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Compressive Sensing
in Healthcare
Advances in Ubiquitous Sensing Applications
for Healthcare

Compressive Sensing
in Healthcare
Volume Eleven

Volume Editors
Mahdi Khosravy
Osaka University, Osaka, Japan

Nilanjan Dey
Techno International New Town, Kolkata, India

Carlos A. Duque
Federal University of Juiz de Fora, Juiz de Fora, MI, Brazil

Series Editors
Nilanjan Dey
Amira S. Ashour
Simon James Fong
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Typeset by VTeX
Contents

List of contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii

CHAPTER 1 Compressive sensing theoretical foundations in a
nutshell . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Mahdi Khosravy, Naoko Nitta, Kazuaki Nakamura,
Noboru Babaguchi
1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2 Digital signal acquisition . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
1.3 Vectorial representation of signal . . . . . . . . . . . . . . . . . . . . . . 4
l1 norm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
l2 norm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
l∞ norm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Spheres made by different lp norms as distance
criterion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Basis/dictionary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
Orthonormal basis/dictionary . . . . . . . . . . . . . . . . . . . 8
Frame/ over-complete dictionary . . . . . . . . . . . . . . . . 9
Alternate/dual frame . . . . . . . . . . . . . . . . . . . . . . . . . 9
1.4 Sparsity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
k-sparse signal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Non-linearity of sparsity . . . . . . . . . . . . . . . . . . . . . . 10
Sparsity and compressibility . . . . . . . . . . . . . . . . . . . 11
1.5 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Compressive sensing model . . . . . . . . . . . . . . . . . . . . 11
1.6 Essential properties of compressive sensing matrix . . . . . . . . . 12
1.6.1 Null space property (NSP) . . . . . . . . . . . . . . . . . . . . . 12
1.6.2 Restricted isometry property . . . . . . . . . . . . . . . . . . . 17
1.6.3 Coherence a simple way to check NSP . . . . . . . . . . . . 18
1.7 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Appendix 1.A ....................................... 20
Null space property of order 2k . . . . . . . . . . . . . . . . . 20
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
CHAPTER 2 Recovery in compressive sensing: a review . . . . . . . 25
Mahdi Khosravy, Neeraj Gupta, Nilesh Patel,
Carlos A. Duque
2.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
2.1.1 Compressive sensing formulation . . . . . . . . . . . . . . . . 26
2.2 Criteria required for a compressive sensing matrix . . . . . . . . . 26

v
vi Contents

2.2.1 Null space property . . . . . . . . . . . . . . . . . . . . . . . . . . 27

2.2.2 Restricted isometry property . . . . . . . . . . . . . . . . . . . 28
2.2.3 Coherence property . . . . . . . . . . . . . . . . . . . . . . . . . . 29
2.3 Recovery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
2.3.1 Recovery via minimization of l1 norm . . . . . . . . . . . . 31
2.3.2 Greedy algorithms . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
2.4 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
CHAPTER 3 A descriptive review to sparsity measures . . . . . . . . 43
Mahdi Khosravy, Naoko Nitta, Neeraj Gupta, Nilesh Patel,
Noboru Babaguchi
3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
3.2 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
3.3 Sparsity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
k-sparse signal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
3.4 Review to sparsity measures . . . . . . . . . . . . . . . . . . . . . . . . . 47
Measure Sl0 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50
Measure Sl0, . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
Measure Stanha,b . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
Measure Slog . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
Measure Sl1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52
Measure Slp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52
Measure S l2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52
l1
Measure κ 4 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
Measure Suθ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
Measures HG , HS , HS , and l− . . . . . . . . . . . . . . . . . .
p
55
Hoyer measure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
pq-mean measure . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
Measure SGini . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
3.5 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
CHAPTER 4 Compressive sensing in practice and potential
advancements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
Ayan Banerjee, Sandeep K.S. Gupta
4.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
4.2 Compressive sensing theory . . . . . . . . . . . . . . . . . . . . . . . . . . 68
4.3 Example compressive sensing implementations . . . . . . . . . . . 69
4.3.1 Compressive sensing in physiological signal
monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
4.3.2 Compressive sensing in THEMIS imaging . . . . . . . . . 71
4.4 Review of CS literature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
4.4.1 Practical manifestations of theoretical bounds . . . . . . 74
 Contents vii

4.5 Advancements in compressive sensing . . . . . . . . . . . . . . . . . . 75

4.5.1 Personalized basis . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
4.5.2 Non-linear model-based compressive sensing . . . . . . . 78
4.5.3 ROI aware compressive sensing . . . . . . . . . . . . . . . . . 82
4.6 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

CHAPTER 5 A review of deterministic sensing matrices . . . . . . . 89

Daniel Ramalho, Katia Melo, Mahdi Khosravy,
Faramarz Asharif, Mir Sayed Shah Danish,
Carlos A. Duque
5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
5.2 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
5.3 Chirp codes compressive matrices . . . . . . . . . . . . . . . . . . . . . 91
5.3.1  for sparse spectrum signals . . . . . . . . . . . . . . . . . . 93
5.4 Second order Reed–Muller compressive sensing matrix . . . . . 93
5.4.1 Fast reconstruction algorithm . . . . . . . . . . . . . . . . . . . 95
5.5 Amini approach to RIP-satisfying matrices . . . . . . . . . . . . . . 96
5.6 Amini–Marvasti binary matrix . . . . . . . . . . . . . . . . . . . . . . . . 97
5.6.1 BCH-code . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
5.6.2 Extremal Set Theory . . . . . . . . . . . . . . . . . . . . . . . . . 101
5.6.3 Unbalanced expander graphs . . . . . . . . . . . . . . . . . . . 103
5.7 Sensing matrices with statistical restricted isometry property . 104
5.8 Deterministic compressive matrix by algebraic curves over
finite fields . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
5.9 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

CHAPTER 6 Deterministic compressive sensing by chirp codes:

a descriptive tutorial . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
Mahdi Khosravy, Neeraj Gupta, Nilesh Patel,
Carlos A. Duque, Naoko Nitta, Noboru Babaguchi
6.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
6.2 The standard formulation compressive sensing . . . . . . . . . . . . 112
6.3 Compressive sensing by chirp codes . . . . . . . . . . . . . . . . . . . 114
6.3.1 Building the compressive sensing matrix by chirp
codes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
6.3.2 Restricted isometry property for the chirp code
compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . 116
6.4 Recovery of chirp code compressively sensed signal . . . . . . . 116
6.4.1 Step by step in one iteration of recovery . . . . . . . . . . . 119
6.5 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
viii Contents

Appendix 6.A . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121

6.A.1 Chirp sinusoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122
CHAPTER 7 Deterministic compressive sensing by chirp codes:
a MATLAB® tutorial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Mahdi Khosravy, Naoko Nitta, Faramarz Asharif,
Katia Melo, Carlos A. Duque
7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
7.2 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
7.3 Chirp codes compressive sensing: MATLAB tutorial . . . . . . . 126
7.3.1 Chirp codes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
7.3.2 The approach for extraction of parameters . . . . . . . . . 130
7.3.3 Bijection between the sets {ri } and {2ri T modK} . . . . 134
7.3.4 Dechirping yl . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
7.3.5 Sensing and recovery . . . . . . . . . . . . . . . . . . . . . . . . . 138
7.4 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142
CHAPTER 8 Cyber physical systems for healthcare applications
using compressive sensing . . . . . . . . . . . . . . . . . . . . . . 145
K. Keerthana, S. Aasha Nandhini, S. Radha
8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
8.2 Related works . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
8.3 Proposed work . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
8.3.1 Image acquisition . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
8.3.2 Pre-processing techniques . . . . . . . . . . . . . . . . . . . . . 149
8.3.3 Block division . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
8.3.4 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . 150
8.3.5 Uploading data to cloud . . . . . . . . . . . . . . . . . . . . . . . 151
8.3.6 GUI (graphical user interface) . . . . . . . . . . . . . . . . . . 152
8.4 Performance evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
8.4.1 Simulation results . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
8.4.2 Experimental results . . . . . . . . . . . . . . . . . . . . . . . . . 157
8.5 Conclusion and scope for future work . . . . . . . . . . . . . . . . . . 163
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
CHAPTER 9 Compressive sensing of electrocardiogram . . . . . . . 165
Felipe Meneguitti Dias, Mahdi Khosravy, Thales
Wulfert Cabral, Henrique Luis Moreira Monteiro, Luciano
Manhaes de Andrade Filho, Leonardo de Mello Honório,
Rayen Naji, Carlos A. Duque
9.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
9.2 Electrocardiogram . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166
 Contents ix

9.2.1 Historical background . . . . . . . . . . . . . . . . . . . . . . . . 166

9.2.2 Heart anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
9.2.3 Conduction system . . . . . . . . . . . . . . . . . . . . . . . . . . 167
9.2.4 Electrophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 168
9.2.5 Electrocardiogram acquisition . . . . . . . . . . . . . . . . . . 168
9.3 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
9.3.1 Compressive sensing signal acquisition . . . . . . . . . . . 170
9.3.2 Compressive sensed signal reconstruction . . . . . . . . . 170
9.3.3 CS importance in tele-medicine . . . . . . . . . . . . . . . . . 172
9.4 Compressive sensing approach to ECG . . . . . . . . . . . . . . . . . 172
9.4.1 ECG signal quality . . . . . . . . . . . . . . . . . . . . . . . . . . 174
9.4.2 Body sensor networks and monitoring systems . . . . . . 174
9.4.3 Dictionary learning . . . . . . . . . . . . . . . . . . . . . . . . . . 175
9.4.4 ECG signal structure . . . . . . . . . . . . . . . . . . . . . . . . . 175
9.4.5 Wavelets and compressive sensing . . . . . . . . . . . . . . . 176
9.4.6 Signal compression . . . . . . . . . . . . . . . . . . . . . . . . . . 176
9.4.7 Reconstruction algorithms . . . . . . . . . . . . . . . . . . . . . 177
9.4.8 Discrete wavelet transform (DWT) vs compressive
sensing (CS) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178
9.4.9 Hardware implementation . . . . . . . . . . . . . . . . . . . . . 178
9.5 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
CHAPTER 10 Multichannel ECG reconstruction based on joint
compressed sensing for healthcare applications . . 185
Sushant Kumar, Bhabesh Deka, Sumit Datta
10.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
10.2 Background and related work . . . . . . . . . . . . . . . . . . . . . . . . . 187
10.2.1 Compressed sensing-based MECG compression . . . . 187
10.2.2 Compressed sensing based MECG reconstruction . . . 188
10.3 Proposed method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
10.4 Results and discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
10.4.1 Experimental setup . . . . . . . . . . . . . . . . . . . . . . . . . . 191
10.4.2 Performance metrics . . . . . . . . . . . . . . . . . . . . . . . . . 192
10.4.3 Performance evaluation . . . . . . . . . . . . . . . . . . . . . . . 193
10.4.4 Healthcare application perspective . . . . . . . . . . . . . . . 195
10.4.5 Power saving . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
10.5 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
CHAPTER 11 Neural signal compressive sensing . . . . . . . . . . . . . . 201
Denise Fonseca Resende, Mahdi Khosravy, Henrique
L.M. Monteiro, Neeraj Gupta, Nilesh Patel,
Carlos A. Duque
x Contents

11.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201

11.2 Compressed sensing theory – a brief review . . . . . . . . . . . . . . 202
11.3 Compressive sensing for energy-efficient neural recording . . . 203
11.4 Compressive sensing in seizure detection . . . . . . . . . . . . . . . . 204
11.5 Compressive sensing in Alzheimer’s disease . . . . . . . . . . . . . 206
11.6 Compressive electroencephalography (EEG) sensor design . . 207
11.7 Compressive sensing in neural recording . . . . . . . . . . . . . . . . 208
11.8 Compressive sensing for fall prevention . . . . . . . . . . . . . . . . . 209
11.9 EEG compressive sensing for person identification . . . . . . . . . 211
11.10 Compressive sensing wireless neural recording . . . . . . . . . . . 212
11.11 Compressive sensing in portable EEG systems . . . . . . . . . . . . 213
11.12 Compressed and distributed sensing of neuronal activity . . . . 215
11.13 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
CHAPTER 12 Level-crossing sampling: principles, circuits, and
processing for healthcare applications . . . . . . . . . . . 223
Nassim Ravanshad, Hamidreza Rezaee-Dehsorkh
12.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
12.2 Basics of level-crossing sampling . . . . . . . . . . . . . . . . . . . . . . 226
12.3 Design considerations in level-crossing sampling . . . . . . . . . . 229
12.3.1 Resolution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
12.3.2 Dynamic range . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
12.3.3 Conversion delay . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
12.3.4 Timer resolution and number of bits . . . . . . . . . . . . . . 234
12.3.5 Accuracy of the converter . . . . . . . . . . . . . . . . . . . . . 236
12.4 Level-crossing analog-to-digital converters . . . . . . . . . . . . . . 238
12.4.1 Floating-window LCADC . . . . . . . . . . . . . . . . . . . . . 239
12.4.2 Fixed-window LCADCs . . . . . . . . . . . . . . . . . . . . . . 241
12.5 Processing of the level-crossing sampled data . . . . . . . . . . . . 244
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245
CHAPTER 13 Compressive sensing of electroencephalogram:
a review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
Mateus M. de Oliveira, Mahdi Khosravy, Henrique
L.M. Monteiro, Thales W. Cabral, Felipe M. Dias, Marcelo
A.A. Lima, Leandro R. Manso Silva, Carlos A. Duque
13.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
13.2 Signal acquisition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
13.2.1 Pulse train sampling . . . . . . . . . . . . . . . . . . . . . . . . . 248
13.2.2 Signal recovery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
13.2.3 Nyquist frequency . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
13.2.4 Aliasing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
13.2.5 Sample-hold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
 Contents xi

13.3 EEG signals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253

13.4 Compressive sensing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
13.4.1 Compressive sensing metrics . . . . . . . . . . . . . . . . . . . 257
13.5 Applications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257
13.5.1 Block sparse Bayesian learning . . . . . . . . . . . . . . . . . 257
13.5.2 Bayesian compressive sensing . . . . . . . . . . . . . . . . . . 258
13.5.3 Slepian basis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
13.5.4 Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
13.5.5 Wireless body area network . . . . . . . . . . . . . . . . . . . . 259
13.5.6 Comparing reconstruction algorithms . . . . . . . . . . . . . 259
13.5.7 Biometric identification . . . . . . . . . . . . . . . . . . . . . . . 259
13.5.8 Dictionary learning . . . . . . . . . . . . . . . . . . . . . . . . . . 259
13.5.9 General applications . . . . . . . . . . . . . . . . . . . . . . . . . 260
13.5.10 Hardware implementation . . . . . . . . . . . . . . . . . . . . . 261
13.5.11 Feasibility of compressive sensing for EEG signals . . 261
13.6 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
CHAPTER 14 Calibrationless parallel compressed sensing
reconstruction for rapid magnetic resonance
imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269
Sumit Datta, Bhabesh Deka
14.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269
14.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270
14.3 Proposed method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
14.4 Results and discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
14.5 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277
Acknowledgment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
List of contributors

S. Aasha Nandhini
Department of ECE, SSN College of Engineering, Kalavakkam, Chennai, India
Faramarz Asharif
School of Earth, Energy and Environmental Engineering, Kitami Institute of
Technology, Hokkaido, Japan
Kitami Institute of Technology, Kitami, Japan
Noboru Babaguchi
Media Integrated Communication Laboratory, Graduate School of Engineering,
Osaka University, Suita, Osaka, Japan
Computer Science and Engineering, Oakland University, Rochester, MI,
United States
Ayan Banerjee
Impact Lab, Arizona State University, Tempe, AZ, United States
Thales W. Cabral
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
Thales Wulfert Cabral
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
Mir Sayed Shah Danish
Strategic Research Projects Center, University of the Ryukyus, Senbaru,
Okinawa, Japan
Sumit Datta
Department of Electronics and Communication Engineering, Tezpur University,
Tezpur, Assam, India
Luciano Manhaes de Andrade Filho
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
Bhabesh Deka
Department of Electronics and Communication Engineering, Tezpur University,
Tezpur, Assam, India

xiii
xiv List of contributors

Leonardo de Mello Honório

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Mateus M. de Oliveira
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Felipe M. Dias
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Carlos A. Duque
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Denise Fonseca Resende

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Neeraj Gupta
School of Engineering and Computer Science, Oakland University, Rochester,
MI, United States
Computer Science and Engineering, Oakland University, Rochester, MI,
United States

Sandeep K.S. Gupta

Impact Lab, Arizona State University, Tempe, AZ, United States

K. Keerthana
Department of ECE, SSN College of Engineering, Kalavakkam, Chennai, India

Mahdi Khosravy
Media Integrated Communication Laboratory, Graduate School of Engineering,
Osaka University, Suita, Osaka, Japan
Graduate School of Engineering, Osaka University, Osaka, Japan

Sushant Kumar
Department of Electronics and Communication Engineering, Tezpur University,
Tezpur, Assam, India

Marcelo A.A. Lima

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
 List of contributors xv

Leandro R. Manso Silva

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Katia Melo
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Felipe Meneguitti Dias

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Henrique L.M. Monteiro

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Henrique Luis Moreira Monteiro

Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil

Rayen Naji
Medical School, Federal University of Juiz de Fora, Juiz de Fora, Brazil

Kazuaki Nakamura
Media Integrated Communication Laboratory, Graduate School of Engineering,
Osaka University, Suita, Osaka, Japan

Naoko Nitta
Media Integrated Communication Laboratory, Graduate School of Engineering,
Osaka University, Suita, Osaka, Japan
Graduate School of Engineering, Osaka University, Osaka, Japan

Nilesh Patel
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
Computer Science and Engineering, Oakland University, Rochester, MI,
United States

S. Radha
Department of ECE, SSN College of Engineering, Kalavakkam, Chennai, India

Daniel Ramalho
Department of Electrical Engineering, Federal University of Juiz de Fora,
Juiz de Fora, Brazil
xvi List of contributors

Nassim Ravanshad
Faculty of Electrical and Biomedical Engineering, Sadjad University of
Technology, Mashhad, Iran
Hamidreza Rezaee-Dehsorkh
Faculty of Electrical and Biomedical Engineering, Sadjad University of
Technology, Mashhad, Iran
12 CHAPTER 1 Compressive sensing theoretical foundations in a nutshell

a vector y in vector space of Rm much shorter in lengthy by the following linear

operation where m << n:
y m×1 = Am×n x n×1 . (1.19)
A is called a compressive sensing matrix. In standard CS, A is a matrix with fixed
rows which previously have been determined, and in adaptive CS, A is depending on
a priori measurements.
There are two fundamental questions in compressive sensing which have been the
main research themes as follows:
1. What is an optimum compressive sensing matrix which maximally preserves the
signal x information after transferring it to the short length measurement y?
2. How do we reconstruct the signal from the compressed sensed vector y?
The focus of this chapter is mainly on the first question as it is answered briefly in
the following.

1.6 Essential properties of compressive sensing matrix

As the n-length signal vector x is compressively sensed by a m × n compressive
sensing matrix as a much shorter m-length signal vector y, in order to maintain the
recovery of x from y as a theoretical possibility, A should possess some properties.
These properties are reviewed here.

1.6.1 Null space property (NSP)

After compressive sensing by the matrix A, we have the compressed sensed mea-
surements y for different k-sparse signal vectors x. Let us consider the two sets:
(i) X = {x}, the set of k-sparse n-length vectors x, and (ii) Y = {y}, the set of mea-
surements by m-length vectors y by the compressive sensing matrix A. As depicted
in Fig. 1.6, the theoretical expectation is that, as the resultant set Y is constituted by
A matrix transfers from the members in X, each member of X can be approximately
recovered by a reverse transfer to . In order to have the theoretical possibility of the
recovery of each signal vector x from its corresponding compressive sensed measure
y, as a matter of fact there must be a bijection between the sets X and Y , as shown in
Fig. 1.7. Mathematically,

∀x, x  ∈ , x = x  ⇒ Ax  =Ax  . (1.20)
k

The above condition is essential for A. To fulfill this necessary bijection in compres-
sively sensing k-sparse signal vectors x, the sensing matrix A must have a property
called the Null Space Property, as explained in the following.
Assuming the unwanted violation of the bijection of X and Y occurs, we have
two different signal vectors of x 1 and x 2 where both are sensed by A as the same
 1.6 Essential properties of compressive sensing matrix 13

FIGURE 1.6
The theoretical expectation of the relations between the members of two sets: X = {x}, the
set of k-sparse n-length vectors x, and Y = {y}, the set of measurements by m-length
vectors y by the compressive sensing matrix A, and the possible recovery transfer .

FIGURE 1.7
Bijection between two sets X = {x}, the set of k-sparse n-length vectors x, and Y = {y}, the
set of measurements by m-length vectors y, by the compressive sensing matrix A is a
theoretical requirement for possible recovery.

measurement y;
∃x 1 = x 2 | y = Ax 1 = Ax 2 . (1.21)
Therefore, the difference vector δ = x 1 − x 2 belongs to the null space of A as Aδ =
A(x 1 − x 2 ) = 0. The null space of A is the set of signal vectors z where their transfer
by A results in a zero vector:

N (A) = {z|Az = 0}. (1.22)

This is the starting point for finding an essential property for the compressive sensing
matrix A which links the null space of A with the level of sparseness of signal vec-
tors k. In the case of a wrong choice of A where Aδ = A(x 1 − x 2 ) = 0, since δ = 0,
some columns in A are linearly dependent. Now the question is how to avoid the un-
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Ulcerative endocarditis, infectious osteomyelitis, pulmonary
gangrene, general pyæmia, and, as is claimed by a few authors,
typhoid fever, are often accompanied by multiple abscesses in the
brain-substance. Usually the foci are small, as may be readily
inferred from the fact that they are of embolic origin, the emboli being
usually so small as to lodge in very small vessels, and that the
fatality of the primary disease is so great as to cut short life before
the abscess can reach larger dimensions. For the same reasons the
symptoms they produce are rarely distinctive. In chronic lung
affections accompanied by putrescence in bronchiectatic or other
cavities cerebral abscesses are not uncommon occurrences. Under
these circumstances, although we must assume an embolic origin,
the abscess is rarely multiple, and the symptoms are as marked as
in the ordinary varieties. Thus a patient suffering from chronic
phthisis, with or without prodromal malaise or somnolence,
experiences formications and pain in his right leg; he then notices a
slight halt in walking; twitches appear in the affected extremity; it
becomes distinctly paretic. The arm then becomes affected in like
manner; the pupils become unequal; a severe chill occurs, followed
by delirium, convulsions, coma, and death.

DIAGNOSIS.—There is little difficulty in recognizing the existence of a

cerebral abscess in which well-marked focal and constitutional
symptoms coincide, or where a distinct abscess-producing cause,
such as an ear trouble, a head injury, or a putrid bronchiectasis,
coexists.59 But there are a number of cases, varying from the latent
form to forms with obscure general symptoms, whose recognition is
impossible or at best a matter of conjecture. Such cases may be
readily confounded with certain tumors. The existence of febrile
symptoms, although not excluding tumor, as some tumors are
accompanied by such, is greatly in favor of abscess. On the other
hand, choked disc, which is rare with abscess and found only with
the very largest, is in favor of tumor.
59 Yet a leading and careful authority was misled into making the diagnosis of
abscess in a case of ear disease complicated by a cerebral tumor.
PROGNOSIS AND TREATMENT.—The majority of cerebral abscesses
must, from the nature of the case, be regarded as not influenceable
by medicinal measures or surgical treatment. The miliary and other
abscesses due to general septic causes or to mycotic invasion,
being in the nature of the case but features of intrinsically dangerous
or fatal primary diseases, do not call for special measures. It is
different with those due to local trouble about the head and to
surgical causes. Remarkable advances have been made in the
operative treatment of cerebral abscesses, chiefly owing to the
increasing accuracy of the localization of the affected areas through
the disturbance of their function, and to the perfection of surgical
methods. A number of cases by Gussenbauer, Wernicke, and others
have shown that some abscesses may be accurately located during
life by the focal symptoms produced by their presence. Wernicke's
observation of a large abscess in the occipital lobe showed two
facts. First, it permitted the study of the effect of large abscesses on
the cerebral movements, as it was found after trephining that the
pulsation movement of the brain was lost and the dura tensely
bulging, thus indicating a high degree of cerebral pressure.
Secondly, the operation showed that an abscess can be emptied of
its contents, under moderate aseptic precautions, without provoking
contiguous inflammatory reaction or infecting the meninges.
Notwithstanding these favorable local conditions, the patient died.
Gussenbauer60 was more fortunate. He surmised from the fluctuation
of some symptoms and the predominance of others that his patient
had an abscess in the frontal lobe. The suspicion was verified: an
abscess of the size of an apple was found, opened, and emptied of
its contents. The patient recovered without any immediate untoward
symptom.61
60 Prager medizinische Wochenschrift, 1885, Nos. 1, 2, and 3.

61 Epileptic and focal spasms subsequently developed, which shows that a new
inflammatory or other destructive process may have set in in the vicinity of the
emptied sac.
The uncertainties of localization in some districts of the brain are so
great that a number of attempts to repeat the explorations and
aspiration of Wernicke and Gussenbauer have failed. In one case
recently operated on in New York City the aspirating-needle was run
into the brain-substance in several different directions without
striking the pus. It is a question under such circumstances whether
the chances of an abscess becoming latent, minimal though they be
in cases with pronounced signs, are not to be preferred to those
which an uncertain operation can give. The superficial encephalitic
foci offer far better opportunities for surgical triumphs. Here not only
the symptoms are much more constant, and point more unerringly to
the site of the morbid spot, but there are often other signs, such as
the evidences of impaction of a foreign body, local tenderness on
percussion, or bone disease, which aid in determining the proper
spot for the application of the trephine. Several operations where
traumatic encephalitis existed with or without leptomeningitis of the
convexity, followed by complete recovery, were performed by
Macewen.62
62 The Lancet, 1885, vol. i. p. 881.

The medicinal treatment of abscess of the brain is limited to

derivative methods, whose aim is the relief of pressure—an aim
whose fulfilment is more frequently illusory than otherwise.

Benefit has been claimed from the energetic use of mercury, chiefly
in the form of calomel, by older writers; and recently Handfield Jones
has endorsed its administration, attributing to it a remission in a case
in which it was employed. It must be remembered, however, that
remissions occur spontaneously in this disease, and that the
purgative action of calomel may act well for the time being in an
affection so apt to be associated with hyperæmia and increased
cerebral pressure as is an abscess of the brain.63 In the nature of the
case, even this latter momentarily beneficial effect is at the best
temporary.
63 Brain, October, 1884, p. 398.
The prophylaxis of cerebral abscess can be carried out only in cases
due to cranial and aural affections. The importance of treating all
scalp and cranial injuries under aseptic64 precautions is recognized
by all surgeons. It is generally admitted that the trephining of a bone
suspected to be the site of an ostitic or necrotic process involves
fewer risks than the allowing it to remain. Similar principles govern
the treatment of the inflammatory involvement of the mastoid cells
often complicating otitis media. If trephined at all, these should be
trephined at the earliest moment. It was a belief among the older
aurists that the sudden cessation of an aural discharge was of evil
augury, and that cerebral complications were more apt to follow
under such circumstances than when the ear discharged freely. Von
Tröltsch, Politzer, Gruber, and Toynbee have opposed the exclusive
application of the old dogma. In so far as the older ear-surgeons
regarded a profuse aural discharge as an encouraging sign, in this
respect they were of course wrong. But their observation of the
frequent concurrence of cerebral sequelæ with suppression of
discharge is, I think, borne out by a large number of cases. It does
not apply, however, to the suppression of discharge by the rational
employment of aseptic injections.
64 This term is used in its widest sense here.

Spinal Hyperæmia.

The spinal cord is found to vary considerably in color in different

individuals. To some extent this difference is influenced by the
position occupied by the body after death, but not as markedly as in
the case of the brain. Thus it will be paler in a body which has been
kept in the prone than in one which has been kept in the supine
position.65 It is usually found more injected in persons who have died
of febrile affection than in those who have died of exhausting
diseases; notably is this the case with typhus fever and with subjects
who die with congestive malarial chill. But the most intense
congestion, where the gray substance instead of having the normal
rosy hue appears like a blood-soaked sponge, and the white
substance instead of the tint to which it owes its name has a pink
shade, is found in subjects dying in convulsive disorders complicated
by asphyxia, such as epileptic status, tetanus, and certain toxic
disorders.
65 I have not seen it noticed anywhere, but it is a fact readily demonstrable in any
autopsy made in a well-preserved body that when a short segment of cord is
observed at the moment of section the section surface appears pale; but if it be again
examined after a few moments, it will show a reddish tinge, marked as a faint injection
would be; this tinge distinctly deepens under the eye. I have observed this in
specimens which were not held in the hand, so that the influence of pressure can be
excluded. Nor do I believe that the elasticity of the tissues is such as to account for
the phenomenon.

In attempting to apply the fact that varying degrees of vascular

injection are found on post-mortem examinations of the spinal cord
to the elucidation of certain clinical phenomena, we encounter the
same difficulties and sources of error that confronted us in the study
of nutritive brain disorders. The majority of writers have therefore
contented themselves with making a careful clinical study of the
mostly subjective signs of disorders which, once designated as
spinal anæmia and hyperæmia, are now classified under the non-
committal titles of spinal irritation and exhaustion (neurasthenia), as
in this volume. A number of these disorders, like the so-called
anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet, Baimer, and
Brandis, would to-day be considered as hysterical or reflex; and a
few of the instances cited by their contemporaries as cases of spinal
hyperæmia have been since demonstrated to resemble the initial
phases of organic diseases of the cord.

The causes of active spinal hyperæmia are either direct, as when the
spinal centres are overtasked by muscular strain either through over-
exertion or through toxic convulsions, surprised by violent shocks,
such as concussion accidents, or collateral, as when a physiological
discharge (menstruation) or a pathological one (hemorrhoidal flux) is
suddenly checked. A few cases are reported where carbonic-oxide-
gas poisoning provoked spinal hyperæmia. But, like the alleged
cases of spinal hyperæmia after continued and exanthematic fevers,
they were probably cases of incipient or established myelitis.
Hammond claims that surface chilling exerts the same congesting
influence on the cord which he claims for the brain; but no definite
observations have been made in this direction.

Passive spinal hyperæmia has been attributed to obstructive cardiac

and chronic pulmonary affections. In such cases, as with most
causes acting on the circulation of blood in the nerve-centres, the
coexisting cerebral congestion usually masks the spinal. It is a
question how far the intense hyperæmia of the cord found in some
cases of tetanus, strychnia-poisoning, and the condition called
hydrophobia66 is primary and an indication of neural hyperexcitability,
and how far it is secondary to the asphyxia attending the last phases
of these convulsive states. The weight of opinion is in favor of an
acceptation of the latter as the chief or only factor.
66 In a case of hydrophobia clinically as well marked as has been recorded, which I
had the privilege of examining through the courtesy of Kretschmar, both brain and
cord were found remarkably anæmic.

Over-exertion and sexual excesses are frequently followed by a

sensation of fulness and tension in the sacral and lumbar regions,
which may be relieved by lying prone, while it is aggravated while
lying supine.67 From the location of this pain it is evident that it is not
due to congestion of the cord or its membranes, but to fulness of the
vertebral and spinal veins of the lower segment of the vertebral
column. A similar sensation, which may be relieved by the same
change in position or by a hemorrhoidal flux, is complained of by
patients suffering from portal obstruction. The veritable symptoms of
hyperæmia manifest themselves in the parts which receive their
nervous supply from the affected districts. The reflexes are usually
more active; paræsthesias of different kinds, such as formication,
tingling, and creeping sensations, are common; and there is more or
less motor weakness, the limbs feeling heavy and sometimes being
the seat of an acute pain. As a rule, these symptoms are limited to
the lower half of the body.
67 Although this fact has been questioned, I have no doubt whatever that it is true,
from a large number of observations. In many subjects suffering from the results of
excessive venery or masturbation, an intolerable, sometimes pulsating, feeling in the
lumbo-sacral region is only relieved by raising the lower end of the trunk with the back
up. This condition is influenced by a change of residence to a district having a
different level above the sea, and consequently a different barometric condition.

There is very little question when these symptoms exist for any
length of time, and become aggravated, that more subtle nutritive
changes than are covered by the single term hyperæmia become
responsible for them. In a pure hyperæmia the position-test of
Brown-Séquard, which shows relief when the patient is upright or
prone and aggravation when he is supine, particularly if the
gravitation of blood to the cord be facilitated by raising the head and
extremities, ought to yield constant results. But in some cases,
particularly those of long-standing, the very opposite is noted: the
patient's symptoms are aggravated by standing or sitting up, and
relieved by lying down. Here there is probably exhaustion or
malnutrition of the nerve-elements, rendering them abnormally
sensitive to exertion. This view is supported by the fact that
molecular disturbances, such as those which probably accompany
simple concussion, predispose the patient to the development of the
symptoms of spinal hyperæmia, and aggravate them if established
previous to such accident.

Hammond,68 who in his chapter on Spinal Congestion and Anæmia

follows rather the older authors, such as Ollivier, than the newer and
either more cautious or more sceptical writers on the subject,
describes the symptoms of congestion as comprising belt
sensations, paraplegia, erections of the penis, muscular twitches,
loss of expulsive power, and incontinence of the bladder, paralysis of
the abdominal muscles, paralysis of the anal sphincter, loss or
abolition of reflex excitability, diminution of electro-muscular
contractility, and occasionally hyperæsthesia and shooting pains. It is
not doubtful for a moment that if such a case were to occur in
hospital experience it would be regarded as one of organic disease,
and not incipient, but well-established organic disease of the cord.
Those making the diagnosis would have their opinion strengthened
if, as Hammond states, the process took place with great rapidity
and had a tendency to extend itself and eventually involve the whole
cord, or if, as Brown-Séquard is by him cited as stating, bed-sores
occurred in addition. Although Hammond describes certain
anatomical changes, such as increased development of blood-
vessels and distension and injection of them, I am unable to find any
cases recorded as spinal congestion during life, and carefully
examined with a due regard to sources of error after death, in which
such changes were found. It is true that after strychnine- and
cocaine-poisoning an intense hyperæmia69 of the cord is found. In
mammals it is of a far more pronounced character than in reptiles,
and usually more marked in proportion to the existing asphyxia. That
the characteristic toxic effects of these drugs is not to be sought for
in their direct or indirect congesting influence is shown by the fact
that exsanguinated frogs can be made to undergo strychnine tetanus
when their blood is replaced by a saline solution according to the
method of Salkowski. Little support, therefore, could be derived from
a pretended analogy between toxic and pathological hyperæmias,
even if the phenomena of both were similar; which is not the case.
68 Diseases of the Nervous System, 7th ed., p. 392.

69 It is true that in animals which are so organized that the congestion cannot be
attributed to asphyxia, as I showed (Hammond Prize Essay of the American
Neurological Association, 1878) in some experiments on strychnine, arterial
congestion and small foci of hemorrhage were found in the upper cervical cord of
frogs who had been kept in continuous strychnine tetanus for over seventy days.

The introduction of subaqueous caissons for workmen engaged in

the building of bridges, in which those employed labor under
abnormal atmospheric pressure, has led to the development of a
previously-unknown cerebro-spinal affection known as the caisson
disease, and in which, it is generally supposed, either congestion or
hemorrhage of the spinal cord occurs in consequence of sudden
changes of vascular pressure resulting from sudden diminution of
the barometric pressure. Clinically, this affection has been studied in
England, France, and above all in America in connection with the
building of the East River Bridge and the one over the Mississippi at
St. Louis.70 Experiments by Hoppe-Seyler, Bert, and I. Rosenthal
have shown that a sudden diminution of pressure leads to
hemorrhages in various tissues, and, according to the two first-
named, a development of gas occurs in the vascular and other fluids
of the body. A number of peculiar symptoms which do not specially
interest us here occur in conjunction with the so-called caisson
disease: these are—pain in the ear, with or without otitis sicca;
peculiar pains in the joints, which occur on leaving the caisson, and
are probably due to hyperæmia of the joint-surfaces and sudden
increase of the intra-articular fluid; and retardation of the pulse-rate.
In some cases cerebral hyperæmia is added, the patients tottering
about as if drunk. The spinal symptoms consist of a paraplegiform
affection. The paralysis is usually sudden; in some cases the patient
a few minutes after stepping from the air-chamber falls down
perfectly helpless as far as the lower half of the body is concerned.
The expulsive power of the bladder is usually weakened, and there
is anæsthesia to all forms of sensation in the affected limbs, as well
as diminished electro-cutaneous sensibility. The patient often
complains of a strange feeling, as if the lower half of his body were a
foreign substance. With this the electro-muscular reactions are
normal. In the majority of cases these symptoms disappear entirely
in from three to ten days, but occasionally they remain longer;
imperfect recovery of motion and sensation occurs, or, as happened
in a few cases, one of which was carefully examined during life by
Lehwess and after death by Leyden, death occurs as in myelitis. In
the only case where an autopsy and careful microscopical
examination were made under these circumstances71 peculiar
fissures were found in the substance of the spinal cord, surrounded
by areas of reactive myelitis and filled with granule-cells. The
absence of any pigmentary relics of a hemorrhage induced Leyden
to assume that the lacunæ were not of hemorrhagic origin. He
inclines to the view that they were due to the escape of gas from the
blood-plasma, and consequent multilocular inflation of the tissue. If
his observation be confirmed, it constitutes a strong objection to the
hyperæmia theory of the caisson disease. There is neither
permanent hyperæmia nor congestive or hemorrhagic myelitis
developed, as far as the limited material thus far studied permits a
conclusion.
70 Clark, St. Louis Med. and Surg. Journ., cited from Hammond, loc. cit.

71 E. Leyden, Archiv für Psychiatrie, ix. p. 316.

Pure spinal hyperæmia rarely presents itself for treatment. The form
due to over-exertion is recovered from by rest in a very short time;
that due to suppressed discharges, by the re-establishment of the
latter or by the application of leeches to the lumbo-sacral and iliac
region. Ergotin is recommended by Hammond in very large doses. It
is a question whether this drug may not exert a bad effect in
protracted cases where its use has to be continued for a long time.72
In using it, it is well to bear in mind that imperfect nutrition of nerve-
elements is perfectly compatible with an increased blood-amount.
72 A young physician, who for a long period took ergotin in twelve-grain doses for the
relief of symptoms regarded as congestive, acquired a tolerance of the drug such as I
have not seen recorded anywhere, and in addition presents some obscure signs of
cerebellar disease and initial optic-nerve atrophy.

Strychnia has been given with benefit in the caisson disease—

another evidence, as this drug is theoretically contraindicated in true
hyperæmia, that this disease is not, as Hammond and the majority of
authors with him regard it, essentially a congestive affection. The
treatment of those numerous cases in which signs of venous fulness
accompany spinal exhaustion and irritation is detailed in the articles
dealing with those affections.

Spinal Anæmia.
Anæmia of the cord-substance proper, like hyperæmia, is practically
inseparable from the corresponding condition of the membranes.
The influence of a reduced blood-amount on the functional activity of
the spinal cord is more susceptible of exact demonstration than the
corresponding nutritive disturbance of the brain. As the functions of
this segment of the nervous axis are far simpler than those of the
higher organ, there is more unanimity among observers as to the
interpretation of their disordered states. In Stenon's experiment, and
the more elaborate modifications made by those who have followed
his method, it is found that interference with the supply of arterial
blood to the spinal cord is followed by abolition of the function of the
gray matter; if the supply be still further diminished, the functions of
the white tracts become eliminated; next the peripheral nerves, and
ultimately the muscles themselves, lose their normal excitability. On
the re-establishment of the circulation these various parts regain
their functional capacity in the inverse order of its suspension—the
muscles first, next the nerves, then the white substance, and last the
gray substance of the cord. The initial symptoms of some cases of
myelitis from refrigeration correspond more nearly to such a result of
artificial anæmia of the cord than they do to anything that is
customarily regarded as hyperæmia.73
73 I have seen distinct pallor of the spinal meninges on dipping the posterior
extremities of a dog, whose cord had been exposed, into water. It is to be remarked,
however, that other observers, notably Hammond, have either obtained different
results or interpreted the consequences of refrigeration differently.

No one has gone farther than Hammond in erecting a theoretical

anatomical framework which elaborately provides for the
accommodation of various symptoms of spinal anæmia. He
describes anæmia of the posterior columns, and sharply
discriminates between it and anæmia of the antero-lateral columns.
It is a question whether the conducting tracts of these columns are
seriously affected in their functions by anæmia as long as the
centres of innervation are well nourished. Undoubtedly, it is the gray
substance of the cord which is most vulnerable to the influence of
disturbed circulation and nutrition, as Stenon's experiment has
shown; and a glance at the distribution of the blood-vessels will show
that a partial anæmia or hyperæmia, limited to special cornua in any
considerable length of the cord, is an exceedingly improbable
occurrence. With regard to isolated anæmia of the white columns, it
is to be admitted that the posterior are most vulnerable to
malnutrition. But it is doubtful whether this vulnerability is so great as
to allow of an exclusively posterior anæmia, or whether a protracted
anæmia of this kind could exist for years as a purely symptomatic—
or, as some designate it, functional—disorder.

Hammond candidly states that in specifically locating the lesions in

these affections he is aware that post-mortem examinations are
wanting to support them, and admits that what he calls anæmia of
special parts of the cord is the spinal irritation of most authors, and in
part the reflex paraplegia of others.

The most clearly-established form of cerebral anæmia is the one

which is indicated by the ischæmic paraplegia of Jaccoud and the
paraplegia following profuse hemorrhages. The former is produced
by all causes which, by obstructing the flow of arterial blood in the
abdominal or thoracic aorta, cut off the proper blood-supply to the
cord, which the latter receives through the intercostal and upper
lumbar arteries. Aneurism, compression by tumors, and embolism of
the aorta produce this result. The consequence is paraplegia
corresponding in all features of its development to the phenomena
observed in Stenon's experiment. These features, already detailed,
suffice to show that it is not the anæmia of the peripheral nerves and
muscles that is chiefly responsible for the paraplegia, but the
insufficient irrigation of the gray and white substance of the cord
itself. The same is true of the paraplegia following hemorrhage which
has been noted after uterine, renal, and enteric hemorrhages. Both
affections are exceedingly rare.

The influence of general anæmia on the functions of the spinal cord

is not susceptible of accurate study. The cerebral enlargement of the
nervous axis is so much more unfavorably situated than the cord that
it suffers first and most when general anæmia is present. The
consequence is that the signs of cerebral anæmia mask those of
spinal anæmia. It is supposed, however, by many authorities that the
effect of anæmia on the cord may be regarded as an auxiliary factor
in the production of hysterical and neurasthenic symptoms.

How far the spinal cord is liable to suffer from arterial spasm is as yet
a matter of conjecture. It is supposable that just as a powerful
psychical impression provokes a sudden spasm of the cerebral
arteries, so a peripheral irritation may provoke a spasm of the spinal
arteries. In this way the reflex paralyses, motor and vaso-motor, are
explained by many writers.

The subject of reflex palsy has been so much confused by improper

cataloguing—if it can be so called—that some of the best authorities
have become sceptical as to its occurrence. Among the chief
sources of error has been the attributing to irritation of the genital
organs various convulsive, psychical, and paralytic disorders.
Adherence of the prepuce and its excessive length were charged
with being responsible for idiocy, imbecility, epilepsy, and every form
of paraplegia and panplegia. It was further claimed that instances of
complete cure of each of these affections had followed the removal
of the exuberant or adherent prepuce. I cannot find a single instance
recorded where such a cure was effected in any of our large medical
centres, so as to prove convincing to critical colleagues. On the
contrary, L. C. Gray74 has shown that various surgical procedures
have been needlessly resorted to on this erroneous theory in cases
of organic diseases of the spinal cord. I have seen two unfortunate
children suffering from the worst forms of anterior poliomyelitis, one
afflicted with pseudo-hypertrophic paralysis, and several
hydrocephalous and microcephalous idiots, whose prepuces had
been sacrificed to the theory alluded to—it is needless to add without
any result, good or bad.
74 Reflex Irritation from Genital Irritation. In this paper written communications from all
or nearly all neurologists in the United States—certainly including all those of national
fame and large experience—are cited, in which they testify to never having seen a
 case of this character cured by operations on the penis (Annals of Anatomy and
Surgery, Jan. and Feb., 1882.)

The possibility of a reflex paralysis occurring from genital irritation in

the male cannot be denied; among the lower animals a ligature
around the spermatic cords sometimes produces paraparesis, and
paraplegia is a common complication of renal and vesical troubles in
others. But analogous observations in man are rare, and becoming
rarer with our increasing acumen in diagnosis. In females peculiar
reflex disturbances are found associated with uterine and ovarian
derangements. In one case of retroflexion, with possible dislocation
of the ovary, referred to me by H. J. Boldt, there is a remarkable
vaso-motor paralysis of the right arm during each menstrual period:
this member becomes greatly enlarged, of a purplish-blue color, and
cold. Equally remarkable are the reflex disturbances resulting from
the presence of worms in the intestinal canal. Every form of spinal
and cerebral paralysis, even aphasia, has been observed in
connection with helminthiasis. Such disorders yield as rapidly as
they are developed to the exhibition of vermifuges.

Special interest has been aroused by the discovery laid down in the
joint treatise of J. W. Mitchell, Morehouse, and Keen of reflex
paralysis following injuries, observed in the War of the Rebellion. The
cases cited by them appear singular on first sight. The paralysis is
often observed in parts of the body which are not only remote from
the seat of injury, but have no direct connection, physiologically or
otherwise, with it. The hand may be injured and the opposite leg
paralyzed.

Since Mitchell, Morehouse, and Keen first announced the existence

of this peculiar form of reflex paralysis a careful search has been
made by military surgeons engaged in other campaigns for like
results. Notably was this done in the Franco-Prussian War. A number
of confirmatory instances have been collected, some of which rival in
singularity those related by the discoverers of the affection. In one
case a unilateral paralysis agitans followed a punctured wound of the
opposite shoulder, and in another reflex aphasia followed a gunshot
wound of the lumbar region.75 A discrimination is to be made
between such cases where the paralysis, anæsthesia, or neuralgia is
an immediate result of the injury, and those where they follow after
weeks or months. In the latter instance we have not true reflex
disorders to deal with, an ascending neuritis having been found in
the few cases which could be carefully followed up.76
75 Sanitäts Bericht über die deutschen Heere im Krieg gegen Frankreich, 1870-71,
vol. vii.—abstracted in Neurologisches Centralblatt, 1886, p. 207.

76 In a case of Mollenhauer's, vesical paralysis and paresis of the right leg occurred
six years ago (1880) in a veteran of our civil war who had a gunshot wound of the
right hand, with signs, which are still present, of occasional exacerbation of brachial
neuritis. Prodromal signs of paresis were noticed at intervals since his return from the
campaign. The bladder trouble and paresis are now apparently stationary. Such a
case can be accounted for only on the assumption of an organic cord-change
secondary to a neuritis.

The theory that the reflex paralysis from utero-ovarian, intestinal, and
surgical affections, when acutely produced, is due to central
anæmia, is as acceptable as any other would be in the absence of
decisive observations.

Spinal anæmia will but rarely present itself as a subject for special
and separate treatment. When not associated with an intrinsically
grave condition, such as aortic obstruction, dysentery, fatal
hemorrhage, or typhoid fever, it is an exceedingly benign affection,
rapidly yielding to tonic and restorative measures combined with
rest.

Embolism, Thrombosis, Hemorrhage, and Abscess of the Spinal

Cord.

Although the spinal cord is a segment of the same central organ as

the brain, nourished in a similar way, and subject to the same
physiological and pathological laws, lesions of the vascular
apparatus, which play so important a part in brain pathology, play a
comparatively insignificant one in that of the spinal cord. Embolic,
thrombic, and primary hemorrhagic lesions of the cord are so rare
that their possible existence has even been denied. A primary
thrombosis of the cord has not yet been satisfactorily demonstrated
to occur independently of syphilitic lesions; and when it occurs the
ensuing tissue-changes, as described by Heubner, Julliard, and
Greiff, are usually in the background as compared to the
gummatous, sclerotic, or meningitic changes which coexist. The
clinical as well as the anatomical picture is accordingly either one of
a myelitis or meningitis, as the cases of Charcot-Gombault, Heubner,
McDowell, Wilks, Wagner, Zambaco, Homolle, Winge, Moxon,
Schultze, Westphal, Julliard, and Greiff show. (See Myelitis and
Spinal Meningitis.)

With regard to the occurrence of hemorrhage into the substance of

the spinal cord (hæmato-myelia), it is so rare an occurrence that I
can recall but a single case in which I entertained the diagnosis of
this lesion; and in that very case I am unable to declare that it was
not a hemorrhagic myelitis. Aneurismal changes of the spinal
arteries are comparatively of rare occurrence, and as other
predisposing causes to primary vascular rupture are rare in the cord,
the probability of its occurrence is very much diminished. Hebold,77
in a young girl who had developed severe cerebro-spinal symptoms
during a period of nine months following an erysipelatous disorder,
found the upper dorsal cord, on section, dotted with numerous
reddish and round points. These points corresponded to aneurismal
dilatations of the vessels. As there were other inflammatory and
vascular lesions in the same subject, the author referred their
causation to a general constitutional vice, the result either of the
phlegmonous or of a tuberculous disorder.
77 Archiv für Psychiatrie, xvi. 3. Rupture of miliary and other aneurisms in the
meninges has been reported by Astley Cooper, Traube, and others. It is remarkable
that such cases are more and more rarely recorded from year to year in inverse ratio
to the accuracy of our spinal autopsies. I have never found a miliary aneurism below
 the uppermost cervical level of the cord. On the other hand, I have found extensive
spinal hemorrhage in cases where the vessels of the cord proper were fairly healthy.

It is claimed that suppression of the menses, over-exertion, lifting

heavy weights, and concussion are causes of spinal hemorrhage.
The same causes are also mentioned for acute hemorrhagic
myelitis; and it is a question whether the supposed hemorrhage is an
initial lesion or secondary to congestive or anæmic softening.78
78 I have never found vascular ruptures, although carefully searching for them, in the
spinal cord of persons dying instantly after falls from a great height, or, as in one case
which I was fortunately able to secure the cord of, where the subject had been
violently thrown down. Where hemorrhages have been found under these
circumstances they were, as far as I am able to learn from the cases recorded,
meningeal.

The symptoms attributed to spinal hemorrhage are the same, taking

the same locality of the cord, as those of a very rapidly-developed
transverse myelitis. It is unnecessary to enumerate these here in
anticipation of the next section. They are described as being much
more sudden. This suddenness is the only diagnostic aid on which
we can rely.79 The fate of the patient is said by Erb to be decided
within a few days. If he survive the immediate consequences of the
hemorrhage, he is apt to recover, as to life, altogether, with such
permanent atrophies, paralyses, and anæsthesias as are entailed by
the destruction of the tracts and gray substance involved in the
hemorrhage. The treatment recommended for this condition consists
of rest, either in the lateral or prone position, local depletion and
derivation to the intestinal canal, as well as the internal use of
ergotin. The local application of ice, which is also advised, is
probably based on illusory views.80 After the immediate danger is
past the case is to be treated as one of myelitis—a very safe
recommendation in view of the probability that it was a case of
myelitis from the beginning.
79 And even this sign is unavailable as a distinguishing feature in supposed
hemorrhage from concussion, as sudden paraplegias of motion and sensation are
 found in some cases of railway spine, and, although a number of cases terminating
fatally have been examined, there was not always hemorrhage even in the meninges.

80 Until authorities shall have agreed as to what effect the exposure of the bodily
periphery to certain temperatures has on the circulation of the cord, it would be
premature to make any special recommendations as to the temperature at which they
should be kept. I am inclined to believe that while, as is universally accepted, a
general cooling of the bodily surface tends to increase vascular fulness in the cord, as
in all other internal organs, a partial cooling, as of the feet, produces local anæmia at
the level of origin of the nerves supplying the cooled part. Certainly, the bilateral
neural effects of unilateral cooling are in favor of this view.

The descriptions given of the hemorrhagic foci as observed after

death strengthen the view that they were in the majority of cases of
myelitic origin. Usually, they are stated to extend up and down the
cord in the direction of least resistance—that is, in the gray
substance—resembling an ordinary apoplectic clot. But in their
neighborhood there was usually considerable softening, and, to
judge by the descriptions given, this softening differed in no wise
from that which is the characteristic feature of acute myelitis;81 and
often the transition from a peripheral zone of white softening, through
an intermediate zone of red softening, to a central compact clot, is so
gradual as to leave it unquestionable that the softening pre-existed,
and that a vessel had broken down in the midst of the myelitic
detritus. Many ancient foci of myelitis betray the hemorrhagic
complication of their initial period by the presence of pigmented
residue of the absorbed clot.
81 In the latest treatise on nervous diseases published in our language (Ross, loc. cit.,
vol. ii. p. 325) the insufficient foundation on which a whole chapter has been built up is
illustrated by the admission that the usual evidence of acute central myelitis may be
observed far beyond the limits of the hemorrhagic infiltration. If a large area of
softening in the brain were found to contain a central or peripheral clot of blood, and
histologically resembling a typical embolic or thrombic softening, no one would be in
doubt as to which of the two was the primary lesion.

Embolisms and embolic softenings of that part of the spinal cord

which is supplied by the small spinal vessels are so rarely observed
in the dead-house that our knowledge of their possible occurrence
and character is almost entirely the result of experimental
observations or based on analogy. The situation of these vessels,
the angle at which their supply-tubes are given off from the aorta, all
act as protectors of the cord against what is one of the chief dangers
to which the brain is exposed. No definite symptoms have been
attributed to the few doubtful cases of simple embolic occlusion of
the spinal arteries found accidentally in human subjects. Even those
emboli which, when once let loose in the circulation, are found
distributed in nearly every organ of the body, those derived from
ulcerative endocarditis and those due to the invasion of micrococci,
are comparatively rare in the cord. Leyden found multiple capillary
emboli in the spinal cord from the former cause. Small grayish white
foci in a similar distribution were found to be due to an invasion of
cocco-bacteria from a decubitus by Rovigli.82 In this latter case an
increase of pain and muscular spasm in the history of the case of
sclerosis which was thus complicated was attributed to the parasitic
affection.
82 Rivista sperimentale di Freniatria, 1884, x. p. 227.

Just as simple and infectious embolic lesions are frequent in the

brain and rare in the cord, so purulent inflammation or abscess is an
exceptional occurrence in spinal as compared with cerebral
pathology, and probably for the same reasons.

Simple Acute Myelitis.

SYNONYMS.—Spontane (primäre) acute Rückenmarkserweichung,

Softening of the spinal cord, Ramollissement blanc de la moelle,
Myélite aiguë.

As Leyden, whose treatise83 may be regarded as the foundation of

our knowledge on this subject, correctly avers, it is to Abercrombie
and Ollivier that we owe the determination of the existence of that
acute structural disease of the spinal cord, now termed myelitis, as
an affection independent of meningeal changes. The anatomical
descriptions given by these older writers may be accepted at the
present day as models of accurate observation by the naked eye.
Their statement that in acute myelitis the substance of the spinal
cord is softened and changed into a puriform, yellowish, diffluent
mass; that while the disorganization is sometimes more marked in
the posterior, at others in the anterior, and occasionally in the lateral
half, it is most pronounced in the axis of the cord, because the
central gray substance is the favorite starting-point of the morbid
process,—requires no modification to-day. Considerable doubt
existed in the minds of the contemporaries of Ollivier and
Abercrombie as to whether this change was the result of a true
inflammation; and one of the clearest thinkers of the day, Recamier,84
regarded myelitic softening as a lesion peculiar to the nervous
apparatus, and different from ordinary inflammation. I believe that
the most profound investigators of the present day have not been
able to rid themselves of a similar doubt. The discovery of Gluge's
so-called inflammatory corpuscles, which was regarded as settling
the question, only served to confuse the student by the confidence
with which it was urged that they were infallible criteria of the
inflammatory process. Under the non-committal designation of
granule-cells these bodies still flourish in the annals of cerebro-spinal
pathology. As we shall see, a number of products of real disease, of
artifice, and of cadaverous change have passed and do pass muster
under this name. The first substantial progress in our knowledge of
the minute processes underlying inflammation of the spinal cord was
made by Frommann and Mannkopf, but it applied altogether to the
chronic inflammatory or cirrhotic affections of the cord. The
difference between acute and chronic myelitis is greater than is the
difference between acute and chronic inflammation in any other
organ; and it must be admitted that if Recamier is to be regarded as
having erred in asserting that acute myelitis is not a true
inflammation, he is justified in so far as he asserted many features of
the process to be altogether peculiar to the organ affected. Leyden
himself attempted to throw light on the subject by provoking myelitis
experimentally in dogs. He injected Fowler's solution into the spinal