Nerve Compromise Research Articles

Monitoring peripheral nerve function during external fixation of upper extremities.

Limb lengthening of the upper extremity using external fixation devices is associated with a high risk of neurovascular impairment. To aid early detection of nerve injury, intraoperative monitoring of neural function was performed in five patients undergoing Ilizarov-type circular external-fixator application. The apparatus was applied to the humerus in two cases and to the forearm in the other three cases. The function of ulnar, median, and radial nerves was assessed continuously throughout the surgery by using sensory-evoked potential (SEP) monitoring technique. The responses were elicited by stimulation of these nerves in the distal forearm with recording at Erb's point and over the anterior cervical spine. During apparatus application, radial-response attenuation was identified in two instances. No corrective actions were performed in one case, and the patient had symptoms of radial nerve deficit postoperatively. In the other case, prompt removal of the offending half-pin after the detection of electrophysiologic abnormalities resulted in subsequent response restoration and the avoidance of postoperative nerve dysfunction. Sensory-evoked potential monitoring proved to be a reliable indicator of nerve compromise during external fixation of upper extremities and may be considered a valuable surgical adjunct.

History and Differential Diagnosis of Carpal Tunnel Syndrome

Carpal tunnel syndrome is the most frequently recognized mononeuropathy of the upper limb; however it was not until the latter part of this century that the site of median nerve entrapment under the carpal ligament was recognized. Previous to that discovery, the symptoms of carpal tunnel syndrome were attributed to proximal nerve compromise at cervical levels, the thoracic outlet, or the distal compromise of the motor branch of the median nerve.

Multiple Compression Neuropathies and the Double-Crush Syndrome

Multiple compressions along a nerve have a cumulative effect on condition, both antegrade and retrograde. This nerve compromise renders the nerve more susceptible to a second source of compression. The proximal source of compression may be subclinical yet partially responsible for the cumulative compression syndrome. The primary "crush" may be anatomic or metabolic in origin. Strict attention to the patient's history and physical findings permit separation of the multiple compressions, making the choice of surgical decompression easier. Provocative testing and work simulation are important in examination, as is EMG testing. Complete medical evaluation can aid in diagnosing patients presenting with peripheral nerve compression and additional risk factors. Surgical decompression of a nerve with multiple levels of compression may not relieve all symptoms. Dynamic compressions in the work place and other nonsurgical types of compression must be identified so the prognosis for complete recovery is improved.

Secondary Muscle and Nerve Impairment in Primary Neuromuscular Disease

Secondary muscle and nerve damage can occur in neuromuscular disease because of muscle, nerve, or soft tissue compromise or degeneration. Examples include chronic compartment syndrome in Duchenne muscular dystrophy (DMD), suprascapular nerve tether in facioscapulohumeral dystrophy (FSH), adhesive capsulitis in the wheelchair- bound child with DMD, carpal tunnel syndrome in FSH or DMD, peroneal neuropa thy from an ill-fitting AFO, ankle injury in DMD due to weakness and proprioceptive loss, piriformis syndrome in the wheelchair-confined patient with neuromuscular dis ease, and ulnar neuropathy due to wheelchair armrest pressure in patients with periph eral neuropathy. Such complications to the primary disorder should be looked for as they often respond to appropriate treatment.

Somatosensory evoked potential monitoring of the brachial plexus to predict nerve injury during internal mammary artery harvest: Intraoperative comparisons of the rultract and pittman sternal retractors

Brachial plexus injury after coronary artery bypass grafting (CABG) continues to be a common problem postoperatively. With the use of somatosensory evoked potential monitoring (SSEP), neurologic integrity of the brachial plexus during internal mammary artery (IMA) harvest was assessed and the Rultract and Pittman sternal retractors were compared to determine what effect they had on SSEP characteristics. Results showed that the Rultract and Pittman retractors caused large decreases in SSEP amplitudes after insertion, (1.25 ± 0.14 versus 0.72 ± 0.09, P < 0.05; and 1.64 ± 0.27 versus 0.91 ± 0.14, P < 0.05) respectively. This decrease was noted in 85% of Rultract and 68.75% of Pittman patients, respectively. Amplitudes increased after retractor removal but never returned to baseline values. Cooley retractor placement in the patients not undergoing IMA harvest (control) produced only mild decreases in amplitude. Waveform latency increased in all groups after retractor placement, but these increases were thought to be clinically insignificant. Postoperatively, three patients in each of the IMA retractor groups had brachial plexus symptoms (18%), whereas only one patient in the control group had symptoms. Somatosensory evoked potential monitoring seems to be a sensitive intraoperative monitor for assessing brachial plexus injury during CABG. The nerve plexus seems to be most at risk for pathologic injury during retraction of the sternum for IMA harvest. Though the Rultract retractor caused greater changes in SSEP characteristics than the Pittman, no clinical outcome differences between the two could be ascertained. Using SSEP monitoring may reduce brachial plexus injury during IMA harvest by allowing early detection of nerve compromise and therapeutic interventions to alleviate the insult while under general anesthesia.

Sixteenth annual AAEM Edward H. Lambert Lecture. Electrodiagnostic aspects of diabetic neuropathies: entrapments. American Association of Electrodiagnostic Medicine.

A MEDLINE review suggested a lack of recent studies about the entrapments seen with underlying diabetic neuropathy. Suggested protocols for research in diabetic peripheral neuropathy have not included the concepts of entrapments as an early--indeed, first manifestation of the neuropathy. Carpal tunnel syndrome is a frequent accompaniment of diabetic peripheral neuropathy. Assessment of the degree of entrapment superimposed on the generalized peripheral neuropathy can be clarified by analysis of the CMAP and the SNAP--particularly with respect to duration of the negative spike of the action potential. Also, analysis of the action potentials elicited by stimulation of the ulnar and radial nerves and their comparison with the median nerve is often helpful. Finally careful inspection of the action potential when stimulating proximal and distal to the entrapment will establish the degree of nerve compromise relative to the underlying diabetic neuropathy.

Profound reductions of flicker sensitivity in the elderly: can glaucoma involve the retina distal to ganglion cells?

Flicker sensitivities were measured for more than 100 people age 60 and older with stimulus-conditions originally designed to obtain estimates of preretinal absorption by the lens and macular pigment. Flicker sensitivities were measured on two chromatic backgrounds: a 1000-td, 480-nm background and a 5800-td, Wratten 33 background (approximately metameric with 633 nm). Testing sessions were administered at 18-month intervals across a 3-yr period. No subject tested had a history of glaucoma or ocular hypertension at the time of entry into the study. For ten subjects, however, flicker sensitivity was sometimes reduced by more than 2.0 log units from the mean norm for at least one of the two backgrounds. For most other subjects, flicker sensitivities were within 0.5 log units of the mean norms. On retrospective analysis, the profound reductions of flicker sensitivity (PRFS) were associated significantly with (a) advanced age (perhaps especially when combined with relatively high intraocular pressure), and (b) the use of cardiovascular medications. The PRFS probably were associated with (c) female sex, and (d) large intraocular pressure fluctuations. In addition, the majority of subjects with PRFS were found to have evidence of glaucomatous cupping or field loss. These results suggest that PRFS result from glaucoma or share etiologies with low-tension glaucoma. The use of cardiovascular medications suggested that PRFS could depend on retinal dysfunction rather than on optic nerve compromise alone. Predicted results from two additional subject populations support this possibility. For young healthy subjects, flicker threshold vs illuminance curves attained very steep slopes for sufficiently short wavelength tests on sufficiently extreme long wavelength backgrounds (655 nm, 50,000 td); the steep slopes coincided with the breakdown of effective M-cone isolation. Reductions of flicker sensitivity on the 5800-td Wratten 33 background depended correspondingly on test wavelength for subjects with well-documented low-tension glaucoma.

Somatosensory-Evoked Potential Monitored During Total Hip Arthroplasty

One hundred consecutive patients were monitored using somatosensory-evoked potential (SEP) monitoring to detect intraoperative sciatic nerve compromise during total hip arthroplasty. The peroneal nerve was stimulated using the contralateral extremity to rule out systemic influences on the SEP tracings. Loss of amplitude or an increase in latency of greater than 10% was considered significant. Of the 18 patients who exhibited changes that met these criteria, 16 were female. Two patients had loss of amplitude of the tracings at the time of closure, and both of these patients exhibited postoperative sciatic nerve palsies. There were no false negatives. Femoral reaming and reduction are the surgical events most commonly associated with nerve reactions. Patients who have had prior hip procedures appear to be at higher risk. There was no correlation with intraoperative SEP changes and age, weight, surgical approach, or leg lengthening. Compared with unmonitored patients, there was no reduction in the incidence of sciatic palsy.

Single fiber EMG evaluation in denervation and reinnervation

SFEMG can be used to follow the course of reinnervation. The parameters of fiber density, mean jitter and percent blocking must each be followed and related to the type of injury to determine the stage of reinnervation. The few reported cases in the literature of SFEMG recordings followed over time after nerve compromise are reviewed and an additional case is presented by the author. Mean jitter values can return to normal approximately 1 1/2 years postonset of reinnervation. Some individual recordings may remain abnormal permanently.

Age covariance between 100-Hue color scores and quantitative perimetry in primary open angle glaucoma.

Color vision tests have shown promise as an early indicator of optic nerve compromise in primary open angle glaucoma (POAG). In this context, it is of interest to know how well color test performance correlates with an accepted measure of glaucomatous optic nerve damage, such as is provided by quantitative static perimetry. We found correlation values for 96 glaucoma suspects (ocular hypertensive patients) and 110 patients with POAG. No significant correlation values were found for the suspect group when age correction was applied to the color variable. Similarly, for the patients with POAG, age correction of the color test scores reduced all age group correlation values below significance, except for the age group 60 to 69 years. These findings conflict with another recent study reporting significant correlation between Farnsworth-Munsell 100-hue color test scores and visual field performance for glaucoma suspects but which did not correct for age. We interpreted our results for the glaucoma suspects and patients with glaucoma to indicate some independence of mechanisms responsible for early color loss compared with visual field loss.

Evaluation of Sciatic Nerve Compromise During Total Hip Arthroplasty

Sciatic nerve function was monitored intraoperatively by somatosensory evoked potentials (SEP) in 50 patients during total hip arthroplasty. There were 12 instances of temporary nerve compromise in ten patients: three during acetabular preparation due to retraction, one due to reamer contact, six during femoral reaming due to positioning, and two during trial reduction due to inadequate shortening of the femoral neck. The technique for monitoring, causes, and incidence of nerve compromise during total hip arthroplasty are discussed. SEP monitoring may be especially useful in revision surgery.

Spasmodic Torticollis as a Cause of Ulnar Nerve Entrapment

Abstract Spasmodic torticollis is thought to be a central nervous system disorder with no peripheral nervous system component. Several consecutive patients with spastic torticollis were found to have ulnar nerve compromise at the elbow on the side ipsilateral to the direction of chin turning. This article describes three such patients in detail. It is postulated that the cause is the stereotypical posture assumed by these patients in using their hand to maintain a neutral head position. The chronic leaning and elbow flexion place the ulnar nerve at risk for the development of pressure neuropathy.

Spasmodic torticollis as a cause of ulnar nerve entrapment.

Spasmodic torticollis is thought to be a central nervous system disorder with no peripheral nervous system component. Several consecutive patients with spastic torticollis were found to have ulnar nerve compromise at the elbow on the side ipsilateral to the direction of chin turning. This article describes three such patients in detail. It is postulated that the cause is the stereotypical posture assumed by these patients in using their hand to maintain a neutral head position. The chronic leaning and elbow flexion place the ulnar nerve at risk for the development of pressure neuropathy.

Optic Nerve Blindness Following Blunt Forehead Trauma

Seven cases of sudden monocular blindness following frontal head trauma are presented. The average age of these patients was 18 years. Four of the seven patients underwent transethmoid-sphenoid nerve decompression with only one of the four achieving a minor return of vision. None of the three out of six patients who failed to respond to megadose steroids regained vision with optic nerve decompression. Three out of six patients had return of good vision with megadose steroids without optic nerve decompression. Two of these three patients had a delayed loss of vision. One of the three patients with visual return developed visual loss again following a facial fracture reduction, which again responded to megadose steroids without optic nerve decompression. Another patient had visual return on steroids but also required removal of a subperiosteal hematoma to obtain near normal vision. This case differs from our other cases in that subperiosteal hematoma is an unusual complication of these injuries and caused the optic nerve compression in the orbital apex in this case. Review of the literature and our clinical and experimental findings suggest that the etiology of the indirect optic nerve injury is secondary to a stretching, tearing, torsion, or contusion of the nerve caused not only from the momentum of the eyeball and orbital contents being absorbed by the fixed canalicular portion of the optic nerve but also by skeletal distortion caused by forces remote from the initial impact. This is well illustrated by the holographic findings. These injuries cause direct injury to the nerve or vascular compromise from tearing, thrombosis, hematoma, or compression of the small nutrient vessels supplying the optic nerve. Megadose steroids appear to be useful in some cases of traumatic monocular blindness secondary to blunt facial trauma and as an adjunct to or an indication for surgery in others. The authors' recommended indications for optic nerve decompression (transethmoid-sphenoidotomy with removal of the medial wall of the optic canal) following blunt trauma are (1) delayed visual loss following frontal head trauma unresponsive to 12 hours of megadose steroid therapy and (2) initial return of vision with megadose steroids followed by visual decrease while on steroids or with the tapering of steroids.

Perineural optic nerve changes in endocrine orbitopathy.

A-scan ultrasonographic measurements of the differences between nerve and dural diameters of the retrobulbar optic nerve were made in 55 eyes of 30 patients with endocrine orbitopathy. This measurement was found to be enlarged in all cases. Extraocular muscle thickness measurements were also made ultrasonically in these eyes, and the degree of intervaginal distension was found to increase with increasing extraocular muscle involvement. These findings were consistent whether the patients were hyperthyroid, hypothyroid, or euthyroid clinically, and the findings occurred in the absence of any detectable functional optic nerve compromise. The cause of this subdural perineural enlargement remains unknown.