Newton MD in Oncology-Neurosurgery / Maschio Epilepsy and Brain Tumors

1. Auflage 2015
ISBN: 978-0-12-417126-8
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 292 Seiten

Patients with brain tumor-related epilepsy (BTRE) suffer from two serious pathologies simultaneously - a brain tumor and a secondary form of epilepsy. Although there has been remarkable progress in BTRE research in recent years, it remains an on-going challenge for clinicians and continues to stimulate much debate in the scientific community. This volume is the first to be completely dedicated to BTRE, and in doing so it explores issues faced by the health care team as well as some of the novel and promising directions that future research may take. Epilepsy and Brain Tumors is not only a complete reference on BTRE but also a practical guide based on clinical experiences, with a comprehensive collection of presentations from international experts who share some of the latest discoveries and their approaches to tackling a wide range of difficult and complex issues. - Includes coverage of epidemiology, pathology and treatment of both primary and metastatic brain tumors - Offers additional insight into supportive care, incidence in children, focal epileptogenesis, clinical evaluation, antiepileptic drugs, surgical treatment, cognitive rehabilitation, and more - Chapters authored and edited by leaders in the field around the globe - the broadest, most expert coverage available

Autoren/Hrsg.

Newton MD in Oncology-Neurosurgery, Herbert B.

Maschio, Marta

Inhaltsverzeichnis

1;Front Cover;1
2;Epilepsy and Brain Tumors;4
3;Copyright;5
4;Dedication;6
5;Contents;8
6;Foreword;12
7;Preface;14
8;Contributors;16
9;Chapter 1: Brain Tumor-Related Epilepsy: Introduction and Overview;18
9.1;Introduction;18
9.2;Epilepsy: Definition, Incidence, Social Context and Treatment Options;19
9.2.1;Epilepsy in the Context of BTs: Epidemiology and Incidence;20
9.2.2;Detection, Classification, and Documentation of Seizures;21
9.2.3;The Unique Role of Epileptogenesis and Drug Resistance in BTRE;21
9.2.3.1;Pharmacoresistance;22
9.2.4;QoL in BTRE Patients;22
9.2.5;Impact of AEDs in BTRE Patients;23
9.2.6;Neurocognitive Evaluation and Possible Rehabilitative Programs;24
9.2.7;Health Economics and BTRE;24
9.3;References;25
10;Chapter 2: Overview of Epidemiology, Pathology, and Treatment of Primary Brain Tumors;28
10.1;Epidemiology of PBT;28
10.2;Pathology of Selected PBT;31
10.2.1;Diffuse Astrocytomas;32
10.2.2;Localized Astrocytomas;33
10.2.3;Oligodendrogliomas and Oligoastrocytomas;34
10.2.4;Medulloblastoma and Other Embryonal Tumors;34
10.2.5;Meningioma and Other Tumors of the Meninges;35
10.2.6;Primary Central Nervous System Lymphoma;37
10.3;Surgical Therapy of PBT;37
10.4;Radiation Therapy of PBT;38
10.5;Chemotherapy of PBT;38
10.6;Molecular or ``Targeted´´ Treatment;41
10.7;References;42
11;Chapter 3: Overview of Epidemiology, Pathology, and Treatment of Metastatic Brain Tumors;46
11.1;Epidemiology of MBTs;46
11.2;Pathology of MBTs;48
11.3;Surgical Therapy of MBTs;49
11.4;Radiation Therapy of MBTs;52
11.5;Chemotherapy of MBTs;54
11.6;Acknowledgments;56
11.7;References;56
12;Chapter 4: Supportive Care of Brain Tumor Patients;62
12.1;Introduction;62
12.2;Seizures and Anticonvulsant Therapy;63
12.3;Corticosteroids;65
12.4;Gastric Acid Inhibitors;67
12.5;Thromboembolic Complications and Anticoagulation;67
12.6;Dysphagia and Swallowing Disorders;68
12.7;Psychiatric Issues;69
12.8;Pain Control Issues;73
12.9;Palliative Care;74
12.10;Ethical Issues;76
12.11;Conclusion;78
12.12;References;78
13;Chapter 5: Brain-Tumor-Related Epilepsy in Children;82
13.1;The Pediatric Perspective;82
13.2;Epilepsy-Associated Brain Tumors;82
13.3;Pathophysiology;84
13.4;Epidemiology;86
13.4.1;Brain Tumors;86
13.4.2;Seizures and Epilepsy;86
13.5;Presentation;87
13.5.1;Brain Tumors;87
13.5.2;Seizures and Epilepsy;87
13.6;General Principles of Management;91
13.7;History and Physical Exam;91
13.8;Diagnostic Evaluation;92
13.8.1;Scalp EEG;92
13.8.2;Intracranial EEG;94
13.8.3;MRI;94
13.8.4;Other Imaging Studies;95
13.8.5;Magnetic and Electrical Source Localization;96
13.8.6;Neuropsychological Assessment and Other Studies Used to Localize Eloquent Brain;96
13.8.7;Genetics;96
13.8.8;Tissue Diagnosis and Molecular Tumor Markers;97
13.9;Medical Management;97
13.9.1;Anticipatory Guidance;97
13.9.2;Maintenance Antiseizure Drugs;97
13.9.3;Rescue Antiseizure Drugs;100
13.9.4;Role of Antiseizure Drugs in Children Without a History of Seizures;101
13.9.5;Chemotherapy, Biologic Agents, and Steroids;102
13.9.6;Dietary Considerations and Alternative Therapies;102
13.10;Surgical Management;102
13.10.1;Goals and Approaches;102
13.10.2;Timing of Surgical Resection;103
13.10.3;Lesionectomy (Tumorectomy) Versus Lesionectomy ``Plus´´;104
13.10.4;Palliative Strategies;105
13.11;Outcome;105
13.12;Future Directions;106
13.13;References;107
14;Chapter 6: Mechanisms of Focal Epileptogenesis;118
14.1;Time Course and Specificity of Acquired Epileptogenesis;119
14.2;References;123
15;Chapter 7: Pathophysiology of Brain Tumor-Related Epilepsy;128
15.1;Introduction;128
15.2;Epidemiology of BTRE;128
15.3;Pathophysiology of BTRE;129
15.4;Treatment of BTRE;131
15.5;References;134
16;Chapter 8: The Neurophysiology of Central Nervous System Tumors;136
16.1;Introduction;136
16.2;EEG Modalities and Applications;137
16.3;EEG Background Changes;138
16.4;Epileptiform Activity;139
16.5;Meningiomas;141
16.6;Generation of Abnormal Cerebral Activity;148
16.7;References;148
17;Chapter 9: Surgical Treatment for Epilepsy;150
17.1;Introduction;150
17.2;Evaluation and Selection of the Surgical Candidate;150
17.3;Resection Procedures;151
17.3.1;Temporal Lobectomy;151
17.3.2;Common Complications;151
17.3.3;Extra-temporal Cortical Resections;151
17.3.4;Hemispherectomy;152
17.4;Nonresective Techniques;152
17.5;Disconnection Surgeries;153
17.5.1;Corpus Callosotomy;153
17.5.2;Multiple Subpial Transections;154
17.5.3;Vagal Nerve Stimulation;154
17.5.4;Deep Brain Stimulation;155
17.5.5;Responsive Neurostimulation;155
17.6;References;156
18;Chapter 10: Clinical Evaluation of Epilepsy in the Brain-Tumor Patient;160
18.1;Differential Diagnosis;162
18.2;Clinical History and Physical Examination;166
18.3;Neuroimaging Evaluation;167
18.4;Clinical and Electrophysiological Work-Up;170
18.5;Effects of Oncological Therapy on Brain Tumor-Related Epilepsy;172
18.6;Acknowledgments;174
18.7;References;174
19;Chapter 11: Antiepileptic Drugs:;176
19.1;Carbamazepine;176
19.2;Ethosuximide;178
19.3;Phenobarbital;180
19.4;Phenytoin;182
19.5;Primidone;183
19.6;Alproate;184
19.7;References;185
20;Chapter 12: Antiepileptic Drugs: Second and Third Generation;188
20.1;Introduction;188
20.2;Clobazam;188
20.3;Eslicarbazepine Acetate;190
20.4;Ezogabine/Retigabine;194
20.5;Felbamate;194
20.6;Gabapentin;195
20.7;Lacosamide;196
20.8;Lamotrigine;197
20.9;Levetiracetam;198
20.10;Oxcarbazepine;200
20.11;Perampanel;201
20.12;Pregabalin;201
20.13;Rufinamide;202
20.14;Tiagabine Hydrochloride;203
20.15;Topiramate;204
20.16;Vigabatrin;205
20.17;Zonisamide;206
20.18;References;207
21;Chapter 13: Antiepileptic Drugs and Brain Tumor Patients;212
21.1;Introduction;212
21.2;Pathophysiology;212
21.3;Type of Seizure;213
21.4;Treatment of Seizures;213
21.4.1;First-Generation AEDs;213
21.4.2;Newer AEDs;215
21.5;Levetiracetam;215
21.6;Oxcarbazepine;217
21.7;Lacosamide;218
21.8;Pregabalin;219
21.9;Topiramate;220
21.10;Zonisamide;220
21.11;Lamotrigine;221
21.12;Conclusion;221
21.13;References;221
22;Chapter 14: Clinical Approach to Brain Tumor-Related Epilepsy;224
22.1;Seizure Prophylaxis in Patients with BTRE;224
22.2;Is There a Best Practice for Seizure Treatment?;228
22.2.1;Introduction;228
22.2.2;Drug Resistance and Epileptogenicity;228
22.2.3;Use of Systemic Treatment for Seizure Control;229
22.2.4;Use of AEDs as Antineoplastic Treatment;230
22.2.5;Efficacy of AEDs on BTRE: An Overview;231
22.2.6;Adverse Events Specific to BTRE Patients;231
22.2.7;Potential Interactions with Systemic Treatments;232
22.2.8;Impact of AED Therapies on Cognition;232
22.2.9;Impact of AED Therapies on QoL;233
22.2.10;How to Choose an AED?;233
22.2.11;Is It Possible to Stop an AED in BTRE, and When?;234
22.3;Clinical Approach to BTRE;234
22.4;Driving and BTRE;234
22.5;References;235
23;Chapter 15: Neuropsychology of BTRE;242
23.1;Introduction;242
23.2;Overview of Neurocognitive Impairment in BT, Epilepsy, and BTRE;243
23.2.1;Neurocognitive Impairment in BT;243
23.2.2;Neurocognitive Impairment in Epilepsy;245
23.3;Neurocognitive Impairment in BTRE;246
23.4;Specific Cognitive Deficits in BT, Epilepsy, and BTRE;246
23.4.1;Specific Cognitive Deficits in BT;246
23.4.2;Specific Cognitive Deficits in Epilepsy;246
23.4.3;Specific Cognitive Deficits in BTRE;247
23.5;Overview of Neuropsychological Assessment Techniques for BT, Epilepsy, and BTRE;247
23.5.1;Neuropsychological Assessment Techniques for BT;247
23.5.2;Neuropsychological Assessment Techniques for Epilepsy;248
23.5.3;Neuropsychological Assessment Techniques for BTRE;249
23.6;Psychological Issues in BT, Epilepsy, and BTRE;249
23.6.1;Psychological Issues in BT;249
23.6.2;Psychological Issues in Epilepsy;250
23.6.3;Psychological Issues in BTRE;251
23.7;Sexual Disturbances in Patients with BT, Epilepsy and BTRE;251
23.7.1;Sexual Disturbances in Patients with BT;251
23.7.2;Sexual Disturbances in Patients with Epilepsy;252
23.7.3;Sexual Disturbances in Patients with BTRE;252
23.8;QoL Assessment and Monitoring in BT, Epilepsy and BTRE;252
23.8.1;QoL Assessment and Monitoring in BT;252
23.8.2;QoL Assessment and Monitoring in Epilepsy;253
23.8.3;QoL Assessment and Monitoring in BTRE;254
23.9;Conclusions;254
23.10;References;254
24;Chapter 16: Cognitive Rehabilitation in Patients with BTRE;260
24.1;Introduction;260
24.2;Goals of Cognitive Rehabilitation;261
24.3;Treatment Modalities in BT;262
24.4;Treatment Modalities in Epilepsy;263
24.5;Treatment Modalities in BTRE;264
24.6;Pharmacological Approaches for Treatment of Cognitive Deficits;264
24.7;Caregivers Issues;265
24.8;Implications for Future Research in BTRE;266
24.9;References;272
25;Chapter 17: Social Cost of Brain Tumor-Related Epilepsy;274
25.1;Introduction;274
25.2;Health Economic Reporting: Terminology and Aims;275
25.3;Health Economics: Funding Priorities;277
25.3.1;Health Technology Assessment;279
25.3.2;BTRE: Economic Burden Within the Context of Neurological Disease;279
25.4;Epilepsy;279
25.5;Brain Tumor;282
25.6;Conclusion;283
25.7;References;284
26;Chapter Appendix: The Prospects of Brain Research within Horizon 2020: Responding Efficiently to Europe’s Societal Needs ...;286
26.1;Summary;286
27;Index;288

Leseproben

Chapter 2 Overview of Epidemiology, Pathology, and Treatment of Primary Brain Tumors
Herbert B. Newton, MD, FAAN1,2,*; Jose J. Otero, MD, PhD3    1 Department of Neurology, Dardinger Neuro-Oncology Center, Division of Neuro-Oncology, Wexner Medical Center at The Ohio State University and James Cancer Hospital and Solove Research Institute, Columbus, Ohio, USA
2 Department of Neurosurgery, Dardinger Neuro-Oncology Center, Division of Neuro-Oncology, Wexner Medical Center at The Ohio State University and James Cancer Hospital and Solove Research Institute, Columbus, Ohio, USA
3 Department of Pathology, Wexner Medical Center at The Ohio State University and James Cancer Hospital and Solove Research Institute, Columbus, Ohio, USA
* Corresponding author: [e-mail] Abstract
Primary brain tumors (PBT) are a pathologically diverse group of neoplasms that remain refractory to treatment. Gliomas are neoplasms of neuroepithelial origin that comprise the largest subgroup and most commonly diagnosed form of PBT. Gliomas usually demonstrate diffuse and infiltrative growth, especially high-grade varieties such as glioblastoma multiforme, anaplastic astrocytoma, and tumors of oligodendroglial origin. Surgical resection is the initial form of therapy for most patients with a PBT. A complete resection should be attempted for all low-grade tumors. For accessible high-grade lesions, gross-total resection of all enhancing tumor and regionally infiltrated brain should be considered. External beam fractionated irradiation should be administered to all patients with high-grade gliomas, and to selected patients with inaccessible or progressive low-grade PBT, especially if symptomatic or older than age 40. The standard regimen consists of 5000-6000 cGy administered in 180-200 cGy daily fractions over 5-7 weeks. Chemotherapy should be considered as adjunctive treatment for all malignant PBT and for selected low-grade gliomas. Temozolomide is an alkylating agent with a broad range of activity, which is often used in combination with irradiation, as well as in the adjuvant setting, for high-grade astrocytomas. Bevacizumab is a monoclonal antibody designed to target vascular endothelial growth factor, which has been shown to have activity against recurrent high-grade gliomas. Molecular therapeutic approaches are under development and have entered clinical trials. Keywords Primary brain tumor Glioma GBM Epidemiology Pathology Treatment Surgery Radiotherapy Chemotherapy Chapter Contents Epidemiology of PBT   11 Pathology of Selected PBT   14 Surgical Therapy of PBT   20 Radiation Therapy of PBT   21 Chemotherapy of PBT   21 Molecular or “Targeted” Treatment   24 Acknowledgments   25 References   25 Acknowledgments
The authors would like to thank Nicole Ghaffari and Shawna Huckell for research assistance. Dr. Newton was supported in part by National Cancer Institute grant CA 16058 and the Dardinger Neuro-Oncology Center Endowment Fund. In this chapter, we will provide an overview of the epidemiology, classification, pathology, and treatment of common primary brain tumors (PBT). PBT remain a significant health problem in the United States and worldwide. Overall, they account for some of the most malignant tumors known to affect human beings and are often refractory to all modalities of treatment. PBT will be diagnosed in approximately 30,000-35,000 patients in the United States this year and are associated with significant morbidity and mortality.1–7 Of the estimated 14 patients per 100,000 population that will develop a PBT this year, 6-8 per 100,000 will have a high-grade neoplasm, usually some form of glioma such as glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA). Epidemiology of PBT
As mentioned above, approximately 14 per 100,000 people in the United States will be diagnosed with a PBT each year, and the majority of those will have a high-grade neoplasm (typically AA or GBM).2–7 Contemporary epidemiological studies suggest an increasing incidence rate for the development of PBT in children less than 14 years of age and in patients 70 years or older.8 For people in the 15- to 44-year-old age group, the overall incidence rates have remained fairly stable in recent years. The cause of the increased incidence of PBT in some age groups remains unclear, but may be due to improvements in diagnostic neuro-imaging such as magnetic resonance imaging (MRI), greater availability of specially qualified neurosurgeons and neuropathologists, improved access to medical care for children and elderly patients, and more aggressive approaches to health care for elderly patients.5,8 In other words, the increase in PBT incidence may be more apparent than real due to ascertainment bias. The prognosis and survival of patients with PBT remains poor.1–7 Although uncommon neoplasms, they rank among the top 10 causes of cancer-related deaths in the United States and account for a disproportionate 2.4% of all yearly cancer-related deaths.9 The median survival for a patient with GBM is approximately 12-16 months, a figure that hasn’t improved substantially over the past 30 years. For patients with a low-grade astrocytoma or oligodendroglioma, the median survival is still significantly curtailed and is about 6-10 years. For PBT patients in the United States as a whole, across all age groups and tumor types, the 5-year survival rate is 20%.3 If a patient with a PBT survives for an initial 2 years, the probability of surviving another 3 years is 76.2%. In general, for any given tumor type, survival is better for younger patients than for older patients. The only exception to this generalization is for children with medulloblastoma and embryonal tumors, in which patients under 3 years of age have poorer survival rates than children between 3 and 14 years of age.10 The 5-year survival rate for all children less than 14 years of age with a malignant PBT is 72%. The median age at diagnosis for PBT is between 54 and 58 years.1–7 Among different histological varieties of PBT, there is significant variability in the age of onset. A small secondary peak is also present in the pediatric age group, in children between the ages of 4 and 9. Overall, PBT are more common in males than females, with the exception of meningiomas, which are almost twice as common in females. Tumors of the sellar region, and of the cranial and spinal nerves, are almost equally represented among males and females. In the United States, gliomas are more commonly diagnosed in whites than blacks, while the incidence of meningiomas is relatively equal between the two groups. Numerous epidemiological studies have been performed in an attempt to define risk factors involved in the development of brain tumors (see Table 2.1).2–7 The vast majority of these potential risk factors have not been associated with any significant predisposition to brain tumors. One risk factor that has proven to be important is the presence of a hereditary syndrome with a genetic predisposition for developing tumors, some of which can affect the nervous system.4,5,11 Several hereditary syndromes are associated with PBT, including tuberous sclerosis, neurofibromatosis types 1 and 2, nevoid basal cell carcinoma syndrome, Li-Fraumeni syndrome, and Turcot’s syndrome. However, it is estimated that hereditary genetic predisposition may be involved in only 2-8% of all cases of PBT. Familial aggregation of brain tumors has also been studied, with conflicting results.5,11 The relative risk for developing a tumor among family members of a patient with a PBT is quite variable, ranging from 1 to 10. One study that performed a segregation analysis of families of more than 600 adult glioma patients showed that a polygenic model most accurately explained the inheritance pattern.12 A similar analysis of 2141 first-degree relatives of 297 glioma families did not reject a multifactorial model, but concluded that an autosomal recessive model fit the inheritance pattern more accurately.13 Critics of these studies suggest that the common exposure of a family to a similar pattern of environmental agents could lead to a similar clustering of tumors. Other investigators have focused on genetic polymorphisms that might influence genetic and environmental factors to increase the risk for a brain tumor.4,5 Alterations in genes involved in oxidative metabolism, detoxification of carcinogens, DNA stability and repair, and immune responses might confer a genetic predisposition to tumors. For example, Elexpuru-Camiruaga and colleagues demonstrated that cytochrome P-4502D6 and glutathione transferase theta were associated with an increased risk for brain...