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Assessing Paediatric Development in Psychiatry
Published in Cathy Laver-Bradbury, Margaret J.J. Thompson, Christopher Gale, Christine M. Hooper, Child and Adolescent Mental Health, 2021
The cerebellum is relatively well developed at birth when compared to the higher cerebral cortex. It receives information from various sensory organs and cognitive areas: the auditory system (vestibular nuclei and the superior olivary nucleus), the optic pathway (inferior olivary nucleus), proprioceptive feedback (spinocerebellar tract), basic autonomic information (from cranial nerve and brainstem nuclei) and higher cortical information (the planning, execution, adjustment in approach and emotional reactions to on-going tasks). The cerebellum, in turn, sends efferents back to all those areas, creating essential feedback loops. This allows the instigation, co-ordination and regulation of both reflex-based movements and higher motor pathways and combines these functions with information from vital sensory systems.
Specific Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Inferiorolivary nucleus (B&K, p. 93) Main olivary nucleus (C&S, p. 331)Olivary nucleus (W&W, p. 904)Principal inferior olivary nucleus (C&S. p. 331)See, also, NS: Inferior olivary complex, NS: Principal nucleus (of the inferior olive), and SS: Nucleus of the corpus trapezoideum.
Dapagliflozin modulates neuronal injury via instigation of LKB1/p-AMPK/GABAB R2 signaling pathway and suppression of the inflammatory cascade in an essential tremor rat model
Published in Expert Opinion on Therapeutic Targets, 2023
Ahmed S. Kamel, Sama M. Farrag, Heba M. Mansour, Noha N. Nassar, Muhammed A. Saad
The harmaline (HAR) animal model is an established model that mimics the mechanisms of ET [10] as it produces postural as well as kinetic tremor with a peak frequency between 10 and 12 Hz in rats [11]. Although, the origins of ET remain elusive, postmortem studies have delved deeply into the anatomical and structural changes found in the cerebellum of ET patients. The cerebellum controls motor coordination through synchronizing oscillations of Purkinje cells (PCs) dendritic arbor. The most prominent pathological marker of the disease is the loss of PCs that reduce gamma amino butyric acid (GABA) levels. Such deficiency of the GABAergic tone leads to glutamatergic neuronal hyperexcitability, which may trigger tremors and apoptotic cascade [12]. Additionally, PCs receive excitatory fibers from the inferior olivary nucleus (ION) and cerebellar granule cells which when fulminated lead to PCs damage [13]. Despite these findings, the management of ET is still symptomatic and the efficacy of the present remedies remains an impediment.
Wernekink commissure syndrome secondary to a rare ‘V’-shaped pure midbrain infarction: a case report and review of the literature
Published in International Journal of Neuroscience, 2020
Mingming Dong, Lishu Wang, Weiyu Teng, Li Tian
Wernekink commissure is firstly described as a horseshoe-shaped commissure by the German anatomist Friedrich Wernekink and actually the decussation of superior cerebellar peduncles (SCP). It mainly consists of two white matter tracts: dentato–rubro–thalamic tract and dentato–rubro–olivary tract [1,8]. The former pathway provides cerebrocerebellum connection by connecting the dentate nucleus through the SCP to the contralateral red nucleus and thalamus. The latter one was formed by the fibers that contacted dentate and interposed cerebellar nuclei to the contralateral red nucleus through the SCP and inferior olivary nucleus in the medulla. The location of this commissure is anterior to the aqueduct and at the paramedian area of upper brainstem (mainly in the caudal midbrain as well as small portion in rostral pontine and midbrain) [9]. The structures adjacent to Wernekink commissure include MLF, reticular formation, trochlear nucleus (at the inferior colliculus level) and the oculomotor nuclei and fibers (at the superior colliculus level). Therefore, the classical symptoms of Wernekink commissure syndrome are described as constant bilateral cerebellar dysfunction along with commonly various ocular signs, and occasionally delayed-onset palatal myoclonus or tremor.
Phoria Adaptation: The Ghost in the Machine
Published in Journal of Binocular Vision and Ocular Motility, 2020
When prisms are placed before one eye of an orthotropic patient, the visual image discordance is interpreted as an error signal. Adaptation and learning to correct motor error signals is modulated at the level of the vestibulocerebellum.10,69 It, therefore, seems likely that phoria adaptation is similarly mediated by both climbing and mossy fibers within the cerebellum, which implement modifiable, adaptive, and “plastic” responses10 (Figure 3).70 The cerebellum receives continuous information via the mossy fiber system. The climbing fiber system originates from the inferior olivary nucleus and provides a powerful timing and error signal to Purkinje cells. The inferior olivary nucleus acts as a comparator of motor commands from the cerebral cortex, brainstem nuclei and receives feedback from receptors via the spinal cord, visual system, or vestibular organs. The inferior olive senses the error and recalibrates the tonic firing of the Purkinje cells. The increased frequency of inferior olivary nucleus discharge and complex spikes in the Purkinje cells triggers long-term depression of the synapse between the parallel fibers and the Purkinje cells, thereby resetting the single spike discharge rate to produce the necessary motor learning and adaptation. The Purkinje cell provides profound inhibition via GABA to the cerebellar nuclei, which provide the output of the cerebellum. It is therefore likely that the neural circuitry subserving phoria adaptation is not localized to a specific area but modulated by cortical, midbrain, and cerebellar circuitry.10,65,66