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  • Pharmacological Treatment of Parkinson Disease: A Review

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    JAMA. 2014; 311(16):1670-1683. doi: 10.1001/jama.2014.3654

    Connelly and Lang provide an evidence-based review of the initial pharmacological management of the classical motor symptoms of Parkinson disease and describe the management of medication-related motor complications as well as selected nonmotor symptoms of Parkinson disease.

  • JAMA April 23, 2014

    Figure 1: Schematic Illustration of Neurologic Pathways Affected in Parkinson Disease and Sites of Action of Medications for the Treatment of Motor Symptoms

    Available medications to treat the motor symptoms of Parkinson disease act on complex neurologic interactions in the striatum that affect motor activity. Dopaminergic afferents from the substantia nigra, glutamatergic afferents from the cerebral cortex and thalamus, and cholinergic striatal interneurons all converge to influence the activity of the main efferent neurons of the striatum, the medium spiny GABAergic neurons. Levodopa is transported from the peripheral circulation across the blood-brain barrier and is converted centrally to dopamine, replacing the neurotransmitter deficient in Parkinson disease. Outside the blood-brain barrier, in the peripheral circulation, dopamine decarboxylase inhibitors (DDCIs) block the conversion of levodopa to dopamine, and catechol-O-methyltransferase inhibitors (COMTIs) block its degradation to 3-0-methyldopa (3-0MD). In the striatum, levodopa, dopamine agonists, and monoamine oxidase type B inhibitors (MAOBIs) all have dopaminergic effects. Anticholinergic drugs and amantadine act on postsynaptic receptors for other neurotransmitters in the striatum. These neurotransmitters bind to and activate multiple different subtypes of receptors present on the various presynaptic afferents in the striatum, as well as on postsynaptic efferent medium spiny neurons. NMDA indicates N-methyl-d-aspartate.aTolcapone, unlike entacapone, is able to cross the blood-brain barrier and block degradation of levodopa and dopamine.bAmantadine has dopamine releasing effects in addition to affecting NMDA glutamate receptors.
  • Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction: The ROSE Acute Heart Failure Randomized Trial

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    JAMA. 2013; 310(23):2533-2543. doi: 10.1001/jama.2013.282190

    To examine the effect of low-dose dopamine or low-dose nesiritide added to diuretic therapy on decongestion and renal function in patients with acute heart failure, Chen and coauthors conducted a randomized clinical trial in 360 patients with heart failure and renal dysfunction in North America.

  • JAMA December 18, 2013

    Figure 2: Dopamine Strategy Subgroup Analysis

    Subgroup analysis of treatment effect. A, Cumulative urine volume during 72 hours. B, Change in cystatin C level from baseline to 72 hours with low-dose dopamine vs placebo.
  • Stem Cells Boost Dopamine

    Abstract Full Text
    JAMA. 2010; 303(24):2464-2464. doi: 10.1001/jama.2010.837
  • JAMA September 9, 2009

    Figure 3: Regression Slopes Between Dopamine D2/D3 Receptor and Dopamine Transporter Availability and Scores on Attention

    The Dimension of the Strengths and Weaknesses of Attention-Deficit/Hyperactivity Disorder (ADHD)–symptoms and Normal-behavior (SWAN) rating scale uses a positive scale for symptoms (1 to 3) and a negative scale for the opposite of the symptoms (−1 to −3) ranging from “far below average” to “far above average.” The negative numbers in some of the regions show that the ratio of the specific to nonspecific binding of the radioligand is very low for these regions. The solid line in each scatterplot corresponds to the regression line (line of best fit).
  • JAMA September 9, 2009

    Figure 2: Regions in the Brain in Which Dopamine Measures Were Lower in Participants With ADHD Than in Controls

    A, Regions showed significantly lower dopamine D2/D3 receptor availability in participants with attention-deficit/hyperactivity disorder (ADHD) than in controls (obtained from [11C]raclopride images).B, Regions showed significantly lower dopamine transporter availability in the participants with ADHD than in controls (obtained from [11C]cocaine images). Significance corresponds to P < .005, cluster >100 voxels. The yellow regions identify the areas in the brain for which the measures differed between controls and participants with ADHD. The location of the region that differed was similar for the dopamine D2/D3 receptor and for the dopamine transporter and included the locations of the left ventral striatum (including accumbens and ventral caudate), left midbrain, and left hypothalamus. The z coordinate maps the superior-inferior position.
  • Effects of Donor Pretreatment With Dopamine on Graft Function After Kidney Transplantation: A Randomized Controlled Trial

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    JAMA. 2009; 302(10):1067-1075. doi: 10.1001/jama.2009.1310
  • Evaluating Dopamine Reward Pathway in ADHD: Clinical Implications

    Abstract Full Text
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    JAMA. 2009; 302(10):1084-1091. doi: 10.1001/jama.2009.1308
  • Spinal Stimulation

    Abstract Full Text
    JAMA. 2009; 301(17):1758-1758. doi: 10.1001/jama.2009.570
  • Effects of Modafinil on Dopamine and Dopamine Transporters in the Male Human Brain: Clinical Implications

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    JAMA. 2009; 301(11):1148-1154. doi: 10.1001/jama.2009.351
  • JAMA September 12, 2007

    Figure: Interrelationships Between Neural Pathways That Mediate Nausea and Vomiting

    Achm indicates muscarinic acetylcholine receptor; D2, dopamine type 2 receptor; GERD, gastroesophageal reflux; GI, gastrointestinal; H1, histamine type 1 receptor; NK1, neurokinin type 1 receptor; 5HT2, 5-hydroxytryptamine type 2 receptor; and 5HT3, 5-hydroxytryptamine type 3 receptor.
  • JAMA December 21, 2005

    Figure: Role of Environment in Addiction Probed

    The environment may alter cocaine's reinforcing effects by dysregulation of the dopaminergic system. An imaging study of dominant and subordinate monkeys housed alone or together shows effects of environment on levels of dopamine D2 receptors (Morgan et al. NatNeurosci. 2002;5:169-174).
  • Research Yields Clues to Improving Cell Therapy for Parkinson Disease

    Abstract Full Text
    JAMA. 2002; 287(2):175-176. doi: 10.1001/jama.287.2.175
  • JAMA November 28, 2001

    Figure: Cocaine Addiction: Neural Pathways and Molecular Mechanisms

    The neural substrates of cocaine action are shown at 3 levels: A, neural pathways on which cocaine acts; B, medium spiny neurons in the nucleus accumbens (ventral striatum) and dorsal striatum (caudate nucleus and putamen), which receive dopamine afferents from the ventral tegmental area and substantia nigra, respectively; and C and D, molecular level, including the synapse (C) between the dopamine terminal and the medium spiny neuron in which cocaine acts to increase dopamine levels, and (D) altered gene expression in the nucleus of the medium spiny neuron that is hypothesized to yield transcripts and eventually proteins that act to remodel synapses. Synaptic remodeling is thought to consolidate addiction-related behaviors.
  • JAMA August 22, 2001

    Figure: Pay Attention: Ritalin Acts Much Like Cocaine

    Representative distribution volume PET images of the radiotracer [11C]raclopride from one of the study participants show that radiotracer binding is reduced at the level of the striatum (bottom left) after oral administration of 60 mg of methylphenidate. Reduced radiotracer binding indicates decreased availability of open dopamine receptors after methylphenidate-induced increases in extracellular dopamine. Cocaine produces a similar effect in those who take it. (Photo credit: Courtesy of Brookhaven National Laboratory)
  • Pay Attention: Ritalin Acts Much Like Cocaine

    Abstract Full Text
    JAMA. 2001; 286(8):905-906. doi: 10.1001/jama.286.8.905
  • Pramipexole vs Levodopa as Initial Treatment for Parkinson Disease: A Randomized Controlled Trial

    Abstract Full Text
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    JAMA. 2000; 284(15):1931-1938. doi: 10.1001/jama.284.15.1931
  • JAMA October 18, 2000

    Figure 2: Percentages of Patients Experiencing Dopaminergic Complications

    First dopaminergic complication is defined as the first occurrence of wearing off, dyskinesias, or on-off fluctuations.
  • JAMA September 8, 1999

    Figure: Several Classes of New Drugs Emerging for Parkinson Disease

    Striatal 18F-dopa uptake in a patient with PD at baseline and again 2 years later shows clear loss of dopamine storage along with clinical progression on the Unified Parkinson's Disease Rating Scale. (Credit: David Brooks, MD)