Jesús Pérez-Nellar

Autonomic, EEG, and behavioral arousal signs in a PVS case after Zolpidem intake.

the paradoxical “arousing” effect of Zolpidem, a highly selective nonbenzodiazepine gamma aminobutyric acid (GABA) agonist acting on the [omega]-1 site of the GABA A receptor, in persistent vegetative state (PVS), in minimally conscious state (MCS) patients, ischemic stroke cases, after brain injury, and in patients suffering hypoxic encephalopathy.1 We describe here this paradoxical arousing effect in a PVS case assessing autonomic, electroencephalographic (EEG), and behavioral changes, after Zolpidem uptake. This case report is the first to show the importance of using heart rate variability (HRV) methodology and EEG to assess autonomic and brain functional changes in a PVS case, during this pharmacological intervention.

QEEG Spectral and Coherence Assessment of Autistic Children in Three Different Experimental Conditions

We studied autistics by quantitative EEG spectral and coherence analysis during three experimental conditions: basal, watching a cartoon with audio (V–A), and with muted audio band (VwA). Significant reductions were found for the absolute power spectral density (PSD) in the central region for delta and theta, and in the posterior region for sigma and beta bands, lateralized to the right hemisphere. When comparing VwA versus the V–A in the midline regions, we found significant decrements of absolute PSD for delta, theta and alpha, and increments for the beta and gamma bands. In autistics, VwA versus V–A tended to show lower coherence values in the right hemisphere. An impairment of visual and auditory sensory integration in autistics might explain our results.

Zolpidem induces paradoxical metabolic and vascular changes in a patient with PVS

Abstract Introduction: Zolpidem is a non-benzodiazepine drug used for the therapy of insomnia, which has selectivity for stimulating the effect of GABA-A receptors. Recently, a paradoxical arousing effect of zolpidem in patients with severe brain damage has been repeatedly reported. Methods: A placebo-controlled magnetic resonance study was conducted to evaluate its effect on BOLD and metabolites spectral signals in a patient with severe brain injuries and an age-matched healthy volunteer. A multi-modal analysis was used to assess aspects in the pharmacologically-induced changes in the resting-state brain metabolism. Results: A significantly increased BOLD signal was transiently localized in the left frontal cortices, bilateral anterior cingulated areas, left thalamus and right head of the caudate nucleus. The healthy subject showed a deactivation of the frontal, parietal and temporal cortices. BOLD signal changes were found to significantly correlate with concentrations of extravascular metabolites in the left frontal cortex. It is discussed that, when zolpidem attaches to modified GABA receptors of neurodormant brain cells, brain activation is induced. This might explain the significant correlations of BOLD signal changes and proton-MRS metabolites in this patient after zolpidem. Conclusion: It was concluded that proton-MRS and BOLD signal assessment could be used to study zolpidem-induced metabolic modulation in a resting state.

TCD diastolic velocity decay and pulsatility index increment in PVS cases.

BACKGROUND Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS. METHODS We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm. RESULTS Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients. CONCLUSIONS We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.

TCD Systolic Spikes in a Malignant MCA Infarct

IntroductionMalignant MCA infarction results in significant space occupying effect and intracranial pressure (ICP) increment. Due to the high mortality rate in such patients, the term malignant MCA infarction was coined.MethodsWe studied a patient who developed a sudden onset of slurred speech, right hemiplegia, and decreased level of arousal. Two days later CT scan showed a massive cerebral infarct, involving the left MCA territory.ResultsA transcranial Doppler exam showed a normal flow pattern in the right hemisphere, but in the left hemisphere systolic spikes without diastolic flow were observed in internal carotid artery, anterior cerebral artery, as well as in the MCA.ConclusionsThe pathophysiologic mechanisms leading to BD might asymmetrically begin in cerebral hemispheres in malignant MCA infarcts.

Residual vasomotor activity assessed by heart rate variability in a brain-dead case

A patient assessed by heart rate variability (HRV) methodology, beginning just after the completion of brain death (BD) diagnosis, showed remaining very low frequency (VLF) waves for approximately 10 min. A time-varying spectral analysis showed that during the first 550 s, a significant power spectral density remained in the high-frequency (HF), low-frequency (LF) and VLF bands. From 550 to 675 s, the HF oscillations totally vanished, and a marked progressive decay of the LF and VLF power density occurred. After 700 s the VLF undulations stopped and remaining small amplitude oscillations at 0.2 Hz coincided with the ventilator frequency. The VLF oscillations recorded in our case might be related to residual sympathetic vasomotor activity that progressively disappeared due to the extension of necrosis affecting the nervous centres of the lower part of the medulla and the first 2–3 cervical spine segments.