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Event-related brain potentials in depressed patients treated with electroconvulsive therapy.

1. As impairment of attention has long been recognized as a clinical feature of depression, we undertook to evaluate in depressed subjects and controls a feature of the event-related brain potentials (ERP) the N100 wave which has been linked to attentional processes. 2. This study involved collection of EEG data in an "auditory oddball" ERP paradigm in 9 depressed subjects prior to and following a course of 6 electroconvulsive therapy (ECT) treatments, as well as 11 controls. Concurrent Hamilton depression rating scales provided a measure of symptomatic severity. 3. Pretreatment N100 amplitude was significantly lower in the depressed group while N100 latency was greater than among controls, with treatment differences from control values disappeared. Further a robust correlation (r = 0.85 p less than or equal to .0038) emerged between N100 amplitude (increased amplitude being lower) and severity of depression. 4. Those results provide evidence for a physiological attentional disturbance in depression and suggest that certain features of this disturbance relate directly to symptom severity.

Adult↗

A common N400 EEG component reflecting contextual integration irrespective of symbolic form.

OBJECTIVE: Electroencephalographic (EEG) waves modulated by context have been identified about 400 ms after presentation of a new semantic stimulus, such as a word or a number, within a prior context. However, it is not known if any component of these waves arises from a common brain system activated by different symbolic forms. METHODS: Multichannel EEG recordings were performed in 10 healthy subjects during the presentation of lexical and numerical series with congruent and incongruent endings. EEG was analysed using a combination of independent component and cluster analysis. RESULTS: Contextual integration of semantic stimuli elicited a negative independent component at around 400 ms that shared the same pattern of spatio-temporal covariation across numerical series and sentences within single subjects. This independent component was bigger following incongruent endings. CONCLUSIONS: These data provide evidence that one element of the activity contributing to the N400 is common to different symbolic forms. SIGNIFICANCE: One component of the brain systems evaluating the semantic inter-relationship of new stimuli with prior context may be common to different symbolic forms.

Acoustic Stimulation↗

The evolution of visual and auditory evoked potentials in infants with perinatal disorder.

The evolutionary changes of evoked potentials (EPs) were studied from the neonatal period up to 1 year of age in 41 infants with various perinatal disorders. Abnormal EPs in the first week of life recovered quickly. In infants with normal outcome, abnormal EPs became normal within a month. In infants with cerebral palsy (CP) or mental retardation (MR), EPs recovered within 2-3 months of age. Infants with more severe neurological damage showed abnormal EPs even beyond 6 months of age. Abnormal EPs beyond 2 weeks of age indicated poor prognosis. As for the wave form of EPs, absent responses or abnormal wave form reflected more severe brain dysfunction. AEPs tended to show more profound abnormalities than VEP. However, some infants with absent AEP in the first week of life had a favorable prognosis. AEPs seemed to be more easily affected by brain dysfunction.

Asphyxia Neonatorum↗

A slow wave investigation of working memory biases in mood disorders.

Mood-congruent working memory biases were examined in a delayed matching to sample paradigm using the slow wave (SW) event-related brain potential (ERP) component. Mood-congruent working memory biases, indexed by SW amplitudes, were demonstrated among individuals experiencing a major depressive episode (MDE) and nondepressed controls but not individuals with dysthymia. However, analyses of symptom severity demonstrated that those with dysthymia exhibited significantly less negative SW amplitudes with increasing depressive mood severity, whereas individuals with major depression demonstrated more negative SW amplitudes with increasing depressive mood severity. These results are discussed in the context of diagnostic specificity for cognitive biases associated with working memory of mood-disordered individuals.

Adult↗

Memory of faces: a slow wave ERP study of major depression.

This study examined slow wave (SW) event-related brain potential (ERP) amplitudes in response to happy, neutral, and sad faces during a working memory task to further identify the associated component processes and physiological changes of mood-congruent memory biases in individuals with and without major depression. The results suggest that individuals with and without a diagnosis of major depressive disorder (MDD) differentially maintain valenced facial information in their working memory. Specifically, the nondepressed individuals displayed a marked reduction in SW amplitude to the negative faces. Individuals with MDD exhibited equivalent SW amplitudes for positive and negative facial stimuli. Results are discussed in terms of avoidance coping, previous ERP studies of working memory, and facial recognition deficits in individuals with MDD.

Adult↗

Electrophysiological models for the study of cognition enhancers.

Electrophysiological approaches range from global EEG studies to single unit recordings. Quantified EEG studies indicate that cognition enhancers increase the power of fast-frequency (beta) EEG activity in humans and the duration of hippocampal theta in animals. A problem here is the distinction between improved cognition and increases in general arousal, although the two might have the same end effect. A second global approach is the use of the evoked potential or even the conditioned evoked potential, for example the P 300 wave. This approach, using defined brain circuits, would appear to be more specific than global EEG models. Both approaches can be used in parallel studies in animals and man. Studies at more cellular levels can only be used in animals and suffer from severe constraints. The most precise approach, single cell recording, cannot be conducted in freely behaving animals, whereas multi-unit approaches in awake animals tend to produce many artefacts. However, techniques using microintophoretically applied drugs in freely moving rodents and monkeys can contribute to the understanding of mechanisms of action. In vitro studies, for example long-term potentiation in hippocampal slices, may represent a neuronal model of learning but its role in normal brain function has still not been elucidated.

Animals↗

Brainstem auditory evoked responses in patients comatose as a result of blunt head trauma.

The brainstem auditory evoked response (BAER) was evaluated as an aid in the early diagnosis and prognosis of 17 comatose blunt head-injury patients. Click stimuli (60 dBSL, 10/sec) were presented monaurally through headphones. BAER's were recorded between Cz and ipsilateral mastoid; contralateral mastoid ground. No BAER waves occurred in three "brain-dead" patients. Two patients with initially abnormal BAER's did not show improvement in followup recordings, and died of their brain injuries. Recovery occurred in 12 patients with normal followup BAER's, regardless of whether initial BAER's had been abnormal (three patients) or normal (nine patients). Apparently, initial BAER's (mean, 31 hours postinjury) can be abnormal as the result of reversible damage. Followup BAER's (3 to 6 days postinjury) did correspond with patient outcome at a time when clinical prognoses were often uncertain. BAER's aided diagnostically in determining the extent of brainstem damage and the effectiveness of treatment.

Acoustic Stimulation↗

Single pulse stimulation of the human subthalamic nucleus facilitates the motor cortex at short intervals.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for Parkinson's disease (PD). The mechanism is poorly understood. High-frequency STN DBS has been reported to affect motor cortex excitability in a complex way, but the timing between STN stimuli and changes in motor cortical (M1) excitability has not been investigated. We examined the time course of changes in motor cortical excitability following single pulse STN DBS. We studied 14 PD patients with implanted DBS electrodes in the STN, 2 patients with electrodes in internal globus pallidus (GPi), and 1 patient with an electrode in the sensory thalamus. Transcranial magnetic stimulation (TMS) was delivered to the M1 ipsilateral to the DBS with induced currents either in the anterior-posterior direction in the brain to evoke indirect (I) waves or in the lateral-medial direction to activate corticospinal axons directly. Single pulse stimulation through the DBS contacts preceded the TMS by 0-10 ms. Surface EMG was recorded from the contralateral first dorsal interosseous muscle. Three milliseconds after STN stimulation, the motor evoked potential (MEP) amplitudes produced by anterior-posterior current were significantly larger than control responses, while the responses to lateral-medial currents were unchanged. Similar facilitation also occurred after GPi stimulation, but not with thalamic stimulation. Single pulse STN stimulation facilitates the M1 at short latencies. The possible mechanisms include antidromic excitation of the cortico-STN fibers or transmission through the basal ganglia-thalamocortical pathway.

Adult↗

Benign focal epileptiform discharges in childhood migraine (BFEDC).

Interictal EEGs were studied in 100 children, ages 3 to 15 years. Records were interpreted independent of history; 89% were normal, 9% had benign focal epileptiform discharges (BFEDC), one had temporal spikes, and one had background slowing. The nine patients with BFEDC did not differ from the others. None had epilepsy. This incidence of 9% is higher (p less than 0.0001) than the incidence of BFEDC in the normal population (1.9%). The significance of this finding is not clear, but migraine and benign focal epilepsy of childhood may be genetically linked, or the vascular abnormality of migraine may cause brain injury to produce sharp waves of low epileptogenicity. These results do not suggest that headaches are epileptic.

Adolescent↗

Fusiform basilar artery aneurysm in a 33-month-old child.

A 33-month-old girl presented with acute subarachnoid hemorrhage from a ruptured multilobulated fusiform aneurysm of the midbasilar artery. This rare lesion was treated surgically by occluding the basilar artery. Intraoperative brain stem auditory evoked potential and somatosensory evoked potential monitoring results did not change with basilar artery occlusion, suggesting that the occlusion would be tolerated. However, the amplitudes of brain stem auditory evoked potential Waves III-V to right ear stimulation were transiently reduced during left pontine retraction during the aneurysm exposure. The patient made a complete clinical recovery.

Aneurysm↗

Nonlinear EEG dynamics during sleep in depression and schizophrenia.

The article deals with the question, whether nonlinear analysis of the sleep EEG may give clues to understanding of disturbed information processing in psychiatric diseases. We point out how the nonlinear approach to EEG dynamics is motivated and review recent investigations concerning nonlinear dynamical properties of physiological systems. We present calculations of the correlation dimension D2 and the principal Lyapunov-exponent lambda 1 for sleep EEG data from 9 depressive and 11 schizophrenic inpatients compared to healthy controls. Combining the findings for D2 and lambda 1 our results point to altered nonlinear brain dynamics mainly during slow wave sleep in depression and during REM sleep in schizophrenia. Finally, possible interpretations of altered nonlinear EEG dynamics during sleep concerning disturbed information processing in depression and schizophrenia are discussed.

Adult↗

Oxidative metabolic activity of cerebral cortex after fluid-percussion head injury in the cat.

To assess the metabolic and vascular effects of head trauma, fluid-percussion pressure waves were transmitted to the brains of anesthetized, paralyzed, and artificially ventilated cats. Changes in the redox state of cytochrome a,a3, and relative local blood volume were measured in situ by dual-wavelength reflection spectrophotometry of the cortical surface viewed through an acrylic cranial window implanted within the closed skull. Initial fluid-percussion impacts of 0.5 to 2.8 atm peak pressure produced consistent transient oxidation of cytochrome a,a3 and increases of cortical blood volume. These changes occurred despite the presence of transient posttraumatic hypotension i some cases. Also, impact-induced alterations of vascular tone occurred, independent of the presence or absence of transient hypertension in the posttraumatic period. These data demonstrate that hypoxia does not play a role in the immediate posttraumatic period in cerebral cortex, and are consistent with the idea that after injury there is increased cortical energy conservation. These data also support the concept that head trauma alters the relationship of metabolism and cerebral circulation in the period immediately after injury.

Animals↗

[Audiologic evaluation in a family showing diabetes mellitus and deafness associated with a mutation in mitochondrial DNA].

An A to G transition at nucleotide 3,243 in the tRNA(Leu)(UUR) gene of mitochondrial DNA has recently been identified as a pathogenic point mutation which is associated with diabetes mellitus and sensorineural deafness in several pedigrees. We have also reported a family showing the association of deafness and diabetes mellitus as the predominant clinical features with this mutation. Audiologic data from two patients in this family are presented. Both had a bilaterally symmetrical sensorineural hearing loss at all frequencies. As is often the case with deafness associated with a mitochondrial disorder, the pure-tone threshold values were maximal at high frequencies in both patients. The audiologic work-up presented not only cochlear characteristics but also signs suggestive of retrocochlear disturbance with poor speech discrimination scores as compared to pure-tone thresholds, although auditory brain-stem responses showed neither wave delay nor prolonged interpeak latencies.

Adolescent↗

Histological study of brain in the rats exposed to 93-days' tail-suspension.

Antiorthostatic position of rats during 93-days' tail suspension induced in the brain strongly pronounced edema of nervous tissue, alteration of structure in horoid plexus, pointing out the decrease in liquor secretion by exocytosis and increase in itraventricular pressure, morphological changes in veins and capillaries, reflecting the development of plethora in veins and tendency to thrombogenesis, and also the appearance of structural signs of prolonged arterial vasoconstriction and narrowing of arterial lumen in surface arteries which be considered as an adaptive process lying the obstacles to excessive blood inflow to brain and dumping the pulse wave during prolonged antiorthostatic state.

Journal Article↗

[Migraine with a combination of aura symptoms as a clinical manifestation of cortical spreading depression].

The pathomechanism of the migraine aura remains unclear. The most probable cause of the aura is cortical spreading depression with associated hypoperfusion. Both the cortical spreading depression and hypoperfusion begin in the occipital lobes and spread forward slowly (2-3 mm/min) in a wave-like mode along the brain convolutions and cross territories of brain arteries. We present a 24-year-old female patient with a combination of aura symptoms. Each migraine attack began with a bright scintillating zig-zag, which crossed the visual field. It was followed by left sided hemiparesthesiae marching from the face to the hand. The last symptom of aura was motor aphasia. Later a unilateral, pulsating headache developed with associated photo- and phonophobia. The stable pattern and duration of aura symptoms in the presented case suggest that the cortical spreading depression plays an important role in the pathomechanism of migraine with aura.

Adult↗

[SPECT-99mTc-HMPAO in a case of epilepsia partialis continua and focal encephalitis].

A case of epilepsia partialis continua (EPC) in a eight year old girl is presented. The episode EPC involved the left side of the face and the left arm and leg with progressive neurologic deficit and mental impairment. The focal seizures did not respond to treatment with a wide variety of antiepileptic drugs. The patient was studied with a 99mTc HMPAO-SPECT in addition to EEG, CT and MRI procedures. During the ictal period the SPECT showed an increased cerebral blood flow in the right hemisphere especially in the Rolandic area and the temporal lobe; during the interictal period a decreased flow was seen in the same regions. The EEG showed marked epileptogenic activity consisting of continued spike and slow wave discharges over the right brain hemisphere; the CT scan was normal and the MRI showed an increased signal intensity in the white and gray matter in the right hemisphere, especially in the frontal and temporal lobes. A temporal lobectomy and a frontal corticectomy were done. The pathologic specimens showed changes consistent with viral encephalitis (Rasmussen's syndrome). The patient has not had seizures in the ten months after surgery. She returned to school three months after surgery, and her IQ was normal. This report illustrates the usefulness of the 99mTc HMPAO-SPECT technique for the diagnosis and the management of EPC cases.

Anticonvulsants↗

Cortistatin is expressed in a distinct subset of cortical interneurons.

Cortistatin is a presumptive neuropeptide that shares 11 of its 14 amino acids with somatostatin. In contrast to somatostatin, administration of cortistatin into the rat brain ventricles specifically enhances slow wave sleep, apparently by antagonizing the effects of acetylcholine on cortical excitability. Here we show that preprocortistatin mRNA is expressed in a subset of GABAergic cells in the cortex and hippocampus that partially overlap with those containing somatostatin. A significant percentage of cortistatin-positive neurons is also positive for parvalbumin. In contrast, no colocalization was found between cortistatin and calretinin, cholecystokinin, or vasoactive intestinal peptide. During development there is a transient increase in cortistatin-expressing cells in the second postnatal week in all cortical areas and in the dentate gyrus. A transient expression of preprocortistatin mRNA in the hilar region at P16 is paralleled by electrophysiological changes in dentate granule cells. Together, these observations suggest mechanisms by which cortistatin may regulate cortical activity.

Animals↗

Pathophysiology of status epilepticus.

The cellular and molecular pathophysiology of status epilepticus (SE) provides a conceptual framework for understanding clinical scenarios and prospectively designing logical therapies. SE is a dynamic process that evolves over time in a predictable manner with an established sequence of EEG, motor, physiologic, and cellular changes. Neuronal injury and death are the result of processes intrinsic to the brain, mediated by a complex neurotoxic cascade consisting of multiple serial and parallel processes. The risk of cell injury depends also on the overall pathophysiologic profile, including the presence of alterations resulting from SE and occurring independent of SE. On neurophysiologic grounds, we divide SE into "spike-wave" and "nonspike-wave" forms. Spike-wave "absence" status epilepticus carries a low risk of epileptic brain damage, and therapy should be adjusted accordingly. All nonspike-wave SE has a theoretical basis for epileptic brain damage, but the actual risk is variable. There is a significant known risk of cell injury during generalized convulsive SE, a variety of nonspike-wave SE, so aggressive treatment is warranted to prevent sequelae. There is also a theoretical basis for epileptic brain damage in nonspike-wave nonconvulsive SE, but prospective studies are needed to determine which of these patients warrant aggressive therapy. Based on pathophysiologic principles, future treatment of nonspike-wave SE may use a combination of anti-ictal agents, including gamma-aminobutyric acid agonists and N-methyl-D-aspartate antagonists, as well as various neuroprotectants.

Animals↗