China
Africa
Explore chapters and articles related to this topic
Contusional brain injury and intracerebral haemorrhage
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
These most commonly are either traumatic in origin, usually in association with cerebellar contusional injury, particularly in the presence of a fracture contusion (Vrankovic et al. 2000), or primarily hypertensive. This latter condition affects the central cerebellum including the dentate nucleus. Other rarer causes include malformations (see later).
Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Macroscopic changes are atrophy of the brainstem and cerebellum (Figure 16.74). Microscopically, there is loss of neurons and degenerative changes in various combinations (Figure 16.75) of sites that include: Pontine and olivary nuclei.Cerebellar dentate nuclei.Cerebellar Purkinje's cells.Basal ganglia (substantia nigra, subthalamic nuclei, and red nuclei).Spinal cord (Clarke's columns, spinocerebellar tracts, and anterior horn cells).Peripheral nerves (dorsal root ganglia).
Examination of the Nervous System
Published in Julian L Burton, Guy Rutty, The Hospital Autopsy, 2010
The pons can be removed from the cerebellum by cutting through the cerebellar peduncles on both sides. The brainstem can then be sectioned at 3 mm intervals from the midbrain, through the pons to the medulla. The cerebellum can be sectioned radially to show the cortex, white matter and cerebellar dentate nuclei.
Current challenges in the pathophysiology, diagnosis, and treatment of paroxysmal movement disorders
Published in Expert Review of Neurotherapeutics, 2021
Cécile Delorme, Camille Giron, David Bendetowicz, Aurélie Méneret, Louise-Laure Mariani, Emmanuel Roze
Clinical studies and animal models support the implication of both basal ganglia and cerebellum in the genesis of paroxysmal dyskinesia. Studies in rodents and primates brought evidence for reciprocal routes of communication between the cerebellum and the striatum [41]. In rodent models, a disynaptic pathway was found from the cerebellar nuclei to the striatum via the central lateral nucleus of the thalamus[42]. Likewise, the main output nucleus of the cerebellum, the dentate nucleus, is at the origin of a disynaptic pathway to the striatum in non-human primates[43]. Aberrant cerebellar activity can percolate through this network and influence activity in the basal ganglia. This may reconcile the apparent dilemma of striatal and cerebellar abnormalities converging into similar manifestations. This concept of network disorder is now a major theory in the pathophysiology of dystonia [44]. Paroxysmal dyskinesia could also be seen as a network disorder, in which either primary striatal dysfunction or aberrant cerebellar output conveyed to the striatum results in the phenotype. Future experimental studies combining neurophysiological and neuroimaging investigations in patients with paroxysmal dyskinesia would help us to better understand the subtle interplay between the cerebellum and the basal ganglia.
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.
Cumulative administrations of gadolinium-based contrast agents: risks of accumulation and toxicity of linear vs macrocyclic agents
Published in Critical Reviews in Toxicology, 2019
Lara Chehabeddine, Tala Al Saleh, Marwa Baalbaki, Eman Saleh, Samia J. Khoury, Salem Hannoun
The issue of Gd deposition in the brain raises new safety questions. In 2016, Welk et al. evaluated the association between Gd exposure and Parkinsonism among the elderly (Welk et al. 2016). Parkinson affects the substantia nigra that directs voluntary movements through signals to the globus pallidus. Since Gd is found to deposit preferentially in the globus pallidus, it is natural to ask whether repeated exposure to Gd will increase the risk of Parkinson disease. Nevertheless, after comparison of patients with Gd exposure to those exposed to non-Gd enhanced MRIs no increased risk of Parkinsonism was found. Gd also deposits in the dentate nucleus which is a part of the cerebellum. Perrotta et al. examined the possible correlation between serial injections of the macrocyclic agent gadoterate and a cerebellar syndrome (Perrotta et al. 2017). This study, however, did not detect the appearance of cerebellar toxicity due to GBCA exposure. That said Perrotta et al. recommended doing a study on lGBCAs with higher brain deposition than gadoterate. In contrast, Forslin et al. noted a decrease in verbal fluency in MS patients with increased signal intensity (SI) in the dentate nucleus even after correction for disease severity (Forslin et al. 2017). Caution is however advised in interpreting these results. The authors note the difficulty of fully correcting for disease severity knowing that MS affects verbal tasks and recognizes that another limitation of their study is the lack of a matched group of MS patients with no (or only macrocyclic) GBCA exposure.