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PubMed2005

Asymmetry of the pitch vestibulo-ocular reflex in patients with cerebellar disease.

Responses to pitch head impulses were measured in 15 patients with cerebellar degeneration and downbeat nystagmus and in 5 control subjects, using three-axis search coils. For each subject, response gains were calculated as (1) the ratio of instantaneous vertical eye velocity to pitch head velocity (at 30 ms and at 70 ms into the response), and (2) the ratio of peak eye velocity to peak head velocity. Gains varied more widely among patients. When calculated at 70 ms and using peak values, patients had higher gains for downward pitch, and normal subjects had symmetric gains. At 30 ms, gains were more symmetric in patients, but at that point control subjects actually had lower gains for downward pitch. Thus, the pitch gain ratio (ratio of downward gain to upward gain) was consistently greater in patients than in normal subjects. Because downward impulses were generally faster, eye velocities during downward and upward pitch for equivalent head speeds were also compared. Again, patients had higher gains for downward pitch. These results are consistent with the authors' hypothesis that cerebellar disease results in a higher sensitivity of anterior than posterior semicircular canal pathways, perhaps through loss of inhibition from the flocculus/paraflocculus complex on anterior canal secondary neurons in the vestibular nuclei. The pitch gain asymmetry was larger than, and did not correlate with, the velocity of spontaneous upward drift. This supports the notion that other mechanisms are likely to contribute to downbeat nystagmus in these patients.

Adult↗
PubMed2005

Cerebellar disease alters the axis of the high-acceleration vestibuloocular reflex.

L. W. Schultheis and D. A. Robinson showed that the axis of the rotational vestibuloocular reflex (RVOR) cannot be altered by visual-vestibular mismatch ("cross-axis adaptation") when the vestibulocerebellum is lesioned. This suggests that the cerebellum may calibrate the axis of eye velocity of the RVOR under natural conditions. Thus we asked whether patients with cerebellar disease have alterations in the RVOR axis and, if so, what might be the mechanism. We used three-axis scleral coils to record head and eye movements during yaw, pitch, and roll head impulses in 18 patients with cerebellar disease and in a comparison group of eight subjects without neurologic disease. We found distinct shifts of the eye-velocity axis in patients. The characteristic finding was a disconjugate upward eye velocity during yaw. Measured at 70 ms after the onset of head rotation, the median upward gaze velocity was 15% of yaw head velocity for patients and <1% for normal subjects (P < 0.001). Upward eye velocity was greater in the contralateral (abducting) eye during yaw and in the ipsilateral eye during roll. Patients had a higher gain (eye speed/head speed) for downward than for upward pitch (median ratio of downward to upward gain: 1.3). In patients, upward gaze velocities during both yaw and roll correlated with the difference in anterior (AC) and posterior canal excitations, scaled by the respective pitch gains. Our findings support the hypothesis that upward eye velocity during yaw results from AC excitation, which must normally be suppressed by the intact cerebellum.

Acceleration↗
PubMed1977

Gaze failure, drifting eye movements, and centripetal nystagmus in cerebellar disease.

Three abnormalities of eye movement in man are described which are indicative of cerebellar system disorder, namely, centripetally beating nystagmus, failure to maintain lateral gaze either in darkness or with eye closure, and slow drifting movements of the eyes in the absence of fixation. Similar eye movement signs follow cerebellectomy in the primate and the cat. These abnormalities of eye movement, together with other signs of cerebellar disease, such as rebound alternating, and gaze paretic nystagmus, are explained by the hypothesis that the cerebellum helps to maintain lateral gaze and that brain stem mechanisms which monitor gaze position generate compensatory biases in the absence of normal cerebellar function.

Adult↗
PubMed1990

Bovine viral diarrhea virus-induced cerebellar disease in a calf.

Bovine viral diarrhea virus (BVDV) was isolated from buffy coat cells of a 10-day-old calf with signs of cerebellar disease--ataxia, hypermetria, and intention head tremor. The tentative diagnosis was BVDV-induced cerebellar hypoplasia. At necropsy, gross lesions were not identified. Histologic findings suggested BVDV-induced diffuse hypomyelination throughout the CNS, as reported in the United Kingdom and The Netherlands.

Animals↗
PubMed1976

Alcoholic cerebellar disease and seizures.

Forty-eight chronic alcoholic patients with a clinical picture consistent with midline cerebellar disease were evaluated regarding alcohol related seizures. These seizures were noted in about 15% of this patient group. This seizure incidence approximates that in the severely alcoholic hospitalized population. Thus, the midline cerebellar degeneration does not appear to influence the seizure diathesis in the chronic alcoholic.

Adult↗
PubMed1996

Lhermitte-Duclos disease (cerebellar gangliocytoma).

We report a case of Lhermitte-Duclos disease (cerebellar gangliocytoma) in a 7-year-old child with café au lait spots and mild cerebellar symptoms. Findings on computed tomography 4 years earlier had been normal. Subsequent development of intracranial hypertension caused by hydrocephalus led to ventriculoperitoneal shunting. The appearance of the cerebellum on magnetic resonance imaging was supportive of the diagnosis, and open biopsy confirmed it.

Cerebellar Neoplasms↗
PubMed2006

Stiff person syndrome with cerebellar disease and high-titer anti-GAD antibodies.

We report five of 38 patients with stiff person syndrome (SPS), who also had cerebellar disease, gait ataxia, dysarthria, and oculomotor dysfunction (SPS-Cer). Cerebellar manifestations either preceded SPS or occurred concurrently. Brain MRI was normal. The intrathecal production of glutamic acid decarboxylase antibodies was elevated. Gamma-aminobutyric acid-enhancing drugs and immunotherapies improved only the stiffness. SPS-Cer is a distinct subset of SPS causing a more severe and complex clinical phenotype.

Adult↗
PubMed1989

On the role of feedback in maintaining constant grip force in patients with cerebellar disease.

The effect of visual feedback on maintaining low finger forces was investigated in patients with chronic cerebellar disease. Precise information about deviation from target force was compared with discrete feedback signaling only 3 states of performance and a condition of withdrawal of feedback. Forces were produced under isometric conditions and against a spring load (anisometric condition). Large performance differences were observed dependent on feedback condition. Maintenance of anisometric force was found to be nearly normal in patients with severe deficits in controlling isometric force.

Biofeedback, Psychology↗
PubMed1988

Control of isometric finger force in patients with cerebellar disease.

Control of isometric forces during grasping or handling of objects is an essential feature of all skilled manual performances. Previous studies of hand function in cerebellar patients were restricted to movements; force control was only investigated under isotonic conditions in combination with movements. Control of isometric forces during voluntary contraction of finger muscles was investigated in 31 patients with chronic cerebellar disease and in 20 normal controls. Eight patients with Friedreich's ataxia were considered to be typical for a disease affecting the afferents to the cerebellum; 4 patients with anterior lobe atrophy, which affects leg movements to a greater extent than finger movements, were compared with 3 patients with hemisphere lesions; 16 patients suffered from diffuse cerebellar atrophy. Using a recently developed microcomputer system for the continuous measurement of finger force, control of isometric force was studied in several tasks within the same subjects. The tasks included the maintenance of constant force output at different force levels with and without visual feedback, fast repetitive force changes, tracking of a sinusoidal target presented visually, and measurement of maximum grip force. The amount of voluntary contraction in terms of muscular power was normal in all patients; in all other tasks clear deficits were observed. The extent of the disturbances was highly variable between patients even within the same clinical subgroup. The detailed analysis of force traces revealed a great variety in types of disturbance. The frequently observed slowing of the speed in repetitive force changes can be attributed to different components in different patients and not only to difficulties at turning points as might be predicted from comparable movement studies. In addition, performance deficits across different tasks were not uniform, indicating dissociation of impairment. Deficits in maintaining force, which may be interpreted as dysmetria or due to tremor, do not necessarily imply an abnormality in diadochokinesis, as measured in fast repetitive force changes, nor does the converse apply.

Adolescent↗
PubMed2002

Dissociation of habit-learning in Parkinson's and cerebellar disease.

Damage to the medial-temporal region is known to result in declarative (explicit) memory deficits but nondeclarative (implicit) memory is largely unaffected by such lesions. Earlier studies have shown that some forms of implicit learning depend on cerebellar circuits but remain preserved following affections of the basal ganglia circuits. It is unknown which forms of implicit learning persist in patients with cerebellar pathology but are affected after basal ganglia lesions. Therefore, we determined if a test sensitive for habit-learning (probabilistic classification task) resulted in normal values for patients with cerebellar disease but resulted in affected results in patients with Parkinson's disease (PD). To this end, 23 patients with PD, 16 patients with familial or idiopathic cerebellar degeneration (CD), and 20 controls were tested for habit-learning. There was no impairment of patients with CD for the early learning period but there was abnormal learning in the PD group. For a later learning period, the patients with the PD showed improved performance. We conclude that the probabilistic learning task is an implicit, nonmotor learning task which is sensitive for basal ganglia pathology but remains unaffected in the case of cerebellar pathology. Such a test may be of special interest for the detection and possible neurobehavioral treatment of cognitive and motor deficits.

Aged↗
PubMed1998

Memory-guided saccadic eye movements: effects of cerebellar disease.

We compared the accuracy of oblique, memory-guided saccades if the eye is stationary or moves horizontally during the memory period. We studied 11 patients with cerebellar disease and 11 age-matched control subjects. Normal subjects showed similar accuracy of saccades for both conditions. In contrast, all patients showed greater errors if the eye moved horizontally during the memory period; however, errors of both vertical and horizontal components of memory-guided saccades were similar. Thus, inaccuracy of memory-guided saccades could not be simply attributed to failure to internally monitor change in horizontal gaze during the memory period. Instead, we propose that the greater saccadic errors which occurred when gaze changed during the memory period reflected a disruption of predictive mechanisms governing eye movements.

Adult↗
PubMedDate not supplied

[Neuropsychological study of 12 patients with pure degenerative cerebellar disease].

INTRODUCTION: The cerebellum has been traditionally associated with motor control learning and performance. However, since 1970 a growing body of clinical and experimental evidences has suggested that the cerebellum may be involved in nonmotor cognitive functions as well. OBJECTIVE: To explore the presence of eventual cognitive impairment in non-demented patients with isolated degenerative cerebellar diseases. PATIENTS AND METHODS: Twelve patients with the diagnosis of selective degenerative cerebellar disorders, either inherited or sporadic, were selected (mean age: 40.42 +/- 13.49 years; mean education level: 9.92 +/- 3.99 years; duration of illness: 12.13 +/- 11.27 years, MMSE: 26.75 +/- 1.5) and evaluated through a standardized neuropsychological tests battery. Normalized Z scores were estimated and compared against 0, employing the t test for one sample. RESULTS: Significant cognitive deficits were found in the following domains: executive, visuo-spatial, memory and attention functions. Performance on the Wisconsin test showed a significative number of perseverative errors. Memory deficits included verbal learning and free recall difficulties, with good recognition of the material presented. CONCLUSIONS: The findings of this study are consistent with the role of the cerebellum as modulator of mental functions. The cognitive deficits resulting from cerebellar pathology may be related with the disruption of cerebello-cortical connexions involving a complex network which includes the prefrontal region, suggesting that the cerebellum may process cortical information coming from different areas linked with the control of cognition.

Adolescent↗
PubMed1991

Ataxia, dysmetria, tremor. Cerebellar diseases.

Diseases affecting the cerebellum typically cause ataxia, coupled with dysmetria and tremor. Dysmetria is a condition in which there is improper measuring of distance in muscular acts; hypermetria is overreaching (overstepping) and hypometria is underreaching (understepping). Tremor refers to an involuntary, rhythmic, oscillatory movement of a body part. The tremor of cerebellar disease typically is exaggerated by goal-oriented movements (intention tremor). Cerebellar lesions also often cause loss of the menace response, despite the presence of normal vision. The anatomic basis for this phenomenon is obscure. The principal disease affecting the cerebellum in cats is cerebellar hypoplasia due to in utero infection with the panleukopenia virus. This disease will be discussed here. Neurologic signs of cerebellar involvement also may be seen in association with those diseases that affect the CNS multifocally. In these cats, there may be additional signs indicating involvement of other anatomic areas or the cerebellar deficits may occur alone (see discussion of multifocal diseases in Multiple Neurologic Deficits: Inflammatory Diseases [page 426] and Multiple Neurologic Deficits: Noninfectious Diseases [page 440]).

Animals↗