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Neuro Week 2 > ICL 4.1: Basal Ganglia & Movement Disorders > Flashcards

ICL 4.1: Basal Ganglia & Movement Disorders Flashcards

1
Q

What are the functions of the basal ganglia?

A
  1. Motor
  2. Oculomotor
  3. Cognitive
  4. Affective (emotions, the limbic system)
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2
Q

What is the motor function of the basal ganglia?

A

The basal ganglia is known as the extrapyramidal tract! It’s the major motor pathway outside of the pyramidal corticospinal tract

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3
Q

What is the motor function of the basal ganglia?

A
  1. Helps select appropriate actions by facilitating the correct motor program

Like if you have to get across the room, there’s lots of ways you can do this like you can walk, run, skip, crawl = all of these are different motor pathways and your basal ganglia helps you select the correct one

Or if you’re outside, you don’t want to run because it’s icy and you’d fall

  1. Active inhibition of competing motor programs

So when it’s appropriate to walk, you’ll only walk and you won’t activate the running, skipping, crawling programs

  1. Increase automaticity over time = learning of habits
  2. Regulates the scale of motor activity by adjusting amplitudes of adjusting duration of posture and movements

So if you’re eating soup, the motion of bringing the spoon to your mouth is the movement you’re doing but you don’t want to do it too fast or the soup will end up everywhere (amplitude)

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4
Q

What is the 4 main structures of the basal ganglia?

A
  1. Striatum
  2. Globus pallidus (external and internal segment)
  3. Substantia nigra (pars reticulata and pars compacta)
  4. Subthalamic nucleus
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5
Q

What are the components of the striatum of the basal ganglia?

A
  1. Putamen
  2. Caudate
  3. Nucleus accumbens

The putamen is separated from the caudate by the anterior limb of the internal capsule

The caudate forms the lateral wall of the lateral ventricle

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6
Q

What is the function of the putamen?

A

Motor activity of the basal ganglia

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7
Q

What is the function of the caudate?

A

Ocular motor and cognitive function of the basal ganglia

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8
Q

What is the function of the nucleus accumbens?

A

Limbic system function

So dopamine and serotonin

Dopamine = desire and exotoxin = satiety

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9
Q

What is the lenticular nucleus?

A

Lenticular nucleus = globus pallidus + putamen

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10
Q

What is the main source of dopamine in the basal ganglia?

A

Pars compacta of the substantia nigra

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11
Q

What is the important excitatory nucleus of the basal ganglia?

A

Subthalamic nucleus

It releases glutamate as a neurotransmitter

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12
Q

What are the inhibitory parts of the basal ganglia?

A
  1. Striatum
  2. Globus pallidus

So these two are mainly inhibitory and release GABA neurotransmitter

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13
Q

Where are the structures of the basal ganglia located in respect to each other?

A

Slide 7 and 8

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14
Q

What is the predominant cell in the striatum?

A

Medium spiny neurons

These are effected in Huntington’s disease; specifically the one’s in the caudate nucleus

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15
Q

How do the medium spiny neurons function?

A

They’re the main cell type in the striatum

The glutametergiv input from the cortex come to the dendritic spines on these cells while the dopaminergic input comes to the neck of the spines to modulate

These cells have projections which are inhibitory so they release GABA

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16
Q

What are the two types of medium spiny neurons?

A

There are two types based on the predominant dopamine receptor expressed

D1 = projects mainly to globus pallidus internal and uses GABA but also substance P and dynorphin

D2 = projects mainly to globus palllidus external and uses GABA but also enkephalin

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17
Q

What is the main input coming into the basal ganglia?

A

Frontal motor cortex in the frontal lobe sends excitatory messages to the striatum and also the substantia nigra compacta

Then the striatum connects to its neighbor, the globus pallidus!

The globus pallidus is inhibitory so it’ll release GABA from its spiny neurons

18
Q

What is the main output from the basal ganglia?

A

The globus pallidus!

It releases GABA which goes to the thalamus

The thalamus then connects to different portions of the frontal lobe like the supplemental motor area (SMA)via the thalamocortical fibers to close the circuit/loop (it started in the cortex of the frontal lobe and it’s back there)

The thalamus also connects to areas in the brainstem for oculomotor control

19
Q

How does the subthalamic nucleus communicate with the globus pallidus?

A

STN provides excitatory input to the globus pallidus external and internal

Then in turn, there’s a negative feedback loop where GPe inhibits STN and GPi

So oscillations can arise in pathologic conditions due to interactions of GPe and STN

Slide 12….

20
Q

What is the template for the circuits involving the basal ganglia?

A

Cortex —> basal ganglia —> thalamus —> cortex (or to the superior colliculus of the midbrain for ocular motor function)

Increased output from the basal ganglia to the thalamus INHIBITS the invitation of movements because the globus pallidus is releasing GABA

21
Q

What is the dual function of the basal ganglia?

A

It facilitates one motor program by transiently interrupting the inhibitory output from the globus pallidus internal and the substantia nigra reticulata while at the same time increasing the inhibition to inhibit all other competing motor programs —> this is what lets you walk instead of trying to walk and run at the same time

The regulators of this are the globus pallidus internal and the SNr —> GPi is inhibitory, subthalamic nucleus is excitatory but it’s exciting the GPi which is inhibitory so it’s actually increasing the inhibition of the OTHER motor programs

The spiny nuclei of the striatum is what actually inhibits the GPi which will allow your body to start a motor program for a short time window

22
Q

What are the 3 motor pathways of the basal ganglia?

A
  1. Direct pathway
  2. Indirect pathway
  3. Hyperdirect pathway
23
Q

What is the direct pathway?

A

Cortex —> striatum —> GPi —> thalamus —> cortex

So the cortex releases glutamate which excites the striatum

The striatum then releases GABA and inhibits the GPi — normally GPi inhibits the thalamus but since it’s now inhibited, the inhibition on the thalamus is gone = double inhibition

So now GPi is no longer inhibiting the thalamus so the thalamus will excite the motor cortex which initiates movement!

So when you initiate the direct pathway, you’re initiating motor action; it’s the go signal for the correct motor program

24
Q

What is the indirect pathway?

A

Cortex —> striatum —> GPe —> STN —> GPi —> thalamus —> cortex

So what happens is the cortex excites the striatum and then the striatum inhibits GPe

Normally GPe would inhibit STN but now GPe is inhibited so STN can do it’s normal excitatory activity and it will go and excite GPi

GPi is inhibitory so it will now really inhibit the thalamus and the thalamus will not be able to excite the cortex which means there will be no movement!

So when this pathway is activated, it prevents initiation of a motor program!

25
Q

What is the hyperdirect pathway?

A

Cortex —> STN —> GPi —> thalamus —> cortex

So the cortex will excite the STN

STN is excitatory so it will go and excite the GPi

GPi is inhibitory so it will go and inhibit the thalamus — normally the thalamus excites the cortex but since it’s inhibited, the cortex can’t be excited and there will be no movement

So if you chose the wrong program on accident and need to stop it really fast, you use the hyperdirect pathway —> so when this pathway is activated, it’s the stop signal for motor programs that are already in progress

26
Q

How does dopamine modulate the basal ganglia?

A

D1 receptors are excitatory

D2 receptors are inhibitory

Medium spiny neurons are normally not active = off state

If you increase dopamine, it maintains the off state which prevents activation; it prevents background static noise randomly coming into the basal ganglia and activating a pathway

However, when you really want to move, you send a strong signal from the motor cortex to the basal ganglia, you turn on the striatal cells and in this situation, the dopamine will actually modulate the on state!

So it prevents involuntary movements and also facilitates voluntary movements too! It helps you initiate the correct motor activity

27
Q

What is reward and motor learning?

A

Motor activity —> positive outcome —> increased dopamine which then goes to basal ganglia and increases that motor activity

Motor activity —> negative outcome —> decreased dopamine which means that motor activity won’t be facilitated as much

So with a baby or kid, they want the reward so they’ll do an activity but eventually they’ll start moving towards a goal after repeated reward

Eventually they’ll figure out what the goal is like walking will get you places without the help of an adult so goal directed activity will eventually become habit! It’s no longer about what will walking bring me, you just walk because you want to

28
Q

What is hypokinetic-rigid syndrome?

A

Aka Parkinson’s!

Due to low dopamine in the striatum due to degeneration of the dopaminergic neurons of SNc which normally make dopamine!

You’ll see Levy body’s due to deposition of alpha-synuclein in the cells!

Because this disease is due to low dopamine, the treatment is dopamine replacement

29
Q

Which pathway is effected in Parkinson’s?

A

Cerebral cortex —> striatum —> GPi which is the direct pathway

Dopamine in the direct pathway produces an excitatory effect and facilitates movement

Dopamine will inhibit the indirect pathway which will allow for movement since the indirect pathway normally inhibits movement

If you get rid of dopamine like in Parkinson’s, the direct pathway doesn’t work as well so the patient won’t be able to start motor programs and they’re can’t easily start a movement! Think about a Parkinson’s patients trying to walk and how much they stutter or get stuck

For the same reason of low dopamine, the inhibiting activity of the indirect pathway has increased which leads to more inhibition of movement! This is because dopamine normally inhibits the indirect pathway

30
Q

Which features suggest a Parkinsonian disorder?

A
  1. Tremor (low frequency resting tremor)
  2. Gait disturbance
  3. Stiffness
  4. Slowness
  5. Handwriting disturbance
  6. Forward bent posture
  7. Pisa syndrome = leaning posture
31
Q

How do you diagnose Parkinson’s?

A

Clinical criteria, there isn’t really a test that will do it

UK Parkinson’s Disease Society Brain Bank’s clinical criteria for the diagnosis of probable Parkinson’s disease

So you have to have bradykinesia = slowness and inability to start movement then you need one of the following: rigidity, resting tremor, or postural instability not caused by primary visual, vestibular cerebellum or proprioception dysfunction

Then you also have to exclude other causes of Parkinsonism

The only way to confirm a diagnose is through biopsy and finding Lewy bodies

32
Q

How do you treat Parkinson’s with medication?

A

Dopamine replacement

  1. Levadopa
  2. Amantadine = helps release dopamine better
  3. Dopamine agonists
  4. anti-cholinergics

Slide 34; go look at where all these drugs act on the basal ganglia and receptors

33
Q

How do you treat Parkinsons?

A
  1. Dopamine replacement
  2. Physical therapy
  3. Electricity therapy which inhibits GPi and subthalamic nucleus
34
Q

What is essential tremor?

A

This happens when the patient is actively doing something so that’s different from Parkinson’s which is a resting tremor

35
Q

What is Archimedes Spiral?

A

Related to essential tremor

The frequency is related to something wrong with a specific nuclei of the basal ganglia

These tremors have a specific axis and at a certain axis, the tremor is the worst and you can see this by telling the patient to draw a spiral

If a spiral doesn’t have an axis, then it is NOT an essential tremor

36
Q

Which medications will help you treat essential tremors?

A
  1. Propranolol
  2. Primidone
  3. Topiramate
  4. Gabapentine
  5. Alprazolam
  6. Clonzepam
37
Q

How do you treat essential tremors?

A
  1. Meds
  2. Chemodenervation is using toxins to block the nerves that are causing the tremors
  3. DBS
  4. MRI focused ultrasound to burn the cells that are messed up
38
Q

What is cervical dystonia?

A

Abnormal muscle spasm that causes abnormal posture of the neck

Sometimes people will describe it as a sensory trick and if they touch a certain part of their neck or head, it will straighten out! This is the hallmark for this disease

So you’d want to turn off the direct pathway in the basal ganglia and activate the indirect pathway to turn off the tick that’s causing the neck spasms

It’s so weird though because if the doctor touches them in the same spot it won’t work but if the patient does it, the tremor or the neck twitch will stop/improve

39
Q

How do you treat cervical dystonia?

A
  1. Oral medications
  2. Botulinum toxin injections
  3. Deep brain stimulation
  4. Rehabilitation
40
Q

What is chorea?

A

A non-respective, random, combination of fast and slow movements

The patient will try to make it a voluntary movement to mask the involuntary movements; initially when this disease is mild they can be successful with hiding it

41
Q

Which disease cause chorea?

A

Huntington’s

This is an AD, CAG trinucleotide repeat disorder on chromosome 4

On MRI scans, you will see caudate nucleus atrophy of the basal ganglia

You can see this happen after a strep infection due to an autoimmune reaction = Sydenham’s chorea

You can also see this happen after pregnancy! = chorea graviderum

42
Q

What is hemiballismus?

A

A lesion of the subthalamic nucleus that causes really big and fast involuntary movements —> the contralateral STN is what’s effected; so if there’s a right STN lesion, then there will be spasms on the left side of the body

STN usually excites GPi which inhibits the thalamus to inhibit involuntary movements

So without STN, GPi isn’t as active so it doesn’t inhibit the thalamus to inhibit involuntary movements

The classic presentation is STN hemorrhage due to hypertension but it can also happen with a stroke (infarct)

Intermittent hemiballismus can also be seen in patients with hyperglycemia or TIA (transient ischemic attack aka a mini stroke)

Neuro Week 2 (10 decks)

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