Brain And Behavior 2011-Cerebellum

Front 1

lenticular nucleus

Back 1

putamen and globus pallidus

Front 2

striatum inputs

Back 2

caudate is more rostral, and thus recieves input from cortical association areas (premotor cortex, supplementary motor area); putamen is more caudal, and thus recieves input from motor cortex

Front 3

internal capsule separates...

Back 3

anterior limb separates caudate from lenticular nucleus; posterior limb separates thalamus from lenticular nucleus

Front 4

direct pathway

Back 4

cortex -> striatum -| GPi and SNr -| thalamus -> cortex ---- i.e. cortex excites striatum which inhibits GPi and SNr which, in response, lower their inhibition of the thalamus and allow excitation of the cortex --- excitation of the cortex ultimately causes excitation of the cortex through the direct pathway

Front 5

indirect pathway

Back 5

cortex -> striatum -| GPe -| STN -> GPi/SNr -| thalamus -> cortex --- i.e. cortex excites striatum which inhibits GPe which, in response, lowers its inhibition of STN, which is then allowed to excite GPi and SNr more so they can inhibit the thalamus and thus prevent cortical excitation --- excitation of the cortex ultimately causes inhibition of the cortex through the indirect pathway

Front 6

substantia nigra pars compacta

Back 6

excites striatum in direct pathway (same as cortical input - facilitates direct pathway and excitation of thalamus as result) and inhibits striatum in indirect pathway (opp of cortical input - prevent indirect pathway and inhibition of thalamus as a result) --- as a result, ALWAYS facilitates movement; acts via dopamine; damaged in PD

Front 7

GPe is part of which pathway; input and output; is it excited or inhibited when cortex excites striatum?

Back 7

indirect; inhibited by striatum, functions to inhibit STN; is inhibited when cortex excites striatum

Front 8

STN is part of which pathway; input and output; is it excited or inhibited when cortex excites striatum?

Back 8

indirect; inhibited by GPe, functions to excite GPi/SNr; is excited when cortex excited striatum

Front 9

GPi is part of which pathway; input and output; is it excited or inhibited when cortex excites striatum?

Back 9

both direct and indirect, inhibited by striatum (direct) and excited by STN (indirect), acts to inhibit thalamus, is inhibited through direct pathway and excited through indirect pathway when cortex excites striatum

Front 10

SNr is part of which pathway; input and output; is it excited or inhibited when cortex excites striatum?

Back 10

both direct and indirect, inhibited by striatum (direct) and excited by STN (indirect), acts to inhibit thalamus, is inhibited through direct pathway and excited through indirect pathway when cortex excites striatum

Front 11

thalamus is part of which pathway; input and output; is it excited or inhibited when cortex excites striatum?

Back 11

both direct and indirect, inhibited by GPi/SNr, acts to excite cortex, is excited through direct pathway and inhibited through indirect pathway when cortex excites striatum

Front 12

medial to lateral anatomy of basal ganglia

Back 12

3rd ventricle -> caudate (anterior) or thalamus (posterior) -> internal capsule -> GPi -> GPe -> putamen -> external capsule -> calustrum (grey matter) -> extreme capsule -> insular cortex

Front 13

substantia nigra location

Back 13

ventral midbrain, just dorsal to cerebral peduncles and ventral to red nucleus (black in unstained sections)

Front 14

STN location

Back 14

ventromedial to GP, rostral and lateral to SN

Front 15

basal ganglia output

Back 15

frontal lobe: motor circuits project to motor, premotor, and supplementary motor areas and frontal eye fields; emotion circuits output to cingulate and orbitofrontal gyri; also outputs to prefrontal association cortex (unknown function)

Front 16

purpose of direct vs indirect pathway

Back 16

direct: initiation of movement, learning of positive outcomes; indirect: termination of movement, learning of negative outcomes

Front 17

Lewy bodies

Back 17

accumulation of alpha-synuclein into cytoplasmic aggregates (in Lewy body dementia and PD)

Front 18

PD motor features (4)

Back 18

bradykinesia, rigidity, resting tremor (asymmetric), stooped and unstable posture

Front 19

PD non-motor features (5)

Back 19

psychiatric symptoms (depression, anxiety, dementia, hallucinations, psychosis, apathy); sleep disorders (restless leg syndrome, REM behavior disorder); autonomic dysfunction (orthostatic hypertension, bladder dysfunction, constipation, drooling, impotence); sensory symptoms (olfactory dysfunction, pain, impaired color discrimination, tingling); miscellaneous (fatigue, double vision, skin changes)

Front 20

DBS in PD

Back 20

inactivate STN or GPi/SNr to stop thalamic inhibition

Front 21

Huntington's etiology

Back 21

autosomal dominant; loss of medium spiny GABAergic neurons of striatum -> causes loss of indirect pathway (striatum cannot inhibit GPe)

Front 22

PD etiology

Back 22

accumulation in Lew bodies causes dopamergic neuron death

Front 23

Huntington's symptoms

Back 23

chorea, athetosis, mental decline, personality changes

Front 24

striate neurotransmitters

Back 24

majority medium spiny GABAergic neurons (to inhibit GPe in indirect pathway or GPi/SNr in direct pathway) while 5% ACh large spiny interneurons (act to inhibit thalamus by favoring indirect pathway and inhibiting direct pathway)

Front 25

ACh in striate

Back 25

facilitates transmission through indirect pathway via excitatory M1 receptors, diminishes transmission through direct pathway via inhibitory M4 receptors -> in both cases, inhibits thalamus and thus cortex (opposite of DA in SNc)

Front 26

substantia nigra parts

Back 26

pars reticularis is like GPi -> inhibited by striatum (direct) and excited by STN (indirect), acts to inhibit thalamus; pars compacta is dopamergic and acts to excite thalamus by favoring direct pathway and inhibiting indirect pathway

Front 27

globus pallidus parts

Back 27

externa is part of indirect pathway (inhibited by striatum, functions to inhibit STN) while interna is like SNr (inhibited by striatum (direct) and excited by STN (indirect), acts to inhibit thalamus)

Front 28

excitatory transmission in basal ganglia

Back 28

Ach used by striate to facilitate indirect pathway (via excitatory M1 receptors); glutamate used by STN to excite GPi/SNr, DA used by SNc to excite striatum in direct pathway

Front 29

M1 vs M4 receptors

Back 29

both muscarinic ACh receptors; M1 is excitatory and used to facilitate indirect pathway while M4 is inhibitory and used to inhibit direct pathway

Front 30

dopamine brain pathways (4 and main disease/feature)

Back 30

mesocortical: ventral tegmental area -> cortex (schizophrenia); mesolimbic: ventral tegmental area -> limbic structures (reward); nigrostrial: SNc -> striatum (PD); tuberoinfundibular pathway: hypothalamus -> pituitary (prolactin)

Front 31

dopamine receptors

Back 31

D1 and D2 used in SNc -> striate synapse; D1 is excitatory and used to facilitate direct pathway while D2 is inhibitory and used to inhibit indirect pathway

Front 32

L-dopa must be administered with

Back 32

peripheral inhibitors of DDC (carbidopa and benserazide) - prevent peripheral breakdown of L-dopa to DA (and thus side-effects) but don't cross blood-brain barrier so L-dopa can be converted to DA in brain

Front 33

L-dopa side effects (4)

Back 33

peripheral conversion to DA (-> nausea, orthostatic hypertension); central stimulation of non-striatal DA receptors (-> hallucinations, disrupted sleep)

Front 34

PD medications

Back 34

L-dopa with DDC inhibitors; DA receptor agonists; blockage of DA metabolism (MAO-B inhibitors, COMT inhibitors); muscarinic cholinergic antagonists (ACh opposes DA in basal ganglia), inactivate GPi or STN via deep brain stimulation

Front 35

PD vs ET

Back 35

PD: asymmetrical, rest tremor, bradykinesia and facial masking, cogwheel rigity, micrographia, shuffling gait; ET: symmetric, action/postural tremor, no bradykinesia not facial masking, no rigidity, shaky-graphia, normal gait, family history in 50%

Front 36

Chorea

Back 36

Irregular, random, abrupt, flowing movement NEWLINE Hereditary - Huntington's, Spinocerebellar ataxia, neuroacanthocytosis NEWLINE Secondary - Hyperthyroid, stroke, SLE, acute renal failure, drugs

Front 37

Athetosis

Back 37

Low amplitude chorea - affects distal muscles (slow, writhing movements)

Front 38

Ballismus

Back 38

High amplitude chorea - affects proxmial muscles

Front 39

Hemiballismus

Back 39

Unilateral High amplitude chorea - affects proximal muscles NEWLINE Usually due to structural lesions - STN

Front 40

Myoclonus

Back 40

Irregular shock-like movements (physiologic - when falling asleep) NEWLINE Fast and slow phase NEWLINE Hereditary - Essential Tremor, epileptic, degenerative NEWLINE Secondary - Metabolic, drugs, lesions (spinal cord lesion leads to segmental myoclonus), degenerative (CJD, CBD) NEWLINE Toxic Metabolic Myoclonus - worsens w/ attempted action

Front 41

Tic

Back 41

Abrupt, brief, stereotyped movement NEWLINE Partial voluntary control - can be temporarily suppressed NEWLINE Motor and vocal

Front 42

Dystonia

Back 42

Sustained muscle contractions w/ twisitng posutres NEWLINE Repetitive movements w/ fixed posture

Front 43

Tourette's

Back 43

motor and vocal tic