Manual Therapy (1998) 3(2), 108-109 © 1998 Harcourt Brace & Co Ltd

Letters to the Editors

B L A D D E R SYMPTOMS: WARNINGS TO PATIENTS

I wish to report on the case of a woman of 29 years of age, with a history of severe back pain and left sciatica, who had an emergency laminectomy for a sudden total loss of function of the sensory components of the sacral nerves 1, 2, 3 and 4 and motor loss in sacral 1.

I was treating her post-surgery and once I got to know her, was able to establish that immediately prior to the onset of numbness and weakness there were none of the 'red flags' that we would normally associate with risk of damage to the sacral roots. She never had any paraesthesia in the legs or saddle area, nor did she have any bilateral pain in the legs.

She reported having had very severe back pain and sciatica for 3 weeks and had sought help from her gen- eral practitioner and a casualty department both of whom told her to rest. In distress she visited a chiroprac- tor who manipulated her. She reported that it appeared to help a little at the time, but 3 hours later she coughed and was immediately relieved of all pain. It seems that she was not alarmed by the sensory loss and was totally unaware of the disastrous consequences of nerve com- pression. She went to bed in compression-induced peace and had the first good night's sleep for weeks. Only the next morning did she realize that she was unable to pass urine, and, on seeking advice, entered the surgical emergency track which confirmed a massive central protrusion at L5 level, compressing all the sacral roots.

Sadly, she has had no recovery after 2 months and is now very distressed that no one had warned her about the consequences of such symptom changes.

In view of this I wonder if we should consider advis- ing more patients about the seriousness of sensory changes and alerting them to potential alterations to bladder function. While we have to be careful not to alarm every patient with back pain perhaps we should include those with signs and/or symptoms of acute nerve root impingement which could be the result of an invertebral disc lesion.

Elizabeth Grieve PhD, MCSR DipTR MMACP

Address supplied

FOCAL DYSTONIA IN A MUSICIAN

Jane Kember has published an interesting report about focal dystonia in musicians. I believe that two refer- ences not cited by Kember are important to this topic (Manual Therapy 1997; 2: 221-225).

Michael Mezernich, Professor of Physiology at University of California, has published two studies demonstrating the neurophysiological basis for focal dystonia and repetitive strain (occupational overuse syndrome or OOS) in monkeys. The OOS produced in monkeys is defined by degradation in motor perfor- mance - only one of their four monkeys had overt pain. Whether monkey OOS is equivalent to human OOS is unknown.

Female monkeys were used in both studies. The rea- son for confining the studies to females was not stated - perhaps this was to match the predominance of OOS in women.

In both studies monkeys were deprived of food for 20-22 hours before each experiment to motivate them to behave in exchange for food rewards. The monkeys had to reach their arm through a tube to fix arm and body position for the task. They were trained to grasp a hand grip made from two half cylinders individually moulded to each monkeys' hand. The monkeys had to grip these cylinders precisely with all five fingers.

The first study involved two monkeys who performed a passive gripping task more than 400 times per day, 6 days a week (Byl et al 1996). When the monkey had grasped its thumb and fingers in the precise position a light flashed and the cylinders moved apart on their own power (a 6.4 mm excursion for the monkeys fingers). If the monkey kept its grip during the opening and closing it was awarded with a food pellet. Hence they were required to maintain a passive grip - very little force was needed. The monkeys trained between 1100 and 3000 hand openings per day to achieve 80-90% accuracy.

After 12-25 weeks both monkeys developed OOS with focal hand dystonia manifest by reduced accuracy, speed and efficiency of movement. Monkey 1 devel- oped tendinitis of the trained hand, manifested by reduced task performance, licking and sucking its thumb. This tendinitis subsided after a rest period of 8 days. Monkey 2 changed her hand dominance outside training activities.

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Letters to the Editors 109

Electrophysiological mapping of the cerebral cortex contralateral to the trained hand showed abnormally large receptive fields within digit segments and between digits, loss of the normal separation between digits, and multiple receptive fields extending across digits. These results suggest that OOS in monkeys is more than a sim- ple peripheral biomechanical problem; there are major cortical changes.

The second study involved two different monkeys in an active gripping task using the same apparatus (Byl et al 1997). When the monkeys squeezed the handpiece with a force of 80 gm, the handpiece vibrated at 250 Hz for 1.5 seconds. A light went on and the monkey had to slide the handpiece towards themselves. To receive a food pellet reward they had to maintain contact with all five fingers during the entire cycle.

Both monkeys initially performed repetitive hand opening and closing with an articulated hand-squeezing technique. Monkey 1 continued this method whereas monkey 2 decided to perform this task using a proximal arm pulling process. Monkey 2 also refused to practise for more than 30 minutes at a time (she could have a brilliant future as an ergonomist!).

Monkey 1 developed overuse signs by 20 weeks of training. These signs included a drop in accuracy from 80-90% to 50%, a 30% fall in task rate, marked diffi- culty opening and closing the hand and difficulty retrieving food from the food tray (the dysfunction spilled over to daily tasks and was not confined to experimental behaviour). However, there was no evi- dence of inflammation or pain in monkey 1 or 2. Monkey 2, who chose the arm pulling strategy, expe- rienced no signs of overuse; accuracy remained 80-90% and speed was maintained. There was no way to determine whether the arm pulling strategy, the break of training in 30 minute periods or both factors in monkey 2 actually prevented focal dystonia and OOS.

The brain mapping required surgery to expose the surface of the sensory cortex. Somatosensory brain maps were severely distorted in both hemispheres of monkey 1, even though the training was with the domi- nant arm. This suggests that the transition of local to dif- fuse OOS could be related to bilateral somatosensory cortical changes. Monkey 2 had only mild changes in the somatosensory cortex.

Mezernich speculates that human focal dystonia associated with OOS may occur through these mecha- nisms:

1. repetitive work that is rigidly stereotyped involving the hand degrades the sensory representation of indi- vidual fingers

2. the potential for OOS is much higher when repetitive motion simultaneously engages body parts which are ordinarily differentiated. Simultaneous stimulation of the thumb, fingers and palm is abnormal

3. to cause OOS, behaviour must be intentional.

Automatic behaviour does not greatly alter neural plasticity.

Mezernich recommends task variation for avoiding human focal dystonia and OOS. Task variation, even if only minor, refines rather than degrades the sensory rep- resentations in the parietal cortex.

Treatment of the cortical sensory disturbance requires re-differentiation of sensory feedback informa- tion and movement, which might be accomplished using repetitive cognitively demanding tasks to restore degraded sensory representations. Thus treatment of focal dystonia with OOS may require sensory re- training.

References

Byl N N, Mezernich M M, Jenkins W M 1996 A primate genesis model of focal dystonia and repetitive strain injury: I. Learning- induced dedifferentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys. Neurology 47: 508-520

Byl N N, Mezernich M M, Cheung S, Bedenbaugh P, Nagarajan S S, Jenkins W M 1997 A primate model for studying focal dystonia and repetitive strain injury: effects on the primary somatosensory cortex. Physical Therapy 77:269-284

Paul Friedman FRACP

Address supplied

Author's response

The research papers by Michael Mezernich show a pos- sible link in the causative factors in human focal dysto- nia. My thanks to Paul Friedman for drawing attention to them as I had not come across them in my literature search.

Looking at the people whom I have treated, a large proportion of players have performed or practised for many hours, over a long period of time before the dysto- nia occurred. The other dominant cause seems to be pre- vious trauma, spinal or peripheral, disturbing the normal function of the limb.

The fact that overuse causes a dysfunction rather than pain is a significant factor when taking a patient's history. Pain may follow later if adaptive movements are used to try to overcome the dysfunction.

The knowledge that disturbed sensory input occurs after continuous, intentional movement patterns gives us an opportunity to restructure practice and playing habits, the emphasis being on preventative measures such as postural awareness and stretches. Specific sensory retraining is an aspect that I shall investigate further as I have dealt with it in a broad sense only.

I should be interested to hear from therapists treating focal dystonia in musicians and can be contacted at The Elgin Physiotherapy Clinic, 4 Elgin Road, Alexandra Park, London N22 4UE, UK.

Jane Kemher MCSE MMACP

© 1998 HarcourtBrace & Co. Ltd Manual Therapy (1998) 3(2), 108-109