S2 Neuro Exam 4: Basal Ganglia

Front 1

Where are the basal ganglia located?

Back 1

located w/i white matter if cerebral hemispheres

Front 2

Obj.
the components of the basal nuclei & associated nuclei

Back 2

Basal nuclei:
caudate nucleus
putamen
nucleus accumbens
ventral striatum
globus pallidus
ventral pallidum
Associated nuclei:
subthalamic nucleus
nigral complex
pedunculopontine tegmental nucleus

Front 3

What does the term basal ganglia refer to?

Back 3

telencephalic gray matter, collection of subcortical nuclei, made up of 2 complexes;
-striatal complex:
caudate & putamen (dorsal)
nucleus accumbens & ventral striatum (ventral)
-pallidal complex:
globus pallidus (dorsal)
ventral pallidum (ventral)

Front 4

What does the term Dorsal striatal complex (neostriatum) refer to?


Ventral striatal complex?

Back 4

Caudate & putamen


nucleus accumbens (NA), ventral striatum, & olfactory tubercle, islands of calleja

Front 5

What does the term dorsal pallidum refer to?

ventral pallidum?

Back 5

Globus pallidus

Ventral extension of globus pallidus below anterior commissure

Front 6

What does the term lenticular nuclei refer to?

Back 6

Putamen and globus pallidus

Front 7

What is the caudate?

Back 7

An elongated C-shaped nucleus that is composed of head, body, and tail.
-Head: bulges into lateral aspect of frontal horn of lateral ventricle
-Body/tail: continue posteriorly, then inferiorly, then anteriorly maintaining a lateral relationship to body and temporal horn of lateral ventricle
-Tail of the caudate ends at the amygdala

Front 8

What is the putamen?

Back 8

Largest and most lateral part of the striatum, lying between external capsule and external segment of globus pallidus.
-Microscopicallly, caudate and putamen are identical
-Rostrally, putamen is continuous with head of caudate

Front 9

What is the globus pallidus?

Back 9

Composed of external(lateral) and internal (medial) segments that are separated by thin internal medullary lamina.
-Many bundles of myelinated fibers give it a paler appearance

Front 10

The nigral complex is made up of the substantia nigra & ventral tegmental area.

What is the substantia nigra?

Back 10

Largest nuclear mass in midbrain. Located anteriorly and extends length of midbrain into caudal diencephalon.
-2 parts: pars compacta (dorsal, cell-rich that contain melanin pigment (from dopamine oxidation) giving SN its black appearance) and pars reticulata (ventral, similar to internal segment of globus pallidus).

Front 11

Obj.
the vessels that supply the basal nuclei

Back 11

*ALL from internal carotid
medial striate artery (blue, from anterior cerebral, A2)

lenticulostriate artery (yellow, from middle cerebral, M1)

anterior choroidal (green)

Front 12

Which artery supplies the following?
Globus Pallidus
Body of caudate nucleus
Most of putamen
Most of anterior capsule

Back 12

Lenticulostriate Arteries

Front 13

Which artery supplies the following?
Ventral Striatal complex (Nucleus accumbens, etc)
Head of caudate nucleus
anterior limb of internal capsule

Back 13

Medial striate artery

Front 14

Which artery supplies the following?
Tail of caudate nucleus
Ventral posterior limb of internal capsule

Back 14

Anterior choroidal artery

Front 15

Obj.
Major Inputs to basal nuclei

Back 15

*arrive via STRATIUM (putamen, caudate, ventral accumbens)

main input from- cerebral cortex
(some from substantia nigra (compacta) & VTA

Front 16

Obj.
Major outputs to basal nuclei

Back 16

*leave via PALLIDUM (globus pallidus internal, substantia nigra (reticulata), & ventral pallidum)

main output to- thalamus (then goes to cortex)
(some to PPTN & superior colliculus via substantia nigra)

Front 17

4 main functions of basal ganglia

Back 17

general motor control (planning & execution)
eye movements (oculomotor)
cognitive functions (prefrontal)
emotions functions (limbic)

Front 18

Obj.
the function of four parallel channels through the basal nuclei

Back 18

1. motor- cortical & brainstem (PPTN) control of body movements & posture
2. oculomotor- cortical & brainstem control of eye movements
3. prefrontal- cognitive control of behavior (memory, etc)
4. reward system, control of biological drives (sex, food)

Front 19

Obj,
the direct and indirect pathway between striatum and outputs and, their influence on movement

Back 19

direct: stratium--> Globus Pallidus Internal (GPi)--> Substantia Nigra Pars Reticularis (SNpr)--> Ventral Pallidum--> Thalamus-->Briainstem

indirect: stratium-->Globus Pallidus external (GPe)*--> Subthalmus*--> SNpr--> Ventral Pallidum--> Thalamus--> Brainstem

Front 20

Obj.
main tracts that carry information in basal nuclei

Back 20

Internal capsule- Corticofugal & Thalamocortical

Thalamic fasiculus- Lenticular fasiculus & Ansa Lenticularis

Subthalamic fasciculus- Pallidosubthalamic & Subthalmopallidal

Front 21

Differentiate btwn the 2 parts of the thalamic fasciculus (lenticular & ansa)

Back 21

*both carry afferents from the GPi to the thalamus*
= Pallidothalamic

Lenticular fasciculus- fibers from medial GPi, travel dorsally THROUGH the internal capsule

Ansa Lenticularis- fibers from lateral GPi, travel ventrally UNDER the internal capsule

Front 22

Obj.
main neurotransmitters of basal nuclei & associated nuclei

Back 22

Stratum:
main inhibitory: GABA
direct- Substance P*
indirect- Enkephalin*
excitatory interneuron: ACh*

Pallidum:
Main inhibitory: GABA

Associated:
subthalamic- excitatory- glutamate
SNpc & VTA- excitatory/inhibitory- dopamine*
SNpr- inhibitory- GABA
PPTN- inhibitory-ACh*
Cortex/Thalamus- excitatory- Glutamate

Front 23

Glutamate is always an activator, while GABA is always an inhibitor, which 2 NTs can be both?

Back 23

Dopamine & Acetylcholine


(substance P & enkephalin are modulators)

Front 24

What is disinhibition?

Back 24

Inhibition of an inhibitor, leading to activation

Front 25

NTs that are in the Direct pathway ultimately lead to.......

Back 25

Increase in cortex (thalamus) activity
= facilitation of movement & suppression of postural reflexes (via disinhibition)

*ACTIVATES PPTN & superior colliculus

Front 26

NTs that are in the Indirect pathway ultimately lead to..........

Back 26

Decrease cortex (thalamus) actvity
= inhibits movement

*INHIBITS PPTN & superior colliculus

Front 27

Acetylcholine & dopamine play a cooperative role in what?

Back 27

habit learning (relative to movement behaviors)



Note: basal nuclei do NOT directly initiate movement

Front 28

Obj.
the role of acetylcholine on basal nuclei function

Back 28

excitatory in BOTH pathways


(when dopamine is high favors direct, when low favor indirect)

Front 29

Obj.
the role of dopamine on basal nuclei function

Back 29

activates direct pathway (via D1)

inhibits the indirect pathway (via D2)

= facilitates movement

Front 30

Obj.
how dysfunction of basal nuclei lead to hypokinetic or hyperkinetic disorders

Back 30

hyperkinetic:
overactivity of direct pathway
underactivity of indirect pathway

hypokinetic:
underactivity of direct pathway
overactivity of indirect pathway

Front 31

What are hyperkinetic disorders characterized by?


hypokinetic?

Back 31

Too much movement, decreased postural reflexes
(Huntington's, Hemiballismus)

Difficult slow movement, increased postural reflexes= rigidity
(Parkinsons)

Front 32

What does parkinsonism symptoms and signs results from?

Back 32

loss of dopamine from deterioration of substantia nigra pars compacts (VTA)

Front 33

Parkinson's disease
symptoms

Back 33

-lewdy bodies (cytoplasmic inclusions)
-loss of dopaminergic neurons in substantia nigra
-major motor symptoms:
tremor at rest
cogwheel rigidity
bradykinesia/akinesia (loss of movement)
postural instability
-non-motor symptoms:
dementia
procedural memory loss
executive dysfuction (attention etc)
mood, sleep, sensory, autonomic disturbances

Front 34

Describe the mechanism of Parkinson's disease

Back 34

loss of dopamine (DA)-->
DA activation via D1 is lost-->direct pathway becomes underactive= reduced activity of spinal motor neurons/less movement (akinesia)

DA inhibition via D2 is lost-->indirect pathway becomes more overactive= increased inhibition of PPTN neurons/ disinhibition of postural spinal reflexes (rigidity)

Front 35

What causes Parkinson's tremors?

What makes them better/ worse?

Back 35

overactive subthalamus


better(dampens)= DA
worse= Ach

Front 36

What is the mesocortical (prefrontal circuit) affect of loss of dopamine?

Back 36

memory loss, dementia, reduced executive funtion

Front 37

What is the mesolimbic (limbic circuit) affect of loss of dopamine?

Back 37

mood disorders

Front 38

Parkinson's treatments:

Back 38

1. Increase dopamine (L-dopa, agonist, MAOI)
2. Decrease ACh (reduce activity of indirect pathway)
3. Surgical lesion of GP or VL thalamus
4. Deep brain (electrical) stimulation of GP, VL, STN

Front 39

What is Huntington Disease (Chorea) caused by?

Back 39

genetic mutation (htt) w/ 100% penetrance
(autosomal dominant)--> glutamate excitotoxicity

leads to loss of caudate & putamen cholinergic neurons--> loss of Ach interneurons

Front 40

Obj.
Huntington's disease
Symptoms & treatments

Back 40

symptoms:
early stage- absentminded, irritable, depressed, clumsy, falls
late stage- bedridden, dementia, loss of speech & cognition--> death

treatments: none

Front 41

Describe the mechanism of Huntington's disease

Back 41

loss of GABA, ENK, & Ach-->
underactivity of indirect pathway (GABA/ENK)-->
excessive & involuntary movement (chorea) & decreased postural reflexes-->
eventual underactivity of direct pathway (GABA/SP)-->
akinesia & rigidity

Front 42

Disruption of the prefrontal & limbic channels from Huntingtons leads to what affects?

Back 42

prefrontal- loss of cognition & memory, dementia

limbic- irritability, depression

Front 43

What is hemiballismus?

Back 43

movement disorder
-Most often seen with lesion of the contralateral subthalamic nucleus
-decreased GPi & SNpr (indirect) activity--> increased thalamic-cortex & PPTN activity

Front 44

Hemiballismus
symptoms & treatments

Back 44

symptoms:
Sudden, involuntary, often violent, flinging movement of one or both extremities of one side.

treatments:
dopamine blockers (reduce direct pathway)
lesions or stimulation of globus pallidus