P14 Potentials Research Articles

The contribution of neurophysiology in the diagnosis and management of cervical spondylotic myelopathy: a review.

Topical review of the literature. The objective of this review article was to assess indications and usefulness of various neurophysiological techniques in diagnosis and management of cervical spondylogenic myelopathy (CSM). The MEDLINE, accessed by Pubmed and EMBASE electronic databases, was searched using the medical subject headings: 'compressive myelopathy', 'cervical spondylotic myelopathy (CSM)', 'cervical spondylogenic myelopathy', 'motor evoked potentials (MEPs)', 'transcranial magnetic stimulation', 'somatosensory evoked potentials (SEPs)', 'electromyography (EMG)', 'nerve conduction studies (NCS)' and 'cutaneous silent period (CSP)'. SEPs and MEPs recording can usefully supplement clinical examination and neuroimaging findings in assessing the spinal cord injury level and severity. Segmental cervical cord dysfunction can be revealed by an abnormal spinal N13 response, whereas the P14 potential is a reliable marker of dorsal column impairment. MEPs may also help in the differential diagnosis between spinal cord compression and neurodegenerative disorders. SEPs and MEPs are also useful in follow-up evaluation of sensory and motor function during surgical treatment and rehabilitation. EMG and NCS improve the sensitivity of cervical radiculopathy detection and may help rule out peripheral nerve problems that can cause symptoms that are similar to those of CSM. CSP also shows a high sensitivity for detecting CSM. Neuroimaging, especially magnetic resonance imaging, represents the procedure of choice for the diagnosis of CSM, but a correct interpretation of morphological findings can be achieved only if they are correlated with functional data. The studies reported in this review highlight the crucial role of the electrophysiological studies in diagnosis and management of CSM.

Mapping the vestibular evoked myogenic potential (VEMP)

Effects of different electrode placements and indifferent electrodes were investigated for the vestibular evoked myogenic potential (VEMP) recorded from the sternocleidomastoid muscle (SCM). In 5 normal volunteers, the motor point of the left SCM was identified and an electrode placed there. A grid of 7 additional electrodes was laid out, along and across the SCM, based upon the location of the motor point. One reference electrode was placed over the sternoclavicular joint and another over C7. There were clear morphological changes with differing recording sites and for the two reference electrodes, but the earliest and largest responses were recorded from the motor point. The C7 reference affected the level of rectified EMG and was associated with an initial negativity in some electrodes. The latencies of the p13 potentials increased with distance from the motor point but the n23 latencies did not. Thus the p13 potential behaved as a travelling wave whereas the n23 behaved as a standing wave. The C7 reference may be contaminated by other evoked myogenic activity. Ideally recordings should be made with an active electrode over the motor point.

Targeting the Pedunculopontine Nucleus

Pedunculopontine tegmental nucleus (PPTg) deep brain stimulation (DBS) has been used in patients with Parkinson disease. To verify the position of the DBS lead within the pons during PPTg targeting. In 10 Parkinson disease patients undergoing electrode implantation in the PPTg, somatosensory evoked potentials were recorded after median nerve stimulation from the 4 DBS electrode contacts and from 2 scalp leads placed in the frontal and parietal regions. The DBS electrode recorded a P16 potential (latency at contact 0, 16.33 ± 0.76 ms). There was a P16 latency shift of 0.18 ± 0.07 ms from contact 0 (lower) to contact 3 (upper). The scalp electrodes recorded the P14 far-field response (latency, 15.44 ± 0.63 ms) and the cortical N20 potential (latency, 21.58 ± 1.42 ms). The P16 potentials recorded by the intracranial electrode contacts are generated by the volley traveling along the medial lemniscus, whereas the scalp P14 potential represents a far-field response generated at the Obex level. Considering that the distance between the electrode contacts 0 and 3 is 6 mm, the distance of the electrode contact 0 from the Obex (ΔObex) was calculated by the equation: ΔObex = 6 × Δlatency P14- PPTg0/Δlatency PPTg0-PPTg3. The Obex-to-brainstem electrode distance obtained by the neurophysiological method confirmed that the electrode was located within the pons in all patients. Moreover, this distance was very similar to that issued from the individual brain magnetic resonance imaging. Somatosensory evoked potentials may be a helpful tool for calculating the macroelectrode position within the pons during PPTg targeting.

18. Neurophysiologic response in newborn as a predictive factor of hearing impairment

Aim: To point on detection lesion with somatosensory evoked potentials SSEP in patients with cervical syndrome. Methods:We evaluate 15 patients with diagnosis of cervical syndrome, mean age 44.9 ± 7.6. In all patients we do NMR and SSEP of median nerve. We analyzed latency, amplitude and left–right difference of N11, N13 and P14 potentials. All parameters were compared with healthy population. Results: NMR diagnostic show a polydiscopathy changes in region C4–C7. All patients had a significantly lower amplitude and prolonged latencies (p < 0.05). Those changes was more statistical significant in patients with myelopathic signal (p < 0.01) on NMR. In 14/15 patients we registered prolonged latency N13 (p < 0.05), in 3 patients left–right difference was pathological, and prolonged latency was on side were we on NMR detect lesion. Conclusions: This kind of noninvasive diagnostic procedure, we can use to detect and evaluate lesion on cervical spine. The greater importance is to evaluate a physical therapy in those patients.

Effects of glutamate receptor agonists on the p13 auditory evoked potential and startle response in the rat.

The P13 potential is the rodent equivalent of the P50 potential, which is an evoked response recorded at the vertex (Vx) 50 ms following an auditory stimulus in humans. Both the P13 and P50 potentials are only present during waking and rapid eye movement (REM) sleep, and are considered to be measures of level of arousal. The source of the P13 and P50 potentials appears to be the pedunculopontine nucleus (PPN), a brainstem nucleus with indirect ascending projections to the cortex through the intralaminar thalamus, mediating arousal, and descending inhibitory projections to the caudal pontine reticular formation (CPRF), which mediates the auditory startle response (SR). We tested the hypothesis that intracranial microinjection (ICM) of glutamate (GLU) or GLU receptor agonists will increase the activity of PPN neurons, resulting in an increased P13 potential response, and decreased SR due to inhibitory projections from the PPN to the CPRF, in freely moving animals. Cannulae were inserted into the PPN to inject neuroactive agents, screws were inserted into the Vx in order to record the P13 potential, and electrodes inserted into the dorsal nuchal muscle to record electromyograms and SR amplitude. Our results showed that ICM of GLU into the PPN dose-dependently increased the amplitude of the P13 potential and decreased the amplitude of the SR. Similarly, ICM of N-methyl-d-aspartic acid or kainate into the PPN increased the amplitude of the P13 potential. These findings indicate that glutamatergic input to the PPN plays a role in arousal control in vivo, and changes in glutamatergic input, or excitability of PPN neurons, could be implicated in a number of neuropsychiatric disorders with the common symptoms of hyperarousal and REM sleep dysregulation.

Absent median nerve P14 far-field somatosensory evoked potential with persistent tibial nerve P30 component in a patient with ischemic pontine lesion

In a patient with an ischemic lesion of the right paramedian region of the pons, somatosensory evoked potential (SEP) recording to median nerve stimulation showed an absent P14 response with still preserved P13 and N18 potentials. The tibial nerve P30 and N33 SEP components were normal. Our results suggest that the median nerve P14 potential, absent in our patient, has a different origin from the tibial nerve P30 response, normal in the present case.

Bilobed splitting of median nerve somatosensory evoked p14 potential under deep hypothermia.

To further elucidate temperature related changes in subcortical components of somatosensory evoked potentials (SEP) in intraoperative monitoring. Intraoperative monitoring of subcortical median nerve SEP under deep hypothermia is described in a patient undergoing intracranial giant aneurysm surgery. The P14 potential was recorded from Fz-Pgz (front to nasopharynx). At a body core temperature of less than 17 degrees C, P14 showed a bilobed splitting that was reversible with rewarming. A comparison with latencies of other subcortical potentials of presynaptic and postsynaptic origin, recorded at the neck, speaks in favor of a presynaptic generation of the first P14 wave and a postsynaptic origin of the latter P14 wave. Deep hypothermia may separate presynaptic and postsynaptic electric activity of evoked potentials that overlap at normal body temperature. Such possible phenomena must be kept in mind to correctly interprete monitoring data at very low body temperatures and may help in better understanding the generation of different SEP components.

Source generators of the early somatosensory evoked potentials to tibial nerve stimulation: an intracerebral and scalp recording study

Objective: To investigate the location of the cerebral generators of the early scalp somatosensory evoked potentials (SEPs) after tibial nerve stimulation. Methods: Tibial nerve SEPs were recorded in 15 patients, suffering from Parkinson's disease, who underwent implantation of intracerebral (IC) electrodes in the subthalamic nucleus, in the globus pallidum or in the thalamic ventralis intermediate nucleus. SEPs were recorded both from the scalp surface and from the IC leads. Results: The lemniscal P30 response was recorded by all the electrodes. The IC waveforms included a negative N40IC response, followed by a positive (P50IC) and a negative (N60IC) potential. The N40IC, the P50IC and the N60IC potentials did not differ in latency from the P40, the N50 and the P60 responses recorded by the Cz electrode. In 6 patients, in which SEPs were recorded also during the voluntary movement of the stimulated foot (active gating), an amplitude reduction of the SEP components following the P30 potential was observed during movement at the vertex and in the IC traces. Instead, in the contralateral temporal traces the SEP components (N40temp and P50temp) were not modified by active gating, and in the ipsilateral parietal traces only the positive potentials at about 60 ms of latency was decreased. Conclusions: Two differently oriented generators are active in the contralateral hemisphere at both 40 and 50 ms of latency after tibial nerve stimulation. One source is oriented perpendicularly to the mesial hemispheric surface and generates the potentials recorded by the contralateral temporal and the ipsilateral parietal leads; the other dipolar source is radial to the hemispheric convexity, and generates the potentials at the vertex and those recorded by the IC electrodes.

Stereotactic recordings of median nerve somatosensory-evoked potentials in the human pre-supplementary motor area.

Median nerve somatosensory-evoked potentials (SEPs) have been recorded using intracortical electrodes stereotactically implanted in the frontal lobe of eight epileptic patients in order to assess the waveforms, latencies and surface-to-depth distributions of somatosensory responses generated in the anterior subdivision of supplementary motor areas (SMAs), the so-called pre-SMA. Intracortical responses were analysed in two latency ranges: 0--50 ms and 50--150 ms after stimulus. In all patients, we recorded in the first 50 ms after stimulus two positive P14 and P20 potentials followed by a N30 negativity. In the hemisphere contralateral to stimulation, the P20--N30 potentials showed a clear amplitude decrease from the outer to the inner aspect of the frontal lobe with minimal amplitudes in the pre-SMA. In the hemisphere ipsilateral to stimulus, P20 and N30 amplitudes were decreasing from mesial to lateral frontal cortex. In the 50--150 ms latency range, contacts implanted in the pre-SMA recorded a negative potential in the 60--70 ms latency range which, in five patients, was followed by a positive response peaking 80--110 ms after stimulus. These potentials were not picked up by more superficial contacts. We conclude that no early SEP is generated in pre-SMA in the first 50 ms after stimulation, while some potentials peaking in the 60--100 ms after stimulus are likely to originate from this cortical area. The latency of the pre-SMA responses recorded in our patients supports the hypothesis that the pre-SMA does not receive short-latency somatosensory inputs via direct thalamocortical projections. More probably the pre-SMA receives somatosensory inputs mediated by a polysynaptic transcortical transmission through functionally secondary motor and somatosensory areas.

Evidence for an abnormal cortical sensory processing in dystonia: selective enhancement of lower limb P37-N50 somatosensory evoked potential.

We evaluated brain stem P30, contralateral frontal N37, and the vertex-ipsilateral central P37, N50 somatosensory evoked potentials (SEPs) obtained in response to stimulation of the tibial nerve in 10 patients with idiopathic dystonia. Results were compared with those obtained in 10 healthy subjects matched for age and sex. The amplitude of the brain stem P30 potential and of the contralateral frontal N37 response in dystonic patients was not significantly different from that recorded in normal subjects. The vertex- ipsilateral central P37-N50 complex, which is thought to originate in the pre-rolandic cortex, was significantly enhanced in patients compared with the control group. These results suggest the enhancement of the vertex-ipsilateral central P37-N50 complex might reflect an abnormal response to somatosensory inputs of a precentral cortex which is excessively activated because of a disorder of the basal ganglia. Such inefficient sensory processing in motor areas might contribute to motor impairment in dystonia.

Midlatency auditory-evoked potentials in the rat: effects of interventions that modulate arousal

The vertex-recorded P13 midlatency auditory-evoked potential in the rat shows the same characteristics as the P1 potential in the human, namely, sleep-state dependence, rapid habituation and blockade by the cholinergic antagonist scopolamine. The P13 potential appears to be generated, at least in part, by projections of the pedunculopontine nucleus, the cholinergic arm of the reticular activating system. On the other hand, the auditory cortex-recorded P7 potential appears to be of primary cortical origin. Simultaneous recordings from the vertex and the auditory cortex showed that (1) the P13 potential was suppressed by administration of the anesthetics ketamine, pentobarbital or halothane in a dose-dependent manner, but the P7 potential was not; (2) the P13 potential was suppressed by intragastric injections of ethanol in a dose-dependent manner, but the P7 potential was not; (3) the amplitude of the P13 potential was negatively correlated with blood ethanol levels; (4) both the P13 and P7 potentials were still present following injections of the neuromuscular blocker pancuronium bromide; and (5) both the P13 and P7 potentials were decreased by diffuse brain injury induced by a weight-drop device in a weight-dependent manner. These findings suggest that the P13 potential is more sensitive than the P7 potential to changes in arousal and that the P13 and P7 potentials are not of myogenic but of neural origin.

Neurophysiological evidence of neuroplasticity at multiple levels of the somatosensory system in patients with carpal tunnel syndrome

The human somatosensory cortex (S1) is capable of modification after partial peripheral deafferentation, but it is not known whether spinal and brainstem changes contribute to this process. We recorded spinal, brainstem and cortical somatosensory evoked potentials following ulnar nerve stimulation in patients affected by unilateral carpal tunnel syndrome with EMG evidence of chronic alterations in median nerve sensorimotor conduction at the wrist lasting at least 4 weeks, and compared them with those from the unaffected hand and with those obtained in a control group. Amplitudes of spinal N13 and brainstem P14 potentials following stimulation of the ulnar nerve ipsilateral to the deafferented median nerve were greater than those following stimulation of the contralateral ulnar nerve. Side-to-side amplitude differences in N13 and P14 were greater in patients than in the control group. Parietal N20 and P27 potentials, supposedly generated in S1, were also significantly increased. The present results suggest that a chronic pathological modification of peripheral sensorimotor inputs is associated with changes in neural activity at multiple sites of the somatosensory system. Changes in spinal and brainstem structures could contribute to the mechanisms subserving changes in the S1. Changes in synaptic strength and unmasking inputs secondary to disconnection of the normally dominant inputs to the 'median nerve' cortex may be the mechanisms underlying ulnar nerve SEP changes.

Generators of short latency human somatosensory-evoked potentials recorded over the spine and scalp.

Somatosensory evoked potentials (SEPs) are most commonly obtained after stimulation of the median nerve and the posterior tibial nerve. SEPs reflect conduction of the afferent volley along the peripheral nerve, dorsal columns, and medial lemniscal pathways to the primary somatosensory cortex. Short-latency SEPs are recorded over the spine and scalp. After posterior tibial nerve stimulation, the following waveforms are recorded: N22, W3, the dorsal column volley, N29, P31, N34, and P37. After median nerve stimulation, the brachial plexus volley, dorsal column volley (N11), N13, P14, N18, N20, and P22 potentials are recorded. We discuss the current state of knowledge about the generators of these SEPs. Such information is crucial for proper interpretation of SEP abnormalities.

Selective gating of lower limb cortical somatosensory evoked potentials (SEPs) during passive and active foot movements

We evaluated subcortical and cortical somatosensory evoked potentials (SEPs) in response to posterior tibial nerve stimulation in 4 experimental conditions of foot movement and compared them with the baseline condition of full relaxation. The experimental conditions were: (a) active flexion-extension of the stimulated foot; (b) active flexion-extension of the non-stimulated foot; (c) passive flexion-extension of the stimulated foot in complete relaxation; (d) tonic active flexion of the stimulated foot. We analyzed latencies and amplitudes of the subcortical P30 potential, of the contralateral pre-rolandic N37 and P50 responses and of the P37, N50 and P60 potentials recorded over the vertex. Latencies did not vary in any of the paradigms. The amplitude of subcortical P30 potential did not change during any of the paradigms. Among the cortical waves, P37, N50 and P60 amplitudes were significantly attenuated in all conditions except active movement of the non-stimulated foot (b). This attenuation was less during passive (c) than during active movements of the stimulated foot (a and d). The contralateral pre-rolandic waves N37 and P50 showed no significant decrease during any of the paradigms. These results suggest that gating occurs rostrally to the cervico-medullary junction, probably at cortical level. The different behavior of N37, P50 and P37, N50 cortical responses during movement of the stimulated foot provides evidence suggestive of a highly localized gating process occurring at cortical level. These potentials could reflect activation of separate, functionally distinct generators.

Potentiels évoqués somesthésiques dans la polyarthrite rhumatoïde avec atteinte radiologique du rachis cervical

Somatosensory evoked potentials (SEP) have been recorded in 11 patients with cervical spine involvement, with or without signs of myelopathy due to rheumatoid arthritis (RA). In three patients, SEP have been recorded both before and after cervical spine surgery. In seven cases, the P14 (particularly the P9/P14 amplitude ratio) or P30 potentials were abnormal, whereas other potentials and conduction times were less often modified. Vertebral luxation sites that were predominantly observed at the upper cervical level account for these findings, thus supporting the diagnostic utility of P14 and P30 potentials which respectively take origin in the lower brain stem, close to or into the nuclei cuneatus and gracilis. Postoperative SEP were strongly correlated with the surgical outcome. SEP could be abnormal in the absence of overt clinical myelopathy or vertebral luxations, thus revealing infraclinical damage to the somatosensory pathways. This suggests that SEP recording is useful to discriminate RA patients with upper cervical cord dysfunction from those in whom vertebral lesion proves to have no direct impact on somatosensory conduction.

Neural generators of tibial nerve P30 somatosensory evoked potential studied in patients with a focal lesion of the cervicomedullary junction.

The tibial nerve P30 potential was studied in 6 patients with focal lesions located in the vicinity of the cervicomedullary junction. P30 potential was unaffected while cortical P39 was abnormal in the patients with a supramedullary lesion affecting the somatosensory pathway just above its decussation. Conversely, P30 was abnormal in the presence of a lesion situated caudally to the cervicomedullary junction affecting the lower limb sensory fibers just below their decussation. Median nerve P14 behaved similarly to the P30 potential in these cases. These clinical observations suggest that P30 potential, as P14 of median nerve somatosensory evoked potentials, is generated in the lower brain stem probably before the decussation of the sensory fibers; nucleus gracilis and medial lemniscus fibers in the lower brain stem are probably the anatomical structures generating P30 potential. This suggests that P30 potential may be used to study intraspinal and intracranial conduction times separately in the afferent somatosensory pathways.

P309 Analysis of latency and amplitude distributions of the median nerve somatosensory evoked P14 potential in derivations from scalp, earlobe and nasopharynx using cephalic and non-cephalic references

P309 Analysis of latency and amplitude distributions of the median nerve somatosensory evoked P14 potential in derivations from scalp, earlobe and nasopharynx using cephalic and non-cephalic references

Brain-stem somatosensory dysfunction in a case of long-standing left hemispherectomy with removal of the left thalamus: a nasopharyngeal and scalp SEP study

We have studied median nerve somatosensory evoked potentials (SEPs) in a patient who had undergone early surgical removal of the left cerebral hemisphere and left thalamus. Stimulation of the right side evoked normal latency P9, P11 and P13 potentials at scalp as well as at nasopharyngeal (NP) leads, while P14 and N18 potentials were absent. These SEP abnormalities, that have been described previously in cervico-medullary lesions and in comatose patients with upper brain-stem involvement, suggest that in our patient the removal of the left thalamus has caused retrograde degeneration of the cuneate-thalamic projections. Moreover, this study confirms that P13 and P14 potentials have different generators.

Scalp, earlobe and nasopharyngeal recordings of the median nerve somatosensory evoked P14 potential in coma and brain death. Detailed latency and amplitude analysis in 181 patients.

Median nerve somatosensory evoked potentials (SEPs) were recorded in a total of 181 patients in coma and brain death. Special attention was paid to derivation of P14 (the positive potential occurring approximately 14 ms after median nerve stimulation) with different electrode montages, using midfrontal scalp (Fz), linked earlobe (A1/2), median nasopharyngeal (Pgz) and non-cephalic reference (NC) electrodes. The P14 amplitude (and, to a lesser extent, latency) were invariably lower in brain death than in coma. The potential was preserved in coma in all patients, but lost in brain death in 9.8% in Fz-NC and Pgz-NC recordings, in 23.2% in Fz-A1/2, and in 100% in Fz-Pgz. Thus, Fz-Pgz was the derivation yielding the most reliable results with respect to the distinction between coma and brain death and is therefore recommended as a confirmatory test, when other diseases interrupting the lemniscal pathway (isolated brainstem death, high cervical transverse cord lesion and focal bilateral lemniscal lesion) are excluded. Theoretical considerations lead to the hypothesis of different (rostral and caudal) segments of the P14 generator dipole being recorded by the different electrode montages. It is assumed that Fz-Pgz picks up the most rostral part of P14 (rP14) that is invariably lost in brain death and preserved in coma.

Origin and distribution of P13 and P14 far-field potentials after median nerve stimulation. Scalp, nasopharyngeal and neck recording in healthy subjects and in patients with cervical and cervico-medullary lesions

We studied median nerve SEPs in 10 healthy subjects, by means of simultaneous recording over the scalp, around the neck and near the ventral surface of the medulla using a nasopharyngeal (NP) electrode. This recording technique enabled us to clearly differentiate P13 and P14 potentials. The former was always found in NP records, while the latter was more evident in scalp traces. The same technique was used to study 9 patients with various lesions of the cervical cord or cervico-medullary junction. Patients with high cervical lesions demonstrated abnormalities of both P13 and P14 potentials, while patients with lesions of the cervico-medullary junction demonstrated a clear dissociation between normal P13 in scalp and NP traces, and abnormal scalp P14. Patients with lower cervical lesions, selectively involving the central grey matter, showed normal P13 and P14 potentials, in spite of abnormal N13 cervical responses. Our findings strongly suggest that both scalp and NP P13 have the same generators in higher segments of the cervical cord, and that NP more than scalp records are effective in analyzing the P13 response. We suggest that the selective recording of the P13 potential could be useful in the assessment of focal lesions of the higher cervical cord or of the cervico-medullary junction.