| Cerebellar vermis | |
|---|---|
 Upper surface of cerebellum. The vermis is highlighted in red. | |
 Vermis (highlighted in red) on the cerebellum. | |
| Details | |
| Part of | Cerebellum |
| Identifiers | |
| Latin | vermis cerebelli |
| MeSH | D065814 |
| NeuroNames | 2463 |
| NeuroLex ID | birnlex_1106 |
| TA98 | A14.1.07.006 |
| TA2 | 5819 |
| FMA | 76928 |
| Anatomical terms of neuroanatomy | |
Thecerebellar vermis (fromLatinvermis, "worm") is located in the medial, cortico-nuclear zone of thecerebellum, which is in theposterior fossa of thecranium. Theprimary fissure in the vermis curvesventrolaterally to thesuperior surface of thecerebellum, dividing it intoanterior andposteriorlobes. Functionally, the vermis is associated with bodilyposture andlocomotion. The vermis is included within thespinocerebellum and receives somatic sensory input from thehead and proximal body parts viaascending spinal pathways.[1]
Thecerebellum develops in a rostro-caudal manner, withrostral regions in the midline giving rise to the vermis, andcaudal regions developing into thecerebellar hemispheres.[2] By 4 months ofprenatal development, the vermis becomes fullyfoliated, while development of the hemispheres lags by 30–60 days.[3] Postnatally,proliferation and organization of the cellular components of thecerebellum continues, with completion of the foliation pattern by 7 months of life[4] and finalmigration, proliferation, andarborization of cerebellar neurons by20 months.[5]
Inspection of theposterior fossa is a common feature ofprenatal ultrasound and is used primarily to determine whether excess fluid or malformations of the cerebellum exist.[6] Anomalies of the cerebellar vermis are diagnosed in this manner and includephenotypes consistent withDandy–Walker malformation,rhombencephalosynapsis, displaying no vermis with fusion of thecerebellar hemispheres,pontocerebellar hypoplasia, orstunted growth of the cerebellum, andneoplasms. Inneonates,hypoxic injury to the cerebellum is fairly common, resulting in neuronal loss andgliosis. Symptoms of these disorders range from mild loss of finemotor control to severeintellectual disability anddeath.Karyotyping has shown that mostpathologies associated with the vermis areinherited through anautosomal recessive pattern, with most knownmutations occurring on theX chromosome.[1][7]
The vermis is intimately associated with all regions of thecerebellar cortex, which can be divided into three functional parts, each having distinct connections with thebrain andspinal cord. These regions are thevestibulocerebellum, which is responsible primarily for the control ofeye movements; thespinocerebellum, involved in fine tune body and limb movement; and thecerebrocerebellum, which is associated with planning, initiation and timing ofmovements.[8]
The vermis is the unpaired, median portion of the cerebellum that connects thetwo hemispheres.[9] Both the vermis and the hemispheres are composed oflobules formed by groups offolia. There are nine lobules of the vermis: lingula, central lobule, culmen, clivus,folium of the vermis, tuber, pyramid, uvula and nodule.[9] These lobules are often difficult to observe during human anatomy classes and may vary in size, shape and number of folia. It has been shown that folia of the cerebellum exhibit frequent variations in form, number and arrangement between individuals.[9]
The lingula is the first lobule of the upper portion of the vermis on thesuperoinferior axis and pertains to thepaleocerebellum together with the central lobule, culmen, pyramid and uvula. It is separated from the central lobule by the pre-centralfissure. The central lobule is the second lobule of the upper portion of the vermis on the superoinferior axis. The culmen is the third and largest lobule of the upper portion of the vermis on the superoinferior axis. It is separated from the declive by the primary fissure and is related with theanterior quadrangular lobule of the hemisphere. The pyramid is the seventh lobule of the vermis on the superoinferior axis. It is separated from the tuber and uvula by the pre-pyramidal and secondary fissures, respectively.[9] This lobule is related with the biventral lobule of the hemisphere. The uvula is the second largest lobule, following the culmen. It pertains to the paleocerebellum and is separated from the nodule by the posterolateral fissure.[9]
The spinocerebellum receivesproprioception input from the dorsal columns of thespinal cord (including thespinocerebellar tract) and from thetrigeminal nerve, as well as from visual andauditory systems. It sends fibers to deepcerebellar nuclei that, in turn, project to both thecerebral cortex and thebrain stem, thus providing modulation of descending motor systems.[8] This region comprises the vermis and intermediate parts of the cerebellar hemispheres. Sensory information from the periphery and from theprimary motor andsomatosensory cortex terminate in this region.Purkinje cells of the vermis project to thefastigial nucleus, controlling theaxial andproximal musculature involved in the execution of limb movements.[10]Purkinje cells in the intermediate zone of the spinocerebellum project to the interposed nuclei, which control the distal musculature components of thedescending motor pathways needed for limb movement. Both of these nuclei include projections to themotor cortex in thecerebrum.[10]
Theinterposed nucleus is smaller than thedentate nucleus but larger than thefastigial nucleus and functions to modulate muscle stretch reflexes of distal musculature.[9] It is locateddorsal to the fourthventricle and lateral to thefastigial nucleus; it receivesafferent neuronal supply from theanterior lobe of the cerebellum and sends output via thesuperior cerebellar peduncle and thered nucleus.[8]
The fastigial nucleus is the most medialefferent cerebellar nucleus, targeting thepontine and medullaryreticular formation as well as thevestibular nuclei.[10] This region deals with antigravity muscle groups and other synergies involved with standing and walking.[11] It is thought that fastigial nucleiaxons areexcitatory and project beyond thecerebellum, likely usingglutamate andaspartate asneurotransmitters.[10]
Malformations of theposterior fossa have been recognized more frequently during the past fewdecades as the result of recent advances in technology. Malformations of the cerebellar vermis were first identified usingpneumoencephalography, where air is injected into thecerebrospinal fluid spaces of thecerebellum; displaced, occluded ordysplastic structures could be identified. Upon the advent ofcomputerized tomography (CT) andmagnetic resonance imaging (MRI), the resolution of cranial structures including the mid-hindbrain regions improved dramatically.[12]
Joubert syndrome (JS) is one of the most commonly diagnosed syndromes associated with the molar tooth sign (MTS),[13] orhypoplasia/dysplasia of the cerebellar vermis accompanied by brainstem abnormalities.JS is defined clinically by features ofhypotonia ininfancy with later development ofataxia, developmental delays,mental retardation, abnormal breathing patterns, abnormal eye movements specific to oculomotorapraxia, or the presence of theMTS on the cranialMRI.[14][15]JS is anautosomal recessive condition with an estimatedprevalence of 1: 100,000.[16]
Dandy Walker malformation is a relatively commoncongenital brain malformation with a prevalence of 1:30,000 live births.[17] Dandy Walker malformation is characterized by enlargedposterior fossa and in which the cerebellar vermis is completely absent, or present in a rudimentary form, sometimes rotated accompanied by an elevation of the fourthventricle. It is also commonly associated withdysplasias ofbrainstem nuclei.[18] DWM has been reported to be in association with a wide array ofchromosomal anomalies, includingtrisomy 18,trisomy 9, andtrisomy 13. Surveys suggest thatprenatal exposure toteratogens such asrubella oralcohol are correlated with development of Dandy Walker malformation.[19][20]
Rhombencephalosynapsis is an anomaly characterized by the absence or severe dysgenesis of the cerebellar vermis with fusion of thecerebellar hemispheres,peduncles, anddentate nuclei. Diagnostic features include fusion of the midbraincolliculi,hydrocephalus, absence of thecorpus callosum other midline structural brain malformations.[21][22][23]
Hypoplasia and other structural alterations of the vermis have been identified in many patients withautism spectrum disorder (ASD). While the exact nature and extent of the impacts ASD has on the vermis remain in question, it has also been shown that other injuries and malformations of the vermis sometimes produce symptoms closely analogous to ASD. Furthermore, several genetic syndromes known to cause autism (such asfragile X syndrome) have also been shown to cause damage to the vermis.[24]
Lesions to the vermis commonly give rise toclinical depression, inappropriate emotional displays (e.g. unwarranted giggling) in addition to movement disorders.[citation needed]
Earlyneurophysiologists suggest thatretinal andinertial signals were selected for about 450 million years ago by primitivebrainstem-cerebellar circuitry because of their relationship with the environment.[25] Microscopically, it is evident thatPurkinje cell precursors arose fromgranule cells, first forming in irregular patterns, then progressively becoming organized in a layered fashion. Evolutionarily, thePurkinje cells then developed extensivedendritic trees that increasingly became confined to a single plane, through which theaxons of granule cells threaded, eventually forming a neuronal grid of right angles.[25] The origin of thecerebellum is in close association with that of thenuclei of thevestibular cranial nerve and lateral linenerves, perhaps suggesting that this part of the cerebellum originated as a means of carrying out transformations of thecoordinate system from input data of thevestibular organ and thelateral line organs.[26] This suggests that the function of the cerebellumevolved as a mode of computing and representing an image relating to the position of the body in space. The cerebellar vermis evolved in conjunction with the hemispheres; this is seen inlampreys and highervertebrates.[27]
Invertebrates, the cerebellar vermis develops between two bilaterally symmetrical formations locateddorsal to the upper end of themedulla oblongata, orrhombencephalon. This is the region of termination for thefibers of thevestibular nerve and lateral line nerves; thus, these are the oldestafferent paths to the cerebellum and cerebellar vermis.[27] In bony fish, orteleosts, it has been proposed that the cerebellar auricles, which receive a large amount of input from the vestibulolateral line system, constitute thevestibulocerebellum and arehomologues of theflocculonodular lobe of higher vertebrates along with thecorpus cerebelli, which receives spinocerebellar and tectocerebellar fibers. Thelabyrinth and the lateral line organs oflampreys have structural and functional similarity. An important difference between the two structures is that the arrangement of the lateral line organs are such that they are sensitive to relative motion of the fluid surrounding the animal, whereas the labyrinths, having very similar sensing mechanisms, are sensitive toendolymph, providing information concerning the animal's ownequilibrium of the body and orientation in space.[27]
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