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50 Cards in this Set
- Front
- Back
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What pathways activate LMNs? |
1. Pyramidal 2. Extrapyramidal |
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What is the pyramidal (direct) pathway? |
1. Pyramidal neurons in primary motor area 2. Axons project via pyramidal tracts 3. Directly synapse on LMNs
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What is the extrapyramidal (indirect) pathway? |
1. Originates in upper motor neurons 2. Axons DO NOT synapse directly with LMNs 3. Axons make connections with motor nuclei in brain stem, which contact the LMNs |
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What are the brain stem nuclei involved in motor function? |
1. Red nucleus (lateral) 2. Vestibular nucleus and reticular formation (medial) |
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What modulates UMN output? Where do these structures project? |
1. Basal ganglia and cerebrocerebellum via the thalamus 2. Also project to LMNs--- can influence activity
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What are the main sensory areas that guide movements in motor areas? |
1. Primary somatosensory cortex 2. Posterior parietal cortex |
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What does the primary somatosensory cortex relay? To where? |
1. Touch 2. Proprioception 3. Relays to primary motor cortex |
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What does the posterior parietal cortex relay? To where? |
1. Visual and auditory information 2. Relays to premotor cortex |
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With what other structures does the premotor cortex form connections? |
1. Primary motor cortex 2. LMNs via pyramidal tract |
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What is the role of the medial premotor cortex? |
1. Control of internally generate movements---thinking about making a movement 2. Active both when thinking about and performing movement |
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What is active concurrently with the medial premotor cortex during movement? |
1. Primary motor cortex |
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What is the role of the primary motor cortex? |
1. Generating movements 2. Control of muscle activity by connecting to LMNs via direct and indirect pathways |
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What will lesions to the primary motor cortex or pyramidal tracts lead to? |
1. Deficits of fine motor control of upper limbs, hands, and fingers
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Why are deficits in the lower limb less severe than the upper limb in lesions of the primary motor cortex/pyramidal tracts? |
1. Control of these muscles can be achieved via the indirect pathway----- brain stem nuclei, cerebellum, and basal ganglia |
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What is the role of the basal ganglia? How is this accomplished? |
1. Control of movement 2. Receives and sends connections with the cerebral cortex via the thalamus 3. Suppression of movements that interfere with selected task 4. Learning motor skills 5. Calculate energy cost/benefit of movement |
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What makes up the basal ganglia? |
1. Caudate nucleus 2. Putamen 3. Globus pallidus internal and external 4. Subthalamic nucleus 5. Subtantia pars nigra compacta |
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Where are cortical inputs to the basal ganglia received? |
1. Striatum |
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What are the subdivisions of the striatum? |
1. Caudate nucleus 2. Putamen 3. Ventral striatum |
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Where is the nucleus acucmbens located? |
1. Ventral striatum |
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What is the function of the putamen? |
1. Receive input from motor control areas of cortex (primary and premotor cortex) |
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What type of connection do cortical axons make on stratal neurons? What is another name for these connections? |
1. Excitatory--- glutamate 2. AKA: medium spiny neurons |
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What are the output tracts from the basal ganglia? |
1. GPi---- major 2. SNr |
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What is the nature of the output from the basal ganglia? What is the target? |
1. Inhibitory 2. Target=thalamus |
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What is the basal ganglia direct pathway? |
1. Medium spiny neurons in putamen project to GPi (direct) 2. Medium spiny neurons from indirect pathway project to GPe (indirect)
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What is the nature of the activity of the medium spiny neurons in the basal ganglia pathways? |
1. Inhibitory--- reduces activity of GPi and GPe |
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To where do GPe neurons project? |
1. GABA connections to GPi and STN |
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What is the function of the connection between the GPe and STN? |
1. Inhibitory control for excitatory input from STN to GPi |
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From where does the STN receive excitatory input? |
1. Motor cortex |
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What is the nature of the output from the GPi? |
1. Inhibitory--- inhibition of activity of thalamic neurons 2. Reduces activity of cortical neurons |
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What do the SNc and VTA provide for the striatum? |
1. SNc-- dopamine for motor areas 2. VTA--- dopamine for non-motor areas |
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What do the dopamine connections target in the striatum? What receptors do they express? |
1. Medium spiny neurons in putamen 2. Direct pathway-- D1--- excited by dopamine 3. Indirect pathway-- D2--- inhibited by dopamine |
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What happens when D1 receptors are activated? |
1. Inhibition of GPi increased 2. Movement increased |
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What happens when D2 receptors are activated? |
1. Inhibition of GPe decreased 2. Inhibition of STN increased 3. Excitation of GPi reduced 4. Movement enhanced |
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How does ACh modulate the direct/indirect pathways? |
1. ACh released from interneurons in striatum 2. Interneurons are inhibited by dopamine released from SNc |
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How are ACh, dopamine, and Parkinson's related? |
1. Loss of dopamine from SNc leads to an increase in ACh release from interneurons 2. Increase in ACh leads to increased activity in indirect pathway 3. GPi activity increased |
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What are the MC disorders associated with basal ganglia dysfunction? |
1. Parkinson's 2. Chorea 3. Hemiballism |
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What is the hypothesized cause of bradykinesia in Parkinson's? |
1. Output form GPi increased to conserve energy |
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What leads to "forgetting" motor skills in Parkinson's? |
1. Destruction of GPi |
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What is the cause of PD? |
1. Progressive loss of dopamine from SNc 2. Dopamine reduced in striatum 3. Direct pathway decreased (less activation) 4. Indirect pathway increased (less inhibition)
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What is the effect of increased GPi activity in PD? |
1. Suppress thalamic neuronal activity and thus cortical activity |
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What leads to the tremor in PD? |
1. Burst of basal ganglia activity |
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What is the surgical tx for PD? |
1. Pallidotomy--- destruction of GPi 2. STN destruction--- reduces GPi output |
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What is the use of deep-brain stimulation in PD? Why is it preferred over surgery? |
1. Electrodes implanted into GPi or STN 2. Under constant stimulation 3. Preferred over surgery due to reversibility and adjustability |
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What leads to chorea in Huntington's? |
1. Preferential loss of medium spiny neurons from indirect pathway 2. Induces inhibition of GPe (less GABA)---- strong suppression of GPi and STN--- reduces excitatory input to GPi |
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What causes hemiballism? |
1. Loss of STN neurons due to highly localized stroke 2. Removes primary excitatory signal to GPi 3. Reduces excitatory input to GPi 4. GABA inhibition in thalamus and corticla motor areas reduced |
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What causes drug-induced dyskinesia? |
1. Anti-psychotic drugs that block dopamine D2 receptors 2. Dopamine receptors supersensitive due to upregulation |
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What is astasia-abasia? MCC? Ssx? |
1. Astasia-- results from inability to maintain body posture 2. Abasia-- results form an inability to use the antigravity muscles to remain upright 3. Ssx: wide stance |
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What causes ataxia? |
1. Spinocerebellum can't error correct/time movements 2. Dysdiadochokinesia--- cannot maintain regular rhythmic movements 3. Cannot stop momentum |
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What leads to decorticate posturing? |
1. Lesions at or above midbrain block medullary or pontine reticular formation 2. Rubrospinal tract undamaged 3. Tonically active neurons activate axial and lower limb extensors with opposition 4. Red nucleus overactive---- hyper-flexion of upper limbs |
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What leads to decerebrate posturing? |
1. Lesions at level of pons-- block input to medullary and pontine reticular formation 2. Damages rubrospinal tract-- no flexors 3. Tonically active extensors are unopposed
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