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Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The cerebellum is connected to the dorsal aspect of the brainstem by three large fiber bundles on either side, referred to as the cerebellar peduncles, and identified as: the inferior cerebellar peduncle, or restiform body, the middle cerebellar peduncle, or brachium pontis, and the superior cerebellar peduncle, or brachium conjunctivum.
General Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
For the more (most) caudal of two or more similar structures in the spinal cord or brain stem. “Caudal” may be used chiefly by some authors who received their primary training in Great Britain. 1a. caudal colliculus (M&M, p. 39)1b. inferior colliculus (B&K, p. 88)2a. caudal cerebellar peduncle (M&M, p. 46)2b. inferior cerebellar peduncle (B&K, p. 157)3a. caudal medullary velum (M&M, p. 46)3b. inferior medullary velum (B&K, p. 86)
Synopsis of the Nervous System
Published in Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner, The Integrated Nervous System, 2017
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner
The human cerebellum is fairly prominent, with easily observed narrow ridges of tissue, called folia. Its cortex has a unique three-layered organization, with the prominent Purkinje neurons occupying the middle layer. A set of output nuclei is located deep within its structure (the deep cerebellar nuclei). The cerebellum is connected to the brainstem by three pairs of bundles of fibers called peduncles – the inferior cerebellar peduncles to the medulla (carrying mainly afferent information from the spinal cord and medulla), the middle ones to the pons (transmitting pontine input from the cerebral cortex) and the superior ones to the midbrain (carrying cerebellar efferents to the thalamus and from there to the cerebral cortex).
Cerebellar degeneration in primary lateral sclerosis: an under-recognized facet of PLS
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Eoin Finegan, We Fong Siah, Stacey Li Hi Shing, Rangariroyashe H. Chipika, Orla Hardiman, Peter Bede
The analyses of white matter diffusion metrics highlight the involvement of the cerebellar peduncles. The superior, middle, and inferior cerebellar peduncles provide the structural connection between the cerebellum and the brainstem. Our region-of-interest diffusivity analyses confirmed increased RD in the bilateral superior and inferior cerebellar peduncles and FA reductions in the inferior cerebellar peduncles. Additionally, our voxelwise analyses detected radial diffusivity alterations in the middle cerebellar peduncles. The superior cerebellar peduncles are the primary output tracts of the cerebellum connecting the cerebellar nuclei to the contralateral cortex via the ventral lateral nuclei, although they also contain spinocerebellar afferents (54,55). It is noteworthy, that the ventral lateral thalamic nuclei have previously been found to be affected in PLS (56,57). Superior cerebellar peduncle involvement has been described in a previous study of 3 PLS patients, in whom significantly lower FA was recorded in comparison with controls (58). Cerebellar peduncle white matter abnormalities have been consistently reported in ALS (59–61) and linked to impaired cerebro-cerebellar connectivity, including projections to the primary and supplementary motor cortices (59). MCP integrity changes have also been consistently described in ALS (59,62). The involvement of the MCP has been demonstrated in PLS patients and has been linked to pseudobulbar affect (PBA), supporting the concept of cerebellar deafferentation in the pathogenesis of PBA (35).
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
Progressive scoliosis is considered a major disability in this disorder. Up to this date, there is no clear genotype-phenotype correlation between the mutations in the ROBO3 gene and the cause of progressive scoliosis, and whether the pathophysiology is related to the nervous or musculoskeletal systems (12). Nevertheless, many authors proposed different theories on why the scoliosis occurs in these patients. One theory is: abnormal control of the axial tone due to the involvement of the central tegmental tract combined with primary dysfunction in the musculoskeletal system as a result of mutations of the ROBO3 gene (13). Maldevelopment of the extrapyramidal projections in the reticular formation is another theory for progressive scoliosis proposed by Jen et al. (3). Agenesis of the afferent fibres within the inferior cerebellar peduncles and of the pontocerebellar tracts proved by MR tractography is another recent explanation (10). The youngest patient in our cases (patient III-2), presented with torticollis before the development of scoliosis. Torticollis was also the initial presentation described in previous cases (14). Although in our patients there was gender predilection for the side of scoliosis; no such correlation was found in the literature and is mostly irrelevant.
Eight-and-a-half syndrome caused by a pontine haemorrhage: a case report and review of the literature
Published in International Journal of Neuroscience, 2018
Nian-ge Xia, Yan-yan Chen, Jia Li, Xi Chen, Zu-sen Ye, Si-yan Chen, Zhen-guo Zhu
A possible ‘nine’ syndrome was described by Rosini et al. [13] which comprised of eight-and-a-half syndrome with contralateral hemiparesis and hemihypesthesia due to the additional involvement of corticospinal tract and medial lemniscus by pontine infarction. Some cases presented eight-and-a-half syndrome with transient hemiparesis due to indirect compression of the medulla oblongata [17] or a transient extension of the peri-infarct oedema as postulated [22]. In 2015, Mahale et al. [19] reported two cases who presented with clinical features suggestive of eight-and-a-half syndrome along with hemiataxia. One patient presented with caudal pontine tegmental demyelination with additional involvement of inferior cerebellar peduncle in rostral dorsolateral medulla responsible for lipsilateral hemiataxia. And the other presented with intracranial haemorrhage of pontine tegmentum with extension into midbrain tegmentum/red nucleus responsible for contralesional hemiataxia. Herein, we present another unusual case of eight-and-a-half syndrome with contralateral hemiparesis due to pontine haemorrhage. Our patient was similar to the second one reported by Mahale et al. Therefore, we classify these clinical manifestations, which presented eight-and-a-half syndrome with hemiparesis or hemiataxia, as ‘nine syndromes’.