Symptomatic ossification of the posterior longitudinal ligament of the cervical spine. Clinical findings.
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Biomedical subjects
Publications and source records attributed to T Mannen.
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Somatosensory evoked potentials (SEPs) to median nerve stimulation were investigated in normal controls and patients with cervical lesions. Attention was paid primarily to the N13 and P13 components in the posterior and anterior cervical records with non-cephalic references. In normal subjects the CV2 and CV6 electrodes registered N13 with almost the same amplitude. Dissociation between N13 at the CV2 electrode (ucN13) and N13 at the CV6 electrode (lcN13) was observed in the patients. In 4 patients with cervical dorsal column lesions, lcN13 was preserved but ucN13 was almost completely absent. Anterior cervical P13 (acP13) was preserved. In a patient with syringomyelia, lcN13 and acP13 were greatly attenuated while ucN13 was relatively well preserved. These results suggested that the origins of ucN13 and lcN13 are different. The generator of lcN13-acP13 was assumed to be the postsynaptic potential of the dorsal horn interneurons. Upon comparison with previous animal studies and intraoperative studies, it was concluded that the generator of ucN13 is the postsynaptic potential of the cuneate nucleus.
Recovery of somatosensory evoked potentials (SEPs) was studied by paired stimulation of the median nerve in patients with various kinds of myoclonus. This technique revealed the hyperexcitability of the central nervous system (CNS) which could not be detected by the conventional SEP technique using a single stimulus. This technique would be useful for studying the excitability of the CNS.
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.
Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).
The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudal most brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.
Tibial nerve stimulation at the ankle elicited a stationary, dipolar potential P15/N15 over the buttock with a reference electrode at the contralateral greater trochanter (GTc). P15 was distributed in the rostral and contralateral region and N15 in the caudal and ipsilateral region. The derivation from the contralateral iliac crest to the ipsilateral greater trochanter (ICc-GTi) registered a large P15 (= P15-N15) potential which was well free from artifacts. The Cz'-contralateral knee lead, which had been employed in previous studies, registered a smaller P15 of poor quality. Sequential bipolar recording along the course of the sciatic nerve indicated that P15 was generated around the greater sciatic foramen. Comparison with a simulation study suggested that P15 is a junctional potential which is generated when the sciatic nerve enters the bone at the greater sciatic foramen. P15 is expected to be a useful tool to evaluate the proximal segment of the tibial nerve.
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