Upper Motor Neuron Lesion Research Articles

F response in vascular and degenerative upper motor neuron lesions

The F response represents the recurrent discharge of a small percentage of the motoneuron pool activated antidromically by any single impulse delivered to the nerve. We studied F waves from median nerve stimulation in 22 controls, in 30 patients with spasticity after cerebrovascular accident (CVA), and in 4 patients with familial spastic paraplegia (FSP). The following parameters were analyzed: median nerve conduction velocity, median nerve M response amplitude (M), average amplitude of 16 F responses (F16); persistence of F response (Fp) defined as the percentage of measurable responses to 16 stimuli, average amplitude of F response expressed as percentage of maximal M amplitude: (F16/M%). Results showed that Fp, F16 and F16/M% values were significantly increased on the spastic side of CVA patients and in FSP. Our findings indicate that after upper motor neuron lesions (whatever etiology and course) a change in the frequency of recurrent discharge and/or in the total number of lower motor neurons capable of backfiring occurs. Therefore, F response reflects the hyperexcitability state of the lower motor neurons in spasticity.

Excessive muscular fatigue in patients with spastic paraparesis

We used intermittent tetanic contractions and 31P magnetic resonance spectroscopy to investigate human tibialis anterior muscle metabolism and fatigability in a group of patients with spastic paraparesis and in normal controls. During intermittent tetanic stimulation, the decline in tension was significantly greater in patients than in controls, and the half-relaxation time of the tetanus was more prolonged. Moreover, the decline in phosphocreatine and intracellular pH was significantly greater in patients than in controls. These observations suggest that biochemical changes in the muscles of patients with upper motor neuron lesions may contribute to their excessive fatigability.

Enhancement of Sexual Function and Fertility in Spinal Cord-Injured Males

Trauma to the spinal cord in males may result in both erectile dysfunction and infertility. Reflex erections may be preserved in upper motor neuron lesions and psychogenic erections in lower motor neuron or incomplete lesions. There are numerous reports of abnormalities of testicular biopsies that may relate to increased scrotal temperature and other factors. Techniques to restore erections include intracavernous injections of vasoactive substances, vacuum tumescence constriction therapy and penile prostheses. All have potential adverse affects. When reflex function in the sacral cord is present, fertility can be improved by vibratory ejaculation. Subcutaneous physostigmine or electroejaculation may benefit individuals with intact fibers from the sympathetic outflow. This paper reviews sexual dysfunction in spinal cord-injured males with a focus on management techniques.

Clonus in man: a rhythmic oscillation maintained by a reflex mechanism

The mechanisms underlying clonus were studied in 7 patients with spasticity of the lower limbs arising from upper motor neuron lesions. Clonus sensitivity to resetting was studied by evoking a soleus H reflex at different time intervals between two successive clonic beats. The relationship between the interval separating the H reflex from the preceding beat and the inter-beat interval in which the H reflex was delivered was used to calculate the resetting index. A high resetting index, close to 1.0, was found. Calf compression, applied to the upper third of the leg to block group I afferent fibres from gastrocnemius-soleus muscle, completely abolished ankle clonus within 10 min of the onset of compression. Clonus disappearance was preceded by a progressive reduction in duration and frequency. Finally, evidence is presented that clonus duration is contingent upon joint angle and therefore presumably on the amount of stretch placed on the triceps surae muscle group. Our findings demonstrate that clonus is largely dependent on reflex and mechanical factors and do not confirm the recent hypothesis that clonus relies on a central spinalgenerator.

Modulation of the bulbocavernosus reflex during voiding: loss of inhibition in upper motor neuron lesions.

The bulbocavernosus reflex (BCR) is a sacral segmental reflex which is suppressed throughout most of micturition. The BCR was evaluated by recording the associated EMG activity using a concentric needle electrode placed in the external urethral sphincter. The influence of the central nervous system (CNS) on the BCR was studied in 29 neurologically normal individuals and in 33 patients with upper motor neuron (UMN) lesions and voiding dysfunction. Ninety percent (26/29) of the neurologically normal patients did not have a BCR during most of micturition. By comparison, all the patients with an UMN lesion had a positive BCR beginning early during voiding. The finding of suprasegmental modulation of the BCR during voiding demonstrated by external urethral sphincter EMG was a more sensitive although slightly less specific sign of UMN bladder dysfunction than detrusor sphincter dyssynergia; uninhibited bladder contractions were neither sensitive nor specific for UMN lesions.

Multi-beat clonus in a patient without an upper motor neuron lesion. A case report

The authors present a case of five-beat clonus in the absence of a central nervous system pathologic condition. As data obtained from the literature demonstrate, clinicians should be aware that multi-beat clonus is not always associated with upper motor neuron lesions.

Spasticity: Quantitative Measurements as a Basis for Assessing Effectiveness of Therapeutic Intervention

Spasticity, a common problem in upper motor neuron lesions, frequently results in uncontrolled involuntary motion that interferes with function. A quantifiable method related to the mechanical output of the muscle is needed to test and improve therapeutic intervention. A sinusoidal displacement of 5 degrees was used to measure elastic and viscous stiffness around the ankle at frequencies from 3 to 12Hz. To isolate viscoelastic response, the influences of inertia and equipment drag were eliminated. Test-retest correlation values were 0.953 for elastic and 0.992 for viscous stiffness. The elastic stiffness in 13 spastic subjects under nerve block was significantly higher than that of 13 healthy subjects (p less than or equal to 0.05), indicating early changes associated with contracture. Elastic and viscous response is expressed by the total stiffness vector containing both components, the Nyquist diagram. This diagram's pathlength from 3 to 12Hz was calculated and showed high test-retest reliability in healthy subjects. The median pathlength value for the spastic group was 98 Newton-meters/radian (N-m/rad) and, for the normal group, 24N-m/rad, a statistically significant difference (p less than or equal to 0.0001). A mathematical model of the spastic response shows that the Nyquist diagram's pathlength relates to reflex loop gain and is independent of the shift in passive properties. The model predicts a shift in passive properties during spastic responses relative to responses measured during nerve block. Thus, subtraction of passive responses measured during nerve block may not isolate the remaining reflex response, but the pathlength measure relating to the reflex response gain was unaffected, allowing evaluation of therapeutic intervention effectiveness.

Therapeutic Electrical Stimulation of the Lower Limb by Epimysial Electrodes

The problem of inadequate hip stability prevents many patients with head trauma, stroke, or spinal injury from balancing on one limb in order to take a step. There is no adequate orthotic substitute for hip instability, and electrical stimulation with surface electrodes cannot effectively activate the deep hip muscles. This report describes a clinical program in which electrical stimulation via surgically placed electrodes is combined with routine tendon lengthening and transfers and physical therapy. The electrodes are fixed to the epimysium and the leads directed subcutaneously to exit the skin at a common site for attachment to a commercially available stimulator. Preliminary results indicate that functional muscle contractions of the deep hip muscles can be obtained with epimysial electrodes and that stimulation can be used to augment walking ability. The results demonstrate the safety and effectiveness of percutaneous electrical stimulation and contribute to the development of a practical, implanted stimulation system for patients who do not regain hip instability after an upper motor neuron lesion.

Neurologic Sequelae Following Interferon Therapy of Juvenile Laryngeal Papilloma

Human leukocyte interferon at doses from 2 million units every two days to 3 million units daily was given to a 2-year-old boy for the treatment of recurrent juvenile laryngeal papilloma. After 7 months of treatment the child developed spastic diplegia, which persisted despite the discontinuation of interferon therapy. The clinical picture was consistent with an upper motor neuron lesion; no evidence of peripheral neuropathy was found.

External Sphincter Dyssynergia: An Abnormal Continence Reflex

Some of the characteristics of detrusor-external sphincter dyssynergia were examined in 14 patients with traumatic upper motor neuron lesions within 44 weeks of injury. The sacral evoked response latencies of the male patients were shortened at any time after injury. A continence reflex could be demonstrated in most patients at any time after injury. Comparing averaged values for the group at 4-week intervals, resting pressure at the external urethral sphincter and post-void residual volumes reached nadirs at 12 weeks while voiding efficiency peaked at this time. Thus, voiding function appears to be optimal 12 weeks after injury. During reflex detrusor activity, increases in external urethral sphincter electromyographic activity and external urethral sphincter pressure were associated clearly with a positive slope of the intravesical pressure trace, whereas decreases in both parameters were associated with a negative slope. Voiding occurred only during a negative slope. Although propantheline induced detrusor areflexia, episodic peaks in external urethral sphincter pressure and electromyographic activity continued to occur. We propose that external sphincter dyssynergia, which is independent of detrusor contraction, is the continence reflex exaggerated owing to the loss of supraspinal influences. We believe that the multiple patterns of dyssynergia described previously by others are variations, largely owing to technique, of the single pattern we have observed. The observation of synergic-like urethral responses in some patients during a negative slope of the intravesical pressure, even with complete suprasacral spinal lesions, implies existence of a pathway for synergic-like voiding in the spinal cord.

Neurogenic vesico-urethral dysfunction in children with cerebral palsy.

20 children with severe cerebral palsy and history of urinary incontinence and recurrent urinary infection underwent radio--and neuro-urologic evaluation. Vesico-ureteral reflux was found in 7 patients. In 9, who had presented episodes of urine sub-retention, a urodynamic study demonstrated detrusor muscle hyperreflexia in all, deficit of vesicourethral sensation in 5 and detrusor-sphincter dyssynergia in 2. These functional findings are compatible with an upper motor neuron lesion, and may be the cause of episodes of altered bladder emptying, and consequently, urinary infection.

Somatosensory conduction in vitamin B12 deficiency

We tested the hypothesis that the somatosensory central conduction time (CCT) can reveal central nervous system involvement in vitamin B12-deficient patients when this cannot be established on clinical grounds alone. Three patients with pernicious anemia and without clinical signs of upper motor neuron lesion had a striking increase of CCT. This increase was shown to be reversible in 1 patient who improved over 3 years of treatment. Detailed analysis of the CCT showed that the decrease of conduction velocity occurred in the posterior columns, whereas the conduction was normal at the thalamo-cortical level. We conclude that CCT is a useful parameter to localize and quantify central nervous system disease in vitamin B12 deficiency.

Respiratory muscle weakness associated with cerebellar atrophy.

Transdiaphragmatic pressures were measured in 3 patients with cerebellar atrophy. Recordings were made during 3 types of voluntary maneuver--maximal sniffs, full inspirations, and maximal static inspiratory efforts, and during bilateral supramaximal phrenic nerve stimulation at 1 Hz. Although diaphragmatic weakness was demonstrated during the voluntary maneuvers, transdiaphragmatic pressures recorded during phrenic nerve stimulation were normal. These findings indicate that diaphragmatic dysfunction, probably caused by ataxia during voluntary maneuvers, may occur in association with cerebellar atrophy. In the presence of diaphragmatic weakness, normal values of transdiaphragmatic pressure during phrenic nerve stimulation may suggest an upper motor neuron lesion affecting the diaphragm.

Long-term follow-up of spinal cord injury patients with vesicoureteral reflux.

The medical records of 32 spinal cord injury patients with 43 vesicoureteral refluxes admitted to our hospital from 1970 to 1982 were retrospectively reviewed. These patients were followed yearly with pyelograms together with cystograms or cystourethrograms. Many of these individuals were on an indwelling Foley catheter at the time reflux was detected, indicating that free urinary drainage such as a Foley catheter did not prevent reflux formation. Further, the majority of refluxes developed 1-2 years post-injury, and some disappeared spontaneously without causing any damage to the urinary tract. However, the indwelling Foley catheter was ineffective for reflux treatment because in the long run it did not prevent progression of vesicoureteral reflux and did not protect the refluxing kidney from damage. We also noticed that the incidence of reflux was statistically higher in patients with complete spinal lesion than in those with incomplete neurological dysfunction. This incidence was also higher in individuals with an upper motor neuron lesion.

Transcutaneous muscle stimulation promotes muscle growth in immobilized patients.

Muscular activity is a fundamental determinant of muscle mass. Transcutaneous muscle stimulation (TMS) may reverse muscle atrophy and lean mass loss in immobile patients by "artificial exercise." Four paraplegic patients with upper motor neuron lesions entered The Ohio State University Clinical Research Center for a 21-day metabolic balance study. After 6 days of baseline monitoring, each underwent isometric tetanic contractions (15 sec on; 45 sec off) of all major lower extremity muscle groups with TMS for 10 hr daily. Cross-sectional areas of muscle plus bone were calculated with CAT scan planimetry at 7 levels in both lower extremities before and after the TMS period. Three patients completed the metabolic balance study. TMS produced significant growth of innervated thigh and calf muscles in all paraplegic patients. Little growth occurred where bone and tendon predominate. No significant changes in nitrogen balance (urine and stool excretion), potassium balance (urine excretion only), or phosphate balance (urine excretion only) could be demonstrated. Two possible explanations are (1) that the patients may have been underfed and (2) that perhaps due to an increase in metabolic rate owing to the stimulation, lean tissue in other locations may have been mobilized to meet leg muscle demands. Future studies will incorporate metabolic monitoring of oxygen consumption and CO2 production during the experiment.

Evaluation and Primary Management of Spasticity

Spasticity is often a lifelong manifestation of central nervous system damage in adults with upper motor neuron lesions. Practitioners who initiate the management of spasticity when damage occurs are more likely to offer the patient a life without permanent joint deformity. Spasticity may be helpful or harmful to the patient, but in either event warrants a careful assessment and management plan based upon current health care concepts. Two general intervention principles and three specific intervention measures, including the use of medication, are discussed.

Urethral sphincter dyssynergia in spinal cord injury patients.

On the basis of several hundreds of urodynamic investigations done in 105 SCI patients the phenomenon of urethral sphincter dyssynergia was studied. In Upper Motor Neuron Lesion (UMNL) patients, dyssynergic contractions of the external urethral sphincter during spontaneous bladder contractions were demonstrated in 86% and, during bladder contractions initiated by suprapubic tapping, also in 86%. CREDE manoeuvre or abdominal straining gave an augmentation of the urethral sphincter activity in 53%. Interrupted tapping could lower a dyssynergic sphincter activity in a great number of UMNL patients. This technique of bladder stimulation was important to acquire a balanced bladder function in 28% of the patients. In patients with a non-contracting detrusor, a non-relaxing sphincter or augmentation of the sphincter spasticity with the crédé manoeuvre or abdominal straining was found in at least 50%. The values of different forms of conservative treatment and of sphincterotomy are discussed. The final outcome of the bladder reeducation is given.

Central motor conduction is abnormal in motor neuron disease.

Conduction in the central motor pathways of the brain and spinal cord was studied in 12 patients with motor neuron disease. Six healthy volunteers served as controls. Transcutaneous electrical stimulation of the cortex, cervical cord, thoracic cord and conus medullaris was used to determine motor latencies to the biceps brachii, thenar eminence and tibialis anterior muscles. Prominent, and often asymmetrical, slowing of central motor conduction was demonstrated in seven of the 12 patients; these findings were most marked in the spinal cord and in most cases correlated with clinical features of corticospinal involvement. In general it was more difficult to excite motor pathways in the central nervous system in the patients with motor neuron disease than in control subjects. Evidence of subclinical involvement of central motor pathways was found in five patients. The central lesion in motor neuron disease may thus contribute more significantly to the clinical deficit than has been realised, since the clinical signs of the upper motor neuron lesion are often masked by the more obvious lower motor neuron features.

Stretch and vibration reflexes of wrist flexor muscles in spasticity.

The surface electromyographic (EMG) reflex responses of the voluntarily contracting flexor carpi radialis evoked by 'stretch' and by tendon vibration have been compared in patients with spasticity of the upper limb, arising from upper motor neuron lesions, and normal subjects. Reflex responses to 'stretch' comprised increases in EMG activity lasting up to 100 ms which were often divided into 'short' and 'long'-latency peaks. The short-latency responses of spastic patients were increased in size compared with those of normal subjects whereas later activity was commonly reduced or absent. In both groups vibration elicited short-latency, essentially phasic responses with activity falling back to or below the background level within 50 ms despite continuing stimulation. These initial reflex responses were exaggerated in the spastics as compared with the normals. In the relaxed state 'stretch' and vibration either failed to elicit reflex responses in normal subjects or reflexes were of small amplitude; in spastic patients both modes of stimulation regularly evoked well developed responses. These findings with 'stretch' and vibration, both of which forms of stimulation powerfully excite primary endings of muscle spindles, support the view that group Ia afferent-mediated reflex action is enhanced in spasticity. The observation that the normal long-latency responses evoked by stretch, which have been attributed to the action of spindle group II afferents (Matthews, 1984a) additionally excited with this stimulus, are depressed in many spastic patients is consistent with reduced group II effects. Observed abnormalities of stretch reflex behaviour did not readily explain the severity of accompanying spasticity of individual patients.

Development of flexor spastic signs in preterm infants.

Fifty-five preterm infants with birthweights between 800 and 2000g and gestational ages between 25 and 33 weeks were repeatedly examined for the Rossolimo and Mendel-Bechterew lower-limb reflexes. Up to 34 weeks conceptional age (CA) an abduction-extension pattern was characteristic. Between 34 and 36 weeks CA the response changed to one implying flexor spasticity, which in some cases lasted throughout the first postnatal trimester. It is thought that this response occurring around 34 to 38 weeks CA is a sign of normal developmental maturation. On the other hand, an extension-abduction response after 38 weeks CA and a flexor response after the first trimester is indicative of delayed motor development and might suggest an upper motor neuron lesion.