Neurophysiological evaluation of the central nervous impulse propagation in patients with sensorimotor disturbances (original) (raw)
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Transcranial cortical stimulation in disorders of the central motor pathways
Journal of Clinical Neuroscience, 1997
Motor evoked potentials (MEPs) were studied in 63 patients with disorders affecting central motor pathways. These were classified into five subgroups: motor neuron disease (16), multiple sclerosis (13), cerebral infarction (19), spinal cord lesions (10) and hereditary spastic paraplegia (5). Three patients with hysterical paraplegia were also studied. Results were compared to those obtained from 30 normal subjects. In normal subjects the mean central motor conduction time (CMCT) was 6.4 ms (range 3.4-8.1 ms, SD 1.0 ms) for abductor digiti minimi and 13.2 ms (range 9.7-17.0 ms, SD 2.3 ms) for tibialis anterior. Amplitude of the cortical MEPs was defined as a percentage of the size of the peripheral compound muscle action potential (CMAP) and ranged from 14 to 85%. Fifteen of 16 patients with motor neuron disease and all patients with cerebral infarction, multiple sclerosis (MS), spastic paraparesis and non-MS spinal lesions had abnormal studies including low amplitude, :dispersed or absent responses and prolonged CMCTs. Patients with MS had markedly prolonged CMCTs. In three cases of hysterical weakness MEPs were within normal limits. MEPs are a useful method to detect pathology in the central motor pathways and may have a significant role in the diagnosis of disorders involving the upper motor neuron.
1997
Motor evoked potentials (MEPs) to magnetic trans cranial stimulation (TCS) were recorded in 47 patients with amyotrophic lateral sclerosis (ALS) in order to evaluate both excitability and conductivity changes relating to central motor pathways. The results were compared with those obtained from a control population of 43 subjects, 34 patients with definite multiple sclerosis (MS) and 15 patients with a rigid early form of Parkinson's disease (PD). The excitability threshold to TCS was higher in ALS patients for both upper and lower limbs compared with both controls and PD patients, but lower than that of MS patients. The Silent Period duration (SP (hand recordings): 80.1 ms, SD: 38.5) was significantly shorter in ALS patients than in all the other examined subjects (P Ͻ 0.001), nor did it increase proportionally to TCS intensity as with control subjects. The abnormal behavior of the SP appears to be specifically linked to the ALS disease, since it was neither observed in PD patients, nor in those with multiple sclerosis, who, on the contrary, displayed a prolonged mean duration of the SP (161.6 ms, SD 77 vs. 115.7 ms, SD 62 for the control group). Due to the neuronal loss of the largest neurons in ALS, MEP latency, amplitude, duration and the motor central conduction time (CCT) were in different proportion found abnormal. Our study shows how different neurological diseases with central motor involvement share broadly similar MEP abnormalities, but a different involvement of the silent period. We suggest that in ALS patients there may be abnormalities of motor cortical inhibitory mechanisms which are detected with the measurement of the SP. The distinctive 'depression' of this parameter in the case of ALS could be a significant marker for diagnosing this disease.
Stimulation of motor tracts in multiple sclerosis
Journal of Neurology, Neurosurgery & Psychiatry, 1988
Percutaneous electrical stimulation of the motor cortex was used to evaluate corticospinal conduction to upper-limb motoneurons in 29 patients with multiple sclerosis. Central motor conduction abnormalities were correlated with clinical signs and somatosensory evoked potentials. Muscle responses to cortical stimulation were altered in 20 patients. The most common abnormality was increased central motor conduction time; in two cases the responses to cortical stimulation were absent. Abnormalities were also present in patients with no clinical evidence of corticomotoneuron deficit. Alterations of muscle responses and of somatosensory evoked potentials were usually correlated, but may appear independently. Both testing methods are useful in the study of patients with multiple sclerosis.
Stimulation of motor tracts in motor neuron disease
Journal of Neurology, Neurosurgery & Psychiatry, 1987
The muscle responses evoked by cortical and cervical stimulation in 11 patients with motor neuron disease were studied. The muscle potential in the abductor pollicis brevis, evoked by median nerve stimulation and the somatosensory potential evoked by wrist stimulation were also studied. In eight of 11 patients there was absence or increased central delay of the responses evoked by cortical stimulation. In four patients muscle responses on cervical stimulation and muscle action potentials on median nerve stimulation were also altered, indicating peripheral abnormalities. Somatosensory responses evoked by wrist stimulation were normal. Electrophysiological techniques are helpful in estimating the site of motor involvement in motor neuron disease.
1987
The complexities of interpreting results of electrical stimulation of the motor cortex in pathological states are discussed and illustrated by reference to results from a variety of patients with diseases affecting the upper motor neurone (multiple sclerosis, cervical spondylosis and myelopathy, motor neurone disease, hemiparesis due to cerebral infarction, and hereditary spastic paraplegia). The abnormalities of the electromyographic (EMG) responses after anodal cortical stimulation consisted of delay in the latency to onset, dispersion or reduction in response size or even absence of EMG responses. These changes were not confine6 to any specific condition or pathology. Previous work has suggested that the sequence of events that follow anodal cortical stimulation involves repetitive excitatory inputs to spinal motoneurones and transmission across at least one central synapse. Accordingly, delayed latencies may not exclusively indicate slowing of motor conduction, while the absence of any response may not indicate complete failure of conduction in corticomotoneurone pathways.
Journal of Neurology, Neurosurgery & Psychiatry, 1988
Magnetic stimulation of the brain and spinal column was used to assess conduction in the descending central motor pathways controlling arm and leg muscles of 20 patients with multiple sclerosis, and 10 normal subjects. The multiple sclerosis patients had relapsing and remitting disease but all were ambulant and in stable clinical remission. Increased central motor conduction times (CMCTs), up to three times normal, were frequently encountered in multiple sclerosis patients and in leg muscles these correlated closely with clinical signs of upper motor neuron disturbance; in the upper limb muscles a higher proportion of subclinical lesions was present. Weak muscles were almost invariably associated with abnormal central conduction but increased CMCTs were also found for 52 of the 104 muscles with normal strength. CMCTs for lower limb muscles were directly related (p < 0-005) to functional motor disability (Kurtzke and Ambulatory Index Scales). No patient developed clinical evidence of relapse during follow-up of at least 8 months. Magnetic brain stimulation is easy to perform, painless, and safe, and provides clinically relevant information in the diagnosis and monitoring of multiple sclerosis patients.
Far-field and cortical somatosensory evoked potentials in motor neuron disease
Muscle & Nerve, 1990
We examined median somatosensory evoked potentials (SEPs) in 26 patients with sporadic motor neuron disease (MND). SEPs were recorded with multiple scalp derivations, using both the midfront and the earlobe as references for each subject. Central conduction time (CCT) was abnormal in three patients, but only when using the midfront reference. Moreover, an exclusive alteration of the early prerolandic potentials (absent or delayed P20 and/or P22) was noted using the earlobe reference in amyotrophic lateral sclerosis and in progressive bulbar palsy (54% and 50% of patients, respectively) but not in progressive muscular atrophy. These findings correlated with clinical evidence of upper motor neuron signs and with the severity of the disease. In agreement with recent views regarding the sources of the early anterior cortical responses, neuronal loss in the motor cortex may be considered as affecting the generator sites of these potentials.