Surgical treatment of Parkinson disease (PD) was described as early as 1940 and, until recently, had focused on ablative procedures of the thalamus and globus pallidus pars interna (GPi). These surgical treatments (especially pallidotomy) rose to prominence in the era before levodopa (LD) but later reemerged as popular approaches in the 1990s. They were rapidly replaced in the late 1990s by deep brain stimulation (DBS), mainly as a result of concerns for adverse effects resulting from bilateral lesions as well as the irreversible effects resulting from poorly placed lesions. Furthermore, a new target, the subthalamic nuclei (STN) was identified to be an effective target and quickly became the most common site for DBS electrode placement.^1-3

Most cases of Parkinson's disease are considered sporadic and idiopathic, although there is evidence of familial aggregation, and several monogenic forms have been identified.¹ Recently, several pathogenic mutations in the highly conserved leucine-rich repeat kinase 2 gene (LRRK2) have been associated with autosomal dominant, late-onset Parkinson's disease.¹ Of these, the G2019S substitution is the most frequently reported.² It occurs in about 1 percent of unselected cases and 3 to 6 percent of familial cases of Parkinson's disease in persons primarily of European ancestry² but in 7 of 17 cases of familial disease in persons from North Africa (41 percent).³ At most, 5 carriers among 10,000 persons without Parkinson's disease have been reported.^2-4

Research from JAMA Neurology — Management of Referred Deep Brain Stimulation Failures — A Retrospective Analysis From 2 Movement Disorders Centers

Spasticity is a disorder of excess muscle tone associated with CNS disease. We hypothesized that botulinum toxin, a neuromuscular blocking agent, would reduce tone in spastic muscles after stroke. This randomized, double-blind, placebo-controlled, multicenter clinical trial evaluated the safety and efficacy of botulinum toxin type A (BTXA) in the treatment of chronic upper limb spasticity after stroke. Thirty-nine patients received IM injections of a total dose of either 75, 150, or 300 units of BTXA or placebo into the biceps, flexor carpi radialis, and flexor carpi ulnaris muscles. At baseline, patients demonstrated a mean wrist flexor tone of 2.9 and elbow flexor tone of 2.6 on the Ashworth Scale (0 to 4). Treatment with the 300-unit BTXA dose resulted in a statistically and clinically significant mean decrease in wrist flexor tone of 1.2 (p = 0.028), 1.1 (p = 0.044), and 1.2 (p = 0.026) points and elbow flexor tone of 1.2 (p = 0.024), 1.2 (p = 0.028), and 1.1 (p = 0.199) at weeks 2, 4, and 6 postinjection. In the placebo group, tone reduction at the wrist was 0.3, 0.2, and 0.0 and at the elbow was 0.3, 0.3, and 0.6 at weeks 2, 4, and 6 postinjection. BTXA groups reported significant improvement on the physician and patient Global Assessment of Response to Treatment at weeks 4 and 6 postinjection. There were no serious adverse effects. In this 3-month study, BTXA safely reduced upper extremity muscle tone in patients with chronic spasticity after stroke.