Neuroscience Poster Session
The cerebellum has complex functions concerned with sensorimotor integration and therefore plays important roles in movement control by refining the motor command with temporal and spatial parameters (1-3). All the inputs and outputs of the cerebellum are conducted via bilaterally paired cerebellar peduncles. Despite the homogeneous cortical structure of the cerebellum, specific motor functions can be ascribed to its functional compartments.
In previous studies, we suggested that lesions in the cortico-cerebello-thalamo-cortical pathway was the primary suspect being responsible for action tremor (AT) and impaired control of visually-guided tracking movements in patients with multiple sclerosis (MS)(4); and AT was weighted predominantly at the distal joint of the arm (5). A major difficulty in interpreting our previous results in a group of patients was that the variable nature of MS in the size, number and localisation of demyelinating lesions not only produced great variations between the patients we studied, but made almost impossible to correlate any specific motor deficits with those multiple and dispersed lesions. Focal lesions, however, provide valuable pathological models for correlating specific impairments in sensorimotor behaviour with certain functional sub-units in the cerebellar connections (6-8).
In the present report, we, therefore, investigated specific impairments in the control of visually guided ramp tracking movements and of pre-programmed pointing movements in one selected patient who had focal MS lesions in the cerebellum and brainstem clearly defined by magnetic resonance imaging (MRI).
Materials and Methods
The patient and normal controls:
Visually-guided motor tasks:
Anatomic location of lesions: Multiple focal lesions of hyperintense signal and a few millimetres in diameter were seen in the white matter of the right cerebellar hemisphere and bilaterally in the inferior/middle cerebellar peduncles (Figure, left half), and the right cerebral peduncle (Figure, right half). The lesions in the right cerebellum were located latero-ventrally around the dentate nucleus, and thus would primarily affect the efferent fibres from the ipsilateral cerebellar cortex. In addition, afferent fibres from the brainstem to the cerebellum could have been affected. The lesions in the bilateral inferior/middle peduncles would have disrupted connections between the cerebellum and neighbouring brainstem structures, including the lateral and inferior vestibular nuclei, reticular formations and the inferior olive. The focal lesion in the right cerebral peduncle would have damaged part of the cerebrospinal tract.
Figure: T2-weighted MRI scan revealed that multiple focal lesions of a few millimetres in diameter with high signal in the white matter ventrally around the right dentate nuclei (white arrow, left half), the centres of bilateral inferior cerebellar peduncles (black arrows) and right cerebral peduncle in which lateral corticospinal tract fibres were mainly involved (white arrow, right half).
Impairments in control of visually guided arm movements: Results of arm tracking and pointing movements from the patient in comparison with normal controls are listed in the table, in which values beyond the 95% confidence range of that in controls are defined as abnormal.
Discussion and Conclusion
In the present report, we investigated specific impairments in visuomotor behaviour of the arm in "on-line" control of visually guided tracking movements and in the "of-line" control of pre-programmed pointing movements in a patient who had focal MS lesions in the cerebellum and brainstem defined by MRI images. The patient had predominantly distal action tremor in both arms with increased tracking errors and prolonged reaction times. Despite being dysmetric with increased spatial variability during pointing movements, the patient was able to adapt his movements amplitude to a gain change in the visual feedback even in the presence of significant visual "noise".
The bilateral arm AT and disturbances in equilibrium and walking in this patient were very likely caused by the symmetrical lesions in the inferior/middle cerebellar peduncles. These lesions would have damaged the fibres connecting the cerebellum and neighbouring brainstem structures including the lateral and inferior vestibular nuclei, reticular formation and inferior olive. These lesions could also be responsible for his detected internuclear ophthalmoplegia in the left. However, he had no palatal tremor despite the obvious axial involvement in his clinical symptoms. The somatotopy within the cerebellar-brainstem connections proposed by Brown and colleagues8 may be an explanation, as the focal lesions appear to have spared the connections to medial cerebellar areas contributing to oculomotor and palatal control.
Lesions in the cortico-cerebello-thalamo-cortical pathway are the primary suspects for causing distal arm tremor in patients with MS (4,5). MS lesions are believed to primarily involve the white matter, and the lesions in this patient may therefore block the afferents and efferents of the cerebellar nuclei, if not damaging them directly. The patient's on-line closed-loop control of tracking movements may have been further impaired by increased delays in the feedback loop caused by possible conduction blockage. Thus, lesions in this part were mainly responsible for the impaired control of movement timing reflected by the delay in visually cued reaction time and decrease in accuracy of tracking velocity. His tracking behaviour was further disturbed by the effect of his AT on the cursor, adding dramatically to the error between target and cursor. Complimentary to previous studies on patients with cerebellar damages due to brain trauma (6) or stroke (7), we propose that in addition to damage in the superior cerebellar peduncles which contain ascending outflow to the motor cortex, the impaired on-line control of visually guided tracking movement can also occur as a consequence of damage in inferior and middle cerebellar peduncles which contain spinal afferents to the cerebellum and the brain stem-cerebellum connections.
The pointing movements of the patient performed "open-loop" with respect to visual feedback were dysmetric with increased spatial variability in pointing to visual targets. However, the average of his movement amplitudes over a number of trials was not significantly different from that of the normal controls, suggesting that he was able to scale his basic motor commands for pointing to the target; in other words, he was able to program his movements even though he had difficult to execute them accurately. He was able to efficiently adapt his movements when the gain of the "off-line" visual feedback of his movement was modified. Based on the results from our patient and another patient studied by Martin and colleagues (7) on a dart-throwing task, it appears that partial damage in the inferior and middle cerebellar peduncles does not significantly affect adaptation to changes in the visual feedback, nor do lesions to the ipsilateral cerebellar nuclei. Interestingly, our patient was able to adapt with much greater random visual noise superimposed on the visual feedback of his movement position (75%, comparing with 30% in the controls). This may be because his arm movements are normally very variable due to AT and dysmetria. Hence the addition of extra visual noise in the experiment may not be as disturbing as it is for the more consistent controls. Together these indicate that his off-line control for pointing movements was almost intact, i.e. he was able to select meaningful visual information from previous movements even in the presence of extra random noise and update his motor commend appropriately.
Finally, we suspect that the focal lesion in the right cerebral peduncle mainly involving the cerebrospinal tract may be the reason that motor impairments are noticeably worse in the left than right side.
Conclusive remarks: We have used two visually guided movement tasks, one dependent on on-line, and the other on off-line visual feedback to contrast the motor performance of a MS patient with focal cerebellar lesions to normal controls. The patient had severe difficulties in the on-line control of his movements, but near-normal control of adaptation of his off-line controlled movements. These results compliment investigations on the role of the cerebellum in motor control and learning.
1. Stein JF. Role of the cerebellum in the visual guidance of movement. Nature 1986;232:217-21.
2. Diener H-C, Dichgans J. Pathophysiology of cerebellar ataxia. Mov Disord 1992;2:95-109.
3. Horne MK, Butler EG. The role of the cerebello-thalamo-cortical pathway in skilled movement. Prog in Neurobiol 1995; 46:199-213.
4. Liu X, Miall RC, Aziz TZ, et al. Analysis of action tremor and impaired control of movement velocity in multiple sclerosis during visually-guided wrist tracking tasks. Mov Disord 1997;12:992-9.
5. Liu X, Miall RC, Aziz TZ, et al. Distal versus proximal arm tremor in multiple sclerosis assessed by visually guided tracking tasks. J Neurol Neurosurg Psychiatry in press.
6. Haggard P, Miall RC, Wade D, et al. Damage to cerebellocortical pathways after closed head injury: A behavioral and magnetic resonance imaging study. J Neurol Neurosurg Psychiatry 1995; 58:433-8.
7. Martin TA, Keating JG, Goodkin HP, et al. Throwing while looking through prisms. I. Focal olivocerebellar lesions impair adaptation. Brain 1996;119:1183-98.
8. Brown P, Rothwell JC, Stevens JM, et al. Cerebellar axial postural tremor. Mov Disord 1997;12: 977-84.
9. England MA, Wakely J. A colour atlas of the brain and spinal cord. Wolfe Publishing Ltd, London, 1991; pp170, 235.
10. Wolpert DM, Ghahramani Z, Jordan MI. Are arm trajectories planned in kinematic or dynamic coordinates? An adaptation study. Exp Brain Res 1995;103:460-70.
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|Liu, X; Ingram, HA; Miall, RC; Palace, JA; (1998). Correlating Selected Impairments in Visuomotor Control with Focal Lesions in the Cerebellum and Brainstem.. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Available at URL http://www.mcmaster.ca/inabis98/neuroscience/liu0134/index.html|
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