Basal Ganglia Flashcards
Basal ganglia
A group of nuclei located (bilaterally) deep in the telencephalon, diencephalon, and midbrain
Primarily located between the cerebral cortex and thalamus, but also in midbrain & near thalamus
Function of basal ganglia
To modify initiation and execution of motor activity
-also cognitive and limbic connections
Helps refine movement signal from cortex by inhibiting “incorrect” motor activity
Brake hypothesis works by Disinhibition. What is disinhibition?
Release from ongoing inhibition
Inhibit the ongoing inhibition
Striatum
-Caudate nucleus
-Nucleus accumbens
-Putamen
Globus pallidus
-External segment (GPe)
-Internal segment (GPi)
Subthalamic nucleus (STN)
-
Sustantia nigra
-Compact part (SNc) - dopaminergic
-Reticular part SNr) - output nuclei
Lenticular nucleus
(aka lentiform nucleus)
-Putamen
Globus pallidus
-External segment (GPe)
-Internal segment (GPi)
Effect of dopamine (on GPe) varies
▪ Excitatory on putamen neurons that are part of the direct pathway (see below)
▪ Inhibitory on putamen neurons that are part of the indirect pathway
➢ basically, dopamine facilitates movement (see Parkinson’s disease below)
Thalamic drive
a theoretical proposal that attempts to predict the motor effects of specific changes within the
basal ganglia – thalamic – cerebral cortical circuitry
a far from perfect
▪ e.g., fails to predict neuronal discharge changes in the thalamus (VA/VL) in various diseases
What is the basic idea behind the thalamic drive?
Basic idea is to understand which regions of the circuit are excitatory or inhibitory and be able
to predict whether damage to those areas will result in increased cortical motor activity
(hyperkinetic; increased thalamic drive) or decreased cortical motor activity (hypokinetic;
decreased thalamic drive)
Direct Pathway
Motor cortex → striatum => GPi/SNr => thalamus → motor cortex
Facilitates movement
Disinhibits the thalamus
▪ increased thalamic drive (thus, damage to this pathway = hypokinetic [Parkinson’s])
Indirect Pathway
Motor cortex → striatum => GPe => STN → GPi => thalamus→ motor cortex
Inhibits movement
Inhibits the thalamus
▪ decreased thalamic drive (thus, damage to this pathway = hyperkinetic [Huntington’s])
Hyperkinetic movement disorders
Extraneous, unwanted movements
e.g., Huntington’s disease, athetosis
Chorea
involuntary, constant, rapid, complex body movements that flow from one body part to
another
Choreiform
resembling chorea
involuntary “dance like” movement of the limbs
Athetosis
slow, writhing movements of the fingers and hands, and sometimes of the toes
Ballismus
violent, flailing movements
damage to subthalamic nuclei of basal ganglia results in hemiballismus
Dystonia
a persistent spasm/posture of a body part which can result in grotesque movements and
distorted positions of the body
Tremor
rhythmic, involuntary, oscillatory movements
Resting tremor
Resting tremor occurs when a body part is at complete rest against gravity
▪ tremor amplitude decreases with voluntary activity
Postural tremor
postural tremor occurs during maintenance of a position against gravity and
increases with action
Essential tremor (familial)
▪ most common form of tremor
▪ tremors occur in a person who is moving or trying to move and no cause can be identified
Intentional tremor
manifests as a marked increase in tremor amplitude during a terminal portion of
targeted movement.
➢ examples of intention tremor include cerebellar tremor/pathology
Hypokinetic movement disorders
difficulty or absence of intended movements
b e.g., Parkinson’s disease
Bradykinesia
slowing of voluntary movement
Difficult initiating movement
use center of gravity to compensate: initiate walking or sit-stand
Increased muscle tone: Rigidity
Lead-pipe rigidity
resistance persists throughout the range of movement of a particular joint
Increased muscle tone: Rigidity
Cogwheel rigidity
periodic resistance at different points throughout the range of movement
Spasticity (speed dependent)
move slow and can move limb through ROM
- often pyramidal system; unidirectional (e.g., only flexion)
Rigidity (not influenced by speed)
move fast or slow and still can’t move limb through ROM
- often extra-pyramidal system; bidirectional
Parkinson’s disease
degenerative hypokinetic disorder
B Extremely common (100-200 per 100,000) >60 yrs old
C Primary symptoms
1 bradykinesia, difficulty initiating movement
a often assume flexed posture
▪ lean forward to compensate for difficultly starting/continuing walking
2 increased muscle tone (rigidity)
3 resting tremor
4 decreased voluntary movement
a micrographia, decreased facial expression “masked expression”, monotone speech
5 potential dementia/depression changes
6 dysautonomic symptoms
a e.g., urge incontinence (loss of bladder control), constipation
D Pathology
1 cell loss in substantia nigra – compact part (SNc)
a reduced dopamine production
▪ inhibits direct pathway = increases inhibition of thalamus = decreases thalamic drive
➢ indirect pathway now dominant (also decreases thalamic drive)
2 note that many other brain regions are involved (e.g., hippocampus, neocortex, brainstem
nuclei)
Huntington’s disease
genetic degenerative hyperkinetic disorder
B Prevalence: 5 per 100,000
a autosomal dominant (children have 50% chance of inheriting)
C Primary symptoms
a appear in adulthood (30-50 yrs)
b gradual onset
2 dementia
a progressive loss of attention & executive function
▪ poor ability to plan, organize, and sequence
▪ short term memory deficits
3 chorea
a initially appears as fidgeting or restlessness
b eventually becomes severe
▪ begins in face & arms; progresses to whole body
D Pathology
1 loss of GABA-ergic neurons in GPe
b eventually includes much of striatum (caudate & putamen)
▪ inhibits indirect pathway = increases thalamic drive
➢ = hyperkinesis
▪ loss of neurons in cortex & striatum also decreases stimulation of direct pathway
➢ = decreased thalamic drive (may result in slowing of the hyperkinetic movements)
2 loss of cortical neurons (esp. prefrontal cortex)
▪ role in attentional and executive symptoms
Emotional
Ventral striatum
- nucleus accumbens
- head of the caudate
- putamen
Limbic connections
- amygdala
- hippocampus
- orbital, cingulate, & entorhinal cortex
- MD thalamus → cingulate cortex
Cognitive
caudate nucleus
- from association cortical areas to prefrontal cortex
Motor
putamen
- from somatosensory cortex to motor cortex
