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Biomedical subjects

M U Manto

Publications and source records attributed to M U Manto.

31 records · Page 2Linked to original sources
PubMed1998

Shift from hypermetria to hypometria in an aberrant recovery following cerebellar infarction.

Cerebellar hypermetria, a classical sign designating the overshoot when the patient attempts to reach rapidly an aimed target, is associated with an imbalance between timing and/or intensity of agonist and antagonist EMG activities. Recovery of hypermetria following a cerebellar ischemia or hemorrhage has been demonstrated to take place in a multistage process, but aberrant recovery following a cerebellar stroke has not been described previously. We report an 85-year-old woman presenting an abnormal recovery following a cerebellar infarction. We identified three successive stages. At stage 1, fast wrist flexion movements were severely hypermetric and associated with three EMG defects: a delayed onset latency of antagonist EMG activity, a reduction of intensity of the agonist EMG activity and a depression of intensity of antagonist EMG activity. At stage 2, movements were characterized by terminal oscillations around the target and the onset latency of the antagonist activity had returned to normal. At stage 3, movements were markedly hypometric, the intensity of the antagonist EMG activity had returned to normal, while the intensity of the agonist EMG activity remained abnormally low. This case illustrates an abnormal reprogramming of the EMG triphasic pattern, resulting in the shift from severe hypermetria to severe hypometria.

Aged↗
PubMed1998

Kinematics of fast wrist movements in manic-depressive illness chronically treated with lithium carbonate.

Lithium salts have been shown to impair kinematics of fast voluntary movements during acute intoxication. The aim of the present study was to determine whether lithium carbonate affected the kinematics of fast movements in patients chronically treated and who did not exhibit signs of neurotoxicity. We analysed fast wrist flexion movements in 6 healthy subjects, in 5 patients presenting a manic-depressive illness without treatment, and in 8 patients receiving lithium carbonate for a manic-depressive disease. The mean duration of treatment was 3.9 +/- 4.1 years, the mean daily dose 837 +/- 341 mg and the mean serum level 0.95 +/- 0.15 mEq/l. Although mean movement amplitudes were similar in the 3 groups, the variability of fast movements was increased in patients receiving lithium salts. The ratio of maximum to average velocities (Vm/Vave) was significantly higher in patients treated, and their movements were temporally asymmetrical, with a ratio of acceleration duration divided by deceleration duration being lower than in the 2 other groups. These kinematic abnormalities show that a chronic treatment with lithium salts is associated with an impairment of the cerebellar control of fast single-joint movements.

Acceleration↗
PubMed1998

Ataxia induced by small amounts of alcohol.

A patient is described who exhibited cerebellar ataxia after drinking small amounts of alcohol. Intake of 5 g alcohol induced a gaze evoked nystagmus, a scanning speech, a body sway after eye closure, and bilateral postural leg tremor. Kinematic and EMG analysis of fast wrist movements showed normal movements before and marked hypermetria after alcohol intake. Dysmetria was due to abnormal programming of antagonist muscle activity.

Alcohol Drinking↗
PubMed1998

[Lesions of ponto-cerebellar and olivo-cerebellar afferents demonstrated by neurophysiologic analysis].

We describe a 52-year-old woman presenting a 2-year history of limb clumsiness and gait difficulties, characterized by progressive worsening. Neurological examination revealed cerebellar intention tremor, cerebellar dysmetria of all 4 limbs and ataxic gait. However, brain MRI was normal. Analysis of fast wrist flexion movements demonstrated hypometric movements, with decreased intensities of agonist EMG activities and increased durations of antagonist EMG activities. Such EMG abnormalities have been demonstrated in patients presenting lesions of the middle cerebellar peduncle, affecting the crossed cerebellopontine projections. Moreover, adaptation motor learning during a pinch task (isometric force) showed a severe inability to adapt motor programming, indicating a disruption of cerebellolivary and cerebellopontine afferent systems. We suggest that our patient presented an exceptional brainstem syndrome involving the function of cerebellar inflow tracts. Such electrophysiological findings are not encountered in patients presenting a cerebellar cortical degeneration or cerebellovlivopontine atrophy, and might have important implications in the treatment of cerebellar ataxia in the future.

Afferent Pathways↗
PubMed1996

Isolated cerebellar dysarthria associated with a heat stroke.

Patients presenting with heat stroke may develop an acute pancerebellar syndrome. A patient presenting with an isolated cerebellar dysarthria after a heat stroke is reported. The dysarthria lasted two weeks. An isolated cerebellar dysarthria has been previously described in lesions of the paravermal zone of the rostral cerebellum. It is suggested that this region of the cerebellum is particularly vulnerable to fever.

Adult↗
PubMed1996

Subacute pancerebellar syndrome associated with systemic lupus erythematosus.

A pancerebellar syndrome of subacute progression associated with cerebellar atrophy is highly suggestive of a paraneoplastic cerebellar degeneration (PCD). We describe a 27-year-old woman with systemic lupus erythematosus (SLE) that presented with a subacute pancerebellar syndrome. Serum and CSF anti-Yo, anti-Hu and anti-Ri antibodies were not found neither in blood, nor in CSF. Brain MRI showed a cerebellar atrophy. The cerebellar ataxia improved markedly following corticosteroids administration. This case probably demonstrates that an antineuronal antibody negative subacute cerebellar disease may not only be a manifestation of paraneoplastic disease, but that it can also be associated with SLE.

Adult↗
PubMed1996

Reversible cerebellar gait ataxia with postural tremor during episodes of high pyrexia.

We describe five patients presenting with high fever and isolated cerebellar gait ataxia. In all these patients, neurological examination revealed dysmetria, intention tremor and postural tremor during sustained posture, all restricted to the legs. Brain MRI was normal. In four of these patients, the recording of leg tremor during sustained postures showed a 3-Hz frequency. Cerebellar gait ataxia resolved within 3-10 days. We suggest that the ataxic gait was due to a reversible dysfunction of the spinocerebellar part of the anterior lobe.

Adult↗