Philip D. Thompson

Electric and magnetic stimulation of human motor cortex: surface EMG and single motor unit responses.

1. The effects of different forms of brain stimulation on the discharge pattern of single motor units were examined using the post‐stimulus time histogram (PSTH) technique and by recording the compound surface electromyographic (EMG) responses in the first dorsal interosseous (FDI) muscle. Electrical and magnetic methods were used to stimulate the brain through the intact scalp of seven normal subjects. Electrical stimuli were applied either with the anode over the lateral central scalp and the cathode at the vertex (anodal stimulation) or with the anode at the vertex and the cathode lateral (cathodal stimulation). Magnetic stimulation used a 9 cm diameter coil centred at the vertex; current in the coil flowed either clockwise or anticlockwise when viewed from above. 2. Supramotor threshold stimuli produced one or more narrow (less than 2 ms) peaks of increased firing in the PSTH of all thirty‐two units studied. Anodal stimulation always produced an early peak. The latencies of the peaks produced by other forms of stimulation, or by high intensities of anodal stimulation, were grouped into four time bands relative to this early peak, at intervals of ‐0.5 to 0.5, 1‐2, 2.5‐3.5 and 4‐5.5 ms later. Peaks occurring within these intervals are referred to as P0 (the earliest anodal), P1, P2 and P3 respectively. 3. At threshold, anodal stimulation evoked only the P0 peak; at higher intensities, the P2 or more commonly the P3 peak also was recruited. The size of the P0 peak appeared to saturate at high intensities. 4. In five of six subjects, cathodal stimulation behaved like anodal stimulation, except that there was a lower threshold for recruitment of the P2 or P3 peak relative to that of the P0 peak. In the other subject, the P3 peak was recruited before the P0 peak. 5. Anticlockwise magnetic [corrected] stimulation, at threshold, often produced several peaks. These always included a P1 peak, and usually a P3 peak. A P0 peak in the PSTH was never produced by an anticlockwise stimulation [corrected] at intensities which we could explore with the technique. 6. Clockwise magnetic [corrected] stimulation never recruited a P1 peak; in most subjects a P3 peak was recruited first and at higher intensities was accompanied by P0 or P2 peaks. 7. On most occasions when more than one peak was observed in a PSTH, the unit fired in only one of the preferred intervals after each shock. However, double firing was seen in five units when high intensities of stimulation were used.(ABSTRACT TRUNCATED AT 400 WORDS)

Rhabdomyolysis: A review

Rhabdomyolysis, a syndrome of skeletal muscle breakdown with leakage of muscle contents, is frequently accompanied by myoglobinuria, and if sufficiently severe, acute renal failure with potentially life‐threatening metabolic derangements may ensue. A diverse spectrum of inherited and acquired disorders affecting muscle membranes, membrane ion channels, and muscle energy supply causes rhabdomyolysis. Common final pathophysiological mechanisms among these causes of rhabdomyolysis include an uncontrolled rise in free intracellular calcium and activation of calcium‐dependent proteases, which lead to destruction of myofibrils and lysosomal digestion of muscle fiber contents. Recent advances in molecular genetics and muscle enzyme histochemistry may enable a specific metabolic diagnosis in many patients with idiopathic recurrent rhabdomyolysis.

Stiff man syndrome and related conditions

The stiff man syndrome (SMS) and its variants, focal SMS, stiff limb (or leg) syndrome (SLS), jerking SMS, and progressive encephalomyelitis with rigidity and myoclonus (PERM), appear to occur more frequently than hitherto thought. A characteristic ensemble of symptoms and signs allows a tentative clinical diagnosis. Supportive ancillary findings include (1) the demonstration of continuous muscle activity in trunk and proximal limb muscles despite attempted relaxation, (2) enhanced exteroceptive reflexes, and (3) antibodies to glutamic acid decarboxylase (GAD) in both serum and spinal fluid. Antibodies to GAD are not diagnostic or specific for SMS and the role of these autoantibodies in the pathogenesis of SMS/SLS/PERM is the subject of debate and difficult to reconcile on the basis of our present knowledge. Nevertheless, evidence is emerging to suggest that SMS/SLS/PERM are manifestations of an immune‐mediated chronic encephalomyelitis and immunomodulation is an effective therapeutic approach.

Changes in corticomotor representations induced by prolonged peripheral nerve stimulation in humans

OBJECTIVE Manipulation of afferent input can induce reorganization within the sensorimotor cortex which may have important functional consequences. Here we investigate whether prolonged peripheral nerve stimulation can induce reorganization within the human motor cortex. METHODS Using transcranial magnetic stimulation, we mapped the scalp representation of the corticospinal projection to hand muscles in 8 normal subjects before and after 2h of simultaneous repetitive electrical stimulation of the ulnar and radial nerves at the wrist. Control mapping experiments were conducted in 6 subjects. RESULTS Following nerve stimulation, larger motor-evoked potentials were evoked from more scalp sites. The induced changes were most apparent in first dorsal interosseous, but were also seen in other hand muscles. The increases in area of the representational maps were accompanied by changes in the location of the optimal site for evoking responses in first dorsal interosseous, and changes in the centres of gravity of the maps. CONCLUSIONS Prolonged afferent stimulation induces an increase in excitability of the corticospinal projection. This is accompanied by a significant shift in the centre of gravity of the stimulated muscles which we propose is evidence of a non-uniform expansion in their cortical representation.

Magnetic stimulation over the spinal enlargements.

Magnetic stimulation over the cervical and lumbar spinal enlargements was performed in 10 normal volunteers using a 9 cm diameter coil. Although the threshold and the amplitude of responses depended on the position of the coil and the direction of current flow within it, the latency was constant. The latencies obtained by magnetic stimulation were compatible with those obtained using high voltage electrical stimulation of the spinal nerve roots and always were shorter than the peripheral motor conduction time estimated by F-wave techniques. The site of activation by magnetic stimulation appears to be very similar to that stimulated by the high-voltage electrical method. Stimulation of descending motor tracts within the cord was not possible using the magnetic stimulator.

Pathophysiology of chorea and bradykinesia in Huntington's disease

This article reviews the neurophysiological abnormalities described in Huntingtons disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median‐nerve somatosensory‐evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long‐latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntingtons disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntingtons disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntingtons disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntingtons disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntingtons disease probably reflect the involvement of direct and indirect pathways in the basal ganglia–thalamus–cortical motor circuit.

Reasons for admission to hospital for Parkinson's disease

The management of Parkinson’s disease (PD) tends to focus on the presenting motor syndrome; yet, in the long term, nonmotor complications of the illness and complications of treatment become increasingly troublesome. The aims of this study were to review the reasons for 761 hospital admissions for patients with a diagnosis of PD and to determine the cause of hospitalization. Only 15% were admitted for primary management of the motor syndrome. PD was the secondary diagnosis in 645 admissions. Of the latter, 39% were admitted because of falls leading to fracture, pneumonia, encephalopathy or dementia and hypotension with syncope. Cardiac and gastrointestinal diseases accounted for a further 22% of admissions. Complications of the later stages of PD and associated treatments are more likely to lead to hospital admission than management of the primary motor syndrome. Some of the emergency hospital admissions for PD may be potentially avoidable with better planning of management in the outpatient and community setting.

The distinctive movement disorder of ovarian teratoma-associated encephalitis

The movement disorder observed in four cases of ovarian teratoma associated encephalitis is described. The illness began with neuropsychiatric symptoms and was followed by prolonged unresponsiveness, respiratory failure, and autonomic instability. The movement disorder consisted of semirhythmic repetitive bulbar and limb movements and persisted during prolonged periods of unresponsiveness, diminishing as awareness returned. The characteristics of the movement disorder differed from recognized dyskinesias. It is suggested that interruption of forebrain corticostriatal inputs by anti‐N‐methyl‐D‐aspartate (NMDA) receptor antibodies removes tonic inhibition of brainstem pattern generators releasing primitive patterns of bulbar and limb movement. Recognition of the distinctive movements should prompt a search for an ovarian teratoma since the condition is responsive to tumor resection and immunomodulation.

Percutaneous electrical stimulation of lumbosacral roots in man.

High voltage percutaneous electrical stimulation over the lumbosacral spinal column was used to assess conduction in the cauda equina of 13 normal subjects. Electromyographic activity elicited by such stimulation was recorded from various muscles of the lower limbs. The stimulating cathode was placed over the spinous process of each vertebral body and the anode kept on the iliac crest contralateral to the studied limb. Shifting the cathode in a rostro-caudal direction shortened the response latency in quadriceps, tibialis anterior and extensor digitorum brevis muscles. At moderate intensities (60% maximum), this occurred abruptly when the cathode was placed at levels corresponding to the exit sites from the spinal canal of the roots innervating these muscles. At these intensities, the size of the response in each muscle was largest when the cathode was placed over the conus medullaris or at or below the exit of the motor roots from the spine. Latencies were always equal to or shorter than those obtained with F-wave measurements, suggesting that peripheral motor axons, rather than intraspinal structures were activated by the stimulus. Collision experiments demonstrated that activation occurred at two sites: near the spinal cord and at the root exit site in the vertebral foramina. Recordings made from soleus indicated that larger diameter proprioceptive afferent fibres also could be activated. This technique might have useful clinical applications in the study of both proximal and distal lesions of the cauda equina and provide a non-invasive method of localising such lesions electrophysiologically.

Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor.

Retrospective surveys of specialist movement disorder clinics suggest that 2.1% to 3.3% of patients have psychogenic movement disorders. 1,2 Some movement disorders are more likely to be psychogenic than others. Around 60% of nonfamilial, idiopathic paroxysmal dyskinesias are psychogenic, 3 whereas less than 0.5% of cases of parkinsonism and chorea attending specialist movement disorder clinics are psychogenic. 1,2 Within the setting of a specialist clinic, tremor, jerks, or abnormal limb postures comprise the majority of psychogenic movement disorders. In our experience, as in that of others, up to 10% of tremor and myoclonus cases have a psychogenic aetiology. 1,4,5