Abnormal primary somatosensory function in unilateral polymicrogyria: an MEG study

The purpose of this study is to investigate the primary somatosensory function in patients with unilateral polymicrogyria. Somatosensory evoked fields (SEFs) due to median and posterior tibial nerve stimulation were compared in the normal and dysplastic cortices of five patients with unilateral polymicrogyria. SEFs were observed in all five normal hemispheres and three dysplastic hemispheres. Latencies of N20m and P38m, the first cortical components of and SEFs for median nerve and tibial nerve stimulation, were all within the normal range in both normal and dysplastic hemispheres. The amplitudes of the N20m and P38m in the dysplastic hemispheres were smaller in one patient and larger in two patients compared to the normal hemispheres. Equivalent current dipoles of N20m and P38m were localized on the anatomical central sulcus of the normal hemispheres and over the central area of the dysplastic hemispheres. P38m dipoles were localized medial and upward to the N20m dipole in both normal and dysplastic hemispheres. N20m dipole orientation was normal in all normal hemispheres and in one dysplastic hemisphere, but abnormally inferior in two dysplastic hemispheres. P38m dipole had normal medial orientation in all hemispheres except one dysplastic hemisphere. Abnormality of the primary somatosensory function in the dysplastic cortex of patients with unilateral polymicrogyria was clearly demonstrated by magnetoencephalography with high resolution in time and space. The normal somatotopic arrangement was preserved.     

Reorganization of the primary somatosensory area in epilepsy associated with focal cortical dysplasia

A 5-year-old boy with focal cortical dysplasia was referred to our hospital because of epileptic seizures. He showed mild weakness of the left hand without sensory disturbance. Brain MRI revealed extensive cortical dysplasia with pachygyria and microgyria around the right central sulcus. On EEG examination, interictal spikes were noted over the right fronto/centro/parietal region. A 37-channel magnetometer revealed that the sources of the spikes were in a small, restricted region of the normal frontal lobe adjacent to the dysplastic brain. Somatosensory evoked magnetic fields indicated that the location of the current source of N2O was in the same area. Our patient shows a unique case of plasticity and reorganization of the somatosensory function due to cortical dysplasia.     

Effect of transcranial DC sensorimotor cortex stimulation on somatosensory evoked potentials in humans.

OBJECTIVE: To study the after-effect of transcranial direct current stimulation (tDCS) over the sensorimotor cortex on the size of somatosensory evoked potentials (SEPs) in humans. METHODS: SEPs were elicited by electrical stimulation of right or left median nerve at the wrist before and after anodal or cathodal tDCS in 8 healthy subjects. tDCS was applied for 10 min to the left motor cortex at a current strength of 1 mA. RESULTS: Amplitudes of P25/N33, N33/P40 (parietal components) and P22/N30 (frontal component) following right median nerve stimulation were significantly increased for at least 60 min after the end of anodal tDCS, whereas P14/N20, N20/P25 (parietal components) and N18/P22 (frontal component) were unaffected. There was no effect on SEPs evoked by left median nerve stimulation. Cathodal tDCS had no effect on SEPs evoked from stimulation of either arm. CONCLUSIONS: Anodal tDCS over the sensorimotor cortex can induce a long-lasting increase in the size of ipsilateral cortical components of SEPs. SIGNIFICANCE: tDCS can modulate cortical somatosensory processing in humans and might be a useful tool to induce plasticity in cortical sensory processing.     

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.     

Evoked potential studies in mitochondrial encephalomyopathy

Evoked potentials were studied in a patient with a mitochondrial encephalomyopathy revealing a defect of nicotinamideadenine dinucleotide dehydrogenase and cytochrome C oxidase in the mitochondria of a muscle biopsy specimen. The biopsy specimen showed myopathic changes with ragged-red fibers and markedly decreased cytochrome C oxidase in the muscle fibers. Subcortical somatosensory evoked potentials to median nerve stimulation were normal in the peak latencies of N9, N11, and N13. Cortical somatosensory evoked potentials to median nerve stimulation revealed significantly delayed peak latencies of N20, P20, P25, and N26, although N16 latency was normal. In particular, the interpeak latency between N16 and N20 was significantly delayed. In topographic maps, N20 and P20 were delayed in the peak latencies with normal scalp distributions. Dysfunction of somatosensory cortex indicated by the delay of cortical somatosensory evoked potentials may be related to a cortical mitochondrial abnormality. The absence of responses to auditory stimulation within 10 milliseconds could be related to the dysfunction of peripheral acoustic nerves.     

Magnetoencephalographic study of giant somatosensory evoked responses in patients with rolandic epilepsy

We report five patients with rolandic epilepsy associated with giant somatosensory responses to median nerve stimulation, in whom we analyzed the pathophysiologic relationship between rolandic discharges and the somatosensory responses using magnetoencephalography. Four of the five patients showed giant P30m, the current source of which was localized in the primary somatosensory cortex, while the first cortical response, N20m, was not enhanced, except in one patient. The current source of the giant middle-latency component, N70m, was localized posterior to that of N20m, possibly in the posterior parietal cortex, in all patients. The initial positive peak and large negative peak of rolandic discharges were identical to P30m and N70m with respect to the current source localization, wave form, topographic pattern, and time relationship in the electroencephalogram and magnetoencephalogram, and somatosensory evoked magnetic field and somatosensory evoked potential records, respectively. In addition, the secondary sensory cortex was considered to be the generator of the middle-latency component in one patient. In one patient, the current intensity of the N70m was normalized along with clinical improvement and the disappearance of rolandic discharges, whereas those of other somatosensory evoked magnetic field components remained unchanged. Our data suggest that the rolandic discharge generator mechanism in these patients could be closely related to the developmental alteration of excitability in the primary somatosensory cortex, posterior parietal cortex, and secondary somatosensory cortex, which decreased with age, and it could share a common neuronal pathway, at least in part, with the giant P30m-N70m (N90m) in the somatosensory evoked magnetic field through the sequential and parallel processing of somatosensory information.     

Frontal component of the somatosensory evoked potential

Electric stimulation of the median nerve at the wrist evokes a series of electric potentials that can be recorded from the scalp or directly from the cortex. These somatosensory evoked potentials (SEP) include a parietal negativity with a maximum 20 ms after the stimulus, which originates in the somatosensory cortex, probably area 3b (Allison et al. [1991a], Brain 114:2465–2503 and Desmedt et al. [1987], Electroenceph Clin Neurophysiol 68:1–19). Thirty milliseconds after the stimulus, a negative potential (N30) occurs at frontal recording sites. Recently it was observed that the amplitude of this potential is altered in patients with dystonia, Parkinson's disease, and Huntington's chorea. It has been argued that the N30 potential stems from cortical areas other than the somatosensory cortex, for example, the supplementary motor area. We used multichannel recordings to investigate the scalp distribution of the N20 and the N30 potentials in healthy subjects. We found that the N20 as well as the N30 potentials were accompanied by a corresponding positivity at frontal and parietal recording sites, respectively. The N20/P20 and the N30/P30 potential fields had a mirrorlike appearance, and both showed a polarity reversal near the central sulcus. This and the results of correlation analyses led us to the conclusion that the N30 generator is located near the central sulcus. © 1995 Wiley-Liss, Inc.     

The significance of somatosensory evoked potentials for localization of unilateral lesions within the cerebral hemispheres

Thirty patients with unilateral lesions of the cerebral hemisphere and clinical signs of an affected somatosensory system (mainly disturbances of kinesthesia and stereoesthesia) were investigated. SEP recordings were abnormal in 27. The degree of sensory loss (especially kinesthesia) correlated well with the SEP abnormalities in 26. These SEP abnormalities could be segregated into 4 groups (types 1-4). A type 1 SEP with pathological evoked potentials from P15 on (but a normal P13/14 complex with ear- or extracephalic reference recordings) correlated with lesions of the thalamus, the internal capsule, and the centrum semiovale. A type 2 SEP characterized by loss or severe attenuation of N20 and the following components was found in patients with lesions of the postcentral gyrus. A variant (type 2a) showed isolated loss of N20, but preserved subsequent components and may be due to lesions restricted to area 3b. A third pattern of SEP abnormality is characterized by a preserved primary cortical response and loss of all the subsequent potentials. It is assumed to correlate with lesions of the parietal association cortex. In only 1 case was a type 4 SEP found, with pathological features from N3 (N55) on, caused by an ischemic stroke in area 39. Loss of all evoked responses after P13/14, including P15, suggests a lesion between thalamus and centrum semiovale. Lesions located close to the postcentral cortex lead to a loss of N20 and a variable cut off of the rising negativity following P15. Preservation of the primary cortical complex and distortion or loss of the later components point to a parietal lesion. Severe disturbances of kinesthesia and stereognosia in patients with a normal primary cortical complex and isolated abnormality of the following potentials suggests that the adjacent association cortex may be important for the perception of this complex somatosensory information. Thus the neuronal activity underlying the primary cortical response does not suffice for perception of motion and for stereoesthesia.     

Parkinson's disease and lower limb somatosensory evoked potentials: apomorphine-induced relief of the akinetic-rigid syndrome and vertex P37-N50 potentials.

We evaluated brainstem P30, vertex-central P37-N50 and contralateral frontal N37 somatosensory evoked potentials (SEPs) from the tibial nerve in 14 patients affected by Parkinson's disease (PD) with akinetic-rigid syndrome. In seven patients SEPs were recorded after administration of apomorphine. The cortical P37-N50 complex was either absent (five patients, eight tested sides) or significantly smaller in patients as compared to the control group (n = 18). There was a relationship between abnormalities of early vertex potentials and degree of motor impairment. Administration of apomorphine was followed by an increase in amplitude of P37-N50 response, which was maximal after 15-30 min and then progressively returned to basal values in parallel with clinical improvement. Amplitude of brainstem P30 and frontal N37 responses was within normal values and did not vary following drug administration. These results suggest that the P37-N50 complex arises from independent cortical generators, probably located in the pre-rolandic cortex, which may be selectively affected by basal ganglia dysfunction. Amplitude decrease of the P37-50 complex may reflect an abnormal processing of somatosensory inputs within the pre-central cortex due to defective modulation exerted by basal ganglia circuitry on cortical excitability. SEP potentiation following apomorphine, besides indicating that this dysfunction is partly reversible, might suggest objective method to measure therapeutic efficacy.     

Cortical and subcortical somatosensory evoked potentials to median nerve stimulation in man

In order to define the precise locations of precentral and postcentral gyri during neurosurgical operations, somatosensory evoked potentials to contralateral median nerve stimulation were recorded from the cerebral cortex in 19 cases with organic cerebral lesions which located near the central sulcus. In addition to that, distribution patterns of early components of SEPs were displayed by Nihonkoden Atac 450 in 3 cases who had bone defects after wide decompressive craniectomy but were without any sensory disturbances In 4 cases, in whom deep electrodes were inserted for the stereotaxic operations or other reasons, frontal subcortical SEPs were recorded in order to know the origins of frontal components of SEPs. From the parietal cortex, N19, P22 and P23 were observed. And from the frontal cortex, P20 and N25 were obtained. Their average peak latencies were as follows; (table; see text) Because all subjects had organic lesion in the brain, the peak latencies were a little bit longer, and their standard deviations were larger than those in normal cases. Usually, clear-cut phase reversal could be observed between N19 and P20 across the central sulcus. So, the precentral and postcentral gyri were easily identified during the operations. N19 and P23 appeared over the wide areas of the parietal cortex. Also, P20 and N25 were recorded almost whole areas of the frontal cortex. On the other hand, P22 appeared from relatively restricted part of the postcentral gyrus where sensory hand area might have been located. Depth recording from the frontal subcortical area revealed that P20 could be recorded from the bilateral frontal subcortical areas and there observed no phase reversal between the cortical and subcortical SEPs.(ABSTRACT TRUNCATED AT 250 WORDS)     

正中神经短潜伏期躯体感觉诱发电位头部分布研究及其临床意义

对46例健康成人,30例缺血性脑血管疾病、10例局灶性皮质病变病人进行4或5道记录,研究正中神经短潜伏期躯体感觉诱发电位(SEP)头部分布。顶 N20波、前额 P20波与中央前 P22波的时间-空间特征明显不同;在缺血性脑血管疾病中,中央前成分异常率(80%)明显比顶成分(30%)高,X~2=9.3,P<0.01;局灶性皮质病变,顶 N20-前额 P20与中央前 P22出现分离性异常现象。多道记录可以明确区分中央前 P22与前额 P20,顶 N20-前额 P20与中央前 P22有不同的神经起源,中央前 P22对缺血性脑血管疾病是一种敏感的诊断指标,同时记录这几个成分将提高 SEP 的诊断敏感性。     

Frontal and parietal components of enhanced somatosensory evoked potentials: a comparison between pathological and pharmacologically induced conditions

Pathologically enhanced somatosensory evoked potentials (giant SEPs) were recorded in 10 patients with cortical myoclonus of various origins. With non-cephalic reference electrodes a giant frontal negativity corresponding to normal N30 was found over the contra- and ipsilateral hemispheres which was not simply a phase reversal of the well-known enhanced parietal P25. The preceding far-field P14, parietal N20 and frontal P22 were of normal size. A similar result was found when SEPs were studied during the action of etomidate, an ultrashort-acting non-barbiturate hypnotic which produced a marked increase of the parietal P25 and frontal N30 after intravenous administration. These increased components, on the other hand, were abolished when recording was repeated immediately after application of electroconvulsive shock whereas P14, N20, and P22 remained more or less unchanged in both conditions. Our results indicate that there are neuronal elements in the sensorimotor cortex which are more resistant to influences such as narcotic drugs and seizure activity than others, being highly modifiable by these alterations. It is speculated whether these highly modifiable cortical systems are those in which giant SEPs, as well as pharmacologically increased SEP components, arise.     

Topography of the initial cortical component of the median nerve somatosensory evoked potential. Relationship to central sulcus anatomy.

The initial cortical component of the median nerve somatosensory evoked potential (SSEP), the parietal N20, is generated in the posterior bank of the central sulcus and inverts in polarity across the sulcus. The inversion is used to identify the central sulcus. The precentral P20 is sometimes not identifiable in scalp recordings, and this has been attributed to a dipole orientation that directs the maximum positivity downward, into the brain. The authors mapped cortical SSEPs during resection of an arteriovenous malformation in the left sensorimotor area. Preoperative scalp SSEPs over the right hemisphere were normal with a frontal P20, but those over the left hemisphere had an unusual topography with a frontal N20. Intraoperative cortical surface recordings demonstrated an N20-P20 inversion in the inferior-superior rather than the usual posterior-anterior direction. This was a result of the trajectory of the central sulcus over the surface of the brain. The section containing the hand representation was coursing in an anterior-posterior direction. This anatomic variant is an additional cause of absent frontal P20 in scalp recordings. Variations in central sulcus anatomy may cause unusual SSEP topographies, but two-dimensional SSEP mapping and correlation with the sulcal anatomy can still permit localization of the central sulcus in such cases.     

Stability of N20 onset or peak latency in median somatosensory evoked potentials

We analyzed onset and peak latencies of the N20 response of median nerve somatosensory evoked potentials (SEPs) in 21 healthy subjects by simultaneous recordings with noncephalic or ear reference from multiple scalp sites. The cortical onset was defined as the fork at which the contralateral parietal and frontal or ipsilateral parietal waves diverged. We found the N20 onset unchanged between noncephalic and ear reference recordings, or among the recordings around the contralateral centroparietal scalp. The N20 peak was prolonged when the recording position moved posteriorly. We suggest that N20 onset latency is more stable than N20 peak.     

Study of early somatosensory evoked potentials by stimulation of the median nerve at the wrist in 6 patients with unilateral thalamic lesions

Somatosensory evoked potentials were recorded at Erb's point, over the cervical spine (C7) and over the cortex: parietal and frontal electrodes were contralateral and ipsilateral to the stimulus which was applied on the median nerve at the wrist. The stimulation was performed on 2 control groups, the first consisting of 10 subjects (average age: 33.6 years), the second of 16 subjects (average age: 66.2 years) and on 6 patients presenting unilateral thalamic lesions. These lesions were circumscribed, ischaemic or haemorrhagic and were visualized by a scanner. In 5 of our patients, a diffusion of the P14 wave with normal latency and a delay in the N20 cortical wave was obtained at the parietal electrode contralateral to the stimulus and homolateral to the lesion. Normal latencies were observed for the diffusion of the N18 wave recorded at the frontal electrode contralateral to the stimulus. In the 6th patient, the evoked potentials were normal. The results of the somatosensory evoked potentials observed in our patients are discussed in the context of the anatomical lesions.     

The evolving MR imaging appearance of lissencephaly: a case report

MR imaging of a patient with epilepsy and psychomotor retardation at 5 months revealed parieto-occipital pachygyria with almost normal cortical appearance and thickness in the frontal region; this appearance evolved into diffuse pachygyria at 7 years. The change of the MR imaging findings may have resulted from myelination in the intracortical and subcortical fibers. It is important for clinicians to be aware of the longitudinal changes of the cerebral cortex in lissencephaly.     

Somatosensory evoked potential recovery in myotonic dystrophy.

OBJECTIVE: To evaluate recovery functions of the sensory cortex using somatosensory evoked potentials (SEPs) elicited by paired stimuli of the median nerve in patients with myotonic dystrophy (MD). SUBJECTS/METHODS: Twelve MD patients were enrolled in the present investigation. Five patients with facioscapulohumeral muscular dystrophy (FSH) and 12 healthy volunteers were studied as control groups. SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Single pulse or paired-pulse stimuli at various interstimulus intervals (ISIs) (10, 20, 40, 60, 80, 100, 150, 200 and 300 ms) were given. Recovery functions of N9, N20onset-N20peak, N20-P25 and P25-N33 components were studied. RESULTS: Conventional SEPs to a single stimulus were normal in the latency and amplitude in all the patients. Recovery functions of both N9 and N20o-N20p components were normal in the patients. In contrast, in MD patients, disinhibited or hyperexcitable recovery pattern was observed in recovery curves of the N20-P25 or P25-N33 components, whereas those were normal in FSH patients. CONCLUSIONS: Disinhibited cortical excitability (or hyperexcitability) is present in the sensory cortex in patients with myotonic dystrophy. This may reflect cortical pathology or functional alteration of the sensory cortex in MD.     

Somatosensory evoked magnetic fields from the primary somatosensory cortex (SI) in acute stroke.

We recorded somatosensory evoked magnetic fields (SEFs) to median nerve stimulation from 15 patients in the acute stage (1-15 days from the onset of the symptoms) of their first-ever unilateral stroke involving sensorimotor cortical and/or subcortical structures in the territory of the middle cerebral artery (MCA). Neuronal activity corresponding to the peaks of the N20m, P35m and P60m SEF deflections from the contralateral primary somatosensory cortex (SI) was modelled with equivalent current dipoles (ECDs), the locations and strengths of which were compared with those of an age-matched normal population. Four patients with pure motor stroke had symmetric SEFs. In one of the 4 patients with pure sensory stroke, and in 5 of the 7 patients with sensorimotor paresis, the SEFs were markedly attenuated or missing. All except one patient with abnormal SEFs had deficient two-point discrimination ability; especially the attenuation of N20m was more clearly correlated with two-point discrimination than with joint-position or vibration senses. Of the different SEF deflections, P35m and P60m were slightly more sensitive indicators of abnormality than N20m, the former being affected in two patients with symmetric N20m. Three patients with pure sensory stroke and lesions in the opercular cortex had normal SEFs from SI. We conclude that the SEF deflections N20m, P35m and P60m from SI are related to cutaneous sensation, in particular discriminative to touch. The results also demonstrate that basic somatosensory perception can be affected by lesions in the opercular cortex in patients with functionally intact SI.     

Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study.

OBJECTIVE: To study the immediate sensorimotor neurophysiological effects of cervical spine manipulation using somatosensory evoked potentials (SEPs). METHODS: Twelve subjects with a history of reoccurring neck stiffness and/or neck pain, but no acute symptoms at the time of the study were invited to participate in the study. An additional twelve subjects participated in a passive head movement control experiment. Spinal (N11, N13) brainstem (P14) and cortical (N20, N30) SEPs to median nerve stimulation were recorded before and for 30min after a single session of cervical spine manipulation, or passive head movement. RESULTS: There was a significant decrease in the amplitude of parietal N20 and frontal N30 SEP components following the single session of cervical spine manipulation compared to pre-manipulation baseline values. These changes lasted on average 20min following the manipulation intervention. No changes were observed in the passive head movement control condition. CONCLUSIONS: Spinal manipulation of dysfunctional cervical joints can lead to transient cortical plastic changes, as demonstrated by attenuation of cortical somatosensory evoked responses. SIGNIFICANCE: This study suggests that cervical spine manipulation may alter cortical somatosensory processing and sensorimotor integration. These findings may help to elucidate the mechanisms responsible for the effective relief of pain and restoration of functional ability documented following spinal manipulation treatment.     

Bilateral frontal polymicrogyria: a newly recognized brain malformation syndrome

BACKGROUND AND OBJECTIVE: Polymicrogyria is a brain malformation characterized by abnormal cortical lamination, excessive cortical folding, and fusion of the cortical molecular layer. Two distinct bilateral localized forms have been described: bilateral perisylvian polymicrogyria, which has proved to be genetically heterogeneous, and bilateral parasagittal parieto-occipital polymicrogyria, which has been described only in sporadic patients. We describe 13 patients with symmetric polymicrogyria of both frontal lobes back to the precentral sulcus: bilateral frontal polymicrogyria (BFP). METHODS: Review of clinical records, brain MRI, and EEG results of 13 patients; correlation with other regional polymicrogyrias. RESULTS: The abnormal cortex extended from the frontal poles anteriorly to the precentral gyrus posteriorly and to the frontal operculum inferiorly and was relatively symmetric in all 13 patients. All patients presented with developmental delay and mild spastic quadriparesis, but variably impaired language development (12/13), mental retardation (11/13), and epilepsy (5/13) also occurred. BFP was sporadic in 13 of 13 patients, but 2 of 13 had consanguineous parents. CONCLUSIONS: BFP extends the spectrum of the recognized bilateral symmetric regional polymicrogyria syndromes.