Articles - Use the links below to find two articles by Professor Leslie J Findley, MD., F.R.C.P, consultant neurologist, and medical advisor to the National Tremor Foundation.

ESSENTIAL TREMOR

TREMOR IS DEFINED as an involuntary rhythmical oscillation of a body part. It occurs as a normal process in all parts of the body, but under normal circumstances is barely visible. This "normal" tremor is caused by the interaction of a number of processes such as the heartbeat and minute, spontaneous contractions of muscle fibres. When a healthy person becomes anxious, frightened or stressed the tremor becomes exaggerated.

It is then clearly visible and can interfere with manual dexterity, e.g., holding a cup and saucer. This exaggeration of normal tremor is produced by increased levels of adrenaline in the blood, resulting in simultaneous and regular contractions of large groups of muscle fibres.

SOME INDIVIDUALS, however, experience continuous tremor, similar to exaggerated normal tremor, even in the absence of stress and anxiety. When other recognised causes of tremor are absent (e.g., thyroid disease, fever, anxiety state and specific disorders of the nervous system) such patients are defined as having essential tremor (ET). This type of tremor frequently runs in families and approximately fifty percent of such patients have an immediate relative with tremor.

ET IS NOW RECOGNISED as an extremely common disorder. Its prevalence in the general population is not known precisely but estimates have varied from three to 55 per thousand, and it is many times more common than Parkinson's disease (PD). Community studies have shown that only a small percentage of people who suffer with ET seek specialist advice and many sufferers simply regard "the shakes" as a family characteristic.

ET CAN OCCUR AT ANY AGE, though it more commonly commences in the older age groups. It is not associated with other symptoms, for example the stiffness and slowness of movement seen in other disorders such as PD. It most commonly presents as tremor of the hands, most noticeable when the hands are held outstretched or engaged in movement, particularly fine movements. Any body part may become affected as well, frequently the head, voice and legs. The term "benign" is often applied as ET does not have the sinister progression seen in some other disorders of the nervous system and it does not affect life expectancy. However, many sufferers find their persistent tremors at best a cosmetic nuisance and, at worst, disabling in many activities of daily living.

MANY PATIENTS, on first noticing tremor, fear that they may have PD or that this condition may convert into PD. It now should be emphasised that a number of studies have shown that patients with ET are not at increased risk of developing PD.

ET, IN IT'S APPEARANCE, is very similar to the exaggeration of normal tremor and thus was once considered to be produced by similar processes. Laboratory studies of normal tremor have shown that it is dependent upon peripheral nerve circuits between the muscles and spinal cord (technically known as peripheral reflex feedback). Studies on patients with ET have shown that although the peripheral nerves are important in the maintenance of tremor, in the majority of cases the tremor is principally "driven" from a higher level of the nervous system, i.e., the brain itself.

THE CENTRE OF ORIGIN OF ET is not known. Unlike PD, in which there are characteristic changes in specific parts of the brain, no structural abnormalities have been found in ET. However, this information is based on only a few studies carried out in the 1960s on brains from patients with ET dying from other causes. Further studies using modern techniques of pathologic examination may provide evidence of structural abnormalities in parts of the brain concerned with the control of movement. For a complete discussion of this subject, see "The Pathology of Essential Tremor" by Dr. Mi H. Rajput.

A FURTHER AVENUE OF INVESTIGATION has been to study tremor mechanisms in laboratory animals. While some success has been achieved in PD, there is no good animal "model" of ET to assist us. It has been shown that certain drugs can produce tremors in animals mimicking ET and that rhythmic electrical discharges in collections of brain cells in the lower part of the brain (brain stem) are responsible for the origin of this tremor. Very recently, using a form of brain scanning called positron emission tomography (PET), it has been possible to show increased activity in these same areas in humans with ET.

SINCE THIS APPARENTLY SIMPLE DISORDER results from many interdependent processes in the brain, spinal cord, peripheral nerves and muscles, it is doubtful whether the mechanism of ET will prove to he entirely attributable to any single structure or functional abnormality.

CLEARLY, MORE RESEARCH into the causes and treatments of ET is needed. Further autopsy studies are required and, to this end, a "brain bank" has been set up in the United Kingdom so that patients can make provision for the use of their brain tissue after their deaths.

NEWER AND HIGHER-POWERED METHODS for brain scanning, including PET, are allowing us to visualise the structure and functioning of the brain in patients with ET. These lines of research will further our understanding of the processes involved in ET and will assist in the development of more effective treatments.

TO DATE, ET RESEARCH has not received a sufficiently high level of interest and financial support from grant-giving institutions and the worldwide pharmaceutical industry. The formation of the International and National Tremor Foundation has provided a voice for patients with ET and its expansion may help to stimulate increased research funding.