Application of duplex Doppler sonography in intracranial carotid dissection.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
P Ashby
Publications and source records attributed to P Ashby.
Intermittent claudication caused by compression of tibial vessels as a result of calf muscle hypertrophy: case report.
We present a case with findings suggestive of popliteal artery entrapment in a patient with intermittent claudication and localized muscle hypertrophy in the calf muscles after removal of a herniated disk. Angiography failed to demonstrate popliteal artery entrapment but instead revealed compression of the tibial vessels caused by calf muscle hypertrophy. The concept of muscle hypertrophy caused by denervation is also discussed.
Humans↗
Bulbo-pontine paralysis with deafness: the Vialetto-Van Laere syndrome.
A Caucasian girl developed slowly progressive sensory neural deafness and bulbar and spinal muscle weakness typical of the Vialetto-Van Laere syndrome. As the condition progressed the major disabilities became dysphagia, respiratory muscle weakness and postural hypotension. Treatment with gastrostomy feedings, oxygen and fludrocortisone acetate produced worthwhile functional improvement.
Adolescent↗
Altered corticospinal projections to lower limb motoneurons in subjects with cerebral palsy.
The projections of cortical neurons activated by transcranial magnetic stimulation to the motoneurons of lower limb muscles were examined in 22 normal subjects and 14 subjects with cerebral palsy (CP). In normal subjects, magnetic stimulation produced strong facilitation of tibialis anterior (TA) motoneurons, but little or no facilitation of soleus (SOL) motoneurons. This differential facilitation of TA and SOL motoneurons was observed at all stimulus sites on the scalp and all stimulus intensities at which responses could be elicited. In subjects with CP, magnetic stimulation produced almost equal facilitation of TA and SOL motoneurons. This could not be explained by differences in the excitability of the respective motoneuron pools. It is postulated that the projections from the motor cortex to spinal motoneurons are altered in CP. These abnormal projections may contribute to the impairment of voluntary movements experienced by these subjects.
Action Potentials↗
Do injuries to the developing human brain alter corticospinal projections?
Experimental lesions of the mammalian brain involving the developing corticospinal pathways may cause these pathways to become redirected. In humans, injury to the developing brain results in disorders of movement known collectively as 'cerebral palsy'. These motor disorders differ from those produced by similar lesions in adults. We present evidence that abnormal corticospinal projections exist in subjects who have had an injury to the brain in the perinatal period. These aberrant connections, which may represent misdirected corticospinal fibers, help to explain the impairment of voluntary movements experienced by these subjects.
Cerebral Palsy↗
An automated technique for measuring the recovery cycle of human nerves.
Action potentials conducted along a nerve fiber leave in their wake consistent alterations in excitability, including the absolute and relative refractory periods, a supernormal period (SNP) and a late phase of subnormality. We describe an automated technique for reliably determining the recovery cycle of human sensory nerve fibers by delivering series of paired stimuli and precisely measuring the latencies (to within 0.5 microseconds) of the compound action potentials. The recovery cycle can be compiled from the differences in latency between the two responses of a pair. Consistent changes in conduction velocity are demonstrated during each phase of altered excitability. Possible physiological mechanisms underlying the recovery cycle are discussed, and the effects of cold, ischemia, prior tetanization and subcutaneous lidocaine are presented. This technique may prove to be a useful and more sensitive tool for the study of certain disorders of peripheral nerves.
Action Potentials↗
Corticospinal projections to upper and lower limb spinal motoneurons in man.
The pattern of muscle activation produced by magnetic stimulation over the human motor cortex has been examined in normal subjects. Magnetic stimulation elicited short latency compound muscle action potentials (CMAPs) from upper limb muscles contralateral to the stimulus and from lower limb muscles bilaterally. In the upper limb, the hand and forearm muscles had the lowest thresholds for activation and the largest CMAPs. There was little or no activation of the more proximal muscles, biceps and tricepts. In the lower limb the extensor digitorum brevis and tibialis anterior had low thresholds and large CMAPs. There was little or no short latency activation of soleus. This pattern of muscle activation remained the same even when the stimulating coil was moved to various locations within a radius of 3 cm from the vertex. Recordings from individual tibialis anterior and soleus motor units indicated that the differential activation of these muscles reflected the relative amplitudes of the short latency postsynaptic potentials produced by magnetic stimulation in their motoneurons. The 'jitter' in the activation of single muscle fibers by magnetic stimulation suggests that these projections are monosynaptic. It is argued that the pattern of muscle activation reflects the projections from the cortex to motoneurons rather than the projections of afferents onto cortical neurons. We conclude that magnetic stimulation can be used to identify the projections of the corticospinal pathways in man.
Action Potentials↗
Monomelic atrophy.
Weakness of distal muscles of one upper limb which progresses over 1 year and then appears to arrest ("monomelic amyotrophy") has been reported mainly in Japan and India. We report 5 cases of a similar syndrome occurring in Canada. In our cases the wasting affected the forearm muscles of one upper limb (sparing brachioradialis and extensor carpi radialis). There was minimal wasting and electromyographic changes in the opposite upper limb. The CT myelogram showed unilateral wasting of the cervical cord.
Adolescent↗
Corticospinal control of soleus motoneurons in man.
Electrical or magnetic stimulation of the human motor cortex causes a strong, short latency facilitation of tibialis anterior (TA) motoneurons but only weak, longer latency changes in the excitability of soleus (SOL) motoneurons. The facilitation of TA motoneurons has been attributed to the monosynaptic action of the "fast" corticospinal pathway. The present study further investigates the cortical control of soleus motoneurons in man. In tests of reaction time to auditory stimuli, normal subjects took significantly longer to activate soleus motoneurons than tibialis anterior motoneurons. Thus we could not demonstrate the existence of a "fast" pathway from the brain to SOL motoneurons that, for some reason, is not activated by magnetic stimulation. The hypothesis that the cortex might control soleus motoneurons indirectly by modulation of the Ia input from muscle spindles was tested. Magnetic stimulation of the cortex was used to condition the facilitation of soleus motoneurons resulting from the stimulation of group I fibres in the tibial nerve. There were no consistent changes in Ia facilitation. We conclude (i) that there is no evidence so far that SOL motoneurons are excited by a direct pathway from the cortex (similar to that projecting to TA motoneurons) and (ii) that the observed changes in firing probability of soleus motoneurons produced by magnetic stimulation over the motor cortex do not result from modulation of presynaptic inhibition of Ia afferents.
Adolescent↗
Alterations in group Ia projections to motoneurons following spinal lesions in humans.
1. The hypothesis that the exaggerated tendon jerks and stretch reflexes that follow chronic spinal cord lesions in humans result from alterations in transmission from group I muscle afferents to motoneurons was tested by making observations on nine normal subjects and 25 patients with spinal cord lesions. All the patients had increased tendon jerks, one-third of them had both increased tendon jerks and increased, velocity-dependent stretch reflexes (i.e.g spasticity). 2. Changes in the firing probability of single, voluntary-activated soleus or tibialis anterior motor units during stimulation of the muscle nerve below the threshold of the alpha-motoneuron axons were used to derive the characteristics of the postsynaptic potentials produced by group I volleys in single motoneurons. Paired stimuli were used to test how multiple volleys in group I muscle afferents were transmitted to motoneurons. 3. Stimulation of the posterior tibial nerve produced a short-latency period of increased firing probability representing the homonymous composite Ia excitatory postsynaptic potential (EPSP) in all soleus motoneurons tested. There was no detectable alteration in the magnitude, duration, or profile of the short-latency facilitation in the patients with spinal lesions when compared with normal subjects. 4. In patients with traumatic spinal cord lesions less than 8 wk in duration the magnitude of the facilitation representing the composite Ia EPSP was significantly larger than normal, although only one out of the four patients in this group had spasticity. 5. In the patients with the greatest spasticity, group I volleys produced a second period of facilitation 11-15 ms after the facilitation representing the composite Ia EPSP. This is presumed to represent enhanced transmission through polysynaptic pathways from group I afferents to motoneurons. 6. In normal subjects the facilitation of motoneurons produced by the second of two group I volleys is greater 5 and 10 ms after the first volley and less 20, 30, and 50 ms after the first volley. These changes involve at least two factors: 1) changes in excitability of peripheral nerves and 2) changes in transmission at the Ia-motoneuron synapse. 7. In patients with spinal lesions the facilitation produced by the second of two muscle-afferent volleys was less depressed at the 30-ms interstimulus interval. 8. Thus two separate abnormalities have been uncovered in human subjects with chronic spinal lesions: 1) a change in the transmission of multiple volleys from muscle afferents to motoneurons and 2) an increase in transmission through polysynaptic pathways from Ia afferents to motoneurons. Both could contribute to the increased tendon jerks and exaggerated stretch reflexes.
Afferent Pathways↗
Reciprocal inhibition in cerebral palsy.
We studied reciprocal inhibition by recording the changes in firing probability of single motor units of the tibialis anterior muscle following stimulation of low-threshold afferents in the posterior tibial nerve. In 15 patients with cerebral palsy, the inhibition was as great or greater than normal. We found no evidence that group I afferents produce "reciprocal facilitation" in cerebral palsy.
Afferent Pathways↗
Cortical-basal ganglionic degeneration.
We report our experience with 15 patients believed to have cortical-basal ganglionic degeneration. The clinical picture is distinctive, comprising features referable to both cortical and basal ganglionic dysfunction. Characteristic manifestations include cortical sensory loss, focal reflex myoclonus, "alien limb" phenomena, apraxia, rigidity and akinesia, a postural-action tremor, limb dystonia, hyperreflexia, and postural instability. The asymmetry of symptoms and signs is often striking. Brain imaging may demonstrate greater abnormalities contralateral to the more affected side. Postmortem studies in 2 patients revealed the characteristic pathologic features of swollen, poorly staining (achromatic) neurons and degeneration of cerebral cortex and substantia nigra. Biochemical analysis of 1 brain showed a severe, diffuse loss of dopamine in the striatum. This condition is more frequent than previously believed, and the diagnosis can be predicted during life on the basis of clinical findings. However, as with other "degenerative" diseases of the nervous system, a definitive diagnosis of cortical-basal ganglionic degeneration requires confirmation by autopsy.
Aged↗
Changes in nerves and neuropeptides in skin from 100 leprosy patients investigated by immunocytochemistry.
The cutaneous innervation is now known to contain neuropeptides including substance P (SP) and calcitonin gene-related peptide (CGRP) in sensory nerves, and vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY), principally in autonomic nerves. Skin biopsies from 100 leprosy patients and equivalent areas from 50 non-leprosy controls were fixed in p-benzoquinone solution for immunofluorescence staining and in Bouin's fluid for classification of leprosy type. Antisera to the neural markers, neurofilaments, and protein gene product 9.5 (PGP 9.5), and to neuropeptides were used. Cutaneous nerves and nerve endings immunoreactive for neuropeptides, neurofilaments, and PGP 9.5 were seen in all non-leprous control cases. In leprosy, PGP 9.5- and neurofilament-immunoreactive nerve fibres were seen in all 14 cases of the indeterminate (early) type and in the majority (33/43) of lepromatous cases, but in a smaller proportion (15/43) of tuberculoid cases. Neuropeptide immunoreactivity was seen in only 2/14 of the indeterminate leprosy specimens and was completely absent in other types. This early disappearance may be of diagnostic significance. Thus, cutaneous sensory and autonomic dysfunctions in leprosy are well reflected by changes in nerve fibres and neuropeptides.
Calcitonin↗
Excitability of corticospinal neurons during tonic muscle contractions in man.
A magnetic stimulus applied to the human scalp over the motor cortex causes a short latency contraction of contralateral limb muscles. This is presumed to result from the indirect excitation of corticospinal neurons with monosynaptic connections to motoneurons. The excitability of these cortical neurons can be estimated from the magnitude of the postsynaptic potentials produced in spinal motoneurons by a given magnetic stimulus. In man the characteristics of these postsynaptic potentials can be derived from changes in the firing probability of single motor units. When a subject increases the level of a sustained voluntary contraction the excitability of the corticospinal neurons estimated in this way becomes less. We conclude that the additional synaptic input to motoneurons required to maintain a stronger muscle contraction comes from fiber systems other than the population of fast corticospinal neurons activated by magnetic stimulation.
Action Potentials↗
Projections of group Ia afferents to motoneurons of thigh muscles in man.
Changes in the firing probability of single motor units in response to electrical stimulation of muscle nerves and to tendon taps were used to derive the projections of large muscle afferents to the motoneurons of various thigh muscles in man. Homonymous facilitation was demonstrated to virtually all of the sampled motor units of biceps (BI), semitendinosus (ST), vastus lateralis (VL) and vastus medialis (VM). Heteronymous facilitation was readily demonstrated between VM and VL but was never obtained from ST to BI and never unequivocally obtained from BI to ST. Reciprocal inhibition was demonstrated from femoral nerve afferents to all of the sampled units of BI, and ST but reciprocal inhibition of VM or VL was never obtained from BI afferents and infrequently from ST afferents. These projections of group I afferents in man show certain specific differences from those of the cat and baboon that may reflect the normal function of the limb.
Action Potentials↗
How synaptic noise may affect cross-correlations.
The relationship between a postsynaptic potential (the 'test PSP') and the profile of the cross-correlation that it produces in a repetitively discharging mammalian motoneuron, with and without synaptic noise, has been explored by computer stimulation. In a noiseless motoneuron the cross-correlation profile represents the first derivative of PSP shape except where 'shadowing' occurs (Eqn. 1a-c). When synaptic noise is present the relationship changes. When the amplitude of spike-like 'noise PSPs' occurring at regular intervals reaches a critical value (Eqn. 2), all threshold crossings involve noise PSPs. Under these circumstances termed 'just maximally effective synaptic noise', the cross-correlation represents test PSP directly (Eqn. 3a). When the interval between noise PSPs is shortened the relationship reverts to the first differential (Eqn. 4a-c). If the amplitude of the noise PSPs is less than the critical value (Eqn. 5) the cross-correlation profile is represented in a complex way by a combination of the first derivative of the upper part and the direct representation of the lower part of the test PSP. The area of the cross-correlation peak above baseline provides the most reliable estimate of EPSP amplitude in a noiseless motoneuron (Eqn. 6a). This area may fall to half for the same triangular test EPSP in the presence of just maximally effective synaptic noise (Eqn. 7a). In general, the presence of synaptic noise leads to underestimation of EPSP amplitude. These general principles remain valid for physiological noise consisting of randomly occurring EPSPs and allow certain experimental findings in cat motoneurons to be understood.
Animals↗
Reciprocal inhibition following lesions of the spinal cord in man.
1. Reciprocal inhibition was studied in normal subjects and patients with spinal cord lesions by stimulating the posterior tibial nerve below the threshold of the soleus alpha-motoneurone axons and recording the changes in firing probability of single tibialis anterior motor units activated by voluntary contraction. A short-latency (about 35 ms) period of decreased firing probability was assumed to represent reciprocal inhibition. 2. For a given stimulus intensity this inhibition was greater in patients with spinal lesions than in normal subjects. 3. The stimulus intensities at which soleus motoneurones and the Ia inhibitory interneurones were brought to threshold provided an estimate of the relative excitability of these two neural populations. In the patients with spinal lesions the Ia inhibitory interneurones were more excitable than soleus motoneurones, whereas in normal subjects the excitabilities were approximately equal. 4. Stimulation of the posterior tibial nerve below the threshold of alpha-motoneurone axons also resulted in a second period of inhibition with a latency of approximately 50 ms. This was less prominent in the patients with spinal cord lesions. 5. It is concluded that transmission through the pathways mediating reciprocal inhibition of flexor muscles during their voluntary contraction is enhanced following a spinal cord lesion in man but that a later inhibitory process is depressed.
Adult↗
Afferents contributing to the exaggerated long latency reflex response to electrical stimulation in Parkinson's disease.
Reflex pathways to tibialis anterior motoneurons from low threshold afferents of the common peroneal nerve were examined in 13 Parkinsonian subjects and 12 age-matched normals. Post-synaptic events occurring in single motoneurons were derived from changes in the firing probability of single voluntarily activated motor units during afferent stimulation. A period of increased firing probability of "monosynaptic" latency (about 33 ms) occurred in all subjects in both groups. A second, later, period of increased firing probability (latency about 64 ms) was seen in 2/12 normals and 8/13 Parkinsonian subjects. Neither of these responses could be produced by cutaneous stimulation. The electrical threshold of the afferents mediating the later effect was 0.82 of the threshold of alpha motoneuron axons which is similar to that of the afferents mediating the shorter latency response. Thus, large non cutaneous afferents contribute to this long latency response in man presumably through polysynaptic pathways. Transmission in these pathways is enhanced in Parkinson's disease.
Adult↗