Tetrabenazine induces acute dystonic reactions.

Four patients suffered acute dystonic reactions caused by tetrabenazine. Because dystonic reactions have previously been reported only after dopamine receptor blockade and not with dopamine depletion, it is likely that the ability of tetrabenazine to induce acute dystonia is due to its dopamine receptor blocking properties. Because tetrabenazine can induce acute dystonia even when combined with alpha-methyl-p-tyrosine, presynaptic dopamine stores may not be necessary for these reactions to occur.

Muscle spasms associated with Sudeck's atrophy after injury.

Four patients developed abnormal involuntary movements of a limb after injury. All subsequently developed sympathetic algodystrophy with Sudeck's atrophy and then abnormal muscle spasms or jerks of the affected limb, lasting years. Sympathetic block in three patients did not relieve the abnormal movements. Two patients obtained partial recovery spontaneously, but the other two required surgery for relief. The pathophysiology of this condition remains to be determined but the evidence suggests that it is a distinct, disabling clinical syndrome.

The behaviour of the long-latency stretch reflex in patients with Parkinson's disease.

The size of the long-latency stretch reflex was measured in a proximal (triceps) and distal (flexor pollicis longus) muscle in 47 patients with Parkinson's disease, and was compared with that seen in a group of 12 age-matched normal control subjects. The patients were classified clinically into four groups according to the degree of rigidity at the elbow or tremor. Stretch reflexes were evaluated while the subject was exerting a small force against a constant preload supplied by a torque motor, and the size of the reflex response was measured as fractional increase over basal levels of activity. When stretches were given at random intervals by increasing the force exerted by the motor by a factor of 2 or 3, there was a clear trend for the more severely affected patients to have larger long latency responses in the triceps muscle, although there was no change in the size of the short-latency, spinal component of the response. In contrast, there was no change in the size of the long-latency response of the flexor pollicis longus in any group of patients with Parkinson's disease. Despite any differences in reflex size, the inherent muscle stiffness of both muscles appeared to be normal in all groups of patients with Parkinson's disease, since the displacement trajectory of the limb following the force increase was the same as control values in the short (25 ms) period before reflex compensation could intervene. In 20 of the patients and in seven of the control subjects, servo-controlled, ramp positional disturbances were given to the thumb. Up to a velocity of 300°/s, the size of the long-latency stretch reflex was proportional to the log velocity of stretch. This technique revealed, in both moderately and severely rigid patients, increases in the reflex sensitivity of the flexor pollicis longus, which had not been clear using step torque stretches alone. However, whether using ramp or step displacements, long latency stretch reflex gain was not closely related to rigidity; reflex size was within the normal range in many patients with severe rigidity. Enhanced long latency stretch reflexes thus contribute to, but may not be solely responsible for, rigidity in Parkinson's disease.

Manual motor performance in a deafferented man.

We have studied manual motor function in a man deafferented by a severe peripheral sensory neuropathy. Motor power was almost unaffected. Our patients could produce a very wide range of preprogrammed finger movements with remarkable accuracy, involving complex muscle synergies of the hand and forearm muscles. He could perform individual finger movements and outline figures in the air with high eyes closed. He had normal pre- and postmovement EEG potentials, and showed the normal bi/triphasic pattern of muscle activation in agonist and antagonist muscles during fast limb movements. He could also move his thumb accurately through three different distances at three different speeds, and could produce three different levels of force at his thumb pad when required. Although he could not judge the weights of objects placed in his hands without vision, he was able to match forces applied by the experimenter to the pad of each thumb if he was given a minimal indication of thumb movement. Despite his success with these laboratory tasks, his hands were relatively useless to him in daily life. He was unable to grasp a pen and write, to fasten his shirt buttons or to hold a cup in one hand. Part of hist difficulty lay in the absence of any automatic reflex correction in his voluntary movements, and also to an inability to sustain constant levels of muscle contraction without visual feedback over periods of more than one or two seconds. He was also unable to maintain long sequences of simple motor programmes without vision.

Reliability and efficacy of the long-latency stretch reflex in the human thumb.

1. The amount of positional compensation afforded by the long-latency reflex in the flexor pollicis longus has been investigated in ten normal human subjects. 2. The interphalangeal joint of the thumb was extended by between 2 and 40 degrees at up to 900 deg/s by suddenly increasing the standing force applied to the lever against which the subject was pressing with the pad of the thumb. 3. Electromyographic (e.m.g.) responses at spinal-latency were very small or absent for stretches of this magnitude. The long-latency stretch reflex produced an average positional correction of about 50% for disturbances in the range of 5-25 degrees. The response began to saturate for disturbances of greater than 25 degrees. 4. The e.m.g. response was pulsatile, lasting only some 50 ms, even during continuously increasing disturbances; frequently it terminated despite a remaining positional error. 5. There was a large variation from subject to subject in the average amount of positional correction provided by the stretch reflex. Examination of single responses to the same stretch in individual subjects showed an even greater variation from trial to trial. 6. Variation in the compensation produced by the long-latency stretch reflex from trial to trial could not be explained by the slight variation in size or maximum velocity of the individual stretches.

A grab reflex in the human hand.

The effect of stretching or unloading flexor pollicis longus indirectly has been investigated by altering the force on the wrist while the subject tracked a moving spot on a cathode ray oscilloscope by flexing the top joint of the thumb against a fixed stiff lever. A radialward pull on the wrist, which lifted the thumb off the lever, thereby indirectly unloading flexor pollicis longus, caused a burst of EMG activity about 50 to 60 ms later, rather than the silent period seen at the same latency when the muscle was unloaded directly. A similar burst of activity occurred in the long finger flexors. Letting the wrist go, which caused the thumb to hit against the lever thereby indirectly stretching flexor pollicis longus, produced an initial burst of EMG activity about 50 ms later, as occurred when the thumb was stretched directly; but this was terminated prematurely after about 10 ms by a paradoxical silent period. The response of flexor pollicis longus to indirect unloading was not altered by anaesthetizing the skin of the wrist under the chain pulling it, nor by anaesthesia of the thumb, so was not due to cutaneous stimuli. Nor was it affected by motor point anaesthesia of flexor pollicis longus, so it was unlikely to be due to changes in spindle input from that muscle. However, it was reduced considerably by bracing the arm, suggesting that it arose as a result of movement proximally at the shoulder. The response to indirect unloading of flexor pollicis longus by a pull on the wrist did not occur if the subject held the lever free in his hand, indicating that it was dependent on and adapted to the task. A similar response to a pull on the wrist occurred if the subject was asked merely to hold his thumb and fingers adjacent to a full sherry glass. In these circumstances wrist release also caused a thumb flexion. Such an automatic flexion response or 'grab reflex' helps the subject to maintain contact of his digits with an object when his hand is displaced from it, provided that is his intent. Although the response occurs too early to be voluntary, it depends on the nature of the task and the subject's prior instruction.

Anticipatory postural reflexes in Parkinson's disease and other akinetic-rigid syndromes and in cerebellar ataxia.

We have examined anticipatory postural responses in calf muscles (triceps surae) in response to a small pull to the arm in standing subjects. This stimulus normally evokes a brisk automatic compensatory contraction of the calf muscles. This is not due to calf muscle stretch, for leg movement occurs after the response has appeared. It appears to be driven centrally by input produced by the pull to the arm. Such anticipatory postural responses were present in every one of the 50 normal subjects studied, but were absent or greatly reduced in many patients with Parkinson's disease when compared to age-matched normal subjects, particularly in those exhibiting postural instability. However, a normal anticipatory postural response was elicited in four patients with progressive supranuclear palsy and in a single patient with an akinetic rigid syndrome due to cerebrovascular disease. Cerebellar truncal ataxia only depressed the response in severe cases. We conclude that although these responses may not be necessary to maintain balance, they may be employed in fine adjustment of posture.

Primary writing tremor.

We describe a patient who complained of jerking of the right forearm on writing. Active pronation of his arm produced several beats of pronation/supination tremor. A burst of tremor also could be elicited by tendon taps to the volar surface of the wrist, to the finger extensors, and to pectoralis major, and by forcible supination of the wrist delivered by a torque motor. The subject's writing difficulty and tremor were temporarily abolished by partial motor point anaesthesia of pronator teres. We conclude that the tremor was caused by an abnormal response to muscle spindle input from pronator teres.

Effect of thumb anaesthesia on weight perception, muscle activity and the stretch reflex in man.

1. We have confirmed the results of Gandevia & McCloskey (1977) on the effect of thumb anaesthesia on perception of weights lifted by the thumb. Weights lifted by flexion feel heavier and weights lifted by extension feel lighter. 2. The change in size of the long-latency stretch reflex in flexor pollicis longus or extensor pollicis longus after thumb anaesthesia cannot explain the effect on weight perception by removal or augmentation of the background servo assistance to muscular contraction. 3. During smooth thumb flexion, thumb anaesthesia increases e.m.g. activity in flexor pollicis longus and extensor pollicis longus for any given opposing torque. 4. During smooth thumb extension the opposite occurs: e.m.g. activity in both extensor and flexor pollicis longus decreases. 5. Clamping the thumb at the proximal phalanx to limit movement solely to the interphalangeal joint reduces or abolishes the effect of anaesthesia on both weight perception and e.m.g. activity during both flexion or extension tasks. 6. Gandevia & McCloskey's findings on the distorting effects of thumb anaesthesia on weight perception cannot be used to support the hypothesis of an efferent monitoring system of the sense of effort. Our results emphasize the close functional relationship between cutaneous and joint afferent information and motor control.