unit 3 - basal ganglia

Basal ganglia

modulates muscle tone and force and rhythmic output

basal ganglia strcutures do not have direct connections with

lower motor neurons (they are NOT UMNs)

basal ganglia influences motor output through

connections to the thalamus and brainstem

basal ganglia lesions will not present with

paralysis - will show disruptions/abnormal movement

basal ganglia connections are a series of

facilitory and inhibitory connections

hypokinetic lesion symptom

diminished movement - parkinsons, parkinsonism, multiple systems atrophy

hyperkinetic lesion symptom

too much movement - huntingtons disease, wilsons disease, tourette's disorder

basal ganglia includes

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

caudate and putamen are classified together a

striatum - input nuclei that receive signals from parts of the brain and send those signals into the BG

putamen and globus pallidus are classified together as

lentiform nucleus (lesions here result in parkinsons)

the globus pallidus has two parts

GP internus and GP externus

GP internus function

output nuclei projecting to thalamus and pons (more medial)

substantia nigra has two parts

compacta and reticulata

SN reticulata function

output nuclei projecting to the thalamus and pons

substantia nigra produces

dopamine

direct BG pathway

facilitates movement, GO

indirect BG pathways

inhibits unwanted movement, NO GO

lesions at different pathways, direct or indirect, determine if symptoms present as

hypokinetic or hyperkinetic

input nuclei - straitum, include

caudate and putamen

output nuclei include

substantia nigra reticulata, and GPi

intrinisic connections of the BG

substantia nigra compacta, GPe, and subthalamic nucleus (connect BG and nuclei)

the direct pathway follows

excitatory signal from cerebral cortex going to the striatum which inhibits GPi and SNr, which blocks inhibitory projections to the thalamus - permitting movement

direct pathway net effect is

disinhibition of thalamus, stimulated movement

indirect pathway follows

excitatory signal from cerebral cortex going to the striatum which inhibits GPe, blocking inhibitory signals to the subthalamic nucleus - subthalamic excites GPi and SNr which inhibits the thalamus and blocks excitatory signal to cortex

indirect pathway net effect

inhibition of thalamus - diminished movement

dopamine modulates

activity of striatum

when dopamine is present to receptors in the striatum

movement is enhanced - facilitates direct path

when the BG inhibits the motor thalamus

motor thalamus excites lateral corticospinal and rubrospinal tracts and permits fractionated movement at MNs

when the BG inhibits the pedunculopontine nucleus (which produces ACh)

pedunculopontine inhibits reticulospinal tract and permits postural and girdle muscle control at MNs

when the BG inhibits the midbrain locomotor region (gait initiation area)

region excites reticulospinal tracts and results in stepping pattern generators (walking)

parkinson's disease is characterized by

death to neurons in substantia nigra causing low dopamine and decreased activity in direct pathway

parkinson's disease symtpoms

bradykinesia, rigidity, stooped posture, resting tremor, freezing/shuffling/initiating/turning gait problems

when substantia nigra compacta's neurons die and dopamine is decreased

leads to GPi excessively inhibiting