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Sc 29 Parkinson's Disease > General > Flashcards

General Flashcards

1
Q

What does the Cortex do?

What is it modulated by?

What are the connections via?

A

Runs executive function; it is the decision making part of the brain

Modulated by Basal Ganglia and Cerebellum via the THALAMUS

Connections betwen the thalamus and the cortex are done via the INTERNAL CAPSULE

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2
Q

What disorders occur with issues of:

Mortex cortex

A

paralysis with spasticity (upper motor sign)

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3
Q

what happens in:

Internal capsule disorder?

A

upper motor sign and sensory deficits

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4
Q

what happens in:

Basal ganaglia

/

cerebellum

disorders?

A

involuntary movements, slowness of movement

disruption to movement execution occurs

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5
Q

Thalamus

A

Swelling on wall of 3rd ventricle

Hub of info flow into the cortex

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6
Q

Cerebellum and pontine nucleus

what do they work as?

A

Work as a single unit

pontine nucleus relays info to cerebellum

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7
Q

Basal Ganaglia

what are the 2 main components?

A
  • Striatum
  • Globus Pallidus
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8
Q

what makes up the Striatum?

A

Putamen

and

Caudate Nucleus

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9
Q

What is the lentiform nucleus

what is it made up of?

A

Made up of the

Putamen

and

Globus Pallidus

called this together since the Putamen & G Pallidus sit together so are collectively called a name

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10
Q

What separates the Caudate and the Putamen?

A

The anterior limb of the I.C

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11
Q

In terms of afferents and efferens

what does the Thalamus contain?

A

Afferents: Thalamus is a SENSORY RELAY

Efferents:

Thalamus is NOT a Motor Relay

  • • cortical efferents by-pass the thalamus
  • • Motor (M):
    • corticospinal and corticobulbar
  • Prefrontal (PF):
    • corticopontine (stops at the PONS)

efferents originate from layer 5 of the cortex

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12
Q

what happens at the genu of the internal capsule

A

it is where the posterior and anterior limbs meet

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13
Q

Visual pathway

A

relayved via the Lateral Geniculate Nucleus

Runs down the Retrolenticular pathway

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14
Q

Auditory pathway

A

Relayed by the Medial Geniculate Nucleus

Runs down the Sub-lenticulat pathway

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15
Q

Posterior Limb of IC

A

Carries descending Motor output and Sensory info from that area

Damage: Catastrophic - both motor and sensory pathways to the limbs would be affected

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16
Q

Genu of the IC

A

Motor and Sensory to the Head region - facial muscles etc

Damage: Loss of motor and sensation to facial area/muscles

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17
Q

Anterior Limb of IC

A

Contain the corticopontine pathway

Parts of the cortex that relate to cognitive functions

Axons which only run to the PONS orginate from this area

Damage:

Cognitive Function defects

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18
Q

What will blockage of the Ant Cerebral Art affect?

A

Genu in particulat

loss of sensation and motor function to the head

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19
Q

Blockage of the MCA

A

Defect affects the Basal Ganglia

Ant and POst limb

20
Q

Damage to the post limb and genu lead to

A

Paralysis

Loss of sensation

Loss of vision and hearing

21
Q

Damage to the anterior limb

A

Leads to

Cognitive defects

22
Q

Basal ganglia send what kind of axons to the Thalamus?

A

Inhibitory axons

Inhibition can either be lifted (increase thalamus excitability )

OR
increased (reduce thalamus excitability)

23
Q

What happens with increased output of the Basal Ganglia

A

Hyperinhibition

Thalamus inhibited and movement suppressed, e.g. in PD

24
Q

Dopamine

from the Sustantia Niagra

A

Modulates overall output of the Basal Ganglia

More dopamine leads to less inhibitory bg output

Less dopamine leads to more inhibition

25
Q

What does Cerebellar damage lead to?

A
  • Hypotonia - pendulous reflexes
  • Astasia - Abasia inability to stand or walk
  • Ataxia - errors in timing and coordination of multi-joint movement
  • Action (intention) tremor
26
Q

Is the cerebellum excitatory or inhibitory?

A

Excitatory

it modifies cortical function by acting on the THalamus

27
Q

What is the difference between Cerebellar and Cortex damage

A

Cerebellar damage = IPSILATERAL

Cortical damage = CONTRALATERAL

28
Q

Cerebrocerebellum

aka neocerebellum

the hemispheres

what does it do and what is its output?

A

Involved in:

  • motor planning
  • cognition

Output:

  • thalamus (ventrolateral)
29
Q

Spinocerebellum

aka palleocerebellum

in the middle

A

Controls: posture

Output:

  • midbrain - red nucleus
  • thalamus - ventrolateral
30
Q

Vestibulocerebellum

aka archicerebellum

A

Involved in: balance

Output: vestibular nuclei

31
Q

what does unilateral cerebellum damage produce?

A

Ipsilateral defects

32
Q

What loops are the basal ganglia and cerebellum part of?

A

Cortical re-entrant loops

33
Q

ACh drugs

blocks storage

blocks release

A

storage - vesamicol

release - Botox

34
Q

Drugs that act on ACh receptors

nicotinics

A

Receptors (nACh)

– Full agonists ACh, - suxamethonium, nicotine,

– Partial agonists – varenacline (α4β2)

– Reversible antagonists - pancronium, vercuronium

– Irreversible antagonist – α-bungarotoxin

35
Q

Drugs that act on ACh receptors

Muscarinics

A

Receptors (mACh)

– Full agonists - ACh, muscarine, oxotremorine

– Partial agonist McN-A-343

– Antagonists - atropine, ipratropium

36
Q

ACh drugs that block

reuptake and degradation

A
  • Reuptake - hemicholinium
  • Degradation – galantamine, rivastigmine (CNS active AChEI)
37
Q

Ach diseases

A
  • dementia
  • myaesthenia gravis
  • parkinsons
  • motion sickness
  • analgesia
38
Q

Ach Function

A
  • learning and memory
  • NMJ
  • motor control
  • vestibular control
  • pain
39
Q

Dopamine synthesis

A

Tyrosine

to DOPA (tyrosine hydroxylase - rate limiting)

to DOPAMINE (dopa decarboxylase)

40
Q

What are the 2 types of ACh receptors?

A

Ligand gated ion channels - pentameric nictonic

G protein coupled receptors - muscarinic

41
Q

Dopamine receptors

A

all Gprotein coupled receptors

D1,D5 coupled to G stimulatory

D2,3,4 coupled to G inhibitory

D receptors either activate or inhibit adenylate cyclase

42
Q

what reuptakes Dopamine?

A

DAT - dopamine active transporter

43
Q

main metabolit of dopamine degradation?

A

Homovanillic acid

44
Q

Dopamine

drugs and disease 1

A
  • Synthesis - Levo DOPA
  • Storage - reserpine, methamphetamine
  • Release – amantadine
  • Receptors

– Full agonist - Dopamine, apomorphine, bromocriptine

– Antagonists - haloperidol, chlopromazine

45
Q

Dopamine

drugs and disease 2

A
  • Reuptake – cocaine, bupropion, methylpenidate (Ritalin®)
  • Degradation

– MAO inhibitors - phenelzine, selegiline (MAO-B)

– COMT inhibitors – entacapone, tolcapone

Sc 29 Parkinson's Disease (1 decks)

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