PBL 5 Flashcards

1
Q

what hierarchies is the control of movement split into and what comes under them?

A

Control of movement is split into various hierarchies:
• Local Control - Spinal Cord & Cord Reflexes
• Subcortical Control - Brainstem, Basal Ganglia & Cerebellum
• Cerebral Control - Cerebral Cortex

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2
Q

describe the function of the supplementary motor area

A

It is involved in programming complex sequences of movements and coordinating bilateral movements based on mental visualisation of remembered sequences.

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3
Q

what makes up the corpus striatum?

A

made up of Caudate Nucleus, Putamen and Globus Pallidus

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4
Q

what makes up the lentiform nucleus?

A

putamen and the globus pallidus

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5
Q

what is the role of Subthalamic Nuclei ?

A

produces the excitatory neurotransmitter, Glutamate.

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6
Q

what is the role of Substantia Nigra?

A

produces the neurotransmitter dopamine

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7
Q

How is the cerebellum anatomically split?

A

The cerebellum consists of two hemispheres which are connected by the vermis, a narrow midline area.

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8
Q

what are the anatomical lobes of the cerebellum? what divides them?

A

the anterior lobe, the posterior lobe and the flocculonodular lobe.
These lobes are divided by two fissures – the primary fissure and posterolateral fissure.

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9
Q

what are the anatomical zones of the cerebellum?

A

intermediate zones on either side of the vermis

lateral zones on either side of intermediate zones

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10
Q

descending motor pathways can be spilt into lateral and ventromedial pathways. what comes under these 2 types of pathways and what is their role?

A

Lateral pathways: corticospinal and rubrospinal tract – control of voluntary movement and distal muscle groups

Ventromedial pathways: tectospinal, vestibulospinal, olivospinal, reticulospinal (pontine + medullary) – mainly control proximal and axial (trunk) muscles and maintain posture

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11
Q

where does the corticospinal tract begin and where does it receive input from?

A
begins in the cerebral cortex
receives input from: 
•	Primary motor cortex
•	Premotor cortex (PMA)
•	Supplementary motor area (SMA)
•	nerves from somatosensory area
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12
Q

describe the path of the corticospinal tract after leaving the cerebral cortex. Describe the decussation of nerve fibres

A

the neurons descend through the internal capsule (a white matter pathway, located between the thalamus and the basal ganglia). The neurons then pass through the crus cerebri of the midbrain, pons and into the medulla.

In the caudal part of the medulla, the tract divides into 2:

  • lateral corticospinal tract (85%) decussate at level of medulla and then descend into the spinal cord, terminating in the ventral horn (at all segmental levels). From the ventral horn, the lower motor neurones go on to supply the muscles of the body.
  • The anterior corticospinal tract (15%) remains ipsilateral, descending into the spinal cord. They then decussate and terminate in the ventral horn of the cervical and upper thoracic segmental levels.
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13
Q

describe the corticobulbar pathway (arises from? input from? passage?)

A

arises from lateral aspect of the primary motor cortex.
They receive the same inputs as the corticospinal tracts.

The fibres converge and pass through the internal capsule to the brainstem.
The neurones terminate on the motor nuclei of 9 pairs of cranial nerves. Here, they synapse with lower motor neurones, which carry the motor signals to the muscles of the face and neck.

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14
Q

Describe dopamine synthesis

A

The amino acid tyrosine (aromatic aa derived from diet) is converted to Leva-dopa by tyrosine hydroxylase. It is then decarboxylated to dopamine by dopa decarboxylase in the brain.

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15
Q

what prevents dopamine from being converted to noradrenaline?

A

Dopaminergic neurons lack dopamine β-hydroxylase

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16
Q

what are the 2 main dopamine rich areas in the brain?

A
  • Substantia nigra

* Ventral tegmental area

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17
Q

name 4 dopamine pathways

A

Nigrostriatal pathway
Mesolimbic pathway
Mesocortical pathway
Tuberoinfundibular/hypophyseal pathway

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18
Q

describe the Nigrostriatal pathway, how much dopamine does it account for and what is its function

A

accounts for 75% of dopamine in the brain, consists of cell bodies in the pars compacta of Substantia Nigra whose axons terminate in the corpus striatum
–> movement control

19
Q

describe the Mesolimbic pathway, what is its function

A

cell bodies found in the ventral tegmental area of midbrain (adjacent to SN) and fibres project via the medial forebrain bundle to parts of the limbic system, especially to Nucleus Accumbens (reward centre) and Amygdaloid Nucleus.
–> involved in behaviour

20
Q

describe the Mesocortical pathway, what is its function

A

cell bodies lie in the ventral tegmental area of midbrain and fibres project via medial forebrain bundle to the frontal cortex.
–> mood/reward = behaviour

21
Q

describe the Tuberoinfundibular pathway, what is its function

A

group of short neurons running from arcuate nucleus in hypothalamus to the median eminence and anterior pituitary gland which inhibits prolactin release in presence of dopamine (endocrine control).

22
Q

describe the dopamine receptor subtypes and mention what type of receptor they are

A

there are 5 subtypes of receptors which are classified into those that increase cAMP production: Type 1 (D1, D5) and decrease cAMP production: Type 2 (D2, D3, D4).

They are G protein coupled receptors

23
Q

list some functions of dopamine

A
  • Movement
  • Processing rewarding experiences
  • Memory + Attention
  • Lactation
  • Sleep regulation
  • Nausea
  • Motivation
  • Pleasure, euphoria, arousal
24
Q

how does dopamine act on chemoreceptor trigger zone?

A

to cause nausea and vomiting

25
Q

mention other monoaminergic systems in the CNS other than dopamine

A

noradrenaline (NA) and serotonin (5-HT).

26
Q

what type of NT is dopamine ?

A

Dopamine is a monoamine and catecholamine neurotransmitter

27
Q

where are noradrenergic neurons found and what are the 2 main nuclei from which they originate?

A

Noradrenergic neurones are only found in the pons and medulla.
The 2 main nuclei where they originate are the locus coeruleus (most important) and the caudal raphe nuclei.

28
Q

what is the role of NA as a neurotransmitter ?

A

Noradrenaline is the primary NT in sympathetic nervous system and has been associated with several brain function e.g. sleep, memory, learning and emotions.

29
Q

how is serotonin formed?

A

It is synthesised from tryptophan first by hydroxylation, then decarboxylation

30
Q

describe the subtypes of serotinin receptors and how many there are

A

There are 7 5-HT receptor subtypes and all of them are G-coupled receptors except receptor subtype 3 which is a ligand gated ion channel receptor.

31
Q

where are Serotonergic neurons found?

A

primarily found in enteric nervous system (GI tract) but Serotonergic neurons are also found throughout most of the brainstem, especially concentrated in raphe nuclei.

32
Q

what do the nuclei containing serotonergic neurones in the caudal region of the brainstem innervate?

A

The nuclei in caudal regions innervate the spinal cord

33
Q

what do the nuclei containing serotonergic neurones in the rostral region of the brainstem innervate?

A

the nuclei in rostral region (in pons/medulla) innervate most of the brain.

34
Q

what is Parkinson’s disease ?

A

a progressive, debilitating neurodegenerative disease which usually occurs in 45-65-year olds.

35
Q

what are the cardinal clinical features of Parkinson’s disease?

A
  • bradykinesia (slowness in initiation of voluntary movement with reduction is speed and amplitude of repetitive actions)
  • tremor at rest (starts unilaterally, looks like they’re rolling a pill, gets better with movement)
  • cogwheel rigidity (increased muscle tone)
  • postural instability (loss of postural reflexes, shuffling, small stridor gait)
36
Q

what is the initial symptom in in 70-80% of Parkinson’s cases ?

A

tremor at rest

37
Q

list some other clinical features of Parkinson’s disease?

A
  • hypomimia (reduced facial expression)
  • dysphagia
  • reduced sense of smell
  • hypophonia (soft speech)
  • blurred vison
  • eyelid opening ataxia
  • shuffling, festination, freezing gait
  • handwriting gets smaller and smaller
  • sleep disturbance, insomnia
  • progression towards general cognitive decline
38
Q

describe the pathology of Parkinson’s disease

A

loss of dopaminergic neurons (which use dopamine as their neurotransmitter) and depigmentation in pars compacta of substantia nigra in basal ganglia. Presence of Lewy bodies – eosinophilic cytoplasmic protein deposits – in this region and in cortical and limbic structures.

39
Q

what proteins are found in the Lewy bodies?

A

The Lewy bodies consist of the protein alpha-synuclein and ubiquitin.

40
Q

Explain the rationale for using L-dopa as a treatment for Parkinson’s disease. what symptoms is it most effective at managing?

A

Levodopa is a precursor for dopamine and is used because dopamine itself cannot cross the blood- brain barrier.

LD is most effective at reducing bradykinesia and rigidity and is less effective at decreasing tremors and motor symptoms.

41
Q

what problem occurs when levo-dopa is taken orally?

A

When administered orally, most of it is decarboxylated peripherally in the GI tract and blood vessels and only a small proportion reaches the brain.

42
Q

what are the central and peripheral adverse effects of Levo-dopa

A
  • Centrally: confusion, hallucinations

- Peripherally: nausea, vomiting, postural hypotension

43
Q

What therapeutic strategies are used to maximise the efficacy of Levo-dopa and its side effects? why is this needed?

A

In the periphery (outside the CNS), levodopa is metabolised to dopamine and then to adrenaline/ noradrenaline, which can cause altered blood pressure.

  • To minimise these side effects, levodopa is combined with carbidopa (dopa decarboxylase inhibitor) which blocks the conversion of levodopa to dopamine in the periphery, thus allowing it to cross the blood-brain barrier
  • Other common side effects include nausea & vomiting, which can be avoided since the dose of levodopa is much lower when combined with carbidopa.
44
Q

what are the 2 most common preparations of Levo-dopa?

A

L-dopa + carbidopa = Sinemet

L-dopa + benserazide = Madopar