Differences in somatosensory hand organization in a healthy flutist and a flutist with focal hand dystonia

CAS

R

PORT

Differences in Somatosensory Hand Organization in a Healthy Flutist and a Flutist with Focal Hand Dystonia: A Case Report Nancy N. ByI, PhD, PT, FAPTA

Professor and Interim Chair Department of Physical Therapy and Rehabilitation Science UCSF/SFSU Graduate Program in Physical Therapy University of Californ ia-San Francisco

Alison McKenzie, PhD, PT

Assistant Professor Department of Physical Therapy Chapman University San Francisco; Assistant Clinical Professor Department of Physical Therapy and Rehabilitation Science UCSF/SFSU Graduate Program in Physical Therapy University of California , San Fra ncisco

Srikantan S. Nagarajan, PhD

Postdoctoral Fellow Keck Centerfor Integrative Neurosciences Coleman Laboratory University of California, San Francisco

Repetitive motion injuries can result from tissue microtrauma, poor posture, nerve compression, and muscle imbalance,l-3 Some patients develop signs of inflammation, swelling, or muscle tension.s whereas others complain of unusual fatigue or awkwardness This research was funded in part by the University of California, School of Medicine, REAC -Dub ois Fund and by program project grant P01-NS34835 from the National Institutes of Health. Correspond ence and reprint requests to Nancy N. Byl, PhD, PT, Professor and Interim Chair, Graduate Program in Physical Therapy, Dep artm ent of Physical Therapy and Rehabilitation Science, University of California-San Francisco, 1320 Seventh Avenue , Box 0736, San Francisco,CA 94143;e-mail:.

302 JOURNAL OF HAND THERAPY 2000

ABSTRACT: Focal hand dystonia is a d isabling, involuntary disorder of movement that can disrupt a successful musician's career. This problem is difficult to treat, to some extent because we do not fully understand its origin. Somatosensory degradation has been proposed as one etiology. The purpose of this case study was to compare the differences in the somatosensory hand representation of two female flutists, one with focal dystonia of the left hand (digits 4 and 5) and one a healthy subject (the control). Nonin vasive magnetic source imaging was performed on both subjects. The somatosensory evoked potentials of controlled taps to the fingers were measured with a 37-ehannel biom agnetometer and reported in terms of the neuronal organization, latency, amplitude, density, location, and spread of the digits on each axis (r, y, and z), The somatosensory representation of the involved hand of the flutist with dystonia differed from that of the healthy flutist. The magnetic fields evoked from the primary somatosensory cortex had a disorganized pattern of firing, with a short latency and excessive amplitude in the involved digits of the affected hand , as well as inconsistency (decreased dens ity). In addi tion, the patterns of firing were different in terms of the location of the d igits on the x, y, and z axes and sequential organizati on of the digits. This study confirms that somatosensory evoked magnetic fields can be used to describe the representation of the hand on the somatosensory cortex in area 3b. Degradation in the hand representation of the flutist with focal hand dystonia was evident, compared with the hand representation of the healthy flutist. It is not clear whether the sensory degradation was the cause or the consequence of the dystonia. The questions are whether re-differentiation of the repr esentation could be achieved with aggressive sensory retraining and whether improvement in structure would be correlated with improvement in function. J HAN D THER. 2000;13:302-309.

of the hand when they perform-a target task. These are often referred to as occupational hand cramps or focal hand dystonia.t" Focal hand dystonia is one of the most disabling limb d ystonias." It is usually associated with a specific target task (e.g., writing, computer work, musical performance).5,7-14 Ordinarily, pain is not present, but problems of involuntary, uncontrollable flexion and extension movements of the digits interfere w ith performance of the target task. 15-22 When the patient is not performing the target task, the findings on traditional neurologic examination may be within normal limits. On examination using currently available

technology,23-30 however, abnormal cortical responses including somatosensory de-differentiation of the hand representation have been reported. 29,3o With more extensive psychophysical assessment, problems in sensory discrimination such a localization, stereo:&nosis, and graphesthesia have been reported .31- Recently, noninvasive magnetoencephalography has been used to confirm somatosensory disorganization in the primary sensory cortex of patients with focal hand dystonia.34-36 Focal hand dystonia is recalcitrant to most treatments. Uncontrollable muscle spasms can sometimes be controlled with repeated injections of botulinum toxin into the affected muscles to reduce the intensity of the contractions and relieve the discomfort of cramping.3~7 Unfortunately, this type of treatment does not restore normal motor control, and patients often cannot return to previous jobs that require fine motor skills. Research in neuroplasticity provides evidence that the primary sensory cortex as well as the motor cortex can be modified by attended, repetitive sensory processing48-52 and motor behaviors.P Some evidence of this plasticity has been demonstrated clinically in a patient with focal hand dystonia who participated in a sensory retraining program.53 The question is whether this serious, involuntary fine motor disorder of focal hand dystonia actually results from an underlying sensory impairment, such as a degradation of the somatosensory representation of the hand. Until recently, it has not been possible to plot an accurate representation of the hand on the somatosensory cortex without using invasive electrophysiologic mapping techniques. Now, magnetoencephalography can be used to document somatosensory evoked magnetic field responses to cutaneous inputs.34-36 However, there is significant variability in testing, based on the patient's age , sex, and type of occupation. Thus, this case study compares the differences in evoked magnetic field responses from the somatosensory cortex in two flutists of the same age and sex, one with focal hand dystonia and the other without central or peripheral neurologic defects. Both were members of a professional orchestra.

cult music for long periods under stressful conditions. In November 1996, she began ha ving difficulty when she played the flute, described as "clumsiness" of digits 4 and 5 of the left hand . After the Christmas-New Year break, the problem seemed to have resolved, but over the next few months after the season began again, her dexterity slowly declined and the diagnosis of focal hand dystonia was made. N.N. investigated the possibility of having botulinum injections, but she came to the conclusion that this was not an option. She was determined to get better. After trying a variety of treatments that were not helpful, however, she came to the United States, to the Peter Ostwald Health Program for Performing Artists in San Francisco. The neurologist confirmed the diagnosis of focal hand dystonia and referred her to a physical therapist for more extensive somatosensory testing.

Presenting Signs and Symptoms When N.N. was playing the flute, extension of the metacarpophalangeal joint and involuntary flexing of the interphalangeal joints of the ring and fifth fingers of the left hand were clearly observable. Biofeedback confirmed that both the flexors and extensors were firing when D4 and D5 were observed curling. She had mild neural tension of the brachial plexus in the area of the thoracic outlet, and postural asymmetry, including a forward head and forward shoulders. She had limited internal rotation of the left shoulder, and she felt that 04 and 05 were weak compared with the other fingers on the involved hand as well as with 04 and 05 on the uninvolved hand. Pronation of the hand with minimal axial loading was evident, flattening the carpal and oblique arches. N .N. was completely independent in personal care, household management, and community integration. She exercised regularly at the gym and enjoyed backpacking.

Medical History N .N. was otherwise healthy, with no other medical problems. In addition to her performance in the symphony, she performed regularly as a soloist and in chamber groups, recorded for radio, and taught flute privately. She recently married but had no children.

CASE HISTORY

Initial Evaluation

History of Injury

Findings from the magnetic resonance image of the brain were normal. Magnetoencephalography was used to measure the somatosensory evoked magnetic fields generated from light taps to the fingers . A 37channel Biomagnetometer (MAGNES Biomagnetic Imaging System, Biomagnetic Technologies Inc. [BTl], San Diego, California) was used to measure these responses. Stimulus-related fields were recorded under a 13.4-cm circular sensory area over the pri-

J.M. is a 36-year-old female flutist without any neuromuscular or musculoskeletal complaints, who plays regularly in an orchestra. N.N. is a 36-year-old female flutist with focal hand dystonia. Both are white, and both have been playing the flute for more than 20 years. N.N. was the second flutist in a symphony orchestra for almost five years, playing diffi-

October-December 2000 303

(8 ) Right hemi . : l "got I

~

(8) . R'gIll hem!. : L dlgll.

~

100

' 00

· ' 00 .~

.,sa .,(1)

' 00

::I.,. . . ,~~~-- : ,. . -,~-: §: .M

. ' 00

-SO

50

leo

150

:PUC lEI l8It hclmI. : R cIgIl 3

'OIl

lC

... ~

C> III . :1OC

~

. Ml:-_~ ,OO::--." -:-::-~--:::"~'-::: OO---::'"

g

20< (G ~ len heml. : R cIgIl 4

W

,oe

50

~ (F) RIghI MmI . : llJgll 3 ' 00

100

E

•

I SO

·200

so

100

' 50

§:

.,

CD lC

g

. ,sa ~.:-:: ,oo::--:... ~~---:': ..::--:'=OO---:':,IO

-g

(HI. RI~I hemi . : L lIgft 4

,

c. . . . .

1::1

ai

' 00 • l ilt

.>DO

.:PUC

. tWJ

. 100

·50

0

50

~

>DO (F) RIghI heml . : L digit 3

' 00

c:

·'00

~

r.-....«J.~

~

. '5O~.~ IDO::---50 -:-::-~--::::-~"-: so ' 00 ISO

g

200 (tt) . Righ t heml. : L dllIft 4

W

' 00

o ~_"''''.11

· ' 00

·200 · ' 00

so

·50

' 00

ISO

'---- -- -so - -

·,so ·'00 -so

200

200 (I) Lell hem!. : R dIg01 5

>DO (J) . Right hem !. : L digit 5

100

'00

100

' 00

· ' 00

· ' 00 .~

· ' 00 . 2OC

-' 00

·200 0

TI"' I'1

so

100

I!.O

. 150

· 100

·50

0 50 Tme(_1

' 00

' SO

C> III -200

(0 ). Left 1Ieml. : R dIgOt •

" 00

(J) Rlg hl hem!. : L di gtl 5

. .~...

. 1\O-'100-.5O---50~-'00---~'"

~

. 1SlO.:--.~ 'OO::--.50 -:-::-~---::::--~-:-:: so '00 150

.

· 150

200 (I) l en hem!. : R ~t 5

.ISO · 100·SO

'DO

.>DO

lC

...

:2

~'"

·'00

' SO

· ' 00

f---".~-

g~

100

dill" 2

' 00

C · 100 C> .>DO

i

so

·so

zoo (0). RIght heml. : l

W ' 00

t ~_ _" "•

.'50 -'00

150

1--............-

. , 5O

~

·,oe

100

o S '-------------,

c

~C

so

.~

~

...

0

(0). RI~1 hem!. : l lIgft 2

~

. 100

-50

,so

' 00

100

' 00

no

·200

.1SO ~.~ ' OO::--:." ~-::O:-:":: ":-'-::: OO---::'50 Tmo I' 1

· ISO · IOO·SO

0

SO

""" 1'1

FIGURE 1. Somatosensory evoked magnetic responses measured by magnetoencephalography for digits 1 through 5 in a normal female flutist. These images represent normal patterns of somatosensory evoked responses following a tap on the finger (the tap stimulus indicated by the rectangle at 00 msec) . The peak amplitude responses (60-67 fT on the left side and 83-92 fT on the right) occurred between 40 and 44 msec and were the second oscillation after stimulus. The neuronal pool was consistent in its response, and the actiVIty quietened quickly after stimulation. On average, three half-cycle oscillations occurred over 150 msec, the defined data collection period. The evoked neuronal response was similar on both sides for latency and density, but the amplitudes of the firing were greatest on the dominant (right) side.

FIGURE2. The degradationof the evoked somatosensory response on the rightand theleft hands ofa flutist with focal hand dystonia. Twofingers were consideredinvolved, the left ringandlittlefingers (digits 4 and 5) of theleft hand. Some backgroundneuronal activity wasevident even during the resting state, making it difficult to see the stimulus onset marker at 00 msec. Bilaterally, the peak amplitudeof thefirst responseoccurred early (approximately 26-3 2 msec on the involvedside and 35-36 msec on the uninvolvedside). The amplitudesof the responses werereducedfor theaffecteddigits and increased for the unaffected digits of the involved hand. The evoked magnetic responses were variable, even in the uninvolved digits. On average, four half-cycle oscillations occurred between 0 and 150 msec. The pattern of firing wastheleast well organized for the involved digits (4 and 5) on the leftside.

mary sensory cortex. The peak amplitude response was selected within 20 to 70 msec post-stimulus (400-500 msec interstimulus interval). The peak response data were fitted to an equivalent current dipole model with a signal to noise ratio greater than 4, a goodness of fit greater than 0.95, and a minimal confidence volume less than 300 mm". From the evoked magnetic field response data, the following parameters were measured: pattern of neuronal response, latency (msec), amplitude (IT), density (nA-m), location (em), and finger spread (em).

Data Analysis

Diagnosis The medical diagnosis was focal dystonia of the hand. The impairment was a loss of motor control of digits 4 and 5 on the left hand during flute playing and the performance of other, similar tasks. The disabilitywas the inability to keep her job as the second flutist in the symphony. 304 JOURNAL OF HAND THERAPY 2000

The differences between the healthy flutist and the flutist with dystonia are reported descriptivel y. Statistical analysis was not suitable for comparing findings from two case studies.

RESULTS The neuronal response of the normal flutist was similar to that of other normal subjects. The latency was between 40 and 44 msec. The initial evoked response after stimulation had a small amplitude. The peak amplitude was 67 to 91 IT. Three half-cycle oscillations followed the sensory stimulus. The evoked magnetic responses were consistent across the excitable neuronal pool. The latency was similar for digits 1 to 3 and digits 4 and 5 on both the right and the left and simi-

lar in amplitude on digits 1 to 3 and 4 and 5. However, the peak amplitude response was greater on the dominant (right) side, and the density was reduced in digits 4 and 5 compared with digits 1 and 3 on both sides (Figure 1]). The evoked magnetic field responses of the flutist with focal ha nd dystonia we re less consistent and were clearly different from those of the control subject (Figure 2]). Specifically, the latencies of the magnetic field responses following stimulation on the TABLE 1. S oma to sen sory Hand Represen tation as Measured b y Magnetic S o u rc e Imaging, f or a Healthy Flutist (C ontrol) and a Flutist with Foc al H and Dystonia (FHD)

Left (Affected) Side Uninv.

Inv.

Dl, D2, D3 D4, D5

Right (Unaffected) Side Uninv.

Inv.

Dl, D2, D3 D4, D5

Latency (rns):

involved and uninvolved sides were shorter for the flutist with focal hand dystonia (26 to 36 msec) than for the control subject (40 to 44 msec). The peak amplitudes of the neuronal responses occu rred earl y and were highest for the uninvolved digits on the involved side for the flutist with focal hand dystonia. The peak amplitude for digits 1 to 3 on the involved side of the flutist with focal hand dystonia (85 fT) was also higher than the peak amplitude for the healthy flutist (68 fT) . For the flutist with dystonia, the peak amplitude of the evoked sensory responses for digits 4 and 5 on both sides was approximately 65% lower than the amplitude for digits 1 to 3. For the healthy flutist, the peak amplitude for digits 4 and 5 was slightly lower (9%) than for digits 1 to 3 . In both flutists, the consistency (density) of the evoked mag netic responses was grea tes t for d igits I , 2, and 3 compared with digits 4 and 5 on both the righ t and left sides (Table 1). This consis tency of the responses was similar for the healthy flut ist and the flutist with focal hand dystonia for the involved as well as the uninvolved digits. The location of the digits was not consistent for the two subjects. On the x axes, the digits of the flutist with dystonia were located more anteriorly than the same digits of the control flutist; this was true on the affected and unaffected sides (Figures 3 and 4). The location of the digits on the y axis for the patient with dystonia was more lateral on both the affected and unaffected sides for all the digits (Figures 5 and 6). On the z axis, the digits for the patient with focal hand dystonia were more superior on the affected side and were not progressively sequential from 01 to 05 (i.e., from inferior to superior), compared with those of the healthy flutist. However, on the right side (the unaffected side for the patient with focal hand dys tonia), the locations of all the digits for both subjects were dis similar on the x and z axes (Figures 7 and 8). The spread of the digits on the x, y, an d z axes (the distance along the axis devoted to the five digits) was greatest on both the affected and the unaffected side in the flutist with hand dystonia compared with the healthy flutist. The spread was determined by subtracting the difference between the location of digit 5 from the locatio n of digit I on each axis.

FHd

32.09 (1.93)

26.06 (5.91)

35.09 (1.71)

36.40 (5.55)

Control

40.66 (8.65)

40.32 (1.59)

43.97 (1.87)

43.12 (0.79)

FHd

84.79 (13.58)

56.44 (6.45)

96.04 (30.90)

58.29 (7.64)

Control

67.58 (5.82)

60.11 ( 13.21)

90.99 (11.37)

82.74 (21.12)

FHd

12.15 (2.11)

9.59 (0.23)

14.98 (5.55)

7.86 (1.32)

Control

11.60 (2.09)

9.82 (3.02)

13.09 (1.58)

10.54 (2.52)

FHd

2.80 (0.54)

2.92 (0.18)

2.24 (0.41)

1.41 (0.04)

Control

1.12 (0.66)

0.68 (0.15)

0.182 (0.03)

0.156 (0.04)

FHd

4.78 (0.25)

4.08 (0.14)

4.00 (0.30)

4.325 (0.445)

Control

3.81 (0.21)

3.69 (0.02)

3.84 (0.20)

3.80 (0.08)

FHd

8.74 (0.47)

9.19 (0.09) .

9.03 (0.01)

9.23 (0.09)

D ISCUSSION

Control

8.15 (0.03)

8.21 (0.71)

9.05 (0.17)

9.57 (0.05)

Variability in hand representation has been reported in musicians who heavily use the left hand, compared with normal subjects/" In addition, the spread of the digits of the left hand was grea ter than the spread on the right hand in string players. In this study, the primary differences in somatosensory representation betw een the flutist with focal hand dys tonia and the he althy flu tist were related to the

Amplitude (IT):

Density (nA-m):

Location (em):

x axis-

y axis -

z axis-

NOTE: Somatosensory evoked potentials were in response to taps to each segment of the finger s. The parameters of the neuronal response are summarized her e. These parameters describe the pattern of firing. Values are expressed as means, with 50s in parenthese s. Uninv. indicates uninvolved; inv., involved. The spreads were as follows: Flutist with FHD--left : x = 1.23, Y = 1.23, z = 1.0; right: x = 1.49, Y =1.36, Z = 1.75; heal thy flutist (controD-left: x = 0.52, Y = 0.80, Z = 0.94; right: x = 0.53, Y = 0.46, Z = 0.84.

October-Decemb er 2000 305

3.5

3 2.5

2

/

/

1.5

2.5

»

~

0.5

0.5

~

"

...

•

•

•

•

01

02

03

04

05

o 02

01

03

04

05

FIGURE 3. Differences in location, on the x axis, of the digits

on the involved (left) side,for the control (solid diamonds) and the subject with focal hand dystonia (open squares). Values are expressed in centimeters.

6

FIGURE 4. Differences in location, on the x axis, of the digits

on the uninvolved (right) side, for the control (solid diamonds) and the subject with focal handdystonia (open squares). Values are expressed in centimeters.

6

--

5

4 3

4

....

:::.:..... ~

1

1

o

o 02

03

04

05

FIGURE 5. Differences in location on the y axis of the digits on

the involved (left) side,for thecontrol (solid diamonds) and the subject with focal hand dystonia (open squares). Values are expressed in centimeters.

9.8 9.6 9.4 9.2

~

»>:...

"U-

3 2

01

<:

5

2

8.8 8.6 8.4 8.2 8

...--"\.

1

o

9

0--"

1.5

.--- .....

1

2

01

02

03

04

05

FIGURE 6. Differences in location on the y axisof thedigits on

the uninvolved (right) side, for the control (solid diamonds) and the subject with focal handdystonia (open squares). Values are expressed in centimeters.

9.6

/

<,

~

»<:>

»<:>

9.4

~ ..0-

~

/

9.2 9

-l-------+------,~------_j

8.8 8.6 8.4

8.2 01

02

03

04

05

FIGURE 7. Differences in location on the z axis of the digits on

the involved (left) side,for the control (solid diamonds) and the subject with focal hand dystonia (open squares). Values are expressed in centimeters. 306 JOURNAL OF HAND THERAPY 2000

01

02

03

04

05

FIGURE 8. Differences in location on the z axisof thedigits on

the uninvolved (right) side, for the control (solid diamonds) and the subject with focal handdystonia (open squares). Values areexpressed in centimeters.

organization of the response, the latency of the response, the amplitude of firing, the consistency of the response pattern (density), and the location. The latency of the neuronal response to a finger tap was shorter for the musician with dystonia than for the healthy flutist. This response was approximately 20% faster in the flutist with dystonia than in the healthy flutist. These findings suggest that the flutist with dystonia had the potential to discriminate between multiple impulses coming rapidly into the skin. However, it is possible that the rapid alternating movements become so fast that the somatosensory cortex interprets them as simultaneous, losing the ability to differentiate the separate and sequential tactile inputs. As sensory differentiation is compromised, the sensorimotor feedback loop is compromised, and normal motor control may be disrupted. The gain may be too high, as in this patient with evoked magnetic fields that have a short latency, a high amplitude, and excessive firing in the late phase (>100 msec) . Thus, there could be excessive motor activity, including involuntary co-contractions of the flexors and extensors or what is defined as a lack of reflex inhibition. In the healthy flutist, the density of the neuronal response was similar across all digits. However, in the flutist with focal hand dystonia, the density of the response in the involved digits (digits 4 and 5) was less than that in the uninvolved digits (digits 1 to 3). Although most people complain of reduced control of digits 4 and 5, no differences in the somatosensory representations of those digits have been documented in otherwise healthy musicians.P" A high-density neuronal response represents consistency of neuronal firing. Therefore, it seems likely that the digits with the least control should have a lower density. It may be hard to draw conclusions about the ability to perform sensory discrimination tasks, but it could be inferred that the quicker response indicates a sort of "heightened state" that allows the cortex to respond more rapidly. It is difficult to interpret variations in the location of the digits. Not only were the locations of the digits different in the flutist with hand dystonia, but the patterns of finger location did not always correspond to the sequential order of the fingers, from digit 1 to digit 5. In other words, the digit order (from digit 1 to 5) should correspond to digit locations, from inferior to superior (z axis), anterior to posterior (x axis) , and medial to lateral (y axis).35,54 Thus, ordinarily, digit 5 would be more superior than the other digits. In the flutist with dystonia, digit 4 was usually more anterior, more lateral, and more superior than digit 5. The differences in latency, amplitude, density, and organization of neuronal responses between the normal healthy flutist and the flutist with focal hand dystonia were apparent on both the affected and unaffected sides. This finding has also been reported in primate studies of focal dystonia.29 It is not clear

whether this represents a risk for potential d egradation and ultimate surfacing of problems on the other side or whether it is compensatory. Reports of patients with bilateral focal hand d ystonia are not uncommon. F In the healthy flutist, there were no differences in latency between digits 1 to 3 and digits 4 and 5 on either the right or the left side or between right and left hands. However, the amplitude of firing for the normal healthy flutist was higher on the right than on the left for all digits. In the subject with focal hand d ystonia, the latency of the involved digits (4 and 5) on the affected side was shorter than for digits 1 to 3. However, the amplitude was reduced for digits 4 and 5 on both the involved and the uninvolved side. In both flutists, the consistency of firing was less for digits 4 and 5 than for digits 1 to 3 on both the right and the left sides. This may be consistent with selfreports by some musicians that they do not feel as coordinated with rapid alternating movements of digits 4 and 5 as with those of digits 1 to 3. In general, the differences in the patterns of the evoked magnetic fields between the healthy flutist and the flutist With dystonia are striking. The normal flutist had a very consistent pattern of response across the digits, with the peak amplitude response occurring as the second half-cycle oscillation, slightly before 50 msec . The evoked magnetic responses of the patient with dystonia were less consistent, with four to five half-cycle oscillations (compared with three to four for the healthy subject) and the peak amplitude response usually the first oscillation, occurring between 25 and 40 msec after stimulus onset.

CONCLUSION This case study reports on the differences in somatosensory organization of the hand in a healthy flutist and a flutist with focal hand dystonia. This comparative study adds to the evidence that a somatosensory sensory deficit underlies the involuntary movement patterns imposed on voluntary task performance of patients with focal hand dystonia. Compared with non-musicians, both musicians in this study had neuronal responses of short latency and high amplitude. Furthermore, the musician with dystonia had bilateral problems in sensorimotor feedback, as indicated bya peak amplitude response before 40 msec and more than four half-cycle oscillations. Sensory degradation was also measured in terms of the digit location on the hand representation. This case report validates the sensitivity of magnetoencephalography for documenting differences in somatosensory representations of the hand. This type of measurement can be used to clarify the level of impairment prior to the initiation of treatment as well as to monitor progress in reorganization following treatment. With more extensive studies, it may also October-December 2000 307

be possible to predict change in voluntary control based on changes in somatosensory representation. Eventually, it might also be possible to use magnetoencephalography to identify patients at risk for focal hand dystonia. For example, if the homunculus of the extremities driven by high levels of repetition were measurably degraded but no abnormal motor movements were present, early attention to modify handuse patterns and begin sensory discrimination training might prevent the onset of disabling focal hand dystonia.

REFERENCES 1. Fry H. Overuse syndromes in musicians 100 years ago: an historical review. Med J Austr.1986;146:62Q-5. 2. The Bureau of National Affairs. Cumulative Trauma Disorders in the Workplace: Costs, Prevention, and Progress. Washington, DC: NBA, 1991. 3. Pitner M. Pathophysiology of overuse injuries in the hand and wrist. Hand Clin.1990;6:355--65. 4. Lederman RJ. Focal dystonia in musicians: clinical features. Med Probl Perform Art. 1991;6:132--{j. 5. Cohen L, Hallet M. Hand cramps: clinical features and electromyographic patterns in focal dystonia. Neurology. 1988;38: 1005-12. 6. Jankovic J, Shale H. Dystonia in musicians. Semin NeuroL 1989;9:131-5. 7. Sheehy M, Marsden C. Writer's cramp: a focal dystonia. Brain. 1982;105:461-80. 8. Newmark J, Hochberg F. Isolated painless manual incoordination in musicians. J Neurol Neurosurg Psychiatry. 1987;50: 291-5. 9. Gilman S, Junek L, Young A. Cerebral metabolic activity in idiopathic dystonia studied with positron emission tomography. Adv NeuroL 1988;50:231--6. 10. Rutledge J, Hilal S, Silver A, Defendini R, Fahn S. Magnetic resonance imaging of dystonic states. Adv NeuroL 1988; 50:265-75. 11. Hochberg F, Harris S, Blartert T. Occupational hand cramps: professional disorders of motor controL Hand Injury Sports Perform Art. 1990;6:427-8. 12. Marsden C, Sheehy M. Writer's cramp. Trends Neurosci. 1990; 13:148-53. 13. Wilson F, Wagner C, Homberg, Moth J. Interaction of biomechanical and training factors in musicians with occupational cramps/focal dystonia. 1991;4(supp l):292--{j. 14. Rhoad R, Ster, P. Writer's cramp-a focal dystonia: etiology, diagnosis, and treatment. J Hand Surg. 1993;18:541-4. 15. Tempel L, Perlmutter J. Abnormal cortical responses in patients with writer's cramp. Neurology. 1993;43:2252-7. 16. Deuschl G, Toro C, Matsumoto J, Hallett M. Movement-related cortical potentials in writer's cramp. Ann NeuroL 1995;38: 861-8. 17. Hallett M. Is dystonia a sensory disorder? Ann NeuroL 1995; 38:139-40. 18. Kaji R, Rothwell J, Katayama M, et aL Tonic vibration reflex and muscle afferent block in writer's cramp. Ann NeuroL 1995; 38:155--{)2. 19. Mavroudais N, Caroyer J, Brunk, E, Zegers de Beyl D. Abnormal motor evoked responses to transcranial magnetic stimulation in focal dystonia. Neurology. 1995;45:1671-7. 20. Nakashima K, Rothwell J, Day B, Thompson P, Shannon K, Marsden C. Reciprocal inhibition between forearm muscles in patients with writer's cramp and other occupational cramps,

308 JOURNAL OF HAND THERAPY 2000

symptomatic hemidystonia and hemiparesis due to stroke. Brain. 1989;112: 681-697. 21. Chen R, Tsai C, Lu C. Reciprocal inhibition in writer's cramp. Move Disord. 1995;10:556--{j1. 22. Ridding M, Sheean G, Rothwell J, Inzelberg R, Kujirai T. Changes in the balance between motor cortical excitation and inhibition in focal, task-specific dystonia. J Neurol Neurosurg Psychiatry. 1995;59:493-8. 23. Rothwell J, Oveso J, Day B, Marsden C. Pathophysiology of dystonias. Adv NeuroL 1983;39:851--63. 24. Bates B. The nervous system. In: A Guide to Physical Examination and History Taking. Philadelphia, Pa: Lippincott, 1987:468-524. 25. Lederman R. Occupational cramp in instrumental musicians. Med Probl Perform Art. 1988;3:45-51. 26. Panizza M, Hallett M, Nilsson J. Reciprocal inhibition in patients with hand cramps. Neurology. 1989;39:85-9. 27. Panizza M, Lelli S, Nilsson J, Hallet M. H-reflex recovery curve and reciprocal inhibition of h-reflex in different kinds of dystonia. Neurology. 1990;40:824-8. 28. Charness M. The relationship between peripheral nerve injury and focal dystonia in musicians. Am Acad NeuroL 1993;162: 21-7. 29. Byl N, Merzenich M, Jenkins W. A primate genesis model of focal dystonia and repetitive strain injury, part I: learninginduced de-differentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys. Ann NeuroL 1996;47:508-20. 30. Byl N, Wilson F, Scott P, Oakes A. Sensory dysfunction associated with repetitive strain injuries of tendinitis and focal hand dystonia: a comparative study. J Orthop Sports Phys Ther. 1996;23;234-44. 31. Byl N, Hamati D, Melnick M, Wilson F, McKenzie A. The sensory consequences of repetitive strain injury in musicians: focal dystonia of the hand. J Back Musculoskel RehabiL 1996;7: 27-39. 32. Byl N, Merzenich M, Cheung S, Bedenbaugh P, Nagarajan S. Jenkins W. A primate model for studying focal dystonia and repetitive strain injury: effects on the primary somatosensory cortex. Phys Ther. 1997;77:269-84. 33. Fahn S, Marsden C. The treatment of dystonia. In: Marsden C, Fahn S (eds), Movement Disorders. London, UK: Butterworths, 1987:359-82. 34. Altenmueller E (1998) Causes and cures of focal limb dystonia in musicians. In: Scott R, Black J (eds). Health and the Musician: Proceedings of the 1997 York Conference. London, UK: BAPAM Publications, 1998. Publication G.1-1-12. 35. Chen R, Hallett M. Focal dystonia and repetitive motion disorders. Clin Orthop Rei Res. 1998;351:102--6. 36. Bara-Jiminez W, Catalan, M, Hallett M. Abnormal somatosensory homunculus in dystonia of the hand. Ann NeuroL 1998; 44:838-1. 37. Brin M, Fahn S, Moskowitz C, et aL Localized injections of botulinum toxin for the treatment of focal dystonia and hernifascial spasm. Move Disord. 1987;2:237-54. 38. Cole R, Hallett M, Cohen 1. Double-blind trial of botulinum toxin for treatment of focal hand dystonia. Move Disord. 1995; 10:466-71. 39. Karp B, Cole R, Cohen L, Grill L, Lou J, Hallet M. Long-term botulinum toxin treatment of focal hand dystonia. Neurology. 1994;44:70--{). 40. Pullman S, Greene P, Fahn S, Pedersen S. Approach to the treatment of limb disorders with botulinum toxin A. Arch NeuroL 1996;53:617-24. 41. Ross MH, Charness ME, Sudarsky L, Logigian E1. Treatment of occupational cramp with botulinum toxin: diffusion of toxin to adjacent noninjected muscles. Muscle Nerve. 1997;20:593-8. 42. Tsui J, Bhatt M, Caine S, Caine D. Botulinum toxin in the treatment of writer's cramp: a double-blind study. Neurology.

1993;43:183-5. 43. Van den Bergh P, Francart J, Mourin S, Kollmann P, Laterre E. Five-year experience in the treatment of focal movement disorders with low-dose Dysport botulinum toxin. Muscle Nerve. 1995;18:720-9. 44. Davis D. Ahlskog J, Litchy W, Root L. Selective peripheral denervation for torticollis: preliminary results. Mayo Clin Proc. 1991;55:365-71. 45. Bertrand C, Molina-Negro P, Bouvier G, Gorczyca W. Observations and analysis of results in 131 cases of spasmodic torticolis after selective denervation. Appl NeurophysioL 1987; 50:319-23. 46. Goetz C, Penn R, Tanner C. Efficacy of cervical cord stimulation in dystonia. Adv NeuroL 1988:50:645-9. 47. Waltz M, Davis J. Cervical cord stimulation in the treatment of athetosis and dystonia. Adv NeuroL 1983;37:225-37. 48. Jenkins W, Merzenich M. Reorganization of neocortical representations after brain injury: a neurophysiological model of the bases of recovery from stroke. Prog Brain Res. 1987;71:249-66. 49. Jenkins W, Allard T, Nudo R. (1988). Cortical representational plasticity. In: Raskic P, Singer W (eds). Neurobiology of the

Neocortex. New York: Wiley, 1988:41-67. 50. Jenkins W, Merzenich M, Ochs M, Allard T, Guic-Robles E. Functional reorganization of primary somatosensory cortex in adult owl monkeys after behaviorally controlled tactile stimulation. J NeurophysioL 1990;63:82-104. 51. Merzenich M, Nelson R, Stryker M, Cynader M, Schoppmann A, Zook ], Somatosensory cortical map changes following digit amputation in adult monkeys. J Comp NeuroL 1984;224: 591-605. 52. Recanzone G, Jenkins W, Hradek G, Merzenich M. Progressive improvement in discriminative abilities in adult owl monkeys performing a tactile frequency discrimination task. J NeurophysioL 1992;67:1015-30. 53. Nudo R, Wise B, SiFuentes F, Milliken G. Neural substrates for the effects of rehabilitative training on motor recovery after ischemic infarct. Science. 1996;272:1791-5. 54. Elbert T, Pantev C, Wienbruch C, Rockstroh B, Taub E. Increased cortical representation of the fingers of the left hand in string players. Science. 1995;270,:305-7. 55. Byl N, Topp KS. Focal hand dystonia. Phys Ther Case Rep. 1998;1:39-52.

New ASHT Officers The JOURNAL of HAND THERAPY congratulates the new officers of the ASHT for 2001:

President . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. President-elect Vice President Secretary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Treasurer Treasurer-elect Historian Board Members at Large . . . . . . . . . . . . . . . . . . . . . . . . . . Associate-Affiliate Board Member at Large

Lauren Rivet Ginger Clark Chris Blake Christine Muhleman Bill Walsh Donna Breger-Stanton Sally Ann Buczek Diane Collins Shelli Lucas-Dellinger Jane Pieper-Ispaso Kathryn Langford

October-December 2000 309