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Biomedical subjects

K R Mills

Publications and source records attributed to K R Mills.

At least 91 records · Page 5Linked to original sources

Magnetic brain stimulation: central motor conduction studies in multiple sclerosis.

Central motor conduction (CMC) was evaluated in 32 normal subjects and 83 patients with multiple sclerosis, and the findings were correlated with clinical signs and evoked potential data. CMC time was obtained from the latency difference in responses from the abductor muscle of the little finger to magnetic stimulation of the motor cortex and electrical stimulation at the C-7/T-1 interspace. Mean CMC time in normal subjects was 6.2 msec (SD 0.86 msec), and amplitudes of responses to cortical stimuli were at least 18% of those obtained with stimuli at the wrist. CMC was abnormal in 60 patients with multiple sclerosis (72%); this correlated well with brisk finger flexor jerks (p less than 0.005). CMC was abnormal in 79% of patients with weakness of the abductor muscle of the little finger and in 54% with a normal muscle. Neurological examination was normal in 7 arms with abnormal CMC. Visual evoked potentials were abnormal in 67%, somatosensory evoked potentials in 59%, and brainstem auditory evoked potentials in 39% of those tested. For each procedure more subjects had abnormal CMC and normal evoked potentials than the reverse. The technique is of value for demonstrating and documenting central motor pathway lesions in multiple sclerosis, especially when physical signs are equivocal.

Action Potentials↗

Chronic demyelinating peripheral neuropathy associated with multifocal central nervous system demyelination.

A series of 6 cases is described in which a chronic demyelinating neuropathy was associated with a relapsing multifocal CNS disorder, the clinical features of which resembled multiple sclerosis. Multifocal CNS lesions were demonstrated by CT and MR imaging and the presence of CNS demyelination was indicated by prolonged central conduction times. These cases are discussed in relation to the occurrence of combined peripheral and central demyelination in chronic relapsing experimental allergic encephalomyelitis and neuritis.

Action Potentials↗

Magnetic and electrical transcranial brain stimulation: physiological mechanisms and clinical applications.

The human brain can be stimulated by electric shocks or by brief intense magnetic fields. The latter cause only a trivial scalp sensation. Stimuli exciting the motor cortex cause contralateral muscle responses, but the threshold for excitation is markedly reduced by slight voluntary contraction of the target muscle. For small hand muscles, the overall latency from scalp to muscle is shorter by 1.8 ms when electrical stimuli are used than when stimuli are magnetic. Central motor conduction time (CMCT) can be estimated by stimulating over the scalp and then over the cervical area. In healthy subjects, the CMCT is 6.1 +/- 0.8 (SD) (n = 29). Physiological studies have shown that the facilitation of responses in hand muscles produced by voluntary contraction is also present when contralateral muscles are used, but not when a leg muscle is contracted. The mechanism of facilitation may involve neural activity at both spinal and cortical levels. Single motor units can be caused to discharge by threshold brain stimuli. These motor units are the same ones activated first during weak voluntary contractions. Clinical studies have shown that the CMCT may be greatly prolonged in patients with multiple sclerosis and that subclinical motor pathway lesions can be detected. Central conduction may also be abnormal in patients with motor neuron disease and cervical myelopathy. Side effects have not been encountered with either type of stimulator.

Electric Stimulation↗

Responses in small hand muscles from magnetic stimulation of the human brain.

1. The magnetic field generated by a brief current in a 9 cm diameter flat circular coil varies rapidly with time and when applied over the human scalp it is capable of exciting motor structures subserving the small hand muscles. With a peak magnetic field at the centre of the coil of 0.9-1.6 Tesla, single scalp stimuli produced twitches in the right abductor digiti minimi (a.d.m.), first dorsal interosseous (f.d.i.) and adductor pollicis muscles. Compound muscle action potentials (c.m.a.p.s) and single motor units from these muscles were recorded. 2. The twitch force and corresponding c.m.a.p. were greatly enhanced by voluntary background contraction of the muscle and depended on the direction and intensity of the magnetic field. Response amplitude was maximal with the stimulating coil centred near the vertex but precise coil position was not critical. 3. When the orthodromic volley set up in the peripheral nerve by magnetic stimulation of the brain collided with a maximal antidromic volley set up by stimulation at the wrist, remaining electromyographic (e.m.g.) activity gave evidence of multiple firing of some spinal motoneurones, provided that the muscle exerted a slight voluntary background contraction and the stimulus intensity was above threshold for relaxed muscle. 4. When the muscle changed from total relaxation to a slightly contracted state the onset latency of the c.m.a.p. was shortened by about 3 ms without further change when the background contraction increased. In slightly contracted muscle, c.m.a.p. onset latency was little affected over a wide range of stimulus intensities and was unaffected by the position of the stimulating coil within an area of 6 X 6 cm over the vertex. 5. Single motor units, recorded with needle electrodes in the a.d.m. or f.d.i. muscle, could be caused to discharge at a constant latency by threshold brain stimuli. Different single motor units had latencies varying from 22.4 to 32.1 ms. The same motor unit was activated from different coil positions up to 7 cm apart. These motor units had the lowest thresholds for voluntary activation. Stronger stimuli caused the same motor unit to discharge 1.5 ms earlier. 6. The threshold for excitation of pathways to the a.d.m. muscle was reduced by voluntary contraction of the contralateral a.d.m. and by contraction of the ipsilateral f.d.i. muscles. Using these procedures, the c.m.a.p. of totally relaxed a.d.m. muscle showed a more than 2-fold amplitude increase, a shortening of onset latency to a similar degree as with contraction of the muscle itself, and single motor units in the a.d.m. muscle discharged 1.5 ms earlier.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

McArdle's sign in multiple sclerosis.

A patient with multiple sclerosis is reported in whom neck flexion produced a reversible deterioration in gait and an increase in the degree of pyramidal weakness of the lower limbs. The name McArdle's sign is proposed.

Female↗

Magnetic stimulation of the human brain: facilitation of motor responses by voluntary contraction of ipsilateral and contralateral muscles with additional observations on an amputee.

An intense rapidly changing magnetic field generated in a coil over the scalp can excite motor pathways to hand muscles. With a suprathreshold stimulus, the amplitude of the muscle action potential of the abductor digiti minimi is increased: by weak contraction of the muscle itself, by weak contraction of the ipsilateral first dorsal interosseus, by stronger contraction of the contralateral abductor digiti minimi, but not by contraction of the contralateral first dorsal interosseus, nor by the ipsilateral quadriceps muscle. This facilitation of response to brain stimulation may occur by two mechanisms, one related to the focussing of attention onto a particular hand, the second involving a rise in excitability of homologous motor pathways.

Amputation Stumps↗

Measurement of central motor conduction in multiple sclerosis by magnetic brain stimulation.

Central motor conduction time (CMCT) to abductor digiti minimi was measured in 18 healthy subjects and in 15 patients with multiple sclerosis. A novel percutaneous magnetic stimulator was used to stimulate the motor cortex painlessly and CMCT was calculated by subtracting the onset latency of muscle responses obtained by electrical stimulation over the C7/T1 interspace from that obtained from stimulation over the scalp. In healthy subjects CMCT was 6.0 +/- 0.76 ms. In multiple sclerosis patients with pyramidal signs in the arms, CMCT was almost always prolonged, the longest conduction time being 39 ms. In 10 patients CMCT was prolonged despite normal strength in the muscle.

Action Potentials↗

Electrical stimulation over the human vertebral column: which neural elements are excited?

Supramaximal percutaneous electrical stimuli applied over the human cervical vertebral column produce maximal compound muscle action potentials (CMAPs) in abductor digiti minimi. It is important to know which neural elements are excited by these stimuli and experiments were performed to answer this question. With stimulating electrodes placed progressively lateral to the midline, submaximal CMAPs with the same latency are produced. With shocks over the cervical vertebrae in the midline, the threshold for excitation of arm muscles is much lower than for excitation of leg muscles. Comparison of conduction time from the cervical column to more distal sites on the ulnar nerve by direct measurement and by F wave latency determination shows that the latter exceeds the former by 1.6 msec. Collision experiments in which paired shocks were given at the wrist and Erb's point or the wrist and cervical column showed that recovery from blocking as interstimulus interval lengthened was similar for the two sites, and that it was possible to detect F waves from the proximal stimulus. The latency of CMAPs evoked from midline surface stimuli was identical to that from a needle stimulus near the C8 root. It is concluded that electrical stimuli applied over the cervical vertebrae in the midline excite the motor roots at their exit from the spinal canal. This finding has implications for clinical studies of pyramidal tract and proximal peripheral nerve conduction.

Action Potentials↗

Neurophysiological evaluation of associated demyelinating peripheral neuropathy and multiple sclerosis: a case report.

A case of combined multiple sclerosis and demyelinating neuropathy is presented. Percutaneous electrical stimulation of the cortex and spinal cord has shown that pyramidal tract conduction time was prolonged and conduction velocity in the cord was 4 m/s. Motor conduction velocity in proximal segments of peripheral nerves was slowed to the same extent as in distal segments.

Evoked Potentials↗

Peripheral neuropathy and myopathy in chronic alcoholism.

Nineteen chronic alcoholics referred for investigation of their medical complications and for alcohol re-education were subjected to quadriceps muscle biopsy and detailed peripheral nerve electrophysiological studies. Thirteen patients showed type II muscle fibre atrophy by histomorphometric analysis. The presence of atrophy did not correlate with peripheral neuropathy as determined by clinical examination or with objective indices of nutritional status. There was no association of muscle atrophy with neurophysiological evidence for neuropathy and both occurred independently of each other. It was concluded that chronic alcoholic myopathy was due to a toxic effect of ethanol on the muscle fibres and was not merely secondary to a peripheral neuropathy.

Adult↗

Corticospinal tract conduction time in multiple sclerosis.

Anodal shocks of 400 to 700 V from a low-output impedance stimulator applied percutaneously over the motor cortex evoke muscle action potentials in partially voluntarily activated contralateral muscles. Cathodal shocks from the same device applied to the cervical spinal cord produce maximal ipsilateral muscle action potentials in a relaxed limb. This technique was used to study the central motor pathway in 15 healthy subjects and 8 patients with clinically definite multiple sclerosis. As stimuli were applied in the axilla, over the C7 vertebral level, and over the arm area of the motor cortex, recordings were made of muscle action potentials of forearm flexor muscles. In controls, cord-to-axilla conduction time was 4.1 +/- 0.61 ms, and cortex-to-cord time was 4.4 +/- 0.75 ms. In patients, cord-to-axilla conduction times were normal, while central conduction times were either markedly prolonged (6.4 to 31 ms) or absent. This technique is a potentially powerful tool for the investigation of central motor pathways in healthy subjects and patients with neurological disease.

Adolescent↗

The relationship between mean power frequency of the EMG spectrum and muscle fibre conduction velocity.

Models of the behaviour of the surface EMG signal during fatigue have assumed that there is a linear relationship between the mean power frequency of the EMG spectrum and muscle fibre conduction velocity. They attribute the fall in mean power frequency during fatigue to a proportionate fall in fibre velocity. Experiments have been performed on human vastus lateralis in which forces ranging from 10% to 90% of the maximum force were sustained for times such that the product of the target force and the time was constant. Muscle fibre conduction velocity was estimated using a cross-correlation technique to determine the lag between two EMG signals. The results confirmed the linearity between mean power frequency and fibre velocity. It is still possible, however, that other factors such as de- and recruitment of fibres and change in motor unit firing rates contribute to the fall in mean power frequency during fatigue. Even if these factors are important, the primary assumption of current EMG models relating mean power frequency and muscle fibre velocity has been confirmed.

Adult↗

Orthodromic sensory action potentials from palmar stimulation in the diagnosis of carpal tunnel syndrome.

It is known that the major slowing of nerve conduction in the carpal tunnel syndrome occurs in the palm to wrist segment. A technique exploiting this fact and easily applicable in the routine laboratory would be useful in diagnosing early examples of the condition. To this end, orthodromic sensory potentials from stimulation of digits II and V, and of the palmar branches of the median and ulnar nerves were recorded at the wrist in 53 healthy hands, 72 hands with a tentative diagnosis of carpal tunnel syndrome and in 20 hands of patients with unrelated neurological conditions. Using conventional criteria, 53% of the 72 hands from those suspected of carpal tunnel syndrome were thought to have median nerve compression. When conduction velocity in median palm wrist fibres was taken into account, 67% of hands were then considered abnormal. It is concluded that orthodromic sensory action potentials from palmar stimulation provide a rapid, sensitive and acceptable method of diagnosing the carpal tunnel syndrome.

Action Potentials↗

Muscle fatigue in myophosphorylase deficiency: power spectral analysis of the electromyogram.

It has been postulated that the power spectral shift in the surface EMG during fatigue is due to accumulation of muscle lactate. This hypothesis has been directly tested by measuring such shift in 3 patients with myophosphorylase deficiency who performed sustained isometric contractions of the quadriceps muscle. It was found that the spectral shift in these patients was greater than that in normal subjects, rendering lactate as a cause of this phenomenon very unlikely. The mechanism of excessive fatiguability in myophosphorylase deficiency is thought to be due to failure of excitation of the muscle membrane; further support for this postulate is provided and it is contended that accumulation of extracellular potassium ions may explain the phenomena of spectral shift in normals and myophosphorylase deficient patients and the excessive fatiguability in the latter.

Adult↗