Textbook Tutorials in Endovascular Neurosurgery and Interventional Neuroradiology 2Nd Edition James Vincent Byrne Auth Ebook All Chapter PDF

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James Vincent Byrne
Tutorials in
Endovascular Neurosurgery
and Interventional
Neuroradiology
Second Edition
123
Tutorials in Endovascular Neurosurgery
and Interventional Neuroradiology
James Vincent Byrne
Tutorials in Endovascular
Neurosurgery and
Interventional
Neuroradiology
Second Edition
James Vincent Byrne
Nuffield Department of Surgical Sciences
Oxford University
Oxford
UK
ISBN 978-3-319-54833-3 ISBN 978-3-319-54835-7 (eBook)

DOI 10.1007/978-3-319-54835-7
Library of Congress Control Number: 2017940860
© Springer International Publishing AG 2017

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
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The use of general descriptive names, registered names, trademarks, service marks, etc. in this
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Acknowledgements 2nd Edition
Writing a second edition of this book has been a chance to update and amend
the text in view of developments in the field since 2012. This process has
taken place in tandem to changes in the curriculum and teaching on the
Oxford University M.Sc. Course in Endovascular Neurosurgery and
Interventional Neuroradiology. During the 5-year interval since the first edi-
tion, the course has expanded to include a clinical attachment at the University
Hospital of Southampton, supervised by Dr. John Millar. As a result, I have
to acknowledge eight former students who have completed the course since
2012, in addition to all the prior graduates whose work has shaped the
course’s tutorial teaching and thereby the content of this book.
These M.Sc. graduates are, in consecutive order, R.P. Brennan, J.K.A.
Hope, J.N.P. Higgins, D.D. Royston, A. Martinez de la Cuesta, D.R. Niemann,
S.T. Lalloo, Z. Hussain, R.A. Corkill, A.P. Mitsos, J. Gralla, F.M. Al-Senani,
R.E. Beltechi, G. Zilani, J.T. Baptista, A. Singh, M. Garcia Alzamora, P.R.
Mordasini, Y.P. Ng, A. Carnerio, T.I. Papasilekas, M.H. Schonfeld, S.H.
Moerkve and A.I. Omar. The course continues to attract other participants,
who whilst training in Oxford or visiting have, along with current teaching
colleagues, contributed to the program. Amongst these people, several made
substantial contributions to the course content, particularly during the early
development of the curriculum. I thank all these people but especially the
following: G. Baltsavias, M. Cellerini, S.C. Coley, N. Deasy, A. Ditchfield, I.
Q. Grunwald, W. Küker, W. Lim, J. Macdonald, J. Millar, S.A. Renowden, N.
Stoodley, V. Young and A. Williams.
No medical text can be written without stealing time which would be better
spent at home and my first thanks goes to my wife Juliet Byrne whose endless
support has been so generous. Next to my colleagues in the Department of
Neuroradiology at the John Radcliffe Hospital and the Nuffield Department of
Surgical Sciences at Oxford University and to Dr. Robert Lenthall for review-
ing the manuscript. My final thanks goes to my collaborating authors: Dr.
Piers Nye, Dr. Paul Giangrande and Henry Byrne. Drs. Nye and Giangrande
have each written chapters covering their specialist areas and Henry Byrne has
produced diagrams and illustrations to aid the reader. This book has been
much improved by their substantial and generous contributions.
Oxford, UK James Vincent Byrne
v
Contents
1 Embryology of the Cranial Circulation �� 1

1.1 Definitions of Terms Used in Embryology �� 2
1.1.1 Timelines in the Embryonic Period�� 2
1.1.2 General Concepts in Vessel Development�� 2
1.2 Closure of the Neural Tube and Development
of the Head Arteries�� 3
1.2.1 Pre-choroidal Stage�� 3
1.2.2 Choroidal Stage�� 4
1.2.3 Branchial Stage �� 4
1.2.4 Development of the Carotid and Vertebrobasilar
System�� 4
1.2.5 Embryological Basis of Variations in the
Carotid Artery �� 9
1.2.6 The Role of the Stapedial Artery�� 12
1.2.7 Development of the Ophthalmic Artery�� 13
1.2.8 Development of the Cavernous Sinus Region�� 17
1.2.9 The Inner and Middle Ear Arteries
and Their Variants �� 19
1.2.10 Vertebral and Vertebrobasilar Anomalies
and Persistence�� 20
1.3 Development of Cerebral Veins�� 24
1.3.1 Superficial Veins and Dural Sinuses �� 24
1.3.2 Deep Veins�� 25
References�� 26
2 Cranial Arterial Anatomy�� 27
2.1 Internal Carotid Artery (ICA) �� 28
2.1.1 The ICA Cervical Portion �� 28
2.1.2 The ICA Petrous Portion�� 28
2.1.3 The ICA Cavernous Portion�� 29
2.1.4 The ICA Intradural Portion�� 31
2.2 The Terminal Branches of the Internal Carotid Artery �� 34
2.2.1 Anterior Cerebral Artery (ACA)�� 34
2.2.2 Middle Cerebral Artery (MCA)�� 36
2.3 The Vertebrobasilar System�� 38
2.3.1 Vertebral Artery (VA)�� 39
2.3.2 Basilar Artery (BA)�� 42
2.3.3 Posterior Cerebral Artery (PCA)�� 42
vii
viii Contents
2.4 External Carotid Artery (ECA)�� 46

2.4.1 Superior Thyroid Artery �� 46
2.4.2 Lingual Artery�� 47
2.4.3 Ascending Pharyngeal Artery (APA)�� 47
2.4.4 Facial Artery (FA)�� 49
2.4.5 Occipital Artery (OA) �� 50
2.4.6 Posterior Auricular Artery (PA)�� 50
2.5 Terminal Branches of the External Carotid Artery �� 51
2.5.1 Superficial Temporal Artery (STA)�� 51
2.5.2 Internal Maxillary Artery (IMA)�� 52
References�� 55
3 Cranial Venous Anatomy�� 57
3.1 Extracranial Veins �� 58
3.1.1 Scalp Veins�� 58
3.1.2 Veins of the Face and Neck�� 58
3.2 Intracranial Veins�� 63
3.2.1 Diploic Veins�� 63
3.2.2 Emissary Veins�� 64
3.2.3 Meningeal Veins�� 64
3.2.4 The Dural Sinuses �� 64
3.3 The Cerebral Veins�� 69
3.3.1 The Supratentorial Superficial (Cortical) Veins�� 69
3.3.2 The Medullary Veins�� 70
3.3.3 Veins of the Posterior Fossa�� 73
References�� 75
4 Spinal Vascular Anatomy�� 77
4.1 Embryology of Spinal Arteries �� 77
4.1.1 Primitive Segmental Arteries�� 77
4.1.2 The Vasa Corona and Longitudinal
Neural Arteries�� 78
4.1.3 Formation of Multimetameric Arteries
and Desegmentation�� 79
4.1.4 Development of Craniocervical Arteries�� 79
4.2 The Spinal Arteries �� 81
4.2.1 The Basic Adult Pattern of Extradural Arteries�� 81
4.3 Arterial Supply to the Spinal Cord�� 82
4.3.1 Radicular Arteries �� 82
4.3.2 Radiculopial Arteries�� 82
4.3.3 Radiculomedullary Arteries�� 83
4.3.4 The Anterior Spinal Artery (ASA) �� 83
4.4 Intrinsic (Medullary) Arteries of the Spinal Cord�� 83
4.4.1 Sulcal Arteries�� 84
4.4.2 Perforator Arteries of the Surface Pial Network�� 84
4.5 The Extradural Multimetameric Spinal Arteries�� 84
4.5.1 Arteries Supplying the Cervical Spine�� 84
4.5.2 Arteries Supplying the Thoracic Spine �� 85
4.5.3 Arteries Supplying the Lumbar Spine�� 85
Contents ix
4.5.4 Arteries Supplying the Sacral Spine �� 86

4.6 Venous Drainage of the Spinal Cord�� 86
4.6.1 Veins of the Spinal Cord �� 86
4.6.2 Epidural Venous Plexus
(Internal Vertebral Plexus)�� 88
4.6.3 External Vertebral Plexus�� 88
References�� 88
5 Control of Cerebral Blood Flow �� 91
5.1 Cerebral Intolerance of Hypoperfusion�� 92
5.1.1 Cerebral Protection of Blood Flow �� 92
5.1.2 Vascular Resistance�� 92
5.2 The Blood–Brain Barrier�� 93
5.2.1 Other Distinguishing Physiological
Responses of Cerebral Vessels�� 94
5.3 Autoregulation�� 95
5.3.1 The Myogenic Response�� 96
5.3.2 Metabolic Responses�� 97
5.4 Neurogenic Influences�� 100
5.4.1 Sympathetic Innervation �� 100
5.4.2 Parasympathetic Innervation�� 101
5.4.3 Sensory Innervation�� 101
5.4.4 Pericytes and Astrocytes �� 101
5.5 Gaseous Vasodilators�� 102
5.5.1 Nitric Oxide: Ascending Vasodilation and Limiting
Intracerebral Steal �� 102
5.5.2 Carbon Monoxide and Hydrogen Sulphide�� 103
5.6 Posture and Its Effects on Cerebral Blood Flow�� 105
5.7 Results Depend upon the Experimental Technique Used �� 106
5.8 Summary of Cerebral Blood Flow Control�� 106
References�� 107
6 Control of Intravascular Thrombosis�� 109
6.1 Blood Coagulation�� 109
6.2 Anticoagulation Therapy�� 110
6.2.1 Warfarin�� 110
6.2.2 Reversal of Warfarin �� 111
6.2.3 Direct-Acting Oral Anticoagulants (DOACs)�� 111
6.2.4 Heparin�� 112
6.2.5 Complications of Heparin Therapy�� 112
6.2.6 Reversal of Heparin�� 113
6.2.7 Thrombophilia�� 113
6.2.8 Anticoagulation in Special Situations�� 114
6.2.9 Precautions Prior to Interventions in
Anticoagulated Patients�� 114
6.3 Antiplatelet Therapy �� 115
6.3.1 Aspirin�� 115
6.3.2 Thienopyridine Agents�� 116
6.3.3 Glycoprotein IIb/IIIa Receptor Inhibitors�� 117
x Contents
6.4 Thrombolytic Therapy�� 118

6.4.1 Clinical Applications of Thrombolytic Therapy�� 119
6.4.2 Complications of Thrombolytic Therapy�� 120
6.4.3 Reversal of Fibrinolysis�� 120
6.5 Prevention of Venous Thromboembolism�� 120
7 Cranial Anastomoses and Dangerous
Vascular Connections�� 121
7.1 Anterior External Carotid Artery:
Superficial Connections�� 122
7.1.1 Anastomotic Branches of the Face and Pharynx�� 123
7.2 Anastomotic Zones of the Face and Pharynx�� 124
7.2.1 Sublingual Anastomosis �� 124
7.2.2 Pharyngeal Anastomosis�� 124
7.2.3 Jugal Anastomosis�� 126
7.2.4 Orbital (Superficial) Anastomosis�� 126
7.2.5 Nasal Anastomosis�� 126
7.3 Anterior External Carotid Artery: Deep Connections�� 126
7.3.1 Anastomotic Branches of the Anterior Skull Base �� 126
7.4 Anastomotic Zones of the Anterior Skull Base�� 128
7.4.1 Eustachian Anastomosis �� 128
7.4.2 Orbital Anastomosis�� 130
7.4.3 Cavernous (Parasellar) Anastomosis�� 130
7.5 Posterior External Carotid Artery: Connections �� 130
7.5.1 Anastomotic Branches of the Posterior Cranium�� 131
7.6 Anastomotic Zones of the Posterior Skull Base �� 133
7.6.1 Clival Anastomosis �� 133
7.6.2 Middle Ear Anastomosis�� 134
7.7 Anastomotic Zones of the Craniocervical
Junction and Cervical Spine�� 136
7.7.1 The Odontoid Arcade�� 136
7.7.2 C3 and C4 Anastomoses �� 136
7.7.3 Posterior Fossa Dural Anastomoses�� 136
7.8 Arterial Supply to the Cranial Nerves�� 138
8 Arterial Aneurysms �� 141
8.1 Arterial Aneurysms: Definitions and Descriptions �� 142
8.1.1 History of Intracranial Aneurysms�� 142
8.1.2 Morphology�� 143
8.1.3 Location�� 144
8.1.4 Unruptured Aneurysms�� 145
8.2 Causes of Intracranial Aneurysms�� 146
8.2.1 Haemodynamic Causes�� 146
8.2.2 Structural Causes�� 147
8.2.3 Genetic Causes�� 148
8.2.4 Specific Causes �� 149
8.3 Pathology of Intracranial Aneurysms �� 151
8.3.1 Histopathology of Small Unruptured Aneurysms�� 151
Contents xi
8.3.2 Histopathology of Large and Giant Unruptured

Aneurysms�� 151
8.3.3 Histopathology of Ruptured Aneurysms�� 152
8.3.4 Histopathology of Fusiform Aneurysms�� 152
8.3.5 Histopathology of Dissecting Aneurysms�� 152
8.3.6 Histopathology of Blister Aneurysms�� 153
8.4 Epidemiology of Intracranial Aneurysms�� 154
8.4.1 Prevalence of Intracranial Aneurysms�� 154
8.4.2 Incidence of Subarachnoid Haemorrhage�� 154
8.4.3 Risk of Aneurysm Rupture �� 155
8.5 Aneurysmal Subarachnoid Haemorrhage �� 163
8.5.1 Clinical Syndromes of Subarachnoid Haemorrhage�� 163
8.5.2 Causes of Subarachnoid Haemorrhage �� 165
8.5.3 Acute Effects of Subarachnoid Haemorrhage�� 165
8.5.4 Grading of Patients After Subarachnoid
Haemorrhage�� 167
8.5.5 Complications of Subarachnoid Haemorrhage �� 169
8.6 Endovascular Treatments of Aneurysms�� 173
8.6.1 Endovascular Treatments with Parent
Artery Occlusion�� 174
8.6.2 Endovascular Treatments with Parent
Artery Preservations�� 175
9 Vascular Malformations of the Brain�� 195
9.1 Types of Vascular Malformations of the Brain �� 196
9.1.1 Early Descriptions of Vascular Malformations
of the Brain �� 196
9.1.2 Definitions of Arteriovenous Malformations�� 196
9.1.3 Classifications of Cerebral Vascular Malformations�� 197
9.2 Capillary Telangiectasia�� 197
9.2.1 Pathology�� 197
9.2.2 Aetiology�� 197
9.2.3 Epidemiology and Natural History �� 198
9.3 Developmental Venous Anomaly (Venous Angioma)�� 198
9.3.3 Epidemiology and Natural History �� 199
9.4 Cavernous Malformations�� 199
9.4.3 Epidemiology�� 199
9.4.4 Symptoms and Natural History�� 200
9.4.5 Treatment�� 201
9.5 Brain Arteriovenous Malformations (BAVM)�� 201
9.5.3 Demography�� 204
xii Contents

9.5.5 Natural History�� 205
9.5.6 Angioarchitecture�� 207
9.5.7 Treatments to Eradicate BAVMs�� 212
10 Cranial Dural Arteriovenous Fistulas�� 225
10.1 Definition�� 225
10.1.1 History�� 225
10.1.3 Epidemiology and Demographics�� 226
10.2 Clinical Consequences �� 227
10.2.1 Classifications �� 227
10.2.2 Clinical Presentation �� 229
10.2.3 Risk of Haemorrhage�� 230
10.2.4 Risks of Clinical Progressive�� 230
10.2.5 Imaging �� 231
10.3 Management �� 232
10.3.1 Indications for Treatment�� 232
10.3.2 Aims of Treatment�� 232
10.3.3 Treatment�� 232
10.4 Treatment Results�� 237
10.4.1 Endovascular Treatment Results�� 238
11 Endovascular Management of Carotid Cavernous Fistulas�� 243
11.1 Definition�� 244
11.1.2 Anatomy of the Cavernous Sinus�� 245
11.2 Diagnosis�� 246
11.2.1 Clinical Symptoms and Signs �� 246
11.2.2 Imaging Diagnosis�� 248
11.3 Treatment�� 248
11.3.2 Risks and Benefits of Balloon Embolisation�� 249
11.3.3 Pre-procedure Assessment�� 249
11.3.4 Endovascular Treatments�� 250
12 Vein of Galen and Non-Galenic Cerebral
Arteriovenous Fistulas�� 255
12.1 Arteriovenous Fistulas and Malformations Involving
the Vein of Galen�� 256
12.1.1 History of the Definition of the Vein of Galen
Malformation�� 256
12.1.2 Embryology�� 256
12.1.3 Early Descriptions of the Vein of Galen
Contents xiii
12.1.4 Current Descriptions of the Vein of Galen

12.1.5 Distinguishing Features of Choroidal and
Mural Types of Vein of Galen Malformation�� 259
12.2 Vein of Galen Malformation�� 260
12.2.1 Presentation�� 260
12.2.2 Pathology of Vein of Galen Malformation�� 261
12.2.3 Incidence/Epidemiology/Natural History �� 261
12.2.4 Imaging Assessments�� 262
12.2.5 Endovascular Treatment of Vein of Galen
12.2.6 Other Interventions for Vein of Galen
Malformations�� 264
12.2.7 Outcomes of Interventions�� 265
12.3 Non-Galenic Cerebral Arteriovenous Fistulas �� 265
12.3.2 Clinical Presentations�� 266
12.3.3 Imaging �� 266
12.3.4 Treatments�� 266
13 Spinal Vascular Malformations�� 269
13.1 History�� 269
13.2 Spinal Vascular Malformations�� 270
13.2.1 Symptoms and Modes of Presentation�� 270
13.2.2 Classifications �� 271
13.3 Spinal Dural Arteriovenous Fistula (SDAVF)�� 271
13.3.1 Aetiology and Pathophysiology�� 272
13.3.2 Presentation and Natural History�� 272
13.3.3 Imaging �� 272
13.3.4 Endovascular Treatment�� 273
13.3.5 Treatment Results and Complications�� 274
13.4 Intradural Perimedullary Fistula �� 274
13.4.3 Imaging �� 275
13.4.5 Treatment Results and Complications�� 276
13.5 Intramedullary Spinal Cord Arteriovenous
Malformation (SCAVM)�� 277
13.5.3 Imaging �� 278
13.5.4 Endovascular and Other Treatments �� 279
13.6 Spinal Aneurysms�� 280
13.7 Metameric Syndromes�� 280
13.8 Cavernous Malformations�� 281
xiv Contents
14 Head and Neck Vascular Lesions �� 285

14.1 Birthmarks and Vascular Lesions of the Head and Neck �� 286
14.1.1 Classification of Vascular Tumours of the
Head and Neck in Children�� 286
14.1.2 Assessment Prior to Treatment of Haemangioma
and Vascular Malformation�� 286
14.2 Haemangioma �� 287
14.2.1 Infantile and Childhood Haemangiomas�� 287
14.2.2 Pathology and Aetiology�� 287
14.2.4 Imaging �� 288
14.2.5 Management and Treatment�� 288
14.2.6 Specific Treatment Indications for Haemangioma
at Different Sites �� 288
14.2.7 Associated Syndromes�� 290
14.2.8 Adult Haemangiomas�� 290
14.3 Vascular Malformation �� 290
14.3.1 Clinical Distinguishing Features�� 291
14.3.2 Capillary Malformation�� 292
14.3.3 Lymphatic Malformation�� 292
14.3.4 Venous Vascular Malformation�� 293
14.3.5 Arteriovenous Malformation (AVM)�� 294
14.3.6 Associated Syndromes�� 296
14.4 Other Vascular Lesions �� 297
14.4.1 Sinus Pericranii �� 297
14.4.2 Thyroid Gland Tumours�� 298
15 Embolisation of Tumours�� 301
15.1 Protocol for Embolisation of Tumours �� 302
15.1.1 Indications for Embolisation�� 302
15.1.2 Aims of Embolisation �� 302
15.1.3 Risks and Benefits�� 303
15.1.4 Preprocedure Assessment �� 303
15.1.5 Procedure Technique�� 304
15.1.6 Postembolisation Care�� 305
15.2 Meningioma�� 306
15.2.3 Histological Grading�� 307
15.2.5 Indications for Endovascular Treatment �� 307
15.2.7 Risks and Benefits�� 307
15.2.9 Embolisation Technique�� 309
15.3 Juvenile Nasopharyngeal Angiofibroma�� 310
15.3.1 Demography, Epidemiology and Aetiology �� 310
15.3.2 Pathology and Natural History�� 310
Contents xv

15.4 Paragangliomas�� 313
15.4.1 Demography, Epidemiology and Aetiology �� 313
15.4.3 Natural History�� 314
15.4.7 Risks and Benefits of Treatment �� 315
15.4.10 Follow-Up �� 319
15.5 Other Cranial Tumours �� 319
15.6 Spinal Tumours�� 320
15.6.1 Vertebral Haemangioma�� 320
15.6.2 Aneurysmal Bone Cysts�� 322
15.6.3 Other Benign Spinal Tumours�� 322
15.6.4 Malignant Spinal Tumours�� 323
16 Embolisation for Epistaxis�� 327
16.1 Epistaxis�� 327
16.1.1 Anterior Epistaxis �� 328
16.1.2 Posterior Epistaxis�� 328
16.2 Causes of Epistaxis �� 328
16.2.1 Vascular Anatomy�� 329
16.2.2 Indications for Embolisation�� 331
16.2.3 Pretreatment Assessment�� 331
16.3 Endovascular Technique �� 331
16.3.1 Preliminary Angiography�� 331
16.3.2 Internal Maxillary Artery Embolisation�� 332
16.3.3 Embolisation in Additional Pedicles�� 332
16.3.4 Following Embolisation�� 332
16.4 Alternative Embolisation Techniques �� 333
16.5 Complications of Embolisation�� 333
16.6 Results of Endovascular Treatment�� 333
17 Re-establishing Blood Flow After
Intravascular Thrombosis �� 337
17.1 Intravascular Thrombosis�� 338
17.1.1 Basis of Intravascular Thrombosis�� 338
17.1.2 Therapeutic Thrombolysis�� 338
17.1.3 Indications for Thrombolysis
and Thrombectomy �� 339
xvi Contents
17.2 Evidence for Thrombolysis and Thrombectomy

After Acute Stroke�� 339
17.2.1 Trails of Intravenous Thrombolysis for
Acute Stroke�� 339
17.2.2 Trails of Intra-arterial Thrombolysis for
17.2.3 Trials of Combined Intravenous and Intra-arterial
Thrombolysis for Acute Stroke�� 341
17.2.4 Trails of Mechanical Thrombectomy for
17.3 Endovascular Treatments of Acute Stroke �� 342
17.3.1 Selection of Patients for
Endovascular Intervention�� 342
17.3.2 Angioplasty and Stent for Thrombectomy
in Acute Stroke �� 343
17.3.3 Stent-Retrieval Devices in Acute Stroke�� 343
17.3.4 Complication of Endovascular Interventions
for Arterial Thrombosis�� 345
17.3.5 Contraindication to Thrombolysis�� 345
17.4 Endovascular Treatment of Cerebral Venous
Sinus Thrombosis �� 345
17.4.3 Imaging �� 346
17.4.5 Outcomes�� 347
17.5 Thrombolysis for Central Retinal Artery Thrombosis�� 347
17.5.2 Indications for Thrombolysis�� 348
17.5.3 Technique for Central Retinal Artery
Thrombolysis�� 348
17.5.4 Results�� 348
18 Embolic Agents�� 353
18.1 General Principles of Embolic Agents �� 354
18.1.1 How Does One Choose the Right Embolic Agent?�� 354
18.2 Classification of Embolic Agents �� 354
18.2.1 Absorbable Materials�� 354
18.2.2 Nonabsorbable Agents�� 355
18.2.3 Particles�� 355
18.3 Coils �� 356
18.3.1 Uncontrolled Release Coils�� 356
18.3.2 Controlled Detachment Coils�� 357
18.3.3 Large Artery Occlusion Devices (Plugs)�� 357
18.3.4 Coated Coils�� 357
18.4 Balloons�� 358
18.4.1 Detachable Balloons �� 358
Contents xvii
18.4.2 Nondetachable Balloons �� 358

18.5 Liquid Embolic Agents�� 359
18.5.1 Quick-Setting Liquids�� 359
18.5.2 Sclerosants�� 360
18.5.3 Chemotherapeutic and Other Agents�� 361
18.6 Intracranial Stents, Flow Diverters and Flow Disruptors �� 361
18.6.1 Stents�� 362
18.6.2 Flow Diverters�� 362
18.6.3 Neck Bridge Devices�� 362
18.6.4 Flow Disruptors�� 363
19 Angioplasty and Stenting for Cranial Vessel Stenosis�� 367
19.1 Carotid Artery Stenosis and Stroke Prevention�� 367
19.1.1 Pathology and Natural History�� 368
19.1.2 Medical Treatment�� 369
19.1.4 Surgical Treatment�� 369
19.2 Endovascular Treatments for Extracranial
Carotid Stenosis�� 370
19.2.1 Carotid Artery Angioplasty�� 370
19.2.2 Carotid Artery Stenting (CAS) �� 370
19.2.3 Vertebral Artery Stenting (VAS)�� 372
19.3 Endovascular Treatment of Intracranial Artery Stenosis �� 372
19.3.1 Natural History of Intracranial Stenosis �� 373
19.3.2 Classification and Techniques of Endovascular
Treatments for Intracranial Artery Stenosis�� 373
19.3.3 Results of Endovascular Treatments
for Intracranial Stenosis�� 373
19.4 Angioplasty for Vasospasm�� 374
19.4.1 Vasospasm After Subarachnoid Haemorrhage�� 374
19.4.2 Timing of Angioplasty for Vasospasm�� 374
19.4.3 Indications for Endovascular Treatment
of Vasospasm�� 374
19.4.4 Imaging for Vasospasm�� 375
19.4.5 Endovascular Treatment Techniques
for Vasospasm �� 375
19.5 Angioplasty and Stenting for Venous Disease �� 376
20 Complications�� 381
20.1 Generic and Specific Complications�� 382
20.1.1 Severity of Complications�� 383
20.2 Complications Caused by Catheter Angiography�� 383
20.2.1 Complications at the Puncture Site �� 383
20.2.2 Complications Caused by Catheters
and Guidewires �� 385
20.2.3 Reactions to Radiographic Contrast Medium
and Periprocedural Drugs �� 386
xviii Contents
20.2.4 Radiation-Induced Skin Damage�� 387

20.2.5 Benchmark Levels for Complications Related
to Angiography �� 387
20.3 Complications Specific to Endovascular Treatments
for Specific Conditions�� 387
20.3.1 Aneurysms�� 387
20.3.2 Arteriovenous Malformations and
Arteriovenous Fistulas�� 390
20.3.3 Angioplasty and Stenting�� 391
20.3.4 Embolisation for Tumours�� 392
20.3.5 Functional Testing and Large Artery Occlusion �� 393
21 Obtaining the Patient’s Consent �� 397
21.1 The Legal Principles of Consent to a Medical Procedure�� 398
21.1.1 Duty of Care�� 398
21.1.2 Level of Risk�� 399
21.1.3 Competency�� 399
21.2 Informed Consent�� 400
21.2.1 Guidance on Obtaining Patients Consent
to Medical Procedures�� 400
21.2.2 The Informed Consent Process Under Ordinary
Circumstances �� 401
21.2.3 Situations in Which Obtaining Informed Consent
Is Impossible or When Patients Are Judged
Incompetent�� 402
Index�� 405
Embryology of the Cranial
Circulation
1
Contents Preamble
1.1 efinitions of Terms Used
D From whence we come…
in Embryology 2 What is the value of studying embryology
1.1.1 Timelines in the Embryonic Period 2 when variant and anomalous vessels are so
1.1.2 General Concepts in Vessel Development 2 uncommon? Surely we always rely on a detailed
1.2 losure of the Neural Tube
C analysis of each patient’s vascular anatomy to
and Development of the Head Arteries 3 guide endovascular treatments.
1.2.1 Pre-choroidal Stage 3
1.2.2 Choroidal Stage 4
For me, anatomy is like a city street map. To
1.2.3 Branchial Stage 4 be more precise, it is like the streets and roads of
1.2.4 Development of the Carotid London, where I grew up. As a child I learnt to
and Vertebrobasilar System 4 navigate those within walking distance of home
1.2.5 Embryological Basis of Variations
in the Carotid Artery 9 and knew only main routes taken by car or bus to
1.2.6 The Role of the Stapedial Artery 12 visit friends, shopping and other excursions. This
1.2.7 Development of the Ophthalmic Artery 13 familiarity of use fundamentally changed when I
1.2.8 Development of the Cavernous Sinus learnt to drive and was no longer a passive
Region 17
1.2.9 The Inner and Middle Ear Arteries observer. Now, consider the role of chauffeur
and Their Variants 19 extended to showing visitors around my city. My
1.2.10 Vertebral and Vertebrobasilar Anomalies priority changed, from learning shortcuts, good
and Persistence 20 parking places and congestion avoidance (though
1.3 Development of Cerebral Veins 24 all very useful to the city guide), to pointing out
1.3.1 Superficial Veins and Dural Sinuses 24 the sites and important historic places.
1.3.2 Deep Veins 25
We should learn the history of the routes we
References 26 travel to deliver our therapy with the intimacy of
the London cab driver and be prepared for the
obscure address which few but they would know.
In embryology we have a chance to marvel at the
compressed evolution of foetal development. By
learning about those processes, we are delighted
when recognising throwbacks and anomalies,
which, like historic sites, provide evidence of ‘from
whence we come’.
In this tutorial the embryology of cranial vas-
cular development is presented in a simplified
© Springer International Publishing AG 2017 1
J.V. Byrne, Tutorials in Endovascular Neurosurgery and Interventional Neuroradiology,
DOI 10.1007/978-3-319-54835-7_1
2 1 Embryology of the Cranial Circulation
overview. Unlike other tutorials, the text contains Table 1.1 Events expected during the second half of the
embryonic period
few citations, since the descriptions are largely
based on the classic works of D. H. Padget which Embryonic period: 4th–8th week
are listed with other source texts, at the end of the 4th week (22–28 days from fertilisation = 4 mm CRL)
tutorial. Readers may find it useful to read this Heartbeat begins
tutorial in conjunction with Tutorials 2 and 7 Branchial arches form
The neural tube closes (day 24)
because it represents the precursor vascular anat-
The ears begin to form as otic pits
omy covered in the subsequent chapters.
5th week (29–35 days from fertilisation = 9 mm CRL)
Optic cups form
Nasal pits form
1.1 efinitions of Terms Used
D The brain divides into five vesicles
in Embryology Rudimentary blood flow starts
6th week (36–42 days from fertilisation = 13 mm CRL)
Embryonic period: The embryonic period is Brain grows
defined as the first 8 weeks after fertilisation or Lymphatic system appears
the first 10 weeks after the last menstrual period 7th week (43–49 days from fertilisation = 18 mm CRL)
which is the gestational age. It is the time when Foetal heartbeat detectable
tissues differentiate to form the principle organs Spontaneous limb movements seen on ultrasound
(i.e. organogenesis). scan
Foundation of all essential organs in place
• Phylogeny: This term refers to the sequence of 8th week (49–56 days from fertilisation = 40 mm CRL)
Adult pattern of cranial arteries established
events involved in the evolutionary development
of a species or taxonomic group of organisms. CRL crown rump length: This measure is variable and
given only a guide to the size of the foetus at each stage.
• Ontogeny: Refers to the development of an
individual organism.
• Foetal period: The time from the end of the
embryonic period until birth. 1.1.2 eneral Concepts in Vessel
G
Development
Anomaly and malformation: An anomaly is a
deviation from the common or normal, whilst Before reviewing the recognised stages of embry-
malformation means badly formed and implies a onic cranial vessel development, it is worth first
defective structure. Both should be distinguished considering how blood vessels grow and adapt to
from abnormality which refers to a given ana- supply tissues. Where no blood vessels exist, as
tomical configuration that is pathological. in the embryo, their growth is termed vasculo-
Variation: Is a modification or different form of genesis. Growth of existing blood vessels is by
something and is used to describe divergence from angiogenesis:
the usual or expected growth pattern. It does not
imply that the result is harmful to the individual. (a) Vasculogenesis occurs from clusters of endo-
thelial cells, which develop from precursor
cells, called angioblasts. Endothelial cells
1.1.1 imelines in the Embryonic
T form vessels that grow and differentiate
Period under the influence of growth factors and the
extracellular matrix. These local clues
The first 4 weeks of the embryonic period precedes include signal proteins, adventitial fibro-
the development of the heart and circulation, so our blasts, pericytes and smooth muscle cells. A
interest in the development of cranial vessels begins primary network forms, by a combination of
at about 22 days, i.e. the start of the fourth week apoptosis and proliferation. Once blood flow
after fertilisation. The relevant milestones in the is established, it stimulates selective remod-
remaining embryonic period are shown in Table 1.1. elling of vessels by angiogenesis in response
1.2 Closure of the Neural Tube and Development of the Head Arteries 3
to the tissue need. Once complete vasculogenesis in the number of endothelial cells
genesis does not occur again under normal required, which is an advantage during embry-
conditions, but certain steps may be reacti- onic development. It is important in the growth of
vated under pathological conditions, such as capillary networks throughout life.
tumour growth.
(b) Angiogenesis refers to the growth of new
vessels in response to tissue growth, wound 1.2 losure of the Neural Tube
C
healing and the formation of granulation tis- and Development
sue. There are two types: sprouting and non- of the Head Arteries
sprouting or splitting angiogenesis.
In the embryonic period, massive changes in the
Sprouting angiogenesis is the growth of new distribution of newly formed vessels take place in
vessel from parent vessels, similar to the growth of a recognisable series of events. D. H. Padget
branches on a plant. It occurs in a well-described divided the development of the cranial vessels
series of events initiated by the activation of endo- into seven stages (see below) after which the
thelial cell receptors and the release of proteases adult configuration of arteries is established. The
that degrade the basement membrane allowing development of veins and dural sinuses takes lon-
endothelial cells into the adjacent matrix. These ger and continues up to and beyond birth.
cells then ‘spout’ through the matrix towards the First we need to review the steps in the devel-
source of the angiogenic stimulus. They migrate in opment of the head and in particular how the
tandem because of adhesion molecules called inte- brain and facial structures appear.
grins and form new vessels linking adjacent ves-
sels. Vascular endothelial growth factor (VEGF) is
the principle driver of angiogenesis and the Notch 1.2.1 Pre-choroidal Stage
receptor pathway for its control.
Non-sprouting or splitting angiogenesis is the Closure of the neural tube occurs at about 24 days
development of a new vessel by the splitting of after the start of the embryonic period. Blood ves-
existing ones. This involves the formation of a sels develop from a mesh of primitive cells
core of pericytes and myofibroblasts between (meninx primitiva) on its surface. Initially, arter-
two vessels. These tissues form the extracellular ies and veins are indistinguishable amongst these
matrix for growth of a new vessel lumen. The vessels, arranged as a network of vascular chan-
process is more economic than sprouting angio- nels (Fig. 1.1). Longitudinal arterial channels
a b
LNS
Dorsal
Aorta
Ventrial
Fig. 1.1 (a) Neural tube and meninx primitiva. (b) Development of the longitudinal neural system (LNS) (Published
with kind permission of © Henry Byrne, 2012. All rights reserved)
develop ventral to the neural tube within the rhombomere has a unique identity provided by
meninx primitiva. These comprise the longitudi- Hox gene expression. The gene products are Hox
nal neural system (LNS). This process is preceded proteins (i.e. transcription factors) which dictate
by the development of the heart and paired ventral the ordered development of facial structures and
and dorsal aortae from the truncus arteriosus. the migration and differentiation of neural crest
During the fourth week, the cranial neural tissue into the first three branchial arches. They
tube develops three expansions termed primary control the orientation of nerves, ganglia, bone,
brain vesicles. These are called prosencephalon cartilage and connective tissue [1].
(forebrain), mesencephalon (midbrain) and Paired connections between the ventral and
rhombencephalon (hindbrain). The ventricles dorsal aortae form between the pharyngeal arches.
form within these expansions. There are six arch arteries, separated by the tran-
sient pharyngeal pouches. The formation of the
heart and great vessels is well described in general
1.2.2 Choroidal Stage texts and will not be covered here. It should be
understood that the six aortic arch arteries arising
The increasing metabolic demand of the neural between the dorsal aorta and the ventral aortic sac
tube prompts invaginations of choroid from the are not present simultaneously. The three rostral
meninx primitiva into ventricles within the vesi- arches concern us since the carotid arterial system
cles so that blood supply occurs from both inner develops from them. The posterior cerebral circu-
(ependymal) and outer (pial) surfaces. lation develops as the meninx coalescences to
During the fifth week, the primary vesicles form segmental and longitudinal arteries. The
develop secondary vesicles. These involve divi- longitudinal intersegmental arteries form a sys-
sion of the prosencephalon into telencephalon tem of vessels termed the longitudinal neural sys-
and diencephalon and the rhombencephalon into tem (LNS) with the adult pattern emerging after
metencephalon and myelencephalon. Thus, there the carotid system (Fig. 1.1).
are now five vesicles. At the same time, the bran-
chial pouches are maturing.
1.2.4 evelopment of the Carotid
D
and Vertebrobasilar System
1.2.3 Branchial Stage
This section will describe the stages in the devel-
The head develops around the rostral end of the opment of the carotid artery. Our understanding
neural tube with the face and neck forming ven- of the cranial artery developments in the embryo
tral to the developing brain. These structures are comes from studies of post-mortem tissue. E. D.
derived from a series of branchial pouches with Congdon in 1922 [2] described the aortic arch
intervening arches (called pharyngeal arches in system and the origins of the major cerebral
humans) and appear in the fourth week. They arteries, i.e. carotid, vertebral and basilar. The
represent an evolutionary period when the organ- details of how the cranial vasculature changes
ism depended on gills. during the embryonic period were described by
The head and neck structures are formed from D. H. Padget [3] in a study of 22 embryos held in
the cranial three branchial arches and develop the Carnegie Collection, Washington.
from neural crest cells together with contribu- She identified the seven stages in this process
tions from paraxial mesoderm, ectoderm and and related these to the size of the embryos at
endoderm. each stage:
The patterning information is provided by the
cranial neural crest cells and can be traced to a Stage 1 = 4–5 mm CRL
transient period of hindbrain segmentation in Stage 2 = 5–6 mm CRL
seven subdivisions called rhombomeres. Each Stage 3 = 7–12 mm CRL
Stage 4 = 12–14 mm CRL 1.2.4.1 Stage 1

Stage 5 = 16–18 mm CRL Six aortic arch arteries connect the dorsal and
Stage 6 = 20–24 mm CRL ventral aorta, of which the upper three develop
Stage 7 = 40 mm CRL into the carotid system. The adult pattern results
from a process of regression of various compo-
The internal carotid artery is established in the nents of the three rostral connections (Fig.1.2a).
first three stages and the vertebrobasilar arteries The dorsal aorta caudal to the third arch invo-
by the fourth stage. These will be described lutes and its rostral portion forms the first section
chronologically. Other developments are easier of the primitive internal carotid artery. Its con-
to describe as systems because they develop in nection with the ventral aorta remains and the
parallel streams. caudal portion of the ventral aorta becomes the
a
Anterior Posterior
ROSTAL division division
VENTRAL DORSAL
CAUDAL
1st Arch
2nd Arch
3rd Arch
Ventral Dorsal
LNS
Aorta Aorta
Fig. 1.2 Stage 1, development of carotid arteries. The now evident. In (c) parts of the first and second arch arter-
three rostral aortic arches connect the ventral and dorsal ies have regressed and branches arising from the dorsal
aorta (a). Regressions result in the arrangement shown in aorta rostral to the first arch artery developed. (Published
(b). Interconnecting arteries between the first and second with kind permission of © Henry Byrne, 2017. All rights
arches and with the longitudinal neural system (LNS) are reserved)
b Anterior Posterior
ROSTAL division division
VENTRAL DORSAL
CAUDAL
trigeminal a.
1st Arch
otic a.
2nd Arch
hypoglossal a.
3rd Arch
Ventral Dorsal LNS

Aorta Aorta
Fig. 1.2 (continued)
common carotid artery. The ventral portions of the posterior communicating artery. These ves-
the first and second arches and the dorsal part of sels supply the developing prosencephalon
the first arch also regress leaving an inter- (subsequently the telencephalon) and mesen-
connecting vessel between the first and second cephalon, respectively. The internal carotid
arches and the dorsal portion of the second arch artery (ICA) also supplies the rhombencepha-
(Fig. 1.2b, c). lon and the emerging LNS by the transient
The most rostral extent of the dorsal aorta, primitive trigeminal, otic and hypoglossal
now the primitive internal carotid artery, divides arteries (Fig. 1.3).
into a ventral branch or anterior division which The dorsal aorta gives three branches rostral
forms the anterior cerebral artery and a dorsal to the first arch – the ventral ophthalmic artery
or posterior division which is the precursor of (VOA), the dorsal ophthalmic artery (DOA) and
c
ROSTAL
VENTRAL DORSAL
CAUDAL Anterior Posterior

division division
vental ophthalmic a.
dorsal ophthalmic a.
primitive maxillary a.
trigeminal a.
1st Arch
otic a.
2nd Arch
hypoglossal a.
3rd Arch
LNS
Ventral Dorsal
Aorta Aorta
Fig. 1.2 (continued)
most caudally the primitive maxillary artery. 1.2.4.2 Stage 2

The primitive maxillary artery supplies Rathke’s The internal carotid artery is thus formed from
pouch,1 from which the anterior pituitary devel- the dorsal aorta and the third arch artery with part
ops. It appears before the optic vesicle of the ventral aorta. The second arch artery
(Fig. 1.2c). becomes the hyoid trunk but maintains a connec-
tion with the first arch. This connection with the
first arch is destined to become the stapedial
1
Martin Heinrich Rathke (1793–1860), professor of zool-
ogy and anatomy at Königsberg who first described the artery, whilst the remnant of the first arch artery
pouch and the arches. becomes the mandibular artery.
Primit. Trigem. A. Int. Carot. A. Bilat. Long. Neur. A.

Pharyng. Pouch 1.
Rathke’s pouch
Primit. Otic a.
Caud. Divis.
And
VIII Primit. Hypoglos. A.
Cran. Divis. V
VII Otic
Of
ves.
Int. Carot. First
A. IX Cerv. Segm. A.
X
XI
XII
Opt.
ves.
Primit. 1
Dors.
Ophth. A.
2
Primit. Olf. A.
Hyoid a. Arter. Tr.
Paired
Olf. Area
Aort. Arch - 3, 4. Aort.
Mand. A. 3
Primit. Max. A.
Fig. 1.3 Graphic reconstruction of cranial arteries in a of vessels and supplied from the internal carotid by tri-
4 mm embryo by Padget [3]. Note the rostral division of geminal, otic and hypoglossal arteries (Reproduced with
the internal carotid arteries, the prominence of the bran- permission)
chial hyoid artery and the LNS emerging from a network
At this time (about 6 mm CRL), paired ventral Finally, because the posterior division of the
pharyngeal arteries develop from the third arch. internal carotid artery, i.e. the posterior commu-
The ventral pharyngeal artery is destined to form nicating artery, consolidates its connection to the
the proximal part of the external carotid artery LNS, the primitive trigeminal, otic and hypoglos-
but it maintains a connection with the second sal arteries regress.
arch (marked * on Fig. 1.4). It will form the
lingo-facial system with lingual and thyroid 1.2.4.3 Stages 3 and 4
branches. These stages encompass the transition from the
The connection to the second arch provides a branchial to post-branchial stages. The cranial
link to the hyoid/stapedial system and is the key divisions of the internal carotid artery (i.e. ventral
to understanding the development of the internal and dorsal branches) develop. The ventral divi-
maxillary artery (second arch) and the middle sion forms the primitive olfactory artery from
meningeal artery (first arch). which the VOA arises. It also gives the anterior
Also in this stage, we see initial signs of the choroidal artery and small branches, which will
two primitive ophthalmic arteries (VOA and coalesce into the middle cerebral artery as the tel-
DOA) as the eye starts to develop. These will encephalon grows. The dorsal or posterior divi-
eventually regress leaving a single ophthalmic sion forms the posterior communicating artery,
artery that follows the course of the VOA, whilst which gives the posterior choroidal artery and
the DOA regresses and forms the precursor of the supplies the mesencephalon and emerging basilar
inferolateral trunk (ILT). The last of these three artery. The paired posterior choroidal arteries
rostral branches of the dorsal aorta is the primi- supply the diencephalon together with the ante-
tive maxillary artery, which is destined to survive rior choroidal arteries.
in the adult pattern as the posteroinferior hypoph- The formation of the internal maxillary artery
yseal artery (PIHA). and middle meningeal artery is complex. This is
ROSTAL
VENTRAL DORSAL
ventral
CAUDAL ophthalmic a.
dorsal ophthalmic a.
primitive maxillary a.
ventral pharyngeal a.
trigeminal a.
mandibular a.
1st Arch
otic a.
hyoid /
stapedial
2nd Arch
hypoglossal a.
3rd Arch
ICA
CCA LNS
Fig. 1.4 Stage 2. The stapedial artery links the first and CCA common carotid artery (Published with kind permis-
second arch arteries and the ventral pharyngeal artery sion of © Henry Byrne, 2012. All rights reserved)
develops from the third arch. ICA internal carotid artery,
because of the development of the face after com- lateral to the LNS and the developing basilar
pletion of the branchial stage causes arteries (and artery longitudinal channels are prominent. These
arterial territories) to establish and then partially transient arteries are called the primitive lateral
or completely regress as new patterns of blood vertebrobasilar anastomoses. They regress as the
supply develop. At the beginning of the fourth more medial basilar and vertebral arteries mature.
stage, the stapedial artery is formed as the con- The vertebral arteries are formed from longitudi-
tinuation of the second arch’s hyoid artery trunk nal channels between the upper six spinal seg-
and an arterial link to the first arch. It divides into ments. Other connections between these segments
dorsal or supraorbital and ventral maxilloman- and the aorta regress as the vertebral arteries
dibular divisions. The supraorbital branch is grow. With growth of the hindbrain vesicles,
taken over by the ophthalmic system and the symmetrical branches of the basilar artery appear.
maxillomandibular trunk annexed by the devel-
oping internal maxillary artery (Fig. 1.5). These
processes will be described in more detail below. 1.2.5 Embryological Basis
The basilar artery is formed by fusion of the of Variations in the Carotid
parallel LNS on the midline surface of the devel- Artery
oping hindbrain. Initially its caudal supply is
from the first segmental artery of the aorta and Before considering potential arterial anomalies,
the primitive hypoglossal artery. At this stage, it is worth revisiting the primitive pattern in
ROSTRAL
DORSAL VENTRAL
CAUDAL
ophthalmic a.
inferolateral trunk
(dorsal ophthalmic)
posterior inferior hypophyseal a.

(primitive maxillary)
trigeminal a.
MMA
otic a.
ventral pharyngeal a.
IMA hypoglossal a.
CCA LNS
Fig. 1.5 Stage 3: Regression of the stapedial artery and lary artery. See Figs. 1.2 and 1.4 for other abbreviations
annexation of its territory by the ventral pharyngeal sys- (Published with kind permission of © Henry Byrne, 2017.
tem. MMA middle meningeal artery, IMA internal maxil- All rights reserved)
which the dorsal aorta and LNS develop from division of the carotid system which connects the
segmental centres. The LNS supplies the devel- rostral LNS with segmental cervical arteries.
oping hindbrain comprising the mesencephalon, Prior to development of the basilar and vertebral
metencephalon and myelencephalon secondary arteries, the LNS is supported by additional tran-
vesicles and the primitive carotid artery the fore- sient arterial connections with the carotid system
brain comprising the telencephalon and dien- via otic, hypoglossal and trigeminal arteries and
cephalon secondary vesicles (Fig. 1.6). by the dorsal aorta via the first cervical segmental
Anastomoses develop and regress between the artery, i.e. proatlantal arteries. Thus, the posterior
carotid system and the LNS. The rostral (and per- communicating artery is the remnant of the pos-
sisting) anastomosis is the dorsal or posterior terior division, and the posterior cerebral arteries
DORSAL
ROSTAL CAUDAL
n
VENTRAL
alo
ph
ce on
len on al
Te
l h on
ha ep al
ce
p c
ep
h on
n en c hal
ie es en ep
D M et nc
M le
ye
M
3
2
5 6 7 8 9
LNS
1 4
11 10
Carotid a.
Fig. 1.6 Development of secondary brain vesicles (5 arteries, 7 superior cerebellar artery, 8 anterior inferior
weeks). The arterial supply to the secondary vesicles are cerebellar artery, 9 posterior inferior cerebellar artery, 10
numbered; 1 anterior division of ICA, 2 anterior cerebral proatlantal artery, 11 primitive trigeminal artery
artery (from which the middle cerebral artery arises – dot- (Published with kind permission of © Henry Byrne, 2012.
ted line), 3 anterior choroidal artery, 4 posterior communi- All rights reserved)
cating artery, 5 posterior choroidal arteries, 6 collicular
represent the supply of this carotid division to the tum. These regress leaving the middle cere-
diencephalon. As the posterior division develops, bral as the dominant vessel but the process is
the primitive trigeminal artery regresses. The otic subject to variations. Similarly, the paired
and hypoglossal arteries normally are present anterior cerebral arteries, which communi-
only at the 4–6 mm stage. cate across the midline via a plexus of ves-
The branches, which develop from the LNS sels, are liable to variations. Regression of the
(and subsequently the basilar artery), are the future midline anastomotic systems usually leaves a
posterior choroidal arteries (assumed by the poste- solitary anterior communication artery, but
rior cerebral arteries), collicular arteries, the supe- duplications are common and the proximity
rior cerebellar arteries, anterior inferior cerebellar of the anterior cerebral arteries creates the
arteries and posterior inferior cerebellar arteries. potential for fusion (see below). The patterns,
resulting from embryological variations,
1.2.5.1 V ariants to the Adult Pattern most commonly involve:
of the Carotid System 1. Duplication(s) of the anterior communicat-
(a) Anterior cerebral artery variants ing artery.
Multiple cortical branches arise from the 2. Dominance of the recurrent artery of
anterior cerebral artery to supply the expand- Heubner.
ing cortical mantle of the telencephalon and 3. Duplication of the middle cerebral artery,
all potentially supply branches to the stria- i.e. persistence of a sister branch of the
anterior division of the primitive internal 4. Absence of the section distal to the primi-
carotid artery. tive maxillary artery. The distal internal
4. A single midline (azygos) anterior cerebral carotid artery is supplied via collaterals
artery. through the DOA remnant, i.e. the ILT.
5. Bi-hemispheric patterns of the anterior 5. Absence of the cavernous section distal to
cerebral artery complex, with one side sup- DOA. The distal internal carotid artery is
plying parts of both hemispheres. reconstituted by the ophthalmic artery (via
(b) Agenesis of internal carotid artery segments branches of the middle meningeal or inter-
The branchial arch arteries and branches nal maxillary arteries).
of the primitive internal carotid artery pro- (c) Anomalous carotid-vertebrobasilar
vide potential routes for the carotid system anastomoses
to be reconstitute if sections fail to develop. The pre-segmental branches of the dor-
To understand these potential variants of the sal aorta supplying the LNS are usually
internal carotid artery (ICA), we return to temporary and have disappeared at around
Fig. 1.4 which is updated in Fig. 1.5. the 15 mm CRL stage. The most common
Potential persistent connections between the persistent artery is the trigeminal artery
LNS and the carotid system (i.e. primitive (Fig. 1.7). The five recognised bridging
trigeminal, otic and hypoglossal arteries) arteries are:
and the definitive ophthalmic artery are 1. Trigeminal artery
shown. Also shown is the annexation of the 2. Otic artery
internal maxillary and middle meningeal 3. Hypoglossal artery
arteries by the ventral pharyngeal artery and 4. Proatlantal artery type 1
regression of the hyoid artery (its remnant 5. Proatlantal artery type 2
being the caroticotympanic artery) and man- If present these persistent embryonic arteries
dibular arteries. This process is described connect the internal carotid artery to the basilar
below. The described patterns of agenesis artery (trigeminal and otic) or the vertebral artery
are as follows: (hypoglossal, proatlantal type 1) or the external
1. Absence of the proximal ICA derived from carotid artery (proatlantal type 2). The otic artery
the third arch and dorsal aorta caudal to the is so rare that its existence as a persistent vessel
second arch. In this variant the distal artery has been disputed. It is described as arising from
is supplied by the ascending pharyngeal the petrous internal carotid artery, running
artery (via its inferior tympanic branch) to through the internal acoustic canal, to anasto-
the caroticotympanic branch of the internal mose with the basilar artery. The others will be
carotid artery within the skull base. described below.
2. Absence of the dorsal aorta section below
the first arch. The distal internal carotid
artery is reconstituted by the distal internal 1.2.6 he Role of the Stapedial
T
maxillary artery (pterygovaginal artery) Artery
via the mandibular artery.
3. Absence of the section above the first arch The stapedial artery arises as a branch of the
and below the primitive maxillary artery. hyoid artery within the rudimentary middle ear.
The distal internal carotid artery is recon- The hyoid artery, which developed at the 9 mm
stituted either by a persistent trigeminal CRL stage, is the second arch artery. It regresses
artery or from transclival arteries at the after the embryological period, and only its ori-
level of the posterior inferior hypophyseal gin remains as the precursors of the caroticotym-
artery (PIHA). panic trunk.
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medicine, or some little thing to eat, put out her candle, open the
window a moment, and then I would return to my task.
After the day of my debut at the Chicago Progressive Lyceum I
continued my dramatic career. The incidents of my performances
would suffice to fill several volumes. For without interruption,
adventures succeeded one another to such an extent that I shall
never undertake the work of describing them all.
I should say that when this first theatrical incident took place I
was just two and a half years old.
III
HOW I CREATED THE SERPENTINE DANCE
I N 1890 I was on a tour in London with my mother. A manager

engaged me to go to the United States and take the principal part
in a new play entitled, “Quack, M.D.” In this piece I was to play
with two American actors, Mr. Will Rising and Mr. Louis de Lange,
who has since then been mysteriously assassinated.
I bought what costumes I needed and took them with me. On our
arrival in New York the rehearsals began. While we were at work, the
author got the idea of adding to the play a scene in which Dr. Quack
hypnotised a young widow. Hypnotism at that moment was very
much to the fore in New York. To give the scene its full effect he
needed very sweet music and indeterminate illumination. We asked
the electrician of the theatre to put green lamps along the footlights
and the orchestra leader to play a subdued air. The great question
next was to decide what costume I was to wear. I was unable to buy
a new one. I had spent all the money advanced me for my costumes
and, not knowing what else to do, I undertook to run over my
wardrobe in the hope of finding something that would be fit to wear.
In vain. I could not find a thing.
All at once, however, I noticed at the bottom of one of my trunks a
small casket, a very small casket, which I opened. Out of it I drew a
light silk material, comparable to a spider’s web. It was a skirt, very
full and very broad at the bottom.
I let the skirt dangle in my fingers, and before this little heap of
fragile texture I lingered in reverie for some time. The past, a past
very near and yet already far away, was summoned up before me.
It had happened in London some months before.
A friend had asked me to dine with several officers who were
being wined and dined just before leaving for India, where they were
under orders to rejoin their regiment. The officers were in handsome
uniforms, the women in low dresses, and they were pretty, as only
English women are.
At table I was seated between two of the youngest officers. They
had very long necks and wore extremely high collars. At first I felt
myself greatly overawed in the presence of people so imposing as
my neighbours. They looked snobbish and uncommunicative.
Presently I discovered that they were much more timid than I, and
that we should never be better acquainted unless one or the other of
us resolved to overcome his own nervousness and, at the same
time, that of his companions.
But my young officers were afraid only in the presence of women.
When I told them I hoped they might never be engaged in a war, and
especially that they might never have to do any killing, one of them
answered me very simply:
“I fancy I can serve as a target as well as any other man, and
certainly the people who draw on me will understand that war is on.”
They were essentially and purely English. Nothing could unsettle
them, provoke them or change them in the least. At our table they
seemed timid. They were nevertheless men of the kind who go into
the presence of death just as one encounters a friend in the street.
At this period I did not understand the English as I have
subsequently come to know them.
I left the table without remembering to ask the names of my
neighbours, and when I thought about the matter it was too late.
I recalled, however, that one of them took the trouble, in the
course of our conversation, to learn the name of the hotel at which I
was staying. I had quite forgotten the incident when, some time after,
I received a little casket, addressed to me from India.
It contained a skirt of very thin white silk, of a peculiar shape, and
some pieces of silk gauze. The box was not more than sixteen
inches long and was hardly taller than a cigar box. It contained
nothing else, not a line, not a card. How odd! From whom could it
come?
I knew no one in India. All at once, however, I remembered the
dinner and the young officers. I was greatly taken with my pretty box,
but I was far from suspecting that it contained the little seed from
which an Aladdin’s lamp was destined to spring for my benefit.
This, of course, was the casket which I had just discovered in my
trunk.
Deep in thought I stooped and gathered up the soft, silky stuff. I
put on the Hindu skirt, the skirt sent me by my two young officers,
those young men who must by this time have “served as targets”
somewhere out there in the jungle, for I never heard from them
again.
My robe, which was destined to become a triumphal robe, was at
least a half a yard too long. Thereupon I raised the girdle and so
shaped for myself a sort of empire robe, pinning the skirt to a
décolleté bodice. The robe looked thoroughly original, perhaps even
a little ridiculous. It was entirely suitable for the hypnotism scene,
which we did not take very seriously.
Photo Sarony
LOIE FULLER IN HER ORIGINAL SERPENTINE DRESS
We “tried the play on the dog” before offering it to the New York
public, and I made my debut as a dancer at a theatre in a small city
of which the average New Yorker had hardly heard. No one, I
suppose, outside its boundaries took the slightest interest in what
went on in that city. At the end of the play, on the evening of the first
presentation, we gave our hypnotism scene. The stage scenery,
representing a garden, was flooded with pale green light. Dr. Quack
made a mysterious entrance and then began his work of suggestion.
The orchestra played a melancholy air very softly, and I
endeavoured to make myself as light as possible, in order to give the
impression of a fluttering figure obedient to the doctor’s orders.
He raised his arms. I raised mine. Under the influence of
suggestion, entranced—so, at least, it looked—with my gaze held by
his, I followed his every motion. My robe was so long that I was
continually stepping upon it, and mechanically I held it up with both
hands and raised my arms aloft, all the while that I continued to flit
around the stage like a winged spirit.
There was a sudden exclamation from the house:
“It’s a butterfly! A butterfly!”
I turned on my steps, running from one end of the stage to the
other, and a second exclamation followed:
“It’s an orchid!”
To my great astonishment sustained applause burst forth. The
doctor all the time was gliding around the stage, with quickening
steps, and I followed him faster and faster. At last, transfixed in a
state of ecstasy, I let myself drop at his feet, completely enveloped in
a cloud of the light material.
The audience encored the scene, and then encored it again—so
loudly and so often that we had to come back twenty times, or more.
We were on the road about six weeks. Then came our opening in
one of the New York suburbs, where Mr. Oscar Hammerstein, who
has since become a famous impresario, owned a theatre.
The play was unsuccessful, and even our hypnotism scene was
not strong enough to save it from the attacks of the critics. No New
York theatre cared to give it house room, and our company broke up.
The day after this opening at Mr. Hammerstein’s theatre a local
newspaper of the little community in which we had successfully
presented this “Quack, M.D.,” which the New York managers refused
to touch, wrote a ridiculously enthusiastic article on what it called my
“acting” in the hypnotism scene. But as the play had not “made
good,” no one thought that it would be possible to take a single
scene out of it, and I was left without an engagement.
Nevertheless, even in New York, and in spite of the failure of the
play, I personally secured some good press notices. The
newspapers were in agreement in announcing that I had a
remarkable string to my bow—if I only knew how to make the most of
it.
I had brought my robe home to sew up a little tear. After reading
these comforting lines I leaped from the bed and arrayed only in my
night-gown, I put the garment on and looked at myself in a large
glass, to make sure of what I had done the evening before.
The mirror was placed just opposite the windows. The long
yellow curtains were drawn and through them the sun shed into the
room an amber light, which enveloped me completely and illumined
my gown, giving a translucent effect. Golden reflections played in the
folds of the sparkling silk, and in this light my body was vaguely
revealed in shadowy contour. This was a moment of intense
emotion. Unconsciously I realised that I was in the presence of a
great discovery, one which was destined to open the path which I
have since followed.
Gently, almost religiously, I set the silk in motion, and I saw that I
had obtained undulations of a character heretofore unknown. I had
created a new dance. Why had I never thought of it before?
Two of my friends, Mrs. Hoffmann and her daughter Mrs.
Hossack, came from time to time to see how I was getting on with
my discoveries. When I found an action or a pose which looked as if
it might amount to something they would say: “Hold that. Try it
again.” Finally I reached a point where each movement of the body
was expressed in the folds of silk, in a play of colours in the
draperies that could be mathematically and systematically
calculated.
The length and size of my silk skirt would constrain me to repeat
the same motion several times as a means of giving this motion its
special and distinctive aim. I obtained a spiral effect by holding my
arms aloft while I kept whirling, to right and then to left, and I
continued this movement until the spiral design was established.
Head, hands and feet followed the evolutions of the body and the
robe. It is very difficult, however, to describe this part of my dance.
You have to see it and feel it. It is too complicated for realisation in
words.
Another dancer will obtain more delicate effects, with more
graceful motions, but they will not be the same. To be the same they
must be created in the same spirit. One thing original, though up to a
certain point it is not so good as an imitation, is in reality worth much
more.
I studied each of my characteristic motions, and at last had
twelve of them. I classed them as Dances No. 1, No. 2, and so on.
The first was to be given under a blue light, the second under red
light, the third under a yellow light. For illumination of my dances I
intended to have a lantern with coloured glass in front of the lens. I
wanted to dance the last one in total darkness with a single ray of
yellow light crossing the stage.
When I had finished studying my dances, I went in search of a
manager. I was acquainted with them all. During my career as singer
and actress I had served all of them more or less frequently.
I was, however, hardly prepared for the reception which they
gave me. The first one laughed me in the face as he said:
“You a dancer! Well, that’s too good! When I want you for a
theatrical part I’ll look you up with pleasure; but as for dancing, good
heavens! When I engage a dancer she will have to be a star. The
only ones I know are Sylvia Gray and Lettie Lind in London. You
cannot outclass them, take my word for it. Good-evening.”
He had lost all respect for my perspicacity and he made fun of
the idea of my being a dancer.
Mrs. Hoffmann had come with me, and was waiting in the lobby,
where I rejoined her. She noted at once how pale and nervous I was.
When we left the theatre it was night. We walked in silence through
dark streets. Neither spoke. Some months later, however, my friend
told me that all that evening I never stopped emitting little groans like
those of a wounded animal. She saw that I was cut to the very quick.
Next day I had to continue my search, for necessity was spurring
me on.
Mrs. Hoffmann offered me the privilege of coming to live with her
and her daughter—an offer which I accepted gratefully, not having
the faintest idea when and how I could ever repay her.
Some time later I had to give in; since I was known as an actress,
nothing could hurt me more than to try to become a dancer.
One manager went so far as to tell me that two years of absence
from New York had caused the public completely to forget me, and
that, in trying to recall myself to their memory, I should seem to be
inflicting ancient history on them. As I had then just passed my
twentieth birthday I was extremely irritated by that insinuation, and I
thought: “Would it then be necessary for me painfully to build up a
reputation and to look old to prove that I was young to-day?”
Unable to restrain my feelings any longer, I told the manager
what I thought.
“Hell,” he replied, “it isn’t age that counts. It’s the time the public
has known you, and you have become too well known as an actress
to come back here as a dancer.”
Everywhere I encountered the same answer, and finally I became
desperate. I was aware that I had discovered something unique, but
I was far from imagining, even in a daydream, that I had hold of a
principle capable of revolutionising a branch of æsthetics.
I am astounded when I see the relations that form and colour
assume. The scientific admixture of chemically composed colours,
heretofore unknown, fills me with admiration, and I stand before
them like a miner who has discovered a vein of gold, and who
completely forgets himself as he contemplates the wealth of the
world before him.
But to return to my troubles.
A manager who, some time before, had done his best to engage
me as a singer, and who had absolutely refused to consider me as a
dancer, gave a careless consent, thanks to the intervention of a
common friend, to an interview at which I was to show him my
dances.
I took my robe, which made a neat little bundle, and I set out for
the theatre.
Mrs. Hoffmann’s daughter accompanied me. We went in by the
stage entrance. A single gas jet lighted the empty stage. In the
house, which was equally dark, the manager, seated in one of the
orchestra chairs, looked at us with an air of boredom, almost of
contempt. There was no dressing-room for my change of clothing,
not even a piano to accompany me. But the opportunity was a
precious one, all the same. Without delay I put on my costume, there
on the stage and over my dress. Then I hummed an air and started
in to dance very gently in the obscurity. The manager came nearer
and nearer, and finally ascended the platform.
His eyes glistened.
I continued to dance, disappearing in the darkness at the rear of
the stage, then returning toward the gas jet. Finally I lifted a part of
my robe over my shoulders, made a kind of cloud which enveloped
me completely and then fell, a wavering mass of fluffy silk, at the
manager’s feet. After that I arose and waited in keenest anxiety to
hear what he would say.
He said nothing. Visions of success were crowding upon each
other in his brain.
Finally he broke his silence and gave my dance the name of “The
Serpentine Dance.”
“There is the name that will go with it,” he said, “and I have just
the music that you need for that dance. Come to my private office. I
am going to play it for you.”
Then for the first time I heard an air which later became very
popular, “Au Loin du Bal.”
A new company was rehearsing “Uncle Celestin” at the theatre.
This company was to go on the road for several weeks before
playing in New York. My new manager offered me, for this tour, an
engagement at fifty dollars a week. I accepted, making it a condition
that I should be featured on the placards, in order to regain in a
measure the prestige I had lost.
A few days after I joined the company and made my first
appearance at a distance from New York. For six weeks I appeared
before country audiences, feverishly counting the hours until I should
at last have my chance in the big city.
During this tour, contrary to the conditions I had imposed, I was
not featured. The posters did not even announce me, and yet my
dance, which was given during an interval and without coloured
lights, was successful from the first.
A month and a half later in Brooklyn its success was
phenomenal. The week following I made my debut in New York, at
what was one of the prettiest theatres in town.
There I was able for the first time to realise my dances just as I
had conceived them; with darkness in the house and coloured lights
on the stage. The house was packed and the audience positively
enthusiastic. I danced my first, my second, my third. When I had
finished the whole house was standing up.
Among the spectators was one of my oldest friends, Marshall P.
Wilder, the little American humourist. He recognised me and called
my name in such a way that everybody could hear it, for they had
neglected to put it on the programme! When the audience
discovered that the new dancer was its old favourite comedian, the
little soubrette of a former day, it gave her an ovation such as, I
suppose, never another human being has received.
They called out, “Three cheers for the butterfly! Three cheers for
the orchid, the cloud, the butterfly! Three cheers!” And the
enthusiasm passed all bounds. The applause resounded in my ears
like the ringing of bells. I was overcome with joy and gratitude.
Next morning I arose early to read the papers. Every New York
newspaper devoted from a column to a page to “Loie Fuller’s
Wonderful Creation.” Numerous illustrations of my dances
accompanied the articles.
I buried my face in my pillow and shed every tear that, for a long
time, had lurked in my discouraged soul. For how many months had
I waited for this good luck!
In one of these articles a critic wrote “Loie Fuller had risen from
her ashes.” Next day the whole city was plastered with lithographs,
reproduced from one of my photographs, representing me larger
than life, with letters a foot high announcing: “The Serpentine Dance!
The Serpentine Dance!” But there was one circumstance came near
giving me heart failure. My name was nowhere mentioned.
I went to the theatre and reminded the manager that I had
accepted the modest salary he offered on condition that I should be
featured. I hardly understood when he remarked drily that he could
not do more for me.
I asked him then whether he supposed that I was going to
continue dancing under such conditions.
“Nothing can compel you to do so,” answered the manager. “In
any case, I have taken my precautions in case you do not care to
keep on.”
I left the theatre in desperation, not knowing what to do. My head
swam. I went home and consulted my friends.
They advised me to go and see another manager, and, if I
secured an engagement, simply to drop the other theatre.
I went to the —— Theatre, but on the way I began to cry, and I
was in tears when I arrived there. I asked to see the manager, and
told him my story.
He offered me one hundred and fifty dollars a week. I was to
make my first appearance at once, and sign a contract dating from
the next day.
On reaching home I asked if nothing had come for me from the
other theatre.
Nothing had come.
That evening my friends went to the theatre, where they saw a
poster announcing, for the following evening, the initial appearance
in the “Serpentine” of Miss —— ——. When they told me that piece
of news I understood that my six weeks on the road had been
profitably employed by my manager and one of the chorus girls to
meet just this situation, and I understood, too, why my name was not
mentioned on the first posters.
They had stolen my dance.
I felt myself overcome, dead—more dead, as it seemed to me,
than I shall be at the moment when my last hour comes. My very life
depended on this success, and now others were going to reap the
benefit. I cannot describe my despair. I was incapable of words, of
gestures. I was dumb and paralysed.
Next day, when I went to sign my new contract, the manager
received me rather coldly. He was willing to sign only if I would give
him the privilege of cancelling at his own discretion. He felt that my
imitator at the Casino, announced for the same day, would diminish
greatly the interest that would be felt in what he ironically called my
“discovery.”
I was obliged to accept the conditions which he imposed, but I
experienced all the while an access of rage and grief as I saw in
what a barefaced manner they had stolen my invention.
Heartbroken, with my courage oozing, I made my appearance at
the Madison Square Theatre and, to my astonishment, to my
immense satisfaction, I saw that the theatre had to turn people away.
And it was that way as long as my engagement lasted.
As for the other theatre, after three weeks of featuring my
imitator, it was obliged to close its doors to rehearse a new opera.
IV
HOW I CAME TO PARIS
A LITTLE while after my appearance at the Madison Square

Theatre I was asked to dance for the benefit of a charity at the
German theatre in New York. I had forgotten all about my
promise until the day of the performance, when a card arrived to call
it to my mind. I had neglected to ask my manager’s permission to
appear on that evening, not thinking that he would refuse to grant the
privilege of my participating in a philanthropic affair.
A short time before there had taken place the first part of a
painful incident which was destined to rupture the pleasant relations
subsisting between the management of the Madison Square and
myself. My manager’s associate had asked me as a great favour to
come to open a ball given by some friends in his honour. Delighted
to be of service to him, I readily agreed to do so. When I asked him
the date of this affair he told me not to bother about that.
It was just then that I asked permission to dance at the German
theatre for the benefit of an actress who was ill. The manager
consented. At the German theatre they had engaged a Roumanian
orchestra for me. The leader of this orchestra, Mr. Sohmers, an
enthusiastic man, as the Roumanians are apt to be, came to see me
after I had danced and foretold for me the wonderful artistic success
which I was sure to meet with in Europe. He advised me to go to
Paris, where an artistically inclined public would give my dances the
reception they deserved. From that moment on this became a fixed
idea with me—to dance in Paris. Then the manager of the German
theatre proposed to me a tour abroad, beginning with Berlin.
I promised to think the matter over and acquaint him with my
decision.
Some days later the famous ball took place which my manager’s
associate had asked me to open. I went to it.
They took us, a friend who accompanied me, and myself, into a
little drawing-room where they begged me to wait until some one
should come and fetch me for my appearance on the stage. More
than an hour passed. Finally a gentleman came to tell me that
everything was ready. Through a corridor I reached the platform,
which had been erected at the top of the ball-room. It was terribly
dark, and the only light perceptible was the little ray that filtered
through from one of my lanterns that was imperfectly closed. The
hall looked totally empty. I saw, when I had taken my bearings, that
the whole audience was disposed in the galleries, forming a balcony
half-way up the room. The orchestra finished its overture and I
began to dance. After having danced three times, as I was
accustomed to do at the theatre, I returned to the scene to
acknowledge the applause and I saw before me in luminous letters a
sign with the words: “Don’t think Club.”
That looked queer to me, but I did not attach much importance to
it. I bowed again to the magnificently gowned women and the men,
who were all in sombre black, and then, walking through the same
passage way, I once more reached the dressing-room, where I put
on my outdoor clothes and left. At the door I entered the carriage
that had brought me there, and while we were on our way home I
kept wondering what the Don’t Think Club could be.
That worried me in spite of myself.
The next morning my friend brought me a newspaper, in which I
found on the first page a long article headed:
“LOIE FULLER OPENS THE DON’T THINK CLUB.”
There followed a description of the affair and of the orgies which
took place there. The article had been written with a deliberate
purpose of creating a scandal. I was exasperated beyond measure. I
had gone there merely to please my manager, and the humiliation
inflicted upon me wounded me deeply.
Possibly he thought that I would never know where I had been. A
single newspaper might print something about the affair; but most
probably my manager thought it would never come to my notice. No
newspaper men had been invited to the performance. There was
one guest, a very little man but with a great reputation, who found
himself among the invited, and he wrote the scandalous article, so I
have been told.
I have since had my revenge, a terrible revenge; for this man,
then at the climax of his career, so mismanaged his affairs and those
of others, that he was imprisoned.
“Everybody is blaming him for the article,” my manager explained
to me when I reproached him for having dragged me to this club.
That was his only excuse. He thought he was lessening the insult
by offering me more money. This offer so increased my anger that I
tendered my resignation. I felt in no wise under obligation to a man
who I thought had morally lost all right to consideration. This was the
reason for my leaving, never to return.
The notion of going to Paris possessed me after that more
completely than before. I wanted to go to a city where, as I had been
told, educated people would like my dancing and would accord it a
place in the realm of art.
I was making at this time one hundred and fifty dollars a week
and I had just been offered five hundred. I decided, nevertheless, to
sign a contract with the manager of the German theatre that
guaranteed me sixty-five dollars instead of five hundred. But the
objective, after a tour in Europe, was Paris!
While I was dancing in New York I had to begin to invent special
robes for my new dances. These were just being made and, when I
was about to leave for Europe, they were ready.
The manager of the German Theatre had gone ahead and had
reserved berths for us on one of the steamers.
After taking leave of my friends I was still full of hope and
ambition. My mother in vain tried to share my feelings; she could not
avoid painful misgivings. As for me, I wanted to think only of the
good things that awaited, and to forget all the past annoyances.
During the voyage an evening entertainment was organised for
the benefit of the seamen and I agreed to dance. A stage was
arranged by the bridge. There with the sea for a background and
with the coloured lights used for signalling as the media of
illumination, I tried for the first time a series of new dances, each with
a special gown.
The enthusiasm of passengers and crew knew no bounds and I
felt that I had taken my first step in the conquest of a new world.
We landed in Germany. My manager came to meet us and took
us to Berlin. But, to my great annoyance, I found that I was not to
make my initial appearance for a month, and I could not discover in
what city I was to make it.
That meant a month of inactivity.
Finally I learned that I was to make my debut, not at the Opera as
my manager had promised, but in a music hall. The Opera was
closed, and the music hall was the only place where I could dance.
In that event I would dance only my first dance and would exhibit
only a single gown, just as I had done in New York. I then chose
three of my numbers and prepared myself for my appearance. But
this debut was made without personal interest. In America the best
theatres offered me engagements on much better terms than those I
had to accept in Europe. In Berlin I was obliged to appear where my
New York manager wished. If, before signing the contract, he had
told me where I should have to dance I should have declined. But
when the time for my appearance was at hand I was without
resources and quite at his mercy. To cap the climax my mother fell
seriously ill.
At the time of which I am writing cholera had just broken out at
Hamburg. My mother’s illness came on so suddenly that it was
thought she was stricken with cholera. Everybody at the hotel was
frightened, and we were obliged to take my poor mother to the
cholera hospital.
All these circumstances, conjoined with frightfully trying weather,
put me in bad shape for the struggle. I renounced everything, my
pride, my highest hopes, and I started in assiduously to gain our
livelihood. But I was disabled and without courage.
After a month my German manager informed me he did not care
to continue my contract. He was going back to the United States with
a company that he had come for the express purpose of engaging in
Germany. It seemed clear to me that his only motive in bringing me
to Europe had been to procure the means with which to engage this
new company and take it back with him. He travelled with his wife, a
pretty American woman, who had become a close friend of mine,
and who reproached him most bitterly on my account.
Our manager left Berlin with his company, leaving me with only
just enough money to pay my bills at the hotel when I had completed
the contract that held me to the music hall in Berlin. I then had
absolutely no engagement in sight. I learned that he was getting ten
thousand marks—about $2,500—a month for me. And yet he had
given me only about $300 a month. What was I to do? My
appearance in Berlin had been deplorable and was likely to have an
unfortunate influence on my whole career in Europe. My purse was
empty, my mother ill. We had not the slightest hope of an
engagement and we had no one to help us.
A theatrical agent, an unknown man at that time, who has since
become a theatrical manager, Mr. Marten Stein, came to see me,
and I tried to continue at the music hall where I was dancing. I was
obliged to make concessions to keep going a week or two more, to
get money enough to go away and to look for a new engagement. I
kept thinking more than ever of Paris. If I could only go there!
In these circumstances Mr. Marten Stein secured for me a dozen
performances in one of the beer gardens at Altona, the well-known
pleasure resort near Hamburg. I earned there several hundred
marks, which allowed us to go to Cologne, where I had to dance in a
circus between an educated donkey and an elephant that played the
organ. My humiliation was complete. Since then, however, occasions
have not been lacking when I have realised that the proximity of
trained horses and music-mad elephants is less humiliating than
intercourse with some human beings.

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Textbook Tutorials in Endovascular Neurosurgery and Interventional Neuroradiology 2Nd Edition James Vincent Byrne Auth Ebook All Chapter PDF

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Tutorials in Endovascular

Neurosurgery and Interventional

The Duke 2nd Edition Kerrigan Byrne

Neurophysiology in Neurosurgery: A Modern Approach 2nd

Spinal Neurosurgery 1st Edition James Harrop Editor

Mecca of Revolution: Algeria, Decolonization, and the

Understanding Digital Culture 2nd Edition Vincent

Otherworlds : fantasy and history in medieval

Oxford Textbook of Interventional Cardiology 2nd

100 Case Reviews in Neurosurgery Rahul Jandial

ISBN 978-3-319-54833-3 ISBN 978-3-319-54835-7 (eBook)

Library of Congress Control Number: 2017940860

© Springer International Publishing AG 2017

Printed on acid-free paper

This Springer imprint is published by Springer Nature

Oxford, UK James Vincent Byrne

1 Embryology of the Cranial Circulation �������������������������������������� 1

2.4 External Carotid Artery (ECA)������������������������������������������������ 46

4.5.4 Arteries Supplying the Sacral Spine ���������������������������� 86

6.4 Thrombolytic Therapy�������������������������������������������������������������� 118

8.3.2 Histopathology of Large and Giant Unruptured

9.5.4 Epidemiology���������������������������������������������������������������� 205

12.1.4 Current Descriptions of the Vein of Galen

14 Head and Neck Vascular Lesions ������������������������������������������������ 285

15.3.3 Clinical Presentation �������������������������������������������������� 311

17.2 Evidence for Thrombolysis and Thrombectomy

18.4.2 Nondetachable Balloons �������������������������������������������� 358

20.2.4 Radiation-Induced Skin Damage�������������������������������� 387

Stage 4 = 12–14 mm CRL 1.2.4.1 Stage 1

Ventral Dorsal LNS

Fig. 1.2 (continued)

CAUDAL Anterior Posterior

Fig. 1.2 (continued)

most caudally the primitive maxillary artery. 1.2.4.2 Stage 2

Primit. Trigem. A. Int. Carot. A. Bilat. Long. Neur. A.

posterior inferior hypophyseal a.

I N 1890 I was on a tour in London with my mother. A manager

A LITTLE while after my appearance at the Madison Square

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Oxford, UK James Vincent Byrne

1 Embryology of the Cranial Circulation �� 1

2.4 External Carotid Artery (ECA)�� 46

4.5.4 Arteries Supplying the Sacral Spine �� 86

6.4 Thrombolytic Therapy�� 118

8.3.2 Histopathology of Large and Giant Unruptured

9.5.4 Epidemiology�� 205

12.1.4 Current Descriptions of the Vein of Galen

14 Head and Neck Vascular Lesions �� 285

15.3.3 Clinical Presentation �� 311

17.2 Evidence for Thrombolysis and Thrombectomy

18.4.2 Nondetachable Balloons �� 358

20.2.4 Radiation-Induced Skin Damage�� 387

Stage 4 = 12–14 mm CRL 1.2.4.1 Stage 1

most caudally the primitive maxillary artery. 1.2.4.2 Stage 2