Lesions In Reticular Formation Research Articles

A patient with unilateral periodic leg movements associated with pontine infarction.

A patient with unilateral periodic leg movements associated with pontine infarction.

Neurotoxic N-methyl- d-aspartate lesion of the ventral midbrain and mesopontine junction alters sleep–wake organization

The dorsal regions of the midbrain and pons have been found to participate in sleep regulation. However, the physiological role of the ventral brainstem in sleep regulation remains unclear. We used N-methyl- d-aspartate-induced lesions of the ventral midbrain and pons to address this question. Unlike dorsal mesencephalic reticular formation lesions, which produce somnolence and electroencephalogram synchronization, we found that ventral midbrain lesions produce insomnia and hyperactivity. Marked increases in waking and decreases in slow wave sleep stage 1 (S1), stage 2 (S2) and rapid eye movement sleep were found immediately after the lesion. Sleep gradually increased, but never returned to baseline levels (baseline/month 1 post-lesion: waking, 30.6±4.58%/62.3±10.1%; S1, 5.1±0.74/3.9±1.91%; S2, 46.2±4.74%/23.1±5.47%; rapid eye movement sleep, 14.1±3.15%/7.2±5.42%). These changes are comparable in magnitude to those seen after basal forebrain lesions. Neuronal degeneration was found in the ventral rostral pons and midbrain, including the substantia nigra, ventral tegmental area, retrorubral nucleus, and ventral mesencephalic and rostroventral pontine reticular formation. We conclude that nuclei within the ventral mesencephalon and rostroventral pons play an important role in sleep regulation.

Disorders of consciousness: the basis for ethical assessment

During the past few years there is an ethical debate about neurological disease entities that are characterised by a) prolongation of life owing to medical treatment, b) limited chances of cure, and c) impaired to unbearable life quality: akinetic mutism, vegetative state ("Wachkoma", apallic syndrome), and locked-in syndrome. These are compared to typical coma and brain death. According to Gerstenbrand (1967) [34] the vegetative state is differentiated into the transitional state following typical coma, the variations of typical and incomplete vegetative state, the remission state and the "Durchgangssyndrom" (characterized by preserved wakefulness with affective lability, disorientation, and amnesia). With regard to pathogenesis we differentiate posttraumatic and posthypoxic origin and variable lesions in cerebral cortex, thalamus or mesencephalic reticular formation. Uncertainty of prognosis is stressed. In respect of brain death we compare a) neocortical death, b) brain stem death, and c) whole brain death, and discuss problems of difficult delimitation and uncertainty of diagnosis. These syndromes are compared to anencephaly and hydranencephaly. Regarding the locked-in syndrome, typical, incomplete and complete (total) forms are distinguished. The differential diagnosis between the complete locked-in syndrome and brain stem death seems problematic. Difficulties in decisions limiting therapeutic effort stem from a) essentially intuitive judgement about observations, b) variability of syndromes and courses, c) uncertainty of prognosis, and d) differences in understanding and valuation throughout society. Emphasis is on a trustful and open colloquy among the persons concerned.

Is subcortical disease associated with a poor response to antidepressants? Neurological, neuropsychological and neuroradiological findings in late-life depression.

Late-life depression is associated with increased subcortical white matter hyperintensities. There is some evidence that they are associated with a poorer response to acute treatment. Neurological signs and neuropsychological dysfunction are further evidence of abnormalities in the brain, but they have not been studied in relation to therapy resistance. A prospective study of 24 normal controls and 75 consecutive elderly (aged 65 to 85) patients with DSM-III-R major depression entered a naturalistic study of treatment. Assessment of response to monotherapy and then lithium augmentation or ECT created three outcome groups. Investigations included magnetic resonance brain imaging, neuropsychological and neurological examination. Response to monotherapy within 12 weeks was shown by 42.7%, a further 37.3% responded to lithium augmentation or ECT within 24 weeks and 20% had responded poorly to all treatments at 24 weeks. Subcortical hyperintensities were significantly increased in the more resistant patients. These included confluent deep white matter, multiple (> 5) basal ganglia lesions and pontine reticular formation lesions. Most of the neuropsychological impairment was restricted to the resistant groups and was of a subcortico-frontal type. Extrapyramidal, frontal and pyramidal neurological signs characterized the resistant groups. The combination of extrapyramidal signs, pyramidal tract signs and impairment of motor hand sequencing strongly predicted resistance to 12 weeks of antidepressant monotherapy with 89% sensitivity and 95% specificity. In late-life depression a poor response to antidepressant monotherapy can be expected in those patients with a frontal lobe syndrome, extrapyramidal signs or if MRI T2-weighted lesions are present in both the basal ganglia and the pontine reticular formation.

Pontile regulation of ventilatory activity in the adult rat

Our purpose was to characterize the pontile components of the brain stem ventilatory control system in rats. This study was precipitated by reports that this pontile component might differ fundamentally from that of other species. Efferent activity of the phrenic nerve was recorded in anesthetized, vagotomized, paralyzed, and ventilated adult rats. As in other species, electrical stimulations of the rostral pons caused premature terminations and/or onsets of phrenic activity in eupnea. Electrolytic lesions of rostrolateral pons resulted in apneusis, characterized by significant prolongations of the phrenic burst. Some effective lesions were in the region of the nucleus parabrachialis medialis and the Kolliker-Fuse nucleus, the site of the pneumotaxic center. Other lesions resulting in apneusis were ventral to the pneumotaxic center. As in cats, lesions in the caudal pontile reticular formation caused the duration of the apneustic neural inspiration to return toward that of eupnea. Again, as in other species, gradual alterations from eupnea to gasping in the rat were recorded during hypoxia, which was induced by ventilation with carbon monoxide. We conclude that the brain stem respiratory control system is similarly organized in rats and other mammalian species. These results have implications for contemporary hypotheses concerning the neurogenesis of ventilatory activity.

POLIOENCEPHALITIS, STRESS, AND THE ETIOLOGY OF POST-POLIO SEQUELAE

Post-mortem neurohistopathologies that document polio virus-induced lesions in reticular formation and hypothalamic, thalamic, peptidergic, and monoaminergic neurons in the brain are reviewed from 158 individuals who contracted polio before 1950. This polioencephalitis was found to occur in every case of poliomyelitis, even those without evidence of damage to spinal motor neurons. These findings, in combination with data from the 1990 National Post-Polio Survey and new magnetic resonance imaging studies documenting post-encephalitis-like lesions in the brains of polio survivors, are used to present two hypotheses: 1) polioencephalitic damage to aging reticular activating system and monoaminergic neurons is responsible for post-polio fatigue, and 2) polioencephalitic damage to enkephalin-producing neurons is responsible for hypersensitivity to pain in polio survivors. In addition, the antimetabolic action of glucocorticoids on polio-damaged, metabolically vulnerable neurons may be responsible for the fatigue and muscle weakness reported by polio survivors during emotional stress.

Mesencephalic reticular formation lesions made after habituation training abolish long-term habituation of the acoustic startle response in rats.

Lesions to the mesencephalic reticular formation (MRF) in rats severely attenuate the acquisition of long-term habituation of the startle response when the lesions are made prior to habituation training. The present experiments extend the finding of habituation deficits to animals with MRF damage made after the animals have habituated to an auditory stimulus. Following habituation training, some animals received lesions to the MRF. The startle amplitudes of these animals immediately changed from control levels to levels indistinguishable from those of animals that never habituated across days--animals with MRF lesions made prior to habituation training. The mechanism responsible for long-term habituation appears to be a progressive increase in activity within a long-term habituation pathway extrinsic to the reflex circuit for the startle response, but the synaptic mechanisms responsible for this change are unknown.

Mesencephalic reticular formation lesions made after habituation training abolish long-term habituation of the acoustic startle response in rats.

Mesencephalic reticular formation lesions made after habituation training abolish long-term habituation of the acoustic startle response in rats.

Hypothalamic afferent connections mediating adrenocortical responses that follow hippocampal stimulation

This study identified some neural pathways which mediate the adrenocortical responses that follow hippocampal stimulation. The increase in plasma corticosterone following dorsal hippocampus stimulation, in rats with electrodes chronically implanted under pentobarbital anesthesia, was blocked by dorsal fornix and lateral septal lesions and by small posterior hypothalamic deafferentation. Fimbria transection, lateral septal lesions, and posterior hypothalamic deafferentation, but not midbrain reticular formation lesions, also blocked the adrenocortical responses to ventral hippocampus stimulation. Our present and previous studies indicate that the dorsal and ventral hippocampal effects on the hypothalamus, which increase plasma corticosterone concentrations, are mediated by the dorsal fornix and fimbria, respectively, as well as by the lateral septum. A posterior hypothalamic input, which does not involve the medial forebrain bundle or the midbrain reticular formation is also essential for the activation of this response.

Lesions of the Mid-Spinal trigeminal complex are effective in producing perioral thermal hypoalgesia

The hypoalgesic effects of lesions in the rat spinal trigeminal complex at the levels of subnucleus interpolaris and caudal subnucleus oralis were investigated. Lesions of the trigeminal tract, nucleus, or adjacent reticular formation resulted in significant elevations in escape latencies to noxious thermal stimulation of the ipsilateral perioral area. The nuclear lesions were significantly more effective in producing latency elevations than were the reticular formation lesions. Behavioral and anatomical evidence is presented suggesting that the mid-spinal trigeminal complex, including the ascending trigeminal intranuclear pathways, participate in perioral thermal nociception.

Bilateral horizontal gaze paralysis due to pontine hemorrhage: A case report

In a case of bilateral horizontal gaze paralysis, vertical gaze was clinically intact but eye movement recordings demonstrated a transient reduction of vertical saccadic velocities. Horizontal caloric vestibulo-ocular responses were absent. CT scanning and NMR imaging showed a hematoma in the median pontine tegmentum. This case provides additional evidence that vertical and horizontal saccade genesis may be independent of caudal paramedian pontine reticular formation lesions.

A generalized learning deficit in albino rats with early median raphe or pontine reticular formation lesions

Recent studies suggest that lesions of the median raphe or pontine reticular formation in adult rats are associated with a nonspecific (generalized) learning impairment. The present study showed that lesions in the region of the median raphe or pontine reticular formation in 21 day old rats likewise produced a nonspecific learning impairment, as evidence by significant deficits on a visual discrimination, nonvisual incline plane discrimination, 3-cul maze, and three simple spatial problems. The finding that relatively large lateral pontomesencephalic lesions did not lead to deficient learning of any of these tasks indicates that lesion locus rather than lesion size is responsible for the production of the learning deficits observed in this study.

Habituation of the acoustic startle response in rats after lesions in the mesencephalic reticular formation or in the inferior colliculus.

Extensive damage to the mesencephalic reticular formation (MRF) in rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. The MRF lesions did not alter initial startle amplitudes, but the animals with lesions were unable to attain as low a long-term asymptote of habituation as could control animals. Subsequent manipulation of stimulus intensity and interstimulus interval revealed no differences in short-term habituation between the two groups. Large lesions to the inferior colliculus (IC) did not disrupt long-term habituation of the acoustic startle response, but these animals were unable to suppress responding as much as controls to intense stimuli presented rapidly. The deficits in long-term habituation following MRF lesions suggested a disruption of an extrinsic, inhibitory mechanism of habituation. The deficits following IC lesions could be due either to a disruption of a short-term habituation mechanism or to an increase in response sensitization produced by the lesions.

Retention of individual spatial reversal problems in rats with nigral, caudoputamenal, and reticular formation lesions

Rats with bilateral nigral, caudoputamenal, or midbrain reticular formation lesions display impairment in learning position reversal problems in a simple T maze. Test trials given after learning each reversal problem disclose defective retention only in the nigral and caudoputamenal groups. This pattern of deficits associated with nigro-neostriatal damage is similar to that reported earlier in rats with bilateral lesions in the vicinity of the parafascicular nucleus. It is proposed that the nigral—parafascicular—neostriatal complex contributes to consolidation of spatial information in rodents.

Effects of mesencephalic reticular formation lesions on habituation of startle and lick suppression responses in the rat.

Extensive damage to the mesencephalic reticular formation (MRF) in rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. Animals with MRF lesions, although initially neither more nor less responsive than controls, could not attain as low a long-term asymptote of habituation as could control animals with repeated presentations of an auditory stimulus. Changing the quality of the auditory stimulus abolished the asymptotic difference in responsiveness. With repeated presentations of the second auditory stimulus, control animals again reached a significantly lower long-term habituation asymptote than did animals with MRF lesions. The course of long-term habituation for the two groups suggested a disruption of an extrinsic, inhibitory habituation process by the lesions. The effects of MRF lesions were specific to the acoustic startle response. Control animals and those with lesions showed comparable response levels, short-term habituation, and long-term habituation of the lick suppression response. responsiveness and habituation to tactile stimuli were comparable for the two groups in both lick suppression and startle response measures.

Medullary reticular formation lesions and lordosis reflex in female rats

Medullary reticular formation lesions and lordosis reflex in female rats

Abolition of hypoxic vagal bradycardia by lateral mesencephalic lesions in spinal cats.

To examine central sites that integrate the vagal bradycardia induced by hypoxia, heart rates were recorded continuously in spinal, precollicular, decerebrated cats during transient hypoxia induced by ventilation with 100% nitrogen. Bilateral lesions in the lateral mesencephalic reticular formation either decreased the extent of bradycardia or caused a reversal to tachycardia; anesthesia induced the same change. In contrast, bilateral lesions in the medial mesencephalic reticular formation failed to alter the bradycardia. Hence, the lateral mesencephalic reticular formation is essential for the appearance of hypoxia-induced vagal bradycardia.

Effects of median raphe nucleus lesions on hippocampal EEG in the freely moving rat

The effects of median raphe lesions on the hippocampal EEG were examined in freely moving rats. First, median raphe lesions, including those restricted to the median raphe nucleus, unequivocally produced hippocampal low-frequency theta activity (5.8 Hz, SD= 0.47 Hz) during relaxed immobility which was not observed under normal conditions. This lesion-induced theta activity during immobility continued for at least 20 days, and was markedly suppressed by atropine sulfate (10 mg/kg, i.p.). On the other hand, reticular formation lesions had little effect on either hippocampal EEG patterns during immobility, movement or PS. Second, the mean frequency of theta activity was significantly reduced during movement and PS on the day following the median raphe lesion. These findings suggest a raphe-hippocampal pathway in which the median raphe nucleus plays a major role in hippocampal desynchronization (irregular pattern) by exerting an inhibitory influence on the hippocompal theta generating or facilitating mechanism. Thus the theta activity will be induced by the disinhibition following median raphe lesions.

BILATERAL RETICULAR FORMATION LESIONS CAUSING COMA: THEIR EFFECTS ON REGIONAL CEREBRAL BLOOD FLOW, GLUCOSE UTILIZATION AND OXIDATIVE METABOLISM*

Annals of the New York Academy of SciencesVolume 315, Issue 1 p. 105-109 BILATERAL RETICULAR FORMATION LESIONS CAUSING COMA: THEIR EFFECTS ON REGIONAL CEREBRAL BLOOD FLOW, GLUCOSE UTILIZATION AND OXIDATIVE METABOLISM* W. K. Hass, W. K. Hass Departments of Neurology and Neurosurgery, New York University Medical Center, New York, New York 10016Search for more papers by this authorR. A. Hawkins, R. A. Hawkins Departments of Neurology and Neurosurgery, New York University Medical Center, New York, New York 10016Search for more papers by this author W. K. Hass, W. K. Hass Departments of Neurology and Neurosurgery, New York University Medical Center, New York, New York 10016Search for more papers by this authorR. A. Hawkins, R. A. Hawkins Departments of Neurology and Neurosurgery, New York University Medical Center, New York, New York 10016Search for more papers by this author First published: November 1978 https://doi.org/10.1111/j.1749-6632.1978.tb50333.xCitations: 2 * This work was supported by Grant No. NS 07366 from the National Institute of Neurological Disease and Stroke. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume315, Issue1Brain Death: Interrelated Medical and Social IssuesNovember 1978Pages 105-109 RelatedInformation

Nonsensory neglect.

Five monkeys trained to perform with the extremity contralateral to a stimulus had unilateral neglect induced by frontal and reticular formation lesions. Postoperatively the performance of the animals was abnormal only on ipsilateral stimulation, which suggests that the mechanism underlying neglect in these subjects is not deafferentation of sensory inattention but a defect of intention.