Ocular Motor Disorders Caused by Lesions in the Cerebrum
■ Receives inputs from the frontal eye field (FEF), supplementary eye field (SEF), dorsolateral prefrontal cortex (DLPC), internal medullary lamina of the thalamus, and substantia nigra pars compacta (SNpc, the dopaminergic portion) ■ Projects to substantia nigra pars reticulata (SNpr) and the globus pallidus ■ Receives inhibitory inputs from the caudate nucleus ■ Sends inhibitory signals to intermediate layers of the superior colliculus Parkinson’s disease is a progressive neurodegenerative disorder that affects about 1% of adults over 60 years of age. 1. Loss of pigmented dopaminergic neurons in the SNpc 2. Presence of Lewy bodies (not specific for Parkinson’s disease) 3. Decreased dopamine reaching the striatum causes increased inhibitory output from the globus pallidus internal segment and SNpr, thereby inhibiting movement 1. Standard therapy: levadopa and carbidopa (a peripheral decarboxylase inhibitor to reduce motor fluctuations and dyskinesia) e.g., such as Sinemet or Sinemet CR 2. Monoamine oxidase-β inhibitor (e.g., Selegiline); may have neuroprotective effect 3. Dopamine agonist (e.g., bromocriptine, a D2 agonist, and apomorphine, a D1 and D2 agonist) 4. Anticholinergics (e.g., Benzhexol) 5. Amantadine (seldom used) 6. Surgery ■ Thalamotomy or thalamic deep brain stimulation of the ventral lateral nucleus to reduce medically refractory tremor. The mechanism of action is unknown; these procedures may destroy autonomous neural activity (synchronous bursts) that has the same frequency as the limb tremor. ■ Pallidotomy or pallidal stimulation to reduce contralateral dyskinesia (e.g., bradykinesia, rigidity, and tremor).