Electrocortical Function Research Articles

Attention, Executive Function, Behavior, and Electrocortical Function, Significantly Improved With 19-Channel Z-Score Neurofeedback in a Clinical Setting: A Pilot Study

Objective: Neurofeedback (NF) is gaining recognition as an evidence-based intervention grounded in learning theory, and 19-channel z-score NF (19ZNF) is a new NF model. This pilot study sought to evaluate the efficacy of 19ZNF in a clinical setting. Method: Outcome measures framed groups such that 19ZNF was evaluated, as it relates to the neuropsychological constructs of attention (n = 10), executive function (n = 12), behavior (n = 14), and electrocortical functioning (n = 21). One-tailed t tests compared pre–post difference scores. Results: For all pre–post comparisons, the direction of change was in the predicted direction, and differences were statistically significant (p = .000 to p = .008, effect sizes 1.29 to 3.42). Conclusion: Results suggest 19ZNF improved attention, executive function, behavior, and electrocortical function. This study provides beginning evidence of 19ZNF’s efficacy, adds to what is known about 19ZNF, and offers an innovative approach for using quantitative electroencephalographic (QEEG) metrics as outcome measures.

Cortical stimulation mapping in a patient with foreign accent syndrome: Case report

Foreign accent syndrome is a rare language output disorder characterized by changes in various speech features leading to a perceived foreign accent. There are few cases reported in the literature. Due to the rarity of this condition, information regarding the functional neuroanatomy of FAS is lacking. We present the case of a 60-year-old woman with a left anterior parietal lobe breast carcinoma metastasis who developed foreign accent syndrome (FAS). This patient presented to the emergency room with right upper extremity weakness, facial weakness, and altered speech. Neurological examination revealed the patient’s speech to be dysarthric and accented, but otherwise appropriate. Brain magnetic resonance (MR) imaging demonstrated a 3 cm × 3 cm × 3 cm lesion in the left anterior parietal lobe. The patient underwent craniotomy for resection of the mass. Intra-operative cortical stimulation mapping demonstrated the lesion to be confined to somatosensory cortex and gross total resection was performed. There were no new neurological deficits post-operatively. To our knowledge, this is a unique case of FAS due to breast carcinoma metastasis. Additionally, this is the first documented case of electrocortical function stimulation mapping of language and Rolandic cortex in a patient with FAS.

Antenatal betamethasone treatment reduces synaptophysin immunoreactivity in presynaptic terminals in the fetal sheep brain

Knowledge of morphofunctional effects on the fetal brain induced by exogenous glucocorticoids is limited. Recently, we reported alterations of both the neuronal cytoskeleton and electrocortical function in the ovine fetal brain after antenatal betamethasone treatment in doses used in perinatal medicine. In the present study we examined whether these changes are accompanied by morphological alterations of synapses. Chronically instrumented fetal sheep at 0.87 of gestation were treated either with isotonic saline ( n=7) or 10 μg/h betamethasone ( n=7) over 48 h administered directly to the fetal jugular vein. Paraffin sections of the frontal neocortex, caudate putamen and hippocampus were stained with a monoclonal antibody against synaptophysin, a specific membrane protein of presynaptic vesicles and quantified morphometrically. Synaptophysin-like immunoreactivity (synaptophysin-LI) showed a widespread granular pattern in the neuropil. Betamethasone exposure reduced synaptophysin-LI in the frontal neocortex, caudate putamen and hippocampus by 46.9, 41.0 and 55.4%, respectively, ( P<0.05) that was not accompanied by irreversible neuronal damage. These results suggest that clinical doses of betamethasone have acute effects on presynaptic terminals in the fetal sheep brain that could contribute to the altered complexity of electrocortical function that we have shown previously to occur following fetal exposure to betamethasone.

Electrocortical brain activity, cerebral haemodynamics and oxygenation during progressive hypotension in newborn piglets

Objective: To investigate the relationships between systemic and cerebral haemodynamics and oxygenation, and electroencephalogram (EEG) amplitude and frequency analysis studied by the cerebral function analyzing monitor (CFAM) during progressive hypovolemic hypotension. Methods: Six piglets of 1 week of age, weighing 1.9–3.4 kg were mechanically ventilated under 1–1.5% halothane anaesthesia. After 1 h stabilization, blood was withdrawn in aliquots of 10 ml/kg over 15 min up to a total of 40–60 ml/kg. Arterial oxygenation was maintained at normal levels. Thereafter, the total blood volume previously withdrawn, was reinfused. Changes in near infrared spectroscopy (NIRS) parameters [cerebral oxidized cytochrome aa3 (Cytaa3), cerebral blood volume (CBV) or total haemoglobin (tHb: oxy- + deoxyhaemoglobin)], carotid blood flow (Q car), maximal EEG amplitude and EEG frequency percentages were analyzed continuously. Results: The EEG amplitude remained stable until the mean arterial blood pressure (MAP), Q car and tHb dropped below 30 mmHg (41% of baseline), 20 ml/min (33% of baseline) and 82% of baseline, respectively. Delta (δ) wave frequency percentage of the CFAM increased significantly at MAP below 30 mmHg. EEG amplitude remained depressed after blood reinfusion and haemodynamic recovery. Cytaa3 changes were not statistically significant, reflecting sufficient neuronal oxygenation. Conclusion: Our results show that electrocortical function is affected only by profound systemic hypotension. This occurred at a higher level of cerebral oxygen delivery than the level associated with neuronal hypoxia and secondary cell damage.

Changes in cortical EEG and cholinergic function in response to NGF in rats with nucleus basalis lesions

We examined whether recovery of cholinergic function in response to nerve growth factor (NGF) results in restoration of electrocortical activity. Rats received unilateral lesions of the nucleus basalis and were infused intracerebroventricularly (i.c.v.) over 3 weeks with NGF or vehicle. Cortical electrical activity was assessed at postoperative days 4, 7, 14, and 21 from 8 epidural electrodes. On day 21, choline acetyl transferase (ChAT) activity was measured in cortical tissue underlying each electrode site. Lesions resulted in increases in slow-wave (δ) power and decreases in high-frequency (β 2) power in the lesioned, as well as the non-lesioned hemisphere. Changes correlated topographically and in magnitude with losses of ChAT activity and suggested that regional electrocortical function was affected by cholinergic activity originating in the ipsilateral, as well as the contralateral hemisphere. NGF attenuated changes in cholinergic and electrocortical function bilaterally, though in the lesioned hemisphere, function did not return to control levels. Likewise, intact animals receiving NGF showed increases in β 2-power, as well as modest increases in ChAT activity. Changes in brain electrical activity in response to NGF occurred within 4–7 days without significant changes during the 2 weeks thereafter. Our results suggest that outcomes of future animal and human trials using unilateral i.c.v. infusions of NGF need to consider the reciprocal influences of hemispheric cholinergic function, as well as possible effects of NGF on intact brain.

Electroencephalographic studies in workers exposed to solvents or pesticides

The qEEG was studied in groups of young and old workers exposed to solvents (house and industrial painters) and in a group of workers exposed to pesticides. Three methods were used: a quantified visual scoring system, the neurometrics method and a multivariate analysis of mean frequencies. Using the visual assessment as well as the neurometrics method, the older painters showed more abnormalities than the younger painters and the pesticide exposed workers. The “profile” of abnormalities differed in all 3 groups. Changes of the mean spectral frequencies were mainly found in the subjects to pesticides. In this study we concluded that the neurometrics method can be useful in neurotoxicological studies. With this technique minor changes in electrocortical function can be detected in seemingly normal workers. However, frequency parameters should be added to the power measures which are usually studied.

Cerebral electrophysiologic effects of resuscitation with hypertonic saline-dextran after hemorrhage

When brain injury accompanies hemorrhage, resuscitation with hypertonic saline (HS) improves intracranial pressure (ICP) and elastance; however, its effect on brain function after a traumatic or ischemic insult has not been assessed. This study compares the electrophysiologic response to hemorrhage and resuscitation with 7.5% NaCl + 6% dextran (HSD), 6% hetastarch (HE), or 0.9% NaCl (NS) using somatosensory evoked potentials (SSEP). Resuscitation with HE resulted in a better return of electrocortical function than with either HSD or NS (SSEP grade 2.0 +/- 0.2 for HE vs. 3.2 +/- 0.3 for HSD and 2.9 +/- 0.3 for NS; p less than .01). SSEP response correlated closet with mean arterial pressure (MAP) (r = -.53). There was no correlation between the SSEP response and cardiac index (r = .06) or ICP (r = -.04). HSD blunted the usual early increase in ICP after fluid infusion, and resulted in a lower ICP throughout resuscitation. However, the restoration of MAP and cerebral perfusion pressure (CPP) after HSD infusion was poor. The vasodilatory properties of hypertonic saline have been well described, both in the systemic and in the pulmonary vascular bed. While these characteristic usually are cited as advantages of this solution, in the case of ischemic cerebral dysfunction, this diminished vascular tone prevents early restoration of the MAP and CPP. The result is suboptimal electrocortical recovery after hemorrhage.

Polyamine inhibition preserves somatosensory evoked potential activity after transient cerebral ischaemia.

We tested the hypothesis that the increase in polyamines observed after cerebral ischaemia is related to deficits in electrocortical function as measured by somatosensory evoked potential (SEP). Adult Mongolian gerbils were anaesthetized with ketamine and prepared for monitoring SEP, cerebral blood flow (CBF) in parietal and frontal regions by H2 clearance, and for bilateral carotid artery occlusion (BCO). Seven animals served as controls and received saline. Another 7 animals were treated with the ornithine decarboxylase inhibitor, difluoromethylornithine (DFMO) (100 mg/kg I.P.) just prior to 40 min BCO followed by 4 h reperfusion. With BCO, both CBF and SEP declined significantly. In control animals, CBF fell from basal 37.8 +/- 4.7 cc/100 g/min to 2.9 +/- 1.2 cc/100 g/min and recovered to 22.7 +/- 3.5 cc/100 g/h over the 4 h reperfusion period. DFMO treatment did not alter this CBF pattern. SEP amplitude declined to 11.3 +/- 3.2% basal during occlusion. DFMO preserved SEP during ischaemia (35.5 +/- 16.8% basal) and remained significantly more preserved during reperfusion (p less than 0.05). These results suggest that polyamines are involved in the progressive decline in neuroelectrical function which occurs during occlusion/reperfusion in the Mongolian gerbil. The observation that polyamine inhibition preserves electrical function despite not altering blood flow indicates that the effects of polyamines are not manifested at the level of the vasculature but perhaps at the neuronal membrane.

Thromboxane synthetase inhibition with imidazole increases blood flow in ischemic penumbra.

Previous studies have indicated that the regional distribution of the arachidonic acid metabolites around a focal ischemic lesion may be important in the pathogenesis of cerebral ischemia. To determine the functional significance of this regionalization, we examined the effect of imidazole (a thromboxane synthetase inhibitor) on the distribution of the vasoconstrictor thromboxane and the vasodilators prostacyclin and prostaglandin E2 (PGE2) and on the distribution of cerebral blood flow (CBF) around a focal ischemic lesion, middle cerebral artery (MCA) occlusion in the cat. The study was conducted in two phases. The first phase examined regional distribution of tissue arachidonic acid metabolites and the effect of imidazole treatment on that distribution. The second phase examined the effect of imidazole treatment on the distribution of blood flow about the focal ischemic lesion as well as on electrocortical function and edema production. MCA occlusion resulted in increased thromboxane, prostacyclin, and PGE2 levels in the ipsilateral hemisphere. These increases were greatest in the region of marginal ischemia and were present both 3 and 6 hours after occlusion. Imidazole pretreatment (50 mg/kg i.p.) significantly inhibited thromboxane production, but augmented production of prostacyclin and PGE2. In the blood flow studies, imidazole was without effect on regions of dense cerebral ischemia (CBF less than 20 ml/minute/100 g for more than 12 of 24 postocclusion hours). In regions of marginal ischemia (20 less than CBF less than 30 ml/minute/100 g for more than 12 of 24 postocclusion hours), imidazole pretreatment significantly increased blood flow in both gray and white matter compared with saline-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

The effects of graded hemorrhagic hypotension on electrocortical function was investigated in 12 cats anesthetized with alpha-chloralose. Cerebral function was assessed both in terms of spontaneous activity (EEG) and the somatosensory evoked response. No significant changes in the EEG trace or in the amplitude of the positive/negative waves of the primary evoked response were observed at mean arterial pressures of between 120 mm Hg and 40 mm Hg. At levels of systemic arterial pressure of less than 40 mm Hg cortical rhythms became slower as pressure was decreased and an isoelectric EEG was recorded in the pressure range 10--30 mm Hg. The earliest sign of any change in the amplitude of the primary evoked responses was observed at arterial pressures of approximately 35--40 mm Hg. Below this value the amplitude decreased with decreasing systemic pressure and became zero in the pressure range 15--25 mm Hg.