Basal Ganglia Flashcards
what is the basal ganglia?
a bunch of nuclei
1st telencephalon structure- deep in the hemispheres- goes through all of the lobes
embedded in white matter of cerebrum
where does the basal ganglia lie?
lateral to the thalamus
what is the corn a radiata?
white matter that is leaving the BG- axons leaving
what are the major functions of the basal ganglia?
the integration of feelings, thoughts and movement occur in the basal ganglia
action selection hypothesis
build up on the “turn up - turn down” effects of the direct and indirect pathways
functions in postural control and descending system to BS that work with locomotion
- any movement you make requires that certain motor commands (raise arm) be executed and opposing commands (lower arm) be suppressed
- promotes proper execution commands and the indirect pathway suppresses commands related to opposing movements
- thus plays a role in the automatic or sub-voluntary integration of the various motor centers where habitual or automatic movement become organized
the sequencing of movements
smooth and accurate movement- performing a motor sequence requires that the movements be executed in the proper order. Thus, the direct pathway may “turn up” the appropriate movement commands when it is their turn while the indirect pathway may “Turn down” the commands when it is not their turn
MOTOR FUNCTION
describe how the integration of feelings, thoughts and movement occur in the basal ganglia:
this is why you jump when you’re excited, tremble when you’re nervous, freeze when you are scared or get tongue-tied when the boss is chewing you out
the basal ganglia allow for a smooth integration of emotions, thoughts and physical movement and when there is too much input they tend to lock up and do not allow a smooth transition
what is action selection hypothesis?
in this model the basal ganglia would be the arbiter of which of the potential actions that cortex might be planning actually gets executed
this fits together well with the idea that dopamine is a system mediating learning based on reward
this could train the basal ganglia to chose behaviors that have been rewarding in the past
what motor function does the BG have?
shifting and smoothing fine motor behavior
involved in suppressing unwanted motor activitiy
control of postural adjustment during voluntary movement
what are the 5 parallel loops of the BG?
how can loops be distinguished?
1- motor (from putamen)
2- cognitive loop
3- limbic loop (motication/emotion)
4-oculomotor loop
5- associative (emotion/social)
1,2,4,5 through the dorsal striatum
3 (limbic) through the ventral striatum
the cortical targets of the four loops through the dorsal striatum include the supplementary motor area, the dorsolateral prefrontal cortex, the frontal eye fields, and the lateral orbitofrontal cortex
what does the cognitive loop play a role in?
spatial memory and motor intentions
head of caudate
what does the limbic loop play a role in?
emotion and motivation function
motor expressions to emotions
what does the oculomotor loop do?
activated when a deliberate saccade is about to be made
disinhibits superior colliculus
comes from cortical eye area to BG to thalamus back to cortical eye area (remember corticobulbars do NOT go to eye)
describe the direct pathway:
what does it do?
what controls it?
what are the steps?
INCREASES EXCITATORY THALAMIC INPUT TO CORTEX
TURNS UP MOTOR ACTIVITY
wants to get rid of associative movements and only pick the right one
1-the dorsal striatum (putamen & caudate) receives excitatory input from the isocortex
“CORTICOSTRIATE FIBERS “= fibers from cortex to striatum
2-the dorsal striatum inhibits the substantia nigra reticulata and the globus pallidus using GABA and enkephalin
3-the substantia nigra and globus pallidus influence the thalamus
4- the direct loop disinhibits (excites) thalamocortical projections to the cortex
through the direct loop, information from several functionally related cortical areas funnels through one sector of the BG and results in recurrent excitation of one of these cortical regions
axons project to the dorsal striatum from neurons in all areas of the isocortex but most heavily from the ?
frontal and parietal lobes
the primary motor (4), premoter (6), supplementary motor (6) and somatosensory (3,1,2) cortices project preferentially to ?
the putamen
these projections have a tomographic organization
the frontal eye fields and association areas of the frontal and parietal lobes project heavily onto the ?
caudate nucleus
these projections have a tomographic organization
the neurons projecting from isocortex too striatum provide…
strong excitation, using glutamate as their neurotransmitter
the excitatory postsynaptic potentials results from the actions of excitatory glutamatergic cortical efferents and the inhibitory
how do the substantia nigra and globus pallidus influence the thalamus?
a major outflow of efferent fibers from the basal ganglia comes from the internal segment of the SN & GP. both these areas develop in the caudal ventral diencephalon region called the SUBTHALAMUS
fibers synapse in the intralaminar nuclei and the in the VL, VA, and MD nuclei of the thalamus.
axons from cells of the intralaminar nuclei provide feedback to the striatum
those of the VL, VA and MD nuclei complete the “basal ganglia loop” by projecting to frontal lobe cortex
each of the basal ganglia loops includes…
both direct and indirect loop fibers
describe the indirect loop:
indirect loop can be viewed as a side arm of the direct loop, through which the sub thalamic nucleus influences the outflow of the globus pallidus interna
striatal efferents reach the external segment of the globus pallidus, and after synaptic articulation, pallidal efferents cross the posterior limb of the internal capsule to reach the SUBTHALAMIC NUCLEUS.
Neurons of the sub thalamic nucleus project EXCITATORY GLUTAMATERGIC fibers back to both parts of the globus pallidus, but primarily to the internal segment and to the substantia nigra reticulate, where they excite GABA projections to the thalamus and THEREBY INHIBIT THE THALAMUS
the sub thalamic nucleus also receives direct input from the cerebral cortex
THE NET RESULT OF ACTIVATION OF THIS INDIRECT LOOP IS TO DECREASE THALAMOCORTICAL ACTIVATION
(extra loop in indirect pathway- 1st part is facilitatory like direct route until you get to the sub thalamic nucleus. sub thalamic is facility- which will facilitate an inhibitory neuron which will inhibit the VA/VL )
how do dopaminergic nigrostriatal connections modulate the direct and indirect loops?
the cells of the substantia nigra compact produce DOPAMINE
their projects to the dorsal striatum enhance cerebral cortical activation through both the direct and indirect loops. This results form differences in the types of stratal receptors that receive nigrostriatal dopaminergic input.
dopaminergic projections EXCITE stratal cells of the direct (excitatory) loop through D1 receptors on these cells
dopaminergic projections INHIBIT stratal cells of the indirect (inhibitory) loop through D2 receptors on these cells
what is dopamine? how is it produced? what effect does it have?
neuromodulator; reward system
produced from the substantia nigra
when dopamine is present it facilitates pathway (D1) or inhibits (D2)
when present you move
not present you are akinetic (Parkinson’s)
SUBSTANTIA NIGRA DOPAMINERGIC:
- Turns UP direct pathway (D1)
- Turns DOWN indirect pathway (D2)
- INCREASED VA/VL drive to cortex
- MORE MOTOR ACTIVITY
what is ACh? what effect does it have?
neuromodulator
opposite effect of dopamine
comes from the medial pontine nucleus; get less movement
facilitates indirect pathway and inhibits direct pathway
too little ACh (or too much dopamine)= hyperkinetic disorders
STRIATAL INTERNEURONS CHOLINERGIC: (ACh) -Turns DOWN direct pathway -Turns UP indirect pathway -DECREASED VA/VL drive to cortex -LESS MOTOR ACTIVITY
describe the blood supply of the BG:
internal carotid divides into anterior and middle cerebral arteries
middle cerebral A goes out into lateral fissure but before it gets there it is called M1 then splits into superior and inferior trunks of M2
Lenticulostriate arteries (at lenticular nucleus) come off of M1 segment and supply the putamen, globus pallidus and part of the internal capsule
medial lenticulostriate arteries do the caudate
projections of substantia nigra reticulata to the superior colliculus contribute to ?
the regulation of saccadic eye movements
the limbic lobe and ventral areas of the temporal lobe project to?
the ventral striatum which includes the nucleus accumbens
modulating the limbic cortex results in participation in ?
motivational and visceral functions associated with emotion
what do the ventral striatum and palladium modulate?
cerebral cortical areas that participate in motivation, mood, affect and in social behaviors and visceral functions associated with emotional states
these structures also participate in behaviors associated with addiction to substances of abuse.
the BG can be viewed as participants in a series of parallel pathways extending from..?
what do these pathways do?
what do they participate in?
cerebral cortex to basal ganglia , then to thalamus and back to the cerebral cortex
these pathways collect info from multiple forebrain structures, process this info through the BG and move it back to the cerebral cortex
these pathways participate in the control of movements and in certain cognitive functions
what does the BG monitor and plan?
monitors the progress of movements and participates in the sequencing and automatic execution of learned motor plans
what are the movements influenced by the BG?
include those related to posture, automatic movements (swinging the arms while walking) and skilled volitional movements of the trunk and limbs, including eye movements
what do diseases of the BG cause?
difficulty in initiating movements
disturbances in continuing or stopping ongoing movements
abnormalities of muscle tone (rigidity)
development of involuntary movements (tremor or chorea)
BG disorders can be divided into what 3 functional categories?
1- parkinsonism
2- hyperkinetic movement disorders (including ballism, chorea, and athetosis)
3- dystonia
how does parkinsonism result?
results from degeneration of the substantia nigra or interference with dopaminergic neurotransmission in the striatum
how do hyperkinetic movement disorders happen?
result from striatal or subthalamic dysfunction
how does dystonia happen?
results from pallidal dysfunction but can occur with disorders of other component parts of the BG
describe parkinsonism:
what are its effects?
what are the symptoms?
neuropathic changes consist of degeneration in the substantia nigra and locus ceruleus with inclusions (Lewy bodies) in remaining neurons
leads to depletion of dopamine in the caudate nucleus and putamen.
End result: decreased cerebral cortical excitation over thalamocortical projection fibers
SYMPTOMS:
-Bradykinesia (slowness of movement)
-rigidity
-gait instability
-tremor
-initially unilateral
-expression becomes fixed “masked face”
-patient stands with head and shoulders stooped and walks with short, shuffling steps
-arms remain at sides and do not automatically swing in rhythm with legs
-Festinating gait- difficulty in starting steps, pace picks up and then difficulty stopping
bradykinesia becomes apparent with difficulty in initiating and performing volitional movements of the most common type (walking, standing, eating, writing)
describe hyperkinetic movement disorders:
how does it happen?
what are its symptoms?
result from striatal or subthalamic dysfunction
disorders include ballism, chorea and athetosis
decreased subthalamic nucleus function can result from destruction of the structure, as when a small stroke affects this structure and causes hemiballismus (series of flinging movements of the arm and leg of one side.)
dysfunction of sub thalamic nucleus neurons causes loss of sub thalamic excitation on the internal segment of the globus pallidus and substantia nigra
The result is DISINHIBITION of thalamocortical neurons that thereby excessively enhances their excitatory effects on the cerebral cortex
diseases are associated with abnormal involuntary movements that occur when? disappear when?
at rest and disappear in sleep
what are discrete lesions in the caudate more likely to produce?
behavioral manifestations (most common pathology)
- abulia- apathy, loss of initiative and spontaneous though and emotional response (head of caudate)
- motor disorders- chorea
what are discrete lesions in the putamen more likely to produce?
motor disturbances
-dystonia
what is dystonia?
twisting, slow, contorting involuntary movement that is somewhat sustained and repetitive
(contact but can’t relax quickly)
no obvious pathology but thought to be related to lesions of the striatum
what are the 2 categories of BG pathologies?
1- hyperkinetic- lesion of the indirect pathway
2- hypokinetic - lesion of the direct pathway
what are hyperkinetic movement? what are the types?
excessive involuntary movement
1- chorea 2- ballism 3- athetosis 4- dystonia 5- tourette syndrome
what is chorea? how is it characterized?
hyperkinetic disorder
characterized by:
- sudden, frequent involuntary purposeless and quick jerks of the trunk, extremities and head associated with facial grimaces
- irregular, rapid, uncontrolled, excessive movement that seems to move randomly from one part of the body to another
- no problems in strength, endurance but these supercede other movements- reflexes would be normal
believed lesions are in caudate nucleus
effects the indirect pathway
Huntington’s chorea- inherited genetic disease; present if 4th/5th decade of life
contralateral if unilateral
what is athetosis? how is it characterized/
hyperkinetic disorder
characterized by:
-slow, writhering, continuous, wormlike movements of distal parts of limbs, chiefly fingers which show bizarre posturing
putamen lesion
what is ballism? how is it characterized?
hyperkinetic disorder
limb movements are sudden, quick continuous, violent and flinging in nature
continuous movements may causes excessive fatigue
subthalamic nucleus lesion
tend to be bilateral lesions
loops are ipsilateral but affect contralateral body
hemiballism= one side of subthalamus degenerates; symptoms are contralateral
what is tourette syndrome?
motor and vocal tics
-motor tic- sudden, breif involuntary movement involving ms in different parts (eyes, shoulder shrugging)
MRIs show volume loss of caudate and lenticular nuclei
Limbic loop- inhibitory limbic system drive acting on motor cortex and motor striatum is thought to generate tics
in general, how can hyperkinetic disorders be treated?
raise ACh levels
OR
lowering dopamine levels in the striatum
(the body gets used to these drugs so you have to keep increasing dose )
deep brain stim- electrodes to drive the parts of the system that you want
what is a hypokinetic disorder?
parkinsonism
what is parkinsonism characterized by?
tremor- 3-6 Hz (rest) (resting tremor= pin rolling)q
cogwheeling- which refers to jerky, ratchet-like movements of the joints
lead pipe rigidity both flexor and extensor so that the resistance to passive movement is intense and consistent through the entire ROM
hypo or akinesia= lack of dopamine, ^ ACh
loss of postural reflexes
-results in balance problems, which can manifest as unstable, stooped or slumped over posture and a shuffling walk of mall steps followed by the need for quicker steps to maintain balance
Palilalia= type of stuttering Hypophonia= softness of speech Bradyphrenia=slowness of thinking Retropulsion= repetition of motor acts Festination= shuffling gait
how are hypokinetic disorders treated?
dopaminergic agonists- L-dopa
lowering ACh levels in striatum
what are the 2 divisions of the peunculopontine tegmental nucleus?
what functions does it have?
1- pars compacta (PPNc)- cholinergic neurons
2- Pars dissipata (PPNd)- glutamatergic neurons
postural control and locomotion- independent of dopamine
sleep
what is the relationship between the basal ganglia and cerebellum?
the output of the cerebellum is excitatory while the BG is inhibitory
the balance b/w these 2 systems allows for smooth, coordinated movement and a disturbance in either system will show up as movement disorders
BG vs. cerebellum
BASAL GANGLIA:
- cognitive and motivational aspects of movement
- effects ms tone and participates in the generation, switching and termination of movement as dictated by situational demands and emotional or attentive states
- activated during memorized motor tasks and therefore contribute to the automatic execution of a learned motor plan
- BG optimize patterns of ms activation so that the desired goal is achieved in the most efficient way
- can suppress unwanted movement
- automatic execution of a learned motor plan. executes learned strategies
- preparation for movement- target location in space, direction of movement and ms pattern
- gating function
CEREBELLUM:
- aides in visual tracking
- helps in predicting movement occurring outside the body (how long a fast ball will take to reach the plate)
- is capable of learning
- permits smooth progression from one movement to the next)
- gives us the ability to adapt to a changing environment quickly and efficiently
- involved with force, frequency, load, velocity and movement direction
what is the nucleus accumbens? what does it play a role in?
plays a central role in the reward circuit
lies just ventral to caudate nucleus
chiefly based on 2 essential neurotransmitters
- dopamine- promotes desire
- serotonin- satiety and inhibition
studies show that drugs that increase the production of dopamine in the nucleus accumbens also reduce serotonin
does not work in isolation- maintains close relations with other centers involved in the mechanisms of pleasure and in particular with the VENTRAL TEGMENTAL AREA
VTA synthesizes dopamine, which their axons then send to the nucleus accumbens. the VTA is also influences by endorphins whose receptors are targeted by opiates
another structure involved in pleasure mechanisms is the PREFRONTAL CORTEX- role in planning and motivating action is well established. the prefrontal cortex is a significant relay in the reward circuit and also modulated by dopamine.
people who are alcoholic, obese or cocaine dependent have..?
fewer dopamine receptors than normal people do
