6. Dedicated to my parents—Avinash and Kanti Prabhakar
The best gifts they stored for me—Kavita and Hemant, who in turn gifted me Sunil and Deepali
To those who mean the world to me—Pallavi, Anavi, and Amyra
To Aishwarya, Avi, and Anav
8. vii
Contents
List of Contributors xvii
Foreword xix
Preface xxi
Acknowledgments xxiii
Introduction and Brief History of Neuroanesthesia
W. S. Jellish xxv
I
NEUROANATOMY
1. Neuroanatomy
D. GUPTA
Introduction 3
Embryological Differentiation of Different Parts of Brain 4
Anatomy of Brain 4
Vascular Supply of the Brain 30
The Meninges and Cerebrospinal Fluid 33
Acknowledgment 39
References 40
2. Neuroembryology
G.P. SINGH
Formation of Zygote 41
Formation of Blastocyst 41
Formation of Embryonic or Germ Disc 42
Formation of Definitive Notochord 44
Development of Nervous System 45
References 50
3. Blood–Brain Barrier
A.K. KHANNA AND E. FARAG
Introduction 51
Permeability at the Blood–Brain Barrier 51
Cellular and Molecular Effects of Anesthetics on the
Blood–Brain Barrier 52
Clinical and Experimental Implications of Anesthetics
on the Blood–Brain Barrier 54
Conclusion 56
References 56
II
NEUROPHYSIOLOGY
4. Neurophysiology
M. SETHURAMAN
Intracranial Pressure 62
Introduction 62
Normal Intracranial Pressure 62
Cerebral Compliance 62
Importance of Intracranial Pressure 63
Summary 68
Cerebral Blood Flow 68
Introduction 68
Vascular Anatomy 68
Summary 74
Brain Metabolism 74
Introduction 74
Normal Cerebral Metabolism 74
Summary 79
Cerebrospinal Fluid 79
Introduction 79
Ventricular System 79
Summary 83
The Spinal Cord 83
Introduction 83
Anatomy 84
Organization of the Spinal Cord 84
Summary 89
References 89
5. Brain Protection in Neurosurgery
H. EL BEHEIRY
Introduction 91
Nonpharmacological Strategies 91
Mild Hypothermia 92
Blood Pressure Control 93
Induced Arterial Hypertension 94
Normoglycemia 94
Target Hemoglobin Concentration 95
Pharmacological Strategies 96
Nonanesthetic Agents 97
Anesthetic Agents 97
Conclusion 98
References 98
9. CONTENTS
viii
III
NEUROPHARMACOLOGY
6. Neuropharmacology
P. GANJOO AND I. KAPOOR
Anesthetic Drugs and Sedatives 104
Intravenous Anesthetic Agents 104
Inhalational Anesthetic Agents 111
Neuromuscular Blocking Agents 115
Local Anesthetic Agents 116
Miscellaneous Drugs 116
Future Directions in Neuropharmacology 116
Conclusion 116
References 118
7. Anesthetic Agents: Neurotoxics or
Neuroprotectives?
J. FIORDA-DIAZ, N. STOICEA AND S.D. BERGESE
Introduction 123
Pharmacological Considerations 124
Anesthesia Practice: Clinical Outcomes 126
Anesthesia and Fragile Brain 127
Conclusion 127
Abbreviations 128
References 128
IV
NEUROMONITORING
8. Neuromonitoring
V.J. RAMESH AND M. RADHAKRISHNAN
Introduction 134
Cerebral Blood Flow 134
Transcranial Sonography 139
Thermal Diffusion Flowmetry 139
Laser Doppler Flowmetry 139
Intra-Arterial 133Xenon 139
CT Perfusion 139
Xenon Enhanced CT 139
Positron Emission Tomography 140
Single Photon Emission Computed Tomography 140
Magnetic Resonance Imaging 140
Intracranial Pressure 140
Electroencephalogram 143
Evoked Potential Monitoring 145
Motor Evoked Potentials 149
Depth of Anesthesia 150
Cerebral Oxygenation Monitoring 152
Jugular Venous Oximetry 152
Regional Cerebral Oximetry 154
Brain Tissue Oxygen Monitoring 156
Cerebral Microdialysis 158
Conclusion 159
References 159
9. Multimodal Monitoring
A. DEFRESNE AND V. BONHOMME
Introduction 161
Temperature 162
Oxygen Transport, Hemodynamics, and Brain
Metabolism 162
Intracranial Pressure Monitoring 171
Electroencephalography and Depth of Anesthesia
Monitoring 173
Miscellaneous 174
Integration of Information and Decision-
Helping Systems 175
Clinical Pearls 176
References 176
V
POSITIONS IN NEUROSURGERY
10. Positioning in Neurosurgery
G. SINGH
Introduction 184
Historical Background 184
Principles of Positioning 184
The Conduct of Positioning 185
Surgical Approach for Craniotomies 186
Positioning for Craniotomy 187
Positions Used for Craniotomies 189
Surgical Approach for Procedures of the Spine 195
Patient Positioning For Spinal Procedures 195
Conclusion 203
Abbreviations 203
References 204
VI
PREANESTHETIC EVALUATION
11. Preanesthetic Evaluation of Neurosurgical
Patients
R. MARIAPPAN
Introduction 209
Preoperative Evaluation of Patient-Related Risk Factors 210
Preoperative Evaluation of Specific
Neurosurgical Conditions 217
References 225
10. CONTENTS ix
VII
NEUROSURGERY
12. Supratentorial Lesions
H. BHAGAT AND S. MAHAJAN
Introduction 231
Classification 232
Pathophysiology and Clinical Correlations 233
Clinical Features 235
Neuroimaging 235
Intraoperative Considerations: The Team
Approach 236
Anesthetic Management 236
Intraoperative Management 238
Emergence From Anesthesia 240
Postoperative Management 241
Awake Craniotomy 242
Conclusions 245
Acknowledgment 245
References 245
13. Emergence From Anesthesia
M. ECHEVERRÍA, J. FIORDA-DIAZ, N. STOICEA AND S.D. BERGESE
Introduction 247
Neurophysiological Response During Emergence in
Neurosurgical Patients 248
Specific Perioperative Considerations 248
Delayed Emergence and Arousal 250
Complications 251
Conclusion 252
References 252
14. Anesthesia for Posterior Fossa Surgery
K. SANDHU AND N. GUPTA
Introduction 255
Anatomy 255
Clinical Presentation 256
Perioperative Management of Patients for Posterior
Fossa Surgery 256
Venous Air Embolism 264
Postoperative Management 271
Complications 272
Abbreviations 272
References 273
15. Transesophageal Echocardiography
A. LELE AND V. KRISHNAMOORTHY
Introduction 277
Basics of Transesophageal Echocardiography 277
Summary 283
References 283
16. Anesthesia for Epilepsy Surgery
N. GUPTA
Introduction 285
Surgical Management of Epilepsy 286
Types of Surgical Treatment 286
Presurgical Evaluation 287
Anesthesia for Epilepsy Surgery 288
Effect of Anesthetic Agents in Patients With Epilepsy 288
Antiepileptic Drug Interactions 290
Preanesthetic Evaluation and Preparation 291
Anesthetic Management of Preoperative Procedures 292
Anesthesia for Intracranial Electrode Insertion 294
Anesthetic Management of Resection of Seizure Focus 295
Awake Craniotomy 295
Resection of Epileptogenic Focus Under General
Anesthesia 300
Neurostimulation for Drug-Resistant Epilepsy 301
Anesthetic Management of the Patient With
Epilepsy for Incidental Surgery 302
Abbreviations 303
References 304
17. Refractory Status Epilepticus
M. PANEBIANCO AND A. MARSON
Introduction 309
Epidemiology 309
Classification 310
Cause 310
Pathophysiology 311
Diagnosis 311
Management 311
Treatment 312
Conclusions 313
References 314
18. Aneurysmal Subarachnoid Hemorrhage
C. MAHAJAN
History 316
Introduction 316
Clinical Presentation and Diagnosis 317
Grading of Subarachnoid Hemorrhage 319
Initial Management Concerns in Neurocritical
Care Unit 321
Timing of Surgery 327
Clipping or Coiling 327
Evaluation of a Patient With Subarachnoid
Hemorrhage for Anesthesia 328
Anesthetic Management 328
Temporary Clipping and Brain Protection Strategy 330
Intraoperative Aneurysm Rupture 330
Giant Aneurysms and Circulatory Arrest 331
Endovascular Management for Aneurysm Ablation 331
Postoperative Management of Patients 333
Conclusion 333
References 333
11. CONTENTS
x
19. Circulatory Arrest
D.E. TRAUL
Introduction 339
Deep Hypothermic Circulatory Arrest 339
Anesthesia Management 340
Complications 341
Adenosine-Induced Circulatory Arrest 341
Anesthesia Considerations 342
Complications 342
Summary 342
References 343
20. Cerebrovascular Disease
M. ABRAHAM AND M. MARDA
Intracerebral Hemorrhage 346
Incidence and Risk Factors 346
Imaging 346
Clinical Presentation 346
Management of Intracerebral Hemorrhage 348
Arteriovenous Malformations 352
Cause and Incidence 352
Natural History 353
Pathophysiologic Effects and Clinical Presentation 353
Grading of Arteriovenous Malformations 353
Imaging 354
Cerebral Hemodynamics in Arteriovenous
Malformation 354
Management 354
Surgical Resection of Arteriovenous Malformation 355
Anesthetic Considerations for Resection of
Arteriovenous Malformation 355
Postoperative Management 356
Anesthetic Considerations for Arteriovenous
Malformation Embolization 356
Complications During Arteriovenous Malformation
Embolization 357
Pediatric Arteriovenous Malformations 357
Pregnancy and Arteriovenous Malformations 358
Vein of Galen Aneurysmal Malformations 358
Dural Arteriovenous Fistula 360
Clinical Presentation 360
Management 360
Carotid Endarterectomy 360
Preoperative Evaluation 362
Management of Carotid Artery Disease 362
Monitoring 362
Intraoperative Management 363
Postoperative Complications and Outcomes 363
Coronary Angioplasty and Stenting 363
Moyamoya Disease 363
Management of Moyamoya Disease 364
References 364
21. Flow Arrest in Cerebrovascular Surgery
M.L. JAMES, M.-A. BABI AND S.A. KHAN
Deep Hypothermic Circulatory Arrest 367
Adenosine-Assisted Cerebral Blood Flow Arrest 370
Rapid Ventricular Pacing–Assisted Cerebral Blood
Flow Arrest 372
References 373
22. Neuroendocrine Lesions
P.K. BITHAL
Hypothalamic-Pituitary–Adrenal
Axis Evaluation 376
Neuroendocrine Response Related to
Anesthesia and Surgery 377
Pituitary Gland Adenomas 377
Physiology of Pituitary Gland 379
Endocrine Diseases 380
Nonfunctioning Tumors 382
Intraoperative Considerations 383
Advantages of Endoscopic Endonasal
Approach 384
Relative Contraindications to
Transsphenoidal Approach 384
Intraoperative Issues 384
Disorder of Water and Electrolytes 387
References 389
23. Pituitary Apoplexy
S.S. THOTA
Clinical Features 395
Management 395
References 397
24. Spinal Surgery
M.S. TANDON AND D. SAIGAL
Introduction 400
Spine 400
Types of Spine Surgeries 401
Surgical Approaches to the Spine 403
Common Spine Disorders 403
Imaging in Spine Lesions 417
Positioning for Spine Surgeries 417
Neurophysiological Intraoperative Monitoring
During Spine Surgeries 418
Preanesthetic Assessment and Optimization 420
Anesthesia Management 423
Postoperative Management 430
Special Considerations 431
Conclusion 437
References 437
25. Postoperative Visual Loss
K.M. KLA AND L.A. LEE
Introduction 441
Central Retinal Artery Occlusion 441
Ischemic Optic Neuropathy 442
Cortical Blindness 442
Recent Advances 443
Conclusion 445
References 445
12. CONTENTS xi
26. Neuroendoscopy
S. MONINGI AND D.K. KULKARNI
Introduction 447
Anesthetic Goals and Management 450
Anesthetic Management of Specific
Neuroendoscopic Procedures 453
Advances in Neuroendoscopy 466
Conclusion 467
Clinical Pearls 467
References 468
27. Pressure Inside the Neuroendoscope
N. FÀBREGAS AND L. SALVADOR
Introduction 471
Indications and Procedures 471
How Do Neurosurgeons Perform an
Intraventricular Endoscopic Procedure? 472
Anesthetic Procedure: What to Take Into Account? 473
Perioperative Complications 475
Conclusion 477
References 477
28. Anesthesia for Functional Neurosurgery
S.K. DUBE
Introduction 479
Procedure 479
Anesthetic Consideration 481
Anesthetic Techniques 484
Complications 485
Anesthesia in Patients With Deep Brain Stimulator In Situ 486
Conclusion 486
References 486
29. Awake Craniotomy
P.H. MANNINEN AND T. Y. YEOH
Introduction 489
Patient Selection 490
Awake Craniotomy for Tumor Surgery 490
Awake Craniotomy for Epilepsy 496
Conclusion 499
References 499
VIII
NEURORADIOLOGY
30. Anesthesia for Neuroradiology
K. SRIGANESH AND B. VINAY
Introduction 505
Issues Relating to Anesthesia Care in Neuroradiology 506
Anesthesia for Computed Tomographic Study 506
Anesthesia for Magnetic Resonance Imaging Study 506
Anesthesia for Diagnostic Angiography 510
Anesthetic Management of Endovascular Coiling 510
Anesthetic Management of Endovascular Embolization of
Arteriovenous Malformation, Arteriovenous
Fistula, and Vein of Galen Malformation 513
Anesthesia for Stroke Interventions 514
Issues Related to Radiation During Neurointervention 515
Anesthesia for Stereotactic Radiosurgery 516
Pregnancy and Neuroradiology 516
Clinical Pearls 517
References 517
31. Magnetic Resonance Imaging: Anesthetic
Implications
F. RABAI AND R. RAMANI
Introduction: The Road From X-Ray to Magnetic
Resonance Imaging 519
Principles of Nuclear Magnetic Resonance and Magnetic
Resonance Imaging 521
Various Types of Signals Recorded 522
Hazards Related to Magnetic Resonance Imaging 524
Magnetic Resonance Imaging Safety:
General Considerations 526
Magnetic Resonance Imaging Safety: Management of Cardiac
Implantable Electronic Devices and Other
Implantable Devices 527
Anesthesia for Magnetic Resonance Imaging 530
Research Applications/Emerging Clinical
Applications of Magnetic Resonance Imaging 531
References 532
IX
NEUROTRAUMA
32. Neurotrauma
D. PADMAJA, A. LUTHRA AND R. MITRA
Traumatic Brain Injury 536
Introduction 536
Definition 536
Epidemiology 536
Classification of Traumatic Brain Injury 537
Physiologic Response to Brain Injury 543
Neuroimaging 545
Severity of Traumatic Brain Injury 549
Management of Traumatic Brain Injury 549
Outcome 559
Emerging Treatment Modalities 559
Conclusion 560
Spine and Spinal Cord Trauma 560
Introduction 560
Epidemiology 560
Classification of Spinal Injury 561
Pathophysiology of Spinal Cord Trauma 563
Systemic Complications of Spinal
Cord Injuries 565
13. CONTENTS
xii
Management of Spine and Spinal Cord Injury 567
Emerging Treatment Modalities 578
References 582
33. Biomarkers in Traumatic Brain Injury
J. ŽUREK
Introduction 587
Conclusion 590
References 590
X
NEUROINTENSIVE CARE
34. Neurological Critical Care
G.S. UMAMAHESWARA RAO AND S. BANSAL
Introduction 595
History of Neurocritical Care 596
Design of a Neurocritical Care Unit 596
Clinical Conditions Requiring Admission to
Neurocritical Care Unit 596
Justification for Neurological Critical Care Units 596
Pathophysiological Issues in Neurological Critical Care 597
Management of Patients in a Neurological
Intensive Care Unit 598
Management of General Systemic Physiology 598
Specific Therapeutic Issues in Individual
Clinical Conditions 603
Advanced Neuromonitoring 603
Outcomes of Neurological Intensive Care Unit 606
End-of-Life Issues in Neurological Critical Care 606
Clinical Pearls 608
References 608
35. Antibiotics: Prophylactic and Therapeutics
S. ERB, L.A. STEINER AND C. OETLIKER
Introduction 613
Principles of Antimicrobial Therapy in Neurosurgery 613
Treatment of Central Nervous System Infections in the
Neurosurgical Patient 616
Antimicrobial Prophylaxis in Neurosurgery 620
References 623
XI
SPECIAL CONSIDERATIONS
36. Pediatric Neuroanesthesia
G.P. RATH
Overview 629
Pediatric Neurophysiology 629
General Principles of Pediatric Neuroanesthesia 630
Intraoperative Management 631
Postoperative Considerations 633
Management of Specific Conditions 633
Conclusion 641
References 641
37. Fluid and Blood Transfusion in
Pediatric Neurosurgery
S. RAJAN AND S. RAO
Introduction 643
Fluid and Electrolyte Choices 644
Type of Fluids for Perioperative Administration in
Pediatric Patients 645
Fluid Management in Pediatric Neurosurgery 645
Osmotherapy 646
Fluid and Electrolyte Disturbances in Pediatric
Neurosurgery 647
Blood Transfusion 647
Blood Components 648
Special Situations 649
Epilepsy Surgery 649
Scoliosis 649
Conclusion 650
References 650
38. Geriatric Neuroanesthesia
S. TRIPATHY
Introduction 653
Implications of Surgical Stress and Anesthesia
on the Elderly 653
Neurosurgical Concerns Unique to the Elderly 654
Conclusion 658
References 658
39. Postoperative Cognitive Dysfunction
A. BOROZDINA, L. PORCELLA AND F. BILOTTA
Introduction 661
Definitions, Epidemiology, and Pathophysiology 661
Risk Factors 663
Prevention 664
Screening Tools 664
Treatment 665
Outcome 666
References 666
40. Pregnancy
V. SINGHAL
Requirement of Neurosurgery During Pregnancy 670
Physiological Alterations During Pregnancy 671
Effect of Anesthetic Agents on Fetal Outcome 673
Uteroplacental Drug Transfer and Neonatal Depression 674
Timing and Method of Delivery 675
Anesthetic Considerations During Pregnancy 675
Induction: Rapid Sequence Versus Slow Neuroinduction 676
Combined Cesarean Delivery and Neurosurgery 678
14. CONTENTS xiii
Intracranial Pressure and Regional Anesthesia 678
Postoperative Management 678
Anesthesia for Interventional Neurosurgical Procedures 679
References 679
41. Cerebral Venous Thrombosis
E.E. SHARPE AND J.J. PASTERNAK
Definition 681
Venous Anatomy 681
Incidence of Cerebral Venous Thrombosis 681
Risk Factors 683
Pathophysiology 684
Clinical Manifestations 685
Diagnostic Evaluation 687
Treatment 688
Anesthetic Management 689
Prognosis 690
Conclusion 690
References 690
42. Neurosurgical Anesthesia in Patients With
Coexisting Cardiac Disease
S. SRIVASTAVA AND A. KANNAUJIA
Introduction 693
Preoperative Evaluation 694
Risk Stratification 694
Perioperative Monitoring 695
Ischemic Heart Disease 695
Valvular Heart Disease 697
Tumors of the Heart 699
Congenital Heart Disease 700
Hypertension 700
Conclusion 701
References 701
43. Intraoperative Cardiopulmonary Resuscitation
R. GORJI AND M. SIDANI
Introduction 703
Incidence, Morbidity, and Mortality 703
Survival From Intraoperative Cardiac Arrest 704
Predictors 704
Cause of Intraoperative Cardiac Arrest 705
Cardiopulmonary Resuscitation Quality 706
Cardiac Arrest and Cardiopulmonary Resuscitation in
Neurosurgical Patients 706
Prognosis 709
Conclusion 709
References 710
44. Coexisting Diabetes Mellitus in Neurosurgical
Patients
N.B. PANDA, S. SAHU AND A. SWAIN
Introduction 714
Incidence of Diabetes Mellitus 714
Glycemic Indices 714
Modes of Glucose Measurement 714
Pathophysiology of Diabetes Mellitus 715
Cerebral Glucose Metabolism 715
Hyperglycemia and the Brain 715
Hyperglycemic Neuropathy 716
Diabetic Dysautonomia 716
Hypoglycemia and the Brain 716
Evidence of Glycemic Control in Important
Neurosurgical Subsets 717
Traumatic Brain Injury 717
Subarachnoid Hemorrhage 717
Cerebrovascular Accidents 717
Tumor Surgery 718
Spine Surgery 718
Blood Sugar Management in Perioperative
Period and Neurocritical Care 718
Intraoperative Management 719
Anesthetic Management 719
Postoperative Glycemic Management 719
Blood Sugar Control in Emergency
Neurosurgical Patient 720
Blood Sugar Control in Intensive Care Setup 720
Nutrition 720
Conclusions 720
Coexisting Hypertension in Neurosurgical Patients 721
Introduction 721
Physiology of Cerebral Circulation 721
Pathophysiology of Arterial Hypertension 722
Hypertension in Patients With Traumatic
Brain Injury 723
Perioperative Management 724
Preoperative Evaluation 724
Antihypertensive Drugs 725
Intraoperative Management 725
Monitoring 725
Induction of Anesthesia 725
Maintenance of Anesthesia 726
Recovery From Anesthesia 726
Postoperative Care 726
Neurocritical Care 727
Conclusion 727
References 727
45. Neuromuscular Disorders
P.U. BIDKAR AND M.V.S. SATYA PRAKASH
Introduction 734
Myasthenia Gravis 735
Myasthenic Crisis 743
Lambert–Eaton Myasthenic Syndrome 747
Guillain–Barré Syndrome 748
Periodic Paralysis 753
Myotonias 755
Muscular Dystrophies 758
Motor Neuron Diseases 759
Multiple Sclerosis 760
Parkinson’s Disease 761
Alzheimer’s Disease 763
Huntington’s Disease 764
References 765
15. CONTENTS
xiv
46. Neuromuscular Electrical Stimulation in
Critically Ill Patients
N. LATRONICO, N. FAGONI AND M. GOBBO
Introduction 771
Neuromuscular Electrical Stimulation: Basic
Concepts and Practical Considerations 772
Neuromuscular Electrical Stimulation in the
Intensive Care Unit 775
Contraindications and Adverse Effects 776
Recommendations for the Use of Neuromuscular
Electrical Stimulation in the Intensive Care Unit 777
References 780
47. Neurological Patients for Nonneurosurgeries
K. JANGRA, V.K. GROVER AND H. BHAGAT
Neurodegenerative Diseases 784
Demyelinating Disease 788
Neuromuscular Disease: Myasthenia Gravis 791
Epilepsy 793
Intracranial Tumors 794
Traumatic Brain Injury 797
References 800
48 Anesthesia for Electroconvulsive Therapy
U. GRUNDMANN
Background 805
Technique of Electroconvulsive Therapy 805
Contraindications 806
Preprocedure Management 806
Anesthesia for Electroconvulsive Therapy 806
Side Effects 809
Special Conditions 809
Conclusion 810
References 810
XII
FLUIDS AND ELECTROLYTE
MANAGEMENT
49. Fluids and Electrolyte Management
J.N. MONTEIRO
Introduction 815
Anatomy and Physiology 815
Pathophysiology 817
Definitions 817
Choice of Fluids 818
Hypertonic Fluids 818
Isotonic Fluids 820
Colloids 820
Hypotonic Fluids 821
Fluid Management 822
Commonly Encountered Fluid Abnormalities 823
Conclusion 824
Clinical Pearls 825
References 825
50. Crystalloid and Colloid Fluids
R.G. HAHN
Crystalloid Fluids 827
Colloid Fluids 829
Which Fluid to Choose? 830
Conclusions 831
References 832
XIII
PAIN MANAGEMENT
51. Pain Management
Z. ALI, S. SINGH, N. HASSAN AND I. NAQASH
Postcraniotomy Pain 836
Introduction 836
Incidence 836
Anatomical and Physiological Basis of Pain
Following Craniotomy 836
Pain-Sensitive Structures of Cranium 838
Pathogenesis of Postcraniotomy Pain 838
Factors Affecting Postcraniotomy Pain 838
Classification and Assessment of
Postcraniotomy Pain 839
Preemption of Pain 840
Treatment of Acute Pain 840
Postcraniotomy Pain Management in the
Pediatric Population 843
Conclusion 843
Acute Pain Management After Spinal Surgery 843
Pathophysiology 844
Treatment Modalities for Acute Postoperative
Spinal Pain 844
Conclusion 848
References 849
XIV
BRAIN DEATH AND ETHICAL ISSUES
52. Brain Death and Ethical Issues in Neuroanesthesia
Practice
M. RADHAKRISHNAN AND S. LALWANI
Part A: Brain Death 856
Introduction 856
Criteria for Diagnosing Death 856
Need for Brain Death Diagnosis 856
Rules Regulating Diagnosis of Brain Death 856
Criteria for Certifying Brain Stem Death 857
Pitfalls/Controversies 859
16. CONTENTS xv
Conclusion 861
Appendix I 861
Part B: Ethical Issues in Neuroanesthesia Practice 863
Introduction 863
Ethical Issues in Clinical Care 863
Ethical Issues Related to Research 867
Ethical Issues Related to Team Work 868
Ethical Issues Related to Training 868
Ethical Issues Related to Innovative Neurosurgery 869
Conclusion 869
References 869
53. Organ Donation
M.J. SOUTER
Introduction 871
Conclusion 876
References 876
XV
EVIDENCE-BASED PRACTICE
54. Evidence-Based Practice of Neuroanesthesia
I. KAPOOR AND H. PRABHAKAR
Introduction 881
Evidence-Based Practice and Neuroanesthesia 883
Evidence and the Brain Trauma Foundation Guidelines 887
Unresolved Issues in the Practice of Neuroanesthesia 887
Conclusion 887
Clinical Pearls 889
References 889
55. Translational Research
M. IDA AND M. KAWAGUCHI
Introduction 891
Definition 891
In Neuroanesthesia 893
Why Not Lead to Clinical 893
To Be a Successful Translation 894
Conclusion 894
References 894
XVI
RECENT ADVANCES
56. Recent Advances in Neuroanesthesiology
T.L. WELCH AND J.J. PASTERNAK
Introduction 897
Endovascular Treatment of Stroke and Perioperative Stroke 897
Indications for Deep Brain Stimulation 898
Anesthetic Neurotoxicity 899
Pre- and Postconditioning 900
Brain Monitoring 901
New Assays for Creutzfeldt–Jakob Disease 902
References 903
57. Stem Cell Therapy
S. SHARMA AND R. AGGARWAL
Hypothesis of Stem Cell Research 907
Stem Cell 907
Historical Background 908
Types of Stem Cells 908
Sources of Stem Cells 908
Mesenchymal Stem Cells 909
Stem Cells in Neurological Diseases 909
Mode of Action of Stem Cell Therapy 910
Ethical Issues 910
Recent Advances 911
References 911
58. Pharmacogenomics
Y.N. MARTIN AND W.T. NICHOLSON
Introduction 913
Basic Genetic Principles 914
Basic Pharmacologic Principles 914
Anesthesia Contribution to the History
of Pharmacogenomics 915
Pharmacogenomics: Current Application
to Clinical Anesthesia 916
Conclusion 921
References 922
XVII
STERILIZATION TECHNIQUES
59. Sterilization and Disinfection
S. MOHAPATRA
Background 930
Recommendation of Preferred Methods for
Various Medical Devices 931
Recommendation for the Cleaning and
Decontamination of Environmental Surfaces 931
Recommendation for Blood Spill on the Surface 932
Cleaning and Disinfection of Medical Instruments 933
Cleaning and Reprocessing of Patient
Care Equipment 933
Reprocessing of Respiratory Apparatus and
Endoscopes 935
Reprocessing of Endoscopes 936
Specific Issues 938
Special Precaution for Inactivation of
Creutzfeldt–Jakob Disease 939
Health Care–Associated Infections 940
Infections in Operating Rooms and Intensive
Care Units 940
Conclusion 943
References 943
17. CONTENTS
xvi
60. Universal Precautions in the Intensive
Care Unit
A.YU LUBNIN AND K.A. POPUGAEV
Introduction 945
Prophylactics of Health Care–Associated Infections
in the Intensive Care Unit 946
Early Diagnosis of Pathogens and Infection
Complications in the Intensive Care Unit 947
Rational Antibiotic Therapy 947
Systemic Approach 948
Conclusion 948
References 948
XVIII
PALLIATIVE CARE
61. Palliative Care to Neurological and
Neurosurgical Patients
S. BHATNAGAR AND S.J. BHARTI
Introduction 953
References 961
62. Quality of Life and Health-Related Issues
L. VENKATRAGHAVAN AND S. BHARADWAJ
Introduction 963
Quality of Life and Health-Related Quality of Life 963
Utility of Health-Related Quality of Life 964
Tools for Measuring Health-Related Quality of Life 964
Uses of Measuring Health-Related Quality of Life 965
Health-Related Quality of Life in Relation to
Neurosurgical/Neurological Conditions 965
Conclusion 970
References 970
XIX
BIOSTATISTICS
63. Biostatistics
M. KALAIVANI, S. AMUDHAN, A.D. UPADHYAY AND V.K. KAMAL
Introduction to Biostatistics 976
Definition of Statistics 976
Biostatistics and Its Applications 976
Uses of Statistical Methods in Medical Sciences 976
Some Basic Statistical Concepts 976
Population and Sample 977
Scale of Measurements 977
Constant 977
Variables 977
Parameter and Statistic 978
Ratio, Proportion, and Rate 978
Statistical Inference 979
Estimation 979
Hypothesis Testing 979
Steps in Hypothesis Testing or Testing the
Statistical Significance 979
Defining the Null and Alternative Hypotheses 980
Calculating the Test Statistic 980
Obtaining, Using, and Interpreting the p-Value 980
Errors in Hypothesis Testing 980
The Possible Mistakes We Can Make 980
Other Important Concepts That Are Essential
in Statistical Inference 981
Parametric and Nonparametric Statistical Methods 981
Basic Principles of Statistics 981
Probability Distributions 982
Study Design 982
Sample Size 985
Data Collection and Preparing Data for Analysis 987
Analysis and Presentation of Data 989
Summarizing Data 989
Comparing Groups: Continuous Data 989
Comparing Groups: Categorical Data 991
Comparing Groups: Time to Event Data 991
Relation Between Two Continuous Variables 992
Multivariable Analysis 994
Conclusion 995
References 995
Index 997
18. xvii
List of Contributors
M. Abraham Max Hospital Panchsheel, New Delhi, India
R. Aggarwal All India Institute of Medical Sciences, New
Delhi, India
Z. Ali SKIMS, Srinagar, India
S. Amudhan NIMHANS, Bengaluru, India
M.-A. Babi Duke University, Durham, NC, United States
S. Bansal National Institute of Mental Health and
NeuroSciences (NIMHANS), Bangalore, India
S.D. Bergese Ohio State University, Columbus, OH,
United States
H. Bhagat Postgraduate Institute of Medical Education
and Research, Chandigarh, India
S. Bharadwaj NIMHANS, Bangalore, India
S.J. Bharti AIIMS, New Delhi, India
S. Bhatnagar AIIMS, New Delhi, India
P.U. Bidkar JIPMER, Puducherry, India
F. Bilotta Sapienza University of Rome, Rome, Italy
P.K. Bithal AIIMS, New Delhi, India
V. Bonhomme CHR Citadelle, Liege, Belgium
A. Borozdina I.M. Sechenov First Moscow Medical
University, Moscow, Russia
A. Defresne CHR Citadelle, Liege, Belgium
S.K. Dube All India Institute of Medical Sciences, New
Delhi, India
M. Echeverría Centro Médico Docente Paraíso, Maracaibo,
Venezuela
H. El Beheiry University of Toronto, Toronto, ON, Canada;
Trillium Health Partners, Toronto, ON, Canada
S. Erb University Hospital Basel, Basel, Switzerland
N. Fàbregas Hospital Clinic Universitari, Barcelona, Spain
N. Fagoni University of Brescia, Brescia, Italy
E. Farag Cleveland Clinic Foundation, Cleveland, OH,
United States
J. Fiorda-Diaz Ohio State University, Columbus, OH,
United States
P. Ganjoo GB Pant Hospital, New Delhi, India
M. Gobbo University of Brescia, Brescia, Italy
R. Gorji Upstate Medical University, Syracuse, NY,
United States
V.K. Grover Postgraduate Institute of Medical Education
and Research, Chandigarh, India
U. Grundmann Saarland University Medical Center,
Homburg/Saar, Germany
D. Gupta Sanjay Gandhi Post Graduate Institute of Medical
Sciences, Lucknow, India
N. Gupta Indraprastha Apollo Hospital, New Delhi, India
R.G. Hahn Södertälje Hospital, Södertälje, Sweden
N. Hassan Government Gousia Hospital, Srinagar, India
M. Ida Nara Medical University, Kashihara, Japan
M.L. James Duke University, Durham, NC, United States
K. Jangra Postgraduate Institute of Medical Education and
Research, Chandigarh, India
M. Kalaivani AIIMS, New Delhi, India
V.K. Kamal AIIMS, New Delhi, India
A. Kannaujia Sanjay Gandhi Post Graduate Institute of
Medical Sciences, Lucknow, India
I. Kapoor All India Institute of Medical Sciences, New
Delhi, India
M. Kawaguchi Nara Medical University, Kashihara, Japan
A.K. Khanna Cleveland Clinic Foundation, Cleveland, OH,
United States
S.A. Khan Duke-NUS Medical School, Singapore,
Singapore
K.M. Kla Vanderbilt University Medical Center, Nashville,
TN, United States
V. Krishnamoorthy University of Washington, Seattle, WA,
United States
D.K. Kulkarni Nizam’s Institute of Medical Sciences,
Hyderabad, India
S. Lalwani All India Institute of Medical Sciences,
New Delhi, India
N. Latronico University of Brescia, Brescia, Italy
L.A. Lee Kadlec Regional Medical Center, Richland, WA,
United States
A. Lele University of Washington, Seattle, WA,
United States
A.Yu Lubnin Neurocritical Care of Burdenko Research
Neurosurgical Institute, Ministry of Health, Moscow,
Russia
A. Luthra PGIMER, Chandigarh, India
C. Mahajan AIIMS, New Delhi, India
S. Mahajan Postgraduate Institute of Medical Education
and Research, Chandigarh, India
P.H. Manninen Toronto Western Hospital, Toronto, ON,
Canada
M. Marda Max Hospital Panchsheel, New Delhi, India
R. Mariappan Christian Medical College, Vellore, India
19. LIST OF CONTRIBUTORS
xviii
A. Marson University of Liverpool, Liverpool, United
Kingdom
Y.N. Martin Mayo Clinic, Rochester, MN, United States
R. Mitra Care Hospital, Bhubhaneswar, India
S. Mohapatra AIIMS, New Delhi, India
S. Moningi Nizam’s Institute of Medical Sciences,
Hyderabad, India
J.N. Monteiro P.D. Hinduja Hospital and Medical Research
Centre, Mumbai, India
I. Naqash SKIMS, Srinagar, India
W.T. Nicholson Mayo Clinic, Rochester, MN, United States
C. Oetliker University Hospital Basel, Basel, Switzerland
D. Padmaja Nizam’s Institute of Medical Sciences,
Hyderabad, India
N.B. Panda Post Graduate Institute of Medical Education
and Research, Chandigarh, India
M. Panebianco University of Liverpool, Liverpool, United
Kingdom
J.J. Pasternak Mayo Clinic College of Medicine, Rochester,
MN, United States
K.A. Popugaev Federal Medical-Biological Agency,
Ministry of Health, Moscow, Russia
L. Porcella Spedali Civili University Hospital, Brescia, Italy
H. Prabhakar All India Institute of Medical Sciences,
New Delhi, India
F. Rabai University of Florida, Gainesville, FL, United
States
M. Radhakrishnan National Institute of Mental Health
and NeuroSciences, Bengaluru, India
S. Rajan Cleveland Clinic, Cleveland, OH, United States
R. Ramani University of Florida, Gainesville, FL,
United States
V.J. Ramesh National Institute of Mental Health and
NeuroSciences, Bengaluru, India
S. Rao Yale New Haven Hospital, New Haven, CT,
United States
G.P. Rath All India Institute of Medical Sciences (AIIMS),
New Delhi, India
S. Sahu Tata Main Hospital, Jamshedpur, India
D. Saigal University of Delhi, New Delhi, India
L. Salvador Consorcio Hospital General Universitario
de Valencia, Valencia, Spain
K. Sandhu Max Superspeciality Hospital, New Delhi, India
M.V.S. Satya Prakash JIPMER, Puducherry, India
M. Sethuraman Sree Chitra Tirunal Institute for Medical
Sciences and Technology, Trivandrum, India
S. Sharma All India Institute of Medical Sciences, New
Delhi, India
E.E. Sharpe Mayo Clinic College of Medicine, Rochester,
MN, United States
M. Sidani Upstate Medical University, Syracuse, NY,
United States
V. Singhal Medanta (The Medicity), Gurgaon, India
G. Singh Christian Medical College, Vellore, India
G.P. Singh AIIMS, New Delhi, India
S. Singh SKIMS, Srinagar, India
M.J. Souter University of Washington, Seattle, WA, United
States
K. Sriganesh NIMHANS, Bangalore, India
S. Srivastava Sanjay Gandhi Post Graduate Institute of
Medical Sciences, Lucknow, India
L.A. Steiner University Hospital Basel, Basel, Switzerland
N. Stoicea Ohio State University, Columbus, OH, United
States
A. Swain Tata Main Hospital, Jamshedpur, India
M.S. Tandon University of Delhi, New Delhi, India
S.S. Thota Upstate Medical University, State University of
New York, Syracuse, NY, United States
D.E. Traul Cleveland Clinic, Cleveland, OH, United States
S. Tripathy All India Institute of Medical Sciences
Bhubaneswar, Bhubaneswar, India
G.S. Umamaheswara Rao National Institute of Mental
Health and NeuroSciences (NIMHANS), Bangalore, India
A.D. Upadhyay AIIMS, New Delhi, India
L. Venkatraghavan University of Toronto, Toronto, ON,
Canada
B. Vinay Gulf Medical University, Ajman, United Arab
Emirates
T.L. Welch Mayo Clinic College of Medicine, Rochester,
MN, United States
T.Y. Yeoh Toronto Western Hospital, Toronto, ON, Canada
J. Žurek University Hospital Brno, Brno, Czech Republic
20. xix
Foreword
There has been substantial flux in the field of neuroanesthesia over the past two decades. This followed what
could be viewed as a relatively quiescent and narrowly focused period in neuroanesthesia. During the latter period
much of the focus was on the roles of hypotension in aneurysm surgery, hyperventilation for head injury, anesthetics
as cerebral protectants, and endless debates about intravenous versus inhaled anesthetics. More recently the purview
of neuroanesthesia broadened substantially partly reflecting the huge expansion in the way patients with neurologi-
cal diseases are managed. Patients are cared for not only in the traditional operating theater and intensive care unit
but also in more complex ways inside and outside the operating theater. Examples include endovascular treatment
of aneurysms, magnetic resonance imaging (MRI)- and computed tomography (CT)-guided surgery, minimally inva-
sive approaches such as deep brain stimulation (DBS), the growth in neurological monitoring from the awake patient
to complex electrophysiology, and the ever increasingly aggressive spine reconstructions. The neuroanesthesiologist
of today is not only a traveler going to different parts of the hospital but needs to be an expert in patient management
in all the newer scenarios. Furthermore, this expansion of the repertoire requires greater refinement in our intimate
knowledge of how drugs and techniques may enhance or adversely affect the nuanced neurosurgical outcomes.
Given the above changes in practice, the novice and experienced neuroanesthesia practitioners now, more than
ever, need an authoritative text not just full of “book knowledge” but written by those who on a daily basis meld
the academic with the practical. To his credit, Hemanshu Prabhakar has brought together an accomplished group of
international experts to contribute to this excellent volume. Their writing is authoritative and up to date while being
practical and easy to understand. There is no doubt that this book is a very useful contribution to the modern practice
of neuroanesthesia.
Adrian W. Gelb
Distinguished Professor
Department of Anesthesia and Perioperative Care
University of California
San Francisco
22. xxi
Preface
Neuroanesthesia is growing fast as a superspecialty as more and more research is being conducted to improve
the practice. The focus is now not restricted to the bench but has also extended to the bedside. There is a need to have
a volume that provides a comprehensive view of various topics and issues related to neuroanesthesia. This book
provides easy understanding of anesthesia related to neurological sciences. This book will be useful for any medi-
cal practitioner associated with neurosurgical and allied branches such as neurology and neuroradiology. This book
also caters to the needs of all those anesthetists who practice neuroanesthesia but do not have a formal training in
it. It will provide a quick and easy access to understand neuroanesthesia. This book will provide an insight into all
possible aspects of anesthetic management of neurosurgical and neurologic patients. This book has been written
mainly for the residents and students appearing for examination and anesthetists practicing neuroanesthesia. This
book includes the basic sciences such as anatomy, physiology, and pharmacology related to brain and spinal cord.
This book also provides an understanding of related issues such as palliative care, evidence-based practice of neuro-
anesthesia, sterilization techniques, and ethical issues.
This book covers all topics related to neuroanesthesia and provides complete knowledge about brain and spinal
cord. The book includes chapters related to allied specialties such as critical care, neurology, and neuroradiology.
This book also contains a section on biostatistics, which would be extremely useful to residents and trainees who
have to submit dissertation or thesis during their course.
This book contains pieces of information that have been brought together, which may have otherwise been avail-
able in different books.
I am grateful to all my authors across the globe, from as many as 14 different countries. The knowledge and infor-
mation shared by the authors through different chapters is the representation of the global practice of neuroanesthe-
sia and not limited to geographical boundaries. I sincerely hope this endeavor will improve our knowledge in the
management of neurologically compromised patients and bring about an improved patient care.
Hemanshu Prabhakar
24. xxiii
Acknowledgments
I wish to acknowledge the support of the administration of the All India Institute of Medical Sciences (AIIMS),
New Delhi, in allowing me to conduct this academic task.
Words are not enough to express my gratitude for the constant support and encouragement from Prof. P.K. Bithal
(Former Head of Neuroanesthesiology and Critical Care, AIIMS, New Delhi). I thank the faculty and staff of the
department of Neuroanesthesiology and Critical Care, for their support.
Special thanks are due to the production team at Elsevier.
26. xxv
Introduction and Brief History of
Neuroanesthesia
W.S. Jellish
Loyola University Medical Center, Maywood, IL, United States
Neuroanesthesia has evolved as a subspecialty of anesthesiology and has continued to evolve in association with
further surgical advancements such as minimally invasive techniques and three-dimensional imaging using neuro-
navigation. Neuroradiology has also advanced with invasive neurovascular procedures, once done in the operating
rooms, now performed in the neurointerventional radiology suite with the support of the anesthesiologists.
Early neuroanesthesia was performed as a method to support the practice of trephination. It was uncertain
whether brain surgery had been performed during this trephination or if it was part of a religious or social ritual
(Fig. 1). Some were obviously related to injury, but the presence of multiple defects in the absence of other apparent
injuries in both young and old suggested a possible therapeutic purpose. A popular aspect was that these openings
were used to alleviate pain or allow the escape of evil spirits and humors or to drain pus or reduce inflammation. No
matter what the reason for the trephination, skulls with these types of defects have been found all over the world.
There are several documented examples, which point out that these skull defects were produced as part of a neu-
rosurgical procedure. The Edwin Smith Papyrus is one of the earliest written records of surgical practice (Fig. 2). The
text may well represent the first neurosurgical practitioner’s manual as it describes 48 cases that consist of 15 head
injuries, 12 facial wounds and fractures, and 7 vertebral injuries. Several other written works produced around 400
BC have been linked to Hippocrates. One of the texts on injuries of the head describes trephination for skull frac-
tures, epilepsy, blindness, and headaches. The practitioner was advised to avoid suture lines and the temporal areas
because of fear of damaging the anatomy that would lead to contralateral convulsions.1 It was also noted that the
inner table should be preserved to protect the dura and this bone fragment would later be extracted by suppuration.
Despite the advanced neurosurgical and neuroanatomical knowledge for the times in Greece and Rome, use and
understanding of neuroanesthesia did not appear to be much different from those of fellow practitioners elsewhere
in the world. In the prehistoric period, anesthesia was probably done by chewing or locally applying a mixture of
coca and yucca.2 Daturas had also been used with its anesthetic effect thought to be produced by its contents of sco-
polamine, hyoscyamine, and atropine. In early cultures, wine making was highly developed. In Egypt the soporific
effects of alcohol had been well documented in hieroglyphic writings. It is considered likely that some analgesia and
amnesic effects were derived from this source. Sometimes just compression of the carotid artery was used to induce
unconsciousness.3
Progress in neurosurgery slowed considerable during the Middle Ages. The Roman Catholic Church became very
influential in medical care and monasteries were the centers for science and knowledge. With the edict of AD 1163
entitled, “Ecclesia abhoret a sanguine,” there were restrictions placed on the use of human bodies for anatomical
studies, and progress in the field of surgery was almost halted. At the beginning of the 10th century, Rhazes com-
piled the Liber Continens, a collection of all literature belonging to the Arab world including medicine, philosophy,
religion, mathematics, and astronomy. Among the several important observations he made with this work, one was
particularly remarkable. He wrote that the pressure on the brain, rather than the presence of the skull fracture itself,
was more important in determining the outcome after head injury.4 It was not until later in the 10th century with the
establishment of a medical school in Salerno, Italy, that this and other medical principles were brought forward to
revive European medicine.
Few references were made on the use of anesthesia, perhaps because pain was mentioned so many times in reli-
gious teachings and was felt to be a noble state that served God’s purpose. When anesthesia was attempted, opium,
hyoscyamine, and sometimes wine were used as agents to alleviate pain.5 On occasion Cannabis indica and henbane
were used, along with a sponge containing opium, marberry, water hemlock, and ivy which was boiled and then
applied to the patient’s nose during the surgery.6 It was thought that wine was added to the sponge during boiling
to enhance its sedative power. The physicians of Myddavi, herbalist from Wales, further advised that to improve
27. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA
xxvi
anesthetic efficiency, when you prepare to operate on a patient, direct them to avoid sleep as long as possible then let
some of the potion be poured into the nostril of the patient who will fall asleep without fail.7
The first account of inducing anesthesia and reversing sedation was attempted by two Hindu brothers who per-
formed a craniotomy in AD 927 to remove an unidentified tumor from the brain of the King of Dhar. They induced
anesthesia with a drug called samohine and reversed the anesthetic effects by pouring an onion compounded with
vinegar into the subject’s mouth.7 Numerous other concoctions both oral and topical were administered to patients
for better outcomes. Some combined puppies boiled in an oil of lilies and earthworms and prepared in turpentine
of Venice.2 Other mixtures used were rose oil, egg yolk, and turpentine, which were either heated in cold weather or
cooled in warm weather to maintain temperature. This was done to produce optimal wound healing.
The major improvements and overall advancement in anesthesia for neurosurgery occurred in the latter half of
the 18th century. The discovery of carbon dioxide, hydrogen, and nitrogen along with experiments by Priestly and
others using several gases including oxygen and nitrous oxide created interest in the use of these agents to support
patients who were sedated or anesthetized for procedures.8 However, the reluctance of surgeons to perform cranial
operations slowed the implementation of anesthesia for neurosurgery. Nevertheless, the accumulation of knowledge
of functional neuroanatomy, establishment of concepts of asepsis, and the discovery of general anesthesia all moved
the process of neurosurgery accompanied by anesthesia forward.
William Macewen was the first neurosurgeon to excise a brain tumor under endotracheal intubation. He was the
first to show the necessity of controlling the airway and ventilation during craniotomy. At the beginning of the 20th
century there was a great deal of controversy as to what was the best inhalational anesthetic, chloroform, or either.
Victor Horsley performed a series of experiments in animals in 1883–85 and concluded that, although ether was the
safer drug, it was not to be recommended in favor of chloroform because it produced a rise in blood pressure and an
FIGURE 2 The Edwin Smith Papyrus. The terms of brain, as original term “iesh,” pointed by an arrow (and depicted below) can be seen. From
James Henry Breasted. The Edwin Smith Surgical Papyrus. Chicago: University Chicago Press; 1930 (reproduced from Eric R Kandel, James H Schwartz,
Thomas M Jessell, editors Principles of Neural Science. 4th ed. New York: McGraw-Hill; 2000).
FIGURE 1 The trephined skulls discovered in paracus, Peru (≈500 BC), and obsidian blades. The surgical holes are covered with roles of cotton
dressing (A). The trepanation had been performed using obsidian blade (B).
28. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA xxvii
increase in blood viscosity with a potential for hemorrhage.9 He also noted a propensity for postoperative vomiting
and concluded it should not be used for neurosurgery. Also, since morphine constricted blood flow, he suggested
that a combination of morphine and chloroform be used. He subsequently abandoned morphine use because of its
recognized depressant effect on respiration.9
Death related to the administration of chloroform was not uncommon, and several commissions were set up to
study the effects of the drug. In 1901, The British Medical Association appointed a special chloroform committee to
study its use. It was known that approximately 2% chloroform vapor in air was sufficient to induce anesthesia with
much less required for maintenance. Some believed that the concentration should be strictly controlled with a vapor-
izer, while others thought it could be administered strictly by sprinkling onto a cloth. Horsley was of the opinion
that the concentration should be controlled and used a vaporizer designed by Vernon Harcourt, which delivered
chloroform at a 2% maximum (Fig. 3). In patients undergoing craniotomy, Horsley felt that chloroform administra-
tion should be reduced to 0.5% once the bone flap was removed.10 Determination of concentration was particularly
important in patients with raised intracranial pressure (ICP) since higher concentrations in these patients could be
fatal.
Horsley also contributed to neuroscience and neurosurgery by his support and defense of surgery done on ani-
mals for scientific research and to advance clinical knowledge. His work and testimony against the Anti-Vivisection
Society helped to defend the use of animal models to advance neurosurgery.11
Around the same time, the use of local anesthesia began to gain prominence. Cocaine had been formally discov-
ered in 1860 and was introduced in surgery in 1884. Procaine was first synthesized in 1905 and immediately became
commonplace among surgical anesthesia. Most neurosurgeons used local anesthetics selectively. However, in 1913
deMartel popularized its use, and it became common practice for use in all craniotomies. By 1917, Harvey Cushing,
considered the founder of neurosurgery, recommended the use of local anesthesia for all neurosurgical cases.7
Besides being one of the leading neurosurgeons of the early 20th century, Cushing introduced numerous new
methods of anesthesiology. His first contracts in providing anesthesia were not entirely successful. He had several
notable patient deaths while providing ether for procedural anesthesia. In all instances, he was told the deaths
occurred due to the patient’s condition, but he remained unconvinced that adverse reactions to anesthesia were
due only to the condition of the patients. At the coaxing of Dr. F. B. Harrington, Cushing and fellow student Amory
Codman tried to determine who gave the best anesthetics. To make the decision objective, they documented their
anesthesia in the form of “ether charts” (Fig. 4).12 Their most important parameters measured were the pulse rate,
FIGURE 3 The Vernon Harcourt vaporizer arranged with a cylinder of compressed oxygen.
29. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA
xxviii
breathing, and temperature of the patients. According to Cushing, “a perfect anesthetic was supposed to be one
in which the patient was sufficiently conscious to respond when left in the ward with the nurse and did not sub-
sequently vomit.” The use of these either charts was a major step toward improvement in what had been a casual
administration of a very dangerous drug.
In 1900, Cushing began an extended tour of Europe, and while in Bern, he recognized the association between
raised ICP and systemic arterial hypertension.13 While in Padua, Italy, at the Ospidale di St. Matteo, he learned the
use of Riva-Rocci’s method of blood pressure measurement (Fig. 5). After returning to Baltimore, he adopted this
method of blood pressure measurement into clinical practice. He gave a lecture in 1903 titled, “Considerations of
Blood Pressure,” only to have a committee of the Harvard Medical School state that, “the skilled finger was of much
greater value clinically for determination of the state of circulation than any pneumatic instrument, and the work
should be put aside, as of no significance.” Even though blood pressure monitoring was not supported by thought
leaders at that time, Cushing still supported the recording of blood pressure during surgery. He also attached great
importance to continuous auscultation of the heart and lungs, a technique he learned from his anesthesiologist,
Dr. S. Griffith Davis.14 The precordial auscultation device used a transmitter of the phonendoscope secured by adhe-
sive strips over the precordium and was connected with a long tube to the anesthesiologist’s ear. The receiver was
held in place by a device similar to a telephone operator’s headgear.15
Cushing remained skeptical about general anesthesia for neurosurgery. Mortality was still high and many of the
anesthetics were performed by students. He began to experiment on work started by Halsted with block anesthesia
using circumferential cocaine infiltration.16 He popularized the use of several local anesthetic techniques and coined
the term “regional anesthesia.” From his first work dealing with regional anesthesia, it was noted that the purpose of
administering it was to avoid side effects in patients with full stomachs and to ensure better cardiovascular stability
in elderly patients.
FIGURE 4 An example of the ether charts made by Cushing.
30. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA xxix
Dr. Fedor Krause, the founder of German neurosurgery, was exposed to combination morphine–chloroform anes-
thesia but was not convinced of its worth for neurosurgery. He felt that controlled hypotension produced by higher
concentrations of chloroform alone were beneficial to reduce bleeding.17 He also noted that sudden death could
occur in patients with intracranial tumors who stopped breathing. He used the Roth-Drager oxygen–chloroform
apparatus which allowed high concentrations of oxygen to be administered. He also noted the brain was insensitive
to pain, and only very light planes of anesthesia were needed to perform these surgeries.18 He concluded a good
neurosurgical outcome required a rapid aseptic technique, minimal blood loss, normothermia, and general narcosis.
During the early 20th century, new delivery systems for anesthesia were being developed. The Junker bottle used
a hand bellows to blow air through a vaporizer and the Ombrédanne ether inhaler could be used in the prone posi-
tion (Fig. 6). Airway management became less supportive and passive and more active with endotracheal intubation
and insufflation of air to maintain oxygenation without ventilation. By 1930, endotracheal anesthesia was recom-
mended for neurosurgery. Inhalational anesthetics such as trichloroethylene with nitrous oxide were developed
as a neuroanesthetic technique,18 while other physicians such as Hershenson used low concentrations of closed
circuit cyclopropane and reported this method in 1942.19 Volwiler and Tabern developed thiopental in 1930 and was
introduced into clinical practice 4years later.20 Halothane was synthesized in 1956 and introduced into practice that
same year.21 Though popular, its propensity to increase ICP and brain size made it a concern to anesthesiologists
and neurosurgeons alike. In 1932, most fluids were given rectally along with a wide variety of anesthetic techniques
including ether-based anesthesia, rectal ether in oil, ethylene, and nitrous oxide.
Certain large centers began to publish their outcomes for neurosurgical procedures and many included a descrip-
tion of the anesthetic techniques used. The Montreal Neurologic Institute showed that of 1000 cases, 700 were per-
formed under general anesthesia and 300 with local anesthetics.22 The major concerns were still airway management
and fluid replacement. A wide variety of agents were used. However, by 1949 and the early 1950s, pentothal was the
induction agent of choice for oral intubation. Throat packing and the use of a nonrebreathing valve to prevent the
buildup of carbon dioxide was also common.
After World War II, great advances in neuroanesthetic techniques were brought on by the development of new
anesthetic agents and advanced knowledge of neurophysiology and pharmacology. Lundy in 1942 noted that in
the presence of hypoventilation it was difficult to reduce ICP unless the patient was artificially ventilated.23 The
effects of hypoventilation on intracranial and systemic dynamics were further elucidated by Keaty and Schmidt
(Fig. 7). They also described methods to measure cerebral blood flow using inhaled N2O.24 Another group used the
injection of intraarterial krypton to measure blood flow in the brain and speed of washout.25 The measurement of
ICP had been discovered by Cannon in 1901 but continuous ICP measurement was not described until 1960.26 The
link between CO2, O2 tension and cerebral blood flow was also developed at this time. Dr. Thomas Langfitt further
FIGURE 5 Dr. Harvey Cushing’s sketch of Riva-Rocci’s blood pressure device.
31. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA
xxx
Venous
Arterial
A-V
1
1 2 3 4 5
Time (minutes)
6 7 8 9 10
N
2
O
Conc
Vol%
2
3
4
5
FIGURE 7 Kety–Schmidt method of arterial and venous nitrous oxide concentration for calculating cerebral blood flow.
FIGURE 6 (A) Ombrédanne inhaler. (B) Ombrédanne inhaler in use.
32. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA xxxi
defined intracranial dynamics based on previous work and developed the pressure volume curves along with the
concept of intracranial compliance.27
Three major anesthesia groups contributed to the development of the specialty, the Glascow Group, Pennsylvania
Group, and the Mayo Clinic Group. All the three centers were considered think tanks in the development of neuro-
anesthetic principles and techniques to help improve intracranial surgery. Most of the principles for neuroanesthesia
have been developed over the last 70years. The term, “neuroanesthesia” was coined by John Michenfelder from the
Mayo Clinic.28
In the 1960s, researchers at the University of Pennsylvania studied the cerebral effects of nitrous oxide, cyclopro-
pane, halothane, enflurane, hypotension, and hyperventilation.29–31 These studies formed many of the basics for neu-
roanesthesia principles today. At the same time, researchers at the University of Glascow studied anesthetic effects
on intracranial dynamics. This group was one of the first to confirm that anesthetic agents did indeed exert a measur-
able effect on cerebral blood flow and metabolism in patients with intracranial mass lesions.32,33 It was some of these
studies that were used to justify the abandonment of the use of halothane because of its vasodilating properties, espe-
cially in patients with mass lesions in the brain. At the Mayo Clinic the only emphasis of research by Michenfelder
was of providing cerebral protection, especially with hypothermia during neurovascular procedures. These same
three centers continued to expand their influence in neuroanesthesia, and at the University of Pennsylvania the role
of the neuroanesthesiologist was expanded to the intensive care unit.
In the 1980s, research continued on glucose control and again on the effects of modest hypothermia. A wide range
of drugs emerged as possible cerebral protective agents. A much clearer understanding of pathways involved in
cell damage was also achieved. Research on brain trauma and survival also became important because of the effects
of war on traumatic brain injury. Despite much of this research, the morbidity and mortality from subarachnoid
hemorrhage, stroke, trauma, and neoplastic lesions have remained largely unchanged in the past several decades.
Nevertheless, neuroanesthesia practice has appreciably changed over the past few decades.
Hyperventilation has long been known to reduce ICP. At the beginning of the 1990s it was widely held that this
had therapeutic value for intracranial procedures. However, with the use of oximetric pulmonary artery catheters,
investigators have been able to do retrograde cannulation of the jugular vein up to the bulb to examine venous Hb
saturation in response to therapeutic hyperventilation in head trauma patients. In some patients, this hyperventila-
tion resulted in increased hypoxia that has resulted in abandonment of hyperventilation unless surgical conditions
dictate. However, other recent studies have demonstrated that hyperventilation, especially for supratentorial brain
tumors, was associated with reduced ICP and a 45% reduction in brain bulk, once again demonstrating its worth,
especially with supratentorial surgery.34
The early 1990s also demonstrated a surge of new anesthetic techniques and drugs. Both desflurane and sevoflu-
rane were introduced and were found to have cerebral metabolic properties similar to isoflurane. However, some
questions still remain regarding desflurane causing an insidious increase in ICP. There are also questions concerning
the metabolism of sevoflurane and possible renal toxicity, especially with the effect of anticonvulsants on hepatic
function. Since both drugs have been accepted and widely used as neuroanesthetics, these concerns do not seem
to hold major importance. Remifentanil was also introduced in the 1990s and was found to be essentially identical
to other opioids with respect to µ-opioid agonist-mediated events. It does have a much more rapid and predictable
emergence compared to other opioid-based techniques. However, the drug produces hypertension and tachycardia
with increased sympathetic activity during emergence which could be especially problematic with large tumor resec-
tions where hemodynamic stability during emergence to prevent bleeding is imperative.
The administration of proper IV fluids and correct fluid replacement therapy was better developed in the 1990s.
There was a widespread acceptance that glucose-containing solutions were not essential in patients undergoing
neurosurgical procedures. Perioperative glycemic control is one of the important topics that have been investigated
in the 1980s and 1990s. Hyperglycemia in ischemic conditions has been proven to be detrimental, and strict control
of plasma glucose has been shown to produce better outcomes in critically ill patients. Many studies have demon-
strated that plasma glucose levels are well maintained at close to normal ranges with nonglucose-containing solu-
tions, while patients who received glucose had high plasma levels which fluctuated dramatically during their care.
Therefore, routine use of glucose-containing solutions should be avoided during neurosurgery.
The use of crystalloid solutions has also been altered by studies from the last 20years. In the 1980s it remained a
standard practice to dehydrate patients with intracranial pathology under the assumption that brain volume would
be decreased. This was often performed at the expense of stable hemodynamics and cerebral perfusion pressure.
However, extensive studies have demonstrated that fluid restriction for neurosurgical procedures may be detrimen-
tal. In addition, many large trials evaluating colloid versus crystalloid solutions, especially with trauma-related injury,
showed that saline resuscitation may be of greater benefit than treatment with albumin. In fact, studies demonstrated
33. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA
xxxii
a detrimental effect of albumin treatment, especially with the relative risk of death within 24months.35 This has led
to a recommendation that colloids not be used for resuscitation in patients with brain injury.
The early 1990s also provided consistent evidence that small changes in brain temperature could have a major
impact on outcome from ischemic or traumatic brain injury.36 These changes did not require overt cooling or the use
of extracorporeal perfusions but were well within the range of routine manipulation by anesthesiologists. The prac-
tice of the use of mild hypothermia increased, but there were other warnings about inadvertent hypothermia from
other patient populations, which caused concerns. In the late 1990s, a multinational consortium of investigators was
formed to examine the risks and benefits of mild hypothermia in patients undergoing aneurysm clipping and was
inconclusive as to the benefit of hypothermia on survival and outcome after a neurologic event producing ischemia.
Based on clinical data, mild hypothermia may still have beneficial effects in patients with good grade subarachnoid
hemorrhage (SAH).37 The latest American Heart Association and American Stroke Association guidelines for the
management of aneurysmal SAH recommend induced hypothermia as a reasonable option in selected cases.38
At the clinical level, no progress has been made in pharmacologic neuroprotection. Despite successful experi-
mental studies, by far no anesthetic technique has been convincingly shown to provide profound neuroprotection in
humans. Barbiturates remain the gold standard, although clinical evidence of efficacy from this class of compounds
is suspected on methodologic grounds. In a post hoc analysis of IHAST (intraoperative hypothermia for aneurysm
surgery trial) data administration of thiopentanil or etomidate was not found to have a demonstrable effect on
postoperative neurological outcomes in patients undergoing temporary clipping.39 Use of etomidate has waned as
a neuroprotective agent as a result of absence of clinical evidence of benefit in both clinical and laboratory studies.
Some of the most exciting and important clinical advances in neuroanesthesia have been in the area of monitor-
ing, both in the operating room and neurointensive care units. With the advancement of near-infrared spectros-
copy (NIRS) and transcranial Doppler, the detection of cerebral ischemia, especially under general anesthesia, has
improved tremendously. Multimodal intraoperative monitoring of spinal cord sensory and motor function during
surgical correction of adult spinal deformity is feasible and provides useful neurophysiological data with an overall
sensitivity of 100% and specificity of 84.3%.40 In the neurointensive care unit, insertion of microdialysis and multipa-
rameter biochemical probes into traumatized human brains has confirmed findings. Cytokine production and pro-
apoptotic markers have been detected during oxidative stress, and these markers have recovered during enhanced
perfusion. Ischemic events have been associated with tissue acidosis, and spontaneous depolarizations have been
observed. Use of these monitors in the operating room has occurred. What remains to be totally defined is what val-
ues constitute thresholds for interventions. These thresholds have been characterized mostly for NIRS monitoring,
and much of this has revolutionized the treatment of patients with the possibility of cerebral hypoperfusion.
The development of neuroanesthesia has paralleled advances in neurosurgery. As techniques and procedures
have become advanced, so have the techniques and protocols to anesthetize and monitor neurologic function. The
overall goal is to provide a good surgical outcome and better quality of life. Procedures will become less invasive
with more functional neurosurgery requiring a cooperative patient. This makes the anesthetic management for these
procedures even more complex. It is also likely that there will be greater integration of neurosurgery and neuroradi-
ology, with greater emphasis on maintaining cerebral vascular function without the effects of inhalational anesthet-
ics and opioids. Neurosurgery is ever evolving; the practice of anesthesiology for these procedures will also have to
evolve to accommodate the demands of the surgeon and improve patient outcomes. Neuroanesthesia practice will
shadow neurosurgical breakthroughs. These changes will accelerate over the next 10years as scientific advances,
and the understanding of the diseases we treat enhance the capacity of the anesthesiologist to develop techniques to
provide an ideal surgical environment with rapid awakening to assess neurologic function.
References
1. Hippocrates on injuries of the head [Adams F, Trans.]. London: The Genuine Works of Hippocrates, in 2 vols.; 1849.
2. Frost EAM. A history of neuroanesthesia. In: Eger E, Saidman LJ, Westhope RN, editors. The wondrous story of anesthesia. New York: Springer;
2014. p. 871–85.
3. Gunther RT. Dioscorides Pedanius. The greek herbal of dioscorides. Oxford: Oxford University Press; 1934.
4. Cooper A. Lectures on the principles and practice of surgery. London: Westley; 1829.
5. Raper HR. Man against pain: the epic of anesthesia. New York: Prentice-Hall; 1945. p. 8.
6. Robinson V. Victory over pain: a history of anesthesia. New York: Henry Schumann; 1945. p. 29.
7. Walker AE. A history of neurological surgery. New York: Hafner; 1967.
8. Priestley J. Experiments and observations on different kinds of air. London: Thomas Pearson; 1790.
9. Horsley V. On the technique of operations on the central nervous system. BMJ 1906;2:411–23.
10. Horsley V. On the technique of operations on the central nervous system. Address in Surgery. Toronto Lancet 1906;2:484.
34. INTRODUCTION AND BRIEF HISTORY OF NEUROANESTHESIA xxxiii
11. Lyons JB. Citizen surgeon. London: Peter Downay; 1966.
12. Beecher HK. The first anesthesia records (Codman Cushing). Surg Gynecol Obstet 1940;71:689.
13. Cushing HW. Concerning a definitive regulatory mechanism of the vasomotor center which controls blood pressure during cerebral compres-
sion. Bull Johns Hopkins Hosp 1901;12:290.
14. Cushing HW. Some principles of cerebral surgery. JAMA 1909;52:184.
15. Shephard DA. Harvey Cushing and anesthesia. Can Anaesth Soc J 1965;12:431–2.
16. Halsted WS. Surgical papers. Baltimore: Johns Hopkins Press; 1924. p. 167.
17. Krause F. [Haubold H, Thorek M, Trans.]. Surgery of the brain and spinal cord based on personal experiences, vol. 1. New York: Rebman & Co.; 1912.
p. 137.
18. Jackson DE. A study of analgesia and anesthesia with special reference to such substances as trichloroethylene and vinesthene together with
apparatus for their administration. Anesth Analg (Curr Res) 1934;13:198.
19. Hershenson BB. Some observations on anesthesia for neurosurgery. NY State J Med 1942;42:2111.
20. Lundy JS. Intravenous anesthesia: preliminary report of the use of two new thiobarbiturates. Mayo Clin Proc 1935;10:536.
21. Johnstone M. The human cardiovascular response to flurothane anaesthesia. Br J Anesth 1956;28:392.
22. Stephen CR, Pasquet A. Anesthesia for neurosurgical procedures. Analysis of 1000 cases. Anesth Analg 1949;28:77.
23. Lundy JS. Clinical anesthesia. Philadelphia: WB Saunders; 1942. p. 3.
24. Kety SS, Schmidt CF. Determination of cerebral blood flow in man by the use of nitrous oxide in low concentrations. Am J Physiol 1945;143:53.
25. Lassen NA, Ingvar DH. The blood flow of the cerebral cortex determined by radioactive krypton. Experientia 1961;17:42.
26. Lundberg N. Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Neurol Scand 1960;36
(Suppl. 149).
27. Langfitt TW. Increased intracranial pressure. Clin Neurosurg 1969;16:438.
28. Michenfelder JD, Gronert VA, Rehder K. Neuroanesthesia. Anesthesiology 1969;30:65–100.
29. Alexander SC, Wollman H, Cohen PJ, Chase PE, Behar M. Cerebral vascular responses to PaCO2 during halothane anesthesia in man. J Appl
Physiol 1964;19:561.
30. Smith AL, Wollman J. Cerebral blood flow and metabolism: Effects of anesthetic drugs and techniques. Anesthesiology 1972;36:378.
31. Pierce Jr EC, Lambertsen CJ, Deutsch S, Chase PE, Linde HW, Dripps RD, et al. Cerebral circulation and metabolism during thiopental anes-
thesia and hyperventilation in man. J Clin Invest 1962;41:1664.
32. Okuda Y, McDowall DG, Ali MM, Lane JR. Changes in CO2 responsiveness and in autoregulation of the cerebral circulation during and after
halothane induced hypotension. J Neurol Neurosurg Psychiatry 1972;39:221.
33. Harper AM, Bell RA. The effect of metabolic acidosis and alkalosis on the blood flow through the cerebral cortex. J Neurol Neurosurg Psychiatry
1963;26:341.
34. Gelb AW, Craen RA, Rao GS, Reddy KR, Megvesi J, Mohanty B, et al. Does hyperventilation improve operating condition during supratento-
rial craniotomy? A multicenter randomized crossover trial. Anesth Analg 2008;106:585–94.
35. SAFE Study Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group, Australian Red Cross Blood Service,
George Institute for International Health, Myburgh J, Cooper DJ, Finfer S, Bellomo R, Norton R, Bishop N, et al. Saline or albumin for fluid
resuscitation in patients with traumatic brain injury. N Engl J Med 2007;357:874–84.
36. Clifton GL, Valadka A, Zygun D, Coffey CS, Drever P, Fourwinds S, et al. Very early hypothermia induction in patients with severe brain
injury (the National Acute Brain Injury Study: Hypothermia II): a randomized trial. Lancet Neurol 2011;10:131–9.
37. Li LR, You C, Chaudhary B. Intraoperative mild hypothermia for postoperative neurological deficits in intracranial aneurysm patients.
Cochrane Database Syst Rev 2012;2:CD008–445.
38. Connolly Jr ES, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al. Guidelines for the management of aneurysmal
subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association. Stroke 2012;43:1711–37.
39. Hindman BJ, Bayman EO, Pfisterer WK, Torner JC, Todd MM. IHAST Investigators. No association between intraoperative hypothermia of
supplemental protective drug and neurologic outcomes in patients undergoing temporary clipping during cerebral aneurysm surgery: find-
ings from the intraoperative hypothermia for aneurysm surgery trial. Anesthesiology 2010;112(1):86–101.
40. Quraishi NA, Lewis SJ, Kelleher MO, Sarjeant R, Rampersaud UR, Fehlings MG. Intraoperative multimodality monitoring in adult spinal
deformity: analysis of a prospective series of one hundred two cases with independent evaluation. Spine (Phil PA 1976) 2009;34:1504–12.
39. 1. NEUROANATOMY
4
I. NEUROANATOMY
basis of his or her clinical practice has adapted well to a vista that emphasizes fundamental sciences as the basis
of all medical education. It helps the person improve his or her procedural skills. Finally, it helps him or her to
be better equipped to deal with a changing and unpredictable world where knowledge empowers and also acts
as a haven of safety.
About 100 billion neurons and 10–50 trillion neuroglias make up the brain, which has a mass of about 1300–
1500 g in adult. On average each neuron forms 1000 synapses with other neurons1. The total number of syn-
apses, about 1000 trillion, is larger than the number of stars in the galaxy. The central nervous system (CNS)
included the brain and the spinal cord and is composed of (1) cerebral hemisphere, (2) diencephalon, (3) basal
ganglion, (4) midbrain, (5) pons, (6) medulla, (7) cerebellum, and (8) spinal cord. This chapter will provide
information of these parts individually, that is integrated, informative, and relevant to educational need of the
neuroanesthesiologists.
EMBRYOLOGICAL DIFFERENTIATION OF DIFFERENT PARTS OF BRAIN
Knowledge of the embryological development of the brain is necessary to understand the terminology used for
the principal part of the adult brain. The development of the brain is dealt with details in the following chapter.
ANATOMY OF BRAIN
Cerebrum
The cerebrum consists of two cerebral hemispheres that are partially connected with each other by corpus cal-
losum. Each hemisphere contains a cavity called the lateral ventricle. The cerebrum is arbitrarily divided into five
lobes: frontal, parietal, temporal, occipital, and insula.2 On the lateral surface three sulci (central, lateral or Sylvian,
and parietooccipital sulci) and two imaginary lines divide the cerebrum into four lobes (Fig. 1.1). The first imaginary
line (lateral parietotemporal line) is drawn from parietooccipital sulcus to preoccipital notch and second (temporo-
occipital line) backward continuation of posterior ramus of lateral sulcus before it turns upward to meet first line.
The central sulcus and posterior ramus of Sylvian fissure (SF) separate frontal lobe from parietal lobe and temporal
lobe. Posteriorly parietooccipital sulcus and lateral parietotemporal line separate occipital lobe from parietal lobe
and temporal lobe. Temporal and parietal lobes are separate by posterior ramus of SF and temporo-occipital line
(Fig. 1.1).
The cerebral cortex is the outermost sheet of neural tissue of the cerebrum whereas white matter lies in the center.
Cerebral cortex is folded into sulci and gyri, which actually increases the surface area of cortex. Sulci include the
central lateral and parietooccipital.
The central sulcus begins by cutting the superomedial border of the hemisphere a little behind the midpoint between
the frontal and parietal lobe. It runs on the superolateral surface obliquely downward and forward for about 8–10cm
and ends a slight above the posterior ramus of lateral sulcus. It separates precentral gyrus (motor area) from postcen-
tral gyrus (sensory area) (Figs. 1.2 and 1.3). It was originally called the fissure of Rolando or the Rolandic fissure.
FIGURE 1.1 Schematic diagram of lateral aspect of left cerebral hemisphere. Line 1. Lateral parietotemporal line; Line 2. Temporooccipital line.
40. ANATOMY OF BRAIN 5
I. NEUROANATOMY
FIGURE 1.2 Brain anatomy. Superior view. 1. Longitudinal fissure of cerebrum. 2. Frontal pole. 3. Superior margin of cerebrum. 4. Superior
frontal sulcus. 5. Inferior frontal sulcus. 6. Precentral sulcus. 7. Central sulcus. 8. Postcentral sulcus. 9. Intraparietal sulcus. 10. Parietooccipital
sulcus. 11. Transverse occipital sulcus. 12. Occipital pole. 13. Superior parietal lobule. 14. Inferior parietal lobule. 15. Paracentral lobule. 16.
Postcentral gyrus. 17. Precentral gyrus. 18. Inferior frontal gyrus. 19. Middle frontal gyrus. 20. Superior frontal gyrus.
FIGURE 1.3 Brain anatomy. Lateral view of right hemisphere. 1. Central sulcus. 2. Precentral sulcus. 3. Precentral gyrus. 4. Superior frontal
gyrus. 5. Superior frontal sulci. 6. Middle frontal gyrus. 7. Middle frontal sulcus. 8. Frontal pole. 9. Orbital gyri. 10. Olfactory bulb. 11. Olfactory
tract. 12. Anterior ramus of lateral sulcus (Sylvian fissure (SF)). 13. Frontal operculum. 14. Ascending ramus lateral sulcus (SF). 15. Frontoparietal
operculum. 16. Posterior ramus lateral sulcus (SF). 17. Superior temporal gyrus. 18. Middle temporal gyrus. 19. Superior temporal sulcus. 20.
Inferior temporal sulcus. 21. Inferior temporal gyrus. 22. Pons. 23. Pyramid (medulla oblongata). 24. Olive. 25. Flocculus. 26. Cerebellar hemi-
sphere. 27. Preoccipital notch. 28. Occipital pole. 29. Postcentral gyrus. 30. Supramarginal gyrus. 31. Angular gyrus. 32. Transverse occipital sulcus.
33. Inferior parietal lobule. 34. Intraparietal sulcus. 35. Superior parietal lobule. 36. Postcentral sulcus.
41. 1. NEUROANATOMY
6
I. NEUROANATOMY
The lateral sulcus or Sylvian fissure (SF) is one of the earliest-developing sulci of the human brain. It first appears
around the 14th gestational week.3 It is the deepest and most prominent of the cortical sulci. The lateral sulcus (SF)
separates frontal and parietal lobes from temporal lobe. It begins on the superomedial margin. The SF starts on basal
and extends to the lateral surface of the brain. It has both a superficial part and a deep part. Superficial part has a
stem and three rami (Figs. 1.2 and 1.3). The anterior portion of the deep part (Sylvian cistern) is called the sphenoidal
compartment and the posterior part is called the operculoinsular compartment. SF is an important corridor in neu-
rosurgery as it connects the surface of anterior part of brain to its depth with all the neural and vascular components
along the way. The structures within the reach through the Transylvian approach include middle cerebral artery; optic
nerves; internal carotid artery; and its branched lamina terminalis, insula, basal ganglia, and interpeduncular fossa.
Parietooccipital sulcus begins on the medial surface of hemisphere nearly 5cm in front of the occipital pole
(Fig. 1.4). The upper end of the sulcus reaches the superomedial border to meet the calcarine sulcus, and a small
part of it is seen on the superolateral surface.
Frontal Lobe
The frontal lobe is an area in the brain of mammals, located at the front of each cerebral hemisphere and positioned
anterior to (in front of) the parietal lobe and superior and anterior to the temporal lobes. A prefrontal sulcus runs
downward and forward parallel to the central sulcus. The area between it and central sulcus is the precentral gyrus.
Two sulcus run horizontally anterior to precentral gyrus, i.e., superior and inferior frontal sulcus and divide the region
into superior, middle, and inferior frontal gyri (Fig. 1.3). The frontal lobe contains most of the dopamine-sensitive
neurons in the cerebral cortex associated with reward, attention, short-term memory tasks, planning, and motivation.
Temporal Lobes
Temporal lobes are bounded by SF superiorly and temporo-occipital and lateral parietotemporal line posteriorly
(Fig. 1.3). The temporal lobe has two sulci, superior and inferior, that run parallel to the posterior ramus of the lateral
sulcus and divide superiolateral surface into superior, middle, and inferior temporal gyri (Fig. 1.3). The temporal
lobes are involved in the retention of visual memories, processing sensory input, comprehending language, storing
new memories, emotion, and deriving meaning.4
FIGURE 1.4 Brain surface anatomy, view of medial surface of right hemisphere. 1. Frontal pole of frontal lobe. 2. Medial frontal gyrus. 3.
Cingulate sulcus. 4. Sulcus of corpus callosum. 5. Cingulate gyrus. 6. Paracentral lobule. 7. Precuneus. 8. Subparietal sulcus. 9. Parietooccipital sulcus.
10. Cuneus. 11. Calcarine fissure. 12. Occipital pole of occipital lobe. 13–16. Corpus callosum (cut surface). (Parts of Corpus callosum 13. Splenium.
14. Trunk. 15. Genu. 16. Rostrum.). 17. Lamina terminalis. 18. Anterior commissure. 19. Septum pellucidum. 20. Fornix. 21. Tela choroidea of the third
ventricle. 22. Choroid plexus of the third ventricle. 23. Transverse cerebral fissure. 24. Thalamus. 25. Interthalamic adhesion. 26. Interventricle foramen
of Monro. 27. Hypothalamus. 28. Suprapineal recess and pineal body. 29. Vermis of cerebellum. 30. Cerebral hemisphere. 31. Choroid plexus of the
fourth ventricle. 32. Medulla oblongata. 33. Pons. 34. Fourth ventricle. 35. Tectal lamina and mesencephalic aqueduct of Sylvius. 36. Mammillary body.
37. Oculomotor nerve. 38. Infundibular recess. 39. Temporal lobe of lateral occipitotemporal gyrus. 40. Rhinal fissure. 41. Hypophysis with adeno-
hypophysis (anterior lobe) and neurohypophysis (posterior lobe) of pituitary gland. 42. Optic chiasma. 43. Optic nerve. 44. Olfactory bulb and tract.
42. ANATOMY OF BRAIN 7
I. NEUROANATOMY
Parietal Lobe
The parietal lobe is positioned superior to the occipital lobe and posterior to the frontal lobe. The parietal lobe
is bounded anteriorly by central sulcus, inferiorly by SF and temporo-occipital line, medially by interhemispheric
fissure, and posteriorly by parietotemporal line. The two main sulci are postcentral sulcus, which run downward
and forward parallel to central sulcus, and intraparietal sulci, which are directed posteriorly and inferiorly toward
occipital pole. Thus divide the parietal lobe into postcentral gyrus, superior parietal lobule, and inferior parietal
lobule (Fig. 1.3). The upturn posterior end of the posterior ramus of lateral sulcus or SF extends into inferior parietal
lobule, also superior and inferior temporal sulci turn upward to enter into this lobule and constitute supramarginal,
angular gyri, and arcus temporo-occipitalis (Fig. 1.3).
The parietal lobe integrates sensory information from different modalities, particularly determining spatial sense
and navigation. For example, it comprises somatosensory cortex and the dorsal stream of the visual system. This
enables regions of the parietal cortex to map objects perceived visually into body coordinate positions. Several por-
tions of the parietal lobe are important in language processing. Just posterior to the central sulcus lies the postcentral
gyrus. This area of the cortex is responsible for somatosensation.5
The occipital lobule occupies space behind the lateral parietotemporal line. It has a number of short lobules
divided by short sulci. A horizontal sulci, lateral to occipital sulcus divides the lobe into superior and inferior occipi-
tal gyri (Fig. 1.3). A vertical strip anterior to curved lunate sulcus is the gyrus descendens. The transverse occipital
sulcus is located in the uppermost part of the occipital lobe. A strip superiolateral to this sulcus is arcus parietooc-
cipitalis. The occipital lobe is the visual processing center of the brain containing most of the anatomical region of
the visual cortex.6
Insula is a portion of the cerebral cortex folded deep within the lateral sulcus. This area grows less than its sur-
rounding areas during development and thus lies deep and not seen from surface view (Fig. 1.5). The surrounding
cortical areas are called opercula such as frontal opercula, frontoparietal opercula, and temporal opercula. The insula
are believed to be involved in consciousness and play a role in diverse functions usually associated to emotion or the
regulation of the body’s homeostasis. These functions include perception, self-awareness, cognitive functioning, and
interpersonal experience.
Two hemispheres are attached with each other by corpus callosum. On the medial surface above the corpus cal-
losum there are many sulci and gyri (Fig. 1.4). The most prominent sulcus is the cingulate sulcus, which follows the
curve course parallel of corpus callosum. The area between the cingulate sulcus and corpus callosum is the gyrus
cinguli. Above the cingulate sulcus, large anterior part is medial frontal gyrus and posteriorly paracentral lobule (Fig.
1.4). Behind the paracentral lobule, two major sulci, parietooccipital sulcus and calcarine sulcus, cut the area into a
triangular area called the cuneus. Between parietooccipital sulcus and paracentral lobule, a quadrangular area is
called precuneus, which is anteriorly separated from gyrus cinguli by suprasplenial sulcus.
FIGURE 1.5 Coronal section through the brain. 1. Longitudinal fissure of the cerebrum. 2. Cingulate sulcus. 3. Cingulate gyrus. 4. Corpus
callosum. 5. Sulcus of corpus callosum. 6. Caudate nucleus. 7. Claustrum. 8. Putamen. 9. Lateral sulcus (Sylvian fissure). 10. Globus pallidus. 11.
Thalamus. 12. Subthalamic nucleus. 13. Mammillary body. 14. Amygdala. 15. Optic tract. 16. Third ventricle and choroid plexus. 17. Body of fornix.
18. Lateral ventricle and choroid plexus. 19. Cortex of insula. 6, 8, and 10. Corpus striatum. 8 and 10. Lentiform nucleus.
43. 1. NEUROANATOMY
8
I. NEUROANATOMY
The majority of the space of cerebral hemisphere deep to the cortex is full of the white matter. There are some
important structures that are embedded within the white matter. On coronal section the corpus callosum is seen as
a strip connecting both the hemispheres (Fig. 1.5). Third ventricle is situated in midline just below corpus callosum.
Thalamus and hypothalamus, which are derived from diencephalon, lie adjacent to lateral wall of the third ventricle.
Caudate nucleus is situated above and lateral to thalamus. Another gray matter mass lentiform nucleus lies more
lateral and just deep to insula. There is a strip of gray matter between insula and lentiform nucleus called claustrum
(Fig. 1.5). The caudate nucleus, lentiform nucleus, claustrum along with some other gray matter nucleus are (derived
from telencephalon) collectively mentioned as basal nuclei or basal ganglia. There is a white matter, an internal cap-
sule that lies between thalamus and lentiform nucleus (Fig. 1.5). The white matter that radiates from the upper part
of internal capsule to the cortex is called corona radiate.
Functional Areas (of Cerebral Cortex)
Korbinian Brodmann was a German neurologist who studied the brain in the early part of the 20th century.7
Brodmann originally defined and numbered (from 1 to 52) different areas of cerebral cortex based on cytoarchitecture
or how the cells were functionally organized (Box 1.1). Brodmann areas have been discussed, debated, refined, and
renamed exhaustively for nearly a century and remain the most widely used and frequently cited cytoarchitectural
organization of the human cortex.8
On the basis of function, regions of the cerebral cortex are divided into three functional categories of areas
(Fig. 1.6). (1) Primary sensory areas, which receive signals from the sensory nerves and tracts by way of relay
nuclei in the thalamus. Primary sensory areas include the somatosensory cortex in the parietal lobe, visual
area of the occipital lobe, and the auditory area in parts of the temporal lobe and insular cortex. (2) Primary
BOX 1.1
I M P O RTA N T B R O D M A N N A R E A S
Frontal lobe contains areas that Brodmann identified
as involved in cognitive functioning and in speech and
language (Fig. 1.8).
t Area 4 corresponds to the precentral gyrus or primary
motor area.
t Area 6 is the premotor or supplemental motor area.
t Area 8 is anterior of the premotor cortex. It facilitates
eye movements and is involved in visual reflexes as
well as pupil dilation and constriction.
t Areas 9, 10, and 11 are anterior to area 8. They are
involved in cognitive processes such as reasoning and
judgment which may be collectively called biological
intelligence.
t Area 44 is Broca’s area.
Parietal lobe plays a role in somatosensory processes
(Fig. 1.8).
t Areas 3, 2, and 1 are located on the primary sensory
strip, with area 3 being superior to the other two.
These are somastosthetic areas, meaning that they are
the primary sensory areas for touch and kinesthesia.
t Areas 5, 7, and 40 are found posterior to the primary
sensory strip and correspond to the presensory to
sensory association areas.
t Area 39 is the angular gyrus.
Temporal lobe: Areas that are involved in the process-
ing of auditory information and semantics as well as the
appreciation of smell (Fig. 1.8).
t Area 41 is the primary auditory area.
t Area 42 is immediately inferior to area 41 and also
involved in the detection and recognition of speech.
The processing done in this area of the cortex
provides a more detailed analysis than that done in
area 41.
t Areas 21 and 22 are the auditory association areas.
Both areas are divided into two parts; one half of each
area lies on either side of area 42.
t Area 37 is found on the posterior–inferior part of the
temporal lobe.
Occipital lobe contains areas that process visual
stimuli (Fig. 1.8).
t Area 17 is the primary visual area.
t Areas 18 and 19 are the secondary visual areas.
44. ANATOMY OF BRAIN 9
I. NEUROANATOMY
motor cortex, which sends axons down to motor neurons in the brain stem and spinal cord and finally inner-
vate voluntary skeletal muscles; (3) remaining parts of the cortex, which are called the association areas. These
areas receive input from the sensory areas and lower parts of the brain which integrate sensory information
with emotional states, memories, learning, and rational thought processes that we call perception, thought, and
decision-making.
Motor areas—The motor area is classically located in precentral gyrus on the superiolateral surface of the hemi-
sphere and in anterior part of paracentral lobule. It is shaped like a pair of headphones stretching from ear to ear
(Fig. 1.6). Specific area within the motor cortex controls voluntary muscle activity on the opposite part of body. The
body is represented on the motor strip in an upside–down fashion (Fig. 1.7). The lower parts of the body, such as the
FIGURE 1.6 Traditional concept of functional areas on the superolateral aspect of the cerebral hemisphere (left sided).
FIGURE 1.7 The motor homunculus in primary motor cortex. Coronal section anterior view of the left hemisphere.
45. 1. NEUROANATOMY
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I. NEUROANATOMY
feet and the legs, receive motor movement commands from the superior part of the precentral gyrus (motor strip).
Parts of the face, on the other hand are innervated by the inferior part of the motor strip. The motor strip extends
down some distance into the longitudinal cerebral fissure. The portion inside this fissure is its medial aspect. The
part on the lateral surface of the hemisphere is called its lateral aspect. The medial cortex controls the movements of
the body from the hips on down while the lateral aspect sends commands to the upper body including the larynx,
face, hands, shoulders, and trunk (Fig. 1.7). The medial and lateral aspects of the motor strip have different blood
supplies. Blood comes to the medial area from the anterior cerebral artery while the lateral cortex is supplied by the
middle cerebral artery.
Premotor Area
There is supplementary motor area on and above the superior part of cingulate sulcus on the medial aspect hemi-
sphere that reaches to the premotor cortex (Brodmann areas 6 and 8) on the lateral surface of brain. The cortical area
in inferior frontal gyrus corresponds to motor speech area or speech area of Broca (Brodmann areas 44 and 45) and
frontal eye area (Fig. 1.8). Lesion into the motor speech area of Broca results in aphasia even the muscles concerned
are intact. In 95% of right-handers do have left-hemisphere dominance for language functions, only around 19% of
left-handers have right-hemisphere language dominance, with another 20% or so processing language functions in
both hemispheres.9
Sensory Areas
From the specific nuclei of the thalamus, neurons are projected into two somatosensory areas of the cortex: somato-
sensory area I in postcentral gyrus and somatosensory area II in the wall of the SF (Fig. 1.6). The arrangement of the
thalamic fibers in somatosensory area I is such that the part of the body is represented in order along the postcentral
gyrus, with leg on the top and head at the foot of the gyrus. The area of the cortex that receives sensation from a part
FIGURE 1.8 Brodmann areas in the neocortex. A number of important Brodmann areas have been marked out in the figure.