Abnormal Brainstem Auditory Evoked Potentials Research Articles

A New Animal Model of Hemolytic Hyperbilirubinemia-Induced Bilirubin Encephalopathy (Kernicterus)

Neonatal hyperbilirubinemia can cause bilirubin encephalopathy (kernicterus). Spontaneously jaundiced (jj) Gunn rats treated with sulfonamide (sulfa) to displace bilirubin from serum albumin, develop bilirubin encephalopathy and abnormal brainstem auditory evoked potentials (BAEPs) comparable with human newborns. We hypothesized phenylhydrazine (PHZ)-induced hemolysis would significantly elevate total plasma bilirubin (TB) in jj Gunn rat pups and produce BAEP abnormalities similar to those observed after sulfa. PHZ 0, 25, 50, or 75 mg/kg was administered intraperitonealy to 15-d-old jjs. An initial TB was recorded in each animal, and a second recorded 1-4 d postinjection to generate a dose-response curve. After PHZ 75 mg/kg, TB peaked at about 30 mg/dL at 48-72 h. A second group of jjs injected with PHZ (0, 25, 50, or 75 mg/kg) and nonjaundiced controls given PHZ 75 mg/kg had HCT and TB at baseline, and HCT, TB, and BAEPs recorded at 48 h. BAEP wave II and III amplitudes decreased, and I-II and I-III interwave intervals increased indicating abnormal central (brainstem) auditory function. PHZ-induced hemolysis in jaundiced Gunn rat pups produces sufficiently elevated TB levels to produce bilirubin encephalopathy. This new model may be a more clinically relevant experimental model of kernicterus- and bilirubin-induced neurologic disorders.

Evaluation of brain stem auditory evoked potentials in stable patients with chronic obstructive pulmonary disease.

Though there are few studies addressing brainstem auditory evoked potentials (BAEP) in patients with chronic obstructive pulmonary disease (COPD), subclinical BAEP abnormalities in stable COPD patients have not been studied. The present study aimed to evaluate the BAEP abnormalities in this study group.MATERIALS AND METHODS:In the present study, 80 male subjects were included: COPD group comprised 40 smokers with stable COPD with no clinical neuropathy; 40 age-matched healthy volunteers served as the control group. Latencies of BAEP waves I, II, III, IV, and V, together with interpeak latencies (IPLs) of I-III, I-V, and III-V, and amplitudes of waves I-Ia and V-Va were studied in both the groups to compare the BAEP abnormalities in COPD group; the latter were correlated with patient characteristics and Mini–Mental Status Examination Questionnaire (MMSEQ) scores to seek any significant correlation.RESULTS:Twenty-six (65%) of the 40 COPD patients had BAEP abnormalities. We observed significantly prolonged latencies of waves I, III, V over left ear and waves III, IV, V over right ear; increased IPLs of I-V, III-V over left ear and of I-III, I-V, III-V over right side. Amplitudes of waves I-Ia and V-Va were decreased bilaterally. Over left ear, the latencies of wave I and III were significantly correlated with FEV1; and amplitude of wave I-Ia, with smoking pack years. A weak positive correlation between amplitude of wave I-Ia and duration of illness; and a weak negative correlation between amplitude of wave V-Va and MMSEQ scores were seen over right side.CONCLUSIONS:We observed significant subclinical BAEP abnormalities on electrophysiological evaluation in studied stable COPD male patients having mild-to-moderate airflow obstruction.

NMDA Channel Antagonist MK-801 Does Not Protect against Bilirubin Neurotoxicity

Background: Bilirubin encephalopathy or kernicterus is a potentially serious complication of neonatal hyperbilirubinemia. The mechanism of bilirubin-induced neurotoxicity is not known. Many neurological insults are mediated through NMDA receptor activation. Objective: We assessed the effect of the NMDA channel antagonist, MK-801 on bilirubin neurotoxicity in vivo and in vitro. Methods: Bilirubin toxic ity in vitro was assessed using trypan blue staining. Sulfadimethoxine injected (i.p.) jaundiced Gunn rat pups ex hibit many neurological sequelae observed in human hyperbilirubinemia. Brainstem auditory-evoked potentials (BAEPs), a noninvasive sensitive tool to assess auditory dysfunction due to bilirubin neurotoxicity, were used to assess neuroprotection with MK-801 (i.p.) in vivo. Results: In primary cultures of hippocampal neurons, 20 min exposure to 64:32 µM bilirubin:human serum albumin reduced the cell viability by approximately 50% ten hours later. MK-801 treatment did not protect the cells. MK-801 pretreatment doses ranging from 0.1–4.0 mg/kg did not protect against BAEP abnormalities in Gunn rat pups 6 h after sulfadimethoxine injection. Conclusion: Our findings suggest that bilirubin neurotoxicity is not mediated through NMDA receptor activation.

Biliverdin-induced brainstem auditory evoked potential abnormalities in the jaundiced Gunn rat

Brainstem auditory evoked potential (BAEP) abnormalities occur in jaundiced Gunn rats given sulfadimethoxine to displace bilirubin bound to serum albumin, releasing it into the tissues. One problem with the model is that after displacement, plasma bilirubin levels drop and do not correlate with neurological dysfunction. In this report, we administered biliverdin, the immediate precursor of bilirubin, in 15- to 17-day-old Gunn rat pups to create an improved model of bilirubin-induced neurological dysfunction. Total plasma bilirubin (TB) levels were measured with a Leica bilirubinometer. Biliverdin (40 mg/kg) or phosphate-buffered saline (PBS) was administered either once and BAEPs recorded 8 h later or twice, 12 h apart, and BAEPs recorded 24 h after the initial injection. A single biliverdin injection produced a significantly decreased amplitude of BAEP wave III, 1.21 ± 0.25 vs. 0.49 ± 0.27 μV (control vs. biliverdin). The two-injection paradigm resulted in a significantly elevated TB (9.9 ± 1.2 vs. 14.9 ± 3.1 mg/dl; control vs. biliverdin), significant increases in I–II (1.15 ± 0.08 vs. 1.42 ± 0.09 ms) and I–III (2.17 ± 0.08 vs. 2.5 ± 0.13 ms) interwave intervals and a decrease in the amplitude of wave III (1.36 ± 0.30 vs. 0.38 ± 0.26 μV). Additionally, there were significant correlations between TB and the amplitude of wave III ( r 2 = 0.74) and TB and the I–III interwave interval ( r 2 = 0.51). In summary, biliverdin administration in jaundiced Gunn rat pups produces BAEP abnormalities consistent with those observed in the sulfadimethoxine model and human newborn hyperbilirubinemia and resulted in increased plasma bilirubin levels that correlate with the degree of neurological dysfunction.

Value of brainstem auditory evoked potential in diagnosing cerebral palsy

目的 通过脑干听觉诱发电位(BAEP)分析探讨脑瘫患儿的听力障碍及脑干功能变化.方法采用意大利MYTO诱发电位仪测定75例脑瘫患儿BAEP.结果BAEP异常者54例(72%),表现为不同程度的脑干波形分化不良,Ⅰ波峰潜伏期,Ⅰ～Ⅲ、Ⅲ～Ⅴ波峰间期延长,Ⅴ/Ⅰ波幅比值异常.结论BAEP能客观反映脑瘫患儿的听力障碍及脑干功能状态。

Study of Brainstem Auditory Evoked Potential (BAEP) in patients with silent brainstem infarction

目的 探讨无症状脑干梗死患者脑干听觉诱发电位(BAEP)变化.方法对影像学诊断明确的21例无明显症状和体征的脑干梗死患者BAEP与20例对照组进行对比分析.结果脑干梗死组18例BAEP异常,异常率为85.71%,其中Ⅲ、V波PL和PⅡ-Ⅴ IPL较对照组明显延长,有非常显著性差异(P＜0.01).结论BAEP可早期发现无症状脑干梗死的存在,对脑干损害有较高的定位诊断价值。

Sensory evoked potentials in infants with Down syndrome

To investigate the sensory functions of the peripheral to central pathways in infants with Down syndrome (DS) by sensory evoked potentials. Fifty-five infants, 30 DS infants and 25 controls, were examined by multimodal evoked potentials, including brainstem auditory evoked potentials (BAEP), visual evoked potentials (VEP) and short-latency somatosensory evoked potentials (SSEP). No obvious difference was found in the peak latencies between the two groups for BAEP. Nine children with DS showed abnormal BAEP; six had hearing loss and three had prolonged wave I latencies. For VEP, the peak latencies of P(2) and N(2) were significantly longer and the amplitudes were smaller in the DS group than in the control group. Of the 30 infants with DS, five had significantly prolonged P(2) latencies and two had lower amplitudes. In SSEP, the mean latencies of N(20) and the interpeak latencies of N(13)-N(20) of the infants with DS showed apparent prolongation compared to the controls. Seven of 30 (23.3%) DS patients had prolonged N(20) latencies. Our results indicate that various sensory deficits occur in patients with DS during the first year of life.

Diagnostic value of multimodal evoked potentials in patients with multiple sclerosis

Different multimodal evoked potentials (MEPs) have a great importance in multiple sclerosis (MS) diagnostics. Previously performed studies have shown different results in MEP application concerning the diagnostic sensitivity. We wanted to show our experiences in diagnostic value of MEPs through a retrospective study of multiple sclerosis patients. During the last 2 years (2002, 2003), visual evoked potentials (VEPs), brain stem auditory evoked potentials (BAEPs), and somatosensory evoked potentials (SEPs) have been performed in 111 patients with probable and definitive forms of MS. Our results indicated abnormalities of BAEPs in 64 patients (57.6%), VEPs in 69 patients (62.1%), median nerve SEPs in 70 patients (67.0%), and tibial nerve SEPs in 97 patients (87.3%). These results show the greatest diagnostic value of SEPs, followed by VEPs, and BAEPs with the lowest sensitivity.

Hereditary Ataxia in the Jack Russell Terrier– Clinical and Genetic Investigations

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2–9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory‐evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.

Brain damage in glycogen storage disease type I

Objective To investigate brain morphology and function in patients with glycogen storage disease type I (GSDI). Study design Nineteen patients (13 females and 6 males, aged 0.9-22.6 years) and 38 sex- and age-matched controls entered the study. Neurological examinations, psychometric tests (IQ, tests of performance and verbal abilities), standard electroencephalogram (EEG), somatosensory (SEPs), visual (VEPs), and brain-stem auditory evoked potentials (BAEPs), and brain magnetic resonance imaging (MRI) were performed. Results The results of tests of performance ability were lower in patients than in controls ( P < .05). The prevalence of abnormal EEG findings (26.3% versus 2.6%), VEPs (38.4% versus 7.7%), SEPs (23.0% versus 0%), and BAEPs abnormalities (15.7% versus 0%) was higher in patients than in controls ( P < .05). MRI pattern was altered in 57.1% of patients and was normal in all controls ( P < .05). Both results of tests of performance ability and BAEPs abnormalities significantly correlated with the frequency of admissions for hypoglycemia, whereas EEG abnormalities correlated with dietary compliance ( P < .05). Conclusions Brain damage, probably caused by recurrent severe hypoglycemia, may be present in patients with GSDI.

Hereditary ataxia in the Jack Russell Terrier--clinical and genetic investigations.

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.

Auditory neuropathy in Friedreich ataxia: A report of two cases

Friedreich ataxia (FA) is a hereditary neurodegenerative disease with autosomical recessive inheritance. The purpose of this paper is to present two cases of FA with auditory neuropathy, demonstrated by Otoacoustic emissions (OAE) and brainstem auditory evoked potentials (BAEP). The patients were two adolescent girls. Both patients underwent behavioral pure-tone audiometry, BAEP, OAE, motor nerve conduction measurement, and magnetic resonance image studies. Both girls showed at least five of nine clinical criteria for FA. They also showed abnormal BAEP and normal OAE indicating auditory neuropathy. One patient showed normal thresholds on behavioral pure-tone audiometry, whereas the other patient showed a mild sensorineural hearing loss. In one case there was absence of peripheral caloric vestibular response, and electronystagmographic abnormalities compatible with cerebellar dysfunction. Cochlear function as assessed by OAE had not been reported previously in cases of FA. We conclude that auditory neuropathy should be considered in patients diagnosed as FA. Furthermore, BAEP and OAE should be included in the diagnostic routine in these patients.

Topographical relationships between the brainstem auditory and somatosensory evoked potentials and the location of lesions in posterior fossa stroke.

The topographical relationships between the location of brainstem lesions detected by magnetic resonance imaging and abnormality of brainstem auditory evoked potentials (BAEPs) and short-latency somatosensory evoked potentials (SSEPs) were studied in 57 patients with stroke in the posterior fossa. Abnormal BAEPs or SSEPs were associated with lesions involving the pontine tegmentum, and abnormal BAEPs also with lesions at the cerebellar peduncle. Absence of the V wave in BAEPs and N20 in SSEPs was associated with a localized overlapping area in the pontine tegmentum contralateral to stimulation. The overlapping area associated with loss of N20 coincided with the location of the medial lemniscus. Lesions widely involving the pontine tegmentum caused the disappearance of multiple waves in the BAEPs and SSEPs. Patients who entered prolonged coma or died had total loss of the III, IV, and V waves, bilateral absence to the contralateral response in BAEPs, or loss of N18 in SSEPs. The loss of N18 in SSEPs had a statistically significant correlation with bad outcome, which suggests the superiority of SSEPs for predicting the outcome of stroke and indicates the involvement of some system excluding the medial lemniscus in the generation of N18.

Somatosensory and brainstem auditory evoked potentials in the Gunn rat model of acute bilirubin neurotoxicity.

Brainstem auditory evoked potentials (BAEPs) are a sensitive indicator of bilirubin neurotoxicity. Somatosensory evoked potentials (SEPs) have been proposed as another measure of toxicity, though the lemniscal pathways that generate the SEP are not involved in kernicterus. In 16 to 17-d-old jaundiced (jj) Gunn rats, serial BAEPs and SEPs were obtained up to 8 h after acute bilirubin toxicity. jjs were injected with 150 mg/kg sulfadimethoxine to displace bilirubin into brain tissue (n = 8); littermate controls were jjs given saline (n = 4) and nonjaundiced given sulfadimethoxine or saline (n = 7). After anesthesia, BAEP and SEP recordings were obtained at baseline and serially after injection. SEPs to median nerve stimulation were recorded from surface electrodes over the brachial plexus (Erb's) and contralateral parietal cortex, and subtracted to obtain central conduction time (CCT). There were no statistically significant different baseline values between groups. Baseline BAEP I, I-II, and I-III were 1.22 +/- 0.13, 1.11 +/- 0.12, and 2.10 +/- 0.15 ms, and SEP Erb's and CCT were 1.48 +/- 0.20 and 5.59 +/- 0.50 ms, respectively (n = 19). At 6.8 +/- 1.5 h after injection BAEP I, I-II, and I-III increased 0.10 +/- 0.08, 0.18 +/- 0.17, and 0.56 +/- 0.33 ms over baseline, respectively (p = 0.005, 0.01, and 0.001, respectively, paired, 1-tailed t-tests), in experimental but not control groups. SEP Erb's decreased slightly, -0.06 +/- 0.04 ms in experimental and -0.08 +/- 0.08 ms in control groups, while CCT did not change significantly. BAEPs were completely abolished in two jjs with no SEP changes. When injection of sulfonamide induced significant peripheral and central BAEP abnormalities in jaundiced rats, no SEP abnormalities occurred. SEPs assess proprioception but not other somatosensory function or sensory integration. The results demonstrate the selectivity of acute bilirubin toxicity for the auditory nervous system.

Somatosensory and Brainstem Auditory Evoked Potentials in the Gunn Rat Model of Acute Bilirubin Neurotoxicity

Brainstem auditory evoked potentials (BAEPs) are a sensitive indicator of bilirubin neurotoxicity. Somatosensory evoked potentials (SEPs) have been proposed as another measure of toxicity, though the lemniscal pathways that generate the SEP are not involved in kernicterus. In 16 to 17-d-old jaundiced (jj) Gunn rats, serial BAEPs and SEPs were obtained up to 8 h after acute bilirubin toxicity. jjs were injected with 150 mg/kg sulfadimethoxine to displace bilirubin into brain tissue (n = 8); littermate controls were jjs given saline (n = 4) and nonjaundiced given sulfadimethoxine or saline (n = 7). After anesthesia, BAEP and SEP recordings were obtained at baseline and serially after injection. SEPs to median nerve stimulation were recorded from surface electrodes over the brachial plexus (Erb's) and contralateral parietal cortex, and subtracted to obtain central conduction time (CCT). There were no statistically significant different baseline values between groups. Baseline BAEP I, I-II, and I-III were 1.22 ± 0.13, 1.11 ± 0.12, and 2.10 ± 0.15 ms, and SEP Erb's and CCT were 1.48 ± 0.20 and 5.59 ± 0.50 ms, respectively (n = 19). At 6.8 ± 1.5 h after injection BAEP I, I-II, and I-III increased 0.10 ± 0.08, 0.18 ± 0.17, and 0.56 ± 0.33 ms over baseline, respectively (p = 0.005, 0.01, and 0.001, respectively, paired, 1-tailed t-tests), in experimental but not control groups. SEP Erb's decreased slightly, −0.06 ± 0.04 ms in experimental and −0.08 ± 0.08 ms in control groups, while CCT did not change significantly. BAEPs were completely abolished in two jjs with no SEP changes. When injection of sulfonamide induced significant peripheral and central BAEP abnormalities in jaundiced rats, no SEP abnormalities occurred. SEPs assess proprioception but not other somatosensory function or sensory integration. The results demonstrate the selectivity of acute bilirubin toxicity for the auditory nervous system.

Agyria-pachygyria: clinical, neuroimaging, and neurophysiologic correlations

Agyria-pachygyria complex is a disorder of neuronal migration and organization. Patients suffer either motor or intellectual retardation. We report our experiences of 10 patients with agyria-pachygyria complex and evaluate their clinical features, electroencephalography, and evoked potentials. Of nine electroencephalography examinations, five patients demonstrated characteristically high-amplitude fast activity. One of nine patients had an abnormal brainstem auditory-evoked potential. Three of seven patients had abnormal goggled visual-evoked potential. Six patients received somatosensory-evoked potential examinations, and five of these were abnormal, including four with prolonged central conduction times. Of the 10 patients, eight survived with variable intellectual and motor retardation; two died of sepsis. Patients with grades 1-4 agyria-pachygyria had high incidences of somatosensory-evoked potential abnormalities and also suffered worse neurologic outcomes. Normal brainstem auditory-evoked potential but abnormal cortical somatosensory-evoked potential components and prolonged central conduction time in these patients indicate that agyria-pachygyria is a supratentorial disease. We conclude that somatosensory-evoked potential examination is supplemental to neuroimaging in predicting the neurologic prognosis of patients with agyria-pachygyria.

Does wave VI of BAEP pertain to the prognosis of coma?

Objectives – The significance of brainstem auditory evoked potential (BAEP) wave VI for the outcome of comatose patients was assessed and compared to the prognostic impact of median nerve evoked somatosensory potential (MSEP) recording. Patients and methods – One hundred sixteen patients in a comatose state due to traumatic brain injury ( n = 57) and to intracerebral hemorrhage or tumours ( n = 59) were investigated prospectively. Outcome was assessed 3 months after the onset of coma using Glasgow Outcome Score (GOS). Standard BAEP and MSEP recordings were obtained within 24 h after coma onset. The frequency of findings was correlated with outcome by means of non-parametric statistical analysis. Additionally, 27 healthy volunteers were studied to confirm the constant presence of wave VI in normal BAEP. Results – In healthy controls, wave VI was present in 53/54 ears stimulated. Outcome correlation analysis revealed a significantly ( p < 0.01) higher frequency of abnormal wave VI in patients with unfavourable outcome (GOS 1-3) irrespective of the underlying pathology. Similarly, abnormal MSEP findings were significantly more frequent in this outcome group. Diagnostic sensitivity for an unfavourable outcome was low for both parameters, whereas specificity and positive predictive value of abnormal wave VI as well as of abnormal MSEP were equally high. Conclusion – Abnormal BAEP wave VI bears prognostic information in comatose patients.

The brainstem auditory evoked potential abnormalities in severe chronic obstructive pulmonary disease.

The aim of the study was to investigate the abnormalities of brainstem auditory evoked potentials (BAEP) in patients with severe chronic obstructive pulmonary disease (COPD). Twenty-one patients with severe COPD (16 men, five women; mean age: 64 +/- 6.5 years), in whom other causes of BAEP abnormalities had been excluded, were studied. Age-matched, non-smoking, healthy subjects acted as a control group. We performed pulmonary function tests, arterial blood gas analysis and bilateral BAEP measurements in COPD patients and control groups. Brainstem auditory evoked potentials were abnormal in 16 (76.1%) of the 21 COPD patients. Most prominent BAEP abnormalities were prolonged wave I peak latencies (42.8%), V wave peak latencies (38.1%), and III-V interpeak latencies (IPL) (38.1%). In five patients, a prolonged central transmission time (I-V IPL) was observed. No significant correlation was evident between the BAEP parameters and pH, PaO2, PaCO2, FEV1%, FEV1/FVC, haematocrit, duration of disease or cigarette consumption. The functions of the eighth cranial nerve and brainstem were highly impaired in severe COPD. These pathological BAEP alterations in severe COPD might be due to the chronic hypoxic-hypercapnic status occurring in the brainstem.

Brainstem size and function at term age in relation to later neurosensory disability in high‐risk, preterm infants

The aim of this study was to measure brainstem size on magnetic resonance imaging (MRI) scans of high-risk. preterm infants, to assess brainstem function by brainstem auditory-evoked potentials (BAEP) and to determine the predictive value of these measures for the neurosensory outcome. A total of 51 preterm infants (gestational age <34 wk, birthweight <1,500 g) underwent examinations at term age; neuromotor outcome and hearing were followed up until a corrected age of 18 mo. Fourteen (27%) infants had neurosensory disability. Those with a later neurosensory disability had a significantly smaller brain stem than those with a normal outcome. The preterm infants had significantly longer peak latency (L) V and interpeak latency (IPL) III-V than the full-term control infants. Most of the preterm infants with severe cerebral palsy or hearing loss had abnormal BAEP. Sensitivity of morphometric dimensions for predicting neurosensory disability was only 20-31%, but specificity was 97-100%. Abnormal L I and IPL III-V in BAEP predicted disability with a sensitivity of 93% and a specificity of 57-59%. We conclude that adverse events during the perinatal period may lead to morphofunctional changes in the brain stem in high-risk, preterm infants, and it seems that functional changes are accurate in predicting neurosensory disability in such patients.

Brainstem size and function at term age in relation to later neurosensory disability in high-risk, preterm infants

The aim of this study was to measure brainstem size on magnetic resonance imaging (MRI) scans of high-risk, preterm infants, to assess brainstem function by brainstem auditory-evoked potentials (BAEP) and to determine the predictive value of these measures for the neurosensory outcome. A total of 51 preterm infants (gestational age <34 wk, birthweight <1500 g) underwent examinations at term age; neuromotor outcome and hearing were followed up until a corrected age of 18 mo. Fourteen (27%) infants had neurosensory disability. Those with a later neurosensory disability had a significantly smaller brain stem than those with a normal outcome. The preterm infants had significantly longer peak latency (L) V and interpeak latency (IPL) III–V than the full-term control infants. Most of the preterm infants with severe cerebral palsy or hearing loss had abnormal BAEP. Sensitivity of morphometric dimensions for predicting neurosensory disability was only 20–31%, but specificity was 97–100%. Abnormal L I and IPL III–V in BAEP predicted disability with a sensitivity of 93% and a specificity of 57–59%. Conclusion: We conclude that adverse events during the perinatal period may lead to morpho-functional changes in the brain stem in high-risk, preterm infants, and it seems that functional changes are accurate in predicting neurosensory disability in such patients.