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 Instructor’s Solutions Manual

Elementary Linear
Algebra with
Applications
Ninth Edition

Bernard Kolman
Drexel University

David R. Hill
Temple University
Editorial Director, Computer Science, Engineering, and Advanced Mathematics: Marcia J. Horton
Senior Editor: Holly Stark
Editorial Assistant: Jennifer Lonschein
Senior Managing Editor/Production Editor: Scott Disanno
Art Director: Juan López
Cover Designer: Michael Fruhbeis
Art Editor: Thomas Benfatti
Manufacturing Buyer: Lisa McDowell
Marketing Manager: Tim Galligan
Cover Image: (c) William T. Williams, Artist, 1969 Trane, 1969 Acrylic on canvas, 108!! × 84!! .
Collection of The Studio Museum in Harlem. Gift of Charles Cowles, New York.

c 2008, 2004, 2000, 1996 by Pearson Education, Inc.

"
Pearson Education, Inc.
Upper Saddle River, New Jersey 07458

c 1991, 1986, 1982, by KTI;

Earlier editions "
1977, 1970 by Bernard Kolman

All rights reserved. No part of this book may be reproduced, in any form or by any means, without permission in
writing from the publisher.

Printed in the United States of America

10 9 8 7 6 5 4 3 2 1

ISBN 0-13-229655-1

Pearson Education, Ltd., London

Pearson Education Australia PTY. Limited, Sydney
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Pearson Education Canada, Ltd., Toronto
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Contents

Preface iii

1 Linear Equations and Matrices 1

1.1 Systems of Linear Equations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2 Matrices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
1.3 Matrix Multiplication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
1.4 Algebraic Properties of Matrix Operations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
1.5 Special Types of Matrices and Partitioned Matrices . . . . . . . . . . . . . . . . . . . . . . . . 9
1.6 Matrix Transformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
1.7 Computer Graphics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
1.8 Correlation Coefficient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

2 Solving Linear Systems 27

2.1 Echelon Form of a Matrix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2.2 Solving Linear Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
2.3 Elementary Matrices; Finding A−1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
2.4 Equivalent Matrices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
2.5 LU -Factorization (Optional) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

3 Determinants 37
3.1 Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
3.2 Properties of Determinants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
3.3 Cofactor Expansion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
3.4 Inverse of a Matrix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
3.5 Other Applications of Determinants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

4 Real Vector Spaces 45

4.1 Vectors in the Plane and in 3-Space . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
4.2 Vector Spaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
4.3 Subspaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
4.4 Span . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
4.5 Span and Linear Independence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52
4.6 Basis and Dimension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
4.7 Homogeneous Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
4.8 Coordinates and Isomorphisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
4.9 Rank of a Matrix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
ii CONTENTS

Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

5 Inner Product Spaces 71

5.1 Standard Inner Product on R2 and R3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
5.2 Cross Product in R3 (Optional) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
5.3 Inner Product Spaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
5.4 Gram-Schmidt Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
5.5 Orthogonal Complements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84
5.6 Least Squares (Optional) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90

6 Linear Transformations and Matrices 93

6.1 Definition and Examples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
6.2 Kernel and Range of a Linear Transformation . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
6.3 Matrix of a Linear Transformation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
6.4 Vector Space of Matrices and Vector Space of Linear Transformations (Optional) . . . . . . . 99
6.5 Similarity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102
6.6 Introduction to Homogeneous Coordinates (Optional) . . . . . . . . . . . . . . . . . . . . . . 103
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

7 Eigenvalues and Eigenvectors 109

7.1 Eigenvalues and Eigenvectors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
7.2 Diagonalization and Similar Matrices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
7.3 Diagonalization of Symmetric Matrices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120
Supplementary Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
Chapter Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126

8 Applications of Eigenvalues and Eigenvectors (Optional) 129

8.1 Stable Age Distribution in a Population; Markov Processes . . . . . . . . . . . . . . . . . . . 129
8.2 Spectral Decomposition and Singular Value Decomposition . . . . . . . . . . . . . . . . . . . 130
8.3 Dominant Eigenvalue and Principal Component Analysis . . . . . . . . . . . . . . . . . . . . 130
8.4 Differential Equations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
8.5 Dynamical Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
8.6 Real Quadratic Forms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
8.7 Conic Sections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
8.8 Quadric Surfaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135

10 MATLAB Exercises 137

Appendix B Complex Numbers 163

B.1 Complex Numbers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
B.2 Complex Numbers in Linear Algebra . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
Preface

This manual is to accompany the Ninth Edition of Bernard Kolman and David R.Hill’s Elementary Linear
Algebra with Applications. Answers to all even numbered exercises and detailed solutions to all theoretical
exercises are included. It was prepared by Dennis Kletzing, Stetson University. It contains many of the
solutions found in the Eighth Edition, as well as solutions to new exercises included in the Ninth Edition of
the text.
Chapter 1

Linear Equations and Matrices

Section 1.1, p. 8
2. x = 1, y = 2, z = −2.

4. No solution.

6. x = 13 + 10t, y = −8 − 8t, t any real number.

8. Inconsistent; no solution.

10. x = 2, y = −1.

12. No solution.

14. x = −1, y = 2, z = −2.

16. (a) For example: s = 0, t = 0 is one answer.
(b) For example: s = 3, t = 4 is one answer.
(c) s = 2t .

18. Yes. The trivial solution is always a solution to a homogeneous system.

20. x = 1, y = 1, z = 4.

22. r = −3.

24. If x1 = s1 , x2 = s2 , . . . , xn = sn satisfy each equation of (2) in the original order, then those
same numbers satisfy each equation of (2) when the equations are listed with one of the original ones
interchanged, and conversely.

25. If x1 = s1 , x2 = s2 , . . . , xn = sn is a solution to (2), then the pth and qth equations are satisfied.
That is,

ap1 s1 + · · · + apn sn = bp
aq1 s1 + · · · + aqn sn = bq .

Thus, for any real number r,

(ap1 + raq1 )s1 + · · · + (apn + raqn )sn = bp + rbq .

Then if the qth equation in (2) is replaced by the preceding equation, the values x1 = s1 , x2 = s2 , . . . ,
xn = sn are a solution to the new linear system since they satisfy each of the equations.
2 Chapter 1

26. (a) A unique point.

(b) There are infinitely many points.
(c) No points simultaneously lie in all three planes.

C2

28. No points of intersection: C1 C2 C1

One point of intersection: C1 C2

C1 C2
Two points of intersection:

Infinitely many points of intersection: C1 = C2

30. 20 tons of low-sulfur fuel, 20 tons of high-sulfur fuel.

32. 3.2 ounces of food A, 4.2 ounces of food B, and 2 ounces of food C.

34. (a) p(1) = a(1)2 + b(1) + c = a + b + c = −5

p(−1) = a(−1)2 + b(−1) + c = a − b + c = 1
p(2) = a(2)2 + b(2) + c = 4a + 2b + c = 7.
(b) a = 5, b = −3, c = −7.

Section 1.2, p. 19
   
0 1 0 0 1 0 1 1 1 1
1 0 1 1 1 1 0 1 0 0
   
   
2. (a) A =  0 1 0 0 0 (b) A =  1 1 0 1 0 .
   
0 1 0 0 0 1 0 1 0 0
1 1 0 0 0 1 0 0 0 0

4. a = 3, b = 1, c = 8, d = −2.
 
5 −5 8 ' (
  7 −7
6. (a) C + E = E + C = 4 2 9 . (b) Impossible. (c) .
0 1
5 3 4
   
−9 3 −9 0 10 −9
(d)  −12 −3 −15 . (e)  8 −1 −2 . (f) Impossible.
−6 −3 −9 −5 −4 3
   
1 2 ' ( 5 4 5 ' (
  1 2 3  −6 10
8. (a) A = 2
T
1 , (A ) =
T T
. (b) −5 2 3 . (c) .
2 1 4 11 17
3 4 8 9 4
Section 1.3 3

 
' ( 3 4 ' (
0 −4   17 2
(d) . (e) 6 3 . (f) .
4 0 −16 6
9 10
' ( ' ( ' (
1 0 1 0 3 0
10. Yes: 2 +1 = .
0 1 0 0 0 2
 
λ−1 −2 −3
12.  −6 λ+2 −3 .
−5 −2 λ−4
14. Because the edges can be traversed in either direction.
 
x1
 x2 
 
16. Let x =  .  be an n-vector. Then
 .. 
xn

      
x1 0 x1 + 0 x1
 x2   0   x2 + 0   x2 
       
x + 0 =  .  +  .  =  .  =  .  = x.
 ..   ..   ..   .. 
xn 0 xn + 0 xn

n )
) m
18. aij = (a11 + a12 + · · · + a1m ) + (a21 + a22 + · · · + a2m ) + · · · + (an1 + an2 + · · · + anm )
i=1 j=1
= (a11 + a21 + · · · + an1 ) + (a12 + a22 + · · · + an2 ) + · · · + (a1m + a2m + · · · + anm )
)m ) n
= aij .
j=1 i=1

n
) n
) n
) n
)
19. (a) True. (ai + 1) = ai + 1= ai + n.
i=1 i=1 i=1 i=1
 
n
) m
) n
)
(b) True.  1 = m = mn.
i=1 j=1 i=1
  
)n )m m
) m
) m
)
(c) True.  ai   bj  = a1 bj + a2 bj + · · · + an bj
i=1 j=1 j=1 j=1 j=1
) m
= (a1 + a2 + · · · + an ) bj
. j=1 /
)n m
) )m )n
= ai bj = ai bj
i=1 j=1 j=1 i=1

20. “new salaries” = u + .08u = 1.08u.

Section 1.3, p. 30
2. (a) 4. (b) 0. (c) 1. (d) 1.
4. x = 5.
4 Chapter 1
√
6. x = ± 2, y = ±3.
8. x = ±5.
10. x = 65 , y = 5 .
12

     
0 −1 1 15 −7 14 8 8
12. (a) Impossible. (b)  12 5 17 . (c)  23 −5 29 . (d)  14 13 . (e) Impossible.
19 0 22 13 −1 17 13 9
' ( ' (
58 12 28 8 38
14. (a) . (b) Same as (a). (c) .
66 13 34 4 41
' ( ' (
28 32 −16 −8 −26
(d) Same as (c). (e) ; same. (f) .
16 18 −30 0 −31
 
0 1 −1 4 2
16. (a) 1. (b) −6. (c) −3 0 1 . (d)  −2 8 4 . (e) 10.
3 −12 −6
 
9 0 −3
(f)  0 0 0 . (g) Impossible.
−3 0 1
18. DI2 = I2 D = D.
' (
0 0
20. .
0 0
   
1 0
 14   18 
22. (a)  
 0 . (b)  .
 3
13 13
           
1 −2 −1 1 −2 −1
24. col1 (AB) = 1  2  + 3  4  + 2  3 ; col2 (AB) = −1  2  + 2  4  + 4  3 .
3 0 −2 3 0 −2

26. (a) −5. (b) BAT

10 0 1
28. Let A = aij be m × p and B = bij be p × n.
(a) Let the ith row of A consist entirely of zeros, so that aik = 0 for k = 1, 2, . . . , p. Then the (i, j)
entry in AB is
)p
aik bkj = 0 for j = 1, 2, . . . , n.
k=1

(b) Let the jth column of A consist entirely of zeros, so that akj = 0 for k = 1, 2, . . . , m. Then the
(i, j) entry in BA is
)m
bik akj = 0 for i = 1, 2, . . . , m.
k=1
 
    x1  
2 3 −3 1 1 2 3 −3 1 1   7
3  x2 
0 2 0 3 3 0 2 0 3     −2 
 
30. (a) 
2
. (b)   x3  = .
3 0 −4 0 2 3 0 −4 0    3
 x4 
0 0 1 1 1 0 0 1 1 1 5
x5
Section 1.3 5
 
2 3 −3 1 1 7
3 0 2 0 3 −2 
(c) 
2

3 0 −4 0 3
0 0 1 1 1 5
' (' ( ' (
−2 3 x1 5
32. = .
1 −5 x2 4

2x1 + x2 + 3x3 + 4x4 = 0

34. (a) 3x1 − x2 + 2x3 =3 (b) same as (a).
−2x1 + x2 − 4x3 + 3x4 = 2
 
   
' ( ' ( ' ( ' ( −1 1 3
3 2 1 4
36. (a) x1 + x2 + x3 = . (b) x1  2  + x2  −1  =  −2 .
1 −1 4 −2
3 1 1
      
' ( x1 ' ( 1 2 1 x1 0
1 2 0   1
38. (a) x2 = . (b)  1 1 2   x2  =  0 .
2 5 3 1
x3 2 0 2 x3 0
39. We have
 
v1
n
) 0 1 
 v2 
u·v = ui vi = u1 u2 · · · un  .  = uT v.
i=1
 .. 
vn

 
1 0 0
40. Possible answer:  2 0 0 .
3 0 0

42. (a) Can say nothing. (b) Can say nothing.

n
) )n
43. (a) Tr(cA) = caii = c aii = c Tr(A).
i=1 i=1
n
) n
) n
)
(b) Tr(A + B) = (aii + bii ) = aii + bii = Tr(A) + Tr(B).
i=1 i=1 i=1
0 1
(c) Let AB = C = cij . Then
n
) n )
) n n )
) n
Tr(AB) = Tr(C) = cii = aik bki = bki aik = Tr(BA).
i=1 i=1 k=1 k=1 i=1

n
) n
)
(d) Since aTii = aii , Tr(AT ) = aTii = aii = Tr(A).
i=1 i=1
0 1
(e) Let AT A = B = bij . Then
n
) n
) n
) n )
) n
bii = aTij aji = a2ji =⇒ Tr(B) = Tr(AT A) = bii = a2ij ≥ 0.
j=1 j=1 i=1 i=1 j=1

Hence, Tr(AT A) ≥ 0.
6 Chapter 1

44. (a) 4. (b) 1. (c) 3.

2' (3
1 0
45. We have Tr(AB − BA) = Tr(AB) − Tr(BA) = 0, while Tr = 2.
0 1
 
b1j
0 1 0 1  b2j 
 
46. (a) Let A = aij and B = bij be m × n and n × p, respectively. Then bj =  .  and the ith
 .. 
bnj
n
)
entry of Abj is aik bkj , which is exactly the (i, j) entry of AB.
k=1
04 4 4 1 0 1
(b) The ith row of AB is k aik bk1 k aik bk2 · · · k aik bkn . Since ai = ai1 ai2 · · · ain ,
we have
04 4 4 1
ai b = k aik bk1 k aik bk2 · · · k aik bkn .
This is the same as the ith row of Ab.
0 1 0 1
47. Let A = aij and B = bij be m × n and n × p, respectively. Then the jth column of AB is
 
a11 b1j + · · · + a1n bnj

(AB)j =  .. 
. 
am1 b1j + · · · + amn bnj
   
a11 a1n
= b1j  ...  + · · · + bnj  ... 
   

am1 amn
= b1j Col1 (A) + · · · + bnj Coln (A).

Thus the jth column of AB is a linear combination of the columns of A with coefficients the entries in
bj .

48. The value of the inventory of the four types of items.

50. (a) row1 (A) · col1 (B) = 80(20) + 120(10) = 2800 grams of protein consumed daily by the males.
(b) row2 (A) · col2 (B) = 100(20) + 200(20) = 6000 grams of fat consumed daily by the females.

51. (a) No. If x = (x1 , x2 , . . . , xn ), then x · x = x21 + x22 + · · · + x2n ≥ 0.

(b) x = 0.

52. Let a = (a1 , a2 , . . . , an ), b = (b1 , b2 , . . . , bn ), and c = (c1 , c2 , . . . , cn ). Then

n
) n
)
(a) a · b = ai bi and b · a = bi ai , so a · b = b · a.
i=1 i=1
n
) n
) n
)
(b) (a + b) · c = (ai + bi )ci = ai ci + bi ci = a · c + b · c.
i=1 i=1 i=1
n
) n
)
(c) (ka) · b = (kai )bi = k ai bi = k(a · b).
i=1 i=1
Section 1.4 7

53. The i, ith element of the matrix AAT is

n
) n
) n
)
aik aTki = aik aik = (aik )2 .
k=1 k=1 k=1
n
)
Thus if AAT = O, then each sum of squares (aik )2 equals zero, which implies aik = 0 for each i
k=1
and k. Thus A = O.
' (
17 2 22
54. AC = . CA cannot be computed.
18 3 23

55. B T B will be 6 × 6 while BB T is 1 × 1.

Section 1.4, p. 40
0 1 0 1 0 1
1. Let A = aij , B = bij , C = cij . Then the (i, j) entry of A + (B + C) is aij + (bij + cij ) and
that of (A + B) + C is (aij + bij ) + cij . By the associative law for addition of real numbers, these two
entries are equal.
0 1 0 1
2. For A = aij , let B = −aij .
n
)
0 1 0 1 0 1
4. Let A = aij , B = bij , C = cij . Then the (i, j) entry of (A + B)C is (aik + bik )ckj and that of
k=1
n
) n
)
AC + BC is aik ckj + bik ckj . By the distributive and additive associative laws for real numbers,
k=1 k=1
these two expressions for the (i, j) entry are equal.
0 1 0 1
6. Let A = aij , where aii = k and aij = 0 if i &= j, and let B = bij . Then, if i &= j, the (i, j) entry of
)n )n
AB is ais bsj = kbij , while if i = j, the (i, i) entry of AB is ais bsi = kbii . Therefore AB = kB.
s=1 s=1
n
)
0 1 0 1
7. Let A = aij and C = c1 c2 · · · cm . Then CA is a 1 × n matrix whose ith entry is cj aij .
j=1
 
a1j
 a2j  )n )m
 
Since Aj =  . , the ith entry of cj Aj is cj aij .
 ..  j=1 j=1
amj
' ( ' ( ' (
cos 2θ sin 2θ cos 3θ sin 3θ cos kθ sin kθ
8. (a) . (b) . (c) .
− sin 2θ cos 2θ − sin 3θ cos 3θ − sin kθ cos kθ
(d) The result is true for p = 2 and 3 as shown in parts (a) and (b). Assume that it is true for p = k.
Then
' (' (
cos kθ sin kθ cos θ sin θ
Ak+1 = Ak A =
− sin kθ cos kθ − sin θ cos θ
' (
cos kθ cos θ − sin kθ sin θ cos kθ sin θ + sin kθ cos θ
=
− sin kθ cos θ − cos kθ sin θ cos kθ cos θ − sin kθ sin θ
' (
cos(k + 1)θ sin(k + 1)θ
= .
− sin(k + 1)θ cos(k + 1)θ
Hence, it is true for all positive integers k.
8 Chapter 1
 
( ' ' ( √1 √1
1 0 0 1
10. Possible answers: A = ;A= ;A= 2 2 .
0 1 1 0 √1 1
− 2
√
2
' ( ' ( ' (
1 1 0 0 0 1
12. Possible answers: A = ;A= ;A= .
−1 −1 0 0 0 0
0 1
13. Let A = aij . The (i, j) entry of r(sA) is r(saij ), which equals (rs)aij and s(raij ).
0 1
14. Let A = aij . The (i, j) entry of (r + s)A is (r + s)aij , which equals raij + saij , the (i, j) entry of
rA + sA.
0 1 0 1
16. Let A = aij , and B = bij . Then r(aij + bij ) = raij + rbij .
n
) n
)
0 1 0 1
18. Let A = aij and B = bij . The (i, j) entry of A(rB) is aik (rbkj ), which equals r aik bkj , the
k=1 k=1
(i, j) entry of r(AB).

20. 1
6 A, k = 16 .

22. 3.

24. If Ax = rx and y = sx, then Ay = A(sx) = s(Ax) = s(rx) = r(sx) = ry.

26. The (i, j) entry of (AT )T is the (j, i) entry of AT , which is the (i, j) entry of A.
0 1
27. (b) The (i, j) entry of (A + B)T is the (j, i) entry of aij + bij , which is to say, aji + bji .
0 1 0 1
(d) Let A = aij and let bij = aji . Then the (i, j) entry of (cA)T is the (j, i) entry of caij , which
is to say, cbij .
   
5 0 −4 −8
28. (A + B)T =  5 2 , (rA)T =  −12 −4 .
1 2 −8 12
   
−34 −34
30. (a)  17 . (b)  17 . (c) B T C is a real number (a 1 × 1 matrix).
−51 −51
' ( ' ( ' (
1 −3 1 2 −1 2
32. Possible answers: A = ;B= 2 ;C= .
0 0 3 1 0 1
' ( ' ( ' (
2 0 0 0 0 0
A= ;B= ;C= .
3 0 1 0 0 1

33. The (i, j) entry of cA is caij , which is 0 for all i and j only if c = 0 or aij = 0 for all i and j.
' (
a b
34. Let A = be such that AB = BA for any 2 × 2 matrix B. Then in particular,
c d
' (' ( ' (' (
a b 1 0 1 0 a b
=
c d 0 0 0 0 c d
' ( ' (
a 0 a b
=
c 0 0 0
' (
a 0
so b = c = 0, A = .
0 d
Section 1.5 9

Also
' (' ( ' (' (
a 0 1 1 1 1 a 0
=
0 d 0 0 0 0 0 d
' ( ' (
a a a d
= ,
0 0 0 0
' (
a 0
which implies that a = d. Thus A = for some number a.
0 a

35. We have

(A − B)T = (A + (−1)B)T
= AT + ((−1)B)T
= AT + (−1)B T = AT − B T by Theorem 1.4(d)).

36. (a) A(x1 + x2 ) = Ax1 + Ax2 = 0 + 0 = 0.

(b) A(x1 − x2 ) = Ax1 − Ax2 = 0 − 0 = 0.
(c) A(rx1 ) = r(Ax1 ) = r0 = 0.
(d) A(rx1 + sx2 ) = r(Ax1 ) + s(Ax2 ) = r0 + s0 = 0.

37. We verify that x3 is also a solution:

Ax3 = A(rx1 + sx2 ) = rAx1 + sAx2 = rb + sb = (r + s)b = b.

38. If Ax1 = b and Ax2 = b, then A(x1 − x2 ) = Ax1 − Ax2 = b − b = 0.

Section 1.5, p. 52
0 1
1. (a) Let Im = dij so dij = 1 if i = j and 0 otherwise. Then the (i, j) entry of Im A is
m
)
dik akj = dii aij (since all other d’s = 0)
k=1
= aij (since dii = 1).

0 1
2. We prove that the product of two upper triangular matrices is upper triangular: Let A = aij with
)n
0 1 0 1
aij = 0 for i > j; let B = bij with bij = 0 for i > j. Then AB = cij where cij = aik bkj . For
k=1
i > j, and each 1 ≤ k ≤ n, either i > k (and so a0ik =1 0) or else k ≥ i > j (so bkj = 0). Thus every
term in the sum for cij is 0 and so cij = 0. Hence cij is upper triangular.
0 1 0 1 0 1
3. Let A = aij and B = bij , where both aij = 0 and bij = 0 if i &= j. Then if AB = C = cij , we
)n
have cij = aik bkj = 0 if i &= j.
k=1
   
9 −1 1 18 −5 11
4. A + B =  0 −2 7  and AB =  0 −8 −7 .
0 0 3 0 0 0

5. All diagonal matrices.

10 Chapter 1
' ( ' ( ' (
7 −2 −9 −11 20 −20
6. (a) (b) (c)
−3 10 22 13 4 76
q summands
7 85 6
8. Ap Aq = (A · A · · · A) (A · A · · · A) = Ap+q ; (Ap )q = A p p p
A A · · · A p
= A p + p + · · · + p = Apq .
5 67 85 67 8 5 67 8
p factors q factors q factors
5 67 8
p + q factors

9. We are given that AB = BA. For p = 2, (AB)2 = (AB)(AB) = A(BA)B = A(AB)B = A2 B 2 .

Assume that for p = k, (AB)k = Ak B k . Then

(AB)k+1 = (AB)k (AB) = Ak B k · A · B = Ak (B k−1 AB)B

= Ak (B k−2 AB 2 )B = · · · = Ak+1 B k+1 .

Thus the result is true for p = k + 1. Hence it is true for all positive integers p. For p = 0, (AB)0 =
In = A0 B 0 .

10. For p = 0, (cA)0 = In = 1 · In = c0 · A0 . For p = 1, cA = cA. Assume the result is true for p = k:
(cA)k = ck Ak , then for k + 1:

(cA)k+1 = (cA)k (cA) = ck Ak · cA = ck (Ak c)A = ck (cAk )A = (ck c)(Ak A) = ck+1 Ak+1 .

11. True for p = 0: (AT )0 = In = InT = (A0 )T . Assume true for p = n. Then

(AT )n+1 = (AT )n AT = (An )T AT = (AAn )T = (An+1 )T .

12. True for p = 0: (A0 )−1 = In−1 = In . Assume true for p = n. Then

(An+1 )−1 = (An A)−1 = A−1 (An )−1 = A−1 (A−1 )n = (A−1 )n+1 .
91 : 91 : 9 : 9 :
13. kA
−1
(kA) = k · k A−1 A = In and (kA) k1 A−1 = k · k1 AA−1 = In . Hence, (kA)−1 = k1 A−1 for
k &= 0.
14. (a) Let A = kIn . Then AT = (kIn )T = kInT = kIn = A.
(b) If k = 0, then A = kIn = 0In = O, which is singular. If k &= 0, then A−1 = (kA)−1 = k1 A−1 , so A
is nonsingular.
(c) No, the entries on the main diagonal do not have to be the same.
' (
a b
16. Possible answers: . Infinitely many.
0 a
' ( ' ( ' (
1 2 5 11 10 14
17. The result is false. Let A = . Then AA =
T
and A A =
T
.
3 4 11 25 14 20
18. (a) A is symmetric if and only if AT = A, or if and only if aij = aTij = aji .
(b) A is skew symmetric if and only if AT = −A, or if and only if aTij = aji = −aij .
(c) aii = −aii , so aii = 0.

19. Since A is symmetric, AT = A and so (AT )T = AT .

20. The zero matrix.

21. (AAT )T = (AT )T AT = AAT .

22. (a) (A + AT )T = AT + (AT )T = AT + A = A + AT .
Section 1.5 11

(b) (A − AT )T = AT − (AT )T = AT − A = −(A − AT ).

23. (Ak )T = (AT )k = Ak .

24. (a) (A + B)T = AT + B T = A + B.
(b) If AB is symmetric, then (AB)T = AB, but (AB)T = B T AT = BA, so AB = BA. Conversely, if
AB = BA, then (AB)T = B T AT = BA = AB, so AB is symmetric.
0 1 0 1
25. (a) Let A = aij be upper triangular, so that aij = 0 for i > j. Since AT = aTij , where aTij = aji ,
we have aTij = 0 for j > i, or aTij = 0 for i < j. Hence AT is lower triangular.
(b) Proof is similar to that for (a).

26. Skew symmetric. To show this, let A be a skew symmetric matrix. Then AT = −A. Therefore
(AT )T = A = −AT . Hence AT is skew symmetric.

27. If A is skew symmetric, AT = −A. Thus aii = −aii , so aii = 0.

k
28. Suppose that A is skew symmetric, so AT = −A. Then (Ak )T = (AT )k = (−A) = −Ak if k is a
positive odd integer, so Ak is skew symmetric.
9 : 9 :
29. Let S = 12 (A + AT ) and K = 12 (A − AT ). Then S is symmetric and K is skew symmetric, by
Exercise 18. Thus 9 : 9 :
S + K = 12 (A + AT + A − AT ) = 12 (2A) = A.
Conversely, suppose A = S + K is any decomposition of A into the sum of a symmetric and skew
symmetric matrix. Then

AT = (S + K)T = S T + K T = S − K
9 :
A + AT = (S + K) + (S − K) = 2S, S = 12 (A + AT ),
9 :
A − AT = (S + K) − (S − K) = 2K, K = 12 (A − AT )

   
2 7 3 0 −1 −7
1 1
30. S = 7 12 3  and K =  1 0 1 .
2 2
3 3 6 7 −1 0
' (' ( ' (
2 3 w x 1 0
31. Form = . Since the linear systems
4 6 y z 0 1

2w + 3y = 1 2x + 3z = 0
and
4w + 6y = 0 4x + 6z = 1

have no solutions, we conclude that the given matrix is singular.

 
1
0 0
4 
 
32. D−1 =  0 − 12 0 .
 
0 0 1
3
 
− 12 1
34. A =  . 2

2 −1
' (' ( ' ( ' (
1 2 4 16 38
36. (a) = . (b) .
1 3 6 22 53
12 Chapter 1
' (
−9
38. .
−6
' (
8
40. .
9
' ( ' ( ' (
1 0 0 0 1 0
42. Possible answer: + = .
0 0 0 1 0 1
' ( ' ( ' (
1 2 −1 −2 0 0
43. Possible answer: + = .
3 4 3 4 6 8

44. The conclusion of the corollary is true for r = 2, by Theorem 1.6. Suppose r ≥ 3 and that the
conclusion is true for a sequence of r − 1 matrices. Then
−1 −1 −1
(A1 A2 · · · Ar )−1 = [(A1 A2 · · · Ar−1 )Ar ]−1 = A−1
r (A1 A2 · · · Ar−1 )
−1
= A−1
r Ar−1 · · · A2 A1 .

45. We have A−1 A = In = AA−1 and since inverses are unique, we conclude that (A−1 )−1 = A.

46. Assume that A is nonsingular, so that there exists an n × n matrix B such that AB = In . Exercise 28
in Section 1.3 implies that AB has a row consisting entirely of zeros. Hence, we cannot have AB = In .

47. Let
 
a11 0 0 ··· 0
 0 a22 0 ··· 0 
 
A= .. ,
 . 
0 0 · · · · · · ann

where aii &= 0 for i = 1, 2, . . . , n. Then

 
1
a11 0 0 ··· 0
 
 
 0 1
a22 0 ··· 0 
A−1 =
 ..



 . 

0 0 ··· ··· 1
ann

as can be verified by computing AA−1 = A−1 A = In .

 
16 0 0
48. A4 =  0 81 0 .
0 0 625
 
ap11 0 0 ··· 0
 0
 ap22 0 ··· 0 
49. Ap =  .. .
 . 
0 0 p
· · · · · · ann

50. Multiply both sides of the equation by A−1 .

51. Multiply both sides by A−1 .

Section 1.5 13
' (' ( ' (
a b w x 1 0
52. Form = . This leads to the linear systems
c d y z 0 1

aw + by = 1 ax + bz = 0
and
cw + dy = 0 cx + dz = 1.

A solution to these systems exists only if ad − bc &= 0. Conversely, if ad − bc &= 0 then a solution to
these linear systems exists and we find A−1 .

53. Ax = 0 implies that A−1 (Ax) = A0 = 0, so x = 0.

54. We must show that (A−1 )T = A−1 . First, AA−1 = In implies that (AA−1 )T = InT = In . Now
(AA−1 )T = (A−1 )T AT = (A−1 )T A, which means that (A−1 )T = A−1 .
 
4 5 0
55. A + B =  0 4 1  is one possible answer.
6 −2 6
   
2×2 2×2 2×1 2×2 2×3
56. A =  2 × 2 2 × 2 2 × 1  and B =  2 × 2 2 × 3 .
2×2 2×2 2×1 1×2 1×3
' ( ' (
3×3 3×2 3×3 3×2
A= and B = .
3×3 3×2 2×3 2×2
 
21 48 41 48 40
 18 26 34 33 5 
 
 
 24 26 42 47 16 
AB =  .
 28 38 54 70 35 
 
 33 33 56 74 42 
34 37 58 79 54

57. A symmetric matrix. To show this, let A1 , . . . , An be symmetric matrices and let x1 , . . . , xn be scalars.
Then AT1 = A1 , . . . , ATn = An . Therefore

(x1 A1 + · · · + xn An )T = (x1 A1 )T + · · · + (xn An )T

= x1 AT1 + · · · + xn ATn
= x1 A1 + · · · + xn An .

Hence the linear combination x1 A1 + · · · + xn An is symmetric.

58. A scalar matrix. To show this, let A1 , . . . , An be scalar matrices and let x1 , . . . , xn be scalars. Then
Ai = ci In for scalars c1 , . . . , cn . Therefore

x1 A1 + · · · + xn An = x1 (c1 I1 ) + · · · + xn (cn In ) = (x1 c1 + · · · + xn cn )In

which is the scalar matrix whose diagonal entries are all equal to x1 c1 + · · · + xn cn .
' ( ' ( ' ( ' (
5 19 65 214
59. (a) w1 = , w2 = , w3 = , w4 = ; u2 = 5, u3 = 19, u4 = 65, u5 = 214.
1 5 19 65
(b) wn−1 = An−1 w0 .
' ( ' ( ' (
4 8 16
60. (a) w1 = , w2 = , w3 = .
2 4 8
(b) wn−1 = An−1 w0 .
14 Chapter 1

63. (b) In Matlab the following message is displayed.

Warning: Matrix is close to singular or badly scaled.
Results may be inaccurate.
RCOND = 2.937385e-018
Then a computed inverse is shown which is useless. (RCOND above is an estimate of the condition
number of the matrix.)

(c) In Matlab a message similar to that in (b) is displayed.

64. (c) In Matlab, AB − BA is not O. It is a matrix each of whose entries has absolute value less than
1 × 10−14 .

65. (b) Let x be the solution from the linear system solver in Matlab and y = A−1 B. A crude measure
of difference in the two approaches is to look at max{|xi − yi | i = 1, . . . , 10}. This value is
approximately 6 × 10−5 . Hence, computationally the methods are not identical.

66. The student should observe that the “diagonal” of ones marches toward the upper right corner and
eventually “exits” the matrix leaving all of the entries zero.

( '
0 0
67. (a) As k → ∞, the entries in A → 0, so A → k
. k
0 0

(b) As k → ∞, some of the entries in Ak do not approach 0, so Ak does not approach any matrix.

Section 1.6, p. 62
2. y

1
f(u) = (3, 0)
x
−3 −1 O 1 3
u = (1, −2)

4. y

1
O x
−2 −1 1 2
f(u) = (6.19, −0.23)

u = ( − 2, −3)
Section 1.6 15

6. y
( − 6, 6)
f(u) = − 2 u 6

u = ( − 3, 3) 2

x
−6 −4 −2 O 1

8. z

u = (0, −2, 4)

f(u) = (4, −2, 4)

1
y
O
1 1

10. No.

12. Yes.

14. No.

16. (a) Reflection about the line y = x.

(b) Reflection about the line y = −x.
  
2 0
18. (a) Possible answers: −1 , 0 .
  
0 1
   
0 1
(b) Possible answers:  4 ,  2 .
4 0

20. (a) f (u + v) = A(u + v) = Au + Av = f (u) + f (v).

(b) f (cu) = A(cu) = c(Au) = cf (u).
(c) f (cu + dv) = A(cu + dv) = A(cu) + A(cv) = c(Au) + d(Av) = cf (u) + df (v).

21. For any real numbers c and d, we have

f (cu + dv) = A(cu + dv) = A(cu) + A(dv) = c(Au) + d(Av) = cf (u) + df (v) = c0 + d0 = 0 + 0 = 0.
16 Chapter 1

    
0 ··· 0 u1 0

22. (a) O(u) =  ..   ..   .. 
.   .  =  .  = 0.
0 ··· 0 un 0
    
1 0 ··· 0 u1 u1

(b) I(u) =  ..   ..   .. 
.   .  =  .  = u.
0 0 ··· 1 un un

Section 1.7, p. 70

2. y

4
2
x
O
2 4 6 8 10 12 14 16

4. (a) y

(4, 16) (12, 16)

16

12

4
(4, 4) (12, 4)
3

1
x
O 1 3 4 8 12
Section 1.7 17

(b) y

1
4
x
1 3
O 4 4 1 2

6. y

1
2

x
O 1

8. (1, −2), (−3, 6), (11, −10).

10. We find that

(f1 ◦ f2 )(e1 ) = e2
(f2 ◦ f1 )(e1 ) = −e2 .

Therefore f1 ◦ f2 &= f2 ◦ f1 .
' (
2 0
12. Here f (u) = u. The new vertices are (0, 0), (2, 0), (2, 3), and (0, 3).
0 3

(2, 3)
3

x
O 2

14. (a) Possible answer: First perform f1 (45◦ counterclockwise rotation), then f2 .
(b) Possible answer: First perform f3 , then f2 .
' (
cos θ − sin θ
16. Let A = . Then A represents a rotation through the angle θ. Hence A2 represents a
sin θ cos θ
rotation through the angle 2θ, so
' (
cos 2θ − sin 2θ
A2 = .
sin 2θ cos 2θ
18 Chapter 1

Since ' (' ( ' 2 (

cos θ − sin θ cos θ − sin θ cos θ − sin2 θ −2 sin θ cos θ
A = 2
= ,
sin θ cos θ sin θ cos θ 2 sin θ cos θ cos2 θ − sin2 θ
we conclude that
cos 2θ = cos2 θ − sin2 θ
sin 2θ = 2 sin θ cos θ.

17. Let ' ( ' ( ' (

cos θ1 − sin θ1 cos(−θ2 ) − sin(−θ2 ) cos θ2 sin θ2
A= and B = = .
sin θ1 cos θ1 sin(−θ2 ) cos(−θ2 ) − sin θ2 cos θ2
Then A and B represent rotations through the angles θ1 and −θ2 , respectively. Hence BA represents
a rotation through the angle θ1 − θ2 . Then
' (
cos(θ1 − θ2 ) − sin(θ1 − θ2 )
BA = .
sin(θ1 − θ2 ) cos(θ1 − θ2 )
Since
' (' ( ' (
cos θ2 sin θ2 cos θ1 − sin θ1 cos θ1 cos θ2 + sin θ1 sin θ2 cos θ1 sin θ2 − sin θ1 cos θ2
BA = = ,
− sin θ2 cos θ2 sin θ1 cos θ1 sin θ1 cos θ2 − cos θ1 sin θ2 cos θ1 cos θ2 + sin θ1 sin θ2
we conclude that
cos(θ1 − θ2 ) = cos θ1 cos θ2 + sin θ1 sin θ2
sin(θ1 − θ2 ) = sin θ1 cos θ2 − cos θ1 sin θ2 .

Section 1.8, p. 79
2. Correlation coefficient = 0.9981. Quite highly correlated.
10

0
0 5 10

4. Correlation coefficient = 0.8774. Moderately positively correlated.

100

80

60

40

20

0
0 50 100
Supplementary Exercises 19

Supplementary Exercises for Chapter 1, p. 80

' (
b1
2. (a) k=1 B= .
0
' (
b11 b12
k=2 B= .
0 0
' (
b11 b12 b13
k=3 B= .
0 0 0
' (
b b b b
k=4 B = 11 12 13 14 .
0 0 0 0
(b) The answers are not unique. The only requirement is that row 2 of B have all zero entries.
 
' ( 1 0 0
1 12
4. (a) . (b)  0 0 0 . (c) I4 .
0 1
0 0 0
' ( ' 2 ( ' (
a b a + bc ab + bd 0 1
(d) Let A = . Then A2 = = = B implies
c d ac + dc bc + d2 0 0

b(a + d) = 1
c(a + d) = 0.
It follows that a + d &= 0 and c = 0. Thus
' 2 ( ' (
a b(a + d) 0 1
A =
2
= .
b d 2
0 0
Hence, a = d = 0, which is a contradiction; thus, B has no square root.
5. (a) (AT A)ii = (rowi AT ) × (coli A) = (coli A)T × (coli A)
(b) From part (a)
 
a1i
0 1   n
 a2i  ) 2
(AT A)ii = a1i a2i · · · ani ×  .  = a ≥ 0.
 ..  j=1 ji
ani
(c) AT A = On if and only if (AT A)ii = 0 for i = 1, . . . , n. But this is possible if and only if aij = 0
for i = 1, . . . , n and j = 1, . . . , n
6. (Ak )T = (A · A · · · A)T = A A 67· · · AT8 = (AT )k .
T T
5 67 8 5
k times k times

7. Let A be a symmetric upper (lower) triangular matrix. Then aij = aji and aij = 0 for j > i (j < i).
Thus, aij = 0 whenever i &= j, so A is diagonal.
8. If A is skew symmetric then AT = −A. Note that xT Ax is a scalar, thus (xT Ax)T = xT Ax. That is,
xT Ax = (xT Ax)T = xT AT x = −(xT Ax).
The only scalar equal to its negative is zero. Hence xT Ax = 0 for all x.
9. We are asked to prove an “if and only if” statement. Hence two things must be proved.
(a) If A is nonsingular, then aii &= 0 for i = 1, . . . , n.
Proof: If A is nonsingular then A is row equivalent to In . Since A is upper triangular, this can
occur only if we can multiply row i by 1/aii for each i. Hence aii &= 0 for i = 1, . . . , n. (Other
row operations will then be needed to get In .)
20 Chapter 1

(b) If aii &= 0 for i = 1, . . . , n then A is nonsingular.

Proof: Just reverse the steps given above in part (a).
' ( ' ( ' (
0 a 0 b −ab 0
10. Let A = and B = . Then A and B are skew symmetric and AB =
−a 0 −b 0 0 −ab
which is diagonal. The result is not true for n > 2. For example, let
 
0 1 2
A =  −1 0 3 .
−2 −3 0
 
5 6 −3
Then A2 =  6 10 2 .
−3 2 13
11. Using the definition of trace and Exercise 5(a), we find that
Tr(AT A) = sum of the diagonal entries of AT A (definition of trace)
 
)n )n )n
= (AT A)ii =  a2ji  (Exercise 5(a))
i=1 i=1 j=1

= sum of the squares of all entries of A

Thus the only way Tr(AT A) = 0 is if aij = 0 for i = 1, . . . , n and j = 1, . . . , n. That is, if A = O.
12. When AB = BA.
' 1(
1 2
13. Let A = . Then
0 12
   
2 2 3
1 1
2 + ( 12 ) 1 1
2 + ( 12 ) + ( 12 )
A2 =  2
 and A3 =  3
.
0 ( 12 ) 0 ( 12 )

Following the pattern for the elements we have

 
1 2 1 n
1 1
2 + ( 2 ) + · · · + ( 2 )
An =  n
.
0 ( 12 )

A formal proof by induction can be given.

14. B k = P Ak P −1 .
15. Since A is skew symmetric, AT = −A. Therefore,
A[−(A−1 )T ] = −A(A−1 )T = AT (A−1 )T = (A−1 A)T = I T = I
and similarly, [−(A−1 )T ]A = I. Hence −(A−1 )T = A−1 , so (A−1 )T = −A−1 , and therefore A−1 is
skew symmetric.
16. If Ax = 0 for all n × 1 matrices x, then AEj = 0, j = 1, 2, . . . , n where Ej = column j of In . But then
 
a1j
 a2j 
 
AEj =  .  = 0.
 .. 
anj
Hence column j of A = 0 for each j and it follows that A = O.
Supplementary Exercises 21

17. If Ax = x for all n × 1 matrices X, then AEj = Ej , where Ej is column j of In . Since

 
a1j
 a2j 
 
AEj =  .  = Ej
 .. 
anj

it follows that aij = 1 if i = j and 0 otherwise. Hence A = In .

18. If Ax = Bx for all n × 1 matrices x, then AEj = BEj , j = 1, 2, . . . , n where Ej = column j of In . But
then    
a1j b1j
 a2j   b2j 
   
AEj =  .  = BEj =  .  .
 ..   .. 
anj bnj
Hence column j of A = column j of B for each j and it follows that A = B.

19. (a) In2 = In and O2 = O

' ( ' (
0 0 1 0
(b) One such matrix is and another is .
0 1 0 0
(c) If A2 = A and A−1 exists, then A−1 (A2 ) = A−1 A which simplifies to give A = In .

20. We have A2 = A and B 2 = B.

(a) (AB)2 = ABAB = A(BA)B = A(AB)B (since AB = BA)
= A2 B 2 = AB (since A and B are idempotent)
(b) (A ) = A A = (AA)
T 2 T T T
(by the properties of the transpose)
= (A ) = A
2 T T
(since A is idempotent)
(c) If A and B are n × n and idempotent, then A + B need not be idempotent. For example, let
' ( ' ( ' (
1 1 0 0 1 1
A= and B = . Both A and B are idempotent and C = A + B = . However,
0 0 1 1 1 1
' (
2 2
C2 = &= C.
2 2
(d) k = 0 and k = 1.

21. (a) We prove this statement using induction. The result is true for n = 1. Assume it is true for n = k
so that Ak = A. Then
Ak+1 = AAk = AA = A2 = A.
Thus the result is true for n = k + 1. It follows by induction that An = A for all integers n ≥ 1.
(b) (In − A)2 = In2 − 2A + A2 = In − 2A + A = In − A.
22. (a) If A were nonsingular then products of A with itself must also be nonsingular, but Ak is singular
since it is the zero matrix. Thus A must be singular.
(b) A3 = O.
(c) k = 1 A = O; In − A = In ; (In − A)−1 A = In
k = 2 A2 = O; (In − A)(In + A) = In − A2 = In ; (In − A)−1 = In + A
k = 3 A3 = O; (In − A)(In + A + A2 ) = In − A3 = In ; (In − A)−1 = In + A + A2
etc.
22 Chapter 1

 
1
1
 
v· .
 .. 
1
24.    
1 1
1 1
   
. · .
 ..   .. 
1 1
) )
25. (a) Mcd(cA) = (caij ) = c aij = c Mcd(A)
i+j=n+1 i+j=n+1
) ) )
(b) Mcd(A + B) = (aij + bij ) = aij + bij = Mcd(A) + Mcd(B)
i+j=n+1 i+j=n+1 i+j=n+1

(c) Mcd(AT ) = (AT )1n + (AT )2 n−1 + · · · + (AT )n1 = an1 + an−1 2 + · · · + a1n = Mcd(A)
' ( ' (
7 −3 1 1
(d) Let A = and B = . Then
0 0 −1 1
' (
10 4
AB = with Mcd(AB) = 4
0 0

and ' (
7 −3
BA = with Mcd(BA) = −10.
−7 3
 
1 2 0 0
3 4 0 0
26. (a) 
0
.
0 0 1
0 0 3 2
'( ' ( ' ( ' ( ' ( ' (
1 2 1 1 0 0 −1 0
(b) Solve y= and z= obtaining y = and z = . Then the solution
3 4 1 2 3 3 1 1
 
−1
' (
 1
to the given linear system Ax = B is x =   where x = y .
 0 z
1

27. Let
' ( ' (
0 a 0 b
A= and B = .
−a 0 −b 0

Then A and B are skew symmetric and

' (
−ab 0
AB =
0 −ab

which is diagonal. The result is not true for n > 2. For example, let
 
0 1 2

A = −1 0 3 .
−2 −3 0
Supplementary Exercises 23

Then
 
5 6 −3
A2 =  6 10 2 .
−3 2 13

28. Consider the linear system Ax = 0. If A11 and A22 are nonsingular, then the matrix
' −1 (
A11 O
O A−1
22

is the inverse of A (verify by block multiplying). Thus A is nonsingular.

29. Let ' (

A11 A12
A=
O A22
where A11 is r × r and A22 is s × s. Let
' (
B11 B12
B=
B21 B22

where B11 is r × r and B22 is s × s. Then

' ( ' (
A11 B11 + A12 B21 A11 B12 + A12 B22 I O
AB = = r .
A22 B21 A22 B22 O Is

We have A22 B22 = Is , so B22 = A−122 . We also have A22 B21 = O, and multiplying both sides of this
equation by A−1
22 , we find that B −1
21 = O. Thus A11 B11 = Ir , so B11 = A11 . Next, since

A11 B12 + A12 B22 = O

then
A11 B12 = −A12 B22 = −A12 A−1
22

Hence,
B12 = −A−1 −1
11 A12 A22 .

Since we have solved for B11 , B12 , B21 , and B22 , we conclude that A is nonsingular. Moreover,
 
−1 −1 −1
A 11 −A A A
11 12 22 
A−1 =  .
O A−1
22

 
  −1 0 3 5
4 5 6  −2 0 6 10 
30. (a) XY T =  8 10 12 . (b) XY T =
 −1
.
0 3 5
12 15 18
−2 0 6 10
0 1T 0 1T
31. Let X = 1 5 and Y = 4 −3 . Then
' ( ' ( ' ( ' (
1 0 1 4 −3 4 0 1 4 20
XY T = 4 −3 = and Y X T = 1 5 = .
5 20 −15 −3 −3 −15

It follows that XY T is not necessarily the same as Y X T .

Another random document with
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SYMPTOMS.—An attack of chorea is usually preceded by more or less
failure of the general health and evidences of some mental
disturbance. It is quite common to be told by the parents of a child
suffering from chorea that the little patient had seemed unwell for
some time previous to the attack; that the appetite had failed, and
that the child had looked pale; that he had been irritable or excitable,
and at school the teacher had complained of restlessness or
inattention in the pupil. In a little girl who was brought to me recently
with her second attack of chorea her mother stated that for several
days before the outbreak the child had been in excessive spirits, and
that she had been singing loudly and in a peculiar manner. The
same symptoms had preceded the first attack. Sometimes nothing is
observed until it is found by the parents or teacher that there are
abnormal twitchings and movements of the limbs.

At first there is a general restlessness and fidgetiness. The child may

be punished at school for not keeping still or for dropping things.
Soon irregular movements of groups of muscles are seen. The
shoulder is shrugged or the fingers move spasmodically. At first the
patient is aware of the movements and tries to control them, but
before long the twitching and jerking are constant, and extend to
most of the voluntary muscles of the body. He is then unable to
control them for any length of time.

The sudden jerk of a limb followed by an odd grimace, the quick

protrusion of the tongue, and the rolling of the eyes or snapping of
the lids give a characteristic picture which can hardly be mistaken.

The extent of the movements varies in different cases. In some they

are slight and affect only certain muscles. Often the disorder is
confined to one lateral half of the body. In other cases the
movements involve all the limbs and the trunk, and are so violent
and constant that the patient does not seem to have a moment's
rest. The trunk may be suddenly drawn backward, then the arms are
extended or thrown up, and the legs flexed and tossed about with
great quickness. Sometimes the patient is thrown off the bed or from
the chair on which he may be to the floor.
The speech is often affected. The patient speaks in a thick or jerky
manner, as if the tongue were too large for the mouth, and saliva
usually flows in great quantities. Sometimes in bad cases there are
involuntary utterances made at frequent intervals.

The features undergo contortions continually, and when at rest

relapse into a condition of vacancy which makes the patient look
almost idiotic. The expression of a child with chorea is so peculiar
that the disease may almost be diagnosticated by this.

During sleep the movements usually cease, but generally the patient
is restless while asleep, and in some instances the irregular
movements continue even at this time.

The mental condition commonly shows some change. The child is

irritable and peevish, cries and laughs readily, or is sullen and
morose. Sometimes he is violent to those about him, but this is rare.
Intellectually the patient suffers somewhat. He is not able to study as
before, and the memory may be impaired. Sometimes there is a mild
form of dementia.

During the course of the disease there may be exacerbations, and

sometimes after convalescence has seemed established there are
relapses.

Recovery is gradual, and as the abnormal movements cease the

mental condition improves, and the patient regains his health without
any traces of the disease remaining.

We will now consider some of the symptoms separately. First, as to

disturbances of motion. As before remarked, the disorderly
movements occur soon after the general restlessness is seen. They
most commonly begin in one upper extremity. The hand is thrown
into various positions, the fingers are flexed and extended or
separated, and all of the movements occur with great rapidity. In a
day or two the whole arm is affected, and then the leg of the same
side is involved in the jerkings and twitchings. In many cases the
facial muscles are contorted, the mouth is pursed up or opened
wide, and then quickly twisted into some other shape. If the patient is
told to put out his tongue, it is protruded after a moment's hesitation,
and then suddenly retracted, the jaws coming together with a snap.
A smacking sound is made with the lips quite often, and words are
uttered involuntarily. The movements may remain confined to one
side of the body, constituting what is called hemichorea. This is quite
common, and the right side is rather more frequently involved than
the left. There is so great difference of opinion among authors on this
point that it is probable that one side is affected about as often as the
other. Of 252 cases which I have examined, 69 were right and 43 left
hemichoreas. Gerhard20 found in 80 cases of chorea that 32 were
unilateral; of these 20 were right and 12 were left. Sée, however,
found that in 97 of 154 cases the movements were either confined to
the left side or were more marked on that side. He states that in his
experience the proportion between left and right hemichorea is as 37
to 27. Pye-Smith in 33 cases of unilateral chorea found 15 on the
right and 18 on the left side. Many cases which begin as hemichorea
soon become general.
20 American Journal of Med. Sci.

The disease reaches its greatest severity in about two weeks, and if
the case is a bad one we find by this time all of the voluntary
muscles are in constant movement. At this time the French name for
chorea, folie musculaire, is most appropriate. Patients are often
unable to walk or to sit up, and sometimes they may be thrown from
the bed by violent spasmodic movements of the trunk. Strange as it
seems, patients rarely complain of fatigue, notwithstanding the
violent muscular exercise. This is probably because each set of
movements is of short duration and is constantly changing its seat.

As a rule, the movements cease completely during sleep or under an

anæsthetic. Sometimes occasional twitchings of muscles are seen in
sleep, and in rare instances we are told by the parents of a child with
chorea that the movements are as active in sleep as in the waking
hours.
The movements of chorea occur either while the limbs are at rest or
under the influence of voluntary effort. This fact has been pointed out
by Mitchell and by Gowers. In some cases the movements are most
marked when the patient is at rest. If a directed effort is made to use
the member for a time, the choreic movements are suspended. For
example, a patient may be able to carry a glass of water to the
mouth without spilling a drop, while a moment before the hand may
have been performing a continual dance. I have often observed that
while the limb to which the whole attention has been directed in
performing some movement has been steadied, the other limbs
become violently agitated.

In another class of cases the movements are comparatively slight

when the part is at rest, but when a motion is attempted the disorder
of the muscles is so much increased that it is almost impossible for
the act to be completed. The patient is told to pick up some small
object: he throws the hand out toward it, and it is jerked away before
he can grasp it. He again puts the hand forward, reaches the object,
and the fingers open and shut and sprawl over the article before it is
taken up. Sometimes it cannot be grasped at all. This has been
called choreic ataxia, but it is only one type of the cases commonly
seen.

This brings us to the influence of the will on the movements in

chorea. There are some cases, as mentioned above, in which the
movements may be controlled by the will for a brief period, but they
will sooner or later return. In other cases it is quite impossible for the
patient to check the movements at all, and one frequently sees in a
case of hemichorea the sound hand used to grasp the other, so as to
control the movements. We have referred to this because of
Niemeyer's opinion that corporeal punishment would shorten an
attack of chorea.

Chorea is sometimes confined to a single muscle or group of

muscles. When limited in this way it is generally in the head, face, or
perhaps in the shoulder. These cases of localized chorea have been
spoken of by Mitchell as habit chorea.21 They are often very
obstinate in resisting treatment, and sometimes last during life.
21 Lectures on Nervous Diseases, p. 146.

PARALYSIS.—Not infrequently in chorea there is paralysis to a greater

or less extent. It is generally one-sided, and most often involves the
upper extremity. The limb affected is the one in which the
movements were most violent. The arm may hang entirely powerless
or it may be only enfeebled, and feeling to the patient like a dead
weight. The paralysis always recovers with the chorea or soon after.

POST-PARALYTIC CHOREA.—Under this term Mitchell and Charcot have

described a variety of chorea which is seen in patients after an
attack of hemiplegia. The movements are chiefly on voluntary effort,
and are those of inco-ordination. They come on from one to several
months after an attack of unilateral paralysis, and are sometimes
seen in cases in which almost complete recovery has taken place.
Mitchell has reported22 a case which was under my care for several
years, and which he saw in consultation with me. This patient had
two attacks of left hemiplegia, the last being fatal. After the first
attack there was great gain of power to use the arm and leg, but the
movements were performed awkwardly and with an irregular jerking
movement. A post-mortem examination revealed a spot of softening
the size of a filbert in the left corpus striatum, which was apparently
recent, and a point of red degeneration in the right crus cerebri. The
vessels at the base of the brain were extensively atheromatous.
22 American Journal of the Med. Sci.

Of the electrical condition of the muscles in chorea but little is known.

Rosenthal23 found increase of faradic contractility in three cases of
hemichorea, and the galvanic test showed a high degree of
excitability, demonstrated by the fact that weak currents gave
contractions at cathodic closure, or even tetanic contractions, and
also contractions were produced at cathodic opening.
23 Ziemssen's Cyclopædia, loc. cit., p. 434.
The affection of speech which is so common in chorea is due to
disordered action of the laryngeal muscles, or it may be from choreic
action of the abdominal muscles. Sometimes it is chiefly from the
awkwardness of the tongue. The usual form of trouble is that the
patient speaks in a staccato manner and the syllables seem as if
they were driven out. When the chorea is in the laryngeal muscles,
the tone and pitch of the voice are altered.

Chorea of the heart is sometimes spoken of, but it has never been
satisfactorily demonstrated that there is any real disorder of cardiac
rhythm in chorea. It is not unusual in chorea to meet with over-action
or palpitation of the heart, but these conditions do not necessarily
depend on the disease.

Valvular murmurs are often met with from the beginning of an attack.
In some instances they are the result of an endocarditis, but
frequently they are functional or anæmic. They are usually heard at
the apex. Sometimes there is a reduplication of the first sound,
giving the idea of a want of synchronism in action of the two sides of
the heart; but this is probably not the result of chorea of the heart. I
recall one patient, a child of seven or eight years, in whom the
reduplication of the first sound was very distinct during an attack of
St. Vitus's dance. She was brought to me at the beginning of a
second attack a year later, and the reduplication of the cardiac
sounds was heard again, so it is likely that it had continued during
the interval, and was probably a congenital condition.

The pupils are commonly dilated in chorea and respond sluggishly to

light.

REFLEXES.—I have examined the condition of the patellar reflex in 50

cases. In 26 of these it was present in normal degree, in 15 it was
diminished, and in 9 it could not be excited. In one patient it was
absent during the height of the choreic movements, but could be
readily produced after the patient had recovered. The condition of
the reflexes has also been examined by Joffroy and Saric,24 and they
found that of 16 cases of chorea the reflexes were abolished or
diminished in 12.
 24 L'Union médicale, Sept. 22, 1885.

SENSIBILITY.—Authors state that disorders of sensation are met with

in chorea, such as localized anæsthesia or a general hyperæsthesia:
I have never met with any such instances. Patients often complain of
pain in the joints or in the limbs, and this may be unaccompanied
with swelling or tenderness on pressure. Tenderness on pressure
over the vertebræ is rare in my experience, although others speak of
its being of frequent occurrence. Mental disorders are generally
present, but only to a slight extent. There is almost always irritability
of temper and peevishness. The most sweet-tempered children
become cross and perverse, laugh immoderately at trifling things, or
cry as readily if they are annoyed. There is generally failure of
memory and incapacity for study or thought. In most cases, however,
this exists to so slight an extent as not to be noticed except on very
close observation. Sometimes there is marked mental disorder
amounting almost to imbecility, and occasionally the mental
weakness remains for some time after the motor disorders have
recovered.

The condition of the pulse is generally unchanged, but sometimes it

is abnormally frequent. The temperature, according to Von
Ziemssen, is unchanged.

The nutrition generally suffers. The patient rapidly loses flesh, and
becomes anæmic; the skin grows dry, and the hair gets harsh. The
digestion is apt to be disordered. The tongue is large, pallid, and
coated thickly, and there is sometimes nausea or vomiting. The
appetite is not good. The bowels are often constipated. The urine
has been examined by several observers. Bence Jones found an
excess of urea at the height of the disease. Albumen is not present
except accidentally, but there is usually an excess of phosphates. In
several cases in which we have examined the urine at the Infirmary
for Nervous Diseases we found that the specific gravity was high
while the chorea was at its height, but fell to normal as the patient
recovered.
Chorea is spoken of as acute and chronic, but all cases are more or
less chronic. Those cases which last eight or ten weeks may be
considered acute, while those running on for months or years are
properly called chronic.

DURATION.—Considerable difference of opinion exists as to the

duration of chorea. Some writers speak of three or four weeks as an
average attack. Gray and Tuckwell, in a series of cases treated by
the expectant plan,25 found an average duration of ten weeks.
Occasionally a patient is seen with an attack of chorea which lasts
only a few days. The parents of a little patient whom I saw a few
days ago assured me that her second attack lasted only a week.
They are educated and intelligent persons whose statement can be
relied upon.
25 Lancet, Nov. 28, 1876.

The course is not always regular. In some cases the disease

gradually reaches a crisis, remains stationary for a few days, and
then by degrees declines; in others there are exacerbations. The
patient will seem to be almost well, and then become very much
worse for a time. Relapses are not infrequent, and are generally
caused by fright or excitement.

The recurrence of attacks of chorea is well known. A child who has

had the disease one year may have it a second or third year. It is
most likely to recur in the spring. Some cases have as many as five
attacks, but as puberty approaches the attacks are lighter, and finally
cease. Of 282 cases to which I have referred, 198 were first attacks,
47 had had chorea twice; 23 were in their third attack, 8 in the fourth,
and 3 in the fifth attack.

TERMINATION.—The disease in most instances terminates in complete

cure, but sometimes there is nervousness or want of co-ordination
remaining for a time. Rarely the inco-ordination or a certain
quickness in movement becomes permanent.
Death is a rare termination of chorea except in pregnancy. If it does
occur, it is usually from some complication. In pregnancy the
mortality is great. Of 64 cases collected by Wenzel, 18 died. In
Philadelphia, in seventy-four years from 1807 to 1881, there have
been but 64 deaths from chorea; of these, 38 were under twenty
years, and 26 over that age.

Hutchinson reports a fatal case in a boy of twelve years.26 After

complaining of headache and rheumatic pains for several days,
choreic movements began. They soon became general and very
violent. At the end of two weeks he was admitted to the
Pennsylvania Hospital. At this time the patient was so extremely
convulsed that it was impossible to keep him in bed without tying
him. The movements continued but little abated, and the child died in
two days.
26 Philadelphia Med. Times, vol. vi. p. 535.

Another case of unusual interest is reported by Hunt.27 The patient, a

man of twenty-nine years, had suffered from chorea of the face and
arms for years. In consequence of a fall on the pavement he
fractured the left humerus. The movements were immediately
exaggerated, and in spite of a carefully adjusted splint it was
impossible to keep the arm at rest. The fragments were in a state of
constant movement, and the points of bone threatened to penetrate
the skin. The skin was so much excoriated that it was determined to
dispense with the splint and attempt to keep the limb at rest by the
administration of morphia hypodermically in half-grain doses three
times daily. This failed to keep the arm quiet, and the seat of fracture
became greatly inflamed. No form of appliance or medication
succeeded in keeping the arm at rest, and the patient finally sank
and died from exhaustion on the tenth day after admission to the
hospital. The post-mortem examination revealed no gross lesion of
the brain or cord. No microscopic examination was made of the
brain.
27 Pennsylvania Hospital Reports, vol. ii.
MORBID ANATOMY AND PATHOLOGY.—In a disease so seldom fatal as
chorea it is not surprising that there have been but few post-mortem
examinations made. In the earlier autopsies, before the microscope
was extensively used, but little of value was recorded. Sée, who
collected 84 cases in which post-mortem examinations were made,
reported that in 16 no changes were found in the nervous system. In
32 there were lesions in the brain and nervous centres, usually
softening and tuberculosis, and in the remainder inflammatory
changes in the serous membranes. In 29 there were evidences of
heart disease. Sée considered that but few cases of death in chorea
were caused by inflammatory diseases of the heart, but that the
majority should be referred to nervous excitement and anæmia.

Ogle28 in a report of 96 cases of chorea mentions 16 which were

fatal. Post-mortem examinations were made in all of these. Cardiac
lesions were found in 13. In 10 of these deposits were found upon
the valves, and in 3 there was some change in the pericardium. He
speaks of having noted congestion of the nervous centres six times,
and softening of the cord once.
28 Brit. and For. Med.-Chir. Review, Jan., 1868.

In all of 11 autopsies reported by Pye-Smith29 there were cardiac

lesions found. In every case old or recent deposits were observed
upon the valves. In two instances the heart was hypertrophied, and
in one there was pericarditis. Changes in the nervous system were
less often found by this writer. In 1 case there was hyperæmia of the
cord, and in 3 cerebral hyperæmia.
29 Guy's Hospital Reports, 1874.

Dickinson found in 22 fatal cases of chorea 17 in which the heart

was diseased. “In every instance making up the large tale of cardiac
disease there were recent vegetations on the mitral valve, and often
also elsewhere.”

In the fatal case of Hutchinson referred to above the heart was found
diseased, the aortic valves were incompetent, the leaflets being
swollen and softened, and the aorta was atheromatous above the
sinus of Valsalva.

Of late years a number of careful autopsies have been made in

cases of chorea. The brain and spinal cord have been closely
examined, and in almost every instance some lesion has been found
in both of these organs.

Steiner reported in 1868 the results of post-mortem examinations in

3 fatal cases of chorea. In 1 case he found cerebro-spinal anæmia,
serous effusion into the spinal canal, and proliferation of the
connective tissue in the upper part of the cord; and in another
hyperæmia of the brain and cord.

Elischer,30 who reports a fatal case in a parturient woman who had

an attack of chorea in her eighth year, two in her sixteenth year, and
another in a previous pregnancy, found at the autopsy hyperæmia
and œdema of the brain and gray substance of the cord.
Microscopically, the brain showed fatty, amyloid, and pigmentary
changes in the nerve-elements and vessels of the large central
ganglia, small secondary extravasations of blood in the connective
tissue, and numerous emboli in the smallest vessels, especially in
the cortex. In the spinal cord there was seen abundant proliferation
of nuclei in the adventitia of the vessels. In the central canal serum
was found, and the surrounding connective tissue was harder than
usual.
30 Cyclopædia of the Practice of Medicine, Von Ziemssen, vol. xiv. p. 450.

Dickinson has contributed an excellent paper on the pathology of

chorea.31 He relates the particulars of the autopsies in 7 fatal cases
in which he personally made microscopical examination of the brain
and spinal cord. He also adds the results of post-mortem
examinations in 17 other cases at St. George's Hospital and at the
Hospital for Sick Children. In all of the 7 cases in which microscopic
examinations of the brain and cord were made there were found
hyperæmia of both of these structures, in many instances
hemorrhages into the substance of the nervous tissues, dilatation of
the smaller vessels, and in chronic cases sclerotic changes in the
course of the vessels. “The first visible change,” he remarks, “would
seem to be the injection or distension of the arteries, succeeded by
extrusion of their contents, to the irritation and injury of the
surrounding tissue.” The changes seemed to affect both brain and
cord in all cases. The parts of the brain most constantly affected lay
between the base and the floor of the lateral ventricles in the track of
the middle cerebral arteries, the substantia perforata, the corpora
striata, and the beginning of the Sylvian fissures. “Of the cord no
region was exempt, but perhaps the cervical and dorsal regions were
usually more affected than the lumbar. With regard to the vertical or
physiological divisions of the cord, these all, whether white or gray,
shared in the vascular destruction; this condition, however, was
usually most marked in the vessels belonging to or in connection
with the lateral part of the gray matter about the root of each
posterior horn. And it is to be observed that this was also the chosen
situation of the more definite and special changes, whether
hemorrhagic (as in two instances), sclerose, or exudatory. Speaking
generally, the chosen seats of the choreic changes are the parts of
the brain which lie between the beginning of the middle cerebral
arteries and the corpora striata—the parta perforata; and in the cord
the central portion of each lateral mass of gray matter comprising the
root of each posterior horn.”
31 Medico-Chirurgical Transactions, vol. xli. p. 1, 1876.

The embolic theory of chorea has been held by several investigators,

among them Hughlings-Jackson. It is undoubtedly an attractive and
reasonable view, especially when we consider the large proportion of
cases in which there is valvular disease of the heart. Dickinson,
however, does not consider this hypothesis tenable. In none of the
cases in which he made post-mortem examinations did he find
evidences of embolism. “In none of the instances described were
decolorized fibrin, detached clots, or signs of impaction detected,
and the erraticism of embolic accident was wanting: the constancy
indeed with which the changes repeated themselves in certain
positions, and the equality with which they affected both sides of the
body, are conclusive objections to this hypothesis. The corpora
striata, for example, were affected with almost absolute symmetry,
notwithstanding that these bodies receive their blood respectively
from the right and left carotids and different parts of the aortic arch.”

Rheumatism is associated with or precedes chorea in a large

proportion of cases, and this was pointed out by Kirkes in 1850 and
again in 1863. This connection between rheumatism and chorea,
and the frequent occurrence of endocarditis in chorea, has led some
authors to believe that the endocarditis is always rheumatic, and that
the chorea is the result of the endocarditis. Dickinson, however,
points out that in cases in which there is a distinct history of the
chorea beginning suddenly from fright there are often well-marked
cardiac murmurs heard. He believes that in all cases of chorea in
which there are cardiac murmurs they are due to endocarditis, and
suggests that in these cases from fright the endocarditis is due to
irregularity of cardiac action. This, of course, is mere hypothesis, and
we must bear in mind that in all cases of chorea there is anæmia,
and that the murmur may be purely functional.

H. C. Wood, in a communication read before the College of

Physicians of Philadelphia,32 gives his views of the pathology of
chorea, based upon the results of post-mortem examinations made
in a number of dogs who had the disease. He believes the history of
chorea to be this: “Owing to emotional disturbance, sometimes
stopping of various vessels of the brain, or sometimes the presence
of organic disease, there is an altered condition of the ganglionic
cells throughout the nerve-centres. If the cause is removed and the
altered condition of the nerve-cells goes only so far, it remains what
we call a functional disease. If it goes so far that the cells show
alteration, we have an organic disease of the nervous system.”
32 Philada. Med. News, May 30, 1885.

In two dogs which were choreic the movements continued after

section of the cord. This shows that in dogs, at any rate, the
movements originate in the cord. In four instances of canine chorea
in which Wool made autopsies there were found in the cords of three
mild grades of infiltration of leucocytes in the gray matter. In the
fourth, in which the dog had died of the disease, the ganglion-cells
were degenerated, and in some places had disappeared. He
concludes, therefore, that choreic movements may depend upon a
diseased condition of the motor cells of the cord.

Although there are several recorded cases of human chorea in which

lesions of the spinal ganglionic cells have been found, we cannot
believe that this can be a constant lesion in chorea. The disease is
too transient in many cases, and presents too many variations and
anomalies, for the cord to be always the seat of the diseased
condition.

In an interesting paper read by Angel Money before the London

Medical and Chirurgical Society in 1885 he detailed some
experiments in which, by injecting a fluid containing arrowroot,
starch-granules, or carmine into the carotids of animals, he produced
movements closely resembling chorea; and this was found to be
associated always with embolism of the capillaries of the cord. In the
discussion which followed Broadbent and Sturges expressed their
disbelief in the embolic origin of chorea in man. Hughlings-Jackson
said that he held the view of the cerebral origin of chorea, one of his
reasons being the frequency with which the face-muscles are
affected in this disease.

The probabilities are that in chorea there is a disordered condition of

the brain and cord more or less general. The lesions are no doubt
slight in mild cases of short duration, but in severe cases of long
standing there occur well-marked changes in portions of both brain
and cord. We cannot do better than to sum up the pathology of
chorea in the words of Dickinson: “A widely-distributed hyperæmia of
the nervous centres, not due to any mechanical mischance, but
produced by causes mainly of two kinds—one a morbid, probably a
humoral, influence which may affect the nervous centres as it affects
other organs and tissues; the other, irritation in some mode, usually
mental, but sometimes what is called reflex, which especially
belongs to and disturbs the nervous system, and affects persons
differently according to the inherent mobility of their nature.”

DIAGNOSIS.—The only diseases for which chorea may be mistaken

are paralysis agitans and disseminated sclerosis. The former occurs
only in adult life, and the tremor is of a regular rhythmical character.
In the latter the tremor occurs only on voluntary effort, and is also
more regular than the movements of chorea. There are forms of
congenital sclerosis seen in children which closely resemble chorea.
Here the duration of the disease and the association of contractures
with it distinguish it from chorea.

Hysterical subjects have a form of chorea which can only be

differentiated from the true disorder by noting the general hysterical
character of the case and the result of treatment, which strongly
influences the will-power of the patient.

PROGNOSIS.—In the great majority of cases this is favorable. If the

disease occurs in childhood and is without complications, recovery
generally takes place spontaneously after a few weeks. Should the
movements be violent and continuous, so as to interfere with sleep
and the taking of food, or should there be any complication, such as
acute rheumatism or cardiac disorder, then the prospect of recovery
is not so good.

The prognosis as to relapses should be given with caution. If in a

child, it is possible that there will be a return of the disease after a
longer or shorter interval. It is not likely to recur until after several
months, usually at about the same season the following year. As the
child grows older the intervals become longer, and it may safely be
asserted that after puberty is passed and bodily development
completed there will be no more returns of the affection.

The cure is usually complete. It must be remembered, however, that

for some time after an apparently complete cure there may be slight
inco-ordination of movements, particularly in the arms and the face.
These are shown in the unnecessary haste in making uncertain
motions or in slight grimaces, or if excited an awkwardness in the
use of the fingers.

Death is a rare termination in uncomplicated cases, especially in

children. The fatal cases are generally when acute rheumatism has
been associated with the chorea or when there has been a fracture
or an injury as a complication.

In Sée's statistics there is a mortality of 5.7 per cent. in 158 cases in

the Children's Hospital. In adults, and more particularly in pregnant
women, death is more common. Wenzel's cases referred to above
gave a mortality of 27.3 per cent.

The cause of death in chorea may be from the intensity of the

disease, and in this case the symptoms are generally violent from
the outset, increase to an extreme extent, and then collapse and
coma come on. The movements may cease when the collapse
occurs, but they may continue to the last, growing gradually less until
death.

TREATMENT.—A vast number of remedies have been popular in this

disease from all ages. The medicine which is most generally
depended upon at the present day is arsenic. It is advised by most
writers, and in my own experience is decidedly the most reliable
remedy for chorea which we know. The best way to administer it is in
the form of Fowler's solution, and it should be given in large doses. I
have given the bromide of arsenic, but did not find it superior to
Fowler's solution. The amount of arsenic which can be safely borne
by children with chorea is surprising to those who have not had
experience in its administration. The medicine should be given in
gradually increasing doses until the toxic effects are well marked or
until the patient is convalescing. In a child of six years three drops
may be given to begin with, three times a day. One drop additional
should be added to the dose each day, and the child soon acquires a
remarkable tolerance of the drug. As much as twelve or fifteen drops
at a dose is borne by a child of eight years. If vomiting or much
œdema of the face occurs, the medicine should be stopped for a day
or two, and then the original dose should be taken, to be again
increased as before.

Seguin recommends that the patient should begin again with the
dose at which tolerance ceased. For instance, if vomiting occurred
after a dose of nine drops, he stops the medicine for a day, and
begins again with eight drops. I have found that sometimes this
causes vomiting again, and I think it preferable to resume the
medicine with a small dose.

It is often seen that a patient becomes worse during the first few
days that the arsenic is taken, but improvement generally begins
after a week of the arsenical treatment, and is well marked after two
weeks.

In obstinate cases it is of marked advantage to give the arsenic

hypodermically. Cases which do not yield to the drug when given by
the mouth often improve at once when it is given hypodermically.
Chronic cases which have resisted all forms of medication
sometimes are cured by hypodermic injections of arsenic. For giving
arsenic in this way it is best to use Fowler's solution, made without
the compound spirit of lavender. It is less likely to cause abscess to
form at the point of puncture.

Other remedies enjoy a reputation in the treatment of chorea.

Sulphate of zinc is relied upon by many, and it is the means which
Ross recommends. It should be given in increasing doses like
arsenic, and very large doses may often be taken without disturbing
the stomach. Trousseau, Hammond, and Hamilton favor strychnia,
but I have had no experience in its use.

Cimicifuga and conium are both often beneficial in their effects. I

have seen the former do good when arsenic had failed. Conium to
be efficacious must be given in large doses. Eserine and
hyoscyamine have both been successfully employed, the former by
Bouchut, and the latter by Oulmont and Laurent. Recently,
DaCosta33 has reported, in a clinical lecture at the Pennsylvania
Hospital, a case of very severe chorea successfully treated with
hyoscyamine. The patient was a boy of eleven years, and the
disorder had followed an attack of acute rheumatism. He was given
1/100 gr. of hyoscyamine three times a day.

33 Philada. Med. Times, Jan. 23, 1886.

Ziegler34 has recorded several cases which recovered under the use
of nitrite of amyl. The bromides and chloral are useful adjuncts to
treatment in case of sleeplessness or mental irritability. Cases of
cure by the use of chloral alone have been reported. Bouchut gave a
girl of fourteen and a half years, with chorea and dementia, 45 grains
of chloral a day for twenty-seven days. She slept most of the time,
but improvement was seen on the fifth day, and cure was completed
on the twenty-eighth day of the use of the chloral. Electricity has
been efficient in the hands of many writers. I have found
galvanization of the spine to produce a quieting effect in some
cases.
34 Ibid., vol. vi. p. 486.

Iron is always of use in chorea; it may be given during the course of

the disease, and is generally necessary in convalescence. Cod-liver
oil or malt extract should be given in feeble persons.

It is scarcely necessary to mention the other remedies which have

been recommended. DaCosta has used the bromide of iron. H. C.
Wood has used a preparation of skunk cabbage, and there are a
great number of other remedies which have been found of value.

Next to the internal means come external applications. Baths and

frictions are useful in their effect on the general health. The ether
spray to the spine or the application of an ice-bag for ten minutes
once or twice daily is sometimes found to assist the other means.
Cold douches have been advised by some, but they may do harm.
The care of the general health of the patient is of first importance,
and his surroundings should be as quiet as possible.
It is of the greatest value in bad cases to place the patient in bed and
keep him there until the symptoms improve. John Van Bibber of
Baltimore has treated a number of cases of chorea successfully by
keeping them secluded in a darkened room. Such an extreme
degree of isolation is not often necessary, and it might make a child
more nervous.

In children the patient should always be taken from school and kept
from exciting play. Plenty of fresh air and wholesome food should be
insisted upon. Change of air to the mountains or to the seashore
often effects a cure in a short time.

Some cases do not appear to be benefited by any treatment. These

are the hereditary form of chorea and some of the localized choreas.
The latter are often helped or cured by the hypodermic use of
arsenic even in long-standing cases.

ATHETOSIS.
 BY WHARTON SINKLER, M.D.

This disease was first described by Hammond in his work on Diseases of the Nervous System in 1871,
and cases have since been reported by many observers, among them Clifford Allbutt, Claye Shaw,
Eulenburg, Oulmont, and Gowers. The disease is named by Hammond from the word ἀθετος, without
fixed position.1 The principal features are an inability to retain the fingers and toes in any position in
which they may be placed, and the continual movements which persist in the parts—a condition called
by Gowers mobile spasm.
1 Diseases of the Nervous System, p. 722.

Athetosis is often connected with impaired mental powers; many of Shaw's cases were in imbecile
children.

The movements of athetosis are not confined to the hand in all cases, but they are sometimes met with
in the foot, and even in the muscles of the face and back.

The following is Hammond's original case:2 “J. P. R——, aged thirty-three, a native of Holland, consulted
Hammond Sept. 13, 1869. His occupation was bookbinding, and he had the reputation, previous to his
present illness, of being a first-class workman. He was of intemperate habits. In 1860 he had an
epileptic paroxysm, and since that time, to the date of his first visit to me, had a fit about once in six
weeks. In 1865 he had an attack of delirium tremens, and for six weeks thereafter was unconscious,
being more or less delirious during the whole period. Soon after recovering his intelligence he noticed a
slight sensation of numbness in the whole of the right upper extremity and in the toes of the same side.
At the same time severe pain appeared in these parts, and complex involuntary movements ensued in
the fingers and toes of the same side.

“At first the movements of the fingers were to some extent under the control of his will, especially when
this was strongly exerted and assisted by his eyesight, and he could, by placing his hand behind him,
restrain them to a still greater degree. He soon, however, found that his labor was very much impeded,
and he had gradually been reduced from time to time to work requiring less care than the finishing, at
which he had been very expert.

“The right forearm, from the continual action of the muscles, was much larger than the other, and the
muscles were hard and developed like those of a gymnast. When told to close his hand he held it out at
arm's length, clasped the wrist with the other hand, and then, exerting all his power, succeeded, after at
least half a minute, in flexing the fingers, but instantaneously they opened again and resumed their
movements.

“In this patient there was impairment of intellect, his memory was enfeebled, and his ideas were dull.
There was no paralysis of any part of the body, but there was slight tremor of both upper extremities.
The involuntary movements were of the right arm, and continued during sleep. Sensation was normal.
The spasm of the muscles causes severe pain in the arm, and keeps him from sleeping at night.”
Hammond used various remedies without relief, and had the patient under his charge for many years.
Finally, he showed the patient to the American Neurological Society at the annual meeting in 1883, with
almost complete relief to the movements as a result of nerve-stretching.
2 Ibid.

Athetosis is found in two forms—the hemiplegic and the bilateral varieties. In the former there has
usually been an attack of hemiplegia more or less marked, or there has been an epileptic fit or
unconsciousness from alcohol, as in Case I. There is often hemianæsthesia or some disorder of