Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
181 Cards in this Set
- Front
- Back
|
Why do we no longer say basal ganglia?
|
because it's a misnomer and these cell bodies are within the CNS
|
|
|
What are the two structures lateral to the external capsule?
|
Clostrum and extreme capsule
|
|
|
What is the grey matter on the cortex just outside of the external capsule?
|
insula
|
|
|
If the insula is the most exterior part of this series of structures out from the basal ganglia, what can we infer about this system's location?
|
It is located right in between the parietal and temporal lobe.
|
|
|
What are the two ways to group structtures in the basal ganglia?
|
Traditional and clinical grouping
|
|
|
Draw the things included in the traditional basal nuclei.
|
|
|
|
List the structures just drawn.
|
Caudate nucleus, lentiform nucleus, amygdala, and clostrum
|
|
|
Draw the things included in the clinical basal nuclei.
|
|
|
|
List the structures just drawn.
|
Caudate nucleus, lentiform, subthalamus, substantia niagra
|
|
|
Why are these things grouped clinically as the basal ganglia?
|
They are all very closely related.
|
|
|
Draw the whole flow chart for basal ganglia types in one.
|
|
|
|
What are the only two parts of the basal ganglia that are the same between the two?
|
caudate nucleus/amygdala and the lentiform nucleus
|
|
|
Draw and name the two parts of the lentiform nucleus.
|
|
|
|
Draw the corpus striatum.
|
|
|
|
What is in the corpus striatum?
|
All parts of the lentiform nucleus and the caudate nucleus
|
|
|
Divide the corpus striatum into the neostriatum and the paleostriatum.
|
|
|
|
Why are the caudate nucleus and putament grouped together? What is another name for the neostriatum?
|
They are structurally similar and are even derived from the same embryological tissue. They just seem separate because the internal capsule goes through them.
Neostriatum = just STRIATUM |
|
|
What constitutes the lentiform nucleus?
|
the putamen and globus palldus
|
|
|
Draw the basic circuit involving the basal ganglia when we are trying to perform a movement.
|
|
|
|
Describe what just happened.
|
The cortex has the intention of a movement, consults the basal ganglia, which pulls a program and sends it back to the cortex via the thalamus.
|
|
|
What else (not shown previously) does the cortex consult?
|
It consults the cerebellum
|
|
|
Show which structures are in the motor cortex and which ones are involved in motor execution (cortex).
|
|
|
|
Show a slightly more detailed pathway of how an idea becomes an action that differentiated between the different parts of the motor cortex.
|
|
|
|
Describe what just happened.
|
1. Idea in prefrontal cortex
2. Sent to motor planning areas (premotor and supplementary) 3. Basal Ganglia is consulted* 4. Program sent to the thalamus 5. Program sent up to all 4 motor/sensory areas 6. Corticospinal tract fires up the action |
|
|
*Remind me of what is happening to the cerebellum during this time?
|
It is also being consulted. The planning area send fibers down the corticopontine pathway to the neocortex, which sends fibers from the denticulate nucleus back via the red nucleus or thalamus to the motor and sensory cortex.
|
|
|
What particular nuclei in the thalamus is activated by this motor pathway?
|
The centromedial thalamic nuclei (the biggest, most central intralaminar nuclei)
|
|
|
NOW WE TALK MORE IN DEPTH ABOUT CONNECTIONS IN THIS SYSTEM!
|
yay!
|
|
|
What is the pathway from the cortex to the basal ganglia and back to the cortex called? Why?
|
The direct pathway because it goes directly from the putamen to the globus palladus internal.
|
|
|
Draw out the direct pathway in detail. Label which neurons are stimulatory vs inhibitory.
|
|
|
|
List the names of the fibers in order of the circuit.
|
1. Cortico-striatal fibers
2. Striaital-Pallidal fibers 3. Palladal-Thalamic fibers 4. Thalamic-cortical fibers |
|
|
Where do most connections from the cortex go in the basal ganglia?
|
The putamen
|
|
|
What are the stimulatory NT's released?
|
Glutamate
|
|
|
What happens to the post synaptic neuron when glutamate is released?
|
there is a cationic influx
|
|
|
What are the inhibitory substances released?
|
Both the inhibitory neurons are GABAnergic, but the striatal (between putamen and GP internal) also releases substance P.
|
|
|
NOW WE TALK ABOUT WHAT HAPPENS IN THE BRAIN WHEN WE ARE AT REST VS INTITIATING A MOVEMENT
|
Yay!
|
|
|
Show which part of the direct pathway becomes more active when we are at rest and not planning any movement.
|
|
|
|
Narrate what just happened.
|
The GP internal got it's inhibition lifted and can fire inhibitory GABA signals to the thalamus now.
|
|
|
Which parts of the thalamus are involved in the direct pathway?
|
Ventral anterior, Ventral lateral, Dorsal medial nucleus
|
|
|
So which fibers become very active at rest?
|
the palladal-thalamic GABAnergic fibers
|
|
|
In my impulse control disorder, which neuronal connections are probably weak?
|
The ones involved with the corpus striatum. (The two inhibitory neurons)
|
|
|
Mnemonic for foot on the brake and direct pathway in terms of initiating an action.
|
Cortical striatal- Impulse to retract foot
Stritatal Pallidum- Foot taken off brake Pallidal thalamic- brake taken off car Thalamic cortical- car moves |
|
|
Mnemonic for default status of direct pathway at rest.
|
We are not sending any impulses to retract our foot so by default our foot is resting on the brake and the car is not moving.
|
|
|
What pathways are represented by having our foot defaultly on the brake?
|
The GP Internal --> thalamic inhibitory fibers are on by default and inhibiting excitatory thalamic--> cortical fibers
|
|
|
What two structures relay info to the thalamus necessary for movement?
|
The globus palladus and the cerebellum
|
|
|
What is the main input and output of the direct pathway in my mnemonic?
|
Input- activate legs to lift off brake
Output- Car moves due to brakes being taken off |
|
|
NOW WE TALK ABOUT THE INDIRECT PATHWAY
|
yay!
|
|
|
When we are writing, we are not only moving the agonist muscles in our hands, but we are also regulating what other muscles?
|
relaxing the antagonist muscles and activating the stabilizing muscles
|
|
|
What structure is responsible for all of the antagonists muscles relaxing? Is it conscious?
|
The basal ganglia, which is not conscious
|
|
|
What pathway is responsible for these supporting movements?
|
The indirect pathway
|
|
|
Why is it called the indirect pathway?
|
The fibers take a detour to the subthalamus so it does not directly go from the putamen to the GP interna.
|
|
|
Draw in the indirect pathway.
|
|
|
|
In the general car mnemonic, what can you say about how the indrect pathway?
|
The person in the driver's seat presses a remote control to signal a driver in the backseat to definitely NOT turn on the backwards drive while he takes his foot off the brake and drives forward.
|
|
|
Take the picture of the indirect pathway and group the pathways more concisely as brakes on or off when the cortex is firing
|
|
|
|
What extra structure is included in the indirect pathway? What happens to it when the indirect pathway is activated?
|
The subthalamus, which has the brakes taken off of it.
|
|
|
What does the subthalamus do when it has the brakes taken off of it?
|
It puts the brake on the thalamic-cortical fibers, thus inhibiting action.
|
|
|
Which pathway is shorter and which one is activated to activate motor movement?
|
The direct pathway
|
|
|
NOW WE TALK ABOUT THE ROLE OF THE SUBSTANTIA NIAGRA
|
woot!
|
|
|
What is the general role of the substantia niagra in all this movement?
|
It modulates the direct and indirect pathways for FINE TUNING OF MOVEMENT
|
|
|
Can you categorize all the structures as being in the telencephalon, diencephalon, and mesencephalon?
|
telencephalon- cortex and lentiform nucleus
diencephalon- thalamus and subthalamus mesencephalon- substantia niagra |
|
|
So if you stimulate the direct and indirect pathway from the cortex, what is the ultimate outcome?
|
stimulation of motor fibers out the direct pathway
inhibition of motor fibers out the indirect pathway |
|
|
How can you contrast this with the end goal of the substantia niagra?
|
The SN's outcome is to stimulate all the motor fibers via modulating the direct and indirect pathways
|
|
|
What NT does the SN use?
|
It uses dopamine
|
|
|
At which point of the indirect and direct pathways does the SN dopaminergic neurons intervene?
|
It goes to the putamen on both.
|
|
|
Is it giving similar input to both pathways at the putamen? What is it?
|
Yes! It is releasing dopamine on both.
|
|
|
How does it manage to give different results than the cortical stimulation of both pathways at the putamen?
|
The two pathways have different receptors. The direct pathway is stimulated by the SN and the indirect pathway is inhibited.
|
|
|
What are the different receptors for dopamine for each pathway?
|
Direct- D1- stimulatory
Indirect- D2- inhibitory |
|
|
How does the SN know when to fire?
|
There are cortico-niagral fibers that inform the SN of what the cortex wants to do.
|
|
|
Which part of the SN is responsible for modulating the lentiform nucleus pathways?
|
The pars compacta part.
|
|
|
What can you say about the effect of the cortex and SN on the indirect pathway?
|
They are antagonistic to one another
|
|
|
What determines whether or not the putamen - subthalamic fiber will fire?
|
the balance of cortical stimulatory and SN inhibitory signals being released to it.
|
|
|
What can we say about the cortex vs SN's effect on the ion channels/membrane potential of the putamen-subthalamus neuron?
|
cortex opens Na channels and raises the membrane potential to threshold whereas the SN does the opposite
|
|
|
SLIGHT DETOUR TO NT FUNCTION TALK
|
YAY!
|
|
|
When GABA inhibition is taken off a neuron, what are two broad reasons that the neuron would then fire?
|
1. Excitatory signals can finally win out
2. The post neuron is Na leaky and can self depolarize to threshold |
|
|
What are two mechanisms by which GABA reduces the membrane potential by acting on membrane channels?
|
1. Opens chloride channels to let it in
2. Opens K channels to let it out (both make the cell membrane more negative) |
|
|
Why would these two things make the cell membrane more negative? (start with the definition of cell membrane potential)
|
cell membrane potential is the charge needed inside of the cell to keep everything where it is.
When Cl channels open- need more negative charge inside to repel them When K channels open- need more negative charge inside to keep them in |
|
|
NOW WE CONTINUE THE TALK ABOUT MODULATION OF THE DIRECT AND INDIRECT PATHWAYS.
|
YAY!
|
|
|
What can you think of the pars reticularis as?
|
An inferiorly displaces GP interna
|
|
|
What does this mean in terms of it's function?
|
It functions the same and will receeive all of the same fibers and connections. Simple, right?
|
|
|
What system counters the effect of the SN pars compacta on the indirect and direct pathways?
|
A cholinergic system within the putamen.
|
|
|
How does it do this? How is this compared to the SN dopaminergic system?
|
It inhibits the direct pathway and stimulates. DIrectly the opposite of the SN dopaminergic pathway.
|
|
|
Now draw the whole pathway to summarize everything and make sure to note which NT's are being released. (they are pathologically very important)
|
|
|
|
NOW WE TALK ABOUT PATHOLOGIES INVOLVING THE BASAL GANGLIA.
|
very interesting stuff!
|
|
|
What are the three main outcomes for basal ganglia dysfunctions?
|
1. Hypokinesia
2. Hyperkinesia 3. Dyskinesia |
|
|
What will happen if there is an underfunctioning of the direct pathway?
|
You will have a hard time initiating movement or you can't at all. (hypokinesia and akinesia)
|
|
|
What kinds of people have an underfunctioning of the direct pathway?
|
People with parkinson's and the people from Awakenings
|
|
|
What disease did the people from awakenings suffer from?
|
Encephalitis lethargica
|
|
|
What was the pathophysiology of encephalitis lethargica?
|
Researchers think the flu that year stimulated autoantibodies against the basal ganglia, which rendered the direct pathway inactive.
|
|
|
What celebrity has Parkinson's that I can thik of when thinking about the pathophysiology?
|
Michael J Fox
|
|
|
What are the three symptoms of Parkinson's?
|
1. Hypokinesia
2. Rigidity 3. Tremors |
|
|
What neuron is initially degenerated in Parkinson's?
|
The dopaminergic neurons
|
|
|
Where are the cell bodies of the affected dopaminergic neurons?
|
The pars compacta of the substantia niagra
|
|
|
What is the net effect on agonist and antagonistic muscles from decreasing dopaminergic firing?
|
they are both decreased
|
|
|
What does this mean as far an initiating movement?
|
It will be very hard to initiate movement without the muscle enhancing effects from the dopaminergic neurons of the substantia niagra pars compacta
|
|
|
What kinds of movements are most affected by hypokinesia? Why?
|
facial expressions because they are so quick. People with Parkinsons may have mask face.
|
|
|
What does this explain about Michael J Fox?
|
Why he doesn't look that great as an actor anymore
|
|
|
Is hypokinesia just a problem with STARTING movement?
|
No it is also a problem with stopping movement.
|
|
|
What would happen if you gently pushed a parkinson's pt forward?
|
They would start shuffing and not be able to stop quickly
|
|
|
What kind of connection does the cortex have with the reticular formation?
|
It will normally inhibit the reticular nuclei.
|
|
|
What happens when you inhibit the reticular nuclei?
|
both the flexor and extensor UMN's coming from there will overfire.
|
|
|
Are these reticular nuclei the main UMN's or just the supporting ones? mnemonic?
|
Just supporting. (they are from the ViP and rubber mat mnemonics)
|
|
|
What will happen if you try to flex and extend the arm them?
|
mild resistance both ways (not enough to stimulate golgi tendon reflex)
|
|
|
So what kind of rigidity will people with parkinson's have?
|
lead pipe rigidity
|
|
|
What happens to the RELATIVE activity of the striatal cholinergic neurons when the dopaminergic neurons underfire?
|
They become more dominant than previous because they are unopposed
|
|
|
What kinds of circuits can get activated when the ACh activity is high?
|
reverberating circuits
|
|
|
Draw a picture of reverberating circuits.
|
|
|
|
What do these reverberating circuits do to your muscles? What is this symptom called?
|
Alternately stimulate agonist and antagonist muscles producing the tremors of Parkinson's.
|
|
|
How can you explain reberberating tremors in terms of overcompensation?
|
Normally you fire just the right amount, but sometimes your brain overshoots it and tries to correct with the antagonizing muscle, but overshoots that as well. This goes back and forth in a tremor.
|
|
|
So what are some classic manifestations of the symptoms of Parkinson's? (use Michael J Fox associations) Show a pic of the woman with parkinson's.
|
1. Stooped posture
2. Shuffling gait 3. Uncontrollable tremors 4. Mask face |
|
|
There are actually many different types of Parkinson's. We just discussed one in which the dopaminergic neurons degraded. Now we discuss more.
|
OK!
|
|
|
What is the type of Parkinson's that started cropping up in some young people?
|
MPTP associated Parkinson's
|
|
|
What was MPTP and what does it do?
|
A contaminant in heroin that would harm the dopaminergic neurons
|
|
|
What kind of medication could cause parkinson's like symptoms? Is this permanent? WHat would happen if you stopped?
|
Dopamine blockers for antipsychotic purposes.
No. You could get tardive dyskinesia during or after because of sensitized neurons with upregulated dopamine receptors. |
|
|
NOW WE TALK ABOUT DAMAGE TO THE INDIRECT PATHWAY.
|
WOOT
|
|
|
Thinking about the final outcome of the direct and indirect pathways, what would you expect to be the symptom is either was damaged?
|
Direct- hypokinesia
Indirect- hyperkinesia and dyskinesia |
|
|
What is the difference in NT's between the GABAnergic neurons in the direct vs indirect pathway?
|
direct- GABA and substance P
indirect- GABA and enkephalins |
|
|
What implication does this have for disease?
|
different diseases can selectively affect the GABAnergic neurons in the direct an indirect pathway
|
|
|
Show what neuron gets affected in Huntington's to produce the chorea.
|
|
|
|
What are the 6 different types of hyperkinesia?
|
1. Chorea
2. Athetosis 3. Dystonia 4. Hemiballismus 5. Tardive Dyskinesia 6. Wilson's disease |
|
|
What are the two types of chorea?
|
1. Huntinton's Chorea
2. Sydenham's chorea (St. Vitus Dance historically) |
|
|
What do all these dysfunctions have in common?
|
they involve lesions of the indirect pathway
|
|
|
How are chorrea movements like michael jackson's dancing?
|
they are very abrupt and spastic and seem purposeless
|
|
|
Show a picture of the picture of the woman with huntington's.
|
|
|
|
Why are these purposeless movements happening?
|
There is random release of motor programs from the basal ganglia
|
|
|
What is the genetic basis for Huntington's?
|
There is an over amplification of trinucleotide CAG repeat in huntington's protein on Chromosome 4.
|
|
|
What does this mutated huntington's protein damage?
|
the dopaminergic neurons
|
|
|
What happens in each successive generation of people with Huntington's?
|
There are more trinucleotide repeats and it gets worse and appears earlier.
|
|
|
Does this happen with all trinucleotide repeat disorders?
|
Yes
|
|
|
Which genetic disease did I learn about previously that had the GAA repeat?
|
Friedrich's ataxia
|
|
|
What symptoms come along with chorea for Huntington's?
|
Depression and dementia
|
|
|
What physical changes happen to structures in the brain of people with Huntington's?
|
The head of the caudate nucleus degenerates and the lateral ventricles enlarge to fill the space.
|
|
|
Mnemonic for Huntington's disease. CAG stands for what?
|
All the things that decrease in Huntington's
Caudate nucleus degeneration Acetyl choline deficit GABA deficit |
|
|
Why is there ACh and GABA deficits?
|
Because these neurons are in the caudate nucleus which gets damaged.
|
|
|
What is the other type of chorea?
|
St. Vitus Dance or Sydenham's Chorea
|
|
|
Who is most likely to get Sydenham's chorea?
|
Young girls
|
|
|
Show the picture of the young girl with Syedenham's chorea. (remember her mother was very light hearted about it so that indicates it is not permanent)
|
|
|
|
Which type of chorea would you prefer to have and why?
|
Sydenham's because it is transient whereas Huntington's is progressive and terminal
|
|
|
Why do people get sydenham's chorea?
|
It is an autoimmune mimicry attack that happens along with rheumatic fever leading to inflammation in the caudate
|
|
|
What percent of children who get strep throat get rheumatic fever?
|
3%
|
|
|
What is WIlson's disease? What causes all the damage?
|
When there is excessive presence of free copper in the blood and it deposits to create oxidative damage.
|
|
|
Where does the copper like to deposit?
|
In the lentiform nucleus, cornea, and the liver.
|
|
|
So what are the symptoms of Wilson's disease?
|
1. liver failure
2. chorea 3. keysa flashner ring in the cornea (copper colored) |
|
|
What carries copper in the blood?
|
ceruloplasmin
|
|
|
So what should the level of ceruloplasmin in the blood of a wilson's disease patient be?
|
low
|
|
|
How do you get Wilson's disease?
|
it is inherited
|
|
|
What is the defect that is inherited and what chromosome is it found on?
|
Chromosome 14 defect of ceruloplasmin
|
|
|
What is athetosis present like? Why?
|
An indian dance because they are more smooth and slow movements. (like how I dance with my hands)
|
|
|
Show the picture of the guy with athetosis
|
|
|
|
Does chorea and athetosis have to be separate?
|
no, often times they are combined and then called choreoathetosis
|
|
|
Show the boy with dystonia.
|
|
|
|
What muscles are being overly active in dystonias? What does this remind you of?
|
The extensor muscles, (arms, back, and neck)
Looks like the exorcist |
|
|
What is dystonia of the neck specifically called? (show a picture)
|
Torticollis
|
|
|
What kind of dance is hemiballismus like?
|
arabic belly dancing
|
|
|
What is the difference between ballismus and hemiballismus?
|
hemiballismus only involves one side of the body
|
|
|
What qualities of ballismus/hemiballismus are like belly dancing?
|
They are continuous and usually rotatory in nature
|
|
|
What is a common cause of ballismus? Why is it usually hemi?
|
a stroke that kills part of the subthalamus controlling the indirect pathway.
|
|
|
In particular, what kinds of movements are affected by subthalamic regions?
|
hip and shoulder girdles
|
|
|
So what kind of "ballistic" movements do these pts have?
|
big rotatory movements of the shoulders and hips.
|
|
|
What is one way in which you can treat psychosis?
|
anti dopaminergic drugs
|
|
|
What happens to the post synaptic dopamine neurons when dopamine is blocked for a long time?
|
They will upreglate dopamine receptors
|
|
|
What kind of dyskinesia does this result in?
|
Tardive dyskinesia
|
|
|
Which demographic is most affected by tardive dyskinesia?
|
older women who have been on antipsychotics for a long time.
|
|
|
What kind of movements are typical in tardive dyskinesia?
|
fly catching movements of the tounge and face
abnormal orofacial movements |
|
|
Give a picture of someone with Tardive dyskinesia.
Mnemonic for the sx? |
tardive- diving in to catch the flies with your mouth
pretty crazy thing to do, which is why crazy old ladies get it. |
|
|
START WHITE'S NEUROANATOMY LECTURE
|
HOPEFULLY THIS WILL CLEAR SOME STUFF UP!
|
|
|
THATHATHA THALAMUS!!!!
|
THALASTIC!
|
|
|
What does DI-ENCEPHALON literally mean?
|
Between brain (hemispheres)
|
|
|
What is the basic essential function of the thalamus?
|
To filter and relay different sensory and motor inputs to the cerebral cortex
|
|
|
What are the most commonly cited 2 nuclei of the thalamus?
|
VPL and VPM
|
|
|
How are VPL and VPM similar? How are they different?
|
They both carry sensation from the body walls to the cortex.
VPM carries sensory info from the face and trigeminal nerve (and taste) VPL carries sensory info from the limbs and trunk |
|
|
What is the somatosensory cortex? What is it getting sensory input from?
|
The place in the cortex getting body wall sensory info.
|
|
|
What is the difference between LGN and MGN?
|
LGN- visual info
MGN- auditory info |
|
|
What do the ventral lateral and ventral anterior nucleus do?
|
They both relay information from both the basal ganglia and the cerebellum
|
|
|
What does the Pulvinar do? Is it well understood?
|
It is a thalamic nuclei that is involved with visual tectal reactions. It is not well understood.
|
|
|
HYPOTHALAMUS CHAT TIMES!
|
WHEEE!
|
|
|
What is the acronym used for the hypothalamus and what does it stand for?
|
HEAL
Homeostasis Endocrine Autonomic Limbic |
|
|
Show the pic of the hpothalamus, pituitary gland, and mamillary body.
|
|
|
|
Show where the optic chiasm is in a real pic compared to the hypothalamus.
|
|
|
|
Are there many hypothalamic nuclei?
|
yes
|
|
|
Which ones give off NT's to the PP?
|
Supraoptic nucleus and paraventricular nucleus.
|
|
|
Show these two nuclei.
|
|
|
|
How does the hypothalamus regulate the AP? What nucleus does this?
|
The arcuate nucleus secretes stiulating and inhibiting factors to the AP.
|
