Medial Bulbar Reticular Formation Research Articles

Brain-stem representation of jaw muscle activities of the dog.

1. The electromyographic discharges of rigid jaw mucles in the decerebrate cat were dominant in the suprahyoid muscle groups and scanty in the jaw closing muscle groups. But the jaw closing muscles were sensitive to stretching and showed strong spastic resistance to even a slight opening of the mouth.2. In spite of the marked extensor rigidity of the limbs, jaw rigidity disappeared readily after decerebration at a level caudal to the mesencephalic trigeminal nucleus.3. Regular spontaneous unit discharges were recorded from and along the mesencephalic trigeminal nucleus and root of the dog. The background activity in these points was remarkably depressed by elevating the lower jaw and accelerated by depressing the jaw. These responses were obtained by strictly localized punctures in the brain-stem, accompanied by a short latency and slow adaptation as shown in goat by Cooper, Daniel and Whitteridge.4. Nearly the same response was recorded in the lateral bulbar reticular formation at points just caudal to the cerebellar peduncles. There were also some localized points in the medial bulbar reticular formation near the hypoglossal nucleus at level rostral to the inferior olive, in which the background activity was inhibited by opening of the mouth.

Ascending fibers in brain stem reticular formation of cat.

Moruzzi and Magoun40in 1949 demonstrated that stimulation of the stem of cats desynchronizes and activates the EEG in a manner paralleling arousal from sleep or alerting to attention. This effect was obtained from the medial bulbar reticular formation, pontine and midbrain tegmentum, dorsal hypothalamus, and subthalamus. From their electrophysiologic observations the authors assumed the structural substrate of the brain stem activating to be a series of ascending reticular relays, which are activated by collaterals from sensory paths. The observations of Moruzzi and Magoun40have subsequently been confirmed and extended by Magoun and his co-workers. The reticular activating system has been identified in the stem of the monkey,17and continued experimental research * has lent support to the assumption that the reticular activating system of the stem is made up of a series of ascending relays coursing forward from the reticular formation of the

Use of phenacemide (phenurone) in treatment of narcolepsy and cataplexy; a preliminary report.

ALTHOUGH the pathogenesis and pathophysiology of idiopathic narcolepsy remain obscure, it is known that symptomatic forms may follow head injury, cerebral arteriosclerosis, encephalitis lethargica, and intracranial tumors involving the posterior portion of the hypothalamus. Ranson 1 in 1939 produced somnolence in monkeys with lesions limited to the subthalamus and hypothalamus. It remained, however, for the recent studies of Magoun and his co-workers 2 clearly to show that afferent stimulation of the ascending activating system of the brain stem underlies wakefulness, while absence of this influence results in sleep. An arousal reaction, or state of wakefulness, was produced by stimulation of the dorsal portion of the hypothalamus, the subthalamus, the related medial bulbar reticular formation, or the tegmentum of the pons and midbrain. Lesions of the ventral portion of the diencephalon and the tegmentum of the midbrain, within the area of distribution of the ascending reticular activating system, produced recurrent electroencephalographic

Brain stem reticular formation and activation of the EEG

1. 1. Stimulation of the reticular formation of the brain stem evokes changes in the EEG, consisting of abolition of synchronized discharge and introduction of low voltage fast activity in its place, which are not mediated by any of the known ascending or descending paths that traverse the brain stem. The alteration is a generalized one but is most pronounced in the ipsilateral hemisphere and, sometimes, in its anterior part. 2. 2. This response can be elicited by stimulating the medial bulbar reticular formation, pontile and midbrain tegmentum, and dorsal hypothalamus and subthalamus. The bulbar effect is due to ascending impulses relayed through these more cephalic structures. The excitable substrate possesses a low threshold and responds best to high frequencies of stimulation. 3. 3. Some background synchrony of electrocortical activity is requisite for manifestation of the response. In the “encephale isole”, reticular stimulation has no additional effect upon the fully activated EEG. With synchrony, in spontaneous drowsiness or light chloralosane anesthesia, the effect of reticular stimulation is strikingly like Berger's alpha wave blockade, or any arousal reaction. In full chloralosane anesthesia, high voltage slow waves are blocked but no increase in lower amplitude, fast activity occurs. With barbiturate anesthesia, the reticular response is difficult to elicit or is abolished. 4. 4. In the chloralosane preparation, the secondary cortical response evoked by a sensory volley is generally unaffected by reticular stimulation. Consequent sensory after-discharge is abolished, however, as is pyramidal tract discharge and jerky movements referable to it. Outside the sensory receiving area, secondary responses themselves may be reduced or prevented. 5. 5. The convulsive spikes produced by local strychnine and those of a fit following supramaximal cortical excitation, are not decreased by stimulating the reticular formation. 6. 6. The cortical recruiting response induced by low frequency stimulation of the diffuse thalamic projection system is reduced or abolished by reticular stimulation. 7. 7. There is some indication that the cortical effect of reticular stimulation may be mediated by this diffuse thalamic projection system, for synchronized activity within it is similarly prevented by reticular excitation, and direct high frequency stimulation of this system, within the thalamus, reproduces the reticular response. It is possible, however, that other mechanisms may be involved in its mediation. 8. 8. The reticular response and the arousal reaction to natural stimuli have been compared in the “encéphale isolé”, in which EEG synchrony was present during spontaneous relaxation or was produced by recruiting mechanisms, and the two appear identical. 9. 9. The possibility that the cortical arousal reaction to natural stimuli is mediated by collaterals of afferent pathways to the brain stem reticular formation, and thence through the ascending reticular activating system, rather than by intra-cortical spread following the arrival of afferent impulses at the sensory receiving areas of the cortex, is under investigation. 10. 10. The possibility is considered that a background of maintained activity within this ascending brain stem activating system may account for wakefulness, while reduction of its activity either naturally, by barbiturates, or by experimental injury and disease, may respectively precipitate normal sleep, contribute to anesthesia or produce pathological somnolence.

Brain stem reticular formation and activation of the EEG

1. 1. Stimulation of the reticular formation of the brain stem evokes changes in the EEG, consisting of abolition of synchronized discharge and introduction of low voltage fast activity in its place, which are not mediated by any of the known ascending or descending paths that traverse the brain stem. The alteration is a generalized one but is most pronounced in the ipsilateral hemisphere and, sometimes, in its anterior part. 2. 2. This response can be elicited by stimulating the medial bulbar reticular formation, pontile and midbrain tegmentum, and dorsal hypothalamus and subthalamus. The bulbar effect is due to ascending impulses relayed through these more cephalic structures. The excitable substrate possesses a low threshold and responds best to high frequencies of stimulation. 3. 3. Some background synchrony of electrocortical activity is requisite for manifestation of the response. In the “encephale isole”, reticular stimulation has no additional effect upon the fully activated EEG. With synchrony, in spontaneous drowsiness or light chloralosane anesthesia, the effect of reticular stimulation is strikingly like Berger's alpha wave blockade, or any arousal reaction. In full chloralosane anesthesia, high voltage slow waves are blocked but no increase in lower amplitude, fast activity occurs. With barbiturate anesthesia, the reticular response is difficult to elicit or is abolished. 4. 4. In the chloralosane preparation, the secondary cortical response evoked by a sensory volley is generally unaffected by reticular stimulation. Consequent sensory after-discharge is abolished, however, as is pyramidal tract discharge and jerky movements referable to it. Outside the sensory receiving area, secondary responses themselves may be reduced or prevented. 5. 5. The convulsive spikes produced by local strychnine and those of a fit following supramaximal cortical excitation, are not decreased by stimulating the reticular formation. 6. 6. The cortical recruiting response induced by low frequency stimulation of the diffuse thalamic projection system is reduced or abolished by reticular stimulation. 7. 7. There is some indication that the cortical effect of reticular stimulation may be mediated by this diffuse thalamic projection system, for synchronized activity within it is similarly prevented by reticular excitation, and direct high frequency stimulation of this system, within the thalamus, reproduces the reticular response. It is possible, however, that other mechanisms may be involved in its mediation. 8. 8. The reticular response and the arousal reaction to natural stimuli have been compared in the “encéphale isolé”, in which EEG synchrony was present during spontaneous relaxation or was produced by recruiting mechanisms, and the two appear identical. 9. 9. The possibility that the cortical arousal reaction to natural stimuli is mediated by collaterals of afferent pathways to the brain stem reticular formation, and thence through the ascending reticular activating system, rather than by intra-cortical spread following the arrival of afferent impulses at the sensory receiving areas of the cortex, is under investigation. 10. 10. The possibility is considered that a background of maintained activity within this ascending brain stem activating system may account for wakefulness, while reduction of its activity either naturally, by barbiturates, or by experimental injury and disease, may respectively precipitate normal sleep, contribute to anesthesia or produce pathological somnolence.