lecture 11: basal nuclei Flashcards
which of the following locations for an UMN lesion would result in symptoms that are ipsilateral to the lesion
1) ventral horn
b) medullary pyramid
c) lateral corticospinal tract
d) decussation of the pyramids
lateral cortcospinal tract
which of the symptoms is/are not associated with a lower motor neuron lesion
a) muscle fascicualtors
b) spastic paralysis/paresis
c) postive babinski
d) decreased or absent deep tendon
c and d
lateral moot pathways are for what movement
appendicular (skilled and voluntary )
medial motor pathways are for what
posture, balance, stance (axial m)
what structure forms are upstream loop with motor cortex
basal nuclei
what is the function of the basal nuclei
responsible for iniating and terminating voluntary motor movement (and making it smooth)
decision to move, the direction and the amplitude is controlled by basal nuclei or cerebellum
basal nuclei
the coordination of movements is basal nuclei or cerebullum
cerebllim
extrapyramidal pathways get cortical input via what fibers
corticofugal fibersw
what are the 4 extrapyramidal pathways
rubro spinal (red nuc)
tectospinal (sup collic)
reticulospinal (reticular formation)
vestibulospinal (vestibular n)
extrapyramidal pathways originate and synapse where
brainstem
the motor pathways cannot start movement without upstream motor loop from where
basal nuclei
basal nuclei communicates with cortex and what other subcortical structure
thalamus
are basal nuclei cortical or subcortical
subcortical
what forms the basal nuclei
caudate nucleus
lentiform nucleus (putamun, GB)
sub thalamic nuclei
substantia nigra
what other subcortical structures are not basal nuclei but have important connections to it
thalamus
nucleus accumenbens
amygdaloid body
what are the two divisions of the globes pallid us
interna and externa
is the head of the caudate located rostral or caudal
rostral
what is the lentiform nucleus
putamen
globus pallidus interna and externa
what forms the most lateral part of the Lentiforn nucleuis
putamen
what forms the inner part of the LN
globus pallisud
what is the black substance in the midbrain called
substantia nigra
what forms the emotion connections for the basal nucleis
amygdaloid body
amygdaloid body is at the head or tail of the caudate
tail
be able to visualize the basal nuclei
the CN follows the curvature of what
the lateral ventricles
is the caudate nucleus a key input or output nuclei of the basal gang and explain
input
(info coming from outside basal nuclei comes to the caudate nucleus first)
what is the function of the caudate nuc
involved in cognitive processes controlled y the basal nuclei
true or false: caudate nucleus is a key output nucleus of the basal nuc
false, input
what forms the dorsal striatum
caudate nucleus and putamen
true or false:> the dorsall striatum is an input nucleus
true
the LN is composed of…
GB and putamen
true or false: putamen is an output nucleus
false, input
true or false: globes pallid us is an input nucleus
false, output
what is the function of the putamen
input nucleus of basal nuc involved in motor function
what is th function of the GP
output nucleus, relate information to the cortex via the thalamus (always happens indirection since it =must pass thru thalamus first)
the GP relays information directly or indirectly to the cortex and explain
always happens indirection since it =must pass thru thalamus first)
true or false: GP is more medial aspect of the LN
true
where is the sub thalamic nuclei located
inferior to the thalamus
superior to the midbrain
caudal to the hypothalamus
(edge of diencephalon, rostral edge of midbrain)
is subthalamic nuclei receiving input or giving output
receiving input
what is the function of the sub thalamic nuclei
receives input from the cortex and other basal nuclei (not a main input nuclei)
described at the clock of the basal nuclei as it regulates the output rhythm
what BN structure regulates the output rhythm
substhalmic nuc
true or false: the sub thalamic nucleus is a main input nuclei
false, not a main
where is the substantial nigra located
rostral midbrain in cerebral peduncle
the substantia nigra is located in rostral midbrain in BLNAK
cerebral peduncle
what are the 2 divisions of the substantia nigra
pars compact and pars reticula
what is the function of the pars compacta (what does it contain)
contains primarily dopaminergic neurons that project to other basal nuclei_
what its he name of the grey matter connection between head of caudate and putamen
nucleus accumens
what is the function of nucleus accumebsn
involved in reward behaviour, addiction, emotions
pleasure cetner
input nucleus of BN
receives limbic input entire the basal nuclei
true or false, the substantia nigra is involved in reward behaviour, addiction, emotions
false, thats nucleus accumebs
what is the pleasure centre of the brain
nucleus accumebns
what is the ventral striatum
nucleus accumbers and olfactory tubercle
what are the input nuclei of the basal
caudate (key)
putamen (key)
sub thalamic (not main)
nucleus accumebns (mostly limbic)
what is the output nuclei of the BG
globes pallidus
what are the 4 main blood supply of the BN
anterior cerebral a (lenticulostriate)
middle cerebral artery (lenticulostriate)
anterior choroidal
posterior cerebral a (deep)
what blood supply supplies the most rostral end of the basal nuc
anterior cerebral a (lenticulostraite)
what does the anterior cerebral a (lenticulostriate) supply
anterior (rostral) putamen and globes pallodus, head of caudate nuc
what does the middle cerebral a (lenticulostriate)
muddle of putamen and GP and body of the caudate
muddle of putamen and GP and body of the caudate
what blood supply
middle cerebral a (lenticulostraite)
anterior (rostral) putamen and globes pallodus, head of caudate nuc
what blood supply
anterior cerebral a (lenticulostraite_
what does the anterior choroidal a supply in BN
posterior (caudal) putamen and GP< and tail of caudate nucleus
posterior (caudal) putamen and GP< and tail of caudate nucleus
what blood s
anterior choroidal
what does posterior cerebral a (deep) supply of Bn
substantia nigra, subthalamic n and thalamus
substantia nigra, subthalamic n and thalamus
what blood supply
posterior cerebral (deep)
be able to locate blood supply on BN
BN form an upstream motor loop with circuit of connections with motor and premotor cortices in IPSILATERAL OR CONTRALATERAL HEMISTEPHRE
IPSILATERAL
true or false, BN forms a circuit of connections with motor and premotor cortices in contralateral hemisphers
false, ipsilateral
what are the main inputs to the basal nucelsu
cortex to dorsal striatum (via corticostriatal fibers)
substantial nigra to dorsal striature (via nigrostriatal gibers)
input to BN from cortex to dorsal striatum is via what fibers
corticostriateal
input to BN fromsubstantial nigra to dorsal striature is via what fibers
(via nigrostriatal fibers)
output from BN is what structure
globes pallidus interna to thalamus (via thalamic fasciculus)
output from BN is from GPi or GPe
GPi
what are the two important thalamic nuclei for the BN pathways
ventral anterior and ventral lateral
what are the 3 NT of the basal nuclei pathway
inhibitory: gaba
excitatory: glutamate
inhib/excite: dopamine
dopamine can be both inhibitory or excitatory, true or false
true, depending on what receptor
know the general basal nuclei pathway
the direct pathway is aka the blank pathways
go pathway
explain the direct pathways
1) excitatory projections: cortex to striate (asking to initiate movement)
2) inhibitory projections: striatum to GPI
3) inhibitory projections: GPi to thalamus
4) inhibition releases tonic inhibition (ie. disinhibition of the thalamus)
5) increase excitatory output from thalamus to the cortex
(dopamine from the Sec enhances excitation of the dorsal striatum though D1 receptions
=pathway will be upreglation, dopamine says more go)
GPi is an inhibitor or excitatory of the thalamus
inhibitor
dorsal striatum is an inhibitor or excitatory of the thalamus
excitator
the cortex sends glutamate or gaba to striatum in the direct pathway
glutamate
the striatum sends gaba or glutameate to the GPI
gaba
GPI sends gaba or glutamate to thalamus
gaba
the thalamus tries to send GABA or glutament back up to cortex
glutameate
the substance nigra sends glutament or gaba in the direct pathway
glutameate
in the direct pathway, dopamine from the Sec enhances excitation or inhibition of the dorsal striatum though D1 receptions
enhances excitation
(=pathway will be upreglation, dopamine says more go))
in the direct or indirect pathway do we get disinhibition of the thalamus
direct pathway
does disinhibition of the thalamus mean more or less excitatory signals to the cortex
more
inhibition of the GPi inhibits or disinhibits the thalamus in direct pathway
disinhibits
know the direct pathway (via the ninja nerd)
1) cortex sends excitation (via glutamate) to the striatum
2) striatum (which is excited) sending a lot of inhibition signals to GPi via gaba
3) GPi is inhibited therefore there a decrease of gaba release from GPi to Thalamus (therefore thalamus is excited )
4) increase in excitation (glutamate) from thalamus to the cortex
5) increase in motor activity
=substantion nigra will act on d1 receptors on striatum to further enhance activity and excite them
explain the pathway of the indirect/stop pathway
1) excitatory projections from cortex to striatum
2) inhibitory projection from striatum to GPE
3) inhibitory projections fro mGPe to STn
4) excitatory projections from Stn to GPI (excitation of the GPI increases inhibition of the thalamus)
5) inhibitory projections from GPI to thalamus (a lot of them)
6) decrease excitatory output from the thalamus to the cortex
=dopamine from Sac inhibits excitatory interneurons in striatum (d2 receptors)
=downregulates the patwath/inhibts
in the indirect pathway, the cortex sends excite or inhibit to striatum
excite (Glut)
in the indirect pathway, the striatum sends excite or inhibit to GPi
does not communicate directly with GPI
in the indirect pathway, the striatum sends excite or inhibit to GPe
inhibitory (GABA)
in the indirect pathway, the SNc sends excite or inhibit to striatum
inhibitory (GABA)
in the indirect pathway, the GPe sends excite or inhibit to STn
inhibitory (GABA)
in the indirect pathway, the STn sends excite or inhibit to GPi
excitatory (GLUT)
in the indirect pathway, the GPi sends excite or inhibit to thalamus
inhibit
true or false, in both pathways, the cortex is always sending inhibitory signals to the striatum
false, always excitatory
true or false, in both pathways, the striatum is always sending inhibitory signals to the GPi
false, always inhibits the GP (but not directly interna in the indirect)
true or false, in both pathways, the GPi is always sending inhibitory signals to the thalamus
true
true or false, in both pathways, the thalamus is always sending excite signals to the cortex
true
by exciting the GPi, do we get increases or decreases in motor activity in the cortex
decreases (we are increasing the inhibition to the thalamus)
by inhibiting the GPi, do we get increases or decreases in motor activity in the cortex
increases (we are decreasing the inhibition to the thalamus)
in what pathway is the sub thalamic nucleus invovled
indirect
understand the indirect pathway (ninja nerd)
1) cortex sends excitatory to the striatum
2) striatum sends inhibit (a lot of it) to the GPe
3) GPe is severely inhibited, but sends inhibitory signals to the Stn (technically activating STN)
4) STN (activated) sends excitatory signals to the GPi
5) Gpi (activtiated) sends inhibitory signals to the thalamus
6) thalamus (inhibited) decreases signals being send to the cortex
7) decreased motor activity
=substainta nigra will act on d2 receptors of striation to decrease inhibition and downregualte pathways
what are the two relay nuclei in the thalamus involved in both pathways
ventral anterior
ventral lateral
true or false: the basal nuclei circuit is purely a motor ciruit
false, also associative and limbic
explain the motor circuit for the BN
motor performance
=inputs from motor and somatosensory cortices are integrated in the putamen
=seperate pathway for oculomotor pathway (input from frontal eye fields pass through caudate nucleus)
in the motor circuit, we get inputs from where and where are they integrates
=inputs from motor and somatosensory cortices are integrated in the putamen
explain the assocaitive circuit of the BN
cognition
inputs from frontal, parietal and temporal association cortices travel to caudate nucleus
involved in complex motor planning, cognitive processes and learning
where do the inputs come from and go to in the associative circuit of the Bn
inputs from frontal, parietal and temporal association cortices travel to caudate nucleus
what is the function of the associative circuit of the BN
involved in complex motor planning, cognitive processes and learning
explain the limbic circuit of the BN
emotion
inputs from frontal assocaition areas and limbic lobe project to nucleus accumebns and ventral striatum
where do inputs from limbic circuit come from and project to
inputs from frontal assocaition areas and limbic lobe project to nucleus accumebns and ventral striatum
motor performance is associated with what circuit
motor cuirucit
cognition is associated with what circuit
associative circuit
emotion is associated with what circuit
limbic circuit
lesions to basal nuclei will result in contralateral or ipsilateral motor deficits
contralateral
true or false: lesions to basal nuclei will result in contralateral motor deficits
true
lesions to the cerebellum will cause ipsilateral or contralateral motor deficits
upsulateral
true or false: basal nuclei lesions and cerebellum lesions will cause opposite motor deficits
true
cerebellum (ipsilat)
basal nuc (contralat)
explain why despite the BN having projections to ipsilateral motor coritices, that a lesion to it will cause contralateral deficits
because downstream corticospinal pathways project primarily to the contralateral side of the body
(ie: right basal nuc = right motor cortex = left side of the body)what
what is the general effect of a lesion to the go pathway/direct
difficulty initiating movement = hypokinesia
difficulty initiating movement = hypokinesia is from a lesion to what pathway
direct
difficulty initiating movement = is known as…
hypokinesia
what is hypokinesia
difficulty initiating movement = is known as…
what is the general effect of a lesion to the stop pathway/indirect
excessive, uncontrollable movement = hyperkinesia
excessive, uncontrollable movement = hyperkinesia is lesion to what pathway
indirect
excessive, uncontrollable movement aka what
= hyperkinesia
what is hyperkinesia
excessive, uncontrollable movement
parkinson’s disease is caused by what
degeneration of substantia nigra, pars compacta
degeneration of substantia nigra, pars compacta assocaited with what condition
parkinsonstr
true or false: degeneration of substantia nigra, pars compacta is associated with hubtingon disease
false, parkinsons
a degeneration of substantia nigra, pars compacta causes what
loss of dopiminergic neurons projection to the basal nuclei
what are the characteric symptoms of parkinsons
akinesia (instability to initiate movement)
bradykinesia (slow execution of movements)
rigidity (esp in flexors)
involuntary tremor (persists as rest)
what is akinesia
nstability to initiate movement)
what is bradykinesia
(slow execution of movements)
in parkinsons, rigidity is most common where
in flexors
loss of dopaminergic neurons projection to basal nuclei causes problems with what pathway
direct pathway (difficukting initiating movement)
be able to udnerstand the effect of parkinsons on BN pathways
what are the treatments for parkinsons
L dopa therapy (precursor of dopamine)
=able to cross the blood brain barrier and be converted to dopamine centrally
deep stimulation of Stn
what treatment can you do to supplement the lack of endogenous dopamine in parkinsons
L dopa therapy since its a precursor of dopamine
Huntington diesease symptoms are usually bilateral or unilateral
bilateral
Huntington disease is usually problems with stop or go pathway
stop
is Huntington hereditary
yes, gets worse over time
huntington diease is caused by degeneration of what
dorsal striatum
degeneration of dorsal striatum is associated with what condition
huntington
true or false: Huntington is a progressive, hereditary disorder that typically manifests later in life
true
true or false: Huntington disease is only degeneration of the dorsal striatum and explain
false, also involves cortical degeneration (ex: frontal and temporal associateion cortices)
what are the characteristic symptoms of Huntington disease
chorea (jerky movements)
cognitive and memory deficits (caudate circuits)
enlargement of ventricles (nuclear degeneration)
true or false: Huntington starts to degenerate the go pathway first
false, stop pathway first
what is chorea
jerky, random and uncontrollable movements
chorea (jerky movements)
cognitive and memory deficits (caudate circuits)
enlargement of ventricles (nuclear degeneration)
associated with what condition
huntington
akinesia (instability to initiate movement)
bradykinesia (slow execution of movements)
rigidity (esp in flexors)
involuntary tremor (persists as rest)
associated with what condition
parkinsons
ballism is usually unilateral or bilateral
unilateral
what part of the BN is affected in ballism
lesion (ex: due to a stroke) affecting the sub thalamic nucleus
what blood vessel rupture could cause ballism
posterior cerebral (since ballism is lesions to the sub thalamic n)
lesions affected the sub thalamic nucleus is associated with what condition
ballism
ballism causes problems with the stop or go pathway first
stop
explain the issue with a lesion to the sub thalamic nucleus
loss of excitatory projections to the GPI (decrease in active thalamic inhibition = a lot of uncontrollable movements)
what are the characters symptoms of ballism
involuntary and uncontrolled flinging/flailing movements of the extremities
typically symptoms are unilateral
involuntary and uncontrolled flinging/flailing movements of the extremities
typically symptoms are unilateral
what condition
ballism
what is the treatment for ballism
dopamine antagonists
surgical interventions
deep brain stimulation of the GPi
what are the treatments for Huntington
dopaminergic antagonists
nutrition (require increase caloric intake)
