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Biomedical subjects

M Manto

Publications and source records attributed to M Manto.

At least 19 recordsLinked to original sources
PubMed2003

Effects of the oral form of ondansetron on cerebellar dysfunction. A multi-center double-blind study.

The aim of this study was to assess the efficacy and the safety of ondansetron administered orally in patients with a cerebellar disorder. The study was a randomised, multi-center, double-blind trial. The patients were randomised either to oral ondansetron 8 mg or to placebo twice daily for seven days. Cerebellar dysfunction was quantified before and after treatment using the International Cooperative Ataxia Rating Scale (ICARS). We performed a global analysis (total scores), we analysed by subscores (4 subscores: oculomotor, speech, kinetic, postural) and subgroups (4 subgroups: Cerebellar Cortical Atrophy (CCA), Multiple Systemic Atrophy (MSA), Familial Cerebellar Degeneration (FCD) and miscellaneous cerebellar disorders), and we also performed an analysis by individual test items. We investigated whether ondansetron and placebo had different effects upon ICARS total scores and subscores in the 4 subgroups considered together or separately. For p values < 0.05, we subsequently applied the Mann-Whitney test to compare ondansetron and placebo effect for each individual item. We evaluated 45 of the 46 patients included. No effect was found in global analysis. We found no difference in the analysis of the ICARS subscores. Concerning the individual test items, there was a significant difference between the placebo and ondansetron for the finger-to-nose test (p = 0.049), the Heel-to-Knee test (HK); (p = 0.03), the Body Sway Eyes Closed (p = 0.017) and the Body Sway Eyes Open (BSEO); (p = 0.014). There was no significant difference for tremor in upper limbs (p = 0.32) or for gait (p = 0.49). The Mann-Whitney test showed a greater effect of ondansetron than placebo for BSEO in miscellaneous disorders (p = 0.013) and for HK in FCD (p = 0.036), but ondansetron was deleterious for HK in CCA (p = 0.019). Our study showed no effect of oral ondansetron on global cerebellar dysfunction. The analysis by subgroups showed that the oral form of ondansetron (a) is deleterious for coordination in patients with CCA, (b) has no effect upon tremor in upper limbs, and (c) has a mild effect upon posture and coordination in lower limbs in some subgroups of ataxic diseases.

Administration, Oral↗
PubMed2002

[The neurology department].

The department of neurology is devoted to the diagnosis and medical treatment of organic diseases of central nervous system (brain and spinal cord) and peripheral nervous system (peripheral nerves and muscles). Basic and clinical research in neuroscience constitute an essential activity of the department that defines its academic character. Over the years, the department of neurology has evolved from providing general neurology services to a multifaceted unit that has developed the several subspecialties of clinical neuroscience. Main research areas have included neurooncology, neurophysiology, neuropsychology, cerebrovascular diseases, childhood epilepsy and conditions affecting the psychomotor development of children. Neurogenetics is a recent addition to the areas of the interest of the department; research in neurogenetics includes basic investigations as well as clinical studies and focuses on inherited ataxias and genetic epilepsies.

Belgium↗
PubMed1999

Cerebellar decompensation following a stroke in contralateral posterior parietal cortex.

We describe here a patient who exhibited cerebellar hypermetria on the left side following a cerebellar ischemia in left cerebellar hemisphere. She subsequently recovered clinically. However, twenty months after cerebellar ischemia, cerebellar symptoms reappeared suddenly. Moreover, kinematic and electromyographic (EMG) abnormalities during fast movements of left wrist were identical to those detected after the initial cerebellar lesion. Surprisingly, the causal lesion of this cerebellar decompensation was found to be a stroke at the level of the right posterior parietal association area.

Adult↗
PubMed1998

Effects of TRH on ballistic wrist movements in cerebellar cortical atrophy: improvement of two genuine deficiencies but not of the major one.

Thyrotropin-releasing hormone (TRH) has been claimed to improve cerebellar ataxia in patients with idiopathic sporadic cerebellar cortical atrophy (CCA). We analysed the effects of intravenous administration of TRH (1 mg) in ballistic wrist flexions movements in 10 healthy subjects and in eight patients with CCA. The associated agonist and antagonist electromyographic (EMG) activities were recorded. In healthy subjects, TRH did modify neither the movement amplitudes, nor the intensity of the agonist and antagonist EMG activities. Before TRH administration, patients with CCA exhibited a hypermetria which was associated with a delayed onset of the antagonist activity. Moreover, the intensity of EMG activity in both the agonist and the antagonist muscles were reduced. After TRH, the hypermetria and the delayed onset latencies of the antagonist EMG activities were unchanged but the intensity of both the agonist and the antagonist EMG activities increased. TRH could increase the magnitude of agonist and antagonist EMG activities in patients with CCA by exerting an excitatory effect directly on motoneurons or by modulating at the supraspinal level the central commands to agonist and antagonist motoneuron pools. Copyright Rapid Science Ltd

Journal Article↗
PubMed1997

Analysis of single-joint rapid movements in patients with sporadic olivopontocerebellar atrophy.

Patients with pure cerebellar cortical atrophy (CCA) present isolated cerebellar signs, whereas patients with sporadic olivopontocerebellar atrophy (sOPCA) present various combinations of cerebellar and extracerebellar signs. However, the differential diagnosis between these two forms of cerebellar degeneration is often a challenge for the clinician. Therefore, any test helping in this differential diagnosis might have a potential clinical interest. In this study, our goal was to investigate the adaptation to increased inertia in patients with sOPCA exhibiting combined cerebellar and pyramidal signs, during the performance of fast wrist flexions. We found that these patients exhibited a hypermetria which remained unchanged after addition of inertia, because they were unable to increase neither their agonist activity (launching force), nor their antagonist activity (braking force). This contrasts with our previous findings in patients with CCA. In these latter, the hypermetria worsened when the inertial load of the hand increased because those patients were able to increase their agonist activity, but not their antagonist activity. The adaptation to inertia might thus help to differentiate CCA and sOPCA.

Adult↗
PubMed1997

Dissociation in the neural control of single-joint and multi-joint movements in the thalamic ataxia syndrome.

We report a patient presenting with a right thalamic ataxia syndrome following a hemorrhage located in the left lateral and posterior thalamus. We investigated the fast goal-directed movements of the wrists (single-joint movements) and the fast pointing movements in the upper limbs (multi-joint movements). On the right side, single-joint movements were markedly hypermetric and characterized by an asymmetry in kinematics, an abnormality of ballistic movements which is considered to be a fundamental cerebellar disorder. By contrast, rapid multi-joint movements were only very slightly impaired. These results suggest that ballistic movements of the wrist are under the strong influence of the cerebello-thalamo-cortical pathway, while rapid pointing multi-joint movements in upper limb are mostly influenced by another pathway emerging from the lateral cerebellum, possibly the dentato-rubral or the dentato-reticular projections in the brainstem. The roles of these neuroanatomical pathways in the control of fast single-joint and multi-joint movements are discussed.

Ataxia↗
PubMed1997

Cerebellar spongiform degeneration induced by acute lithium intoxication in the rat.

Cerebellar syndrome has been described after acute lithium intoxication in human. Neuropathological studies have demonstrated neuronal loss and spongiosis in the cerebellum. We describe an animal model of acute lithium-induced cerebellar degeneration. Five hours following administration of lithium chloride (250 mg/kg, i.p.), the cerebellar white matter of seven rats out 14 exhibited extensive spongiform changes. Microdialysis study in the rat cerebellar cortex demonstrated basal concentrations of dopamine (DA), hydroxy-3-methoxyphenylacetic acid (HVA) and 5-hydroxy-3-indolacetic acid (5-HIAA). These metabolites were unaffected by acute lithium intoxication suggesting that the cerebellar toxicity is not due to a modification of dopaminergic or serotoninergic neurotransmission.

Acute Disease↗
PubMed1996

Cerebellar hypermetria associated with a selective decrease in the rate of rise of antagonist activity.

Classically, cerebellar hypermetria observed during fast and accurate movements is ascribed to a delayed onset of the electromyographic activity of the antagonist muscle. We describe here 3 patients presenting a late-onset cerebellar degeneration and exhibiting a hypermetria during their fast and accurate movements in spite of a normal onset latency of the antagonist activity. Hypermetria was found to be due to a slower rate of rise of the antagonist activity.

Adult↗
PubMed1996

Analysis of cerebellar dysmetria associated with lithium intoxication.

By contrast to the permanent cerebellar sequelae developing over the weeks following a lithium intoxication, the cerebellar dysfunction occurring in the acute phase is poorly documented. In this study, we analysed the fast and accurate wrist flexion movements and the associated electromyographic activities in 6 patients as soon as possible after a lithium intoxication and three months later. Movements were recorded before and after increasing the inertial load of the moving hand. During the acute phase of the disease, three patients performed dysmetric movements, which became hypermetric when the inertia was increased. In the three other patients, the overshooting of the target which was already observed in the basal condition (no load), was even larger when masses were added. In all the patients, addition of loads increased the onset latency of the antagonist activity during the acute stage of the intoxication. Three of the six patients who presented fever, renal failure and did not undergo hemodialysis developed permanent cerebellar deficits. The three others who presented no fever, no renal failure and underwent hemodialysis recovered completely.

Acute Disease↗
PubMed1996

Hypoglycemia associated with phenytoin intoxication.

BACKGROUND: Diphenylhydantoin, a widely used antiepileptic agent, can alter carbohydrate tolerance, and acute intoxication with diphenylhydantoin can be associated with hyperglycemia. CASE REPORT: We describe a patient who experienced a prolonged episode of hypoglycemia secondary to an acute voluntary intoxication with diphenylhydantoin 20 g and zopiclone 225 mg. This hypoglycemic episode was presumptively attributed to diphenylhydantoin and might be due either to an escape from the inhibitory effects of diphenylhydantoin on insulin secretion or an increased sensitivity of the tissues to insulin. Zopiclone was considered less likely since zopiclone overdoses have been only exceptionally associated with hyperglycemia.

Adult↗
PubMed1996

[Cerebellar syndrome associated with Hashimoto's encephalopathy].

A 38-year-old man presented with an acute confusional state associated with cerebellar signs in left upper limb. Hashimoto's thyroiditis was discovered. Brain magnetic resonance imaging with T2-weighted sequences revealed a high-intensity signal in the left cerebellar hemisphere. The patient received corticosteroids and thyroid hormonal therapy, which was followed by a rapid clinical improvement. The association of an acute confusional state and of cerebellar signs should suggest a Hashimoto's encephalopathy.

Adult↗
PubMed1996

Analysis of ballistic movements in ataxic hemiparesis following a pontine stroke.

Although cerebellar-like ataxia is a well known component of the ataxic hemiparesis (AH), the mechanism of hypermetria in AH has not been established. We describe a patient presenting a left AH following a right pontine infarction. We investigated the ballistic flexion movements of both wrists and the associated agonist and antagonist electromyographic (EMG) activities, before and after addition of inertial loads. At the time of motion analysis, neurological examination showed cerebellar-like dysmetria of the left side but the patient had recovered a normal strength. In the basal state (without addition of loads), movements of the left wrist were hypermetric. The duration of the agonist EMG activity was prolonged and the onset latency of the antagonist EMG activity was not delayed. Moreover, when a mass was added, the hypermetria was unchanged because the patient was unable to adapt appropriately neither the agonist, nor the antagonist EMG activity. We suggest that the hypermetria was due to an imbalance between the duration of the agonist EMG activity (the launching force) and the duration of the antagonist EMG activity (the braking force).

Aged↗
PubMed1996

[Mechanism of hypometria caused by pontocerebellar infarction].

By contrast to cerebellar hypermetria, the pathophysiology of cerebellar hypometria associated with a focal lesion is poorly understood. We describe a patient presenting an ischemic stroke involving the left lateral pons and middle cerebellar peduncle and exhibiting severely hypometric ballistic movements of the left wrist. Hypometria was associated with two distinct abnormalities of the triphasic electromyographic (EMG) pattern: a prolongation of the duration of the antagonist EMG activity and a reduced intensity of the agonist EMG activity. The first mechanism has been described previously in patients with a cerebellar disease and exhibiting hypometria, but not the second. The concomitant presence of these two elementary mechanisms contributed to the severity of hypometria in our patient. Moreover, this case illustrates that the integrity of the crossed pontocerebellar fibers passing through the middle cerebellar peduncle is necessary to generate an adequate agonist EMG activity.

Cerebellopontine Angle↗
PubMed1995

Detection of silent cerebellar lesions by increasing the inertial load of the moving hand.

In a previous study, we analyzed the hypermetria of wrist flexion movements in patients with a cerebellar syndrome. We found that hypermetria augmented when the inertial load of the moving hand was artificially increased. In the present study, we applied the same protocol to patients with an apparently normal neurological examination, in spite of a cerebellar lesion documented by magnetic resonance imaging. In all of these patients, the addition of a mass to the moving hand caused the appearance of a hypermetria. This lack of adaptation of fast and accurate movements to an increased inertia thus appears as a new diagnostic tool enabling the detection of silent cerebellar lesions.

Adaptation, Physiological↗
PubMed1995

Recovery of hypermetria after a cerebellar stroke occurs as a multistage process.

In a prospective study, we repeatedly recorded fast goal-directed wrist movements of 8 patients who had experienced an acute cerebellar hypermetria due to a stroke and who had subsequently recovered clinically. Movements and the associated agonist and antagonist electromyographic (EMG) activities were recorded before and after addition of inertial loads. Four stages characterized the recovery process. At stage 1, hypermetria was present in the basal state and was not modified by the addition of inerital loads. At stage 2, hypermetria, which was present in the basal state, was enlarged by mass addition. At stage 3, hypermetria was absent in the basal state, but was revealed by an inertial load increase. At stage 4, as in healthy subjects, there was no hypermetria without or with addition of inertial loads. At stage 1, the patients presented several defects. (1) Facing an increased inertia, they could not increase their agonist EMG activity. (2) The onset latency of their antagonist EMG activity was delayed. (3) Facing an increased inertia, they could not increase their antagonist EMG activity. Among these three defects, the first disappeared at stage 2, the second at stage 3, and the third at stage 4.

Adult↗