Effects Of Brainstem Lesions Research Articles

Effects of brainstem lesions on amino acid levels in the rat cochlear nucleus

There is evidence for glutamate, γ-amino butyric acid (GABA), and glycine as neurotransmitters of centrifugal pathways to the cochlear nucleus, but the quantitative extent of their contributions to amino acid neurotransmission in cochlear nucleus regions has not been known. We used microdissection of freeze-dried tissue sections of rat cochlear nucleus, with mapping of sample locations, combined with a high performance liquid chromatography (HPLC) assay, to measure amino acid levels in cochlear nucleus subregions of rats with unilateral lesions of centrifugal pathways to the cochlear nucleus. In rats with lesions transecting all or almost all pathways to the cochlear nucleus from brain stem regions, GABA, aspartate, and glutamate levels were reduced, compared to contralateral values, in almost all ipsilateral cochlear nucleus regions. The largest reductions, in dorsal (DCN), anteroventral (AVCN), and posteroventral (PVCN) cochlear nucleus regions, approached 50% for GABA, 40% for aspartate, and 30% for glutamate. In contrast, glutamine and taurine levels were typically higher in lesioned-side cochlear nucleus regions than contralaterally. Effects on glycine levels were mixed but usually included increased lesioned-side values compared to contralateral, probably reflecting a balance between increases during protein breakdown and decreases of free glycine in transected pathways. More limited lesions transecting just dorsal pathways showed much less effect on amino acid levels. Lesion of the ipsilateral trapezoid body connection plus ipsilateral superior olivary nuclei resulted in decreases of GABA, aspartate, and glutamate levels especially in ventral cochlear nucleus regions. No clear contralateral effects of this lesion could be shown. The results most strongly support centrifugal GABAergic pathways to the cochlear nucleus, providing almost half of GABAergic neurotransmission in most regions. Our results support and extend previously published measurements of lesion effects on GABA uptake and release in cochlear nucleus subdivisions.

Effects of brain stem lesions on cochlear function: Mechanism of hearing improvement after removal of a brain stem tumor

EOAEs are well correlated with changes of hearing sensitivity during the clinical course of brain stem lesions, as shown in this case study. They may serve as sensitive indicators to evaluate the possible effects of a brain stem lesion on cochlear function and monitor the attempted preservation of hearing during CPA or brain stem surgeries. It is thereby suggested that EOAEs should be included in an audiologic test battery in a differential diagnosis of retrocochlear lesions.

Effects of Brain Stem Lesions on Cochlear Function: Mechanism of Hearing Improvement after Removal of a Brain Stem Tumor

Effects of Brain Stem Lesions on Cochlear Function: Mechanism of Hearing Improvement after Removal of a Brain Stem Tumor

Dextrorphan effects on cocaine and brainstem perturbation.

Dextrorphan is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors. Since NMDA blockers are known to reduce the locomotor stimulatory and toxic effects of cocaine, it was speculated that dextrorphan would attenuate cocaine-induced behavioral excitatory motor activity associated with and without mechanical perturbation of the brainstem. Motor activity was recorded following dextrorphan and/or cocaine challenge in 25 SHR rats. Ten were naive subjects. Mini-osmotic pumps delivering cocaine (2.5 mg/0.49 ul/hr) were placed in 15 subjects, and infusion was halted after the third infusion day. On the fifth day either a dextrorphan (25 mg/kg, subcutaneous) or a dextrorphan and cocaine (40 mg/kg, intraperitoneal) challenge was done. Ten rats had bipolar electrode implants in the bilateral brainstem. Five were treated with DC current lesions in each of 12 days over a 3-week period. The effects of brainstem lesions on escape behavior were also evaluated in those five subjects. In the naive subjects, dextrorphan reduced motor activity (P = .0001), whereas combined cocaine and dextrorphan increased motor activity (P = 0.04). In lesioned subjects, dextrorphan decreased motor activity (P = 0.0001). In electrode implant subjects, combined dextrorphan and cocaine challenge decreased the motor activity (P = 0.04). Hyperactivity in the electrode implant group was greater than in the lesioned subjects. Midbrain electrolytic lesions attenuated escape behavior. A variety of behaviors were produced by brainstem lesions. Dextrorphan and brainstem lesions reduced motor hyperactivity and escape behavior. In electrode implant subjects dextrorphan counteracted the expected cocaine excitatory motor effects. Dextrorphan did not activate nor facilitate seizures.

Effects of brain stem lesions on 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge.

We studied the effects of brain stem lesions or transection on the 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge (SND) in baroreceptor-denervated unanesthetized decerebrate cats. The results indicate that these two rhythms depend in part on different brain stem regions. The 10-Hz rhythm was eliminated by ablation of the rostral ventrolateral medulla (RVLM), medullary raphe complex, or pontine parabrachial and Kölliker-Fuse complex (PB/KF) or by pontomedullary border transection. Except for RVLM lesions, these procedures did not disrupt the 2- to 6-Hz rhythm in SND. In fact the power in SND at frequencies less than 6 Hz was increased by raphe or PB/KF lesions. Total power in SND was not significantly affected by raphe or PB/KF lesions, but mean arterial pressure was significantly reduced. Field potentials recorded from the RVLM (11 of 26 sites) and raphe (10 of 20 sites) were correlated to the 10-Hz rhythm in SND, further supporting a role of these areas in either generating or relaying this rhythm to sympathetic nerves. In contrast, field potentials recorded from the PB/KF were not correlated to the 10-Hz rhythm in SND. Thus this region may provide a tonic drive to the 10-Hz generator located elsewhere in the brain stem.

The effect of brainstem lesions on brainstem auditory evoked potentials in the cat

Brainstem auditory evoked potentials (BAEPs) were recorded before and after cuts were made in either the midline trapezoid body (TB), the lateral lemniscus (LL), or the combined dorsal and intermediate acoustic striae (DAS/IAS) in 23 anesthetized cats. Monaural and binaural rarefaction clicks were presented at a rate of 10 per s, and the potentials recorded from a vertex electrode referenced to either earbar or to the neck. The potentials were filtered so that fast and slow components could be examined separately and special efforts were exerted to obtain stable conditions so that small changes in waveforms could be significant. Lesions of the DAS/IAS produced negligible changes in either the fast or slow waves. Lesions of the midline TB reduced the amplitudes of peaks P3 through P5, while greatly reducing the amplitude of the slow wave. Complete lesions of the LL always reduced the amplitude of the slow wave. Lesions of the ventral part of the LL were more likely to reduce the amplitude of P4-P5. Our interpretations of these lesion experiments are based on the idea that individual fast peaks of the BAEP represent compound action potentials of fiber pathways. According to this view, only synchronized activity generated in populations of neurons that are both favorably oriented in space and significant in number, will contribute to the fast peaks.

Effects of electrolytic lesions of the superior olivary complex and trapezoid body on brainstem auditory-evoked potentials in the guinea pig. II. Three-channel Lissajous' trajectory analysis.

Brainstem auditory-evoked potentials (BAEP) were studied both with vertex (positive) - tragus (negative) derivation and three-channel Lissajous' trajectory (3-CLT) planar analysis in guinea pigs (GP) after destruction of the ipsilateral superior olivary complex (SOC) (6 GP), contralateral SOC (8 GP) referred to the stimulation side, and trapezoid body (TB) in the sagittal line (8 GP). The size of the lesion was evaluated on histological examination. The right ear was locally destroyed with aminoside instillation. The left ear was stimulated with unfiltered clicks and tone bursts of different frequencies at 100 dB SPL. Three questions were the basis of this study: (i) What are the effects of brainstem lesions on 3-CLT? (ii) Is there a relationship between planar segments and underlying sources? (iii) What is the generator of planar segment C (P3) in GP? 3-CLT analysis was made on plane A (corresponding to P1 on a vertex-tragus channel), plane B (N1-P2) and plane C (P3.) Plane C disappeared after TB lesions and remained after ipsi- and contralateral SOC destructions. However, plane C disappeared after extensive lesions to the contralateral SOC affecting the TB. Planes A and B were always observed whatever the lesion, with sometimes a modification of their orientation. A localized brainstem lesion induced a local modification of the three-dimensional trajectory. These data are in agreement with the assumption that some planes of 3-CLT reflect the activity of underlying generators. However, the loop which contains the planar segment is a better indicator of the global electrical activity of the source. Plane C (P3) would have a contralateral source which is probably not the SOC but the afferent curved fibers of the TB close to the contralateral SOC.

The effects of brainstem lesions on vocalization in the squirrel monkey

The present study is an attempt to find out the brain areas involved in the motor coordination of species-specific vocalization. For this purpose, high-frequency coagulations were placed in a systematic manner throughout the brainstem and posterior diencephalon in altogether 43 squirrel monkeys ( Saimiri sciureus). The effect of these lesions on different call types elicited by electrical brain stimulation was studied spectrographically. It was found that bilateral destruction of the ventrolateral, ventroposterior and intralaminar thalamus, periventricular and rostral periaqueductal gray, ventral tegmental area of Tsai, nucl. interpeduncularis, nucl. ruber, anterodorsolateral midbrain tegmentum, superior and inferior colliculi, pontine gray, cerebral peduncles, medial pontine reticular formation, raphe and vestibular nuclei did not affect the acoustic structure of the calls tested. On the other hand, lesions in the ventrolateral midbrain involving the substantia nigra and overlying reticular formation, in the midbrain tegmentum just below the inferior colliculus, in the lateral pons and almost the whole medulla (minimal lesion size: 2.5 mm 3) changed vocalization significantly. It is suggested that the latter areas are more or less directly involved in the motor coordination of vocalization, while the first are not.

Brachium conjuntivum and rubrobulbar tract: Brain stem projections of red nucleus essential for the conditioned nictitating membrane response

The trajectory of the rubrobulbar tract in rabbit to the level of the accessory abducens nucleus is described: orthograde labeling of fibers of the rubrobulbar tract following horseradish peroxidase implants into red nucleus of 8 animals permitted ad hoc analysis of the effects of brain stem lesions on the rabbit's conditioned nictitating membrane response. Twenty-four rabbits, trained to give conditioned NM responses from both eyes, received unilateral lesions of the right pontine brain stem. Six of the 7 cases of post-lesion disruption of ipsilateral conditioned responding involved either ipsilateral brachium conjunctivum or the rubrobulbar tract. This finding, together with a reexamination of data from two related studies from this laboratory [1,12] strongly support the conclusion that an essential premotor component of the conditioned NM response is a doubly decussating circuit from the interpositus nucleus of the cerebellum to magnocellular red nucleus, via brachium conjunctivum and its decussation, and from red nucleus caudally, via the ventral tegmental bundle and the rubrobulbar tract, to the accessory abducens nucleus, where motoneurons involved in the NM response are located. These findings are consistent with published reports on the essential role of interpositus nucleus of the cerebellum in NM conditioning [4,9]. The possible role of the supratrigeminal reticular formation [2] in this learned behavior is also discussed.

Effects of brainstem lesions on the nasopharyngeal reflex in the conscious rabbit.

The cardiovascular responses evoked through the nasopharyngeal reflex by the inhalation of formaldehyde vapour were studied in conscious rabbits after bilateral electrolytic lesions of the ventrolateral medulla coinciding with the A1 group of catecholamine cells. Arterial blood pressure was measured in the central ear artery, heart rate was determined from the arterial pressure trace, and iliac blood flow was determined using a Doppler ultrasonic flow meter placed around the lower abdominal aorta. There were no significant changes in the heart rate, blood pressure and iliac conductance responses elicited through the nasopharyngeal reflexes of sham operated animals in which electrodes were inserted without the passage of current. The blood pressure changes produced by inhalation of formaldehyde in control rabbits were not significantly altered in animals with ventrolateral medullary lesions. However, the magnitude of the bradycardia and of the fall in iliac conductance evoked by the inhalation of formaldehyde were approximately halved 4 h and 1 day after the lesions but were fully restored at 2 weeks. These experiments suggest that the A1 group of catecholamine neurones help mediate the bradycardia and vasoconstriction elicited through nasopharyngeal reflexes in terrestial animals exposed to noxious vapours.

Effects of brainstem lesions on tonic immobility in the rabbit ( Oryctolagus cuniculus)

Lesions were placed in discrete brainstem areas implicated in the generation of both tonic immobility (TI) and paradoxical sleep (PS) to examine postulated state and event correspondences between these states in the rabbit. Lesions were concentrated in the region of the nucleus locus coeruleus (LC)—an area implicated in the mediation of muscular atonia during PS—but also included other reticular (pontine gigantocellular tegmental field: FTG), and nonreticular (vestibular, cerebellar, central grey, collicular) areas. Polygraphic recordings of EEG, EMG and EOG activities were taken during sleep-waking states and measures of the TI response were obtained before (1 day prior) and after (5 and 14 days) lesions were made. None of the lesions was followed by a sustained, significant variation in either frequency of induction or duration of TI. Following LC lesions, and to a lesser extent after FTG lesions, sleep patterns were fragmented, with a reduction or absence of PS and the occurrence of phasic motor activation at times when PS periods might be expected to occur. The absence of PS and persistence of TI following specific brainstem lesions indicate a fundamental difference in mechanisms underlying these states. It is suggested that a major determinant of these results is the activation of phasic activity during PS but not TI, and that the possibility remains that both states may share a common mechanism of tonic motor control.

Brainstem lesions dissociate neural mechanisms of morphine analgesia in different kinds of pain

The effects of brainstem lesions on morphine analgesia were examined using the formalin test which produces moderate pain that lasts about 2 h, and the tail-flick test which measures brief threshold-level pain. Lesions of the nucleus raphe magnus attenuated and small lesions of the central tegmental nucleus potentiated the effects of morphine in the tail-flick test. Lesions of the median raphe nucleus potentiated the effects of morphine in the formalin test. Large lesins of the pontine reticular formation had no effect in either pain test. These results indicate that the neural mechanisms underlying morphine analgesia are different in different kinds of pain.

Auditory brain stem responses in the cat. II. Effects of lesions

Discrete lesions of the brain stem auditory pathway in cats were found to have complex effects on the auditory brain stem response (ABR). These effects ranged from an amplitude change on only a single component of the ABR to latency and amplitude changes for that component plus some or all of the subsequent components. Lesions of certain portions of the classical primary auditory pathway (i.e., the dorsal cochlear nucleus, the dorsal acoustic stria, the lateral superior olivary nucleus, the posterior portion of the lateral lemniscus and the inferior colliculus) were not associated with changes in the ABR prior to component P5. Except for midline lesions, the effects of a brain stem lesion on the ABR were quite different for ipsilateral and contralateral stimulation. The predominant effect of brain stem lesions on the ABR was an attenuation of the amplitudes of the components and only an occasional increase in their latency. Opposite effects, i.e., increases in amplitude or decreases in latency, were rare. The acute effects of brain stem lesions on the ABR could be transient and not persist in chronic recordings. The components of the ABR were primarily affected by the following lesions. Component P0.8 was attenuated by a lesion of the eighth nerve. N1.0, P1.2 and N1.5 were unaffected by lesions of the cochlear nucleus but were affected by lesions of the eighth nerve, suggesting that the eighth nerve was the generator of these components. Except for one lesion of the trapezoid body component P1.7 was only affected by lesions of the cochlear nucleus or eighth nerve, suggesting its origin in one or both of these structures. N2.0 was affected by lesions of the ventral cochlear nucleus, the region of the superior olivary complex and the trapezoid body. P3 was affected by lesions in the region of the superior olivary complex and the trapezoid body. N3 and N4 were affected primarily by lesions of the lateral lemniscus, but also by lesions of the superior olivary complex and trapezoid body. The results suggest that except for the first few components (P0.8, N1.0, P1.2 and N1.5) each of the components has substantial contributions from more than one auditory brain stem structure. Component P0.8 was determined to have substantial contributions from both cochlear microphonic and neural activity.

The effect of brain stem lesions on vasomotor nerves and the smooth muscle of the cerebral arteries--a morphological study.

A morphological study was performed on the nerve fibers and the smooth muscle of the cerebral arteries in human brains with hypertensive intracerebral hematomas. In addition, an experimental study was also performed on dogs. Immediately after autopsy, the nerve fibers on the Willis circle and its main branches in five patients with hypertensive intracerebral hematomas were examined with Falck and Hillarp's fluorescent method and with Koelle's thiocholine method. The smooth muscle of the main cerebral arteries from ten brains with intracerebral hematomas, which had been preserved in 10% formalin, was studied with histochemical examinations. Bilateral hypothalamic lesions were made experimentally in 16 dogs, and the nerve fibers and the smooth muscle of the main cerebral arteries were examined by the histochemical method and with an electron-microscope. No adrenergic fibers were seen with the fluorescent method in any of the five patients. The cholinergic nerve fibers on the same arteries were observed with the thiocholine method. Examinations for cholinergic nerve fibers of arteries from the affected cerebral hemispheres of two patients did not show any enzymatic activity, while it was shown to be present in the intact hemisphere. Ten brains showed degeneration of the smooth muscle cells in the tunica media. Animal studies showed a decrease of the adrenergic and cholinergic nerve fibers from experimental hypothalamic injuries. The degeneration of the nerve fibers was observed with electron-microscopic examinations. Thus our findings in this study suggest that brain stem damage leads to the degeneration of the smooth muscle together with the adrenergic and cholinergic nerve fibers of the cerebral artery.

Effects of brainstem lesions on temperature regulation in hot and cold environments.

ARTICLESEffects of brainstem lesions on temperature regulation in hot and cold environmentsJM Lipton, PE Dwyer, and DE FosslerJM Lipton, PE Dwyer, and DE FosslerPublished Online:01 Jun 1974https://doi.org/10.1152/ajplegacy.1974.226.6.1356MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 226Issue 6June 1974Pages 1356-1365 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.226.6.1356PubMed4833992History Published online 1 June 1974 Published in print 1 June 1974 Metrics

The role of the raphe nuclei in the regulation of ponto-geniculo-occipital wave activity

A study has been made of the effect of brain stem lesions upon ponto-geniculo-occipital PGO) wave activity. The results include the following. (1) Midline lesions, in the region of the raphe nuclei, caused a transient increase in waves having the characteristics of PGO REM. After 1–4 days these waves were suppressed during wakefulness but continued to appear during slow wave sleep, as well as during REM sleep. (2) The disturbance in the regulation of PGO REM was greatest in the animals with large lesions, involving several raphe nuclei. (3) Unilateral parasagittal cuts, 1.5 mm lateral to the midline in the region of the raphe nuclei, caused changes in PGO wave activity similar to those following midline lesions of comparable extent. (4) Pentobarbital, administered several days after a raphe lesion, gave rise to a transient increase in PGO wave activity. The recordings resembled those obtained s shortly after the lesion was made. (5) The onset of drug-induced wave activity, following treatment with PCPA, was accelerated in animals with midline lesions of the raphe area. (6) Stimulation of the pacemaker region of the pons, on the side ipsilateral to an extensive parasagittal cut, consistently evoked lateral geniculate responses during slow wave sleep, as well as during REM sleep. Stimulation of the pacemaker on the opposite side of the pons evoked lateral geniculate responses only during REM sleep. These results support the hypothesis that 5-HT containing neurons, having their perikarya in the raphe nuclei, play an important role in the normal their perikarya in the raphe nuclei, play an important role in the normal regulation of PGO REM.

Effects of brain-stem lesions on instrumental conditioning in cats

The effects of two-stage brain-stem lesions on formation of avoidance motor conditioned reflexes (AMCR) to visual and auditory stimuli were studied in cats. Most animals survived the large two-stage bilateral lesions of the central brain-stem which included the mesencephalic reticular formation. In the postoperative period all the animals showed many changes in unconditioned behavior which seemed to depend on the extent and location of the lesions. With great difficulty it was possible in some cats to form an AMCR. However, there seems to be a critical size and configuration of the lesion limiting the possibility of successful conditioning. As a rule the learning was prolonged and unstable. Difficulties in transfer from one modality to another and unsuccessful differentiation also indicate serious impairment in learning.

Effect of brain-stem lesions on retention of a conditioned reflex in cats

The effects of central brain-stem lesions on memory was studied in eight animals with previously acquired avoidance motor conditioned reflexes. The prelesion training included conditioning to flashes or clicks, differentiation and transfer. After extensive bilateral, two-stage electrolytic lesions of the central mesencephalon and after subsequent recovery for 5–12 weeks, the animals were subjected to reconditioning, redifferentiation and retransfer. The lesions did not produce loss of the previously established conditioned response. The memory of training prior to the lesion was perfect and comparable to that in normal cats with equal intervals in the training.

Effect of brain-stem lesions on metrazol-induced seizures in cats

1. 1. The chronic effect of bilaterally paired lesions in the cat's brain-stem on Metrazol-induced seizures was studied in order to clarify the intracerebral mechanism for the maintenance of epileptic excitability. 2. 2. The results seem to indicate that there are two systems of facilitatory and inhibitory functions in the brain-stem rostral to the pons as far as Metrazol-induced seizure activity is concerned. The facilitatory system consists of the caudal mesencephalon extending rostrally to the posterior hypothalamus through the ventral part of the rostral mesencephalon and posterior sub-thalamus, and also of the medio-dorsal nucleus of the thalamus. the inhibitory system consists of the dorsal part of the rostral mesencephalon extending rostrally to the thalamus and also of the anterior hypothalamus. 3. 3. It may be suggested that this facilitatory system plays a significant role in the onset and generalization of the Metrazol seizure.

The effect of brain stem lesions on tyrosine and tryptophan hydroxylases in various structures of the telencephalon of the cat

A la suite de le´sions unilate´rales inte´ressant la re´gion tegmentaire ventrome´diane de la partie supe´rieure du tronc ce´re´bral, l'on constate une diminution conside´rable des hydroxylases de la tyrosine et du tryptophane sans modification de la de´hydroge´nase succinique au niveau de diverses structures du te´lence´phale de meˆme coˆte´. Par contre la destruction des noyaux intralaminaires du thalamus ne modifie pas la concentration de ces enzymes au niveau des meˆmes structures. Ces re´sultats sugge´rent que la synthes de la dopamine et de la se´rotonine s'e´labore aux de´pens de circuits neuronaux distincts qui ont leur origine dans des amas cellulaires spe´cifiques du tronc ce´re´bral.