“…The hemorrhage (hypointense, black) centered in the midline between the deep cerebellar nuclei and extended rostrally into the vermal lobules IV and V and the right hemispheric lobules V and VI ( 40 , 41 ). The edema (hyperintense, light gray) involved bilaterally the fastigial nucleus (F, blue) anteriorly to the hemorrhage at the roof of the fourth ventricle, most likely impairing inter-fastigial projections ( 15 ), and laterally the interpositus composed of the globose (G) and emboliform (E) nuclei, and the medial part of the dentate nucleus (D). The lesion did not comprise (oculomotor) hemispheric lobule VI (simple lobule), the posterior oculomotor vermal lobules VI and VI (OMV), flocculus, paraflocculus, and caudal vermal uvula and nodulus.…”
Section: Resultsmentioning
confidence: 99%
“…Noticeably, as pursuit and saccade fibers cross the midline at the rostral level and project to the contralateral side, unilateral FOR lesions may have bidirectional effects. A recent anatomical study has shown inter-fastigial projections along the roof of the fourth ventricle in mice ( 15 ) but these projections have neither been identified in the non-human primate yet nor been functionally characterized as related to the control of eye movements.…”
Background“Central dizziness” due to acute bilateral midline cerebellar disease sparing the posterior vermis has specific oculomotor signs. The oculomotor region of the cerebellar fastigial nucleus (FOR) crucially controls the accuracy of horizontal visually-guided saccades and smooth pursuit eye movements. Bilateral FOR lesions elicit bilateral saccade hypermetria with preserved pursuit. It is unknown whether the initial acceleration of smooth pursuit is impaired in patients with bilateral FOR lesions.ObjectiveWe studied the effect of a cerebellar lesion affecting the deep cerebellar nuclei on the initial horizontal pursuit acceleration and investigated whether saccade dysmetria also affects other types of volitional saccades, i.e., memory-guided saccades and anti-saccades, which are not performed in immediate response to the visual target.MethodsWe recorded eye movements during a sinusoidal and step-ramp target motion paradigm as well as visually-guided saccades, memory-guided saccades, and anti-saccades in one patient with a circumscribed cerebellar hemorrhage and 18 healthy control subjects using a video-based eye tracker.ResultsThe lesion comprised the FOR bilaterally but spared the posterior vermis. The initial pursuit acceleration was low but not significantly different from the healthy control subjects and sinusoidal pursuit was normal. Bilateral saccade hypermetria was not only seen with visually-guided saccades but also with anti-saccades and memory-guided saccades. The final eye position remained accurate.ConclusionWe provide new insights into the contribution of the bilateral deep cerebellar nuclei on the initial acceleration of human smooth pursuit in midline cerebellar lesions. In line with experimental bilateral FOR lesion data in non-human primates, the initial pursuit acceleration in our patient was not significantly reduced, in contrast to the effects of unilateral experimental FOR lesions. Working memory and neural representation of target locations seem to remain unimpaired. Our data argue against an impaired common command feeding the circuits controlling saccadic and pursuit eye movements and support the hypothesis of independent influences on the neural processes generating both types of eye movements in the deep cerebellar nuclei.
“…The hemorrhage (hypointense, black) centered in the midline between the deep cerebellar nuclei and extended rostrally into the vermal lobules IV and V and the right hemispheric lobules V and VI ( 40 , 41 ). The edema (hyperintense, light gray) involved bilaterally the fastigial nucleus (F, blue) anteriorly to the hemorrhage at the roof of the fourth ventricle, most likely impairing inter-fastigial projections ( 15 ), and laterally the interpositus composed of the globose (G) and emboliform (E) nuclei, and the medial part of the dentate nucleus (D). The lesion did not comprise (oculomotor) hemispheric lobule VI (simple lobule), the posterior oculomotor vermal lobules VI and VI (OMV), flocculus, paraflocculus, and caudal vermal uvula and nodulus.…”
Section: Resultsmentioning
confidence: 99%
“…Noticeably, as pursuit and saccade fibers cross the midline at the rostral level and project to the contralateral side, unilateral FOR lesions may have bidirectional effects. A recent anatomical study has shown inter-fastigial projections along the roof of the fourth ventricle in mice ( 15 ) but these projections have neither been identified in the non-human primate yet nor been functionally characterized as related to the control of eye movements.…”
Background“Central dizziness” due to acute bilateral midline cerebellar disease sparing the posterior vermis has specific oculomotor signs. The oculomotor region of the cerebellar fastigial nucleus (FOR) crucially controls the accuracy of horizontal visually-guided saccades and smooth pursuit eye movements. Bilateral FOR lesions elicit bilateral saccade hypermetria with preserved pursuit. It is unknown whether the initial acceleration of smooth pursuit is impaired in patients with bilateral FOR lesions.ObjectiveWe studied the effect of a cerebellar lesion affecting the deep cerebellar nuclei on the initial horizontal pursuit acceleration and investigated whether saccade dysmetria also affects other types of volitional saccades, i.e., memory-guided saccades and anti-saccades, which are not performed in immediate response to the visual target.MethodsWe recorded eye movements during a sinusoidal and step-ramp target motion paradigm as well as visually-guided saccades, memory-guided saccades, and anti-saccades in one patient with a circumscribed cerebellar hemorrhage and 18 healthy control subjects using a video-based eye tracker.ResultsThe lesion comprised the FOR bilaterally but spared the posterior vermis. The initial pursuit acceleration was low but not significantly different from the healthy control subjects and sinusoidal pursuit was normal. Bilateral saccade hypermetria was not only seen with visually-guided saccades but also with anti-saccades and memory-guided saccades. The final eye position remained accurate.ConclusionWe provide new insights into the contribution of the bilateral deep cerebellar nuclei on the initial acceleration of human smooth pursuit in midline cerebellar lesions. In line with experimental bilateral FOR lesion data in non-human primates, the initial pursuit acceleration in our patient was not significantly reduced, in contrast to the effects of unilateral experimental FOR lesions. Working memory and neural representation of target locations seem to remain unimpaired. Our data argue against an impaired common command feeding the circuits controlling saccadic and pursuit eye movements and support the hypothesis of independent influences on the neural processes generating both types of eye movements in the deep cerebellar nuclei.
“…Two sets of axons transverse contralaterally the roof of the V, subventricular axons (SV axons, red) from the fastigial nucleus and supraventricular axons (SupraV axons, green) form the vellum medularis that project from the IV cranial nerve. Voogd, 1967;Voogd and Glickstein, 1998;Gómez-González and Martínez-Torres, 2021). These axons are generally formed by neurons with a dense myelin sheath, and show diverse neurochemical identity either glutamatergic, glycinergic or GABAergic (Robinson et al, 1993;Uusisaari et al, 2007;Bagnall et al, 2009).…”
Section: Subventricular Zonementioning
confidence: 99%
“…Axons from the descending section of the fastigial nucleus (FN) cross contralaterally along the roof of the ventricle mainly projecting to the vestibular system (Walberg et al, 1962 ; Voogd, 1967 ; Voogd and Glickstein, 1998 ; Gómez-González and Martínez-Torres, 2021 ). These axons are generally formed by neurons with a dense myelin sheath, and show diverse neurochemical identity either glutamatergic, glycinergic or GABAergic (Robinson et al, 1993 ; Uusisaari et al, 2007 ; Bagnall et al, 2009 ).…”
Section: The Neural Componentmentioning
confidence: 99%
“…These axons are generally formed by neurons with a dense myelin sheath, and show diverse neurochemical identity either glutamatergic, glycinergic or GABAergic (Robinson et al, 1993 ; Uusisaari et al, 2007 ; Bagnall et al, 2009 ). Interestingly, in a study conducted by Gómez-González and Martínez-Torres ( 2021 ), it was demonstrated that the medial portion of the FN located between the cerebellar lobules I-II, form an inter-fastigial direct pathway composed mostly by GABAergic axons, adding complexity to this circuit. Functionally, the rostral region of the FN is associated with regulation of ocular movements (initiation, consistence, and accuracy of saccades), in addition its stimulation increases the systemic blood pressure (Nisimaru and Kawaguchi, 1984 ; Robinson et al, 1993 ; Takahashi et al, 2014 ).…”
The roof of the fourth ventricle (4V) is located on the ventral part of the cerebellum, a region with abundant vascularization and cell heterogeneity that includes tanycyte-like cells that define a peculiar glial niche known as ventromedial cord. This cord is composed of a group of biciliated cells that run along the midline, contacting the ventricular lumen and the subventricular zone. Although the complex morphology of the glial cells composing the cord resembles to tanycytes, cells which are known for its proliferative capacity, scarce or non-proliferative activity has been evidenced in this area. The subventricular zone of the cerebellum includes astrocytes, oligodendrocytes, and neurons whose function has not been extensively studied. This review describes to some extent the phenotypic, morphological, and functional characteristics of the cells that integrate the roof of the 4V, primarily from rodent brains.
The present review aims to provide a short update of our understanding of the inhibitory interneurons of the cerebellum. While these cells constitute but a minority of all cerebellar neurons, their functional significance is increasingly being recognized. For one, inhibitory interneurons of the cerebellar cortex are now known to constitute a clearly more diverse group than their traditional grouping as stellate, basket, and Golgi cells suggests, and this diversity is now substantiated by single-cell genetic data. The past decade or so has also provided important information about interneurons in cerebellar nuclei. Significantly, developmental studies have revealed that the specification and formation of cerebellar inhibitory interneurons fundamentally differ from, say, the cortical interneurons, and define a mode of diversification critically dependent on spatiotemporally patterned external signals. Last, but not least, in the past years, dysfunction of cerebellar inhibitory interneurons could also be linked with clinically defined deficits. I hope that this review, however fragmentary, may stimulate interest and help focus research towards understanding the cerebellum.
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