basal ganglia

helps select movement, suppress competing movement, and scale movement appropriately

basal ganglia

subcortical nuclei (basal ganglia)

caudate nucleus, putamen, globus pallidus, substantia nigra, subthalamic nucleus

subcortical nuclei located in the cerebrum

caudate, putamen, globus pallidus

subcortical nuclei located in the diencephalon

subthalamic nucleus

subcortical nuclei located in the midbrain

substantia nigra

basal nuclei

gray matter areas deep within the white matter of the cerebral hemispheres

Striatum consists of

caudate and putamen

major input from cortex to BG

caudate and putamen (striatum)

lenticular nucleus is composed of

putamen and globus pallidus

primary output from basal ganglia, sending back to cerebral cortex

GPi and substantia nigra

caudate nucleus blood supply

deep branches of MCA

putamen blood supply

deep branches of MCA

globus pallidus blood supply

anterior choroidal artery

subthalamic body blood supply

PCA

anterior choroidal artery comes from

ICA

basal ganglia involved in

motor control

-motor output

BG also involved in psychological functions of

goal-directed behavior, social behavior, and emotions

BG Non-Motor Functions

-decision-making

-judgement

-prioritizing info

-emotional processing and responses

-learning

-spatial attention

BG also involved in ___ movements

eye

Like the cerebellum, the basal ganglia influences activity in the

descending motor tracts without direct connections

doesn't have connections with LMN

BG

affects movement via thalamus

BG

neurotransmitters involved in afferent transmission of BG

-glutamate (excitatory)

-Ach (excitatory)

-serotonin (inhibitory)

efferent transmission neurotransmitters of BG

GABA (inhibitory)

cortical motor areas produce excitation of the striatum by delivering the transmitter

glutamate

w/in the BG, signals are mediated by the release of

glutamate, GABA, and DA

dopamine from substantia nigra to striatum adjusts the

signals to the output nuclei

output nuclei provide the appropriate level of

inhibition to their target nuclei

Output nuclei of basal ganglia

GPi and SNr

Output nuclei of basal ganglia are

inhibitory

nonmotor circuits of BG

-goal-directed behavior circuit

-social behavior circuit

-emotion/motivation circuit

motor circuits of basal ganglia

-oculomotor circuit

-stop (hyper direct), go (direct), and no-go (indirect) pathways

loops contribute to

prediction of future events, selecting desired behaviors, preventing undesired behaviors, motor learning, shifting attention, and spatial working memory

Goal directed behavior loop

Lateral Prefrontal Cortex (cerebral cortex) to Head of Caudate (basal ganglia) to Ventral anterior (Thalamic nuclei)

evaluates information for making perceptual decisions, planning, and choosing actions in context; evaluates potential actions and selects the appropriate one to take

goal directed behavior loop

active in learning, changing its activity before the cortex when reward contingencies are reversed

goal directed behavior loop

not involved in controlling movements

goal directed behavior loop

recognizes social cues, regulates self control, and analyzes from irrelevant information

social behavior loop

maintains attention, stimulates response learning, decision making, judgement

social behavior loop

uses rewards and emotional behavior to guide behavior and inhibit undesirable behaviors

social behavior loop

no motor deficits present

social behavior loop

social behavior loop

ventral prefrontal cortex -> head of caudate, substantia nigra reticularis -> mediodorsal thalamic nuclei

emotion loop

medial prefrontal cortex, ventral striatum, ventral pallidum, mediodorsal

ventral striatum loops with

medial prefrontal cortex; participates in emotions and motivation; acts as a link b/t emotional, cognitive, and motor systems

integrates emotion with roles of other loops and alters locomotor activity an approach/avoidance behaviors w/ its connections to the thalamus

emotion/motivation loop

partially responsible for the perception and experiences of emotions

emotion/motivation loop

essential function of emotion loop of BG

seeking rewards

body of caudate= part of an

oculomotor loop

-that makes decisions about spatial attention and eye movements

-gaze and orienting movements

rapid movement of eyes

saccade

fast eye movements away from an object

antisaccades

Impaired saccades

BG pathology

BG motor circuit output regulates

skeletal muscle contraction

muscle force

multi joint movements

movement sequence

Motor loop of basal ganglia

motor and pre motor cortex

putamen, globus pallidus, ventral lateral thalamic nuclei

no direct output to LMN

BG

Functionally, motor loop regulates three activities via three pathways

voluntary muscle activity (motor thalamus)

postural and girdle muscle activity (PPN)

walking (midbrain locomotor region)

BG output to motor thalamus from which output goes to the

supplementary motor area of cortex (plans, coordinates, initiates)

occurs when another neuron inhibits the inhibitory neuron, thus allowing

increasing activity in the target neuron

- allows for fine tuning of neural output

These three pathways process signals within the cortico-basal ganglia-thalamic loop

hyper direct (stop)

go (direct)

no-go (indirect)

normal movement requires activity in all 3 pathways b/c all 3 pathways

converge on the GPi which is the output nucleus

GPi inhibits

motor thalamus

motor thalamus excites the

motor cerebral cortex

hyperdirect pathway final result

powerful inhibition of the motor thalamus resulting in suppressed voluntary movement

hyper direct pathway mechanism

-conveys powerful excitation from the CC directly to the STN

-STN excites the GPi

-GPi inhibits the motor thalamus resulting in

hyper direct pathway inhibits

ongoing motor programs eliminating irrelevant movements when voluntary movement is initiated

direct pathway activation

"accelerator"

direct pathway disinhibits

the motor thalamus

direct pathway mechanism

-putamen inhibits GPi

-inhibited GPi provides less inhibition to motor thalamus

-motor thalamus signals motor areas in CC to activate specific corticospinal neurons

facilitates specific movements

direct pathway

indirect pathway also begins in putamen but

in different cells than the direct pathway

indirect pathway

"brakes"

indirect pathway mechanism

-putamen inhibits GPe

-GPe provides less inhibition to STN

-STN excites the GPi

-GPi inhibitory output is increased

end result is suppression of unwanted movements

indirect pathway

which pathway explains why movement initiation can fail?

stop/hyper direct pathway

motor loop is dependent on

dopamine supplied by the substantia nigra

DA binding to D1 receptors excites the

inhibitory neurons in the Go pathway facilitating specific movements

DA binding to D2 receptors inhibits the neurons from

putamen to the GPe; disinhibits the STN and facilitates the GPi- decreasing unwanted movements

hypokinetic

too little movement

Hyperkinetic

excessive movement

differences in abnormal movements are due to dysfunction in the

motor pathways w/in the BG and in the PPN

most common basal ganglia motor disorder

Parkinson's disease

interferes w/ both voluntary and automatic movements

parkinson's

2 common subtypes of Parkinson's disease

postural instability gait difficulty (PIGD) and tremor-dominant (TD)

characterized by muscular rigidity, drooping posture, rhythmic tremors, and a mask-like facial expression

PIGD

difficulty coming to standing from sitting; gait is characterized by flexed posture, shuffling of feet, and decreased/absent arm swing

PIGD

distinctive signs of PIGD

-akinesia/hypokinesia/bradykinesia

-ridigity

-postural unsteadiness

-resting tremor

-freezing during movment

-visuoperceptual impairments

-mask-like facial expression

-nonmotor signs

deep brain stimulation surgery STN

parkinson's

freezing episodes that are made better with visual cues

parkinson's

both resting and active tremors

TD PD

rigidity and slowing of movement are relatively mild

TD

experience a slower progression of signs and symptoms that those with PIGD

TD

pathology in PD

the death of DA-producing cells in the substantia nigra and GABA producing cells in PPN

effect of loss of DA is increased

inhibition from the putamen to the GPi; GPi excessively inhibits all 3 BG output routes

cell death occurs long before clinical signs of PD become evident

PD

treatments for parkinson's

-levodopa: converts into DA in brain

-carbidopa: taken w/ levo to prevent its breakdown in blood

-dopamine agonists: mimic effects of dopamine

-MAO inhibitors: prevent breakdown of dopamine

-COMT inhibitors: extend duration of levo

invasive treatments of PD

deep brain stimulation, neuronal transplantation, destructive surgery

PD rehab

-PT, OT improves mobility and functional status

-must think about on-off phenomenon

-intense resistance training produces greater muscle hypertrophy and functional gains than standard exercise

Hyperkinetic disorders

-huntington's disease

-dystonia

-tourette's disorder

-dyskinetic CP

signs of disease include chorea and dementia

huntingtons disease

autosomal dominant hereditary disorder causes degeneration in many areas of the brain, most prominently in the striatum and CC

huntingtons

genetic, nonprogressive movement disorders are characterized by

-involuntary sustained muscle contractions

-abnormal posture, twisting, and repetitive movements