Surgical Treatment of Parkinson’s Disease and Other Movement Disorders pot

Surgical Treatment of

Parkinson’s Disease

and Other Movement Disorders

HUMANA PRESS

Surgical Treatment of

Parkinson’s Disease

and Other Movement Disorders

EDITED BY

Daniel Tarsy, MD

Jerrold L. Vitek, MD, PhD

Andres M. Lozano, MD, PhD

EDITED BY

Daniel Tarsy, MD

Jerrold L. Vitek, MD, PhD

Andres M. Lozano, MD, PhD

HUMANA PRESS

Surgical Treatment of Parkinson’s Disease

and Other Movement Disorders

C URRENT CLINICAL N EUROLOGY

Daniel Tarsy, MD, SERIES EDITORS

The Visual Field: A Perimetric Atlas, edited by Jason J. S. Barton and

Michael Benatar, 2003

Surgical Treatment of Parkinson’s Disease and Other Movement Disorders,

edited by Daniel Tarsy, Jerrold L. Vitek, and Andres M. Lozano, 2003

Myasthenia Gravis and Related Disorders, edited by Henry J. Kaminski, 2003

Seizures: Medical Causes and Management, edited by Norman Delanty, 2002

Clinical Evaluation and Management of Spasticity, edited by David A.

Gelber and Douglas R. Jeffery, 2002

Early Diagnosis of Alzheimer's Disease, edited by Leonard F. M. Scinto

and Kirk R. Daffner, 2000

Sexual and Reproductive Neurorehabilitation, edited by Mindy Aisen, 1997

Surgical Treatment

of Parkinson’s Disease

and Other Movement Disorders

Edited by

Daniel Tarsy, MD

Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Jerrold L. Vitek, MD, PhD

Emory University School of Medicine, Atlanta, GA

and

Andres M. Lozano, MD, PhD

Toronto Western Hospital, Toronto, ON, Canada

Humana Press

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the information published and to describe generally accepted practices. The contributors herein have

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Library of Congress Cataloging in Publication Data

Surgical treatment of Parkinson's disease and other movement disorders / edited by

Daniel Tarsy, Jerrold L. Vitek and Andres M. Lozano.

p. ; cm. Includes bibliographical references and index.

ISBN 0-89603-921-8 (alk. paper)

1. Parkinson's disease--Surgery. 2. Movement disorders--Surgery. I. Lozano, A. M.

(Andres M.), 1959– II. Tarsy, Daniel. III. Vitek, Jerrold Lee.

[DNLM: 1. Parkinson Disease--surgery. 2. Movement Disorders--surgery. 3.

Neurosurgical Procedures. 4. Stereotaxic Techniques. WL 359 S9528 2003]

RC382.S875 2003

617.4'81--dc21

2002068476

v

Preface

There has been a major resurgence in stereotactic neurosurgery for the treat￾ment of Parkinson’s disease and tremor in the past several years. More recently,

interest has also been rekindled in stereotactic neurosurgery for the treatment of

dystonia and other movement disorders. This is based on a large number of

factors, which include recognized limitations of pharmacologic therapies for

these conditions, better understanding of the functional neuroanatomy and

neurophysiology of the basal ganglia, use of microelectrode recording techniques

for lesion localization, improved brain imaging, improved brain lesioning tech￾niques, the rapid emergence of deep brain stimulation technology, progress in

neurotransplantation, better patient selection, and improved objective methods

for the evaluation of surgical results. These changes have led to increased col￾laboration between neurosurgeons, neurologists, clinical neurophysiologists,

and neuropsychologists, all of which appear to be resulting in a better therapeu￾tic result for patients afflicted with these disorders.

The aim of Surgical Treatment of Parkinson's Disease and Other Movement Disor￾ders is to create a reference handbook that describes the methodologies we

believe are necessary to carry out neurosurgical procedures for the treatment of

Parkinson’s disease and other movement disorders. It is directed toward neu￾rologists who participate in these procedures or are referring patients to have

them done, to neurosurgeons who are already carrying out these procedures or

contemplating becoming involved, and to other health care professionals

including neuropsychologists and general medical physicians seeking better

familiarity with this rapidly evolving area of therapeutics. Several books con￾cerning this subject currently exist, most of which have emerged from symposia

on surgical treatment of movement disorders. We have tried here to provide a

systematic and comprehensive review of the subject, which (where possible)

takes a “horizontal” view of the approaches and methodologies common to

more than one surgical procedure, including patient selection, patient assess￾ment, target localization, postoperative programming methods, and positron

emission tomography.

We have gathered a group of experienced and recognized authorities in the

field who have provided authoritative reviews that define the current state of the

art of surgical treatment of Parkinson’s disease and related movement disorders.

We greatly appreciate their excellent contributions as well as the work of Paul

Dolgert, Craig Adams, and Mark Breaugh at Humana Press who made this work

a reality. We especially thank our very patient and understanding families

whose love and support helped to make this book possible. Finally we dedicate

this book to our patients whose courage and persistence in the face of great

adversity have allowed the work described in this book to progress toward some

measure of relief of their difficult conditions.

Daniel Tarsy, MD

Jerrold L. Vitek, MD, PhD

Andres M. Lozano, MD, PhD

vii Preface

Contents

Preface ...........................................................................................................................v

Contributors ............................................................................................................... ix

Part I Rationale for Surgical Therapy

1 Physiology of the Basal Ganglia

and Pathophysiology of Movement Disorders ........................................ 3

Thomas Wichmann and Jerrold L. Vitek

2 Basal Ganglia Circuitry and Synaptic Connectivity .................................. 19

Ali Charara, Mamadou Sidibé, and Yoland Smith

3 Surgical Treatment of Parkinson’s Disease: Past, Present, and Future ......... 41

William C. Koller, Alireza Minagar, Kelly E. Lyons, and Rajesh Pahwa

Part II Surgical Therapy for Parkinson’s Disease and Tremor

4 Patient Selection for Movement Disorders Surgery .................................. 53

Rajeev Kumar and Anthony E. Lang

5 Methods of Patient Assessment in Surgical Therapy

for Movement Disorders ............................................................................ 69

Esther Cubo and Christopher G. Goetz

6 Target Localization in Movement Disorders Surgery ............................... 87

Michael Kaplitt, William D. Hutchison, and Andres M. Lozano

7 Thalamotomy for Tremor ............................................................................... 99

Sherwin E. Hua, Ira M. Garonzik, Jung-Il Lee, and Frederick A. Lenz

8 Pallidotomy for Parkinson’s Disease.......................................................... 115

Diane K. Sierens and Roy A. E. Bakay

9 Bilateral Pallidotomy in Parkinson’s Disease: Costs and Benefits .......... 129

Simon Parkin, Carole Joint, Richard Scott, and Tipu Z. Aziz

10 Subthalamotomy for Parkinson’s Disease ................................................. 145

Steven S. Gill, Nikunj K. Patel, and Peter Heywood

11 Thalamic Deep Brain Stimulation for Parkinson’s Disease

and Essential Tremor ................................................................................ 153

Daniel Tarsy, Thorkild Norregaard, and Jean Hubble

12 Pallidal Deep Brain Stimulation for Parkinson’s Disease ...................... 163

Jens Volkmann and Volker Sturm

13 Subthalamic Deep Brain Stimulation for Parkinson’s Disease .............. 175

Aviva Abosch, Anthony E. Lang, William D. Hutchison,

and Andres M. Lozano

vii

14 Methods of Programming and Patient Management

with Deep Brain Stimulation ................................................................... 189

Rajeev Kumar

15 The Role of Neuropsychological Evaluation

in the Neurosurgical Treatment of Movement Disorders .................. 213

Alexander I. Tröster and Julie A. Fields

16 Surgical Treatment of Secondary Tremor.................................................. 241

J. Eric Ahlskog, Joseph Y. Matsumoto, and Dudley H. Davis

Part III Surgical Therapy for Dystonia

17 Thalamotomy for Dystonia .......................................................................... 259

Ronald R. Tasker

18 Pallidotomy and Pallidal Deep Brain Stimulation for Dystonia ........... 265

Aviva Abosch, Jerrold L. Vitek, and Andres M. Lozano

19 Surgical Treatment of Spasmodic Torticollis

by Peripheral Denervation ....................................................................... 275

Pedro Molina-Negro and Guy Bouvier

20 Intrathecal Baclofen for Dystonia and Related Motor Disorders.......... 287

Blair Ford

Part IV Miscellaneous

21 Positron Emission Tomography in Surgery

for Movement Disorders .......................................................................... 301

Masafumi Fukuda, Christine Edwards, and David Eidelberg

22 Fetal Tissue Transplantation for the Treatment

of Parkinson’s Disease .............................................................................. 313

Paul Greene and Stanley Fahn

23 Future Surgical Therapies in Parkinson’s Disease................................... 329

Un Jung Kang, Nora Papasian, Jin Woo Chang, and Won Yong Lee

Index .......................................................................................................................... 345

viii Contents

AVIVA ABOSCH, MD, PhD • Division of Neurosurgery, Toronto Western Hospital,

Toronto, Ontario, Canada

J. ERIC AHLSKOG, MD, PhD • Department of Neurology, Mayo Clinic, Rochester, MN

TIPU Z. AZIZ, MD • Department of Neurosurgery, The Radcliffe Infirmary,

Oxford, UK

ROY A. E. BAKAY, MD • Department of Neurosurgery, Rush Medical College,

Chicago, IL

GUY BOUVIER, MD • Hôpital Notre-Dame, University of Montreal, Montreal,

Quebec, Canada

JIN WOO CHANG, MD, PhD • Department of Neurosurgery, Yonsei University

College of Medicine, Seoul, South Korea

ALI CHARARA, PhD • Yerkes Primate Research Center, Emory University,

Atlanta, GA

ESTHER CUBO, MD • Department of Neurological Sciences, Rush Medical College,

Chicago, IL

DUDLEY H. DAVIS, MD • Department of Neurosurgery, Mayo Clinic, Rochester, MN

CHRISTINE EDWARDS, MA • Center for Neurosciences, North Shore-Long Island

Jewish Research Institute, Manhasset, NY

DAVID EIDELBERG, MD • Center for Neurosciences, North Shore-Long Island

Jewish Research Institute, Manhasset, NY

STANLEY FAHN, MD • Neurological Institute, Columbia-Presbyterian Medical

Center, New York, NY

JULIE A. FIELDS, BA • Department of Psychiatry and Behavioral Sciences,

University of Washington School of Medicine, Seattle, WA

BLAIR FORD, MD • Neurological Institute, Columbia-Presbyterian Medical Center,

New York, NY

MASAFUMI FUKUDA, MD • Center for Neurosciences, North Shore-Long Island

Jewish Research Institute, Manhasset, NY

IRA M. GARONZIK, MD • Department of Neurosurgery, Johns Hopkins Hospital,

Baltimore, MD

STEVEN S. GILL, MS • Department of Neurosurgery, Frenchay Hospital, Bristol, UK

CHRISTOPHER G. GOETZ, MD • Department of Neurological Sciences, Rush Medical

College, Chicago, IL

PAUL GREENE, MD • Neurological Institute, Columbia-Presbyterian Medical Center,

New York, NY

PETER HEYWOOD, PhD • Department of Neurosurgery, Frenchay Hospital, Bristol, UK

SHERWIN E. HUA, MD, PhD • Department of Neurosurgery, Johns Hopkins

Hospital, Baltimore, MD

JEAN HUBBLE, MD • Department of Neurology, The Ohio State University,

Columbus, OH

WILLIAM D. HUTCHISON, PhD • Division of Neurosurgery, Toronto Western

Hospital, Toronto, Ontario, Canada

ix

Contributors

x Contributors

CAROLE JOINT, RGN • Department of Neurosurgery, The Radcliffe Infirmary,

Oxford, UK

UN JUNG KANG, MD • Department of Neurology, The University of Chicago,

Chicago, IL

MICHAEL KAPLITT, MD, PhD • Department of Neurosurgery, Weill Medical College

of Cornell University, New York, NY

WILLIAM C. KOLLER, MD, PhD • Department of Neurology, University of Miami

School of Medicine, Miami, FL

RAJEEV KUMAR, MD • Colorado Neurological Institute, Englewood, CO

ANTHONY E. LANG, MD • Department of Neurology, Toronto Western Hospital,

Toronto, Ontario, Canada

JUNG-IL LEE, MD • Department of Neurosurgery, Johns Hopkins Hospital,

Baltimore, MD

WON YONG LEE, MD, PhD • Department of Neurology, Samsung Medical Center,

Seoul, Korea

FREDERICK A. LENZ, MD, PhD • Department of Neurosurgery, Johns Hopkins

Hospital, Baltimore, MD

ANDRES M. LOZANO, MD, PhD • Division of Neurosurgery, Toronto Western

Hospital, Toronto, Ontario, Canada

KELLY E. LYONS, PhD • Department of Neurology, University of Miami School

of Medicine, Miami, FL

JOSEPH Y. MATSUMOTO, MD • Department of Neurology, Mayo Clinic, Rochester, MN

ALIREZA MINAGAR, MD • Department of Neurology, University of Miami School

of Medicine, Miami, FL

PEDRO MOLINA-NEGRO, MD, PhD • Hôpital Notre-Dame, University of Montreal,

Montreal, Quebec, Canada

THORKILD NORREGAARD, MD • Division of Neurosurgery, Beth Israel Deaconess

Medical Center, Boston, MA

RAJESH PAHWA, MD • Department of Neurology, University of Kansas Medical

Center, Kansas City, KS

NORA PAPASIAN, PhD • Department of Neurology, The University of Chicago,

Chicago, IL

SIMON PARKIN, MRCP • Department of Neurology, The Radcliffe Infirmary,

Oxford, UK

NIKUNJ K. PATEL, BS • Department of Neurosurgery, Frenchay Hospital, Bristol, UK

RICHARD SCOTT, PhD • Department of Neurosurgery, The Radcliffe Infirmary,

Oxford, UK

MAMADOU SIDIBÉ, PhD • Yerkes Primate Research Center, Emory University,

Atlanta, GA

DIANE K. SIERENS, MD • Department of Neurosurgery, Rush Medical College,

Chicago, IL

YOLAND SMITH, PhD • Yerkes Primate Research Center, Emory University,

Atlanta, GA

VOLKER STURM, MD, PhD • Department of Stereotactic and Functional

Neurosurgery, University of Cologne, Cologne, Germany

DANIEL TARSY, MD • Department of Neurology, Beth Israel Deaconess Medical

Center, Boston, MA

RONALD R. TASKER, MD • Department of Neurosurgery, Toronto Western

Hospital, Toronto, Ontario, Canada

ALEXANDER I. TRÖSTER, PhD • Department of Psychiatry and Behavioral Sciences

and Department of Neurological Surgery, University of Washington

School of Medicine, Seattle, WA

JERROLD L. VITEK, MD, PhD • Department of Neurology, Emory University

Medical Center, Atlanta, GA

JENS VOLKMANN, MD, PhD • Department of Neurology, University of Christian￾Albrechts University, Kiel, Germany

THOMAS WICHMANN, MD • Department of Neurology, Emory University

Medical Center, Atlanta, GA

Contributors xi

Basal Ganglia and Movement Disorders 1

I Rationale for Surgical Therapy

Basal Ganglia and Movement Disorders 3

3

From: Current Clinical Neurology:

Surgical Treatment of Parkinson's Disease and Other Movement Disorders

Edited by: D. Tarsy, J. L. Vitek, and A. M. Lozano © Humana Press Inc., Totowa, NJ

1

Physiology of the Basal Ganglia

and Pathophysiology of Movement Disorders

Thomas Wichmann and Jerrold L. Vitek

1. INTRODUCTION

Insights into the structure and function of the basal ganglia and their role in the pathophysiology

of movement disorders resulted in the 1980s in the development of testable models of hypokinetic and

hyperkinetic movement disorders. Further refinement in the 1990s resulted from continued research

in animal models and the addition of physiological recordings of neuronal activity in humans under￾going functional neurosurgical procedures (1–7). These models have gained considerable practical

value, guiding the development of new pharmacologic and surgical treatments, but, in their current

form, more and more insufficiencies of these simplified schemes are becoming apparent. In the fol￾lowing chapter we discuss both models, as well as some of the most important criticisms.

2. NORMAL ANATOMY AND FUNCTION OF THE BASAL GANGLIA

The basal ganglia are components of circuits that include the cerebral cortex and thalamus (8).

These circuits originate in specific cortical areas, pass through separate portions of the basal ganglia

and thalamus, and project back to the frontal cortical area from which they took origin. The cortical

sites of origin of these circuits define their presumed function and include “motor,” “oculomotor,”

“associative,” and “limbic.” In each of these circuits, the striatum and subthalamic nucleus (STN) serve

as the input stage of the basal ganglia, and globus pallidus interna (GPi) and substantia nigra, pars retic￾ulata (SNr) serve as output stations. This anatomic organization is consistent with the clinical evi￾dence for motor and nonmotor functions and the development of cognitive and emotional/behavioral

disturbances in diseases of the basal ganglia.

The motor circuit is particularly important in the pathophysiology of movement disorders. This

circuit originates in pre- and postcentral sensorimotor fields, which project to the putamen. These

projections either are direct connections to the putamen from the cortex, or reach the putamen via the

intercalated centromedian nucleus (CM) of the thalamus (9–15). Putamenal output reaches GPi/SNr

via two pathways, a “direct” monosynaptic route, and an “indirect” polysynaptic route that passes

through the external pallidal segment (GPe) to GPi directly or via GPe projections to the STN (16,17).

Although the main neurotransmitter of all striatal output neurons is GABA, one difference between

the source neurons in the direct and indirect pathways is that neurons in the indirect pathway contain

the neuropeptide substance P, whereas source neurons of the indirect pathway carry the neuropeptides

enkephalin and dynorphin.

4 Wichmann and Vitek

In addition to changes in the cortico-striatal pathway, the cortico-subthalamic pathway (18–20)

may also influence basal ganglia activity (14,21). The importance of this pathway is underscored by

the fact that neuronal responses to sensorimotor examination in GPe and GPi are greatly reduced

after lesions of the STN, suggesting that this pathway is largely responsible for relaying sensory

input to the basal ganglia (22). The close relationship between neuronal activity in the cerebral cortex

and the STN is suggested by the fact that oscillatory activity in the STN and the pallidum is closely

correlated to oscillatory activity in the cortex (23). Furthermore, cortical stimulation results in a com￾plex pattern of excitation-inhibition in GPi, which is likely mediated by the STN and its connection

to both pallidal segments (24).

Basal ganglia output is directed toward the thalamic ventral anterior, ventral lateral, and intralam￾inar nuclei (ventralis anterioris [VA], ventralis lateralis pars oralis [VLo], centromedian and parafasci￾cular nucleus CM/Pf) (25–34), and to the brainstem, in particular to portions of the pedunculopontine

nucleus (PPN), which may serve to connect the basal ganglia to spinal centers (35–39). Portions of

the PPN also project back to the basal ganglia, and may modulate basal ganglia output. Basal ganglia

output to the thalamus remains segregated into “motor” and “nonmotor” functions. Even within the

movement-related circuitry, there may be a certain degree of specialization. Output from the motor

portion of GPi reaches predominately VA and VLo, which, in turn, project to cortical motor areas that

are closely related to the sequencing and execution of movements (34). Motor output from SNr, on

the other hand, reaches premotor areas that are more closely related to the planning of movement

(34). In addition, output from the SNr reaches areas closely related to eye movements, such as the

frontal eye fields (34), and the superior colliculus. The latter is the phylogenetically oldest basal gan￾glia connection, whose more general relevance may lie in a contribution to the control of orienting

behaviors (40–45). STN, PPN, thalamus, and cortical projection neurons are excitatory (glutamater￾gic), whereas other neurons intrinsic to the basal ganglia are inhibitory (GABAergic).

The neurotransmitter dopamine plays a central role in striatal function. The net effect of striatal

dopamine is to reduce basal ganglia output, leading to disinhibition of thalamocortical projection

neurons. This may occur, however, via a number of different mechanisms, including a “fast” synap￾tic and a slower modulatory mode. The fast synaptic mode modulates transmission along the spines

of striatal neurons, which are the major targets of cortical and thalamic inputs to the striatum (46). By

this mechanism, dopamine may be important in motor learning or in the selection of contextually

appropriate movements (47–49). The slower mode may modulate striatal activity on a slower time

scale via a broad neuromodulatory mechanism. Changes in this neuromodulatory control of striatal

outflow may underlie some of the behavioral alterations seen in movement disorders (5). Although

under considerable debate (50,51), it appears that dopamine predominately facilitates transmission

over the direct pathway and inhibits transmission over the indirect pathway via dopamine D1 and D2

receptors, respectively (52,53).

By virtue of being part of the aforementioned cortico-subcortical re-entrant loops that terminate in

the frontal lobes, the basal ganglia have a major impact on cortical function and on the control of

behavior. Both GPi and SNr output neurons exhibit a high tonic discharge rate in intact animals (54–

57). Modulation of this discharge by alteration in phasic and tonic activity over multiple afferent

pathways occurs with voluntary movement, as well as involuntary movements. Details of the basal

ganglia mechanisms involved in the control of voluntary movements are still far from clear, but it is

thought that motor commands generated at the cortical level are transmitted to the putamen directly

and via the CM. Stated in the most simple terms, phasic activation of the direct striato-pallidal path￾way may result in reduction of tonic-inhibitory basal ganglia output, resulting in disinhibition of

thalamocortical neurons, and facilitation of movement. By contrast, phasic activation of the indirect

pathway may lead to increased basal ganglia output (18) and to suppression of movement.

The combination of information traveling via the direct and the indirect pathways of the motor cir￾cuit may serve basic motor control functions such as “scaling” or “focusing” of movements (8,58–60).