From
Dr. Amr Moursi
Movement Disorder Exam Questions for Neurosurgeons | MCQs, Concepts and Key Topics
With Dr. Amr Moursi
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Parkinson's Disease 3 items
Chapter 5 of 6 · Complications
Side effects
Stimulation Side Effects and Anatomical Correlates
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What the experts said
Functional neurosurgery is under-taught in basic training and most units don't do much of it.
Examiner expectations for functional neurosurgery are low and basic knowledge is sufficient.
Functional neurosurgery splits into three exam topics: movement disorders, pain surgery, and epilepsy.
Bradykinesia is mandatory for the diagnosis of Parkinson's disease.
Tremor responds best to deep brain stimulation in Parkinson's disease.
Gait freezing, speech, and cognition respond poorly to deep brain stimulation.
Cognition can be worsened by deep brain stimulation.
Balance, speech, and postural instability all respond poorly to deep brain stimulation.
The subthalamic nucleus is the first choice target for deep brain stimulation in Parkinson's disease.
The globus pallidus internus is the second choice target for deep brain stimulation in Parkinson's disease.
When dyskinesia dominates in Parkinson's disease, the globus pallidus internus is the preferred target because it smooths dyskinesia directly.
When tremor dominates in Parkinson's disease, the ventral intermediate nucleus of the thalamus is the preferred target.
The anterior limb of the internal capsule is an obsessive compulsive disorder target, not a Parkinson's disease target.
Inclusion criteria for deep brain stimulation include disease over 5 years, a meaningful levodopa response, disabling fluctuations, or refractory tremor.
Exclusion criteria for deep brain stimulation include dementia, untreated depression or psychosis, and atypical Parkinsonism like progressive supranuclear palsy and multiple system atrophy.
The levodopa challenge predicts the response to deep brain stimulation, not severity of disease.
Stimulation of the subthalamic nucleus roughly reproduces the patient's best medication on state.
A good levodopa response predicts a good stimulation response to deep brain stimulation.
Atypical Parkinsonism does not respond to deep brain stimulation and is a contraindication.
At the subthalamic nucleus, medial spread of stimulation hits the third cranial nerve and red nucleus, causing diplopia.
At the subthalamic nucleus, lateral spread of stimulation hits the internal capsule, causing contralateral twitching and dysarthria.
At the globus pallidus internus, ventral spread of stimulation hits the optic tract, causing phosphenes (flashes of light).
At the globus pallidus internus, posteromedial spread of stimulation hits the internal capsule, causing muscle contraction.
The side effect during stimulation tells you where the electrode is, and you correct by moving away from the structure you're hitting.
Motor fibers run in the internal capsule just lateral to the subthalamic nucleus.
Twitching during subthalamic nucleus stimulation means the electrode is too lateral and should be moved medially.
Reducing voltage during stimulation just shrinks the therapeutic window and doesn't fix electrode position.
Diplopia during subthalamic nucleus stimulation is the medial side effect from spread toward the third cranial nerve and red nucleus.
The optic tract is ventral to the globus pallidus internus, so ventral spread produces phosphenes.
The dopamine transporter scan separates Parkinson's disease from essential tremor and drug-induced tremor by showing reduced uptake in the posterior putamen.
The dopamine transporter scan does not distinguish Parkinson's disease from atypical Parkinsonism.