TL;DR: An easy method of measuring facial movement has been developed by one of us and is intended for use when a patient's facial nerve recovery is being assessed.
Abstract: Normal Normal facial function in all areas Mild dysfunction Gross: slight weakness noticeable on close inspection; may have very slight synkinesis At rest: normal symmetry and tone Motion Forehead: moderate to good function Eye: complete closure with minimum effort Mouth: slight asymmetry III Moderate dysfunction Gross: obvious but not disfiguring difference between two sides; noticeable but not severe synkinesis. contracture. and/or hemifacial spasm At rest: normal symmetry and tone Motion Forehead: slight to moderate movement Eye: complete closure with effort Mouth: slightly weak with maximum effort rv Moderately severe dysfunction Gross: obvious weakness and/or disfiguring asymmetry At rest: normal symmetry and tone Motion Forehead: none Eye: incomplete closure Mouth: asymmetric with maximum effort V Severe dysfunction Gross: only barely perceptible motion At rest: asymmetry Motion Forehead: none Eye: incomplete closure Mouth: slight movement VI Total paralysis No movement From the Otologic Medical Group. Supported by funds from the House Ear Institute, affiliated with the University of Southern California School of Medicine. Submitted for publication Dec. 7, 1984; accepted Jan. 29, 1985. Reprint requests: John W. House, MD, The Otologic Medical Group, 2122 W. Third St., Los Angeles, CA 90057. At the Annual Meeting of the Table 1. Facial nerve grading system American Academy of Otolaryngology-Head and Neck Surgery, the Facial Nerve Disorders Committee adopted a universal standard for grading facial nerve recovery. This standard is based on articles by US. •2 It is intended for use when a patient's facial nerve recovery is being assessed. The system involves a six-point scale with I being normal and VI total, flaccid paralysis (Table 1). Those who have their own method of assessing facial nerve recovery are encouraged to convert their results to this six-point scale, which will be required when results are reported in Otolaryngology-Head and Neck Surgery. To assist in placing patients in the proper group, an easy method of measuring facial movement has been developed by one of us (D.E.B.). This system involves
TL;DR: Ectopic multiunit nerve activity correlating in intensity and time course to the positive sensory symptoms was recorded and paresthesiae were non‐painful except in the patient with Lasegue's sign and the ectopic impulses were probably recorded from large myelinated afferent fibers.
Abstract: Ectopically generated and antidromically conducted nerve impulses were recorded in 5 patients with tungsten microelectrodes inserted into skin nerve fascicles. All patients had mainly positive sensory symptoms and reported paresthesiae which could be provoked by different maneuvers which suggested increased mechanosensitivity of the primary sensory neurons at different anatomic levels. Ectopic multiunit nerve activity correlating in intensity and time course to the positive sensory symptoms was recorded: (1) when Tinel's sign was elicited in a patient with entrapment of the ulnar nerve at the elbow, (2) when paresthesiae were provoked by elevation of the arm in a patient with symptoms consistent with a thoracic outlet syndrome, (3) when paresthesiae were evoked by straining during chin-chest maneuver in a patient with an S1 syndrome due to a herniated lumbar disc, (4) when a painful Lasegue's sign occurred during the straight-leg raising test in a patient with an S1 syndrome due to root fibrosis, and (5) when Lhermitte's sign was elicited by neck flexion in a patient with multiple sclerosis. The sites for the ectopic impulse generation in these cases are suggested to be peripheral nerve, brachial plexus, dorsal root or dorsal root ganglion and dorsal columns. The paresthesiae were non-painful except in the patient with Lasegue's sign and the ectopic impulses were probably recorded from large myelinated afferent fibers.
TL;DR: An animal model of stretch injury to nerve in order to study in vivo conduction changes as a function of nerve strain has clinical implications in nerve repair, limb trauma, and limb lengthening.
Abstract: We developed an animal model of stretch injury to nerve in order to study in vivo conduction changes as a function of nerve strain. In 24 rabbits, the tibial nerve was exposed and stretched by 0%, 6% or 12% of its length. The strain was maintained for one hour. Nerve conduction was monitored during the period of stretch and for a one-hour recovery period. At 6% strain, the amplitude of the action potential had decreased by 70% at one hour and returned to normal during the recovery period. At 12% strain, conduction was completely blocked by one hour, and showed minimal recovery. These findings have clinical implications in nerve repair, limb trauma, and limb lengthening.
TL;DR: The low level of spontaneous activity does not suggest permanent spinal sympathetic hyperactivity, but the prolonged episodes of vasoconstriction may contribute to attacks of high blood pressure in patients with spinal cord lesions.
Abstract: Microelectrode recordings were made in peroneal muscle nerve fascicles in 9 patients with traumatic spinal cord lesions at the C5 to T8 level. In 4 patients the lesion was incomplete with some sensibility but no voluntary motor function below the level of the lesion. All patients had increased tendon jerks. EMG was recorded in 5 patients and showed signs of some peripheral denervation. Simultaneous recordings from nerves to skin and to muscle were made in 2 patients and control recordings were made in 19 normal subjects. In the patients, spontaneous neural activity was sparse but after a latency of 0.5-1.1 s strong mechanical and electrical stimuli applied to the skin below the level of the lesion, stimulation of the urinary bladder and deep breaths induced bursts of efferent impulses with a conduction velocity of 0.65 m X s-1. The discharges were often followed by cutaneous vasoconstriction and/or reduction of skin resistance. It is concluded that the neural bursts contained sympathetic impulses of spinal origin. The main differences between patients and normal subjects were spontaneous muscle sympathetic activity was much lower in the patients; no evidence of arterial baroreflex modulation of muscle sympathetic activity was obtained in the patients; and in the patients a given stimulus induced sympathetic reflex discharges which occurred synchronously in muscle and skin nerve branches. Increases of intravesical pressure induced only weak increases of muscle sympathetic activity in the patients but nevertheless marked hypertensive reactions occurred. It is suggested that the excitability of decentralized spinal sympathetic neurons to muscles is usually decreased and that mechanisms other than exaggerated sympathetic outflow must be important for evoking episodes of high blood pressure in patients with spinal cord injuries.
TL;DR: 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.
Abstract: 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.