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At least 55 records · Page 3Linked to original sources
PubMed1997

Double-blind crossover study with physostigmine in patients with degenerative cerebellar diseases.

OBJECTIVE: To determine whether treatment with physostigmine can improve the conditions of patients with ataxia. DESIGN: A double-blind crossover study with physostigmine was performed in 19 patients with degenerative cerebellar diseases. SETTING: Patients were selected from an ongoing prospective follow-up study at the university hospital in Lübeck, Germany. PATIENTS: Eleven patients with autosomal dominant cerebellar ataxia and 8 patients with idiopathic cerebellar ataxia. INTERVENTION: Physostigmine was administered by using a transdermal system (patch) containing 30 mg of physostigmine as a base, of which about 6 mg is released during 24 hours along a diffusion gradient. Each treatment phase with the physostigmine patch or the placebo lasted 4 weeks, after which the treatment of patients was crossed over to the other phase. MAIN OUTCOME MEASURES: Ataxia was documented and quantified by using a clinical score and posturographic measures. RESULTS: Physostigmine patches had no significant effect on cerebellar symptoms. CONCLUSION: Treatment with physostigmine does not improve the conditions of patients with ataxia.

Cerebellar Ataxia↗
PubMed1990

Associated postural adjustments with body movement in normal subjects and patients with parkinsonism and cerebellar disease.

Sequential postural adjustments associated with the task of rising on tip-toes were investigated in a reaction time paradigm in 30 normal subjects, 10 patients with Parkinson's disease and 2 patients with cerebellar lesions. The typical motor pattern observed in normal subjects consists of preparatory activity in tibialis anterior (TA, shifting the body forward) and quadriceps femoris (QUA, stabilizing the knee joint) followed by executional activity in triceps surae (TS) resulting in the movement itself. Shortening of TS without preparation would result in shifting the body backward and in flexion of the knee. The coordinated pattern of motor activities is obviously adapted to functional demands. Leaning forward or backward prior to the movement results in additional adaptive changes in the timing of preparatory versus executional EMG activity, and in the amount of preparatory muscle force. The basic pattern of preparatory (TA and QUA) and executional (TS) activity was preserved in most patients with Parkinson's disease. Reaction times were normal or only moderately delayed. Time intervals between postural preparation and execution were also normal. But trial to trial variation of reaction times was increased. In the two patients with cerebellar disorders, motor preparation in QUA was delayed beyond TS onset. EMG activity was tonic and cocontraction of antagonistic muscles occurred. The basic pattern of motor preparation and execution was again preserved. It must therefore be generated outside the basal ganglia and the cerebellum. The temporal coordination of muscular activity within each and between the two components and scaling of muscle force are under cerebellar control.

Adult↗
PubMed1993

The execution of bimanual movements in patients with Parkinson's, Huntington's and cerebellar disease.

Patients with Parkinson's disease have difficulty in performing two different tasks simultaneously. The present study tested whether this deficit was specific to the disease or was found in other patient groups. An identical pattern of performance was shown by a group of patients with cerebellar disease and, to a lesser extent, by a group of patients with Huntington's disease. Further research should focus on clarifying the nature of the deficits and the reasons for the similar performances in the various patient groups.

Female↗
PubMed1995

Double-blind crossover study with levorotatory form of hydroxytryptophan in patients with degenerative cerebellar diseases.

OBJECTIVE: To determine whether treatment with the levorotatory form of hydroxytryptophan (L-5-hydroxytryptophan), a controversial experimental drug, can improve the conditions of patients with ataxia. DESIGN: A double-blind crossover study with the levorotatory form of hydroxytryptophan was performed in 39 patients with degenerative cerebellar diseases. SETTING: Patients were selected from an ongoing prospective follow-up study at two university hospitals. PATIENTS: We studied 19 patients with Friedreich's ataxia, 13 with cerebellar atrophy, and seven with olivoponto-cerebellar atrophy. INTERVENTION: The levorotatory form of hydroxytryptophan was given orally in a dose of 1000 mg/d. Each treatment phase, with the levorotatory form of hydroxytryptophan or the placebo, lasted 10 months, after which the treatment of patients was crossed over to the other phase. MAIN OUTCOME MEASURES: Ataxia was documented and quantified by using a clinical score, posturography, and measurement of grip force and the rapid-syllable repetition rate. RESULT: The levorotatory form of hydroxytryptophan had no significant effect on cerebellar symptoms. CONCLUSION: Long-term treatment with a high dose of the levorotatory form of hydroxytryptophan does not improve the conditions of patients with ataxia.

5-Hydroxytryptophan↗
PubMed1965

CEREBELLAR DISEASE IN CATS INDUCED BY INOCULATION OF RAT VIRUS.

Rat virus selectively destroys the external germinal layer of the cerebellar cortex when inoculated intracerebrally into newborn cats. The lesions are marked by numerous intranuclear inclusion bodies and a rise of virus titers. These effects suggest that the spontaneous ataxia of cats which is accompanied by cerebellar hypoplasia, may be of viral origin.

Animals↗
PubMed1999

Directional abnormalities of vestibular and optokinetic responses in cerebellar disease.

Directional abnormalities of vestibular and optokinetic responses in patients with cerebellar degeneration are reported. Three-axis magnetic search-coil recordings of the eye and head were performed in eight cerebellar patients. Among these patients, examples of directional cross-coupling were found during (1) high-frequency, high-acceleration head thrusts; (2) constant-velocity chair rotations with the head fixed; (3) constant-velocity optokinetic stimulation; and (4) following repetitive head shaking. Cross-coupling during horizontal head thrusts consisted of an inappropriate upward eye-velocity component. In some patients, sustained constant-velocity yaw-axis chair rotations produced a mixed horizontal-torsional nystagmus and/or an increase in the baseline vertical slow-phase velocity. Following horizontal head shaking, some patients showed an increase in the slow-phase velocity of their downbeat nystagmus. These various forms of cross-coupling did not necessarily occur to the same degree in a given patient; this suggests that different mechanisms may be responsible. It is suggested that cross-coupling during head thrusts may reflect a loss of calibration of brainstem connections involved in the direct vestibular pathways, perhaps due to dysfunction of the flocculus. Cross-coupling during constant-velocity rotations and following head shaking may result from a misorientation of the angular eye-velocity vector in the velocity-storage system. Finally, responses to horizontal optokinetic stimulation included an inappropriate torsional component in some patients. This suggests that the underlying organization of horizontal optokinetic tracking is in labyrinthine coordinates. The findings are also consistent with prior animal-lesion studies that have shown a role for the vestibulocerebellum in the control of the direction of the VOR.

Adult↗
PubMed1994

[Quantitative approach of postural asynergia in cerebellar diseases].

In his original description of cerebellar asynergia, Babinski, in 1899, presented a patient with cerebellar dysfunction performing a backward upper trunk bending. When the patient tried to bend his head and trunk, his lower limbs stayed almost motionless, because the associated flexion of the knee and hip, usually observed in a normal subject, did not take place. To reassess the possibility that asynergia may actually be a symptom of cerebellar dysfunction, a combined kinematic and electromyographic (EMG) analysis of the upper-trunk bending was performed on 3 patients suffering from progressive cerebellar ataxia of late onset and showing a significant atrophy of the vermis on MRI examination. Compared with 3 age and sex-matched control subjects, a significant slowing down of the upper-trunk displacement and a marked reduction of the associated displacement of hip and knee was observed. EMG recordings of three pairs of antagonistic muscles at trunk level (rectus abdominis, erectores spinae), at thigh level (vastus lateralis, semi membranosus), and at leg level (tibialis anterior, gastrocnemius lateralis), showed that the reciprocal activation pattern characteristic of a normal fast movement was absent at the thigh level in the cerebellar patients. This lack of reciprocal activation of the thigh muscles during the upper-trunk bending might explain the reduction of the compensatory displacement of the hip and knee. It might also represent an essential feature of cerebellar dysfunction in provoking axial asynergia between the upper-trunk, which is the moving segment, and the leg, which is the supporting segment during equilibrium control and during whole body displacement.

Adult↗