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The Sleeping Brain
Published in Hanno W. Kirk, Restoring the Brain, 2020
PET scans obtained during REM sleep have consistently demonstrated increased activity in the pontine tegmentum and the limbic and paralimbic areas as noted in NREM.17 The medial prefrontal cortex (MPFC) shows metabolic activity similar to that of wakefulness. The MPFC is a key component of the Default Mode Network (DMN), our principal resting state network. Additionally, the temporal and occipital cortices are active during REM, probably reflective of sensory experiences that arise with dreaming. The findings of enhanced metabolic activity in focal areas during sleep are consonant with the synaptic homeostasis model of sleep thought critical for the cerebral plasticity, which underpins a healthy homeostasis as well as learning and/or responses to novel stimuli.
Integrated physiology of the lower urinary tract
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Naoki Yoshimura, Jeong Yun Jeong, Dae Kyung Kim, Michael B. Chancellor
The dorsal pontine tegmentum has been firmly established as an essential control center for micturition in normal subjects. First described by Barrington,112 it has subsequently been called “Barrington’s nucleus,” the “pontine micturition center” (PMC),113 or the “M region”78,92,114 because of its medial location.
Neuro-Ophthalmological Findings in Patients with Posterior Circulation Stroke
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
When the medial pontine tegmentum has bilaterally lesions, patients are usually comatose and have bilateral horizontal gaze palsies. Reflex vertical gaze is preserved if the more rostral mesencephalic-diencephalic tegmental structures are spared. Often in this situation, ocular bobbing, an intermittent brisk downward movement of one or both eyes, occurs.19,20 Bobbing can be asymmetric especially if the horizontal gaze abnormalities are asymmetric. Bobbing is more likely to affect eyes in which ocular abduction is lost. Bobbing is best understood as a form of vertical roving eye movement. Comatose patients with bilateral cerebral hemisphere lesions have free roving side-to-side movements of their eyes. The supratentorial gaze centers have both horizontal and vertical vectors, but ordinarily horizontal gaze predominates because most of the visual action is more on an eye plane than up or down. When the left frontal eye field is stimulated ordinarily, the eyes would conjugately deviate to the right. If the right sixth nerve is paralyzed, stimulation of the left frontal eye field causes the right eye to deviate downward instead of to the right. Bilateral simultaneous stimulation of the supratentorial gaze centers results in vertical gaze because horizontal vectors are canceled. Similarly, bilateral simultaneous irrigation of both ear canals results in up or down gaze depending on whether warm or cold water is used. When horizontal gaze to one or both sides is abolished by a medial pontine lesion, then the vertical downgaze vectors predominate and bobbing occurs. At times, vergence movements are seen when patients attempt to look in the direction of a gaze palsy. In these patients, vergence movements are substituted for paretic movements.
Complete Horizontal Gaze Paresis Due to Medial Pontine Haemorrhage
Published in Neuro-Ophthalmology, 2023
Joan Pei Yun Sim, Jackie Jia Lin Sim, Sameer Saleem, Dennis Cordato
Horizontal gaze is controlled by specific pathways and nuclei in the pontine tegmentum. The abducens nucleus receives projections from the ipsilateral paramedian pontine reticular formation (PPRF) to mediate abduction of the ipsilateral eye. It also projects efferent fibres that innervate the contralateral oculomotor nuclei through the medial longitudinal fascicle (MLF) to coordinate simultaneous adduction of the contralateral eye in the same direction.2,6 Pathological lesions arising in the PPRF or abducens nucleus can result in a gaze palsy.7 Given the role of the PPRF in the initiation of conjugate horizontal eye movements, damage to this structure will result in impairment of horizontal gaze towards the side of the lesion (including horizontal pursuit, vestibulo-ocular reflex, and saccades), and very occasionally bilateral conjugate horizontal gaze palsies should both PPRFs be affected.1,8 Additionally, complete horizontal gaze palsy may also be attributed to damage to bilateral abducens nuclei and MLFs.9,10 Our patient demonstrated impaired vertical gaze consistent with involvement of vertical gaze pathways as well as a skew deviation, which is a well-documented finding in lesions involving the MLF. Our patient’s gaze palsy was at the nuclear level, which can be distinguished from a supranuclear gaze palsy by the demonstration of a negative doll’s head manoeuvre.
Pitolisant for the treatment of cataplexy in adults with narcolepsy
Published in Expert Opinion on Orphan Drugs, 2021
Gerard J. Meskill, Ulf Kallweit, Donna Zarycranski, Christian Caussé, Olivier Finance, Xavier Ligneau, Craig W. Davis
In the absence of adequate hypocretin activity, patients with NT1 experience not only EDS but also REM sleep dysregulation, which manifests as elements of REM sleep occurring during wakefulness or sleep-wake transitions (i.e. cataplexy, sleep paralysis, hypnagogic hallucinations) [2,9,10]. Muscle atonia is a normal characteristic of REM sleep [18]. During wakefulness, muscle tone is maintained by activity in several neural pathways, including REM sleep-suppressing neurons in the ventrolateral periaqueductal gray and lateral pontine tegmentum (vlPAG/LPT), norepinephrine neurons of the locus coeruleus, serotonin neurons of the dorsal raphe nucleus, and acetylcholine neurons in the lateral dorsal tegmental/pedunculopontine tegmental (LDT/PPT) nuclei [10,12,18–20]. Cataplexy is thought to result from the intermittent activation of REM sleep atonia circuitry, which allows the intrusion of this REM sleep manifestation (i.e. muscle atonia) into wakefulness [9,10,18,21]. Strong emotions activate neural pathways in the prefrontal cortex and amygdala, and hypocretin functions to suppress atonia during normal wakefulness [12,20,21]. Due to the lack of adequate hypocretin activity in patients with NT1, the experience of strong emotions can lead to disinhibition of neurons in the REM sleep atonia circuit and reduced activity in neural pathways that maintain normal muscle tone, which results in the occurrence of muscle atonia during wakefulness (i.e. cataplexy; Figure 1) [9,10,12,18,20,21].
Horizontal gaze palsy and progressive scoliosis with two novel ROBO3 gene mutations in two Jordanian families
Published in Ophthalmic Genetics, 2019
Liqa A. Rousan, Abu Baker L. Qased, Ziad A Audat, Laila T. Ababneh, Saied A. Jaradat
All six patients in our study presented with the typical clinical manifestations, and the pathognomonic imaging findings of horizontal gaze palsy and progressive scoliosis reported in the literature: paralysis in the horizontal gaze with preservation of the vertical gaze and convergence with progressive scoliosis. Many theories proposed that the palsy in the horizontal gaze was attributed to abnormally decussated medial longitudinal fasciculus projections and abnormal innervation of the supranuclear abducens nerve (5). The abducens nuclei which are located in the lower part of the pontine tegmentum control the coordinated activity of the lateral and medial recti muscles responsible for the horizontal gaze (6). This was proved by neuroanatomical, electrophysiological, and clinical studies (7–10). Brain MRI shows the characteristic congenital anatomical abnormalities of the brainstem that explain the clinical manifestations in these patients: split pons sign, butterfly medulla, and absence of the facial colliculi. The split pons sign is a result of abnormally developed medial longitudinal fasciculus and abducens nuclei (11). The butterfly appearance of the medulla oblongata is a result of uncrossed corticospinal tracts (5). Thus, recognition of the characteristic imaging findings by the radiologist may be the first step for the clinical diagnosis of horizontal gaze palsy and progressive scoliosis.