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Neuroanatomy of basic cognitive function
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Mark J. Ashley, Jessica G. Ashley, Matthew J. Ashley
Cholinergic neurons (Figure 6.15) project from the mesopontine tegmentum and the basal forebrain. The neurons of the pontine region provide a descending projectional pathway to the nuclei of the pontine and medullary reticular formation. They also project in a major ascending pathway to the thalamus. The ascending pathway to the thalamus exerts an arousal effect that is mediated indirectly by excitatory projections from the thalamus to the cortex.177 Projections arising in the basal forebrain provide indirect cholinergic input to the cortex. By contrast, cholinergic projections arising from the nucleus basalis neurons project entirely to nearly all the cerebral cortex. The hippocampal formation is fed by projections from the medial septal nuclei and the nucleus of the diagonal band of Broca. Cholinergic neurons of the descending pathway are thought to impact the sleep–wake cycle via these projections. Cholinergic blockade of central cholinergic transmission results in delirium, and blockade of the striatal neurons results in movement disorders.177 The primary function of acetylcholine is found in attention, memory, and learning.
The Biology of Dream Formation
Published in Milton Kramer, The Dream Experience, 2013
The control of REM dreaming is described anatomically, physiologically, cellularly, and chemically. The anatomic control is in the pons; therefore, it is subcortical in the brainstem. Physiologically, it is represented by PGO waves from the pons to the lateral geniculate body to the occipital cortex. At the cellular level in the pons, the REM-on cells are in the mesopontine tegmentum. The REM-off cells are in the Nucleus Locus Coeruleus and Dorsal Raphe Nucleus. The chemical control of dreaming is a consequence of REM-on cells secreting acetylcholine while the REM-off cells secrete norepinephrine and serotonin.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
The term mesopontine is used to describe an area of tissue the lies around the junction of the MESENCEPHALON (hence meso-) and PONS. The mesopontine tegmentum (see TEGMENTUM) is the dorsal area of this. The most prominent structure in this region is the PEDUNCULOPONTINE TEGMENTAL NUCLEUS.
Spinal cord involvement in Lewy body-related α-synucleinopathies
Published in The Journal of Spinal Cord Medicine, 2020
Raffaele Nardone, Yvonne Höller, Francesco Brigo, Viviana Versace, Luca Sebastianelli, Cristina Florea, Kerstin Schwenker, Stefan Golaszewski, Leopold Saltuari, Eugen Trinka
The locomotion requires the integration of several intentional or automatic processes at different levels. Intentional locomotion initiation arises in the cerebral cortex or in the limbic-hypothalamic system when triggered emotionally. Locomotion regulation processes originate in the cerebral cortex, basal ganglia, and cerebellum. The automatic basic locomotion execution processes are located in the brain stem and in the spinal cord. Two areas located in the mesopontine tegmentum, the midbrain locomotor region and the muscle tone inhibitory region, are involved in the control of locomotion. Two pathways arise from the midbrain locomotor region, descend in the ventrolateral and dorsolateral funiculi, and activate the interneurons of the locomotor central pattern generator located in laminae VII, VIII, and X of the lumbar cord. In contrast, inputs originating from the ventrolateral part of the pedunculopontine tegmental nucleus have inhibitory effects upon the motoneurons.95 LB-like inclusions have been observed in the lumbar spinal cord’s motoneurons of a patient affected by autosomal juvenile PD.33 Unlike in animal models of PD,96 in humans the epidural electrical stimulation of the dorsal columns failed to restore locomotion.97
Resting-state fMRI reveals increased functional connectivity in the cerebellum but decreased functional connectivity of the caudate nucleus in Parkinson’s disease
Published in Neurological Research, 2020
Oliver Kaut, Clemens Mielacher, René Hurlemann, Ullrich Wüllner
The underlying pathophysiology leading to falls in PD is highly complex and still not fully understood. A multifactorial etiology, with contributions from both primary and secondary disease processes, as well as various compensatory mechanisms, is likely to be implicated [5]. Multi-sensory information, such as somatosensory, visual and vestibular sensation, is integrated in different areas of the brain to enable a delicate control of posture and gait. There are two levels of control involved: 1) an automatic process of gait control mediated by the descending pathways from the brainstem to the spinal cord, particularly the reticulospinal pathways arising from the lateral part of the mesopontine tegmentum and spinal locomotor network, 2) a cognitive process of postural control required when walking in unfamiliar surroundings or circumstances, located in the temporoparietal association cortex. In addition, the basal ganglia and cerebellum may modulate both the automatic and cognitive processes through reciprocal connections with the brainstem and cerebral cortex [6]. This interplay enables the regulation of muscle tone and rhythmic limb movements [7]. Consequently, dysfunction at the level of cortex, basal ganglia, or cerebellum could impair posture and gait control and thereby induce falls [6].