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Biomedical subjects

D Laplane

Publications and source records attributed to D Laplane.

At least 37 records · Page 2Linked to original sources
PubMed1990

Kearns-sayre syndrome. Two clinico-pathological cases.

Two clinico-pathological cases of Kearns-Sayre syndrome are reported. In both cases the typical triad (progressive external ophthalmoplegia, heart block, retinitis pigmentosa) was present and spongiosis was the main pathological finding. In one case there was also a marked capillary proliferation, significance of which is discussed. A deletion of the mitochondrial DNA was found in the muscle, spinal cord and brain of this last case.

Adolescent↗
PubMed1990

[Loss of psychic self-activation].

Loss of motivation is a well-known disorder in patients with frontal lesions or, as more recently described, with bipallidal lesions. Some of these patients also report a kind of fading of their mental life when they are without exogenous stimulation. Yet their performances return to normal (or almost normal) levels under the influence of a social stimulation. It is this dissociation which we propose to call "loss of psychic self-activation" (LPSA). Comparisons with disorders produced by similar lesions suggest that this is not an "all or none" phenomenon. The purpose of this paper is to discuss the originality, usefulness and validity of the loss of psychic self-activation concept and to evaluate its heuristic value, notably in its application to Janet's psychasthenia and to obsessional neurosis. An interpretation of this disorder based on the available anatomical data is also tentatively proposed.

Activities of Daily Living↗
PubMed1990

Neurosarcoidosis: signs, course and treatment in 35 confirmed cases.

Thirty-five cases of biopsy-proven sarcoidosis with neurologic manifestations are reported. Neurosarcoidosis was the presenting symptom in 31% of cases and the only clinical manifestation in 17%. Mean follow-up time was 48 months. Central nervous system involvement was observed in 37% and meningitis in 40% of patients. Other manifestations were cranial nerve palsies (37%), peripheral neuropathy (40%), and myopathy (26%). Multiple neurologic manifestations were present in 51% of cases. All but 4 were treated with corticosteroids. Another immunosuppressive agent or cerebral irradiation was added in 6 and 2 patients, respectively. Complete recovery was observed in 46%, improvement in 46%, 4% remained stable, and 4% worsened. There were no deaths. We advocate treating neurosarcoidosis with corticosteroids as early as possible. If the patient's condition worsens, additional immunosuppressive agents or cerebral irradiation is warranted.

Adolescent↗
PubMed1990

[Is there a correlation between motor neglect and unilateral sensory neglect].

Similarities between motor neglect and unilateral sensorial neglect are so striking that their mechanisms are likely to be almost the same. As the attentional interpretation is no longer possible for motor neglect, and the intentional interpretation may be dismissed in man because of the loss of automatic movements, the psychological interpretation must be abandoned. A purely physiological hypothesis is put forward for motor neglect. When applied to unilateral neglect, it suggests that sensorial signals treated by the right hemisphere do not reach a significant functional level. In such case, the left hemisphere assumed to be dominant for awareness of body and space would receive from the right hemisphere a message interpreted as nul and would neglect information coming from the left.

Brain Diseases↗
PubMed1989

[Practical management of Alzheimer's disease].

In patients with confirmed Alzheimer's disease--a condition for which no active treatment is available--the practitioner's first duty is to abstain from prescribing useless of harmful drugs that would make the situation worse. There is a long list of such potential nuisances. The most badly tolerated drugs unquestionably are anticholinergics, but one must also beware of tricyclic antidepressants, neuroleptics (sometimes unavoidable, however) and also, to a lesser extent, benzodiazepines, beta-blockers and so forth. Yet medical support is far from being ruled out. The benefits of placebos and drugs of undemonstrated value are not negligible, but above all it is mandatory to help the relative understand the truly pathological nature of almost unbearable behaviours. It is also very useful to advise the family on the life organization at home in order to perdure, on the legal safeguards, on whether or not the patient should be institutionalized, and similar topics. Inside institutions, keeping a sensible attitude between relentless therapy and euthanasia is the best way to ensure that the dignity of the demented patient will be preserved.

Alzheimer Disease↗
PubMed1989

Peripheral neuropathies during treatment with almitrine: report of 46 cases.

Almitrine bismesylate is thought to cause sensory peripheral neuropathy. Forty-six patients are reported who received almitrine bismesylate alone for chronic respiratory failure or in combination with raubasine for various cerebrovascular diseases. Polyneuropathy appeared between 9 and 25 months after the onset of treatment. Sensory signs and symptoms were confined to the distal parts of the lower limbs and involved large and small fibres. Histological and electrophysiological findings indicated axonal degeneration. Respiratory failure could have caused the polyneuropathy in some cases but many had no chest disease. Patients began to improve between 3 and 6 months after withdrawal of the drug. Recovery was usually complete after 12 months.

Aged↗
PubMed1989

Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study.

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.

Adult↗
PubMed1989

[Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases].

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1988

[Peripheral neuropathies with neural vasculitis. Clinical and electrophysiological aspects of 33 cases].

Lesions of vasculitis of nerve were found in 33 of 140 patients hospitalized for peripheral neuropathy over a little less than 2 years, and in 113 specimens from neuromuscular biopsies. A first group of 7 patients had histological lesions suggestive of systemic necrotizing vasculitis (periarteritis nodosa in 4 cases and Churg and Strauss disease in 2 cases); the 7th patient was treated for myeloproliferative syndrome. The clinical and electromyographic signs were those of an axonal polyneuropathy which was improved by various treatments in 6 cases. A second group of 26 patients had histological lesions of vasculitis of nerve. Ten of these patients presented with single or multiple neuritis (of unknown origin in 5 cases), 11 with distal polyneuropathy (of unknown origin in 5 cases) and 3 with chronic polyradiculoneuritis; in 2 cases, clinical and electromyographic findings were in favour of an anterior horn lesion. The duration of the disease varied from 6 months to 10 years. The principal causes identified were connective tissue diseases, solid cancer or lymphoma and isolated gammapathy. Two patients with multiple neuritis recovered spontaneously. The finding of vasculitis of nerve at biopsy therefore is of unequivocal significance outside the better known but smaller group of systemic necrotizing vasculitis.

Adult↗
PubMed1988

The clinical spectrum of alcoholic pellagra encephalopathy. A retrospective analysis of 22 cases studied pathologically.

A retrospective clinical study of 22 heavy alcohol drinkers is reported in which postmortem study showed diffuse chromatolysis of neurons identical to that found in neurological pellagra, associated in 13 cases with Marchiafava-Bignami disease and/or Wernicke-Korsakoff disease. The clinical features included confusion and/or clouding of consciousness, marked oppositional hypertonus ('gegenhalten') and myoclonus. Because of the frequent coexistence of other alcoholic encephalopathies in the same patient, alcoholic pellagra was often unrecognized. Fifteen patients received thiamine and pyridoxine therapy without niacin. It appeared to aggravate the neurological state or to trigger the development of alcoholic pellagra encephalopathy in 9 cases. The relationship between pellagra occurring during thiamine and pyridoxine therapy and 'nicotinic acid deficiency' is discussed. Multiple vitamin therapy should be given in the treatment of undiagnosed encephalopathies in alcoholic patients.

Adult↗
PubMed1988

Duplex scanning in extracranial vertebral artery dissection.

Ultrasonic (duplex scanning and continuous-wave Doppler) and angiographic findings in three patients with bilateral extracranial vertebral artery dissection are reported. A pattern of ultrasonic anomalies diagnostic of dissection is described, including association of a localized increase in diameter of the artery with hemodynamic signs of stenosis or occlusion at the same level and decreased pulsatility and presence of intravascular echoes in the enlarged segment.

Adult↗
PubMed1988

[Benign cerebral angiopathies and phenylpropanolamine].

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.

Adult↗
PubMed1988

[Loss of psychic self-activation and stereotyped mental activity caused by a frontal lesion. Relation of the obsessive-compulsive disorder].

A case of frontal lobe lesions is reported, its interest being that it is similar to a syndrome that we have previously described as the consequence of lenticular nucleus lesions. This syndrome includes primarily a loss of psychic self-activation (psychic akinesia) and compulsive or pseudo-compulsive activities. In the present case the lesions involved the deep white matter of the prefrontal cortex on both sides, and were most extensive in the depth of the middle frontal gyrus. This similitude brings further support to the notion that subcortical damage of the lenticular nuclei can induce a frontal-like syndrome. The similitude with some of the behavioural aspects or depressive of hebephrenic states is emphasized. The occurrence of stereotyped mental activities is the basis for a discussion of the relationships with some features of obsessive-compulsive neurosis.

Activities of Daily Living↗