Neuro Basal Ganglia Ssom Keifer 4/22/10

Front 1

Basal Ganglia
(group of _ nuclei,
general function is _)

Back 1

subcortical brain nuclei
generation and control of voluntary movements:
internal generation of movement
automatic execution of motor plans and
to some degree the acquisition and retention of learned motor skills

Front 2

Basal Ganglia
(name all components)

Back 2

striatum (caudate + putamen)
pallidum (globus pallidus)
substantia nigra
amygdala
subthalamic nucleus

Front 3

Basal Ganglia
(dysfunction notable in what 2 diseases)

Back 3

Parkinson's disease
Huntington's disease

Front 4

Striatal connections
(major input from what structures)

Back 4

major inputs to caudate and putamen from:
cerebral cortex
intralaminar thalamic nuclei
substantia nigra

Front 5

Striatal connections
Major inputs
(name fibers)

Back 5

Corticostriate fibers
Thalamostriate fibers
Nigrostriatal fibers

Front 6

Striatal inputs
Corticostriate fibers
(input originate from)

Back 6

widespread regions of neocortex that terminate in mosaic pattern of patches or clusters
inputs from widely separate cortical areas are overlapping
somatosensory and motor are somatotopically organized

Front 7

Striatal inputs
Corticostriate fibers
(excitatory and/or inhib?, NT)

Back 7

excitatory
glutamate

Front 8

Striatal inputs
Thalamostriate fibers
(inputs originate from)

Back 8

intralaminar nuclei of thalamus and project to caudate and putamen

Front 9

Striatal inputs
Thalamostriate fibers
(excite and/or inhib?)

Back 9

excitatory

Front 10

Striatal inputs
Nigrostriatal fibers
(inputs originate from)

Back 10

substantia nigra pars compacta (SNc)
both caudate and putamen receive these inputs

Front 11

Striatal inputs
Nigrostriatal fibers
(pathway important for?,
disease correlation)

Back 11

important afferent input conveying dopamine (DA) to the striatum
striatum is deprived of DA in Parkinson's

Front 12

Striatal inputs
Nigrostriatal fibers
(excite and/or inhib?)

Back 12

dopamine has both excite and inhit actions on striatal neurons

Front 13

Striatal outputs
(outputs to what structures)

Back 13

globus pallidus
substantia nigra pars reticulata (SNr)

Front 14

Striatal outputs
(name fibers)

Back 14

Striatonigral fibers
Striatopallidal fibers

Front 15

Striatal outputs
Striatonigral fibers
(project from _ to _)

Back 15

striatum to SNr
(caudate projects to rostral part of SNr, putamen projects to more caudal parts)

Front 16

Striatal outputs
Striatonigral fibers
(excite/inhib?, NT)

Back 16

inhib
GABA

Front 17

Striatal outputs
Striatopallidal fibers
(project to)

Back 17

massive fiber system projects to:
GPi
GPe

Front 18

Striatal outputs
Striatopallidal fibers
(NTs, disease correlation)

Back 18

GABA
enkephalin to GPe
substance P to GPi
signif reductions in enkephalin and substance P in the GP in patients with Huntington's

Front 19

GP
(physical appearance and why?)

Back 19

paler appearance than putamen in fresh tissue
bundles of myelinated fibers traverse it
(globus pallidus means "pale globe")

Front 20

GP
(divisions, NT)

Back 20

GPi (internal division)
GPe (external division)
GP mainly GABAergic

Front 21

GP
(major inputs from what structures)

Back 21

striatum: (striatopallidal fibers are principal afferents)
subthalamic nucleus

Front 22

Does the GP receive inputs from the cerebral cortex?

Back 22

NO NO NO
Unlike the striatum, the GP does NOT NOT NOT receive afferents from the cerebral cortex

Front 23

Does the GP receive inputs from the thalamus?

Back 23

NO NO NO
Unlike the striatum, the GP does NOT NOT NOT receive afferents from the thalamus
(subthalamus is NOT part of thalamus)

Front 24

GP
Other inputs

Back 24

receives dense DA projections from SNc

Front 25

GP inputs
Striatopallidal fibers
(projection, NT, disease correlation)

Back 25

Striatum to GPi and GPe
GABA
enkephalin to GPe
substance P to GPi
signif reductions in enkephalin and substance P in GP in Huntington's

Front 26

GP inputs
Subthalamopallidal fibers
(project to, excite and/or inhib?)

Back 26

project to:
GPe
GPi
excitatory

Front 27

Major GP outputs
GPi projects to _ _

Back 27

thalamus
pedunculopontine nucleus

Front 28

Major GP outputs
GPe projects to _

Back 28

subthalamic nucleus

Front 29

Major GP outputs
(name the 4 efferent pathways from pallidum)

Back 29

Ansa lenticularis
Lenticular fasciculus
Pallidotegmental fibers
Pallidosubthalamic projection

Front 30

Efferent pathways from GP
Initial pathways taken on way to thalamus

Back 30

Ansa lenticularis
Lenticular fasciculus
(output fibers initially take one of these two pathways from GPi either thru or around the internal capsule on the way to the thalamus

Front 31

Efferent pathways from GP
How to thalamus?

Back 31

from GPi
thru or around internal capsule using either:
ansa lenticularis or lenticular fasciculus
They come together as thalamic fasciculus and
project to ventral thalamus
(thus, GP linked to motor cortex)

Front 32

Efferent pathways from pallidum
Pallidotegmental fibers
(from _ to _)

Back 32

from GPi descend and terminate in
pedunculopontine nucleus (PPN) of brainstem

Front 33

Efferent pathways from pallidum
Pallidotegmental fibers
(feedback connection,
excite and or inhib, NT)

Back 33

PPN provides feedback to GPi
excite
ACh

Front 34

Efferent pathways from pallidum
Pallidosubthalamic projection
(projection from _ to _ via _)

Back 34

GPe to subthalamic nucleus
via subthalamic fasciculus

Front 35

Subthalamic Nucleus
(major inputs from)

Back 35

GPe
cerebral cortex (particularly frontal lobe)

Front 36

Subthalamic Nucleus
(major outputs)

Back 36

are excitatory connections
back to GPe and to
GPi and SNr

Front 37

Ventral Thalamus (VA, VLo)
(input from)

Back 37

GPi
SNr

Front 38

Ventral Thalamus (VA, VLo)
(project reciprocally to)

Back 38

cerebral cortex (excitatory)
striatum

Front 39

Functional organization of BG
(organization
each circuit engages separate regions of _ _ _,
output of each circuit centered on _)

Back 39

organized in parallel but remain segregated in structure and function
each circuit engages separate regions of BG, thalamus, cortex
output of each centered on different part of frontal lobe

Front 40

Functional Organization of BG
(how many circuits (loops))

Back 40

At least 5 basal ganglia-thalamocortical circuits (loops)

Front 41

Name 5 basal ganglia-thalamocortical circuits (loops)

Back 41

"Motor" circuit
"Oculomotor" circuit (links cortical eye fields to BG)
2 "Prefrontal" circuits
"Limbic" circuit (links ant cingulate and medial orbitofrontal cortex to BG)
**Organization suggests a functional specificity of info processing in BG**

Front 42

Functional Organization of BG
(organization suggests _)

Back 42

functional specificity of info processing in the BG

Front 43

"Motor" Circuit
(strongly implicated in pathophys of _)

Back 43

movement disorders

Front 44

"Motor" Circuit
(putamen receives somatotopic projections from)

Back 44

primary motor cortex and from
premotor areas including
supplementary motor area (M2)
also from somatosensory cortex
(motor and sensory somatotopic maps are in register such that "arm" regions of putamen receive input from "arm" regions of motor and somatosensory cortex)

Front 45

"Motor" Circuit
(putamen projects somatotopically to specific regions of _ _ _,
these regions then send projections to specific nuclei in _,
this motor loop completed by _ projections back to _ _ _)

Back 45

GPe
GPi
SNr

ventral thalamus

motor loop completed by
thalamocortical projections back to:
primary motor cx
premotor cx
supplementary motor cx

Front 46

"Motor" Circuit
(There are _ and _ pathways)

Back 46

"direct"
"indirect"

Front 47

"Motor" Circuit
"Direct" pathway
(primary function)

Back 47

facilitate movement by allowing
disinhibition of the thalamocortical neurons by
GPi/SNr

Front 48

"Motor" Circuit
"Indirect" pathway
(role)

Back 48

inhibit movement by increasing the
inhibition of thalamocortical neurons

Front 49

"Motor" Circuit
"Direct" and "Indirect" pathways
(how the two pathways are differentially affected is thought to lead to _ and _)

Back 49

hypokinetic and
hyperkinetic
movement disorders

Front 50

Pathophys Model of Parkinson's based on Motor circuit
It is thought that the direct and indirect pathways are differently affected by dopamine loss
direct pathway becomes _ resulting in _
indirect pathway becomes _ resulting in _
Overall result is _

Back 50

direct pathway:
**underactive**
resulting in reduced disinhibition and increased inhib of thalamocortical neurons

Indirect:
**overactive**
resulting in increased inhib of thalamocortical neurons

Overall result is increased activity in GPi and increased inhibition to ventral thalamus

Front 51

Parkinson's
(Overall result of direct pathway underactive and
indirect pathway overactive,
this is thought to cause _ _ _ which are associated with the disease,
Which nucleus plays a key role and why)

Back 51

overall result is increased activity in GPi and
increased inhib to ventral thalamus

akinesia
rigidity
tremor

subthalamic nucleus b/c
symptoms ameliorated by blockage of activity or stimulation of this nucleus

Front 52

Disorders of BG
(spectrum of movement abnormalities ranging from _ to _, give an example of each)

Back 52

hypokinetic (Parkinson's) to
hyperkinetic (Huntington's)

Front 53

Hypokinetic disorders
(characterized by _ _)

Back 53

akinesia = absence of movement
bradykinesia = slowness of voluntary movements

Front 54

Hypokinetic disorders
(2 symptoms are _ _)

Back 54

***resting tremor***
muscle rigidity

Front 55

Hyperkinetic disorders
(characterized by _)

Back 55

dyskinesia = excessive involuntary motor activity

Front 56

Types of Dyskinesia
(associated with lesions of _)

Back 56

corpus striatum

Front 57

Types of Dyskinesia
(name)

Back 57

tremor
athetosis
chorea
ballismus

Front 58

Dyskinesias
Tremor
(what, involves what body parts in Parkinson's and occurs at _)

Back 58

most common form
rhythmical involuntary movement

Parkinson's:
involves primarily the digits, hands, head, lips
occurs at rest at 4-8 Hz

Front 59

Dyskinesias
Athetosis
(what)

Back 59

slow, twisting movements involving limbs, face, or trunk
movements blend together into continuous spasm

Front 60

Dyskinesias
Chorea
(what, seen in what disease)

Back 60

(means dance)
brisk series of successive involuntary movements that resemble fragments of purposeful voluntary movement
often involve distal extremities, muscles of facial expression and tongue
example is Huntington's disease (chorea)

Front 61

Huntington's disease

Back 61

inherited
adult-onset
progressive
involves choreiform activity of the face and hands and eventually severe behavioral disturbances with dementia
patient's generally die about 15 years after onset
genetic screening available

Front 62

Dyskinesias
Ballismus
(what, most common type, *usually associated with discrete lesions of _, side affected*)

Back 62

violent forceful flinging movement of the arms or legs caused by contractions of the proximal muscles
the most violent form of dyskinesia
**hemiballismus** is the most common
***usually associated with discrete lesions of subthalamic nucleus or its connections
effects are contralateral***

Front 63

Ballismus
(usually associate with _, side affected)

Back 63

***usually associated with discrete lesions of subthalamic nucleus or its connections
effects contralateral

Front 64

Parkinson's Disease
(a _ disorder, *caused by _)

Back 64

hypokinetic disorder

caused by:
loss of dopamine containing neurons in SNc (pars compacta of SN)

Front 65

Parkinson's Disease
(symptoms)

Back 65

mask-like face
infrequent eyeblinks
slow dysarthric speech
stooped posture
slow shuffling gait
loss of associated movements like swinging the arms during walking
slowness and general poverty of movement
4-8 Hz resting tremor

Front 66

Parkinson's Disease
levodopa
(aka, positive effects, problems, does not stop _, current research)

Back 66

L-dopa, a precursor to DA
exerts antirigidity and antikinesia

Problems:
large amounts = choreiform movements
L-dopa effects only transitory

does not stop cell death (the cause of the disease)

neural tissue transplants

Front 67

MPTA story

Back 67

accidentally formed in illegal drug lab
individuals on it showed classic signs Parkinson's
found to induce pathological hallmark of Parkinson's - loss of DA containing SNc neurons
provided the much-needed animal model

Front 68

Neurosurgical approaches to treating Parkinson's disease
(name 2)

Back 68

Ablative
Deep brain stimulation (DBS)

Front 69

Neurosurgical approaches to treating Parkinson's Disease
Ablative
(types)

Back 69

thalamotomy (not common)
pallidotomy (most common)

Front 70

Neurosurgical approaches to treating Parkinson's Disease
DBS
(what do they stimulate)

Back 70

thalamic (Vim)
GPi
subthalamic nucleus (most common)

Front 71

Treatment of choice for Parkinson's

Back 71

DBS but pallidotomy continues to be performed worldwide

Front 72

DBS
(long term _ benefits,
decline in _)

Back 72

long term motor benefits

decline in:
oral and visuomotor info processing
verbal fluency
verbal recognition memory