Auditory evoked potentials in children and adolescents with multiple sclerosis and neuromyelitis optica spectrum disorders

Barbosa, Dayane Aparecida Nascimento; Samelli, Alessandra Giannella; Oliveira, Danielle Patriota de; Paz, José Albino da; Matas, Carla Gentile

doi:10.1016/j.ijporl.2021.111013

Cited by 6 publications

(5 citation statements)

References 33 publications

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“…Barbosa et al 33 also found a significant decrease only in P2-N2 amplitude in children and adolescents with MS. On the other hand, regarding adults, there are reports of increased latencies in N1, 14,28 P2, 12,14 N2, 12,14 and P3, 5,12,14,18,26,28 as well as increased amplitudes in P2, 14,28 N2, 28 and P3. 14 These results suggest that MS patients may have slowed neural processing and decreased neural activity in sensory, inattentional, 5 and attentional discrimination of acoustic stimuli, due to demyelination 18 -which slows down conduction, while axonal degeneration attenuates the amplitude of the potential.…”

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 88%

“…8,19,21,25 As for children and youth, a study assessed a small group of 11 children and adolescents aged 9 to 17 years and found increased III-V and I-V interpeak latencies, suggesting changes in the high brainstem. 33 However, another study assessed 10 adolescents aged 13 to 17 years and reported increased latencies in waves III and V and increased interpeak intervals I-III and I-V, suggesting changes in the low brainstem. 34 Such results may suggest a gradual impairment of the auditory pathways, progressing from the most central region of the auditory system to future impairments in more distal regions of the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

“…As for children and youth, a study assessed a small group of 11 children and adolescents aged 9 to 17 years and found increased III-V and I-V interpeak latencies, suggesting changes in the high brainstem. 33 However, another study assessed 10 adolescents aged 13 to 17 years and reported increased latencies in waves III and V and increased interpeak intervals I-III and I-V, suggesting changes in the low brainstem. 34…”

Section: Discussionmentioning

confidence: 99%

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Auditory central pathways in children and adolescents with multiple sclerosis

Barbosa,

Silva,

Samelli

et al. 2023

Arq Neuropsiquiatr

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Background Multiple sclerosis (MS) is an inflammatory demyelinating disease. Auditory evoked potential studies have demonstrated conduction and neural processing deficits in adults with MS, but little is known about the electrophysiological responses in children and adolescents. Objective to evaluate the central auditory pathway with brainstem auditory evoked potentials (BAEP) and long-latency auditory evoked potentials (LLAEP) in children and adolescents with MS. Methods The study comprised 17 individuals with MS, of both sexes, aged 9 to 18 years, and 17 healthy volunteers, matched for age and sex. All individuals had normal hearing and no middle ear impairments. They were assessed with click-BAEP and LLAEP through oddball paradigm and tone-burst stimuli. Results Abnormal responses were observed in 60% of electrophysiologic assessments of individuals with MS. In BAEP, 58.82% of MS patients had abnormal responses, with longer wave V latency and therefore longer III-V and I-V interpeak latencies than healthy volunteers. In LLAEP, 52.94% of MS patients had abnormal responses. Although statistical differences were found only in P2-N2 amplitude, MS patients had longer latencies and smaller amplitudes than healthy volunteers in all components. Conclusion Children and adolescents with MS had abnormal BAEP responses, with delayed neural conduction between the cochlear nucleus and the lateral lemniscus. Also, abnormal LLAEP results suggest a decrease in neural processing speed and auditory sensory discrimination response.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Auditory central pathways in children and adolescents with multiple sclerosis

Barbosa,

Silva,

Samelli

et al. 2023

Arq Neuropsiquiatr

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“…To further evaluate the impairment of neuronal transmission by hypoxia clinically, we subsequently used the objective BAEP test, a traditional method to help the diagnosis of paediatric neurologic diseases [17] and reveal neuronal transmission in the auditory system with respect to investigating hypoxia‐induced neurological damage [18], which reflects the state of the entire nervous system [19–21] (Fig. 2A,B) ( n = 122 and n = 44 in the neonatal hypoxia and control groups, respectively).…”

Section: Resultsmentioning

confidence: 99%

Upregulation of A‐type potassium channels suppresses neuronal excitability in hypoxic neonatal mice

Liu

Lai

et al. 2023

The FEBS Journal

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Neuronal excitability is a critical feature of central nervous system development, playing a fundamental role in the functional maturation of brain regions, including the hippocampus, cerebellum, auditory and visual systems. The present study aimed to determine the mechanism by which hypoxia causes brain dysfunction through perturbation of neuronal excitability in a hypoxic neonatal mouse model. Functional brain development was assessed in humans using the Gesell Development Diagnosis Scale. In mice, gene transcription was evaluated via mRNA sequencing and quantitative PCR; furthermore, patch clamp recordings assessed potassium currents. Clinical observations revealed disrupted functional brain development in 6‐ and 18‐month‐old hypoxic neonates, and those born with normal hearing screening unexpectedly exhibited impaired central auditory function at 3 months. In model mice, CA1 pyramidal neurons exhibited reduced spontaneous activity, largely induced by excitatory synaptic input suppression, despite the elevated membrane excitability of hypoxic neurons compared to that of control neurons. In hypoxic neurons, Kcnd3 gene transcription was upregulated, confirming upregulated hippocampal Kv4.3 expression. A‐type potassium currents were enhanced, and Kv4.3 participated in blocking excitatory presynaptic inputs. Elevated Kv4.3 activity in pyramidal neurons under hypoxic conditions inhibited excitatory presynaptic inputs and further decreased neuronal excitability, disrupting functional brain development in hypoxic neonates.

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