Midbrain ataxia: an introduction to the mesencephalic locomotor region and the pedunculopontine nucleus.
ABSTRACT OBJECTIVE: Although gait ataxia is usually associated with cerebellar lesions, we review a less familiar cause. We present three patients with dorsal midbrain lesions and correlate these presentations with recent findings in the functional anatomy of the midbrain. CONCLUSION: We suggest that these lesions involve a well-studied but generally unfamiliar area of the dorsal midbrain known as the mesencephalic locomotor region. More specifically, we hypothesize that involvement of the pedunculopontine nucleus, a major component of the mesencephalic locomotor region, may be at least partially responsible for producing midbrain ataxia.
SourceAvailable from: Paolo Nichelli[Show abstract] [Hide abstract]
ABSTRACT: We investigated structural brain differences between a group of early-mild PD patients at different phases of the disease and healthy subjects using voxel-based morphometry (VBM). 20 mild PD patients compared to 15 healthy at baseline and after 2 years of follow-up. VBM is a fully automated technique, which allows the identification of regional differences in the gray matter enabling an objective analysis of the whole brain between groups of subjects. With respect to controls, PD patients exhibited decreased GM volumes in right putamen and right parietal cortex. After 2 years of disease, the same patients confirmed GM loss in the putamen and parietal cortex; a significant difference was also observed in the area of pedunculopontine nucleus (PPN) and in the mesencephalic locomotor region (MLR). PD is associated with brain morphological changes in cortical and subcortical structures. The first regions to be affected in PD seem to be the parietal cortex and the putamen. A third structure that undergoes atrophy is the part of the inferior-posterior midbrain, attributable to the PPN and MLR. Our findings provide new insight into the brain involvement in PD and could contribute to a better understanding of the sequence of events occurring in these patients.01/2015; 2015:378032. DOI:10.1155/2015/378032
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ABSTRACT: In severe spinal cord injuries, the tracts conveying motor commands to the spinal cord are disrupted, resulting in paralysis, but many patients still have small numbers of spared fibers. We have found that excitatory deep brain stimulation (DBS) of the mesencephalic locomotor region (MLR), an important control center for locomotion in the brain, markedly improved hindlimb function in rats with chronic, severe, but incomplete spinal cord injury. The medial medullary reticular formation was essential for this effect. Functional deficits of rats with 20 to 30% spared reticulospinal fibers were comparable to patients able to walk but with strong deficits in strength and speed [for example, individuals with American Spinal Injury Association Impairment Scale (AIS)-D scores]. MLR DBS enabled close to normal locomotion in these rats. In more extensively injured animals, with less than 10% spared reticulospinal fibers, hindlimbs were almost fully paralyzed, comparable to wheelchair-bound patients (for example, AIS-A, B, and C). With MLR DBS, hindlimb function reappeared under gravity-released conditions during swimming. We propose that therapeutic MLR DBS using the brain's own motor command circuits may offer a potential new approach to treat persistent gait disturbances in patients suffering from chronic incomplete spinal cord injury.Science translational medicine 10/2013; 5(208):208ra146. DOI:10.1126/scitranslmed.3005972 · 14.41 Impact Factor