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Biomedical subjects

A M Bonnet

Publications and source records attributed to A M Bonnet.

At least 55 records · Page 3Linked to original sources
PubMed1998

Chromosome 6-linked autosomal recessive early-onset Parkinsonism: linkage in European and Algerian families, extension of the clinical spectrum, and evidence of a small homozygous deletion in one family. The French Parkinson's Disease Genetics Study Group, and the European Consortium on Genetic Susceptibility in Parkinson's Disease.

The gene for autosomal recessive juvenile Parkinsonism (AR-JP) recently has been mapped to chromosome 6q25.2-27 in Japanese families. We have tested one Algerian and 10 European multiplex families with early-onset Parkinson disease for linkage to this locus, with marker D6S305. Homogeneity analysis provided a conditional probability in favor of linkage of >.9 in eight families, which were analyzed further with eight microsatellite markers spanning the 17-cM AR-JP region. Haplotype reconstruction for eight families and determination of the smallest region of homozygosity in two consanguineous families reduced the candidate interval to 11.3 cM. If the deletion of two microsatellite markers (D6S411 and D6S1550) that colocalize on the genetic map and that segregate with the disease in the Algerian family is taken into account, the candidate region would be reduced to <1 cM. These findings should facilitate identification of the corresponding gene. We have confirmed linkage of AR-JP, in European families and in an Algerian family, to the PARK2 locus. PARK2 appears to be an important locus for AR-JP in European patients. The clinical spectrum of the disease in our families, with age at onset <=58 years and the presence of painful dystonia in some patients, is broader than that reported previously.

Age of Onset↗
PubMed1998

[Clinical diagnostic criteria for multiple system atrophy].

What are the distinctive criteria for the diagnosis of multiple system atrophy? The combination of motor, dysautonomic, neuropsychological and eyes movements may help to distinguish, at a early stage, multiple system atrophy from other neurodegenerative diseases such as Parkinson's disease, progressive supranuclear palsy or corticobasal degeneration. Thus, these criteria are suitable both for clinical care and drug trials.

Cognition Disorders↗
PubMed1997

Urinary disturbances in striatonigral degeneration and Parkinson's disease: clinical and urodynamic aspects.

Although urinary disturbances are more frequent in multiple system atrophy (MSA) than in Parkinson's disease (PD), the striatonigral degeneration (SND) type of MSA is difficult to distinguish from PD, especially when the latter is associated with orthostatic hypotension or urinary symptoms. The pattern of urinary symptoms and urodynamic dysfunction was analyzed in 15 SND and 35 PD patients with urinary complaints. In SND, dysuria with or without chronic retention, frequently associated with a hypoactive detrusor and low urethral pressure, permitted early and reliable diagnosis. In PD, urgency to void, with or without difficulty voiding, but without chronic retention, associated with detrusor hyperreflexia and normal urethral sphincter function, predominated. In clinical practice, the study of urinary symptoms and bladder function may help to distinguish SND from PD in patients with urinary disturbances.

Aged↗
PubMed1997

Memory for spatial location in 'de novo' parkinsonian patients.

A deficit in memory for spatial location was recently reported in typical non-demented parkinsonian patients ('standard'). Is this deficit related to dopamine depletion? Such an association would reinforce the suggestion that striato-frontal neuronal circuits are implicated in memory for item-specific spatial coordinates. To answer this question, we compared the performance of 10 recently diagnosed and not yet treated parkinsonian patients ('de novo'), in which the neurobiochemical deficit is considered to involve mainly the nigrostriatal dopaminergic system, to that of 14 controls matched for age, global cognitive efficiency and mood, on a visuospatial learning test. The task required little motor or constructive functions and was designed to allow control of encoding and comparison of free recall, cued recall and recognition. Compared to controls, 'de novo' patients displayed a lower performance in memory for visuospatial location of pictures, contrasting with relative preservation of verbal memory, perceptive visuospatial and executive functions. These results confirm the sensitivity of visuospatial memory even at an early stage of Parkinson's disease and suggest the implication of the nigrostriatal dopaminergic system, and associated striato-frontal neuronal circuits, in executive processes needed for spatial location learning.

Analysis of Variance↗
PubMed1997

Low-dose clozapine improves dyskinesias in Parkinson's disease.

The severity of parkinsonian motor disability and dyskinesias was evaluated in seven levodopa-responsive patients with Parkinson's disease after an acute challenge with the mixed dopamine agonist apomorphine, before and after low-dose clozapine (50 mg) for 18 +/- 2 days. There was a significant 59% improvement (p < 0.05) of apomorphine-induced dyskinesias without aggravation of parkinsonian motor disability following clozapine treatment. The results suggest that low-dose clozapine, already shown to improve psychotic symptoms, may help to reduce severe levodopa-induced dyskinesias in parkinsonian patients.

Aged↗
PubMed1997

Pallidal stimulation for Parkinson's disease. Two targets?

There has been renewed interest in functional surgery as treatment for Parkinson's disease (PD). Although pallidotomy and chronic pallidal stimulation are highly effective in suppressing levodopa-induced dyskinesia (LID), both methods also seem to be effective in reducing parkinsonian disability. However, the simultaneous improvement of LID and motor signs is hard to explain with the classic model of basal ganglia circuitry. Taking advantage of the fact that deep brain stimulation is reversible and that implanted electrodes contain four discrete stimulation sites, we investigated the effect of stimulation on different sites of the globus pallidus (GP) in five PD patients. Stimulation in the dorsal GP (upper contact) significantly improved gait, akinesia, and rigidity and could induce dyskinesia when patients were in the "off" state. In contrast, stimulation in the posteroventral GP (lower contact) significantly worsened gait and akinesia, although the reduction in rigidity remained. For patients in the "on" state, stimulation in the posteroventral GP dramatically reduced LID but, as in the "off" state, worsened gait and akinesia, thus canceling out the antiparkinsonian effect of levodopa. Our results indicate that stimulation had a striking different effect on parkinsonism and dyskinesia when applied at two different loci of the GP and that stimulation applied in the posteroventral GP produced opposite effects on rigidity and on akinesia. We conclude that parkinsonian signs and LID are a reflection of at least two different anatomofunctional systems within the GP and that this functional organization of the GP needs to be considered when determining the optimal target for surgical treatment of PD.

Adult↗
PubMed1996

Improvement of levodopa-induced dyskinesia by propranolol in Parkinson's disease.

Seven patients suffering from Parkinson's disease (PD) with severely disabling dyskinesia received low-dose propranolol as an adjunct to the currently used medical treatment. There was a significant 40% improvement in the dyskinesia score without increase of parkinsonian motor disability. Ballistic and choreic dyskinesia were markedly ameliorated, whereas dystonia was not. This study suggests that administration of low doses of beta-blockers may improve levodopa-induced ballistic and choreic dyskinesia in PD.

Adrenergic beta-Antagonists↗
PubMed1995

"Pure" striatonigral degeneration and Parkinson's disease: a comparative clinical study.

Striatonigral degeneration (SND) is difficult to diagnose in vivo. The purpose of this study was to detect the best indicators for an early and reliable diagnosis of the disease. Eighteen patients clinically diagnosed as having SND were selected with rigorous inclusion criteria and compared to 18 patients with Parkinson's disease (PD) matched for age and disease duration. Apart from dysautonomia, the principal discriminant clinical features that distinguished SND from PD were the early appearance of the following symptoms and signs: (a) severe and atypical progressive parkinsonism characterized by bilateral bradykinesia and rigidity, slowness of gait, postural instability, and falls, and poor or absent response to adequate levodopa treatment; (b) increased tendon reflexes associated or not with frank pyramidal signs, severe dysarthria, and less consistently, dysphagia, stridor, antecollis, and stimulus-sensitive myoclonus, which, when present, are highly suggestive of the disease.

Aged↗
PubMed1995

A "combined" levodopa test as a useful method for evaluating the efficacy of dopamine agonists: application to pergolide and bromocriptine.

The efficacy of pergolide as adjunct to levodopa therapy was compared to that of bromocriptine in 12 parkinsonian patients with fluctuating motor disability and levodopa-induced dyskinesias (mean age of onset, 50.6 +/- 8 years; Hoehn and Yahr stage between II and IV; mean basal UPDRS motor score, 30.6 +/- 8.6), in a double-blind crossover study. After an 8-day habituation to each agonist, an acute challenge of a supraliminal dose of levodopa ("levodopa test") was performed in association with either 1 mg pergolide or 10 mg bromocriptine. The delay to onset and the duration of therapeutic benefit, the percentage improvement in motor disability, and the severity of onset and peak-dose dyskinesias were evaluated. Both agonists significantly increased the duration of therapeutic benefit, but pergolide more so than bromocriptine (p = 0.02). Pergolide also tended to reduce the severity of dyskinesias and was globally perceived by the patients to be more efficacious than bromocriptine on parkinsonian symptoms and fluctuations. This study illustrated the usefulness of the "levodopa test" in evaluating, objectively, the effects of dopamine agonists.

Aged↗
PubMed1995

Levodopa-induced dyskinesias are improved by fluoxetine.

We evaluated the severity of motor disability and dyskinesias in seven levodopa-responsive patients with Parkinson's disease after an acute challenge with the mixed dopamine agonist, apomorphine, before and after the administration of fluoxetine (20 mg twice per day) for 11 +/- 1 days. After fluoxetine treatment, there was a significant 47% improvement (p < 0.05) of apomorphine-induced dyskinesias without modification of parkinsonian motor disability. The dyskinesias were reduced predominantly in the lower limbs during the onset and disappearance of dystonic dyskinesias (onset- and end-of-dose dyskinesias) and in the upper limbs during choreic mid-dose dyskinesias. The results suggest that increased brain serotoninergic transmission with fluoxetine may reduce levodopa- or dopamine agonist-induced dyskinesias without aggravating parkinsonian motor disability.

Antiparkinson Agents↗
PubMed1994

Eye movements in parkinsonian syndromes.

Eye movements were recorded in 14 patients with Parkinson's disease (PD) in the "off" condition, 14 patients with striatonigral degeneration (SND), 10 patients with corticobasal degeneration (CBD), and 10 patients with progressive supranuclear palsy (PSP), with comparison with 12 control subjects. Vertical saccade paralysis was not observed in the PD, SND, and CBD groups but was present in 9 patients of 10 in the PSP group. In the PD and SND groups, horizontal reflexive visually guided saccade latency and accuracy were similar, and differed only slightly from those of controls. In the CBD group, saccade latency was significantly increased and correlated to an "apraxia score"; whereas, in the PSP group, saccade amplitude was significantly decreased. Thus, the abnormalities of both horizontal saccade parameters in the PSP group contrasted with those observed in the CBD group. The percentage of errors in the antisaccade task, an index of prefrontal dysfunction, was markedly increased only in the PSP group. The smooth pursuit gain was decreased in all groups but more severely in the PSP group. It may be concluded that saccade abnormalities are clearly different in SND, CBD, and PSP, and might help in early differential diagnosis in individual patients, but that SND cannot be differentiated from PD on the simple basis of eye movement abnormalities.

Aged↗
PubMed1994

Sequences of memory-guided saccades in Parkinson's disease.

Sequences of ocular saccades were studied in 8 patients with Parkinson's disease, with (i.e., "on") and without (i.e., "off") levodopa treatment. The amplitude of single saccades was decreased and not improved by treatment. The chronology of saccades during sequences was impaired in patients in the "off" state, but significantly improved during the "on" period. These results are compatible with a decreased activation of the supplementary motor area, which can be reversed by levodopa.

Electrooculography↗
PubMed1994

Levodopa-induced dyskinesias in Parkinson's disease phenomenology and pathophysiology.

The aim of this study was to provide further insight into the phenomenology and pathophysiology of monophasic and biphasic dyskinesias induced by levodopa in Parkinson's disease. For this purpose, the type, localization, severity, and timing of dyskinesias were evaluated in 15 parkinsonian patients in relation to motor disability after administration of levodopa using a video-electromyographic recording device. Foot-dystonia, myoclonus, and akathisia were observed in most patients. The dyskinesias started in the foot, usually on the side most affected by the disease, and spread in an "ascending wave" to the contralateral side, the trunk, and upper extremities. In a few patients, onset was axial, spreading almost instantaneously to all limbs. The dyskinesias were dystonic and ballistic at the start, and became increasingly choreic as they attained the upper limbs. Their intensity was maximal in the lower limbs, then progressively decreased, while increasing in upper limbs and head. The results indicate that there is no strict dichotomy between biphasic and monophasic dyskinesias. In other words, there is a "continuum" between the first dyskinesias and those observed during the period of maximal clinical improvement. These dyskinesias can also appear in reverse order, as if there were an "oscillator" determining a sequence of alternating patterns.

Activities of Daily Living↗
PubMed1994

Do parkinsonian symptoms and levodopa-induced dyskinesias start in the foot?

Parkinsonian symptoms and levodopa-induced dyskinesias (LIDs) are often considered to occur first, and to predominate, in the upper limbs. We studied the topography, type, sequence, and severity of LIDs in 20 consecutive patients with Parkinson's disease (PD) experiencing LIDs for less than 6 months (Hoehn and Yahr stage II-III; average age at onset of PD, 57 years; average duration of PD, 7.2 years; percent of improvement with levodopa > 50) and compared them with the initial site, form, and evolution of the patient's motor disability. Parkinsonism started in the foot in six of 20 patients. Motor disability in the "off" state was similar in upper and lower extremities, except for akinesia, which was worse in the lower limbs. A careful interview indicated that LIDs had started in the foot in all patients. After administration of a single dose of levodopa ("levodopa test"), LIDs appeared in all patients as dystonia of the foot homolateral to the side most affected by PD (onset-of-dose dyskinesia). LIDs were preceded by "off" dystonia (dystonic foot) in six patients and were followed by mid-dose dyskinesia in eight. This is consistent with an early loss of dopaminergic innervation corresponding somatotopically to the foot area. The similarities among initial LIDs, early morning dystonia, and onset-of-dose dyskinesia suggest a similar pathophysiology.

Adult↗