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G Fénelon

Publications and source records attributed to G Fénelon.

At least 19 recordsLinked to original sources
PubMed2005

[Primary central nervous system lymphoma presenting with central neurogenic hyperventilation. A case report and review of the literature].

INTRODUCTION: Central neurogenic hyperventilation (CNH) in an awake patient is a rare entity. OBSERVATION: We report here a 54-year-old patient who developed central neurogenic hyperventilation as the initial presentation of a primary central nervous system lymphoma located in the brainstem. CONCLUSION: The patient's hyperventilation resolved completely with chemotherapy for primary CNS lymphoma. Most of the cases reported in the literature are related to a diffuse tumor of the brainstem with an intriguing overrepresentation of primary CNS lymphoma. The pathogenesis of CNH is discussed.

Brain Stem Neoplasms↗
PubMed2004

Low-frequency repetitive TMS of premotor cortex can reduce painful axial spasms in generalized secondary dystonia: a pilot study of three patients.

Dystonia is associated with excessive corticospinal motor output. Motor cortex excitability may be reduced by low-frequency repetitive transcranial magnetic stimulation (rTMS) of premotor cortical areas. We report the effects of 1 Hz rTMS applied at 90% of resting motor threshold over the left premotor cortex in an open pilot study of three patients with severe, generalized, secondary dystonia including painful spasms in the proximal and axial musculature. A 20-min session of premotor rTMS was daily performed during 5 consecutive days. The series of rTMS sessions dramatically reduced the painful spasms, for 3-8 days after the last session, without any other significant beneficial effects. However, a slight reduction of the Movement score of the Burke, Fahn and Marsden rating scale was observed for two patients, and of the Disability score for the third one. Low-frequency rTMS of the premotor cortex may improve some specific motor symptoms in severe, generalized dystonia. These results should prompt confirmation in a larger placebo-controlled study.

Adult↗
PubMed2004

[Hallucinations and dementia. Prevalence, clinical presentation and pathophysiology].

Hallucinations are a common feature of certain degenerative diseases with a risk of dementia such as Alzheimer's disease, Lewy body dementia, and Parkinson's disease. Obtaining valid epidemiological data is nevertheless quite difficult because of methodological problems. As a rule, hallucinations are more prevalent in Lewy body disease than Parkinson's disease or Alzheimer's disease. The prevalence in parkinsonian dementia is about the same as in Lewy body disease. Complex visual hallucinations predominate, auditory or tactile hallucinations are more exceptional. Minor forms (illusions, sensation of presence) are also observed. Recurrence is common, mainly in the evening or at night. Patients with advanced mental impairment generally take the hallucinations for reality. The hallucinations can be associated with psychological and behavioral disorders such as delusionnal idea or identification disorders. It is important to search for other causes of hallucinations such as drugs, ocular disorders, or depression, but many of these disorders are common comorbidities in elderly patients with degenerative disease. There is no unique model fitting all the hypothesized pathogenic mechanisms. Complex visual hallucinations most likely arise from abnormal activation of the extra-striat temporal associative regions, but only hypothetical mechanisms have been proposed. Genetic studies and functional imaging have not provided convincing evidence. Current focus is placed on an imbalance between deficient cholinergic transmission and preserved or augmented monoaminergic transmission at the cortical level, but other neurotransmission systems could be involved. The dream dysregulation mechanism proposed in Parkinson's disease cannot be generalized. The link between cognitive disorders and hallucination is also poorly understood: hallucinations are associated with more severe cognitive impairments or more rapid cognitive deline in Parkinson's disease and Alzheimer's disease, but the association with specific cognitive disorders remains to be fully explored.

Cognition Disorders↗
PubMed2003

Efficacy and tolerability of entacapone in patients with Parkinson's disease treated with levodopa plus a dopamine agonist and experiencing wearing-off motor fluctuations. A randomized, double-blind, multicentre study.

The efficacy and tolerability of entacapone was investigated in a randomized, double-blind, placebo-controlled, 3-month study of 162 patients with Parkinson's disease (PD) treated with levodopa and a dopamine agonist and experiencing wearing-off motor fluctuations. Patients were randomized in a 3 : 2 ratio to entacapone 200 mg or placebo, administered with each dose of levodopa. Efficacy was judged on the improvement of "on" and "off" time while awake (Patient Diary and UPDRS part IV Item 39), Investigators' Global Assessment, the SF-36 Health Survey, and changes in levodopa dosages. Patients were monitored for adverse events, laboratory safety and vital signs throughout the study. Improvements in "on" time as assessed using patient diary data showed a trend in favour of entacapone, however these did not reach statistical significance. "Off" time while awake (UPDRS part IV Item 39) showed an improvement of at least one category in 36% of entacapone-treated patients, compared with 22% in the control group (p = 0.0038). The proportion of patients showing an improvement at the Investigators' Global Assessment was significantly higher (p = 0.0006) in the entacapone-treated group of patients. Also, the proportion of patients with a reduction in their daily levodopa dose was significantly higher (p = 0.02) in the entacapone group (28%) compared with placebo (13%). As expected, the most frequent adverse events were dopamine-mediated (dyskinesia: entacapone 31% versus placebo 13%), and harmless urinary discoloration. The modest increase in dyskinesias could be readily managed by levodopa down-adjustment, and, at study end there was no significant difference for the UPDRS "overall dyskinesia score" between entacapone and placebo. In conclusion, although the primary efficacy variable did not reach statistical significance, the present results demonstrate that entacapone provides additional antiparkinsonian benefits to levodopa therapy and is well tolerated in levodopa-treated PD patients experiencing wearing-off motor fluctuations despite adjunct dopamine agonist therapy.

Aged↗
PubMed2003

[Secondary parkinsonian syndromes].

Secondary parkinsonism (SP) is caused by an identified structural, toxic, or metabolic mechanism. The first group of SP syndromes includes disorders caused by a primary pathological process in the brain. The second group includes disorders with a primary extrinsic or ubiquitous causal factor resulting either from reversible dysfunction of the basal ganglia or structural disorders related to the predominant or selective vulnerability to aggression of the basal ganglia. The pathophysiological aspects SP are developed here, particularly vascular syndromes and syndromes secondary to hydrocephalus. In both conditions, it is rare that SP resembles Parkinson's disease. The pathophysiology is poorly understood, but would involve, in most cases, corticostratial and/or thalamocortical connections in the basal ganglia system. For the clinician, the practical problem is frequently to determine whether a patient's parkinsonism can be related to an identifiable cause or whether there is an associated Parkinson's disease or other degenerative disease. When both a known cause of parkinsonism and Parkinson's disease are present, the cause may be asymptomatic, reveal Parkinson's disease, have an aggravating effect on the underlying disease, or modify its clinical expression.

Antipsychotic Agents↗
PubMed2001

Increased plasma neurotensin concentrations in patients with Parkinson's disease.

Plasma neurotensin (NT) was measured by radioimmunoassay in propanol extracted and unextracted plasma from 16 parkinsonian patients (four before treatment) and 16 age and sex matched controls. Mean plasma NT concentrations were consistently higher in parkinsonian patients than in controls and higher in the four untreated patients than in levodopa treated patients suggesting that plasma NT measurement may represent an easy detectable additional index in diagnosing parkinsonism and provides a novel approach to research in this field.

Aged↗
PubMed2000

Hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors.

Hallucinations, mainly of a visual nature, are considered to affect about one-quarter of patients with Parkinson's disease. They are commonly viewed as a side-effect of antiparkinsonian treatment, but other factors may be involved. The aim of this study was to determine the phenomenology, prevalence and risk factors of hallucinations in Parkinson's disease. Two-hundred and sixteen consecutive patients fulfilling clinical criteria for Parkinson's disease were studied. Demographic and clinical variables were recorded, including motor and cognitive status, depressive symptoms and sleep-wake disturbances. Patients with and without hallucinations were compared using non-parametric tests, and logistic regression was applied to significant data. Hallucinations had been present during the previous 3 months in 39.8% of the patients, and fell into three categories: minor forms, consisting of a sensation of a presence (person), a sideways passage (commonly of an animal) or illusions were present in 25.5% of the patients (an isolated occurrence in 14.3%), formed visual hallucinations were present in 22.2% (isolated in 9.3%) and auditory hallucinations were present in 9.7% (isolated in 2.3%). Patients with minor hallucinations had a higher depression score than non-hallucinators but did not differ in other respects. Logistic regression analysis identified three factors independently predictive of formed visual hallucinations: severe cognitive disorders, daytime somnolence and a long duration of Parkinson's disease. These findings indicate that, when minor hallucinations are included, the total prevalence is much higher than previously reported. A simple side-effect of dopaminergic treatment is not sufficient to explain the occurrence of all visual hallucinations. The main risk factor in treated patients is cognitive impairment, although sleep-wake cycle disturbances, and possibly other factors related to the duration of the disease, act as cofactors.

Aged↗
PubMed2000

[Spinal cord compression secondary to extramedullary hematopoiesis in a patient with thalassemia].

A 19-year-old man with homozygous beta thalassemia presented with signs of thoracic spinal cord compression secondary to extramedullary hematopoiesis. The patient was treated with hypertransfusion and hydroxyurea. After two months, clinical signs had resolved and magnetic resonance imaging showed significant regression of the extradural mass. Pathophysiology and therapeutic options in this condition are briefly discussed.

Adult↗
PubMed1998

Neuropsychological prediction of dementia in Parkinson's disease.

OBJECTIVE: To identify neuropsychological characteristics predictive of later dementia in Parkinson's disease. METHODS: A comprehensive neuropsychological test battery was administered to a cohort of 89 initially non-demented patients with Parkinson's disease consecutively enrolled at a specialised Parkinson's disease clinic. They were reassessed after a mean of 3.5 years for the diagnosis of dementia. The Cox proportional hazards model was used to identify baseline characteristics predictive of dementia. RESULTS: Only four of the baseline clinical characteristics of Parkinson's disease and neuropsychological variables remained independently linked to subsequent development of dementia: the age of onset of Parkinson's disease (>60 years; relative risk (RR) 4.1, 95% confidence interval (95% CI) 1.8-24.0, p<0.03), the picture completion subtest of the Wechsler adult intelligence scale (score<10; RR 4.9, 95% CI 1.0-24.1, p<0.02), the interference section of the Stroop test (score<21; RR 3.8, p=0.08), and a verbal fluency task (score<9; RR 2.7, 95% CI 0.8-9.1, p=0.09). Depressive symptoms and the severity of motor impairment were not predictive of dementia. CONCLUSION: These features are different from the neuropsychological characteristics predictive of Alzheimer's dementia in healthy elderly people (mainly memory and language performance). They are in keeping with the well known specificity of the impairments in Parkinson's disease for visuospatial abilities and difficulties in inhibiting irrelevant stimuli. It is postulated that the composite nature of the picture completion subtest, involving several cognitive abilities impaired in Parkinson's disease, explains its sensitivity.

Aged↗
PubMed1998

[Vascular Parkinson syndromes: a controversial concept].

The concept of arteriosclerotic parkinsonism has created some confusion due to the absence of a precise definition of the parkinsonian syndrome and to a prolonged absence of knowledge concerning the topography of the lesions in "idiopathic" Parkinson's disease as well as the anatomic relations of the basal nuclei. Although certain authors at the beginning of the century suggested that Parkinson's disease could have a vascular origin, an opposition rapidly developed between Parkinson's disease and arteriosclerotic parkinsonism, largely based on the work by Cricthley (1929). The concept of arteriosclerotic parkinsonism is a quite ambiguous notion, but was generally accepted up to the sixties before severe criticisms were made when the anatomo-clinical characteristics of Parkinson's disease were identified. Recent work has again suggested that parkinsonism can be of vascular origin but the observations reported show a heterogeneous collection of lesions with different localizations, clinical expression and clinical courses. Clinically, two rare circumstances can be identified (vascular parkinsonism similar to Parkinson's disease and unilateral vascular parkinsonism due to contralateral lesions) and inversely much more frequent "atypical" parkinsonism syndromes. These differ from Parkinson's disease by their parkinsonism symptomatology (no resting tremor, predominance of gait disorders), the presence of associated neurological signs and lower sensitivity to levodopa. The attribution of the parkinsonism disorders to vascular lesions identified at imaging is often quite hazardous, but a few anatomo-clinical observations have confirmed that vascular parkinsonism does exist. The heterogeneous nature of the observations hinders the development of diagnostic criteria.

Arteriosclerosis↗
PubMed1997

[Diagnosis and course (under treatment) of Parkinson disease].

Diagnosis of Parkinsonism is made in two steps: 1. identification of the Parkinson syndrome, a combination of rest tremor, hypertonia, akinesia and postural disturbances; 2. then essentially on the basis of clinical observations, relation to Parkinson's disease. The main risks during the course with L-dopa treatment are, on the one hand, the appearance of akinetic changes and movement disorders, more common in the younger affected patients, and on the other hand, disorders that do not respond to L-dopa, especially postural and cognitive, that are favoured by old age. Anxiety, depression pain, autonomic disorders and insomnia increase the repercussions of the disease and complicate its management.

Antiparkinson Agents↗