Background: Pathological gambling is a rare potential complication related to treatment of Parkinson disease (PD). However, the etiology of this behavior is poorly understood.Objective: To examine the relationship between medical therapy for PD and pathological gambling.Methods: In our routine movement disorders practice (2002)(2003)(2004), we encountered 11 patients with idiopathic PD who had recently developed pathological gambling. We assessed the relationship to their medical therapy and compared them with cases identified by systematic review of the existing literature on pathological gambling and PD.Results: All 11 patients with PD and pathological gambling were taking therapeutic doses of a dopamine ago-nist; 3 of these patients were not treated with levodopa. In 7 patients, pathological gambling developed within 3 months of starting to take or escalating the dose of the agonist; in the other 4 with a longer latency, gambling resolved after the agonist use was discontinued. Pramipexole dihydrochloride was the agonist in 9 of 11 cases in our series and 10 of 17 in the literature (68% in total).Conclusions: Dopamine agonist therapy was associated with potentially reversible pathological gambling, and pramipexole was the medication predominantly implicated. This may relate to disproportionate stimulation of dopamine D 3 receptors, which are primarily localized to the limbic system.

We conclude that QTc dispersion appears to be a valid predictor of arrhythmias.

In patients referred for ECT, baseline QTc dispersion does not correlate with presence of cardiac illness or concomitant psychotropic usage.

Research in the neurosciences in recent decades has shown that the central nervous system is not a structurally static organ as was believed previously, but instead is a dynamic system that constantly undergoes structural and functional reorganization. The term brain plasticity refers to the constant cellular and intercellular modifications that occur during normal development and after neurologic R esearch in the neurosciences in recent decades has revealed that the brain is not a structurally static organ as was believed previously, but instead is a dynamic system that continuously changes in structure and function. The term brain plasticity refers to the inherent capacity and resiliency of the brain to undergo structural and functional modifications. These changes are especially evident during development and after neurologic injury and can be best conceptualized as spanning throughout various levels: brain level (glial and vascular support), network level (changes in interconnection between neurons), intercellular level (qualitative and quantitative changes at the synaptic level, including synaptic sprouting), intracellular level (changes in mitochondrial and ribosomal function), biochemical level (protein conformation, enzyme mobilization), and genetic level (transcription, translation, and posttranslation modifications). 1 Because the brain is the source and end organ for neurologic, cognitive, and psychological functions, modifications in the brain's structure and function are mirrored by changes in these areas.Brain plasticity is of particular interest to neurologists because plastic changes are seen clearly after neurologic injury, and these changes correlate with either improvement or deterioration of neurologic function. Function is the cognitive and/or physical activity through which individuals interact with self and the external world and includes mobility, communication, cognition, and sexual ac-injury and result in changes in neurologic function. The discovery that central nervous system plasticity after injury can be directed toward functional improvement with use of specific modalities has opened up a new dimension in the care of the neurologically impaired patient, termed restorative neurology. Mayo Clin Proc. 2004;79:796-800 tivity. From a functional perspective, it is helpful to divide cortical reorganization after neurologic injury into functionenabling plasticity, which leads to an improvement in neurologic function, or function-disabling plasticity, which results in deterioration of function. Examples of functionenabling plasticity include changes in cortical representation and improved function seen with forced use of the affected extremity after injury. Examples of function-disabling plasticity include modifications in the cortical representation for a specific motor function after nonuse, which results in decreased motor capabilities. Other examples include late development of dystonias and other movement disorders seen after injury. Also, phantom limb and phantom sensation after spinal...