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The cerebellar vermis (from Latin vermis, "worm") is located in the medial, cortico-nuclear zone of the cerebellum, which is in the posterior fossa of the cranium. The primary fissure in the vermis curves ventrolaterally to the superior surface of the cerebellum , dividing it into anterior and posterior lobes .
Cerebellar cognitive affective syndrome (CCAS), also called Schmahmann's syndrome [1] is a condition that follows from lesions (damage) to the cerebellum of the brain. It refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum.
Cerebellar degeneration is a condition in which cerebellar cells, otherwise known as neurons, become damaged and progressively weaken in the cerebellum. [1] There are two types of cerebellar degeneration; paraneoplastic cerebellar degeneration , and alcoholic or nutritional cerebellar degeneration. [ 2 ]
Research is still needed in the area of cerebellar stroke management; however, several factors may lead to poor outcomes in individuals who have a cerebellar stroke. These factors include: Declining levels of consciousness; New signs of brainstem involvement; Progressing Hydrocephalus; Stroke to the midline of the cerebellum (a.k.a. the vermis) [4]
Neuroimaging evidence of cerebellar atrophy, especially in the vermis. C. The following clinical features cast doubt on the diagnosis of alcohol-related dementia: The presence of language impairment, especially dysnomia or anomia. the presence of focal neurologic signs or symptoms (except ataxia or peripheral sensory polyneuropathy).
In those with cerebral atrophy, Purkinje cells, or the cerebellar output neurons, in the vermis are reduced in number by 43%. [8] This large reduction in Purkinje cells causes a decrease in high order cerebral cortex organization. The cerebellum is also responsible for refining crude motor output from the primary motor cortex.
SCA1 positive mice haplodeficient in 14-3-3ε +/-were shown not to exhibit cerebellar degeneration but still exhibited lethal bulbar degeneration, suggesting that cerebellar atrophy may be related to increased stability of the expanded ataxin 1 protein and that there may be different pathogenic mechanisms for different regions of the brain. [26]
There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others.