Serial visual evoked potentials and outcome in term birth asphyxia

Birth asphyxia is a major cause of neonatal mortality and morbidity. It remains difficult to predict accurately neurologic outcome among survivors, particularly infants with moderate hypoxic-ischemic encephalopathy. Visual evoked potential (VEP) is a reproducible measure of cortical function and reflects acute changes in central nervous system status secondary to asphyxial insult. We performed serial VEPs on 36 term infants with documented birth asphyxia to investigate the relationship between VEPs and neurodevelopmental outcome at 18 months of age. Fourteen infants were neurologically intact at subsequent examination; all had normal VEPs during the first week of life. Twenty-two infants had died or were significantly handicapped at 18 months of age; 20 had abnormal VEPs persisting beyond day 7 of life. Abnormal VEPs accurately predicted abnormal outcome (100%) and were both sensitive (91%) and specific (100%). In 20 infants who were classified as moderately asphyxiated according to the criteria of Sarnat and Sarnat, even greater accuracy, sensitivity, and specificity (all 100%) were observed. VEPs demonstrate good correlation with neurodevelopmental outcome in term infants with birth asphyxia and provide accurate prognostic information useful in the clinical management of these infants.     

Somatosensory evoked potentials in the term newborn.

Median nerve somatosensory evoked potentials (SEPs) were recorded from surface electrodes in 40 healthy term infants (range 36.5-43 weeks postmenstrual age). Electrical stimulation at 5 Hz was used, averaging the response to several runs of 1024 stimuli to each median nerve, bandpass 10-3000 Hz, sweeptime 100 msec. Identifiable potentials were collected over the cervical cord on all runs in all 40 infants and from the cortex in at least some runs in 39 out of 40 infants. The cervical response showed little variation and consisted of a clear negative wave with up to 3 peaks, mean latency of the largest 10.2 +/- 0.7 msec, followed by a positive deflection. The cortical response was very variable in form and latency between infants and to a lesser degree within infants. Four types of cortical wave form were found, symmetrical, asymmetrical, plateau and M shaped, of increasing complexity. In 11% of trials the response was absent or indistinct but could usually be uncovered by alteration in stimulus frequency or intensity. In the whole group, the mean latency for N1 was 30.0 +/- 6.8 msec and for the central conduction time 19.8 +/- 6.5 msec. Significant differences were found between the 4 cortical wave forms in the main variables measured, which gave support for form S being the most primitive and form M the most mature response.     

Somatosensory evoked potentials in term and preterm infants in relation to postconceptional age and birth weight

The effect of age on the maturation of median nerve somatosensory evoked potentials (SEPs) was studied in 103 normal neonates (24 preterm, 79 term) at the postconceptional age (PCA) of 36-48 weeks. The influence of birth weight was evaluated in 44 term neonates, aged 0-7 days, according to their gestational age (GA) stratified into three groups: A: 38-39 weeks (n = 15); B: 39.5-40.5 weeks (n = 15); C: 41-43 weeks (n = 14). The mean birth weight was not different in the three groups. For all infants the N13 latency recorded at cervical (CS2-Fz) level as well as the N19 onset and peak latency at cortical (C3'/C4'-Fz) level were measured. For these parameters and for the N13 latency divided by arm length (N13/AL) and the N19 ascending time (N19AT) the P50, P97 and P3 were calculated as a function of PCA. They were all decreasing in the 36-48 weeks period, fast before 40 weeks and slowly thereafter. The SEP values of groups, A, B and C were not different, but in each group the wave pattern of the cortical SEPs was more mature in the larger than in the smaller infants. For the groups A, B and C together birth weight (in SDS) correlated inversely with the N13/AL and the N19AT (both in SDS) (r = 0.73 and 0.52 respectively, p less than 0.001). Our data indicate that the progression of maturation of the various SEP components in the period of 36-48 PCA is non-linear.(ABSTRACT TRUNCATED AT 250 WORDS)     

Somatosensory evoked potentials in abetalipoproteinemia

Visual, brain-stem auditory, and somatosensory evoked potentials (SEPs) were obtained on a patient with known abetalipoproteinemia. Only the SEP was abnormal, and it correlated with the reported neuropathology of this disease. Serial SEP studies remained stable, as had the clinical condition of this patient on vitamin E therapy. The SEP may supplement clinical examination in follow-up of patients under treatment.     

Prognostic value of early somatosensory evoked potentials for adverse outcome in full-term infants with birth asphyxia.

SEPs were examined during the first weeks of life in 34 infants with mild to severe birth asphyxia, in an attempt to provide a more accurate prediction of neurodevelopmental outcome. Normal, delayed and absent responses were compared with the infant's acute clinical condition, imaging findings using different imaging techniques and neurodevelopmental outcome. All infants with normal SEPs were normal at follow-up. All but two of the infants with a delayed or absent response died or suffered from severe neurological sequelae. A delayed or absent N1 latency carried a risk for death or severe handicap of 71 and 100%, respectively, compared with 25 and 89% for moderate or severe encephalopathy on neurological assessment, and 29 and 85% for moderate or severe changes seen using different imaging techniques. SEPs may provide useful additional information when assessing the infant with birth asphyxia.     

Somatosensory evoked potentials after experimental head injury in the awake rat

Experimental acceleration concussion was induced in 30 male rats who were immobilized with curare, artificially ventilated but not anaesthetised. Serial recordings of cortical somatosensory evoked potentials (SEPs) were made from the onset of concussion and for the following 30 min. Immediately after the head blow the initial three components of the SEP (P1, N1 and P2) were all either absent or markedly increased in latency. The late negative component (N2) was always abolished. All components reappeared and returned to approximately pre-concussion latencies within 5-6 min. The most persisting abnormality was in N2 whose post-concussion amplitude stabilized and remained depressed at only 50% of baseline value. The results suggest that experimental head injury produces a significant abnormality in every component of the evoked potential. The findings are therefore inconsistent with the theory that concussion differentially affects the diffuse nonspecific pathways whose activity is mediated by the reticular formation while leaving the lemniscal system comparatively intact. It is also shown that the morphology of the post-concussion SEP waveform can be quite accurately simulated by recording SEPs from normal animals at high rates of stimulation (50/s). This implies that the pathophysiology of concussion involves a temporary dysfunction in synaptic transmission although the level at which this is occurring has yet to be determined.     

Somatosensory evoked potentials in Huntington's chorea

Somatosensory evoked potentials were measured in 21 patients with Huntington's chorea and 12 controls. Central brain conduction time was normal. Early cortical component amplitudes were reduced in the patient group, latencies were normal. These abnormalities probably can be attributed to cortical dysfunction in Huntington's chorea. No indication of brain-stem dysfunction was found.     

Somatosensory evoked potentials in Charcot-Marie-Tooth disease

SEPs by median nerve stimulation have been performed in 18 adult patients (12 males and 6 females) affected by CMTD (type I, 13 patients; type II, 5 patients). All patients underwent MCV studies (median, ulnar, peroneal nerve), SCV studies (median and sural nerve), VEP, BAEP. N9 and N13 peaks were not detectable in 7/13 and 5/13 cases (HMSN type I) while cortical N19 were always recorded. Latency values of all responses were moderately or markedly delayed in all cases with HMSN type I, but proved normal or slightly delayed in HMSN type II cases. The prolonged latencies were mainly related to slowing of peripheral conduction. N9-N13 inter-peak was abnormally prolonged in 2 cases and N13-N19 in 2 other cases; both were prolonged in another case. In another 3 cases an abnormal BAEP was recorded. The few patients with abnormal CCT and BAEP probably belong to a borderline form between HMSN and hereditary ataxias.     

Somatosensory evoked potentials in Arnold-Chiari malformation

Nearly all patients with repaired myelomeningoceles have an Arnold-Chiari (AC) malformation and about 20% of these patients develop clinical signs of brainstem dysfunction. The management of symptomatic AC malformation is still controversial and techniques are needed to provide an objective assessment of brainstem function. We recorded somatosensory evoked potentials (SEPs) in 52 patients aged between 8 months and 20 years (median 7.3 years) with AC malformation, to determine whether the SEPs discriminate patients with symptomatic AC malformation from those without symptoms. The subcortical far-field components P13, P14 and N18, which are generated within the brainstem, were recorded with non-cephalic reference electrodes and the cortical N20 with a frontal reference. Fourteen patients (27%) had signs and symptoms of brainstem dysfunction, which were related to the AC malformation. Abnormal SEPs were mainly recorded in symptomatic patients (sensitivity 0.7, specificity 0.9). The SEPs were particularly useful in patients from 4 years of age (sensitivity 0.9, specificity 0.9), but not in the younger age group. Abnormal somatosensory conduction reflects dysfunction of the brainstem or the upper cervical cord and may be clinically useful to assess patients with late onset symptomatic AC malformation.     

Somatosensory evoked potentials in Huntington's disease

Scalp recorded somatosensory evoked potentials (SEPs) elicited by left and right median nerve stimulation were obtained in 21 patients with Huntington's disease (HD), 14 individuals at risk (AR) for HD, and 21 non-patient controls matched for age and sex. Although SEP abnormalities were not uniform in the HD group, no HD patient had SEPs that conformed fully to the normal configuration with respect to peak latencies, presence of all components and spatial distribution. The most common abnormality was non-specific in nature, consisting of amplitude reduction or virtual abscence of components after 100 msec. More specific deviations were noted in the early SEP events. In half of the HD patients, peak P30 seemed to occur at approximately 45 msec poststimulus; this peak could have been taken as the normal P45 had it not reversed in phase between the central and frontal leads. In these cases peak P45 prepared to be missing. Peak N20 latency values were longer in the HD group than in the non-patient controls, whereas the P15 latencies did not differ significantly. The conduction time between P15 and N20 was significantly longer in HD patients than the non-patient controls. SEPs of the majority of the ARs were similar to those of the non-patients controls in terms of overall configuration, although mean amplitudes were generally lower for ARs than non-patient controls and 4 ARs exhibited prolonged P15-N20 latency differences.     

Somatosensory evoked potentials in lacunar syndromes

Summary Parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from 40 patients with lacunar syndromes due to CT-verified lacunar infarcts. The control group consisted of 30 age-matched normal controls. Nineteen patients showed SEP abnormalities, mainly an increase of height-covariated latency of cortical components and/or of the central conduction time. Such changes occurred independently of the clinical features of lacunar syndromes, being related more to the lesion location than to its size. SEP studies may be a useful adjunct to the clinical diagnosis of lacunar infarct, possibly also when the CT scans are normal.     

Somatosensory evoked potentials in syringomyelia.

The two types of upper limb somatosensory evoked potential abnormality observed in nine patients with syringomyelia were reduced amplitude or absent cervical potentials and an abnormal central conduction time. Although this pattern of abnormalities resembles that observed in other intrinsic spinal cord lesions, it differs from peripheral nerve diseases and cervical radiculopathy in which the central conduction time is normal.     

Somatosensory evoked potentials in intraspinal tumors

SEPs have been recorded in 15 patients with spinal cord tumors (mostly ependymomas) and in 5 patients with cord compression due to meningiomas (3 cas), neuromas (1 case) or neurosarcoma (1 cas). All the patients have been operated on so that precise informations were available on the histology and the location of the tumor. SEPs were monitored during surgery in 8 patients. The main conclusions of this study are as follows: There was a good correlation between the somatosensory troubles for touch, vibration sense and joint position sense, and SEPs abnormalities, however, SEPs may be clearly abnormal in the absence of any somatosensory deficit when the dorsal columns are compressed and not infiltrated by the tumor. In the latter situation the reverse dissociation (i.e., normal SEPs with somatosensory troubles) may be observed. The possibility of a dissociation between normal N11 and N13 cervical components and absent P14 far field components (non-cephalic reference) has been confirmed in 6 patients with cervicomedullary tumors. In 3 of them, this dissociation was found to be reversible and early SEPs returned to normal after surgery. Peroperative monitoring of scalp SEPs recorded with a non-cephalic reference electrode allowed the detection of transient SEP abnormalities related with a traction on the dorsal columns of the cord. SEP monitoring is recommended for any surgical removal of tumor that needs a posterior myelotomy.     

Somatosensory evoked potentials following severe head injury: loss of the thalamic potential with brain death

The thalamic component (P17) of the short-latency somatosensory evoked potential (SEP) was assessed to determine its usefulness in patients with severe head injury. Subjects were a group of patients admitted to the Auckland Hospital Critical Care Unit who subsequently died from head injury. In all instances where brain death was unequivocally established and a SEP recording made in close temporal proximity to the time of brain death the P17 potential was absent. When there was evidence of continuing brainstem activity and particularly where prolonged survival occurred following the last SEP recording the P17 potential remained intact bilaterally. This study shows that the presence or absence of the thalamic component of the short-latency SEP provides a reliable electrophysiological measure of brainstem function in patients where brain death has been suspected.     

Seizure-associated brain injury in term newborns with perinatal asphyxia

BACKGROUND: There is controversy over whether seizures, the most common manifestation of neonatal brain injury, may themselves damage the developing brain. OBJECTIVE: To determine if neonatal seizures are independently associated with brain injury in newborns with perinatal asphyxia. METHODS: Ninety term neonates were studied with MRI and single-voxel (1)H-MRS on median day of life 6 (range 1 to 13 days). The severity of MR abnormality in the (1)H-MRS regions of interest was scored using a validated scale. Seizure severity was scored based on seizure frequency and duration, EEG findings, and anticonvulsant administration. Multivariable linear regression tested the independent association of seizure severity with impaired cerebral metabolism measured by lactate/choline and compromised neuronal integrity measured by N-acetylaspartate/choline in both regions. RESULTS: Clinical seizures occurred in 33 of 90 infants (37%). Seizure severity was associated with increased lactate/choline in both the intervascular boundary zone (p < 0.001) and the basal nuclei (p = 0.011) when controlling for potential confounders of MRI abnormalities and amount of resuscitation at birth. Each increase in seizure score was independently associated with a 21% increase in lactate/choline in the intervascular boundary zone (95% CI, 5.1-38.2%) and a 15% increase in the basal nuclei (95% CI, 0.1-31.7%). Seizure severity was independently associated with diminished N-acetylaspartate/choline in the intervascular boundary zone (p = 0.034). CONCLUSION: The severity of seizures in human newborns with perinatal asphyxia is independently associated with brain injury and is not limited to structural damage detectable by MRI.     

The prognostic value of somatosensory evoked potentials in traumatic primary and secondary brain stem lesions

To estimate the prognostic value of somatosensory evoked potentials elicited via stimulation of the median nerve (M-SSEP) in cases of primary and secondary brainstem lesions 126 patients with traumatic brainstem lesions (GCS < or = 6) were investigated on admission to our hospital. Various parameters of the patients' M-SSEP were compared with the corresponding data of 40 healthy persons. Latency and amplitude of the cervical (N14) and cortical (N20) derived potentials and the central conduction time (CCT) were taken into account. Changes or a loss of the N20 signal and of the CCT were related to clinical outcome for up to two years. All patients had a normal N14 bilaterally. Most patients with a primary brainstem lesion (n = 25) showed symmetrical N20 changes bilaterally. However, the majority of patients with a secondary brainstem lesion (n = 62) showed asymmetric N20 changes in M-SSEP which became more symmetrical in cases with marked progressive brainstem compression. Irrespective of a primary or secondary traumatic brainstem lesion, marked changes of N20 represented an unfavourable clinical prognosis. A loss of N20 was closely correlated with a very poor outcome (GOS 1-2) if the N20 potential had not recovered within 48 hours. The recovery of this potential, however, was not necessarily correlated to a recovery of the brain function.