinical expression of bilateral lesions of these structures differs according to whether they affect the posterior Ammon's horn region or lie more anteriorly in the trigonomammillothalamo-cingular complex. Clinical features of hippocampic amnesia include continuous anterograde amnesia with successive periods of forgetfulness, retrograde deficit of variable duration, parallel alterations of verbal and visuospatial memory and absence of fabulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Alcohol Amnestic Disorder↗
PubMed1985

[Cavitary orthochromatic leukodystrophy with oligodendroglial changes. A sporadic adult case].

A 39 year-old man with mild stable mental retardation, without family history, developed progressively a gait disturbance and intellectual deterioration. CT scan showed a low density of the periventricular hemispheric white matter which increased on subsequent examinations. Eight months before death he presented with several Grand Mal seizures. He died 29 months after the onset of the clinical disorders. Neuropathological studies included light and electron microscopy of a cerebral biopsy and a post-mortem examination of the brain. It showed a sudanophilic leukodystrophy with unusual features: cavitation of the white matter, oligodendrocyte proliferation and lamellar "fingerprint" dense cytoplasmic inclusions in the oligodendrocytes. Only 3 similar cases have been previously reported.

Adult↗
PubMed1980

[Association of Pick's disease and amyotrophic lateral sclerosis. Pathological study of one case and review of the literature (author's transl)].

An anatomoclinical case of Pick's Dementia secondarily complicated with Amyotrophic Lateral Sclerosis (A.L.S.) has been compared with twelve similar cases from the litterature. These comparisons drive to three hypotheses:--coincidence of two distinct diseases;--extension to motor cortex of the Pick's atrophy;--atypical onset of ALS outside of motor cortex, secondarily reaching the motor area. Against the last hypothesis, one could argue that, in "Pick's disease + ALS", there is no superficial spongiosis such as seen generally in ALS + Dementia in frontal or temporal cortex, or in ALS simplex in motor cortex. Also, there are marked focal lesions, i.e. in uncus hippocampi, similar to that of Pick's disease. However, if the second hypothesis seem to be the best one, there are actually no definite evidence for it.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

[Post-traumatic Korsakoff's syndrome: clinical and anatomical report].

Clinical and anatomical report of a post traumatic amnestic syndrome (Korsakoff's syndrome), associating anterograde amnesia persisting for fifteen years, with temporal disorientation, false recognitions, initially intense transitory confabulation and secondarily bursts of confabulation, intact remote memory and persistence of old learnings. Death after twelve years from mesenteric infarction. Anatomically, post-traumatic sequellae are limited to both cingulate gyri in their anterior part. This cingula involvement is easy to understand if one knows that post-traumatic Korsakoff's syndrome appears after severe cranial traumatisms, with at least three days of coma, and develops constantly, even if transitory, after long duration comas with 20 to 30 days of loss of consciousness. Anatomical explanation depends on the fact that Korsakoff's syndromes from various etiologies need, to be produced, a bilateral damage of the limbic circuit and that severe head traumatisms, when dying early in the evolution without possibility of a neuro-psychological investigation, have always a destruction of corpus callosum or cingulate gyri or both, resulting from crushing of these structures by the edge of the faulx cerebri. Consistent with these constatations, it is logical that a Korsakoff's syndrome develops after severe head traumas with bilateral lesions of the limbic circuit and especially of the cingulate gyri. But anatomical evidence remains rare, because early fatal evolution does not permit psychological evaluation and, reversely, long survivals who may die from another pathology would not have brain examination. We prefer the name of "Korsakoff's syndrome" rather than that of "amnesic syndrome" to denominate the anterograd amnesia (amnésie des faits récents) encountered in nutritional disorders due to B1 deficiency in true Korsakoff's disease, but also with other etiologies such as cerebral tumours, vascular cerebral disorders, post-commital anoxia, herpetic encephalopathy, head traumas, all of them developing amnesia for recent events, formerly classified under the title of "korsakowian syndrome" or "mental syndrome of Korsakoff" and more recently under the denomination of "amnesic syndrome". But whatever is the etiology of the memory disorder, the amnesic syndrome remains identical and the advanced small differences, such as euphoria in alcoholics or mood depression in tumours, are often fallacious, so that the only way of differentiation deals with accessory symptoms such as intracranial hypertension in tumours, sudden onset in vascular etiologies or polyneuritis in B1 deficiency. Post-traumatic Korsakoff's syndrome joins with this scheme, for its clinical aspect is so similar to that of nutritional disorders that it might be difficult to reach the exact diagnosis when an alcohol addict develops, after a head trauma, an amnesia which could be the consequence of the trauma but also of a nutritional disorder developed after the accident with inadequate parenteral treatment. Our case, which is the first well documented observation of this disease reported with long clinical survey and final pathological examination, was presented in 1981 at a joint meeting of the French and Dutch neurological societies. It gives the proof of the importance, in limbic circuit, of the cingulate gyri. A comparison is made with four other clinical cases of post traumatic amnestic syndrome with MNR procedures which show, for two of them, cingula lesions explaining the clinical features, for one of them a bilateral lesion of Ammon's homs and for the last one extra-limbic lesions, with destruction of the inferior part of both frontal lobes, associated with a possible deafferentation of the right cingula cortex.

Adult↗
PubMedDate not supplied

[A case report of mania precipitated by use of DHEA].

Dehydroepiandrosterone (DHEA) and its sulfate ester metabolite (DHEA-S) are precursors to testosterone and, to a lesser extent, to estrogen, and, for both sexes, they are produced in the adrenal cortex. They are among the most abundant steroids in the human body, yet their physiological roles remain unknown. DHEA and DHEA-S appear to have diverse biochemical activities, including actions within the central nervous system. So DHEA is produced in the central nervous system as well as the human adrenals and is present in the brain, concentrated in limbic regions, in levels much higher than other steroids. DHEA has been postulated to function as an excitory neuroregulator, antagonizing g-aminobutyric acid transmission. The main characteristic of DHEA is that its level of concentration in plasma varies throughout life, such level being low during the early childhood and after the age of 60 years. Adrenal production and serum concentrations of DHEA are then known to peak between ages 25 and 30 years and thereafter decrease with age, severe illness and chronic stress. The decrease of DHEA over time would appear to be responsible for morbidity related to aging process. Previous reports have found low levels of DHEA in association with physical and with frailty in the elderly (immunosenescence, increased incidence of osteoporosis, atherosclerosis and cancer, decreased cognitive functions and/or well-being). As it has been touted as a fountain of youth and a sexual tonic and promoted for a variety of illnesses associated with aging, DHEA is widely available over all the United States (since 1994) as a dietary supplement. In France, as a result of a massive advertising campaign, DHEA is already the subject of a widespread use and a growing demand although it has not yet been approved by the relevant authorities for sale as drug to the public. In practice, DHEA is prescribed and delivered under the sole responsibility of both doctor and chemist who ascertain the benefit-risk ratio and the quality of the product. DHEA may then be purchased on the internet or in the form of magistral preparations delivered on the basis of such prescription. Accordingly, there is little information or data on efficacy, drug interactions, results of long-term use, abrupt discontinuation or potential adverse effects related to the use of DHEA. We report a case of mania possibly precipitated by the use of high doses of DHEA (150-200 mg/day at the time of presentation) during several weeks in a 68 years old man who had already been hospitalized for an acute mania many years ago. Although, in this case, the patient suffered a bipolar diathesis in the past, oral DHEA may have played a role in the induction of his acute manic episode. Further research is required to assess the mood effects of DHEA, including its potential risk for patients with bipolar disorder.

Adult↗
PubMedDate not supplied

[Interaction between cotrimoxazole and antidepressive agents].

The association cotrimoxazole-tricyclic antidepressants seems to involve a rapid relapse of the depressive states continuously treated with the latter drugs. Five cases are reported. Mechanisms of this unknown drug interaction are discussed. The hypothesis of an enzymatic induction is not the most probable. A central inhibition of the tricyclic antidepressants seems to be possible but needs to be supported by further evidence.

Anti-Infective Agents↗
PubMedDate not supplied

[Lesions of the motor cortex in amyotrophic lateral sclerosis].

The lesions of the spinal cord and the medulla in ALS, have been known for a long time. However the existence of cortical lesions in this disease, and their description, remain debated questions. This study deals with ten anatomical cases of ALS, with a special attention to the precentral gyrus. Three kinds of lesions are described in most cases: a disappearance of Betz cells with shrinkage and ghost cells of some other neurons; principally a subcortical gliosis, and also a laminar spongiosis located in the second cortical layer. The value and the signification of these lesions, which are strictly located in the motor cortex, are discussed. This could be compared to diffuse cortical lesions which are described in some cases of ALS with dementia state.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

[Alzheimer's disease and Meynert's nucleus basalis. An anatomo- clinical point of view].

The existence of a lesion in the nucleus basalis (NbM), in Alzheimer's disease, which has been brought up again by Whitehouse et al. (1981), is not doubted anymore. The lesion is correlated with the disease's cholinergic deficit. The histology of the lesion isn't much described, and its importance not very clear. This study compares ten cases of Alzheimer's disease, and six cases of "senile dementia". A cellular count and a histologic observation of the NbM are done on slides imbedded in paraffin. The cortex is studied in the classical way. There are neuro-fibrillary tangles "en boules" in the NbM of the two types of dementia, but more frequently in Alzheimer's disease. No senile plaques are observed. The neuronal loss appears much more important in the group of Alzheimer's disease than in the senile dementias. But a typical clinical and histological case of Alzheimer's disease did not show neuronal loss in the NbM. The final results invite to further discussions concerning the present knowledge of Alzheimer's disease and senile dementia.

Aged↗
PubMedDate not supplied

[Aneurysms of the anterior communicating artery. Diagnostic, clinical and anatomic difficulties].

Aneurysm in the anterior communicating artery always presents diagnostic difficulties of a clinical and sometimes neuropathological nature. The authors describe the anatomic aspects of 21 cases of this type of aneurysm, together with the clinical background: anatomic recognition of clinically undetected aneurysms is not always straightforward. An inferior frontal inter-hemispheric hematoma suggests the diagnosis, but only macroscopic dissection of the whole hematoma and large vessels allows confirmation. Histological examination often reveals a hemorrhagic lesion in the fronto-polar area. Clinical investigation of these cases shows the reasons for certain classic diagnostic errors. Although this exercise reveals no original concepts, it draws attention to some classic facts that are often unexplainably overlooked. An uncommon speech disorder is described in two cases, but the mechanism of development is not clear.

Adolescent↗
PubMedDate not supplied

[Dementia in diffuse cortical Lewy body disease].

Diffuse Lewy body disease has not been yet described in France, although some authors, essentially Japanese ones reported cases of this disease. A man began at age 56 to be very apathetic with memory disturbances. Later, he developed aphasia, stereotypies, and mild parkinsonian rigidity. He died in cachexia, three years after the onset of the disease. Post-mortem examination showed diffuse senile plaques and tangles in the cortex. But there was also a striking widening of Lewy bodies, in the pons and in the frontal, temporal and cingular cortex. These Lewy bodies were located in the 5th cortical layer, and their immature and irregular shape made them difficult to identify. The authors discuss the role of each lesions on the clinical disturbances, in regard to other described cases.

Alzheimer Disease↗
PubMedDate not supplied

[Depression and calcinosis of the basal ganglia: apropos of a case].

Idiopathic basal ganglia calcifications is a heterogeneous entity characterized by the association of bilateral and symmetric calcifications of the basal ganglia and the dentae nuclei in the cerebellum, polymorphous neuropsychiatric symptomatology. It is rare, of unknown etiology and often hereditary. We report the case of a 48 years old man, who presented with melancholic depression which has been steadily worsening for more than a year and which had led to a serious suicide attempt. Clinical observation revealed apragmatism, affective dullness and impoverished spontaneous expression; the theme of incapacity predominated but guilt feelings were absent. Neurologic examination was normal except for extra-pyramidal signs. CT-scan revealed the presence of bilateral and extensive calcifications of caudate nuclei, lenticular nuclei and thalamus, which indicated a diagnosis of idiopathic basal ganglia calcification characterized by depression. Moreover, MRI revealed an hypersignal of the white periventricular substance. Phospho-calcic results and the parathormone dosage were normal. Psychometric tests showed that although intellectual capacity seemed to be intact, it was not utilised in practice. Unresponsive to antidepressants and sismotherapy, the patient is still the same one and a half year later, and needs to remain in an institution. Subsequent tests indicate that intellectual deterioration has begun. This case poses the problem of the relationship between depressive syndrome and basal ganglia lesions. We look at studies bearing on this subject and on other clinically similar syndromes (athymhormia, loss of psychic self-activation), in which the interruption or cortico-striato-pallido-thalamo-cortical circuits (particularly the limbic loop), is a physiopathologic mechanism currently invoked.

Basal Ganglia↗