| Term 
 
        | What is the cerebellum derived from? |  | Definition 
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        | Term 
 
        | Give control of and input for; -Vermis
 -Intermediate hemisphere
 -Lateral hemisphere
 -Flocculonodular lobe
 |  | Definition 
 
        | -Vermis; axial and proximal musculature (via spinal chord) 
 -Intermediate/paravermal hemisphere; distal musculature (spinal chord)
 
 -Lateral hemisphere; motor planning (cerebral cortex for what the planned action is, and inferior olivary nucleus which is the "error detector" augmenting future movement)
 
 -Flocculonodular lobe; balance and eye movements (Vestibular nuclei; VIII)
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        | Term 
 
        | How does info go into and out of the cerebellum? What uses the MCP? |  | Definition 
 
        | -Inf. & middle cerebellar peduncles (ICP & MCP); input -Sup. cerebellar peduncle (SCP); output
 
 -Two ways in, one way out
 
 -MCP is used mainly by the *pontocerebellar tract with input from cerebral cortex (rest pretty much uses the ICP)
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        | Term 
 
        | What are the layers and cells of cerebellum? What do the cells do? |  | Definition 
 
        | 1. Molecular layer; parallel fibers (from granule cells), stellate cells, and basket cells (PSB) 2. Purkinje layer; **purkinje cells (only ones exiting) (P)
 3. Granule cell layer; granule cells (only ones excitatory), & golgi cells
 
 PS Brain Parts Get Gooey
 
 -See slide 419 and try to get the flow of the cells (stellate and basket inhibit purkinje, golgi inhibits granule, granule excites everything)
 |  | 
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        | Term 
 
        | What are the fibers projecting into the cerebellum and tracts that make them up? What do they stimulate? |  | Definition 
 
        | -All are excitatory and use glutamate as signal -Both send collaterals to deep cerebellar nuclei also
 
 1. Climbing fibers;
 -From *olivocerebellar tract
 -Powerful direct stimulation of *purkinje cells
 
 2. Mossy fibers;
 -From everywhere else (vestibulocerebellar, spinocerebellar, and pontocerebellar tracts)
 -Stimulate *granule cells, which in turn indirectly stimulate the purkinje cells and most other cells (which are inhibitory and cause the more diffuse activation)
 |  | 
        |  | 
        
        | Term 
 
        | What are the neurotransmitters used in the cerebellum? |  | Definition 
 
        | -*GABA; inhibitory, all but *granule cells -Glutamate; excitatory, granule cells only (also two incoming fibers)
 |  | 
        |  | 
        
        | Term 
 
        | Where do the Purkinje cells project? Where are they coming from in the cerebellum cortex? What is their action? |  | Definition 
 
        | To the deep cerebellar nuclei; -Vermal & Flocculonodular-->*Fastigial nucleus
 -Paravermal-->*Interposed nuclei (Emboliform + Globus)
 -Lateral-->**Dentate nucleus
 (Nuclei given med to lat);  FID
 |  | 
        |  | 
        
        | Term 
 
        | What all can excite the Purkinje cells? |  | Definition 
 
        | -Climbing fibers and parallel fibers from granule cells |  | 
        |  | 
        
        | Term 
 
        | ***Give the paths overall for all four areas of the cerebellum (to and from)?*** |  | Definition 
 
        | -Axial skeletal muscles-->Vermis-->Fastigial N.-->Vestibular N. 
 -Vestibular nuclei-->Flocculonodular Lobe-->Fastigial N.-->Vestibular N. (similar, both for positional changes)
 
 -Distal musculature-->Paravermal Hem.-->Interpositus N.-->Red N.-->Rubrospinal tract
 
 -**Cerebral cortex & ION-->Lateral Hem.-->Dentate N.-->Thalamus (VA & VL)-->Motor Cortex (influences upper motoneurons in corticospinal tract)**
 
 -Also, see *illustration and table on page 421
 |  | 
        |  | 
        
        | Term 
 
        | What do we see with a cerebellar dysfunction? |  | Definition 
 
        | -**Tremor with intended movement (no fine tuning) -Without weakness or paralysis
 -On **ipsilateral side (will fall towards the lesioned side)
 |  | 
        |  | 
        
        | Term 
 
        | What do we see with vermus dysfunction? What do we need to differentiate this from? |  | Definition 
 
        | -Messed up posture and ataxic gait -Will present the same as a dorsal column lesion (input to vermis) but will not give a ***Romberg sign
 
 -Romberg sign is when they only sway/fall with eyes closed (sensory problem, but cerebellum is okay because it can use the visual info)
 |  | 
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        | Term 
 
        | What are the typical causes of vermal damage? What part? Difference in symptoms? |  | Definition 
 
        | -Anterior vermis; from alcohol abuse-->gait ataxia 
 -Post vermis; from tumors (meduloblastomas & ependymomas)-->truncal ataxia
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        | Term 
 
        | What will we see with a lesion of the hemisphere region (many symptoms)? |  | Definition 
 
        | -More distal ataxia with **intention tremors (like when trying to touch target) -*Dysmetria; can't stop movement at right place (literally, can't measure)
 -Dysdiadochokinesia; can't do alternating movements (***trouble jerking off haha***)
 -Speech problems; divide words into syllables
 -Gaze problems; cerebellum help in tracking
 -Hypotonia; lower reflexes (but no weakness)
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