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At least 667 records · Page 37Linked to original sources
PubMed2003

Auditory brain stem responses in the detection of brain death.

OBJECTIVES: We evaluated comatose patients by auditory brain stem responses (ABR) to determine the role of ABR in the diagnosis of impending brain death. PATIENTS AND METHODS: Sixty comatose patients in the intensive care unit were evaluated by brain stem evoked response audiometry. Correlations were sought between the absence or presence of ABRs and the presenting pathology, the Glasgow Coma Scale (GCS) scores, and ultimate diagnoses. RESULTS: The brain stem responses were totally absent in 41 patients. Presence of wave I could be obtained in only 10 patients. All the waveforms were found in nine patients; however, in eight patients the potentials disappeared as the GCS scores decreased to 3. Detection of wave I alone strongly suggested dysfunction of the brain stem. However, loss of wave I particularly in trauma patients aroused doubt as to whether the absence was associated with auditory end organ injury or brain stem dysfunction. CONCLUSION: The results suggest that evaluation of ABR may support brain death in a comatose patient (i) when wave I is present alone, (ii) the absence of wave I is accompanied by a documented auditory end organ injury, or (iii) when previously recorded potentials are no longer detectable.

Adolescent↗
PubMed1999

[Effects of lead exposure on their brain-stem auditory evoked potential in children].

OBJECTIVE: To determine if low lead exposure can influence auditory development in children. METHODS: Children were divided into two groups, i.e., low (< 0.483 micromol/L) and high (>or= 0.483 micromol/L) blood lead levels with atomic spectrophotometry (AAS). Latencies and latent intervals between peak waves of their brain-stem auditory evoked potentials (BAEP) in the two groups were measured and compared. RESULTS: There was positive correlation between blood lead levels and BAEP in wave III at right ear, wave V at both right and left ears and latent intervals between peak waves I to V, with correlation coefficients of 0.2991, 0.2748, 0.3248, 0.2064 and 0.2412, respectively. There was significant difference in latencies of wave III at right ear, wave V at both right and left ears and latent intervals between peak waves I to V at both right and left ears and those between waves of III to V at right ear in the low blood lead group. Latencies and latent intervals between peak waves were longer in the high blood level group (with a mean of 0.78 micromol/L and a range of 0.58 to 1.42 micromol/L) than those in the low one (with a mean of 0.30 micromol/L and a range of 0.17 to 0.45 micromol/L). CONCLUSION: Elevated blood lead level could cause prolongation of latencies and latent intervals between peak waves of BAEP and slowdown of the nerve conduction velocity, and so auditory development was influenced.

Child↗
PubMed1998

C-Fos, Jun D and HSP72 immunoreactivity, and neuronal injury following lithium-pilocarpine induced status epilepticus in immature and adult rats.

In order to follow the maturation-related evolution of neuronal damage, cellular activation and stress response subsequent to Li-Pilo seizures in the 10- (P10), 21-day-old (P21) and adult rat, we analyzed the expression of the c-Fos protein as a marker of cellular activation, HSP72 immunoreactivity as the stress response and silver staining for the assessment of neuronal damage in 20 selected brain regions. The early wave of c-Fos measured at 2 h after the onset of seizures was present in most structures of the animals at the three ages studied and particularly strong in the cerebral cortex, hippocampus and amygdala. The late wave of c-Fos measured at 24 h after the onset of seizures and that was shown to correlate to neuronal damage was absent from the P10 rat brain, and present mainly in the cerebral cortex and hippocampus of P21 and adult rats. The expression of the stress response, assessed by the immunoreactivity of HSP72 at 24 h after the seizures was absent from the P10 rat brain and present in the entorhinal cortex, amygdala, hippocampus and thalamus of P21 and adult rats. The expression of Jun D at 24 h after the seizures was discrete and present in most brain regions at all ages. Neuronal injury assessed by silver staining at 6 h after the onset of seizures was very discrete in the brain of the P10 rat and limited to a few neurons in the piriform and entorhinal cortices. In older animals, marked neuronal degeneration occurred in the cerebral cortex, amygdala, hippocampus, lateral septum and thalamus. Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage.

Age Factors↗
PubMed2006

[Changes in the rabbit brain cortex redox potential accompaning episodes of ECoG-arousal during slow-wave sleep].

Local cortex E variations are well expressive indices of rate and peculiarities of energy metabolism. The brain E is determined by the ratio of processes occurring in two energy compartments in glycolysis, in whish glucose is split without oxygen utilization and in oxidative metabolism. In the present investigation, the brain cortex E changes were recorded with implanted platinum electrodes during slow wave sleep. Under such conditions, the E lowering detects acceleration in glycolytic compartment, whereas the E local rising shows acceleration in oxidative metabolism in the tissue surrounding the electrode. Earlier in rats, we have found that E significantly lowered in metabolic active cortical sites during episodes of SWS, and supposed that acceleration of glycolysis increased. Slow oscillations (a 20-40-sec prolongation of the amplitude up to several dozens millivolts) appeared at the same time. We considered these E slow oscillations to reflect changes in the rate in compartment of glycolysis. In this research, we have found the E slow oscillations to be created by regular episodes of ECoG-arousal which were accompanied by E decreases, i. e. by acceleration in glycolysis. We think the data presented show existence of functional system supporting a low level of arousal. As in any complex system with feed back connections, this system works in oscillatory regime.

Animals↗
PubMed2006

[Auditory evoked potentials].

Auditory evoked potentials (AEPs) are an electrical manifestation of the brain response to an auditory stimulus. The waveform represents the passage of electrical activity provoked by auditory stimuli from the cochlea to cortex. The waves represented by I-VII are generated mainly in the brainstem. These waves are called the brain stem auditory evoked potentials (BAEPs) or the auditory brain stem response (ABR). The middle latency AEPs (MLAEP) are generated from the medial geniculate and primary auditory cortex. The long latency AEPs (LLAEP) are generated from the frontal cortex and association areas. The BAEPs appear to be an exquisitely sensitive monitor for pathological events during surgery. Anesthetics and mild hypothermia have minimum effect, if any, on the BAEPs. The BAEPs are useful during the microvascular decompression of the fifth or seventh cranial nerve, resection of acoustic neuroma and posterior fossa operations. Because the auditory pathway occupies a small area in the brainstem, combined use of other evoked potentials such as short latency sensory evoked potentials is recommended. The MLAEPs are most promising evoked responses for monitoring awareness or depth of anesthesia. When the concentration of anesthetics is increased, the amplitudes of the MLAEP's peaks are decreased and their latencies are elongated. Commercially developed A-line AEP monitor or aepEX can extract the AEPs waveform in a short period and automatically analyze the changes in the MLAEPs. These AEP based monitors may be superior to bispectral index (BIS) in detecting the transition from unconsciousness to consciousness.

Anesthesia↗
PubMed1990

Spinal cord responses to feline transcranial brain stimulation: evidence for involvement of cerebellar pathways.

The physiological characteristics of spinal cord responses recorded from the spinal epidural space of the cat to transcranial brain stimulation were studied, in comparison with the spinal cord responses to direct stimulation of the motor cortex or cerebellum. The conduction velocity of the initial wave of the responses to transcranial brain stimulation (122.3 +/- 16.3 m/sec mean +/- SD, n = 5) was much faster than the conduction velocity of the initial wave of the responses to motor cortex stimulation (68.3 +/- 14.7, n = 5) and similar to the conduction velocity of the initial wave of the responses to cerebellar stimulation (120.2 +/- 16.2, n = 5). Furthermore, the conduction velocity of any component in the subsequent polyphasic waves at any intensity was not similar to the conduction velocity of the initial wave of the responses to motor cortex stimulation. All components of the responses to motor cortex stimulation disappeared after intercollicular transection. In contrast, the initial wave of the responses to cerebellar stimulation and transcranial brain stimulation remained unaffected by intercollicular transection. The initial wave caused by anodal transcranial brain stimulation was eliminated by ablation of the cerebellum. However, cathodal transcranial brain stimulation sometimes can produce an initial wave that can be eliminated only by transection at the medullospinal junction. The initial wave of the responses to cerebellar stimulation was largest in amplitude when the vicinity of the dentate nucleus was stimulated. These results suggest that responses to activation of the cerebellum, rather than corticospinal neurons arising from the motor cortex, represent a major component of the spinal cord responses to transcranial brain stimulation in cats. The data obtained indicate that it is difficult to activate the motor cortex selectively by transcranial brain stimulation in cats.

Animals↗
PubMedDate not supplied

[Characteristics of the ultraslow activity and temperature of the brain as affected by neurotropic substances].

It has been demonstrated in experiments on rabbits with golden electrodes and thermocouples implanted to the brain that ethimizol (1.5 mg/kg) and 1-ethyl-4,5-di-(N.-methylcarbamoyl)-pyrazole (IEM-476, 3 mg/kg) altered the amplitude and frequency of ultraslow wave potentials and decreased the temperature of the hypothalamus, dorsal hippocamp and neocortex. Allylnorantifein (1-allyl-4,5-di-(N-methylcarbamoyl)-imidazole, 3 mg/kg) and 1-allyl-4,5-di-(N-methylcarbamoyl)-pyrazole (IEM-474, 3 mg/kg) altered the amplitude and frequency of ultraslow wave potentials of middle brain reticular formation nuclei, medial thalamic nuclei and of the neocortex, the structures of the nonspecific ascending system of the brain, and did not influence the temperature of the brain. The effects of IEM-476 and IEM-474 on the indicators under study were less powerful than those of ethimizol and allylnortifein.

Animals↗
PubMed1997

State-dependent fluctuations of low-frequency rhythms in corticothalamic networks.

We have studied the variations in the degree of correlated firing within the low-frequency sleep rhythms (< 15 Hz) between cortical, thalamic reticular and thalamocortical neurons during changes in the amplitude and frequency of brain electrical activity in anaesthetized cats. Extracellular discharges of neuronal groups of two to five physiologically identified cortical and thalamic units were recorded simultaneously with independent microelectrodes. The firing patterns and the temporal correlation between spike-trains were evaluated by auto- and crosscorrelograms. Although the animals were under deep anaesthesia, additional doses of the same or different anaesthetics were able to alter the electroencephalographic pattern, inducing waves with higher amplitude. Similar transitions occurred spontaneously. We found that the presence of rhythmic behaviour in cells of corticothalamic networks, as well as their degree of correlated firing, was extremely sensitive to even slight alterations in the state of the electroencephalogram. Cells belonging to the same functional system, but located distantly, became highly synchronized upon the increased amplitude of brain waves. Thus, an electroencephalogram characterized by slow waves corresponds to a state of rhythmic and correlated firing among cortical and thalamic neurons. The highly coherent activity during sleep patterns transcends the borders which limit the functioning during the waking brain.

Anesthetics, General↗
PubMed1982

[Early evoked auditory potentials for the assessment of prognosis in cerebral resuscitation].

Four patients who fulfilled all the clinical criteria for brain death, and 17 patients who did not, were tested with brainstem auditory evoked responses (BAER). Of the brain-dead patients, 3 had no waves present in the BAER, including wave. I. Initially BAER were intact in none of the brain-dead patients and then showed a decrease in amplitude and a prolongation of latency of the later components (7 cases) until finally wave I alone was present (6 cases). Normal data suggested toxic or metabolic comatose patients (2 cases). BAER are an objective measure of one of the sensory pathways traversing the brainstem and can be used to evaluate the functional states of the brainstem in patients in whom brain death must be considered. The association of short-latency somatosensory evoked responses (SER) has greater clinical utility in the brain death setting because it is important to have a wave present which establishes that the input signal has reached the central nervous system.

Brain Death↗
PubMedDate not supplied

[An analysis of evoked brain activity by computing the average duration of the wave half-period].

Poststimulus spectral EEG changes and their relation to averaged evoked potential (AEP) were analysed using average wave half period length (AWHL) computation method. In 5 healthy subjects increase of AWHL in the latency range of slow AEP components was revealed during simple motor reaction to visual stimuli. It was shown that AWHL increase could not be explained by AEP contribution to single realizations and/or by the process of suppression of EEG rhythms.

Brain↗
PubMed2001

Spontaneous oscillations in cerebral blood flow velocity give evidence of different autonomic dysfunctions in various types of headache.

OBJECTIVES: Our objectives were to determine if: (1) patients with migraine have B wave abnormalities in comparison to normal controls and patients with chronic tension headache and (2) patients with chronic tension headache have an imbalance in autonomic activity that is reflected in differences in Mayer wave activity in comparison to normal controls. BACKGROUND: B waves and Mayer waves are spontaneous oscillations in cerebral blood flow velocity with a frequency of 0.5 to 3 or 4 to 7 cycles per minute, respectively, and can be measured by transcranial Doppler sonography. There is experimental evidence that B waves are generated by certain brain stem nuclei which modulate the lumen of the small intracerebral vessels via monoaminergic nerve endings. In contrast, Mayer waves in cerebral blood flow velocity have no central generator but mirror the Mayer waves in arterial blood pressure which represent peripheral autonomic activity. Migraine may be attributed to a neurotransmitter imbalance in brain stem nuclei. Dysfunctions of the peripheral autonomic nervous system are known in patients with chronic tension headache. METHODS: Using bilateral transcranial Doppler monitoring of the middle cerebral artery B waves and Mayer waves were studied in 30 patients with migraine without aura, 28 subjects with tension-type headache, and 30 normal controls. Coefficient of variation as a quantitative parameter for amplitude of waves and the mean frequency were calculated from the envelope curves of the Doppler spectra. RESULTS: The coefficient of variation of B waves was higher in migrainous patients compared with patients with tension-type headache and normal controls (P<.05), indicating an increase in activity of brain stem nuclei in migraine only. Patients with chronic tension headaches had lower values for Mayer wave activity in comparison with normal controls (P<.05), a sign of an impairment of sympathetic activity. CONCLUSIONS: Our data support the dysfunction of the brain stem monoaminergic/serotonergic system in migraine. In contrast, patients with chronic tension headache have an autonomic dysfunction of peripheral origin presenting as a decrease of sympathetic activity.

Adult↗
PubMed2002

Cellular telephones and effects on the brain: the head as an antenna and brain tissue as a radio receiver.

Headache and other neuropsychological symptoms occur in users of cellular telephones, and controversy exists concerning risks for brain cancer. We hypothesize these effects result from the head serving as an antenna and brain tissue as a radio receiver. The frequencies for transmission and reception by cellular telephones, about 900 MHz for analog and 1800 MHz for digital transmission, have wavelengths of 33-35 and 16-17 cm, respectively. Human heads are oval in shape with a short axis about 16 to 17 cm in length. Near the ear there will be a cross-section in the head with an axis half the wavelength of RF/MW transmissions of 900 MHz and equal to the wavelength of RF/MW transmissions at 1800 MHz. Therefore, the human head can serve as a lossy resonator for the electromagnetic radiation emitted by the cellular telephone, absorbing much of the energy specifically from these wavelengths. Brain cells and tissues demodulate the cell-phone's audio frequencies from the radio frequency carrier. Low audio frequencies in the ranges of alpha and beta waves affect these waves and thereby influence brain function. These effects state the case for a precautionary policy.

Auditory Perception↗
PubMed2004

Long-lasting novelty-induced neuronal reverberation during slow-wave sleep in multiple forebrain areas.

The discovery of experience-dependent brain reactivation during both slow-wave (SW) and rapid eye-movement (REM) sleep led to the notion that the consolidation of recently acquired memory traces requires neural replay during sleep. To date, however, several observations continue to undermine this hypothesis. To address some of these objections, we investigated the effects of a transient novel experience on the long-term evolution of ongoing neuronal activity in the rat forebrain. We observed that spatiotemporal patterns of neuronal ensemble activity originally produced by the tactile exploration of novel objects recurred for up to 48 h in the cerebral cortex, hippocampus, putamen, and thalamus. This novelty-induced recurrence was characterized by low but significant correlations values. Nearly identical results were found for neuronal activity sampled when animals were moving between objects without touching them. In contrast, negligible recurrence was observed for neuronal patterns obtained when animals explored a familiar environment. While the reverberation of past patterns of neuronal activity was strongest during SW sleep, waking was correlated with a decrease of neuronal reverberation. REM sleep showed more variable results across animals. In contrast with data from hippocampal place cells, we found no evidence of time compression or expansion of neuronal reverberation in any of the sampled forebrain areas. Our results indicate that persistent experience-dependent neuronal reverberation is a general property of multiple forebrain structures. It does not consist of an exact replay of previous activity, but instead it defines a mild and consistent bias towards salient neural ensemble firing patterns. These results are compatible with a slow and progressive process of memory consolidation, reflecting novelty-related neuronal ensemble relationships that seem to be context- rather than stimulus-specific. Based on our current and previous results, we propose that the two major phases of sleep play distinct and complementary roles in memory consolidation: pretranscriptional recall during SW sleep and transcriptional storage during REM sleep.

Animals↗
PubMed1980

[The auditory evoked brain stem potential andits value for clinical diagnosis].

Auditory evoked brain stem potentials (seven waves within the first 10 milliseconds after the stimulus) obtained from the intercalated nuclei within the auditory pathway by averaging are suitable for a functional diagnosis of the brain stem. Disorders affecting the auditory pathway (direct or indirect tumour pressure or infiltrates, demyelinisation processes, traumatic brain stem injuries, ischemia) from the acoustic nerve through the cochlear nuclei, the superior olivary nuclei, the nuclei of the lateral lemnisci, the inferior collicular nuclei, to the medial geniculate bodies can be identified and used for the topical diagnosis.

Adolescent↗
PubMed2006

Developmental expression of neural Wiskott-Aldrich syndrome protein (N-WASP) and WASP family verprolin-homologous protein (WAVE)-related proteins in postnatal rat cerebral cortex and hippocampus.

The actin cytoskeleton plays a critical role in the cellular morphological changes. Its organization is essential for neurite extension and synaptogenesis under the processes of neuronal development. Recently, neural Wiskott-Aldrich syndrome protein (N-WASP) and WASP family verprolin-homologous protein (WAVE) have been identified as key molecules, which specifically participate in regulation of actin cytoskeleton through small GTPases. The functions of these factors have been investigated using cultured cells; however, in vivo developmental changes in these factors are not fully understood. In this study, we examined the expression levels and distributions of N-WASP, WAVE and their related proteins in the rat cerebral cortex and hippocampus during postnatal development. Protein levels of these factors were progressively increased during development, and actin was accumulated in membranous fractions. Immunoreactivities for these factors were widely but differentially observed in entire brain. In the developing brain, N-WASP and WAVE seemed to exist in the synapse-rich areas, such as stratum radiatum of hippocampal CA1 subfield. A similar tendency in the distributions of these factors was observed in the mature brain. Taken together, N-WASP, WAVE and their related proteins may participate in normal brain development and synaptic plasticity by regulating the actin cytoskeleton.

Actins↗
PubMedDate not supplied

[Shifts in the constant potential in the structures of the rat brain in focal ischemia and systemic hypoxia].

The role of spreading depression (SD) in the development of ischemic brain damage in rats was studied in two models: focal cortical ischemia provoked by a photothrombotic occlusion of the middle cerebral artery (MCA) and systemic hypoxia induced by breathing with 0.8% carbon monoxide (CO). Spontaneous cortical SD waves occurring during illumination were found to delay the irreversible MCA occlusion. Thrombosis was probably prevented by episodes of striking vasodilation and hyperemia lasting for 1-2 min and accompanying every SD wave. The SD-induced hyperemia after permanent MCA occlusion seems to improve the oxygen supply of the penumbra zone. During hypoxia induced by one-hour respiration with 0.8% CO, COHb saturation of the blood reached 50-60%. SD waves occurred in different brain regions of lightly anesthetized rats (pentobarbital, 20 mg/kg) changed under the above conditions into prolonged depolarizations (HDs) which led to a substantial increase in animals' mortality (60%). The SDs evoked in the cortex and hippocampus of deeply anesthetized rats (pentobarbital, 50 mg/kg) showed that hippocampus became highly vulnerable by CO hypoxia. Duration of the SD-provoked HDs often reached 30-60 min after a single SD wave. Decreased cell density was found in CA1 area of the hippocampus 20-30 days after the CD-enhanced CO hypoxia. Cerebrolysin (2.5 ml/kg daily, during 10 days) prevented from severe hippocampal injury (formation of granulomas) usually seen in the left hemisphere of rats not treated with cerebrolysin.

Acute Disease↗