Basal Ganglia And Cerebellum

Front 1

functions of cerebellum

Back 1

serve as a filter system for sensory input to other areas of brain
filter inputs from visual, auditory, proprioceptive, pain, touch, taste
receives and modifies cardiovascular respiratory inputs

Front 2

where does the cerebellum lie?

Back 2

posterior fossa
below occipital cortex
under tentorium, falx cerebelli

Front 3

part of what developmental structure?

Back 3

metencephalon
above 4th ventricle
dorsal to pons and medulla

Front 4

how many lobules in cerebellum?

Back 4

10

Front 5

what are folia?

Back 5

small gyri

Front 6

cerebellar cortex has how many layers?
what is it made of?

Back 6

3 layers
neurons and fibers

Front 7

cerebellar white matter

Back 7

lies beneath cortex and composed of afferent (incoming) and efferent (outgoing) axons

Front 8

deep cerebellar nuclei

Back 8

lie deep within white matter

Front 9

cerebellum integrates activity of cerebral cortex with brainstem and spinal motor systems to:

Back 9

coordinate movement

Front 10

how many central cerebellar nuclei?

Back 10

4 pairs deep within center of cerebellar white matter
send axons out of cerebellum proper

Front 11

Name the cerebellar nuclei

Back 11

DONT EAT GREASY FOODS
fastigial: near the midline, receives afferents from vermis and sends ouput to vestbular nuclei
interposed noclei: globose and emboliform nuclei
dentate nuclei

vestibular nuclei - displaced deep cerebellar nuclei

Front 12

the cerebellum has roughly the same surface are as a single cerebral hemisphere even though it takes up much less space
cerebellum has an extroadinary number of neurons that rivals rest of brain.
cerebellar neurons esp granule cell make up how much of all neurons in brain?

Back 12

1/2 of all neurons in brain
cerebellum is 10% of total brain

Front 13

PICA infarct will affect

Back 13

lateral medulla
inferior half of cerebellum
inferior vermis

Front 14

AICA infarct will affect

Back 14

inferior (tegmental) lateral pons
middle cerebellar peduncle
strip between PICA and SCA
flocculonodular lobe

Front 15

SCA infarct will affect

Back 15

upper lateral pons
superior cerebellar peduncle
most of the superior half of cerebellar hemisphere
superior vermis
deep cerebellar nuclei

Front 16

what is fatal gastoenteritis?

Back 16

cerebelllar hemorrhage that presents with GI symptoms: nausea, vomiting
quickly lead to upward transtentorial herniation
*dizziness in ER always ask them to walk before sending them home

Front 17

unilateral/ipsilateral ataxis with little or no brainstem signs are most common with what artery infarct?

Back 17

SCA

Front 18

infarction of lateral medulla or pons can cause what symptoms?

Back 18

ataxia (involve cerebellar peduncles)

Front 19

pt with vertigo, nausea, vomiting, horizontal nystagmus, limb ataxia, unsteady gait, headache

Back 19

cerebellar infarcts

Front 20

PICA brainstem signs

Back 20

Decreased pain & temperature on ipsilateral face- trigeminal tract & N,
Decreased pain & temperature on contralateral body- spinothalamic
Ipsilateral Horner’s syndrome- descending sympathetics
Hoarseness, dysphagia- Ambiguus N
Decreased taste ipsilateral-NTS
Ipsilateral ataxia, vertigo, nystagmus, nausea – Inferior peduncle

Front 21

what are the three lobes of cerebellum called?

Back 21

anterior lobe
posterior lobe
flocculonodular lobe

Front 22

where is vermis?

Back 22

midline
worm

Front 23

hemispheres are divided into

Back 23

lateral and intermediate (paravermal) part

Front 24

phylogenetically the oldest lobe
located on anterior (ventral) cerebellum

Back 24

flocculonodular lobe

Front 25

smallest lobe
tucked under cerebrum
subject to degenderation

Back 25

anterior lobe

Front 26

largest lobe
primary fissure separates posterior lobe from anterior lobe

Back 26

posterior lobe

Front 27

intermediate hemisphere
site of herniation

Back 27

tonsil

Front 28

what are the three layers of cerebellar cortex?

Back 28

molecular layer - outermost, composed of few neurons but many fibers
Purkinje layer - middle
Granular layer - innermost

Front 29

molecular layer

Back 29

contains dendrites of Purkinje neurons
stellate and basket inhibitory interneurons
parallel fibers

Front 30

purkinje layer

Back 30

monolayer composed only of Purkinje cell bodies
lie in a single row

Front 31

granular layer

Back 31

high density neurons reside here

Front 32

parallel fibers

Back 32

run parallel to long axis of folia after bifurcating into molecular layer to innervate dendrites of Purkinje cells
dendrites of Purkinje cells run perpendicular to the parallel fibers

Front 33

what are the sole output of the cerebellar cortex?

Back 33

Purkinje cells

Front 34

axons of Purkinje neurons run in underlying white matter and provide an inhibitory input via what to neurons in what nuclei?

Back 34

GABA
cerebellar nuclei
vestibular nuclei in brainstem

Front 35

neurons of deep cerebellar nuclei provide output of cerebellum and is predominantly excitatory or inhibitory?

Back 35

excitatory

Front 36

granule cells are densely packed in the inner layer with few larger what?

Back 36

inhibitory Golgi cells interneurons

Front 37

what is the major source of afferent input to the cerebellum and terminate in the granular layer?

Back 37

mossy fibers

Front 38

mossy fibers' bulbous terminals contact granule cells and golgi neurons in synaptic complexes called

Back 38

cerebellar glomeruli

Front 39

inputs of the cerebellum

Back 39

climbing fibers
mossy fibers- excite granule cells

Front 40

outputs of cerebellum

Back 40

Purkinje neurons for cortex
deep cerebellar neurons for cerebellum

Front 41

internal circuitry of cerebellar cortex are composed of

Back 41

inhibitory interneurons

Front 42

what are climbing fibers?

Back 42

climb onto Purkinje neuron dendrites and provide strong excitatory input

Front 43

what are mossy fibers?

Back 43

excite granule cells (in glomerulus) that send their axons (parallel fibers) to Purkinje neuron dendrites

Front 44

what types of inhibitory interneurons are found in the internal circuitry of the cerebellar cortex?

Back 44

basket - form a basket around cell body of Purkinje neuron leadin to a strong inhibitory influence
stellate - found in molecular layer next to dendrites of Purkinje neurons, exert an inhibitory influence
golgi cells - provide feedback inhibition onto granule cells

all use GABA inhibition

Front 45

golgi dendrites are excited by

Back 45

parallel fibers (GCs axons
their axons provide feedback inhibition onto granule cells

Front 46

ALL acons that go up in cortex are excitatory or inhibitory?
what axons do they include?
what neurotransmitter?

Back 46

excitatory
mossy fibers, climbing fibers, parallel fibers (axons of Granular cells)
glutamate excitation

Front 47

all axons that go downward in cortex aare excitatory or inhibitory?
what cells?
what neurotransmitter?

Back 47

inhibitory
PNs, basket, stellate, golgi
GABA

Front 48

majority of inputs to cerebellar cortex are

Back 48

mossy fibers

Front 49

what is the sole source of climbing fibers?

Back 49

inferior olive

Front 50

afferents synapse on neuron in both the

Back 50

deep cerebellar nuclei and the cerebellar cortex

Front 51

the outflow from most regions of the cerebellar cortex projects first to_____ and __________

Back 51

deep cerebellar nuclei
vestibular nuclei (floccolonodular lobe)

Front 52

what leads to long term depression?

Back 52

loss of AMPA receptors

Front 53

what decreases purkinje neuron excitation in cerebellar motor learning?

Back 53

Coincident CF & MF activity
leads to long term depression (LTD)
Loss of AMPA receptors
Decreases its inhibitory tone
on DCN neurons
Allows increase in deep nuclei activity to promote motor learning

Front 54

what is the cellular mechanism of LTD (long term depression)

Back 54

increases Ca and 2nd messengers within Purkinje neurons
decrease AMPA receptor activity
decrease excitatory tone on purkinje neurons

Front 55

Purkinje neurons receive excitation from

Back 55

parallel fibers
climbing fibers

Front 56

when bother excitatory inputs occur coincident a lot of glutamate is released onto metabotropic receptors which will cause a massive increase in

Back 56

calcium and 2nd messengers

Front 57

what causes loss of AMPA (excitatory glutamate receptor analog)

Back 57

massive increase in calcium and 2nd messengers due to excitatory input of glutamate onto metabotropic receptors

Front 58

purkinje neurons are inhibitory or excitatory to deep cerebellar nuclei neurons?

Back 58

inhibitory

Front 59

what structure assists in motor learning
acts as a movement error
-motor error

Back 59

inferior olive

Front 60

increase the number of climbing fibers will

Back 60

suppress parallel fiber activity
motor error
During a movement the climbing fibers (CF) from inferior olive will provide an error signal that will depress parallel fibers that are active concurrently and allow correct movements with no error to emerge

Front 61

damage to IO

Back 61

loss of motor learning
loss of error correction

Front 62

motor adaption and learning which the cerebellum is concerned requires trial and error practice
once the behavior is adapted as learned, it is

Back 62

automatic

Front 63

what detects differences between expected and actual sensory inputs rather than simply monitoring afferent information

Back 63

CF

Front 64

what are the 2 overall functions of the cerebellum?

Back 64

commander of movements
detector and corrector of errors in movement

Front 65

lesion will cause contralateral or ipsilateral damage?

Back 65

ipsilateral
lesions are seen on the same side of the body as damage crebellum

Front 66

projection to red nucleus is to parvocellular portion
it gives rise to the

Back 66

inferior olive
not the rubrospinal tract

Front 67

what provides important information capable of triggering activity of primary motor cortex

Back 67

dentate nucleus

Front 68

what cells project onto neurons in dentate nucleus?

Back 68

purkinje

Front 69

bulk of the dentate neurons travel in the _____ and synapse in the ______

Back 69

SCP
cross to synapse in contralateral VL thalamus

Front 70

cerebellar projection to the cerebral cortex

Back 70

cerebellum --> SCP --> red nucleus --> VL of thalamus --> motor and premotor cortex

Front 71

pathway from cerebellum to cortex
where are the two POSSIBLE crossings
they can never cross OR double cross

Back 71

1st crossing - SCP
2nd crossing - CST/rubrospinal tract

Front 72

3 cerebellar divisons

Back 72

spinocerebellum
vestibulocerebellum
cerebrocerebellum

Front 73

vestibulocerebellar afferents

Back 73

vestibular system: vestibular nucleus and vestibular ganglia
cue to control standing and walking
This cerebellar division receives info from semicircular canals and otolith organs of the vestibular system. The vestibular system of the inner ear senses head motion and the body’s and head’s position relative to gravity.

Front 74

vestibulocerebellar efferents

Back 74

flocculonodular lobe --> vestibular and fastigial nuclei --> medial and lateral descending path --> proximal and trunk muscles --> error detector/corrector and gain setter --> standing upright, eye movements, extensor tone and EQ

Front 75

function of vestibulocerebellum

Back 75

controls all the dynamic and static reflexes: fine tunes the vestibular system
resets the gain of the VOR
resets the gain of increased limb extensor tone

Front 76

VOR

Back 76

maintains orientation of eye on a fixed target when head is rotated

Front 77

lesion of the flocculonodular lobe would prevent what in VOR?

Back 77

ability to modify the gain of his VOR

Front 78

lateral vestibular nucleus facilitates motorneurons innervating

Back 78

antigravity muscles/extensors

Front 79

medial vestibular nucleus facilitates motoneurons innervating

Back 79

trunk and neck muscle and feeds into MLF for VOR gain
involved in smooth muscle pursuit
receives input from vermis/flocculus which received input from cortex

Front 80

what tract provides unconscious information from upper and lower limbs to the ipsilateral cerebellum
involved unconscious proprioception

Back 80

spinocerebellar tract

Front 81

what tracts:
send internally generated information about the central locomotor rhythm as well as the rhythmic discharge of somatic sensory receptors

Back 81

ventral and rostral spinocerebellar tracts

Front 82

what tracts provide the cerebellum with sensory feedback only during evolving movements
provide proprioceptive input from muscle and joints from upper and lower limbs to ipsilateral spinocerebellum

Back 82

dorsal spinocerebellar tract (lower body)
cuneocerebellar tract (upper body)

Front 83

external feedback

Back 83

actual movement info

Front 84

internal feedback

Back 84

intended movement info

Front 85

what tract arises from proprioceptive touch and pressure from the lower body (gracile fasciculus) and innervates the nucleus dorsalis of Clarke (C8-L2/L3)

Back 85

dorsal spinocerebellar

Front 86

the upper body proprioceptive touch and pressure sensation that innervates the clarke's nucleus
provides proprioceptive feedback, part of spinocerebellum
concerns evolving movement from upper body via inferior cerebellar peduncle

Back 86

dorsal spinocerebellar tract

Front 87

internal spinal cord feedback (intended movement) - ventral spinocerebellar tract involve

Back 87

leg spinal interneurons
intersegmental circuits: innervate medial and lateral motor neurons
central locomotor pattern generators - running/walking
-convey UMN info

Front 88

spinocerebellar division for motor execution (error detector/corrector) - vermis pathway

Back 88

vermis --> fastigial nucleus --> thalamus (VL), motor nucleus --> medial descending motor paths --> trunk and proximal limb muscle posture and balance and gaze --> motor execution (error detector and corrector)

Front 89

spinocerebellar division for motor execution - intermediate hemisphere

Back 89

intermediate hemisphere --> interposed nucleus --> thalamus (VL), motor cortex, red nucleus --> lateral descending motor paths --> distal limb muscles (skilled movements) --> motor execution: error detector/corrector

Front 90

what are the 3 cues in testing balance and posture?

Back 90

vestibular
proprioceptive visual

Front 91

what is the positive romberg sign?

Back 91

sway when eyes are closed not when eyes are open
indicate sensory ataxis where you have a loss of proprioceptive input/processing or it can indivate vestibular problem
balance require 2 od 3 inputs

Front 92

will cerebellar lesion get romberg sign?

Back 92

no because they are unsteady when eyes are closed OR open

Front 93

cerebrocerebellar afferents - major input/pathway

Back 93

Major Input-
Premotor cortex (motor planning)

travels in internal capsule to cerebral peduncle to pons

crosses into contralateral middle cerebellar peduncle

terminates as mossy fibers
on GCs that excite PCs
DCN neurons

Front 94

cerebrocerebellum is arranged in a _____ loop modifies action before it takes place

Back 94

feed forward

Front 95

what is the major input to the cerebrocerebellum?

Back 95

premotor cortex?

Front 96

efferents of cerebrocerebellum

Back 96

The cerebro-cerebellum has motor programs or subprograms to interface with motor Cx. It is involved in the preparation of movement and in programming movements requiring multi-joint movements, especially with hand movements. The Dentate Nucleus projects to the contralateral red nucleus (parvocellular portion), the portion of the red nucleus that projects to inferior olivary nucleus which then sends climbing fibers to the contralateral cerebellum. Interestingly, this portion of the red nucleus also receives input from premotor cortex. This circuitry suggests that the premotor-cerebello-rubrocerebellar loop is involved in mental rehearsal of movements and motor learning.

Front 97

what is the function of the cerebrocerebellum?

Back 97

plans and initiates motor programs for extremities
skilled learned movement necessary for rapid limb and digit movements

Front 98

lesions of dentate N

Back 98

interfere with coordinated movements of distal and proximanl components of hand movements - require precise and coordinate motions

Front 99

lateral cerebellar lesions

Back 99

disrupt the timing of various component causing a decomposition of movements
causes increases in reaction time and abnormalities in hand paths

Front 100

lesions of the midline cerebellum (vermal cortex, fastigial nuclei flocculonodular lobe)

Back 100

truncal ataxia - titubation, nystagmus
wide based gait - tandem walk impaired, increase base support
unable to walk in tandem because it requires patient to assume a more narrow stance (heel to toe)

Front 101

wernicke-korsakoff is due to what deficiency?

Back 101

thiamine
B1

Front 102

Wernicke-korsakoff causes damage where?

Back 102

damages midline to anterior portion of intermediate hemisphere
-ataxia of gait, trunk, stance
-spares arms
-damage to purkinje and granule cells
oculomotor and vestibular nuclei
mammillary nuclei (hallmark)

Front 103

wernicke-korsakoff damage to oculomotor and vestibular nuclei causes

Back 103

nystagmus
oculomotor paralysis
paralysis of conjugate gaze

Front 104

mammillary nuclei (hallmark)

Back 104

mental problems
retrograde and anterograde amnesia
confusion

Front 105

ataxia

Back 105

inability to coordinate voluntary muscle movements
unsteady movements and staggering gait

Front 106

dysdiadochokinesia

Back 106

inability to perform rapid and alternating movements

Front 107

dysmetria

Back 107

a lack of coordination of movement typified by undershoot and/or overshoot of intended position
difficult to measure

Front 108

dyssynergia

Back 108

failure of muscles to work in unison leading to ataxias

Front 109

scanning speech

Back 109

singsong intonation in which vowels are abnormally prolonged

Front 110

terminal intension tremor

Back 110

arises or which is intensified when a voluntary coordinated movement is attempted and intensifies when you come close to your target

Front 111

truncal titubation

Back 111

tottering side to side
staggering

Front 112

lesions of cerebellar hemisphere will cause

Back 112

Ataxia
Dysmetria
Terminal intension tremor
Dysdiadochokinesia
Scanning speech
Hypotonia

Front 113

cerebellum is needed to: comprehensive list

Back 113

Maintain proper posture and balance
for walking and running
Damage causes truncal titubation, wide stance gait, unsteady

To execute sequential movements
for eating, dressing, writing
damage causes finger to nose movement failure

To participate in rapidly alternating repetitive movements
Participates in smooth pursuit movements
Damage causes saccadic breakdown with ocular smooth pursuit
Control trajectory, velocity and acceleration of movements
Damage causes the foot and leg to fling while walking

Front 114

medulloblastoma

Back 114

vestibulocerebellum
widebased stance
gait
eq probs

Front 115

: A 38-yr woman can no longer control the use of her hands, stand, or walk. On exam, there is severe saccadic breakdown of ocular smooth pursuit (normal smooth following movements of eyes have been replaced by a series of small, quick, saccadic jerks). When asked to alternate gaze between the examiner's nose and the examiner’s raised hand, her eyes consistently shoot past the target, following which she has to saccade back (hypermetric saccades). Her speech has a singsong intonation in which vowel sounds are frequently abnormally prolonged (scanning speech). When asked to perform a finger-to nose maneuver, her hand and arm irregularly accelerate and decelerate and the hand follows a ragged trajectory (dyssynergia- failure to work in unison). She tends to swing her hand back and forth as she tries to zero in on the target (ataxia/cerebellar tremor) and she typically misses the target by several cm (dysmetria -difficulty arresting movements). On the heel-to shin maneuver, she is also very ataxic and dysmetric. As she sits on the side of the bed, she totters from side to side (truncal titubation). Her balance is so bad that she is completely unable to stand. Her strength is normal.

Back 115

pareneoplastic cerebellar degeneration

Front 116

A 16 yr girl is brought to neurology clinic because of clumsiness. On examination there is mild saccadic breakdown (eyes advance by small jerks when she visually follows slow-moving objects) of ocular smooth pursuit. The finger-to-nose maneuver is moderately dyssynergic (failure to work in unison) and slightly dysmetric (overshoots and undershoots). She exhibits mild truncal titubation (staggering) while on the exam table and her gait is wide-based and unsteady. She is barely able to walk at all with her eyes closed and nearly falls in the attempt. She has severe impairment of position sense. Deep tendon reflexes are lost.

Back 116

Friedreich’s ataxia- a disorder characterized by degeneration of dorsal root ganglia neurons and spinocerebellar projection cells.

Front 117

basal ganglia include what nuclei?

Back 117

caudate
putamen
globus pallidus
subthalamic nucleus
substantia nigra

Front 118

the striatum consists of

Back 118

caudate
putamen

Front 119

the lenticular nucleus consists of

Back 119

globus pallidus
putamen

Front 120

does the basal ganglia contain lower motor neurons?

Back 120

no

Front 121

basal ganglia projects to some brainstem motor areas but does it have classical UMNs?

Back 121

no

Front 122

what are the input nuclei of the BG?

Back 122

striatum (caudate and putamen)
subthalamic nucleus

Front 123

what are the intrinsic nuclei of the BG?

Back 123

globus pallidus
external segment
substantia nigra
pars compacta
subthalamic nucleus

Front 124

what are the output nuclei of the BG?

Back 124

globus pallidus
internal segment
substantia nigra
pars reticulata

Front 125

what are the major afferent projections to the basal ganglia?

Back 125

neostriatum is the primary site where extrinsic inputs to basal ganglia synapse

Front 126

corticostriatal projection goes from

Back 126

most of cerebral cortex to neostriatum

Front 127

thalamostriatal projection

Back 127

intralaminar thalami nuclei --> neostriatum

Front 128

striatopallidal projection

Back 128

neostriatum --> globus pallidus

Front 129

striatonigral projection

Back 129

neostriatum --> substantia nigra

Front 130

nigrostriatal projection

Back 130

substantia nigra pars compacta --> neostriatum

Front 131

subthalamopallidal and subthalamonigral projections

Back 131

subthalamic nucleus --> output nuclei

Front 132

major internuclear connections of basal ganglia

Back 132

striatopallidal
striatonigral
nigrostriatal
pallidosubthalamic
subthalamopallidal
subthalamonigral

Front 133

major efferent projections of basal ganglia

Back 133

nigrothalamic
pallidothalamic

Front 134

the major output nuclei of basal ganglia

Back 134

globus pallidus
substantia nigra

Front 135

almost all of cerebral cortex projects onto striatum in a _____ manner

Back 135

topographic manner

Front 136

basal ganglia channels

Back 136

cortex --> basal ganglia --> thalamus --> back to cortex

Front 137

convergence onto output nuclei

Back 137

: ≈100 million striatal neurons project onto about
≈1 million neurons in output nuclei = convergence, with individual striatal projections terminating heavily on a small number of neurons.

Front 138

what are motor channels?

Back 138

plays a role in selection and initiation of motor programs
conveys this information to motor cortex
suppresses unselected movements
collaborates with motor cortex in initiating learned movements

Front 139

what are non-motor channels?

Back 139

analogous to motor function for cognitive and affective processing channels

Front 140

what are the 3 parallel channels through basal ganglia

Back 140

motor channel
oculomotor channel
prefrontal channel
limbic channel

Front 141

oculomotor channel

Back 141

input: caudate/body
output: GP, SN
target: frontal eye fields supplementary eye fields

Front 142

motor channel

Back 142

input: putamen
output: GP/SN
thalamic relay: VL/VA
target: supplementary motor area
premotor cortex
primary motor cortex

Front 143

prefrontal channel

Back 143

input: caudate
output: GP/SN
thalamic relay: VA/MD
target: prefrontal cortex

Front 144

limbic channel

Back 144

input: nucleus accumbens, ventral caudate, ventral putamen
output: ventral pallidum, GP, SN
thalamic relay: MD/VA
target: anterior cingulate, orbital frontal cortex

Front 145

firing rate change models

Back 145

standard model = antagonistic parallel pathways
center-surround model = motor program selection

Front 146

firing pattern change models

Back 146

abnormal firing pattern model

Front 147

standard model (parallel pathways) - two parallel pathways

Back 147

direct and indirect emanate from striatum
direct: striatum --> GP/SN
indirect: striatum --> GPe --> subthalamus --> Gpi/SNpr
pathways have antagonistic effects on output nuclei

Front 148

what is released in the striatum, has opposite effects on direct and indirect pthways?

Back 148

dopamine

Front 149

imbalance in direct and indirect pathway causes pathophysiology and movement disorders such as:

Back 149

hypokinesia (parkinson's)
hyperkinesia (huntington's, hemiballism)

Front 150

direct pathway

Back 150

Increased activity by striatal neurons in the Direct pathway  inhibition of basal ganglia output nuclei  decreased motor thalamus inhibition (disinhibition)  increased excitation of motor cortical areas = facilitates generation of movements

Front 151

indirect pathway

Back 151

Increased activity in Indirect pathway  excitation of output nuclei  increased inhibition of thalamus  disfacilitation of motor cortex = inhibits generation of movements

Front 152

normal function of basal ganglia requires

Back 152

balance of activity in direct and indirect pathways
imbalance leads to pathophysiology and clinical motor symptoms

Front 153

what does the standard model explain?

Back 153

signs and symptoms of parkinson and huntington's
provides rationale for surgical intervention in treating Parkinson's such as what nuclei in which deep brain stimulating stimulating electrode should be implanted

Front 154

what does the standard model NOT explain?

Back 154

tremor in Parkinson's disease
not terribly useful for understanding normal function of basal ganglia

Front 155

center-surround model

Back 155

motor program selection
an elaboration of standard model
basal ganglia disinhibits wanted movement and inhibits undesirable movements

Front 156

center surround model emphasizes which projection?

Back 156

motor cortex --> subthalamic nucleu which is the hyperdirect pathway
comprises a short latency cortical projection within indirect pathway

Front 157

together what three pathways mediate the role of the BG in selecting motor programs?

Back 157

direct
indirect
hyperdirect

Front 158

what the clinical consequences of disease and pathophysiology of motor channel of BG range from:

Back 158

impaired generation of spontaneous movements (akinesia or hypokinesia) to abnormal involuntary movements (dyskinesia or hyperkinesia)

Front 159

motor pathologies involving the basal ganglia are often referred to as

Back 159

movement disorders

Front 160

unilateral lesions in basal ganglia give rise to _______ movement disorders

Back 160

contralateral

Front 161

basal ganglia movement disorder usually disappear during _____ and are exacerbated during _____

Back 161

sleep
stress

Front 162

firing rate models of BG pathophysiology

Back 162

simple models that take into account anatomy and phys of basal ganglia to explain motor disorders

Front 163

parkinson's disease is a ____ movement disorder

Back 163

hypokinetic

Front 164

____ is a progressive motor disorder of the elderly involving about 1% of the population over 65 yrs of age

Back 164

Parkinson's

Front 165

what are the signs and symptoms of Parkinson's?

Back 165

Tremor at rest
Rigidity
Akinesia/bradykinesia
Postural instability and festinating gait
other signs:
Mask-like face, reduced blink rate, pill-rolling motion of fingers, autonomic dysfunction, sleep disorders, micrographia

Front 166

tremor at rest

Back 166

rhythmic 4-8 Hz tremor is present at rest
most evident in hands
often first sign of PD
often improves with intentional movement

Front 167

bradykinesia --> akinesia

Back 167

slowed movement
voluntary movements suffer from marked retardation
muscular strength is preserved

Front 168

postural instability and festinating gait

Back 168

occurs secondary to tremor and bradykinesia

Front 169

rigidity in PD

Back 169

more common at end stage
both rigidity and spasticity are forms of hypertonia but rigidity differs from spastric paralysis from a UMN lesion
-affects all muscles to same degree and is velocity-independent
-typically of cogwheel or leadpipe type
involves increased resistance to passive movement involves both flexors and extensors
spinal stretch reflexes are not appreciably altered
likely results from increased supraspinal descending excitatory drive onto alpha motor neurons in the SC that innervate flexor and extensor muscles

Front 170

PD arises from bilateral degeneration of what?

Back 170

dopamine neurons in substantia nigra pars compacta
(>90%)

Front 171

etiology of degeneration is

Back 171

unknown

Front 172

dopamine neurons project to the

Back 172

striatum and elsewhere in forebrain

Front 173

depletion of striatal dopamine in PD alters

Back 173

basal ganglia circuitry --> altered activity in BG output nuclei

Front 174

in pathology, PD pt have no

Back 174

melanin -indicating DA neuron loss

Front 175

what is the precursor of dopamine that is radiolabeled?

Back 175

L-DOPA
decreased in PD in striata

Front 176

dopamine excites what pathways?

Back 176

dopamine excites the direct and indirect pathway

Front 177

Rational Treatments for Parkinson’s disease based on these Firing Rate Models

Back 177

Dopamine Replacement therapies- Intracranial stimulation - Neuron replacement therapies

Front 178

what is a common drug therapy given systemically as a pill

Back 178

L-Dopa therapy

Front 179

does dopamine cross the BBB?

Back 179

no

Front 180

does l-dopa cross the BBB?

Back 180

yes
once in the CNS, L-dopa diffuses into the striatum -converted to dopamine by an enzyme located in dopaminergic axons

Front 181

deep brain stimulation in BG

Back 181

Based on insights from the Firing Rate models, the subthalamic nucleus and GPi are common sites for implanting deep brain stimulating electrodes for high frequency (100-180 Hz) intracranial electrical “stimulation.”

Front 182

temporal information processing (firing pattern model)

Back 182

patterns of spike activity instead of changes in firing rate
loss of striatal dopamine results in abnormal 10-30 Hx oscillatory synchronized activity within BG

Proposed mechanism:
Dopamine reduces lateral spread of activity in striatum.
With absence of dopamine, basal ganglia neurons to transition to natural state of oscillatory synchronization.

Front 183

according to temporal information processing, what might be related to PD motor impairments?

Back 183

synchronization (via suppression of beta oscillations for PD)
beta oscillations underlies bradykinesia and rigidity

Front 184

what is deep brain stimulation used for?

Back 184

PD
help control tremors and chronive movement disorders
tiny electrodes are surgically implanted in brain and are connected via a subcutaneous wire to a neurostimulator, implanted under skin near clavicle

Front 185

Huntington's disease is a _____movement disorder

Back 185

hyperkinetic

Front 186

early signs of huntington's are

Back 186

clumsiness
mild involuntary muscle contractions that evolve into more prominent irregular jerky choreiform movement

Front 187

dementia occurs later in disease as ______ becomes prominent

Back 187

cortical atrophy

Front 188

signs usually become apparent by ____ yrs of age

Back 188

40

Front 189

Huntington's disease results from degeneration of

Back 189

striatal neurons that project to the globus pallidus with concomitant enlargement of adjacent lateral ventricles

Front 190

early in the disease there is preferential degeneration of

Back 190

enkephalinergic striatal neurons that project to globus pallidus external segment = indirect pathway

Front 191

Huntington's etiology

Back 191

Degeneration is related to autosomal genetic mutation in the huntingtin gene (unknown function; is a transcription factor for trophic factor, and possible cytoskeletal role) on chromosome 4, involving an excessive number of ‟trinucleotide repeats” (CAG, which codes for glutamine).
HD is one of a growing list of polyglutamine Trinucleotide Repeat Expansion Disorders (TREDs) = unstable DNA segments.
CAG repeat of AT LEAST 36 CAG or greater

Front 192

mutant form of huntingtin misfolds leads to accumulation of

Back 192

nuclear and cytoplasmic inclusions in striatal output neurons and cortical pyramidal neurons

Front 193

Degeneration (usually bilateral) of striatal neurons in the Indirect pathway in early stages of HD ......leads to

Back 193

decreased activity in basal ganglia output nuclei  hyper-kinesia.