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BACKGROUND: We have observed that the reduction in cerebral blood flow (CBF) of patients with chronic subdural hematomas is always most pronounced in the thalamus and has a linear correlation with the degree of brain deformity caused by the compression from the hematoma. When the brain is markedly displaced by a hematoma, electroencephalography (EEG) shows delta waves in the frontal region. We theorized that the flow reduction begins in the thalamus, spreading throughout the hemisphere as displacement progresses. METHODS: We measured CBF using the xenon/computed tomography (CT) method in 10 patients with chronic subdural hematomas who had hemiparesis and/or a mental disturbance and radiographic evidence of a midline shift or herniation. We correlated their flow reductions with topographic encephalograms. RESULTS: Flow reductions were more pronounced in the thalamus than in the hemisphere and cortex. Slow waves dominated over fast waves, especially in the frontopolar and frontal regions bilaterally. Flow values correlated negatively with the presence of delta and theta waves and positively with that of alpha and beta waves. On the side of the hematoma, the brain wave activity correlated significantly with thalamic flow, and the correlation was greater than with the hemispheric or cortical flow. Thalamic flow correlated more consistently with delta and alpha waves in the central, temporal, and occipital regions, and with beta waves in the frontopolar, frontal, and central regions. On the nonhematoma side, the correlation between brain wave activity and hemispheric flow was significant and greater than with cortical or thalamic flow. CONCLUSIONS: The correlation of EEGs with thalamic flow, which was maximally reduced, seems to substantiate the concept that the thalamus is primarily injured by brain distortion due to the compression from hematoma and that the remote areas are secondarily deactivated by a transneural depression ("diaschisis") originating from the dysfunctioning thalamus. Thalamic involvement seems to be the cause of the neurologic dysfunction and the abnormal EEG activity in chronic subdural hematomas.
The authors studied brain blood flow with single photon emission computed tomography (SPECT) in two patients with plateau waves. The intracranial pressure and blood pressure were also monitored continuously in these patients. They included one patient with brain-tumor (rt. sphenoid ridge meningioma) and another with hydrocephalus after subarachnoid hemorrhage due to rupture of lt. internal carotid aneurysm. The intracranial pressure was monitored through an indwelling ventricular catheter attached to a pressure transducer. The blood pressure was recorded through an intraarterial catheter placed in the dorsalis pedis artery. Brain blood flow was studied with Headtome SET-011 (manufactured by Shimazu Co., Ltd.). For this flow measurement study, an intravenous injection of Xenon-133 of about 30 mCi was given via an antecubital vein. The position of the slice for the SPECT was selected so as to obtain information not only from the cerebral hemisphere but also from the brain stem: a cross section 25 degrees over the orbito-meatal line, passing through the inferior aspect of the frontal horn, the basal ganglia, the lower recessus of the third ventricle and the brain stem. The results indicated that, in the cerebral hemisphere, plateau waves were accompanied by a decrease in blood flow, whereas, in the brain stem, the blood flow showed little change during plateau waves as compared with the interval phase between two plateau waves. These observations may explain why there is no rise in the blood pressure and why patients are often alert during plateau waves.
Wave forms of canine brain stem auditory-evoked potentials (BAEP) and the effects of electrode positions on the wave forms were studied as a basis for experimental and clinical use of BAEP recording. The BAEP regularly consisted of 5 waves (I to V) with latencies and polarities similar to those of other species. In some dogs, waves II, III, and IV contained distinct subpeaks (a, b, c). Waves similar to waves VI and VII of other species were recorded in some dogs. With respect to BAEP, no site on the head was electrically inactive and BAEP could be recorded as far caudally as the caudal cervical region in some dogs. Wave I, positive in recordings from the dorsal midline of the calvaria (vertex) underwent polarity reversal and increased amplitude and duration in recordings made from caudal ventrolateral regions of the head (mastoid region). As a result, wave I partially or totally obscured wave II so that the latter could no longer be clearly identified. Waves IIIa and IIIb were differentially affected by moving the recording site, indicating that their generators were spatially separated. Waves IV and V were also affected by electrode site, consistent with previous reports that they have spatially separated generators in other species. In recordings made with vertex electrodes referenced to the mastoid region ipsilateral to the stimulated ear, wave I appeared as a high-amplitude positive peak with onset latency equalling that in noncephalic reference recordings, but with somewhat later peak latency and longer duration. As a result, wave II was partially or totally obscured so that only 4 major peaks were evident in the BAEP. In contralateral mastoid reference recordings, latency to peak of wave I was unchanged; however, amplitude of all waves was reduced and waves IIa and IIb were not as clearly differentiated as they were in noncephalic reference recordings.
A 10-year-old boy had gait and speech disturbances 17 days after the initial symptoms of a fever, headache and cough. Four days later he was admitted to a hospital with mild disturbances of gait, speech, writing, visual acuity, left facial nerve, nystagmus and consciousness. Impairments of cranial nerves (II, III and VII), pyramidal sign and cerebellar sign were noticed. EEG showed generalized slow waves. Auditory brain stem response showed prolongation of the interval between I and V waves and poor differentiation between them. Brain CT could not find any abnormalities. Brain stem encephalitis was diagnosed. Clinical signs and symptoms continued for two weeks when steroid therapy was started and it was effective to improve the disease. He was discharged from the hospital without sequelae. Herpes simplex virus (HSV) type 1 was detected from cells in CSF on admission by fluorescence antibody method. HSV antibody titers in sera changed from 1/8 to 1/64 during three months by complement fixation test. Specific IgG and IgA by enzyme linked immunosorbent assay (ELISA) was high in CSF. Specific antibody in CSF/total antibody in CSF: specific antibody in serum/total antibody in serum for IgG and IgA classes were more than 1. Reports of mild type of HSV brain stem encephalitis seemed to be rare. Our case which was followed for several months carefully would be important to discuss.
Eye movement-related brain activity was studied in 14 subjects by recording EEG topographically in 16 channels over the occipital brain areas. Potential fields obtained with or without the simultaneous presentation of a visual stimulus during the time course of horizontal saccades were compared. Without visual stimulation, eye movements were followed at a mean latency of about 65 ms by a lateralized occipital dominant component whose topography was determined by the direction of the saccade but whose latency was independent of the time course of the eye movements. This component was reminiscent of lambda waves, however, it could also be elicited in complete darkness. When stimuli were presented during saccades, component latencies increased significantly, and there were also topographic changes in the evoked potential fields. Negative centroids were located more anteriorly and positive ones more posteriorly on the scalp when compared to brain activity recorded with stable eye positions and visual stimulation. All subjects reported no suppression of visual stimuli when presented during saccades occurred. This was confirmed by testing the discrimination performance of an independent group of 27 subjects. Our data show that the execution of saccades elicits electrophysiological patterns of activation in the visual cortex even without visual input. The increase of component latency observed during saccades as well as topographical differences suggest that visual information is processed by different neuronal elements during saccadic eye movements.
Auditory brain-stem response (ABR) waveforms from 61 patients with eighth nerve or cerebellopontine angle tumors were analyzed for wave presence or absence. Eighteen patients yielded ABRs lacking any readable waves; 27 patients revealed ABRs in which waves were partially present (ie, one or two waves present); and 16 patients demonstrated ABRs with all waves (I, III, and V) present. In the partially present ABR group, waves I and V were most prevalent. The group lacking waves (absent ABR group) had significantly poorer hearing sensitivity and larger tumors than the partial ABR group. Various additional group comparisons for hearing sensitivity and tumor size did not yield any significant differences among the three groups.
During ischaemia neurons depolarize and release the neurotransmitter L-glutamate, which accumulates extracellularly and binds to postsynaptic receptors. This initiates a sequence of events thought to culminate in immediate and delayed neuronal death. However, there is growing evidence that during ischaemia the development of spreading depression (SD) can be an important determinant of the degree and extent of ischaemic damage. In contrast, SD without metabolic compromise (as occurs in migraine aura) causes no discernible damage to brain tissue. SD is a profound depolarization of neurons and glia that propagates like a wave across brain tissue. Brain cell swelling, an early event of both the excitotoxic process and of SD, can be assessed by imaging associated intrinsic optical signals (IOSs). We demonstrate here that IOS imaging clearly demarcates the ignition site and migration of SD across the submerged hippocampal slice of the rat. If SD is induced by elevating [K+]O, the tissue fully recovers, but in slices that are metabolically compromised at 37.5 degrees C by oxygen/glucose deprivation (OGD) or by ouabain exposure, cellular damage develops only where SD has propagated. Specifically, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity. In contrast to OGD, bath application of L-glutamate (6-10 mM) at 37.5 degrees C evokes a non-propagating LT increase in CA1 that reverses without obvious cellular damage. Moreover, application of 2-20 mM glutamate or various glutamate agonists fail to evoke SD in the submerged hippocampal slice. We propose that SD and OGD together (but not alone) constitute a 'one-two punch', causing acute neuronal death in the slice that is not replicated by elevated glutamate. These findings support the proposal that SD generation during stroke promotes and extends acute ischaemic damage.
Slow wave sleep is a condition for paradoxical sleep (PS) expression. The lower brain stem is able to produce the known PS phenomena but, in order to do so in all its functional magnitude, it depends on the rest of the brain. There are physiological conditions that appear as necessary to develop the PS. A group of basic functions, i.e., respiration, cardiovascular, brain oxygen availability, temperature, etc., have to go on in a non-homeostatic fashion during this state. Other conditions to be met are: the cut-off of the motor output and a different central control of the sensory input. During PS, phasic pO2 changes were observed in some nuclear structures characterized by a dramatic increase in the amplitude of oscillations. These changes were found in a number of subcortical, cerebellar and brain stem regions and were never observed neither in the neocortex, the specific thalamic nuclei nor in the white matter. It is postulated that these variations are due to a local increase in neuronal activity in PS during a decrease of the local homeostatic oxygen control. All the physiological changes above mentioned have a common anatomical denominator: the pons and medulla. Upon this region, proposed as the PS FINAL COMMON REGION, conveges rostral and caudal information making it the executor of all PS phenomena. The pons, on the other hand, has a bioelectrical activity of its own during PS, i.e., the ponto-geniculo-occipital spikes (PGO). This activity spreads through the brain and cerebellum. The cerebellum also participates in sleep physiology: the pO2 oscillations pattern and PGO are present in all of its parts, cortex and nuclei, being, the spike activity, dependent of a cholinergic pontine region. The pons shows a particular duality during PS. It is part of the FINAL COMMON REGION for PS phenomena and, at the same time, it is the origin of the PGO activity.
The BSEPs elicited by monaural and binaural click stimuli were studied using a variety of monopolar and bipolar montages. The wave form of the evoked response was different on separate montages. Evidence is presented that there are multiple generators responsible for the evoked potential recorded. Furthermore binaural stimulation evoked activity in a generator not excited from either ear alone. A method of presentation of the data in terms of a vectogram is given and the use of this in disease illustrated. The implication of complex interactions of many generators upon the assessment of the record in patients is discussed.
The generators of the several components of the auditory brain stem evoked response (ABR) have yet to be completely identified. However, there is compelling evidence to suggest specific generators for waves I and II, namely the distal and proximal portions of the auditory nerve, respectively. Although there is no question concerning the origin of wave I, there remains some uncertainty as to whether or not wave II arises entirely from the auditory nerve. The purpose of this study was to examine the behavior of wave II, as recorded via vertical versus horizontal derivations, in an effort to determine if wave II in both derivations is equally affected by stimulus manipulations (i.e., as would be presumed from a single generator theory). ABR recordings were obtained from normal-hearing young adults using vertical (hairline-to-ipsilateral mastoid and hairline-to-contralateral mastoid) and horizontal (mastoid-to-mastoid) derivations of responses to clicks presented at a variety of stimulus levels (40-80 dB nHL) and rates (19.9-59.9/sec.). The results indicate a shorter latency for wave II recorded in the horizontal derivation (wave IIa), compared to the vertical derivation (wave IIb). Also, wave IIa was found to be more susceptible to increased stimulus rate and exhibited a different latency behavior than wave IIb. These findings seem difficult to reconcile on the basis of a single generator for waves IIa and IIb.
Variations of the brain cortex redox state potential (E) were recorded in freely moving white rats (mass of 300-350 g) with implanted platinum electrodes (with the platinum reference electrode in the nasal bone) during sleep-wake cycles. It was found that transitions from the slow-wave sleep to wakefulness were accompanied in the number of cortical areas (metabolic-active sites) by the E rise, while the transitions from the wakefulness to slow-ware sleep were associated with a drop of E. However, the episodes of the short-term arousals during the slow-wave sleep were accompanied by the respective decreases in E thus forming the irregular E variations (1.5-3 min in duration). It was also found that the oscillations of a typical pattern (quasisinusoidal with the frequency of 10-20 osc/min and the amplitudes up to several mV) could take place in the metabolic-active cortical sites. These oscillations were defined as fast E oscillations. During the slow-wave sleep, the less regular oscillations with the lower frequency (1.2-10 osc/min) and higher amplitude were recorded in the same cortical sites. These oscillations were defined as slow. It is suggested that the fast metabolic oscillations of wakefulness are mainly controlled by the mitochondria of neuronal populations, whereas the slow metabolic oscillations which occur in the slow-wave sleep are related with glycolysis in populations of glial cells.
PURPOSE: To illustrate a functional interpretation of blood oxygen level-dependent (BOLD) signal changes associated with generalized spike-and-wave discharges in patients with absence seizures and to demonstrate the reproducibility of these findings in one case. METHODS: In a 47 year-old patient with frequent absence seizures, BOLD signal changes during generalized spike-and-wave discharges (GSWD) were mapped by using simultaneous and continuous electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) at 1.5 T and 6 months later at 3 T. GSWDs were modeled as individual events and as blocks. RESULTS: The patient studied exhibited frequent generalized spike-wave activity with temporal properties ideal for study with EEG/fMRI. Highly reproducible GSWD-associated fMRI signal decreases (deactivations) were seen in bilateral frontal and temporoparietal cortices and the precuneus, in addition to activations in occipital cortex and, at 3 T, the posterior thalamus. CONCLUSIONS: The GSWD-associated changes seen here involve cortical regions that have been shown to be more active at conscious rest compared with sleep and with various types of extroverted perception and action. These regions have been proposed to constitute the core of a functional "default mode" system. We propose that the findings of deactivation of this distributed brain system during GSWDs mirrors the clinical manifestation of GSWDs (i.e., absence seizures). Furthermore, we suggest that these deactivations may reflect the functional consequences of GSWDs on physiologic brain activity at rest rather than direct hemodynamic correlates of epileptic discharges.
PURPOSE: To investigate the effect of 2450 MHz pulsed-wave microwaves on the induction of DNA damage in brain cells of exposed rats and to discover whether proteinase K is needed to detect DNA damage in the brain cells of rats exposed to 2450 MHz microwaves. MATERIALS AND METHODS: Sprague-Dawley rats were exposed to 2450 MHz pulsed-wave microwaves and sacrificed 4 h after a 2-h exposure. Rats irradiated whole-body with 1 Gy (137)Cs were included as positive controls. DNA damage was assayed by two variants of the alkaline comet assay on separate aliquots of the same cell preparation. RESULTS: Significant DNA damage was observed in the rat brain cells of rats exposed to gamma-rays using both versions of the alkaline comet assay independent of the presence or absence of proteinase K. However, neither version of the assay could detect any difference in comet length and/or normalized comet moment between sham- and 2450 MHz pulsed-wave microwave-exposed rats, regardless of the inclusion or omission of proteinase K in the comet assay. CONCLUSIONS: No DNA damage in brain cells was detected following exposure of rats to 2450 MHz microwaves pulsed-wave at a specific absorption rate of 1.2 W kg(-1) regardless of whether or not proteinase K was included in the assay. Thus, the results support the conclusion that low-level 2450 MHz pulsed-wave microwave exposures do not induce DNA damage detectable by the alkaline comet assay.
Blood-gas (pO2, pCO2) and pH-changes of venous (v.jugularis interna) and arterial (A.femoralis) blood samples, furthermore glucose utilization and lactate-, pyruvate-production of brain were investigated during electroconvulsive treatment in relaxation of 45 psychotic patients. The blood-gas values and substrate concentrations were statistically evaluated and represented in a function of the characteristic phases of the postconvulsive EEG-activity. A correlation was found between the glucose metabolism of the brain and the postconvulsive recovery of EEG. The restitution of postconvulsive brain metabolism runs discontinuously in the first 12 minutes of postconvulsive state. In the phase of electric silence and periodic delta-waves the brain metabolism was shifted to anaerobic direction. During the treatment no anoxic anoxia or acidosis takes place during the seizure activity and restitution, the measurable metabolic changes are moderate and supposedly play no important role in the "effect" of treatment.
Estimates of cochlear traveling wave velocity (TWV) were computed from derived band auditory brain-stem response (ABR) latencies in 24 normal-hearing subjects. Wave V latencies were determined for each of six derived frequency bands (unmasked-8 kHz, 8-4 kHz, 4-2 kHz, 2-1 kHz, 1 kHz-500 Hz, and 500-250 Hz). Representative frequencies were assigned to the derived bands by estimating their energy midpoints, and cochlear positions corresponding to these frequencies were determined using Greenwood's [J. Acoust. Soc. Am. 33, 1344-1356 (1961)] place-frequency function for humans. Two procedures were used to estimate TWV. In one procedure, an exponential function of the form l = A + BeCd was fitted to each subject's latency-by-distance data using a least-squares algorithm, and a TWV function was generated by taking the inverse derivative of the latency function with respect to time. In the second procedure, average TWVs between adjacent derived bands were computed directly from subjects' ipsilateral wave V latencies. Values obtained with the two procedures were similar for middle and apical cochlear loci; however, TWV functions produced lower estimates of TWV at the most basal of five cochlear sites. TWVs based on ipsilateral wave V latencies ranged from 5.6 to 78.0 m/s (geometric mean 11.2 m/s) in the cochlear base (7.53 mm from the stapes) and from 1.2 to 3.4 m/s (geometric mean 1.96 m/s) in the cochlear apex (24.1 mm from the stapes). Intersubject variability was large at the most basal point of TWV estimation but was progressively smaller at more apical sites. Mean TWV estimates were lower than those reported by several previous investigators. The range of values obtained in various studies may stem from differences in the procedures used to estimate TWV.
If the interpeak intervals in the auditory brain stem response (ABR) are assumed to be statistically independent variables that represent the neural transmission time between loci, then the absolute latency of an ABR wave is the sum of the transmission times between successive loci. Consequently, the correlations between the absolute latencies of the ABR waves would be part-whole correlations whose expected values are appreciably different from r = 0. We derived the expected values of the correlations between the latencies of the ABR waves on the assumption that their latencies are the sum of independent elements (transmission times) and found them to be 0.707, 0.577, and 0.816 for I.III, I.V, and III.V, respectively. In addition, the expected values of the correlations between the latencies of the ABR waves assuming that the absolute wave latencies themselves are independent variables (e.g., rI.III = 0) were derived. Several of the correlations among interpeak and between the interpeak and absolute latencies were demonstrated to be appreciably different from r = 0. It would appear that it is more reasonable to assume that the elements (transmission times) rather than the component latencies are the variables of choice for statistical analysis of ABR data.
This study is concerned with the question of whether the late, slow negative wave 2 (SNW2) component of the event-related brain potential is a component of the orienting response (OR). As habituation of the SNW2 would be an argument for such a link with the OR, it was investigated using a variant of the classical repetition/change paradigm. Results supported major claims to be made for a component of the OR: the amplitude of the vertex SNW2 exhibited roughly the typical exponential decline with repeated stimulations (six numeric verbal stimuli presented seriatim in an ascending order) and responded incrementally to a change, at least in a narrow time slot, i.e. it exhibited partial recovery to an out-of-sequence stimulus. These findings were accompanied by similar effects on an exemplary OR component, the skin conductance response, and on such possible components of the OR as heart rate deceleration and the vertex P3 of the event-related brain potential. In so far as OR components should behave in comparable fashion in response to orienting stimuli, it is thus reasonable to suppose that the SNW2 relates to the OR.