Widespread N18 in median nerve SEP is preserved in a pontine lesion

Widespread N18 potential to median nerve stimulation was preserved in a patient who had profound unilateral disturbance of deep sensation and a lesion of the pontine medial lemniscus confirmed by MRI. It was concluded from this result that at least a significant part of the N18 potential was generated caudal to the pontine level or at higher levels via extralemniscal pathways. Careful review of studies in man with intraoperative recordings seemed to support that the N18 potential already exists at the medullary level. We suggested that the potential generated at the cuneate nucleus which was described in cats may correspond to part of the N18 potential.     

The N18 component of the median nerve SEP is not reduced by vibration

Objective: To study the interference of mechanical vibration of the palm of the hand on the median nerve short-latency SEP components.Methods: Electrically-elicited short-latency median nerve SEP were obtained before and during mechanical vibration (120 Hz) of the palm in two groups of normal individuals (6 in group I and 9 in group II). The amplitude of the different components was compared between the two conditions through non-parametric statistical tests.Results: A significant reduction in the amplitude of the N9, P13/14 and N20 components was detected, however no overall significant changes were detected for the N18 component.Conclusions: Vibration interference reduced all studied components except the N18, these findings are interpreted as supporting evidence for the proposed association between the N18 component and the inhibitory activities elicited in the dorsal column nuclei.     

Origin of scalp far-field N18 of SSEPs in response to median nerve stimulation

To identify the origin of scalp-recorded far-field negativity of short-latency somatosensory evoked potentials to median nerve stimulation (designated N18), direct records were made from the thalamus and ventricular system during 4 stereotaxic and 3 posterior fossa operations.In the thalamus a negative potential with almost the same latency as the scalp N18 was restricted to the Vim nucleus, but there was a large positive potential in the VC nucleus and medial lemniscus. Vim negativity increased in amplitude when high frequency stimulation was given to the median nerve, indicative of a facilitation effect. In contrast, the amplitude of scalp N18 decreased at high frequency stimulus.Direct recordings made through the medulla oblongata to the mid-brain showed a negative potential with gradually increasing latency. Above the upper pons, there was stationary negativity with no latency shift. The similarity between this negative potential and N18 is shown by their having the same latency and same response to the amplitude reduction and latency prolongation produced by high frequency stimulus.Our data suggest that scalp N18 comes from brain-stem activity between the upper pons and the mid-brain rather than from the thalamus.     

P30 and N33 of posterior tibial nerve SSEPs are analogous to P14 and N18 of median nerve SSEPs

Generator sources of far-field P30 and N33 components produced bosterior tibial nerve stimulation were compared with those of the P14 and N18 components of median nerve stimulated somatosensory evoked potentials. Intracranial spatio-temporal distributions of P30 and N33 were similar to those of the P14 and N18 obtained by median nerve stimulation. In clinical cases, the changes in P30 and N33 were correlated with those in P14 and N18, indicative that P30 and N33 are derived from activities similar to those that produce P14 and N18.     

Amplitude abnormalities in the scalp far-field N18 of SSEPs to median nerve stimulation in patients with midbrain-pontine lesion

Various amplitude ratios were measured in 20 normal controls and 36 patients with midbrain-pontine, thalamic or putaminal lesions in order to evaluate the amplitude abnormalities in scalp far-field N18 following median nerve stimulation. A study of normal controls showed that the distributions of P9/N18, P14/N18 and N18/P14 + N18 resembled a gaussian distribution and could be used as criteria for determining the decrease in N18 amplitude in each patient. There was a decrease in N18 amplitude, or the absence of N18, in patients with midbrain-pontine lesions, but not in those with thalamic or putaminal lesions.Nine amplitude ratios (P11/P9, P14/P9, N18/P9, P9/P11, P9/P14, P9/N18, N18/P14, P14/N18 and N18/P14 + N18) were compared statistically for normal controls and 3 groups of patients based on non-parametric, Wilcoxon's non-pairs and signed-rank tests. A decrease in N18 amplitude in midbrain-pontine lesion was shown by significant changes in N18/P9, P9/N18, N18/P14, P14/N18 and N18/P14 + N18, no amplitude decreases in P11 and P14 being found from the amplitude ratios of P11/P9, P9/P11, P14/P9 and P9/P14. No significant changes were seen in any of the 9 amplitude ratios when the normal controls and patients with thalamic and putaminal lesions were compared.The amplitude ratios of N18 can be used to detect a decrease in N18 amplitude in patients with midbrain-pontine lesions. The data obtained support the hypothesis that N18 originates in the midbrain-pontine region and that neither the thalamus nor thalamocortical radiation make major contributions to the formation of the N18 peak.     

Scalp, basal epidural and intravascular far-field recordings after median nerve stimulation: evidence for a separate N18a potential

Far-field somatosensory evoked potentials (SSEPs) after median nerve stimulation were recorded from scalp- (Fz), epidural- (ED) and intravascular electrodes (basilar artery [Bas]) to study the nature of the controversial N18a component of the widespread N18 potential. In healthy volunteers frequently an N18a potential was recorded at Fz. Simultaneous Fz and ED recordings at the pontomesencephalic junction as well as Bas-recordings at the caudal basilar artery showed N18a components identical in latency and shape. With intravascular recordings the shapes differed between the top of the basilar artery and the caudal artery recordings. These findings support the existence of a separate N18a potential. The generator of the N18a is likely to be localized within the upper brainstem.     

Scalp,basal epidural and intravascular far-field recordings after median nerve stimulation: evidence for a separate N18a potential

Far-field somatosensory evoked potentials (SSEPs) after median nerve stimulation were recorded from scalp- (Fz), epidural(ED) and intravascular electrodes (basilar artery [Bas]) to study the nature of the controversial N18a component of the widespread N18 potential. In healthy volunteers frequently an N18a potential was recorded at Fz. Simultaneous Fz and ED recordings at the pontomesencephalic junction as well as Bas-recordings at the caudal basilar artery showed N18a components identical in latency and shape. With intravascular recordings the shapes differed between the top of the basilar artery and the caudal artery recordings. These findings support the existence of a separate N18a potential. The generator of the N18a is likely to be localized within the upper brainstem.     

Intraneural perineurioma involving the median nerve

Intraneural perineurioma is a rare clinical entity, which tends to affect major nerve trunks in the upper extremities. On light microscopy, numerous pseudo-onion-bulb structures having a central clear area are surrounded by concentric layers of eosinophilic elongate cells having spindled nuclei. Immunohistochemistry of concentric cells stains positive for epithelial membrane antigen but negative for S100 protein. Because of the small number of cases, no consensus has been made on proper treatment of this entity. Although none of the patients who have had excision of tumor with nerve grafting have had sensory nerve recovery, we believe each patient should be individualized until more data are available regarding this tumor.     

Modification of median nerve somatic evoked potentials by prior median nerve,peroneal nerve,and auditory stimulation

In a recovery function design, changes were measured in the somatic evoked potentials (SEP) to right median nerve (RMN) shocks preceded by stimulation of: the same nerve (RMN-RMN); the left median nerve having primary input to the homologous sensory area in the contralateral hemisphere (LMN-RMN); the right peroneal nerve having primary input to a different region of the same hemisphere (RPN-RMN); and the auditory nerve with primary input to a different sensory modality (AUD-RMN). Eight inter-stimulus intervals ranged from zero (simultaneous) to 2.5 sec. It was assumed that the degree of interaction between evoked potentials would be related to the degree to which common neural structures are activated or modulated in response to the stimuli. Results were: (a) the primary somatosensory response N20-P30 was little influenced by other somatic or auditory stimulation, interaction occurring predominantly in the RMN-RMN condition; (b) with increasing latency, components showed increasing interaction across modalities; (c) preceding homolateral stimulation (RPN-RMN) showed no greater interaction than preceding contralateral stimulation (LMN-RMN); (d) N55-P100 differed from the primary somatosensory response N20-P30 by showing greater interaction with other somatic stimuli; and (e) N140-P190 showed similarly shaped recovery functions across stimulus pairs but significant differences in magnitude of interaction. These results show that components with similar wave form and topographical characteristics can have different neurophysiological properties.     

Lipofibromatous hamartoma of the median nerve and macrodactyly

A case of lipofibromatous hamartoma of the median nerve with macrodactyly of 2 digits is described. Nerve stripping resulted in a growth control.     

Origin of the extra chromosome in trisomy 18

Summary The parental origin of an extra chromosome in five patients with trisomy 18 was traced using a restriction fragment length polymorphism (RFLP) of the human prealbumin (PA) gene, localized to 18p11.1–q12.1, as a genetic marker. MspI digests of the genomic DNAs of the five patients, their parents and normal controls were hybridized with the PAcDNA. Densitometric analysis on the gene dose of the polymorphic fragments of these patients revealed that three had originated from a maternal meiotic error. The other two patients were uninformative for the parental origin of trisomy 18. Our results indicate that nondisjunctional errors leading to trisomy 18 may occur predominantly at the maternal meiosis, consistent with the results of previous studies on the parental origin of trisomies 21 and 13.     

Arteriovenous malformation of a persistent median artery with a bifurcated median nerve

A patient with arteriovenous malformations of the volar forearm and hand arising from a persistent median artery with an associated bifid median nerve is presented. Surgeons should be aware of high median nerve bifurcations, particularly when a persistent median artery is identified, and should remember that additional structures that can lead to nerve compression may be present in the carpal tunnel. Specifically, more than one median nerve may need to be identified and protected in such cases.     

Latency and amplitude abnormalities of the scalp far-field P14 to median nerve stimulation in multiple sclerosis. A SEP study of 122 patients recorded with a non-cephalic reference montage

The frequency and characteristics of P14 abnormalities were investigated in 122 patients with probable (68), or definite (54) multiple sclerosis by recording SEPs to median nerve stimulation with a non-cephalic reference montage. The most frequent SEP abnormality found in our series (62% of abnormal results) combined latency increase and amplitude reduction of P14. Interindividual variability, inherent in absolute amplitude measurements, was by-passed by calculating the ration between the amplitudes of far-field P9 and P14 components, which proved to be normally distributed in controls. In spite of the strong association (P ⪡ 0.001) between the P9–P14 interpeak interval (IPL) and the P9/P14 amplitude ratio in MS patients, the latter parameter was found to be the only abnormality in 12 patients whose P9–P14 and P14–N20 IPLs were normal. Also IPLs were increased in 12 patients with normal P14 amplitudes. These results suggest that adding the P9/P14 amplitude criterion to standard IPL data might be useful to detect conduction troubles in MS patients.     

Management of synovial sarcoma of the median nerve at the elbow

Synovial sarcoma is a high-grade malignancy with a marked propensity for local recurrence and a moderate rate of regional lymph node involvement. It usually causes death from massive pulmonary metastases. Despite its aggressive biologic behavior, en bloc wide local resection of small extremity tumors rather than amputation may be indicated if removal of all gross disease is possible. Extremity morbidity from resection of vessels, nerves, and soft-tissue bulk can be minimized by the use of composite reconstruction techniques currently available. A case report is presented to illustrate aggressive limb-sparing surgical therapy of a small, favorably located synovial sarcoma with immediate neurovascular and soft-tissue reconstruction. The literature is reviewed to aid subsequent surgeons faced with management of this uncommon tumor.     

Ontogenetic appearance of somatostatin-containing nerve terminals in the median eminence of rats

Summary The development of immunoreactive (ir) somatostatin-containing nerve terminals in the rat median eminence (ME) has been examined electron-microscopically. Nerve fibers containing ir particles scattered throughout the axoplasm are first seen in the external layer of the ME on day 18.5 of gestation, and, on day 21.5 appear to terminate on the basement membrane of the perivascular space of the portal vessels. After birth, the fiber terminals contain several membrane-limited granules, which are labeled with ir PAP particles. Ultrathin, Epon-embedded sections of ME, treated by the protein A gold-labeling method for somatostatin, demonstrate positively labeled granules in the nerve fibers in the postnatal ME, but in the prenatal tissue, no specific gold-labeling is found. These findings show that, in the external layer of the ME, somatostatin storing occurs in the granules in the axonal terminals after birth.