Parkinson Disease Medication

  • Author: Robert A Hauser, MD, MBA; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: May 10, 2012
 

Medication Summary

The cornerstone of symptomatic treatment for Parkinson disease (PD) is dopamine replacement therapy. The criterion standard of symptomatic therapy is levodopa (L-dopa), the metabolic precursor of dopamine, in combination with carbidopa, a peripheral decarboxylase inhibitor (PDI). This combination provides the greatest symptomatic benefit with the fewest short-term adverse effects.

Dopamine agonists such as pramipexole and ropinirole can be used as monotherapy to improve symptoms in early disease or as adjuncts to levodopa in patients whose response to levodopa is deteriorating and in those who are experiencing fluctuations in their response to levodopa.

Monoamine oxidase (MAO)-B inhibitors inhibitors such as rasagiline and selegiline provide symptomatic benefit as monotherapy in early disease and as adjuncts to levodopa in patients experiencing motor fluctuations.

Catechol-O -methyl transferase (COMT) inhibitors inhibitors such as entacapone and tolcapone may be used to increase the peripheral half-life of levodopa, thereby delivering more levodopa to the brain over a longer time.

Anticholinergic medications can be used for the treatment of resting tremor. However, they are not particularly effective for bradykinesia, rigidity, gait disturbance, or other features of advanced Parkinson disease; and cognitive side effects are common. Therefore, anticholinergics are usually reserved for the treatment of tremor that is not adequately controlled with dopaminergic medications.

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Dopamine Agonists

Class Summary

Dopamine agonists are effective as monotherapy in early PD and as adjuncts to levodopa/PDI (peripheral decarboxylase inhibitor) in moderate to advanced disease. Dopamine agonists directly stimulate postsynaptic dopamine receptors to provide antiparkinsonian benefit. All available dopamine agonists stimulate D2 receptors, an action that is thought to be clinically beneficial. The role of other dopamine receptors is currently unclear.

Dopamine agonists are effective to treat motor features of early PD, and they cause less development of motor fluctuations and dyskinesia than levodopa. For patients with motor fluctuations on levodopa/PDI, the addition of a dopamine agonist reduces off time, improves motor function, and allows lower levodopa doses.

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Carbidopa/levodopa (Sinemet, Sinemet CR, Parcopa)

 

Carbidopa/levodopa is approved for the treatment of symptoms of idiopathic PD, postencephalitic parkinsonism, and symptomatic parkinsonism that may follow injury to the nervous system by carbon monoxide and/or manganese intoxication. Levodopa, combined with a peripheral decarboxylase inhibitor (PDI) such as carbidopa, is the criterion standard of symptomatic treatment for PD; it provides the greatest antiparkinsonian efficacy in moderate to advanced disease with the fewest acute adverse effects. When administered alone, levodopa causes a high incidence of nausea and vomiting due to the formation of dopamine in the peripheral circulation. Carbidopa inhibits the decarboxylation of levodopa to dopamine in the peripheral circulation thereby reducing nausea and allowing for greater levodopa distribution into the CNS. Carbidopa does not cross the blood-brain barrier.

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Apomorphine (Apokyn)

 

Apomorphine is a nonergoline dopamine agonist indicated for the acute, intermittent treatment of hypomobility "off" episodes ("end-of-dose wearing off" and unpredictable "on/off" episodes) associated with advanced PD. It is administered by a subcutaneous injection. Although the exact mechanism by which apomorphine exerts its therapeutic effects in PD is unknown, it is thought to occur via activation of postsynaptic D2 receptors in the striatum.

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Pramipexole (Mirapex, Mirapex ER)

 

Pramipexole is approved as monotherapy in early disease and as adjunctive therapy to levodopa/PDI in more advanced stages. The mechanism of action of pramipexole as a treatment for Parkinson disease is unknown, although it is believed to be related to its ability to stimulate D2 dopamine receptors in the striatum. It is available as an immediate-release and an extended-release tablet.

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Ropinirole (Requip and Requip XL)

 

Ropinirole is approved as monotherapy in early disease and as adjunctive therapy to levodopa/PDI in more advanced disease. Ropinirole is a nonergot dopamine agonist that has high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine receptors; it binds with higher affinity to D3 than to D2 or D4 receptor subtypes. The mechanism of action of ropinirole is stimulation of dopamine D2 receptors in striatum. It is available as an immediate-release and an extended-release tablet.

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Amantadine

 

Amantadine is approved for the treatment of idiopathic PD, postencephalitic parkinsonism, and symptomatic parkinsonism, which may follow injury to the nervous system by carbon monoxide intoxication. It is also indicated in those elderly patients believed to develop parkinsonism in association with cerebral arteriosclerosis. The usual dosage is 100 mg given twice a day when used alone.

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Rotigotine (Neupro)

 

Dopamine agonist stimulating D3, D2, and D1 receptors. Improvement in Parkinson-related symptoms thought to be its ability to stimulate D2 receptors within the caudate putamen in the brain. Indicated for the treatment of the signs and symptoms of idiopathic Parkinson disease (PD). Dosage ranges differ for early-stage PD and advanced-stage PD. Available as transdermal patch that provides continuous delivery for 24 h

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Anticholinergic

Class Summary

Anticholinergics are commonly used as symptomatic treatment of PD, both as monotherapy and as part of combination therapy. Anticholinergic agents provide benefit for tremor in approximately 50% of patients but do not substantially improve bradykinesia or rigidity. If one anticholinergic does not work, try another.

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Trihexyphenidyl

 

Trihexyphenidyl is indicated as an adjunct in the treatment of all forms of parkinsonism (postencephalitic, arteriosclerotic, and idiopathic). It is often useful as adjuvant therapy when treating these forms of parkinsonism with levodopa.

It is a synthetic tertiary amine anticholinergic agent. It has a direct antispasmodic action on smooth muscle and has weak mydriatic, antisecretory, and positive chronotropic activities. In addition to suppressing central cholinergic activity, trihexyphenidyl may also inhibit reuptake and storage of dopamine at central dopamine receptors, thereby prolonging the action of dopamine. It is commonly used in combination with other antiparkinsonian agents. Generally, anticholinergic agents can help control tremor but are less effective for treating bradykinesia or rigidity.

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Benztropine mesylate (Cogentin)

 

Benztropine mesylate is approved for use as an adjunct in the therapy of all forms of PD. It partially blocks striatal cholinergic receptors, and by blocking muscarinic cholinergic receptors in the CNS, benztropine reduces the excessive cholinergic activity present in parkinsonism and related states. It can also block dopamine reuptake and storage in CNS cells. In general, anticholinergic agents can help control tremor but are less effective for treating bradykinesia or rigidity.

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MAO-B inhibitors

Class Summary

MAO-B inhibitors inhibit the activity of MAO-B oxidases that are responsible for inactivating dopamine.

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Selegiline (Eldepryl)

 

Selegiline is approved as adjunctive therapy to levodopa/carbidopa in patients who exhibit deterioration in response to that therapy. For patients who are experiencing motor fluctuations on levodopa/carbidopa, the addition of selegiline reduces off time, improves motor function, and allows levodopa dose reductions. If a patient experiences an increase in troublesome dyskinesia, reduce the levodopa dose. Selegiline blocks the breakdown of dopamine and extends the duration of action of each dose of levodopa.

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Rasagiline (Azilect)

 

Rasagiline is indicated for the treatment of the signs and symptoms of idiopathic PD as initial monotherapy and as adjunctive therapy to levodopa. Rasagiline is an irreversible MAO-B inhibitor that blocks dopamine degradation. Rasagiline at a dosage of 1 mg once daily is given as monotherapy. When it is given as adjunctive therapy, an initial dose of 0.5 mg once daily is administered. Dosage adjustments are required if clinical response is not seen.

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Acetylcholinesterase Inhibitors, Central

Class Summary

Pathologic changes in dementia associated with PD involve cholinergic neuronal pathways that project from the basal forebrain to the cerebral cortex and hippocampus. These pathways may be involved in memory, attention, learning, and other cognitive processes. Acetylcholinesterase inhibitors may exert their therapeutic effect by enhancing cholinergic function through inhibition of acetylcholinesterase.

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Donepezil (Aricept)

 

Donepezil is a reversible inhibitor of ACh and exerts its beneficial effects by enhancing cholinergic function. It is indicated for the treatment for dementia of the Alzheimer type.

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Rivastigmine (Exelon)

 

Rivastigmine is indicated for the treatment of mild to moderate dementia associated with PD. In addition, it is also approved for the treatment of mild to moderate dementia of the Alzheimer type.

Rivastigmine is a selective, competitive, and reversible acetylcholinesterase (ACh) inhibitor. It may reversibly inhibit cholinesterase, which may, in turn, increase concentrations of ACh available for synaptic transmission in CNS and thereby enhance cholinergic function. The effect may lessen as the disease process advances and fewer cholinergic neurons remain functionally intact.

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Galantamine (Razadyne, Razadyne ER)

 

Galantamine is a competitive and reversible inhibitor of ACh. It is approved for the treatment of mild to moderate dementia of the Alzheimer type.

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NMDA Antagonists

Class Summary

Persistent activation of CNS N-methyl-D-aspartate (NMDA) receptors by the excitatory amino acid glutamate has been hypothesized to contribute to the symptomatology of dementia. Agents such as memantine, which is an NMDA receptor antagonist, can prevent activation of the NMDA receptors.

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Memantine (Namenda, Namenda XR)

 

Memantine is approved for the treatment of moderate to severe dementia in Alzheimer disease. Initial dosage is 5 mg once daily for immediate-release tablets and 7 mg once daily for extended-release tablets. Dosage titration may be required based on clinical response.

Memantine is postulated to exert its therapeutic effect through its action as a low- to moderate-affinity, uncompetitive NMDA receptor antagonist. Blockade of NMDA receptors by memantine slows the intracellular calcium accumulation and helps prevent further nerve damage.

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COMT Inhibitors

Class Summary

Catechol-O -methyl transferase (COMT) inhibitors inhibit the peripheral metabolism of levodopa, making more levodopa available for transport across the blood-brain barrier over a longer time. For patients with motor fluctuations on levodopa/carbidopa, the addition of a COMT inhibitor decreases off time, improves motor function, and allows lower levodopa doses.

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Tolcapone (Tasmar)

 

Tolcapone is an adjunct to levodopa/carbidopa therapy in PD in patients who are experiencing motor fluctuations. Because of the risk of hepatotoxicity, tolcapone is reserved for patients who have not responded adequately to, or are not appropriate candidates for, other adjunctive medications. If improvement is not apparent within 3 weeks, this medication should be withdrawn.

Tolcapone is a selective and reversible inhibitor of COMT. In the presence of a decarboxylase inhibitor such as carbidopa, COMT is the major degradation pathway for levodopa. By inhibiting COMT, there are more sustained plasma levels of levodopa, as well as enhanced central dopaminergic activity.

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Entacapone (Comtan)

 

Entacapone is approved as an adjunct to levodopa/carbidopa for patients who are experiencing signs and symptoms of end-of-dose "wearing-off." The mechanism of action of entacapone is related to its ability to inhibit COMT and alter plasma pharmacokinetics of levodopa. When given in conjunction with levodopa and an aromatic amino acid decarboxylase inhibitor (eg, carbidopa), plasma levels of levodopa are more sustained than after administration of levodopa and an aromatic amino acid decarboxylase inhibitor alone. These sustained plasma levels of levodopa may result in more constant dopaminergic stimulation in the brain. This may lead to greater effects on signs and symptoms of PD, as well as increased levodopa adverse effects (which sometimes require a levodopa dose decrease).

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Carbidopa, levodopa, and entacapone (Stalevo)

 

Carbidopa/levodopa/entacapone is indicated for the treatment of PD to substitute (with equivalent strengths of each of the 3 components) for immediate-release carbidopa/levodopa and entacapone previously administered as individual products. It is also used to replace immediate-release carbidopa/levodopa therapy (without entacapone) when patients experience the signs and symptoms of end-of-dose "wearing-off" (only for patients taking a total daily dose of levodopa of 600 mg or less and not experiencing dyskinesias).

Carbidopa inhibits dopa decarboxylation, thereby allowing more complete levodopa distribution to the CNS. Levodopa is a dopamine precursor capable of crossing the blood-brain barrier, thereby increasing CNS dopamine following conversion. Entacapone inhibits COMT, another enzyme that metabolizes levodopa. COMT inhibition increases and sustains levodopa plasma levels, enabling more blood-brain barrier penetration.

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Contributor Information and Disclosures
Author

Robert A Hauser, MD, MBA  Professor of Neurology, Molecular Pharmacology and Physiology, Director, Parkinson's Disease and Movement Disorders Center, University of South Florida College of Medicine; Clinical Chair, Signature Interdisciplinary Program in Neuroscience

Robert A Hauser, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, and Movement Disorders Society

Disclosure: Ingelheim Pharmaceuticals, Inc Honoraria Advisory Board; Teva Neuroscience Honoraria Advisory Board; Impax Pharmaceuticals Honoraria Advisory Board; UCB, Inc Honoraria Advisory Board; GE Healthcare Honoraria Advisory Board; IPSEN Pharmaceuticals Honoraria Advisory Board; Novartis Pharmaceuticals Advisory Board; Parkinson Study Group Honoraria Advisory Board; Solvay Pharmaceuticals Honoraria Advisory Board; Quintiles Honoraria Advisory Board

Coauthor(s)

Kelly E Lyons, PhD  Research Associate Professor of Neurology, Director of Research and Education, Parkinson's Disease and Movement Disorder Center, University of Kansas Medical Center

Kelly E Lyons, PhD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Novartis Honoraria Speaking and teaching; Teva Neuroscience Honoraria Speaking and teaching; St Jude Medical Honoraria Board membership

Theresa A McClain, RN, MSN, ARNP-BC  Advanced Registered Nurse Practitioner and Investigator, Parkinson's Disease and Movement Disorders Center, University of South Florida College of Medicine

Theresa A McClain, RN, MSN, ARNP-BC is a member of the following medical societies: Sigma Theta Tau International

Disclosure: Teva Consulting fee Consulting; GSK Consulting fee Consulting; Valeant Pharm Consulting fee Consulting; Solvay Consulting fee Consulting; Shering Plough Consulting fee Consulting

Rajesh Pahwa, MD  Professor of Neurology, Director, Parkinson Disease and Movement Disorder Center, Department of Neurology, University of Kansas Medical Center

Rajesh Pahwa, MD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Additional Contributors

Ron L Alterman, MD Associate Professor of Neurosurgery, Mount Sinai School of Medicine; Consulting Surgeon, Department of Neurosurgery, Mount Sinai School of Medicine, Elmhurst Hospital, and Walter Reed Army Medical Center

Ron L Alterman, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Medical Society of the State of New York, and New York County Medical Society

Disclosure: Nothing to disclose.

Heather S Anderson, MD Assistant Professor, Staff Neurologist, Department of Neurology, Alzheimer and Memory Center, University of Kansas Medical Center

Heather S Anderson, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Jeff Blackmer, MD, FRCP(C) Associate Professor, Medical Director, Neurospinal Service, Division of Physical Medicine and Rehabilitation, The Rehabilitation Centre, University of Ottawa Faculty of Medicine; Executive Director, Office of Ethics, Canadian Medical Association

Jeff Blackmer, MD, FRCP(C) is a member of the following medical societies: American Paraplegia Society, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Thomas L Carroll, MD Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, Tufts University School of Medicine and Director, The Center for Voice and Swallowing, Tufts Medical Center

Thomas L Carroll, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Bronchoesophagological Association, American Laryngological Association, and American Medical Association

Disclosure: Merz aesthetics inc. Consulting fee Speaking and teaching

Richard J Caselli, MD Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale

Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi

Disclosure: Nothing to disclose.

Arif I Dalvi, MD Director, Movement Disorders Center, NorthShore University HealthSystem, Clinical Associate Professor of Neurology, University of Chicago Pritzker Medical School

Arif I Dalvi, MD is a member of the following medical societies: European Neurological Society and Movement Disorders Society

Disclosure: Nothing to disclose.

Nestor Galvez-Jimenez, MD, MSc, MHA Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society

Disclosure: Nothing to disclose.

Stephen T Gancher, MD Adjunct Associate Professor, Department of Neurology, Oregon Health Sciences University

Stephen T Gancher, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, and Movement Disorders Society

Disclosure: Nothing to disclose.

Michael Hoffmann, MBBCh, MD, FCP(SA), FAAN, FAHA Professor of Neurology, University of Central Florida College of Medicine; Director of Cognitive Neurology, Director of Stroke Program, James A Haley Veterans Affairs Hospital

Michael Hoffmann, MBBCh, MD, FCP(SA), FAAN, FAHA is a member of the following medical societies: American Academy of Neurology, American Headache Society, American Heart Association, and American Society of Neuroimaging

Disclosure: Nothing to disclose.

Daniel H Jacobs MD, FAAN, Associate Professor of Neurology, University of Florida College of Medicine; Director for Stroke Services, Orlando Regional Medical Center

Daniel H Jacobs is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience

Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Robert M Kellman, MD Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York Upstate Medical University

Robert M Kellman, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Rhinologic Society, American Society for Head and Neck Surgery, Medical Society of the State of New York, and Triological Society

Disclosure: GE Healthcare Honoraria Review panel membership; Revent Medical Honoraria Review panel membership

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Kat Kolaski, MD Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Jose G Merino, MD Medical Director, Suburban Hospital Stroke Program

Jose G Merino, MD is a member of the following medical societies: American Heart Association and American Stroke Association

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting; GYRUS ACMI Honoraria Consulting

Lorraine Ramig, PhD Professor, Department of Speech Language Hearing Sciences, University of Colorado at Boulder; Senior Scientist, National Center for Voice and Speech (NCVS); Adjunct Professor, Department of Biobehavior, Columbia University Teacher's College

Disclosure: Nothing to disclose.

Alan D Schmetzer, MD Professor Emeritus, Interim Chairman, Vice-Chair for Education, Associate Residency Training Director in General Psychiatry, Fellowship Training Director in Addiction Psychiatry, Department of Psychiatry, Indiana University School of Medicine; Addiction Psychiatrist, Midtown Mental Health Cener at Wishard Health Services

Alan D Schmetzer, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Clinical Psychiatrists, American Academy of Psychiatry and the Law, American College of Physician Executives, American Medical Association, American Neuropsychiatric Association, American Psychiatric Association, and Association for Convulsive Therapy

Disclosure: Eli Lilly & Co. Grant/research funds Other

Roy Sucholeiki, MD Director, Comprehensive Seizure and Epilepsy Program, The Neurosciences Institute at Central DuPage Hospital

Roy Sucholeiki, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and American Neuropsychiatric Association

Disclosure: Nothing to disclose.

Margaret M Swanberg, DO Assistant Professor of Neurology, Uniformed Services University; Chief of Neurobehavior Service, Walter Reed Army Medical Center; Assistant Chief, Department of Neurology, Walter Reed Army Medical Center

Margaret M Swanberg, DO is a member of the following medical societies: American Academy of Neurology and American Neuropsychiatric Association

Disclosure: Nothing to disclose.

Michele Tagliati, MD Associate Professor, Department of Neurology, Mount Sinai School of Medicine; Division Chief of Movement Disorders, Mount Sinai Medical Center

Michele Tagliati, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Movement Disorders Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

B Viswanatha, MBBS, MS, DLO Professor of Otolaryngology (ENT), Chief of ENT III Unit, Sri Venkateshwara ENT Institute, Victoria Hospital, Bangalore Medical College and Research Institute; PG and UG Examiner, Manipal University, India and Annamalai University, India

B Viswanatha, MBBS, MS, DLO is a member of the following medical societies: Association of Otolaryngologists of India, Indian Medical Association, and Indian Society of Otology

Disclosure: Nothing to disclose.

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Schematic representation of the basal ganglia - thalamocortical motor circuit and its neurotransmitters in the normal state. From Vitek J. Stereotaxic surgery and deep brain stimulation for Parkinson disease and movement disorders. In: Watts RL, Koller WC, eds. Movement Disorders: Neurologic Principles and Practice. New York: McGraw-Hill, 1997:240. Copyright, McGraw-Hill Companies, Inc. Used with permission.
Schematic representation of the basal ganglia - thalamocortical motor circuit and the relative change in neuronal activity in Parkinson disease. From Vitek J. Stereotaxic surgery and deep brain stimulation for Parkinson disease and movement disorders. In: Watts RL, Koller WC, eds. Movement Disorders: Neurologic Principles and Practice. New York: McGraw-Hill, 1997:241. Used with kind permission. Copyright, McGraw-Hill Companies, Inc.
Parkinson disease diary. The patient or caregiver should place 1 check mark in each half-hour time slot to indicate the patient's predominant response during most of that period. The goal of therapeutic management is to minimize off time and on time with troublesome dyskinesia. Copyright Robert Hauser, 1996. Used with permission.
Stages in the development of Parkinson disease (PD)-related pathology (path.). Adapted from Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K. Stages in the development of Parkinson's disease-related pathology. Cell Tissue Res. 2004 Oct;318(1):121-34.
Schematic diagram of the basal ganglia circuitry. Represented are the following: inhibitory (red arrows) and excitatory (green arrows) projections between the motor cortex, the putamen, the globus pallidus pars externa (GPe) and globus pallidus pars interna (GPi), the subthalamic nucleus (STN), the substantia nigra pars reticulata (SNr) and substantia nigra pars compacta (SNc), and the ventrolateral thalamus (VL). D1 and D2 indicate the direct (regulated by dopamine D1 receptors) and indirect (regulated by dopamine D2 receptors) pathways, respectively.
Sagittal section, 12 mm lateral of the midline, demonstrating the subthalamic nucleus (STN) (lavender). The STN is one of the preferred surgical targets for deep brain stimulation to treat symptoms of advanced Parkinson disease.
The deep brain stimulating lead is equipped with 4 electrode contacts, each of which may be used, alone or in combination, for therapeutic stimulation.
Axial, fast spin-echo inversion recovery magnetic resonance image at the level of the posterior commissure. The typical target for placing a thalamic stimulator is demonstrated (cross-hairs).
Implantation of the deep brain stimulation (DBS) lead.
Insertion of an electrode during deep brain stimulation for Parkinson disease.
Postoperative coronal magnetic resonance image (MRI) demonstrating desired placement of bilateral subthalamic nuclei-deep brain stimulation (STN-DBS) leads.
Radiograph of the skull depicting a deep brain stimulator and leads in a patient with Parkinson disease.
Lewy bodies in the locus coeruleus from a patient with Parkinson disease.
A: Schematic initial progression of Lewy body deposits in the first stages of Parkinson disease (PD), as proposed by Braak and colleagues. B: Localization of the cluster of significant volume reduction in PD compared with health control subjects. The significant cluster located in the medulla oblongata/pons is superimposed as a red blob on the mean normalized anatomic scan of all participants. The axial and sagittal sections are centered on the peak of significance (–1; –36; –49). This image using voxel-based morphometry (VBM), which searched for regional atrophy in idiopathic PD by comparing a group of subjects with the disease and a group of healthy controls. Jubault T, Brambati SM, Degroot C, et al. Regional brain stem atrophy in idiopathic Parkinson's disease detected by anatomical MRI. PLoS ONE. 2009;4(12):e8247.
Gross comparison of the appearance of the substantia nigra between a normal brain and a brain affected by Parkinson disease. Note the well-pigmented substantia nigra in the normal brain specimen on the left. In the brain of a Parkinson disease patient on the right, loss of pigmented substantia nigra due to depopulation of pigmented neurons is observed.
Lewy bodies are intracytoplasmic eosinophilic inclusions, often with halos, that are easily seen in pigmented neurons, as shown in this histologic slide. They contain polymerized alpha-synuclein; therefore, Parkinson disease is a synucleinopathy.
 
 
 
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