Long-term continuous positive airway pressure therapy improves cardiac autonomic tone during sleep in patients with obstructive sleep apnea.

BACKGROUND: Cardiac autonomic tone after long-term continuous positive airway pressure therapy in patients with obstructive sleep apnea remains unexplored. METHODS: Thirty patients with obstructive sleep apnea (14 with moderate and 16 with severe obstructive sleep apnea) were studied during a baseline polysomnographic study, after a full night of acute continuous positive airway pressure treatment, and after long-term (~2 years) chronic continuous positive airway pressure therapy. Twenty age- and gender-matched controls with baseline sleep study were selected for comparison purposes. Cross-spectral analysis and the low-frequency (LF) and high-frequency (HF) components of the heart rate variability were computed separately over 10-min ECG epochs during rapid eye movement sleep, non-rapid eye movement sleep, and wakefulness. RESULTS: During the baseline study, obstructive sleep apnea patients exhibited increased LF, decreased HF, and increased LF/HF ratio during sleep when compared to controls. In a multiple regression model, the mean oxygen saturation explained the increased LF during rapid and non-rapid eye movement sleep in obstructive sleep apnea patients. Acute continuous positive airway pressure therapy decreased the LF modulations and the LF/HF ratio and increased the HF modulations during sleep in patients with severe obstructive sleep apnea. Long-term continuous positive airway pressure therapy decreased LF modulations and LF/HF ratio with increased HF modulations during sleep in patients with moderate and severe obstructive sleep apnea. CONCLUSIONS: Long-term continuous positive airway pressure reduces the sympathovagal imbalance in patients with moderate and severe obstructive sleep apnea, both during rapid and non-rapid eye movement sleep. Continuous positive airway pressure seems to exert its changes in cardiac autonomic modulation by decreasing the burden of nocturnal hypoxia.

Abnormal functional connectivity between motor cortex and pedunculopontine nucleus following chronic dopamine depletion.

The activity of the basal ganglia is altered in Parkinson's disease (PD) as a consequence of the degeneration of dopamine neurons in the substantia nigra pars compacta. This results in aberrant discharge patterns and expression of exaggerated oscillatory activity across the basal ganglia circuit. Altered activity has also been reported in some of the targets of the basal ganglia, including the pedunculopontine nucleus (PPN), possibly due to its close interconnectivity with most regions of the basal ganglia. However, the nature of the involvement of the PPN in the pathophysiology of PD has not been fully elucidated. Here, we recorded local field potentials in the motor cortex and the PPN in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD under urethane anesthesia. By means of linear and nonlinear statistics, we analyzed the synchrony between the motor cortex and the PPN and the delay in the interaction between these two structures. We observed the presence of coherent activity between the cortex and the PPN in low (5-15 Hz)- and high (25-35 Hz)-frequency bands during episodes of cortical activation. In each case, the cortex led the PPN. Dopamine depletion strengthened the interaction of the low-frequency activities by increasing the coherence specifically in the theta and alpha ranges and reduced the delay of the interaction in the gamma band. Our data show that cortical inputs play a determinant role in leading the coherent activity with the PPN and support the involvement of the PPN in the pathophysiology of PD.

High beta activity in the subthalamic nucleus and freezing of gait in Parkinson's disease.

OBJECTIVE: Oscillatory activity in the beta band is increased in the subthalamic nucleus (STN) of Parkinson's disease (PD) patients. Rigidity and bradykinesia are associated with the low-beta component (13-20Hz) but the neurophysiological correlate of freezing of gait in PD has not been ascertained. METHODS: We evaluated the power and coherence of the low- and high-beta bands in the STN and cortex (EEG) of PD patients with (p-FOG) (n=14) or without freezing of gait (n-FOG) (n=8) in whom electrodes for chronic stimulation in the STN had been implanted for treatment with deep brain stimulation. RESULTS: p-FOG patients showed higher power in the high-beta band (F=11.6, p=0.002) that was significantly reduced after l-dopa administration along with suppression of FOG (F=4.6, p=0.042). High-beta cortico-STN coherence was maximal for midline cortical EEG electrodes, whereas the low-beta band was maximal for lateral electrodes (χ(2)=20.60, p<0.0001). CONCLUSIONS: The association between freezing of gait, high-beta STN oscillations and cortico-STN coherence suggests that this oscillatory activity might interfere in the frontal cortex-basal ganglia networks, thereby participating in the pathophysiology of FOG in PD.

Basal cardiac autonomic tone is normal in patients with periodic leg movements during sleep.

The relationship between the autonomic nervous system and periodic leg movements during sleep (PLMS) is not completely understood. We aimed to determine whether patients with PLMS exhibit any changes in their basal heart rate variability (HRV), excluding episodes of leg movements and arousals. To investigate this, we conducted a cross-sectional study including 13 patients with PLMS (PLMS ≥ 20) and 13 matched controls, free of cardiovascular diseases and medications. Time-and frequency-domain HRV measures [mean R-R interval, low frequency (LF), high frequency (HF), LF/HF] were calculated across all sleep stages as well during wakefulness just before and after sleep during one-night polysomnography. We only took ECG segments of sleep without arousals and excluded periods of 30 s before and after the leg movements. No statistical differences between PLMS and control subjects were found in any of the time- or frequency-domain HRV measures across sleep stages. Basal cardiac autonomic modulation in patients with PLMS is similar to that of control subjects. Our results argue against a role for a basal disturbance of the cardiac autonomic nervous system in the pathogenesis of PLMS.

Pharmacological inhibition of the integrated stress response accelerates disease progression in an amyotrophic lateral sclerosis mouse model.

BACKGROUND AND PURPOSE: The integrated stress response (ISR) regulates translation in response to diverse stresses. ISR activation has been documented in amyotrophic lateral sclerosis (ALS) patients and ALS experimental models. In experimental models, both ISR stimulation and inhibition prevented ALS neurodegeneration; however, which mode of ISR regulation would work in patients is still debated. We previously demonstrated that the ISR modulator ISRIB (Integrated Stress Response InhiBitor, an eIF2B activator) enhances survival of neurons expressing the ALS neurotoxic allele SOD1 G93A. Here, we tested the effect of two ISRIB-like eIF2B activators (2BAct and PRXS571) in the disease progression of transgenic SOD1G93A mice. EXPERIMENTAL APPROACH: After biochemical characterization in primary neurons, SOD1G93A mice were treated with 2BAct and PRXS571. Muscle denervation of vulnerable motor units was monitored with a longitudinal electromyographic test. We used a clinical score to document disease onset and progression; force loss was determined with the hanging wire motor test. Motor neuronal survival was assessed by immunohistochemistry. KEY RESULTS: In primary neurons, 2BAct and PRXS571 relieve the ISR-imposed translational inhibition while maintaining high ATF4 levels. Electromyographic recordings evidenced an earlier and more dramatic muscle denervation in treated SOD1G93A mice that correlated with a decrease in motor neuron survival. Both compounds anticipated disease onset and shortened survival time. CONCLUSION AND IMPLICATIONS: 2BAct and PRXS571 anticipate disease onset, aggravating muscle denervation and motor neuronal death of SOD1G93A mice. This study reveals that the ISR works as a neuroprotective pathway in ALS motor neurons and reveals the toxicity that eIF2B activators may display in ALS patients.

Subthalamic activity during diphasic dyskinesias in Parkinson's disease.

BACKGROUND: Diphasic dyskinesias are a subtype of levodopa-induced dyskinesias that appear typically at the onset and end of levodopa antiparkinsonian action. The pathophysiology of diphasic dyskinesias is not well understood. METHODS: We analyzed local field potentials recorded from the subthalamic nucleus in 7 Parkinson's disease (PD) patients who showed typical diphasic dyskinesias during postoperative recordings through a deep brain stimulation electrode. The evolution of the different oscillatory activities related to the onset and end of diphasic dyskinesias was studied by windowed fast Fourier transforms. RESULTS: Typical "off"-state beta activity disappeared with the onset of diphasic dyskinesias, whereas gamma activity was absent or minimal until their end. Theta activity during diphasic dyskinesias was similar to that observed during peak-dose dyskinesias. CONCLUSIONS: From a neurophysiological viewpoint, patients exhibited oscillatory activity typical of the "on" medication state during diphasic dyskinesias. The minimal presence of gamma activity during diphasic dyskinesias, however, suggests that this "on" state might be incomplete or limited to dopaminergic mechanisms affecting the lower limbs.

Involvement of the subthalamic nucleus in impulse control disorders associated with Parkinson's disease.

Behavioural abnormalities such as impulse control disorders may develop when patients with Parkinson's disease receive dopaminergic therapy, although they can be controlled by deep brain stimulation of the subthalamic nucleus. We have recorded local field potentials in the subthalamic nucleus of 28 patients with surgically implanted subthalamic electrodes. According to the predominant clinical features of each patient, their Parkinson's disease was associated with impulse control disorders (n = 10), dyskinesias (n = 9) or no dopaminergic mediated motor or behavioural complications (n = 9). Recordings were obtained during the OFF and ON dopaminergic states and the power spectrum of the subthalamic activity as well as the subthalamocortical coherence were analysed using Fourier transform-based techniques. The position of each electrode contact was determined in the postoperative magnetic resonance image to define the topography of the oscillatory activity recorded in each patient. In the OFF state, the three groups of patients had similar oscillatory activity. By contrast, in the ON state, the patients with impulse control disorders displayed theta-alpha (4-10 Hz) activity (mean peak: 6.71 Hz) that was generated 2-8 mm below the intercommissural line. Similarly, the patients with dyskinesia showed theta-alpha activity that peaked at a higher frequency (mean: 8.38 Hz) and was generated 0-2 mm below the intercommissural line. No such activity was detected in patients that displayed no dopaminergic side effects. Cortico-subthalamic coherence was more frequent in the impulsive patients in the 4-7.5 Hz range in scalp electrodes placed on the frontal regions anterior to the primary motor cortex, while in patients with dyskinesia it was in the 7.5-10 Hz range in the leads overlying the primary motor and supplementary motor area. Thus, dopaminergic side effects in Parkinson's disease are associated with oscillatory activity in the theta-alpha band, but at different frequencies and with different topography for the motor (dyskinesias) and behavioural (abnormal impulsivity) manifestations. These findings suggest that the activity recorded in parkinsonian patients with impulse control disorders stems from the associative-limbic area (ventral subthalamic area), which is coherent with premotor frontal cortical activity. Conversely, in patients with l-dopa-induced dyskinesias such activity is recorded in the motor area (dorsal subthalamic area) and it is coherent with cortical motor activity. Consequently, the subthalamic nucleus appears to be implicated in the motor and behavioural complications associated with dopaminergic drugs in Parkinson's disease, specifically engaging different anatomo-functional territories.

Sustained enzymatic correction by rAAV-mediated liver gene therapy protects against induced motor neuropathy in acute porphyria mice.

Acute intermittent porphyria (AIP) is characterized by a hereditary deficiency of hepatic porphobilinogen deaminase (PBGD) activity. Clinical features are acute neurovisceral attacks accompanied by overproduction of porphyrin precursors in the liver. Recurrent life-threatening attacks can be cured only by liver transplantation. We developed recombinant adeno-associated virus (rAAV) vectors expressing human PBGD protein driven by a liver-specific promoter to provide sustained protection against induced attacks in a predictive model for AIP. Phenobarbital injections in AIP mice induced porphyrin precursor accumulation, functional block of nerve conduction, and progressive loss of large-caliber axons in the sciatic nerve. Hepatocyte transduction showed no gender variation after rAAV2/8 injection, while rAAV2/5 showed lower transduction efficiency in females than males. Full protection against induced phenobarbital-attacks was achieved in animals showing over 10% of hepatocytes expressing high amounts of PBGD. More importantly, sustained hepatic expression of hPBGD protected against loss of large-caliber axons in the sciatic nerve and disturbances in nerve conduction velocity as induced by recurrent phenobarbital administrations. These data show for the first time that porphyrin precursors generated in the liver interfere with motor function. rAAV2/5-hPBGD vector can be produced in sufficient quantity for an intended gene therapy trial in patients with recurrent life-threatening porphyria attacks.

An interactive framework for the detection of ictal and interictal activities: Cross-species and stand-alone implementation.

BACKGROUND AND OBJECTIVE: Despite advances on signal analysis and artificial intelligence, visual inspection is the gold standard in event detection on electroencephalographic recordings. This process requires much time of clinical experts on both annotating and training new experts for this same task. In scenarios where epilepsy is considered, the need for automatic tools is more prominent, as both seizures and interictal events can occur on hours- or days-long recordings. Although other solutions have already been proposed, most of them are not integrated on clinical and basic science environments due to their complexity and required specialization. Here we present a pipeline that arises from coordinated efforts between life-science researchers, clinicians and data scientists to develop an interactive and iterative workflow to train machine-learning tools for the automatic detection of electroencephalographic events in a variety of scenarios. METHODS: The approach consists on a series of subsequent steps covering data loading and configuration, event annotation, model training/re-training and event detection. With slight modifications, the combination of these blocks can cope with a variety of scenarios. To illustrate the flexibility and robustness of the approach, three datasets from clinical (patients of Dravet Syndrome) and basic research environments (mice model of the same disease) were evaluated. From them, and in response to researchers' daily needs, four real world examples of interictal event detection and seizure classification tasks were selected and processed. RESULTS: Results show that the current approach was of great aid for event annotation and model development. It was capable of creating custom machine-learning solutions for each scenario with slight adjustments on the analysis protocol, easily accessible to users without programming skills. Final annotator similarity metrics reached values above 80% on all cases of use, reaching 92.3% on interictal event detection on human recordings. CONCLUSIONS: The presented framework is easily adaptable to multiple real world scenarios and the interactive and ease-to-use approach makes it manageable to clinical and basic researches without programming skills. Nevertheless, it is conceived so data scientists can optimize it for specific scenarios, improving the knowledge transfer between these fields.

Coupling between beta and high-frequency activity in the human subthalamic nucleus may be a pathophysiological mechanism in Parkinson's disease.

In Parkinson's disease (PD), the oscillatory activity recorded from the basal ganglia shows dopamine-dependent changes. In the "off" parkinsonian motor state, there is prominent activity in the beta band (12-30 Hz) that is mostly attenuated after dopaminergic therapy ("on" medication state). The on state is also characterized by activity in the gamma (60-80 Hz) and high-frequency (300 Hz) bands that is modulated by movement. We recorded local field potentials from a group of 15 PD patients (three females) treated with bilateral deep brain stimulation of the subthalamic nucleus, using a high sampling rate (2 kHz) and filters suitable to study high-frequency activity (0.3-1000 Hz). We observed high-frequency oscillations (HFOs) in both the off and on motor states. In the off state, the amplitude of the HFOs was coupled to the phase of the abnormal beta activity. The beta-coupled HFOs showed little or even negative movement-related changes in amplitude. Moreover, the degree of movement-related modulation of the HFOs correlated negatively with the rigidity/bradykinesia scores. In the on motor state, the HFOs were liberated from this beta coupling, and they displayed marked movement-related amplitude modulation. Cross-frequency interactions between the phase of slow activities and the amplitude of fast frequencies have been attributed an important role in information processing in cortical structures. Our findings suggest that nonlinear coupling between frequencies may not only be a physiological mechanism (as shown previously) but also that it may participate in the pathophysiology of parkinsonism.

Sound analysis of catathrenia: a vocal expiratory sound.

PURPOSE: Catathrenia (nocturnal groaning) is a rare and relatively little-understood parasomnia. The characteristics of the sound and the recordings are not similar in all the relevant research papers. Indeed, there is currently some discussion regarding whether or not this is a single entity. For some authors, catathrenia is a particular form of parasomnia; for others, it may be a variant of snoring or a respiratory problem. The goal is to establish whether or not catathrenia may be regarded as an expiratory vocal sound. An attempt was made to classify the origin of this sound according to its sound structure. METHODS: We present the sound analysis of two patients, a man and a woman, with clinically diagnosed catathrenia and we compared them with the analysis of snoring. We use the spectrogram and the oscillogram. We classified the sounds according to the Yanagihara criteria. RESULTS: The vocal nature of the sound was confirmed, and several significant differences to some snoring sounds were discovered. The analysis of the catathrenia samples demonstrated that these signals are type II according to Yanagihara classification; these signals had a very short jitter, and had formants and harmonics. However, snoring is a type III, very irregular and had formants but not harmonics. CONCLUSIONS: The oscillogram and the spectrogram in these patients show that the origins of the sounds are clearly different: catathrenia is laryngeal, while snoring is guttural. Catathrenia cannot be considered as expiratory snoring.

Abnormal brain gamma oscillations in response to auditory stimulation in Dravet syndrome.

OBJECTIVE: To evaluate the capability of children with Dravet syndrome to generate brain γ-oscillatory activity in response to auditory steady-state stimulation. METHODS: Fifty-one subjects were included: 13 with Dravet syndrome with SCN1A gene alterations, 26 with non-Dravet epilepsies and 12 healthy controls. Responses to auditory steady-state stimulation elicited with a chirp-modulated tone between 1 and 120 Hz were collected in subjects and compared across groups. RESULTS: Subjects with Dravet syndrome showed weak or no responses in the 1-120 Hz frequency range. Healthy controls showed oscillatory responses following the frequency of the modulation that were maximal in the low (30-70 Hz) and high (80-120) γ-ranges both, in the power and inter-trial coherence estimates. Non-Dravet epileptic children showed differences in the auditory responses when compared with the healthy controls but were able to generate oscillatory evoked activities following the frequency-varying stimulation. CONCLUSIONS: The ability to generate brain γ-oscillatory activity of children with Dravet in response to a chirp-modulated auditory stimulus is highly impaired, is not due to epilepsy and is consistent with the Nav1.1 channel dysfunction affecting interneuron activity seen in Dravet mouse models. SIGNIFICANCE: The reported deficits in the brain oscillatory activity evoked by chirp modulated tones in children with Dravet is compatible with Dravet syndrome disease mechanisms and constitutes a potential biomarker for future disease-modifying interventions.

Beta activity in the subthalamic nucleus during sleep in patients with Parkinson's disease.

The recordings of local field potentials in the subthalamic nucleus in patients with Parkinson's disease (PD), carried out through the stimulators implanted to treat the motor symptoms of the disease, show a prominent basal ("off") activity in the beta range, which is attenuated after dopaminergic therapy. A recent study described improvement of parkinsonian features during rapid eyes movements (REM) sleep. We describe, for the first time, the changes in activity of the subthlamic nucleus (STN) during different sleep stages in Parkinson's disease with special interest in the beta band. Ten patients with PD treated with deep brain stimulation of the STN were studied. Subthalamic local field potentials (LFPs) were recorded through the stimulation electrodes during wakefulness ("off" medication) and different sleep stages. In Stage 2 and slow-wave sleep, a significant decrease of beta activity was recorded. During REM sleep, beta power values were similar to wakefulness values or even higher. These findings indicate that STN activity is modulated and modified during different sleep stages. The increased beta activity during REM sleep is a new but unexpected finding, which requires further analysis.

Late-onset periodic asystolia during vagus nerve stimulation.

Cardiac changes may occasionally occur during vagus nerve stimulation (VNS) used in epileptic patients. As they can be potentially life-threatening, it is important to detect them, and this is why an intraoperative test is performed during the implantation. Few cases of asystole during this test have been described. Only one patient with late-onset bradyarrythmia caused by VNS has been reported. This patient had been implanted 2 years and 4 months before the episode. We present another case of late asystole in a patient whose VNS had been implanted 9 years before the arrhythmia onset. In our patient, each run of stimulation produced bradyarrhythmias and very often severe asystolia due to atrium-ventricular block.

Epilepsy and neuropsychiatric comorbidities in mice carrying a recurrent Dravet syndrome SCN1A missense mutation.

Dravet Syndrome (DS) is an encephalopathy with epilepsy associated with multiple neuropsychiatric comorbidities. In up to 90% of cases, it is caused by functional happloinsufficiency of the SCN1A gene, which encodes the alpha subunit of a voltage-dependent sodium channel (Nav1.1). Preclinical development of new targeted therapies requires accessible animal models which recapitulate the disease at the genetic and clinical levels. Here we describe that a C57BL/6 J knock-in mouse strain carrying a heterozygous, clinically relevant SCN1A mutation (A1783V) presents a full spectrum of DS manifestations. This includes 70% mortality rate during the first 8 weeks of age, reduced threshold for heat-induced seizures (4.7 °C lower compared with control littermates), cognitive impairment, motor disturbances, anxiety, hyperactive behavior and defects in the interaction with the environment. In contrast, sociability was relatively preserved. Electrophysiological studies showed spontaneous interictal epileptiform discharges, which increased in a temperature-dependent manner. Seizures were multifocal, with different origins within and across individuals. They showed intra/inter-hemispheric propagation and often resulted in generalized tonic-clonic seizures. 18F-labelled flourodeoxyglucose positron emission tomography (FDG-PET) revealed a global increase in glucose uptake in the brain of Scn1aWT/A1783V mice. We conclude that the Scn1aWT/A1783V model is a robust research platform for the evaluation of new therapies against DS.

Successful thalamic deep brain stimulation for orthostatic tremor.

We report a patient with severe orthostatic tremor (OT) unresponsive to pharmacological treatments that was successfully controlled with thalamic (Vim, ventralis intermedius nucleus) deep brain stimulation (DBS) over a 4-year period. Cortical activity associated with the OT revealed by EEG back-averaging and fluoro-deoxi-glucose PET were also suppressed in parallel with tremor arrest. This case suggests that Vim-DBS may be a useful therapeutic approach for patients highly disabled by OT.

Influence of filters in the detrended fluctuation analysis of digital electroencephalographic data.

The technique named detrended fluctuation analysis (DFA) has been used to reveal the presence of long-range temporal correlations (LRTC) and scaling behavior (SB) in electroencephalographic (EEG) recordings. The occurrence of these phenomena seems to be a salient characteristic of the healthy human brain and alterations in different pathologies has been described. Here we show how the filtering stages implemented in the systems for digital EEG influence the estimation of the DFA parameters used to characterize the brain signals. In consequence, we conclude that it is important to consider these filtering effects before interpreting the results obtained from digital EEG recordings.

Effect of reduced attention on auditory amplitude-modulation following responses: a study with chirp-evoked potentials.

The amplitude of the auditory amplitude-modulation following responses (AMFR) is variable, depending on the modulation rate. Although 40-Hz responses have higher amplitudes in adults, the AMFR in the 80- to 120-Hz range are less influenced by sleep and more consistent in children. The effect of attention on 40-Hz responses has been addressed in some studies; however, no study to our knowledge has investigated the effect of attention on other stimulation rates. Our aim was to test the effect of attention on the AMFR to different frequencies of stimulation, using a chirp-modulated tone as stimulus. We recorded chirp-evoked responses in 12 subjects while attending to the sound (first condition) and reading a novel (second condition), in a randomly determined sequence. The energy of the response and the intertrial coherence (ITC) were measured by means of time-frequency transforms. The frequency range of response was similar in both conditions. No significant differences were found in the ITC values in the 40-Hz and the 80- to 120-Hz ranges, nor in the energy of the 40-Hz response. The only statistically significant difference found was the lower energy of the response in the 80- to 120-Hz range in the reading condition. Our results suggest that attention may affect auditory steady-state clinical testing using amplitude values. Phase measures may be preferable in this context.

Theta-phase closed-loop stimulation induces motor paradoxical responses in the rat model of Parkinson disease.

BACKGROUND: High-frequency deep brain stimulation (DBS) has become a widespread therapy used in the treatment of Parkinson's Disease (PD) and other diseases. Although it has proved beneficial, much recent attention has been centered around the potential of new closed-loop DBS implementations. OBJECTIVE: Here we present a new closed-loop DBS scheme based on the phase of the theta activity recorded from the motor cortex. By testing the implementation on freely moving 6-OHDA lesioned and control rats, we assessed the behavioral and neurophysiologic effects of this implementation and compared it against the classical high-frequency DBS. RESULTS: Results show that both stimulation modalities produce significant and opposite changes on the movement and neurophysiological activity. Close-loop stimulation, far from improving the animals' behavior, exert contrary effects to those of high-frequency DBS which reverts the parkinsonian symptoms. Motor improvement during open-loop, high-frequency DBS was accompanied by a reduction in the amount of cortical beta oscillations while akinetic and disturbed behavior during close-loop stimulation coincided with an increase in the amplitude of beta activity. CONCLUSION: Cortical-phase-dependent close-loop stimulation of the STN exerts significant behavioral and oscillatory changes in the rat model of PD. Open-loop and close-loop stimulation outcomes differed dramatically, thus suggesting that the scheme of stimulation determines the output of the modulation even if the target structure is maintained. The current framework could be extended in future studies to identify the correct parameters that would provide a suitable control signal to the system. It may well be that with other stimulation parameters, this sort of DBS could be beneficial.

[Vestibular evoked myogenic potentials and benign paroxysmal positional vertigo]. / Resultados de los potenciales evocados miogénicos vestibulares en el vértigo posicional paroxístico benigno.

OBJECTIVE: Benign paroxysmal positional vertigo (BPPV) seems to occur because of otoconia migration into the semicircular canals or their adherence to the cupula. Although the origin of these otoconia lies in the macula of the utricle, vestibular evoked myogenic potentials (VEMPs) can be used assess saccular function. The aim of this study is to assess the saccular function in patients diagnosed with BPPV. PATIENTS AND METHOD: Nineteen patients diagnosed with BPPV of the posterior semicircular canal were included in this study. Their auditory function and their caloric, rotatory chair, and VEMP responses were tested. Ipsilateral and contralateral VEMP thresholds, ipsilateral and contralateral p13 and n23 latencies at 100 dB, inter-peak amplitude and the interaural amplitude difference were determined. RESULTS: We found a lack of VEMP response in 52 % of the ears with BPPV. When adjusted for bilateral absence, VEMP response was absent in 20.3 % of ears. CONCLUSIONS: Some patients with idiopathic BPPV show a degree of saccular dysfunction.