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  • Pharmacological Treatment of Parkinson Disease: A Review

    Abstract Full Text
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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.
  • JAMA April 23, 2014

    Figure 4: Algorithm for the Treatment of Parkinson Disease With Predominant Postural Instability and Gait Impairment

    aSuboptimal benefit is defined as improvement in parkinsonian symptoms following initiation of therapy, but the patient still experiences a bothersome or disabling degree of symptoms either continuously or intermittently. In these cases, increase the dose of current medication if the patient is not receiving a maximal dose or add another medication. If benefit is absent, stop the current medication and try another.bIf the patient experiences inadequate symptom control while on current therapy and there was more than 1 treatment option in the previous step, go back to previous step and try an alternate treatment option. If all options in the previous step fail to provide adequate symptom control, move to the next step in the algorithm.cPersistent ambulatory problems including freezing, postural instability, and falls despite optimal dopaminergic therapy are generally refractory to other treatments. Trials of amantadine or a cholinesterase inhibitor, added to ongoing dopaminergic therapy for other symptoms of Parkinson disease, can be considered.dConsider deep brain stimulation if motor fluctuations are refractory to medical therapy and postural instability and/or gait impairment remains responsive to levodopa.
  • Treatment of Parkinson Disease: A 64-Year-Old Man With Motor Complications of Advanced Parkinson Disease

    Abstract Full Text
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    JAMA. 2012; 307(21):2305-2314. doi: 10.1001/jama.2012.4829
    Mr L, a 64-year-old man with advanced Parkinson disease, was experiencing increasing difficulty buttoning, tying his shoe laces, and periodic gait freezes. He has found some relief after an increase in his carbidopa-levodopa-entacapone regimen. Tarsy discusses treatment options including deep brain stimulation.
  • Neurological Studies Launched

    Abstract Full Text
    JAMA. 2005; 293(16):1966-1966. doi: 10.1001/jama.293.16.1966-c
  • JAMA January 21, 2004

    Figure 3: Imaging Results of the REAL-PET and CALM-PD-CIT Studies

    At each time point in both studies, the rate of decline in the surrogate imaging marker of nigrostriatal function is greater in patients treated with levodopa compared with those treated with the dopamine agonist. REAL-PET indicates Requip as Early Therapy versus L-dopa; CALM-PD, parallel-group, double-blind comparison study of pramipexole and carbidopa/levodopa in the treatment of PD; and CIT, 2β-carbomethoxy-3β-(4-iodophenyl)tropane.
  • Neuroprotection in Parkinson Disease: Mysteries, Myths, and Misconceptions

    Abstract Full Text
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    JAMA. 2004; 291(3):358-364. doi: 10.1001/jama.291.3.358
  • Dopamine Transporter Brain Imaging to Assess the Effects of Pramipexole vs Levodopa on Parkinson Disease Progression

    Abstract Full Text
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    JAMA. 2002; 287(13):1653-1661. doi: 10.1001/jama.287.13.1653
  • JAMA April 3, 2002

    Figure 1: Patient Flow Diagram

    PD indicates Parkinson disease; CALM-PD, parallel-group, double-blind comparison study of pramipexole and carbidopa/levodopa in the treatment of PD; CIT, 2β-carboxymethoxy-3β(4-iodophenyl)tropane.
  • JAMA April 3, 2002

    Figure 3: Change From Baseline in β-CIT Uptake

    β-CIT indicates 2β-carboxymethoxy-3β(4-iodophenyl)tropane. The rate of loss of striatal β-CIT uptake (specific/nondisplaceable activity) is reduced for those subjects initially treated with pramipexole compared with those initially treated with levodopa. The mean (SE) percentage loss of uptake from baseline is indicated during a 46-month period.
  • 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 14, 2001

    Figure 2: Two-Point Maximum Parametric Lod Scores (MLODs) Stratified by Age at Onset of PD and Levodopa Response

    Each point represents the MLOD at 1 of the 344 markers analyzed in each subset. Regions of interest (see the "Methods" section) are located above the dotted horizontal line (MLOD >1.5). cM indicates centimorgans; PD, Parkinson disease.
  • Complete Genomic Screen in Parkinson Disease: Evidence for Multiple Genes

    Abstract Full Text
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    JAMA. 2001; 286(18):2239-2244. doi: 10.1001/jama.286.18.2239
  • 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 3: Unified Parkinson's Disease Rating Scale

    Scores are expressed as mean (SE). In each case, a lower score indicates less severe features of the disease. Scores were calculated over the course of the trial by treatment assignment. Significant differences (P≤.002) were evident between the pramipexole and levodopa groups at week 10 and at all subsequent visits.
  • JAMA October 18, 2000

    Figure 4: Mean Changes in Quality-of-Life Scores Over the Course of the Trial

    Quality-of-life scores improved by approximately 2 units during the first 6 months of the trial. At the end of the trial (23.5 months), the group difference in the mean change was statistically significant (P = .006) for the Parkinson's Disease Quality of Life Scale and marginally significant for the EuroQol (P = .06), with the scores higher for those in the levodopa group. Differences in mean changes were not significant at any other time points.
  • Dopamine Agonists in Early Therapy for Parkinson Disease: Promise and Problems

    Abstract Full Text
    JAMA. 2000; 284(15):1971-1973. doi: 10.1001/jama.284.15.1971
  • Several Classes of New Drugs Emerging for Parkinson Disease

    Abstract Full Text
    JAMA. 1999; 282(10):929-931. doi: 10.1001/jama.282.10.929-JMN0908-2-1