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Phase 1 > Neuro physiology 🧠 > Flashcards

Neuro physiology 🧠 Flashcards

1
Q

What is the McGurk effect?

A
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2
Q

What can we hear?

A

Range of human hearing
20Hz-

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3
Q

What is the function of the middle ear?

A

Acoustic impedance match
Between air and fluid filled inner ear
Amplifies the movement and so makes the sound louder
Because
Ratio area TM: stapes 14:1
Lever action of ossicles
Total gain is 20-35 db
200fold increase in transfer of energy

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4
Q

What is the loss of energy transferring from air to fluid?

A

97%

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5
Q

What is the role of the muscles of the middle ear

A

Protect inner ear from acoustic trauma
Stiffens ossciular chain
Stapedius stimulated acoustically
Reflex arc- 3 or 4 neurones

Tensir tympani

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6
Q

What is the role of the eustacian tube

A

Ventilation of the middle ear space
Drainage of secretions
Grommits

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7
Q

What are the cochlear fluids?

A

Endlolymph- High K+
Perilymph- Like ECF and CSF Na+ rich

Gradients maintained by Na, K-ATPase
and NKCC1 CIC-K chlorine channels
Ion channel abnormalities- deafness

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8
Q
A

Pressure wave in cochlear
Moves basilar membrane

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9
Q

What does the organ of corti do

A

basilar membrane moves
inner hair cells move and move tectorial membrane

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10
Q
A

Inner hair cells- mechanical transduction
Outer hair cells- fine tuning (stiffens the basilar membrrane so hair cells either side don’t move and so the sound is sharpened

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11
Q
A

Stereocillia move
Rapid response required
Mechanically gated K+ channels opened causing depolarisation

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12
Q
A

frequency
Amplitude intensity

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13
Q

What does the brainstem do for hearing

A

Localisation of sound

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14
Q

Interaural time differences

A
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15
Q

What are neurons

A
  • Specialised for electrical signalling
  • Inputs via dendrites
  • Action potentials propagate along the
    axon from the axon hillock
  • Mainly formed during development
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16
Q

What are neurons stained with?

A
  • Tissue sections can be stained with
    histological stains
  • e.g. H&E:
  • Haemotoxylin, stains nucleic acids
    blue
  • Eosin – stains proteins red
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17
Q

Neuronal communication

A
  • Neurons communicate via synapses - 2 types
  • Chemical – majority – via neurotransmitters (glutamate, GABA, dopamine, serotonin,
    etc.)
  • Electrical – less abundant – via direct flow of ions
  • enable synchronized electrical activity, e.g brainstem (breathing) and hypothalamus (hormone secretion)
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18
Q

Describe chemical synaptic transmission

A
  • Axon potential depolarises synaptic
    terminal membrane
  • Opening of voltage-gated calcium
    channels leads to calcium influx
  • Calcium influx triggers
    neurotransmitter release
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19
Q

Electrical synapse structire

A

Electron dense material on both sides
rings called connecins
gap junctions

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20
Q

Excitatory synapses

A

Concentrated on dendritic spines

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21
Q

What is neural plasticity?

A

-changes in neuronal/synaptic structure and function in response to neural activity
-basis of learning and memory

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22
Q

Describe spines

A
  • Spines are dynamic structures – number, size, composition
  • Spine remodelling linked to neural activity
  • Relevant to disease – e.g. schizophrenia & Alzheimer’s - ↓spine density
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23
Q

Describe neuronal heterogeneity

A

Neurons differ in their:
* Size
* Morphology
* Neurotransmitter content
* Electrical properties
* E.g. neocortex (right)

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24
Q

Examples of neuronal heterogeneity

A
  • Betz cells = upper motor neurons –
    large, excitatory (glutamatergic,) long
    projections, pyramidal cells
  • Vulnerable in MND
  • Medium spiny neurons = striatal
    interneurons – small, inhibitory
    (GABAergic)
  • Vulnerable in Huntington’s disease
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25
Q

Describe arborisation of axons and dendrites

A

Cortical projection neuron
Cerebellar Purkinje cell

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26
Q

What are oligodendrocytes?

A
  • Myelinating cells of the CNS
  • Unique to vertebrates
  • Myelin insulates axon segments,
    enables rapid nerve conduction
  • Myelin sheath segments interrupted by
    nodes of Ranvier – saltatory conduction
  • Provide metabolic support for axons
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27
Q

Describe myelin sheath

A
  • Formed by wrapping of axons by
    oligodendrocyte processes
    (membranes)
  • Highly compacted – 70% lipid, 30%
    protein
  • Myelin specific proteins, e.g. myelin
    basic protein (MBP) can be used as
    “markers
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28
Q

Describe microglia

A
  • Resident immune cells of the CNS
  • Originate from yolk sac progenitors
    that migrate into the CNS
  • “Resting” state, highly ramified, motile
    processes survey environment (2-3
    µm/min)
  • Upon activation (e.g. by ATP), retract
    processes, become “amoeboid” &
    motile
  • Proliferate at sites of injury -
    phagocytic

Not like the other types- more like macrophages

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29
Q

What are the functions of microglia?

A
  • Immune surveillance
  • Phagocytosis – debris/microbes
  • Synaptic plasticity – pruning of spine
  • “bad” (M1) and “good” (M2) microglia
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30
Q

What are astrocytes?

A
  • “Star-like cells”
  • Most numerous glial
    cells in the CNS
  • Highly heterogeneous –
    not all star-shaped
  • Common “marker” glial
    fibrillary acidic protein
    (GFAP)

Contribute to the blood-brain barrier

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31
Q

Describe how astrocytes contribute to blood brain barrier

A

Processes of astrocytes wrap around capillaries

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32
Q

What are the functions of astrocytes?

A
  • Structural - define brain micro-architecture
  • Envelope synapses – “tripartite synapse” – buffer K+, glutamate, etc
  • Metabolic support – e.g. Glutamate-Glutamine shuttle
  • Neurovascular coupling – changes in cerebral blood flow in response to neural
    activity
  • Proliferate in disease = gliosis or astrocytosis
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33
Q

What are some specialised astrocytes?

A
  • Radial glia –important for brain development
  • Bergmann glia (cerebellum) - green
  • Müller cells (retina)
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34
Q

CNS terminology

A
  • Abundance of neuronal cell bodies in nuclei
  • Axons gathered into tracts
  • Tracts that cross midline = commissures
  • Grey matter abundant in neural cell bodies & processes – neuropil contains few cell
    bodies
  • White matter contains abundance of myelinated tracts & commissures
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35
Q

PNS terminology

A
  • Cell bodies & supporting cells located
    in ganglia – e.g. dorsal root ganglia
    (DRGs)
  • Axons bundled into nerves
  • Many PNS axons are enveloped by
    Schwann cells (myelinating cells
    of the PNS – neural crest derived c.f.
    oligodendrocytes, derived from CNSresident neural progenitors)
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36
Q

Describe the blood brain barrier

A
  • Dyes injected into blood penetrate
    most tissues, but not the brain
  • Dyes injected into CSF – brain stains →
    specialised blood-brain barrier
  • Formed by endothelial cell tight junctions, basement membrane (few
    fenestrations), astrocyte end feet &
    pericytes (contractile, aid blood flow)
  • Sensitive to inflammation,
    hypertension, trauma, ischaemia
  • Problem for drug delivery!
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37
Q

Describe ependymal cells

A
  • Epithelial-like, line ventricles & central
    canal of spinal cord
  • Functions - CSF production, flow &
    absorption
  • Ciliated – facilitates flow
  • Allow solute exchange between
    nervous tissue & CSF
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38
Q

Describe the choroid plexus

A
  • Frond-like projections in ventricles
  • Formed from modified ependymal cells - villi form
    around network of capillaries
    → highly vascularised with a large surface area
  • Main site CSF production by plasma filtration driven
    by solute secretion
  • Gap junctions between ependymal cells form bloodCSF barrier
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39
Q

What are 3 different levels of defence and the part of the CNS activated?

A

Learned threat- cortex and limbic system
Loom- Sensorimotor midbrain
Pain- spinal cord

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40
Q

Describe dualism

A

“There are two kinds of foundation: mental and body”

“The mental cannot exist outside of the body; and the body cannot think”

“Thus: mental events cause physical events and vice-versa

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41
Q

Critiques of dualism 1

A

What is this “non physical” substance which is not brain?
How can an “immaterial” mind cause anything in a “material” body and vice versa
Theory leads to explanations involving another being - soul, animal spirits, deity?
Lack of scientific evidence for this

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42
Q

Critiques of dualism 2

A

What about “inexplicable” symptoms? Or where “biological reductionism” does not explain symptoms?
“functional, conversion, psychosomatic, medically unexplained, persistent physical symptoms, overlay, psychogenic, hysterical, manipulative, factitious, Munchausen’s ”

How do we reflect the importance of the fact that the individual is part of a range of larger (social /political /cultural) systems?

What is the impact of environment /society is critical in our perception of self and our wellbeing

How do we think about dualism when the WHO defines health in positivist terms as:
“a state of complete physical, mental and social well-being” or
“the capacity, relative to potential and aspirations, for living fully in the social environment” (Tarlov)

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43
Q

Why does dualistic thinking persist?

A

Familiar: 300 years of medical experience
Economics: private enterprise (Big Pharma?) rely on this paradigm
Power: health is traditionally the business of doctors (or is it – currently being challenged)
Convenience: ability to design experiments to test
NB not only biological reductionism, can also have social reductionism (e.g postnatal depression is not “valid” as the experiences can be understood as the adaptation to a significant environmental change??)

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44
Q

Advantages of classification in health/ ill health

A

Facilitate reporting and inform public health issues such as allocation of resources
Facilitate meaningful communication and debate between patients, professionals, organisations and legislators
Promote a feeling of being understood (“we’ve seen this before – your problems are not unique”)
Provide a framework for research
Offer evidence for treatment options and some information about natural history and prognosis

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45
Q

Problems with using classification systems and diagnosis?

A

Improved scientific understanding makes a mockery of previous attempts to classify (e.g. phrenology)
Categorisation means defining thresholds which are arbitrary
depression / dysthymia / fed up
obese / well built / chubby / slender
Categorisation can lead to stigma and prejudice
Economy of thought may lead to oversimplification, reductionism and ultimately inhumane action

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46
Q

Role of emotion

A

Motivator for learning
Means of best obtaining rewards/ avoiding punishment
- Stimulus-reinforcer associations
- Instrumental (action-outcome) learning

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47
Q

Movement and emotion

A

Ability to act s

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48
Q

Basic theory

A

-Biologically privileged emotion automatically triggered by oblects and events
-Hard-wired circuits
-Variability: cultural

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49
Q

Appraisal

A
  • Meaningful interpretation of an object or a situation by an individual
  • Action readimess
  • May be automatic
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50
Q

Psychological constructionist

A

Psychial compounds of basic ingredients (affect and ideational component)
Same ingredients involved in other mental states
Internal state subject of meanig analysis

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51
Q

Baysian model

A
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52
Q

Neuroanatomy of emotion

A

-limbus
-described by broca
- emotion result of network of sirect and trans synaptic connections-#
- no single limbic system
network of connections

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53
Q

Appraisal: Orbitofrontal cortex

A

-Appraisal - input: ventral cortical streams (identity)
0 Medial- reward- activation: subjective to pleasantness
Lateral- punishment/ non reward- negative reward prediction error- expectation of punishment

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54
Q

Mesolimbic pathway

A
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55
Q

Appraisal amygdala

A
  • Older brain overshadowed by OFC
  • conditions responses to stimuli predicting harm
  • facial expression recognition
  • Little involved in subjective emotional experience
  • slower response in verbal? learning tasks
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56
Q

Reactivity: cingulate cortex

A

Action- outcome learning
Anterior- outcome- subgenual reward signals from ofc
Supracallosal punishment/ non reward from lateral ofc
posterior- action- input from parietal lobes (spatial/ action related info
output hippocampus
mid output to premotor area

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57
Q

Reactivity: hypothalamus and insula

A

Modulated by: OFC via anteroventral insula and subgenual cingulate cortex, amygdala- hypothalamus and periaqueductal grey
feedback from autonomic output not needed for emotional behaviour/ feelings

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58
Q

What layer of the embryo gives rise to the nervous system?

A

Ectoderm

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59
Q

What happens in the 4th week to the ectoderm and what will it become

A

Ectoderm thickens in midline to form the neural plate- neural tube and then eventually spinal canal

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60
Q

Step 1 of

A

Notochord forms from mesoderm cells soon after gastrulation is complete

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61
Q
A

Signals from the notochord cause inward folding of the ectoderm at the neural plate

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62
Q
A

Ends of neural plate fuse and disconnect to form an autonomous neural tube

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63
Q

What are the presumptive neural crest cells and where are they?

A

Stem cells
Lateral to the neural groove lie presumptive neural crest cells
in ectoderm form- melanocytes, schwann cells and neurons
in mesoderm- osteoblasts, adipocytes and chondrocytes

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64
Q

Main things that the neural crest cells form

A

Sensory dorsal root ganglia of spinal cord and V/VII/IX/X

Schwann cells

Adrenal medulla

Bony skull

Meninges

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65
Q

What are some abnormalities of the spinal cord?

A

The neural tube usually closes at the end of 4th embryonic week

Failure to close cephalic region – anencephaly

Failure to close spinal region – spina bifida

Collectively called – neural tube defects

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66
Q

What is hydrocephalus?

A

Accumulation of CSF with increased intracranial pressure
Can cause macrocephaly in children (therefore always scan increasing head size)

Obstructive (non-communicating): e.g. tumour, haemorrhage.

Non-obstructive (communicating): e.g. increased CSF production

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67
Q

Describe the cerebrospinal fluid circulation

A

CSF circulates through the subarachnoid spaces and through the ventricles

CSF cushions the brain and helps circulate metabolites

Around 120 mLs

Produced as filtrate of blood at choroid plexuses in ventricules

Absorbed via arachnoid granulations in superior sagittal sinus

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68
Q

Brain structures in week 4

A

Prosencephalon-cerebral hemispheres and thalamic structures
Mesencephalon – midbrain
Rhombencephalon – medulla, pons and cerebellum

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69
Q

What are the areas of the brain in week 6

A

Telencephalon
Diencephalon
Mesencephalon
fourth ventricle
rhombencephalon

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70
Q
A

cortex is thin in development but complicated layered structure in adults

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71
Q

What are microcephaly and macrocephaly?

A

Microcephaly – reduced head circumference

Macrocephaly – increased head circumference

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72
Q

Give a brief overview of the neuron

A

Basic cellular unit of the nervous system
Huge range - specialised for different functions
All have same basic components
Approximately 100 billion (109) neurons in the ‘average’ brain
But, 0.15 quadrillion (1015) connections between them (synapses)

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73
Q

Basic components of a neuron

A

Dendrites
Cell body/soma
Axon
Presynaptic terminals

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74
Q

Neuron types

A

Multipolar neuron
Bipolar neuron
Pseudo-unipolar neuron
Unipolar-neuron

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75
Q

What is axonal transmission?

A

Transmission of information from location A to location B

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76
Q

What is synaptic transmission?

A

Integration/processing of information and transmission between neurons

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77
Q

What is the charge inside a neuron at rest?

A

Negative

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78
Q

Describe the semi-permeability of neuronal cells

A

Some substances which are electrically charged (+ve or –ve) cross readily – potassium (K+) and chloride (Cl-)
Some cross with difficulty – sodium (Na+)
Some not at all – large organic proteins (-ve charge)

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79
Q

WHat is a force determining the distribution of charged ions?

A

Diffusion – the force driving molecules to move to areas of lower concentration

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80
Q

What is the force determining the distribution of CHARGED ions?

A

electrostatic attraction/repulsion
Electrostatic pressure - ions (like magnets) move according to charge – Like ions repel and unlike attract
Ions:
A- (anions - protein)
Na+ (sodium ions)
+ (potassium ions)
Cl- (chlorine ions)

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81
Q

Ion distribution in neurons at rest

A

A- (anions - protein) - restricted to inside of cell
Na+ (sodium ions) - mostly outside neuron
K+ (potassium ions) - mostly inside neuron
Cl- (chlorine ions) - mostly outside neuron

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82
Q

Forces determining sodium and potassium conc.

A

Active process to transport Na+ ions out of neuron & K+ in
Three Na+ for every two K+
Require energy supplied by ATP

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83
Q

Describe final resting potential

A

Result is NA+ high concentration outside but with both forces pushing in
Membrane and pump resists Na+ inward movement
K+ & Cl- can move backward and forward across membrane so reach steady state determined by opposing forces of diffusion and electrostatic pressure
Some sodium leaks back in but is expelled by the pump

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84
Q

Describe an action potential

A

Neuron fires – a sudden pulse where the negative resting potential is temporarily reversed
Transmits information i.e. the message [digitally / all or none / 0 or 1]

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85
Q

What are the events within the action potential?

A

Depolarization & threshold
Reversal of membrane potential
Repolarisation to resting potential
Refractory period

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86
Q

Describe the action of neurotransmitters

A

The membrane potential remains in this resting ‘stable’ state until something disturbs the balance:Membrane permeability changes

Neurotransmitters initiate such changes at the dendrites of neurons

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87
Q

Describe the process of changing action potential in the neuron

A

Neurotransmitters activate receptors on dendrites / soma
Receptors open ion channels
Ions cross plasma membrane, changing the membrane potential
The potential changes spread through the cell
If the potential changes felt at the axon hillock are positive (+mV), and large enough, an action potential is triggered

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88
Q

WHat does whether an action potential is reached

A

The voltage of the potential spread thru the cell

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89
Q

What do excitatory neurotransmitters do?

A

Excitatory neurotransmitters depolarise the cell membrane
increases probability of an action potential being elicited
cause an Excitatory Post Synaptic Potential (EPSP)

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90
Q

What do inhibitory neurotransmitters do

A

Inhibitory neurotransmitters hyperpolarise the cell membrane
decreases probability of an action potential being elicited
cause an Inhibitory Post Synaptic Potential (IPSP)

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91
Q

When will an action potential occur?

A

An action potential will be elicited if the membrane potential is depolarised beyond the threshold of excitation

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92
Q

What is passive conduction?

A

Voltage changes spread away (decrementally) from point of origin (Passive Conduction).
Whether AP is generated depends on what reaches the axon hillock.

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93
Q

Spatial summation

A

Inhibitory post synaptic potential

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94
Q

Temporal summation

A

Excitatory post synaptic potential

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95
Q

Describe the action potential

A

EPSPs begin to depolarise cell membrane
Threshold ~ -60mV
When reached Na+ channels open (Na+ rushes in) and polarity reverses to +30 inside
Membrane potential reverses with the inside going positive
…at which point voltage-gated Na+ channels close and K+ channels open (K+ rushes out)
…which restores resting membrane potential

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96
Q

Describe the self perpetuating nature of the action potential

A

The voltage changes are caused by the opening or closing of ion channels
In the cell membrane there are channels which are opened by voltage changes…thus
voltage changes control the ion channels which control the voltage changes……….
The action potential is therefore self perpetuating

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97
Q

Initiation and propagation of the action potential

A

Receptors- (neurotransmitter activated ion channels)
Summation
Voltage activated ion channels open

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98
Q

What does myelination do?

A

Speeds up axonal conduction
Allows the conduction of current as it means it can jump from nodes of ranvie

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99
Q

Unmyelinated neuron

A

Signal loss due to lack of insulation –could be overcome by continual opening of next ion channel
But SLOW due to time to activate each channel.
Mainly short axon interneurons

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100
Q

Myelinated neuron

A

Saltatory Conduction
Decremental conduction between nodes (but ‘re-boosted’ each time)
But very fast along axon.
Most CNS neurons.

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101
Q

How does a synapse work

A

action potential triggers opening of voltage gated Ca+ channels to open
This causes the vesicles in presynaptic terminal release neurotransmitter into the synapse

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102
Q

Why synapse

A

allows for modulation of signal
charge spread
charge slowed

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103
Q

What happens to the neurotransmitter after it has crossed the synapse?

A

Would remain active in synapse if it wasn’t for:
Enzymatic Degradation
Reuptake

Acetylcholinesterase is the name of the enzyme that breaks down the neurotransmitter acetylcholine

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104
Q

What afre bottom up and top down processing

A

Bottom up processing- sensation
Top down processing- perception

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105
Q

What is sensation

A

A mental process resulting from immediate external stimulation of a sense organ
Touch, smell, taste, sight hearing

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106
Q

WHat is perception

A

The ability to become aware of something or understand something following sensory stimulation
Tactile, olfactory, gustatory, visual, auditory

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107
Q

What is perceptual set?

A

Psychological factors that determine how you perceive your environment

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108
Q

What determines how we perceive things?

A

Context, culture, expectations, mood & motivation

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109
Q

what is gestalt theory

A

Proximity, common fate, continuity, similarity, closure, common region, symmetry

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110
Q

What is illusion?

A

An instance of a wrong or misinterpreted perception of
a sensory experience

Realise quickly

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111
Q

What is a hallucination?

A

Experiences involving the
apparent perception of
something not present

Cannot shake it quickly like illusion

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112
Q

What areas of the brain with most activity in hallucinations?

A

Visual and auditory cortices

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113
Q

What causes hallucinations

A

Drugs, delerium, sleep deprivation, psychiatric illness

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114
Q

Psychiatric conditions that cause hallucinations

A

SCHIZOPHRENIA
DEPRESSION WITH PSYCHOSIS
BIPOLAR AFFECTIVE DISORDER
SCHIZOAFFECTIVE DISORDER
DRUG INDUCED PSYCHOSIS
ACUTE TRANSIENT PSYCHOSIS

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115
Q

Bio-psychosocial model of care for hallucinatory disorders

A

Medication
Psychologists
Social networks

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116
Q

What are the categories of mental illness/conditions?

A

The organic illnesses
The dependency states – alcohol; drugs
The mood disorders
The anxiety states
The psychoses
The behavioural disorders
Neurodiversity
Childhood disorders
Personality disorders

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117
Q

What are the organic illness types?

A

Dementias
Delerium

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118
Q

What are the types of dementia?

A

Alzheimer’s
Rx - Acetylcholine esterase inhibitors
Rx - Glutamate blockade
Vascular dementia
Subcortical
Stoke related
Multi-infarct
Lewy body
Frontotemporal

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119
Q

What are some causes of delerium?

A

B12 and Folate deficiency
Cushing’s disease
Thyrotoxic storm
Wilson’s disease
And many more physical illnesses

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120
Q

Give an overview of the types of drugs used in dependency states

A

Drugs: Key examples
Heroin
Cocaine
Marijuana
Alcohol

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121
Q

Give an example of physical dependency

A
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122
Q

What are the mood disorders?

A

Depressive illness (Unipolar)
Mania (Unipolar)
Bipolar (Manic-depression)
Cyclothymia
Low mood (adjustment disorders, burnout, life setting)

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123
Q

What are some key examples of the anxiety states?

A

Generalised anxiety disorder
Panic attacks
OCD
Derealisation-depersonalisation

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124
Q

What are the psychoses?

A

Schizophrenia
Acute and transient psychosis
Monosymptomatic delusion
Post-natal (Puerperal) psychosis
Drug induced psychosis

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125
Q

What are the behavioural disorders?

A

Sleep
Sex
Eating
Habits

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126
Q

What us the bed nucleus involved in?

A

Anxiety
Gender identity
Appetite
Dampens startle response
Social recognition
Parental bonding

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127
Q

Give some examples of neurodiversity

A

The developmental ‘disorders’
Autistic spectrum
ADHD
Learning disability

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128
Q

What is involved in the default mode network?

A

Medial PFC
Posterior CC
Angular gyrus
Precuneus

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129
Q

What are some psychiatric conditions related to childhood?

A

Separation anxiety
General anxiety states
School refusal
Other behavioural problems
Sexual, psychological and physical abuse

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130
Q

What are some examples of personality disorders?

A

Many recognised types
Two key examples
Borderline PD
Dissocial PD

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131
Q

What is eustress (good stress)?

A

Positive stress which is beneficial and motivating; typically, the experience of striving for a goal which is within reach

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132
Q

What is distress (bad stress)?

A

Negative stress which is damaging and harmful. Typically occurs when a challenge (or threat) is not resolved by coping or (rapid) adaptation.

The type of stressor is less important than how it is experienced ie negative (threat) or positive (challenge), whether it is experienced physically and/or psychologically and how long it goes on.

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133
Q

What are stresses?

A

Stresses are physical and psychological. Different neuronal networks are involved but these are connected.

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134
Q

What are stress responses?

A

Stress responses are often characterised as either physiological or psychological (mind). But these overlap and both are mediated via the brain.

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135
Q

What are physical stressors?

A

(processed in brainstem & hypothalamus: reflexive)
Insults or injuries that produce direct physiological effects eg damage of body tissue and/or bodily threat (eg pain, haemorrhage or inflammation).

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136
Q

What is psychological stress?

A

(Involving PFC, amygdala and hippocampus)
Stimuli that are perceived as excessively demanding or threatening, often involving anticipation.

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137
Q

What are the 3 phases of stress response?

A

Alarm, adaptation, exhaustion

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138
Q

Alarm

A

Threat identified; body’s response is state of alarm (fight or flight)

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139
Q

Adaptation

A

Body engages defensive countermeasures

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140
Q

Exhaustion

A

Body runs out of defences and resources are depleted

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141
Q

General adaptation syndrome

A

Stress as “non-specific response of the body to any demand for change”.

Selye (1907-1982) found that different insults caused the same disease (eg heart attacks, stroke, kidney disease and rheumatoid arthritis).
Early evidence of neuroendocrine mechanisms and role of HPA axis.

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142
Q

Homeostasis

A

Maintaining internal environment necessary for cell functioning

143
Q

Allostasis

A

How complex systems adapt (eg via HPA axis) to changing environments by changing set-points (“adaptation through change”).

144
Q

Allostatic load

A

refers to cumulative exposure to stressors (and cost to the body of allostasis), which if unrelieved leads to systems ‘wearing out’.

145
Q

What happens if there is continued attempts to restore balance?

A

Continued attempts to restore balance have long-term effects on physiological systems, including structural changes (eg to the CNS).

146
Q

What is acute stress?

A

Brief response to a novel but short-lived situation experienced by the body as a danger. Conscious perception of threat is not always involved.

The acute stress response (‘fight or flight’) is healthy & adaptive and necessary for survival.

147
Q

What is chronic stress?

A

Arises from repeated or continued exposure to threatening or dangerous situations, especially those that cannot be controlled. More likely than acute stress response to involve appraisal and conscious perception.

148
Q

What are some of the examples of chronic stressors?

A
  • Physical illness, disability & pain
  • Physical or sexual abuse
  • Poverty including poor housing, hunger, cold or damp, debt
  • Unemployment
  • Bullying or discrimination
  • Caregiving
149
Q

Describe the importance of individual differences

A

Individual differences are important, including differences in perception of threat & control and physiological differences in the timing and duration of the stress response

150
Q

What are the 5 elements of the human stress response?

A

Biochemical
Physiological
Behavioural
Cognitive
Emotional

151
Q

Key facts about stress responses

A

Stress responses are generic and not stressor-specific.

Stress responses mediated via autonomic nervous system (ANS) and the hypothalamo-pituitary (HPA) axis.

These responses lead to changes that influence future responses to stress, also reflecting brain plasticity.

152
Q

Describe the sympathomedullary pathway

A

hypothalamus activates adrenal medulla ->
Adrenal medulla releases adrenaline and noradrenaline into the bloodstream ->
Body prepares for fight or flight, adrenaline and noradrenaline reinfordes bthe pattern e.g increased hr and bp ->
Energy

153
Q

Pituitary adrenal system

A
154
Q

Chemicals released in the blood in stress

A

Steroids especially glucocorticoids (cortisol)
Catecholamines (adrenaline & noradrenaline)
The so-called sympathetic nervous system (SNS) ‘fight-or-flight’ chemicals

155
Q

Inflammation and the immune response

A

are important & complex, mediated and modified by adrenaline and cortisol. Effects can be pro- and anti-inflammatory, and GCCs also have direct effects on the CNS.

Balance between immune activation & autoimmunity disrupted in chronic stress response (NB reduced vaccination response)
Immunosenescence?

156
Q

Immune response in acute stress

A

Immune suppression (anti-inflammatory)

157
Q

Chronic stress immune response

A

Partial immune suppression + low-grade chronic inflammatory response, possibly through epigenetic effects on gene expression

158
Q

What are some fast psychological stress responses?

A

Breathing more rapid to increase oxygen
Blood flow increases up to 400%, directed to heart & muscles
Increased heart rate & blood pressure
Muscles tense
Glucose released, insulin levels fall: boost energy to muscles
Red blood cells discharged from the spleen
Mouth becomes dry & digestion is inhibited
Sweating
Cytotoxic & surveillance WBCs go where injury & inflammation may occur i.e. bone marrow, skin, lymph nodes

159
Q

Physical (somatic) effects of chronic stress

A

Headache
Chest pain
Stomach ache
Musculoskeletal pain
Low energy
Loss of libido
Colds & infections
Cold hands & feet
Clenched jaw & grinding teeth

160
Q

Behavioural responses to stress

A
  • Easily startled & hypervigilant
    Change in appetite – both directions
    Weight gain (obesity) or weight loss
    Procrastinating and avoiding responsibilities
    Increased use of alcohol, drugs & smoking
    Nail biting, fidgeting and pacing
    Sleep disturbances especially insomnia
    Withdrawal
161
Q

Cognitive responses to stress

A
  • Constant worrying
  • Racing thoughts
  • Forgetfulness and disorganisation
  • Inability to focus
  • Poor judgement
  • Being pessimistic or seeing only the negative side
  • Altered learning
162
Q

Emotional responses to stress

A
  • Depression & sadness
  • Tearfulness
  • Mood swings
  • Irritability
  • Restlessness
  • Aggression
  • Low self-esteem and worthlessness
  • Boredom & apathy
  • Feeling overwhelmed
  • Rumination, anticipation & avoidance
163
Q

Unhealthy stress responses

A

Anticipatory reaction
Lack of recovery- stress decreases at normal rate but doesn’t fully stop
Lack of habituation response continues for a while but does decrease
Lack of habituation and recovery- response doesn’t decrease and doesn’t go away

164
Q

How does stress affect us?

A

Ppl vary
Different parts of the brain mediate responses to different types of stressor (but amygdala and hippocampus are key).

Context, appraisal, vulnerability and learning (past experience) modify perception of threat and hence the stress response. People exposed to adversity in early life are more sensitive to stress later on.

Stress mechanisms alter affect (mood, anxiety levels). This is likely to mediate the effects of stress on other bodily systems including through behaviours (eg alcohol, diet etc).

165
Q

Link between stress and illness

A

Stress is related to a host of illnesses, esp of cardiovascular and GI systems, ie those with strong ANS connections.

Stress exacerbates physical illnesses and slows recovery and increases susceptibility to infection.

Strong evidence of association between depression and mortality following an MI.

Evidence of causal association between stress and physical illness is still limited, though note emerging evidence that chronic stress increases ‘immune ageing’.

Exposure to stress (trauma)

166
Q

Possible links between stress and various illnesses

A
  • Cancer: stress linked to survival rather than incidence
  • Cardiovascular disease: high blood pressure, abnormal heart rhythms, MI and stroke
  • Obesity & eating disorders
  • Infertility, recurrent miscarriage & menstrual problems
  • Rheumatoid arthritis
  • Skin & hair problems eg acne, psoriasis, eczema
  • Gastrointestinal problems: inflammatory bowel disease, irritable bowel syndrome.
  • Medically unexplained symptoms (MUS)
  • Infectious diseases especially covid-19
167
Q

PTSD symptoms

A
  • Vivid flashbacks & nightmares
  • Intrusive thoughts and images
  • Sweating
  • Nausea
  • Trembling
  • Hypervigilance & increased startle response
  • Agoraphobia
  • Insomnia
  • Irritability
  • Impaired concentration
168
Q

Ways to manage stress

A
  • Shiatsu, T’ai Chi, Yoga
  • Mindfulness
  • Meditation
  • Exercise
  • Sleep hygiene
  • Friends and family
  • Healthy diet
  • Exposure to natural environments
  • Aromatherapy
  • Cognitive Behavioural Therapy
169
Q

What is evolutionary psychiatry?

A

Ask questions about why natural selection has left us vulnerable to developing mental disorders

170
Q

Four areas of biology

A

Ontogeny
mechanism
phylogeny
adaptive significance

171
Q

Why did natural selection leave us vulnerable to disease?

A

Mismatch- body unable to cope with modern environment
Infection- bacteria and viruses evolve faster than us
Constraints- some things evolution can’t do
Trade off- everything has advantages and disadvantages
Reproduction- ns maximises reproduction not health
Defensive responses- responses such as pain and anxiety are useful in the face of threats

172
Q

Smoke detector principle

A

Want alarm system to go off if there is an actual fire- benefits
So false alarms happen to err on the side of caution

173
Q

5 fundamental processes of synaptic transmission

A

Manufacture – intracellular biochemical processes
Storage – vesicles
Release – by action potential
Interact with post-synaptic receptors – diffusion across the synapse
Inactivation – break down or re-uptake

174
Q

Fast neurotransmitters

A

– short lasting effects
Acetylcholine (ACh)
Glutamate (GLU)
Gamma-aminobutyric acid (GABA)

175
Q

Neuromodulators

A

slower timescale
Dopamine (DA)
Noradrenalin (NA) (norepenephrine)
Serotonin (5HT) (5-hydroxytryptamine)

176
Q

Problems for drug design

A

A region of the brain engaged in a particular function uses several neurotransmission systems e.g. basal ganglia
Glutamate
GABA
Dopamine
Acetylcholine
Substance P
Enkephalin
Regions of the brain engaged in different functions use the same neurotransmission systems
Glutamate
GABA
Acetylcholine
Serotonin
Dopamine/Noradrenalin

177
Q

How do hallucinogenic drugs work?

A

Hallucinogenic drugs include LSD, Magic Mushrooms, Ketamine

They mimic serotonin, and can activate numerous different serotonin receptor subtypes

But the hallucinogenic effect itself appears to be specifically related to the way they target the serotonin ‘2a’ receptor (5-HT2a)

178
Q

Types of motor control

A
  • Involuntary: eye movements, facial expressions, jaw, tongue, postural muscles throughout trunk, hand and fingers, diaphragm, cardiac, intercostals (around lungs), digestive tract……
  • Goal-directed: conscious, explicit, controlled.
  • Habit: unconscious, implicit, automatic
  • Voluntary: running, walking, talking playing guitar etc.,……
179
Q

Key concepts in the sensorimotor system

A

Motor control governed by lower and upper motor neurons.

The lower motor neuron begins (has its cell body) in brainstem or spinal cord and projects to the muscle

The upper motor neurons originate in higher centres and project down to meet the lower motor neurons

180
Q

Key facts about muscles

A

Muscles can only contract or relax (i.e. stop contracting)
The activation of muscle fibres is all or none
So how do we achieve such a range of movements and forces ??
Antagonistic arrangement – combined co-ordinated action
Recruitment of muscle fibres – fast/slow twitch, small and large motor units (see later)

181
Q

INdividual differences in muscles

A

The number of muscle fibres varies across individuals, but changes little with either time or training – appears to be genetically determined

Muscle size (+ strength) is more about cross sectional area of individual fibres and different proportions of the different types of fibre (see later)

182
Q

How do muscles contract?

A

A skeletal muscle is attached to the bone by the tendon
A skeletal muscle comprises several muscle fasciculi (group of muscle fibres)
A muscle fasciculus comprises several muscle fibres (= muscle cells)
A muscle fibre is constituted of several myofibrils
Myofibrils contain protein filaments: Actin and Myosin myofilaments
When the muscle fibre is depolarised actin and myosin slide against each other which produce muscle contraction

183
Q

Describe rigor mortis

A

The release of acetylcholine causes a cascade of events resulting in the release of packets of calcium from inside the muscle cell (fibre)

This causes the myosin head to change shape, enabling it to bind with the actin filament

ATP (provides energy for cells) is required to break the bond between the myosin head and the actin filament

ATP is produced by oxidative metabolism, which stops upon death

So the muscle become contracted and remain that way until enzymes begin to disrupt the actin/myosin

184
Q

What is the motor unit?

A

Single alpha () motor neuron + all the muscle fibres it innervates – Different motor neurones innervate different numbers of muscle fibres – fewer fibres means greater movement resolution - those innervating finger tips and tongue

185
Q

Key facts about the motor unit

A

The motor unit is the final common pathway for motor control
Activation of an alpha motor neuron depolarises and causes contraction of all muscle fibres in that unit (all or none)
Muscle fibres innervated by each unit are the same type of fibre and often distributed through the muscle to provide evenly distributed force (and may help reduce effect of damage)
More motor units fire – more fibres contract – more power

186
Q

Control of muscle force

A

Average number of muscle fibres innervated by single motor neuron (a motor unit) varies according to two functional requirements for that muscle:
1. Level of control
2. Strength
Typically a range of motor units in a muscle, some with few, some with many fibres.

187
Q

Size principle

A

Units are recruited in order of size (smallest first)
Fine control typically required at lower forces
Try playing the violin with weights attached to your arms!!

188
Q

What are the 3 types of muscle fibres?

A

Slow
Fast fatigue resistant
Fast fatigable

189
Q

What is the motor pool?

A

All the lower motor neurons that innervate single muscle

The motor pool contains both the alpha and gamma motor neurons (see later)

Motor pools are often arranged in a rod like shape within the ventral horn of the spinal column

190
Q

Describe innervation of the muscles

A

Cell bodies in the ventral horn: activated by:
Sensory information from muscle
Descending information from brain

191
Q

Sensing in muscles

A

Muscles can be contracted or relaxed to provide movement, but a good control system (the CNS) needs to know two things:
how much tension is on the muscle- golgi tendon organs sense tension
what is the length (stretch) of the muscle- muscle spindles sense stretch

192
Q

Describe golgi tendon organs- muscle tension (force)

A

The GTO is within the tendon (where the muscle joins to bone)
Mostly, it sends ascending sensory information to the brain via the spinal cord about how much force there is in the muscle
Critical for proprioception
Under conditions of extreme tension, it is possible that GTOs act to inhibit muscle fibres (via a circuit in the spinal cord) to prevent damage

193
Q

Muscle spindles- muscle strength (stretch)

A

Muscle spindles sense the length of muscles, i.e. the amount of stretch

This information forms a key part of reflex circuits…….

194
Q

Extrafusal muscle fibres

A

Ones that do stuff

195
Q

Intrafusal muscle fibres

A

Sensory neuron connected so it can sense stretch

196
Q

Complex reflexes in quadrapeds

A

Quadrupeds will walk on treadmill if weight supported if spinal cord damaged at thoracic level
Will change to appropriate patterns of limb movement as treadmill speed is altered
Complex reflex system responding to nothing more than stretch of muscle spindles!!

197
Q

Withdrawal reflex?

A

Reciprocal Innervation

Principle described by Sherrington (also called Sherrington’s Law of reciprocal innervation)

Reciprocal innervation of antagonistic muscles explains why the contraction of one muscle induces the relaxation of the other

Permits the execution of smooth movements

198
Q

Brainstem importance

A

Pathways and nuclei within the brainstem (and midbrain) connect sensory input to motor output in quite direct ways, providing an evolutionarily ancient but still very important control system. E.g balance and speech

199
Q

Motor cortex overview

A

Primary motor cortex exerts quite direct, top down control over muscular activity, with as few as one synapse (in the spine) between a cortical neuron and innervation of muscle cells

200
Q

Describe descending projections from cortical motor areas

A

Motor command originates in motor cortex pyramidal cells (in layer 5-6, grey matter).
These are the upper motor neurons.
Pyramidal cell axons project directly or indirectly (e.g. via brainstem) to spinal cord, where they synapse with lower motor neurons.
The axons of these upper motor (pyramidal) neurons form the pyramidal tract
Most cortical projections innervate contralateral motor units

201
Q
A

Basal ganglia- inhibitory
Cerebellum- excitatory

202
Q

Describe the homunculus

A

Homunculus is a reasonable representation, but an oversimplification: damage to a single finger area doesn’t mean loss of voluntary control of that finger.
Representations are more complex and overlapping
After all, few motor commands require isolated activation of a single motor unit

203
Q

What is the dorsolateral tracts?

A

In spinal white matter
Innervate contralateral side of one segment of spinal cord
Sometimes project directly to alpha motor neuron

Project to distal muscles, e.g. fingers

204
Q

Ventromedial tract

A

Direct route

Diffuse innervation projecting to both sides and multiple segments of spinal cord

Project to proximal muscles of trunk and limbs

205
Q

Give an overview of the basal ganglia through the lens of the motor system

A

A group of structures beneath the cortex that act as a ‘gate-keeper’ for control of the motor system (muscles)
- The basal ganglia are a group of nuclei lying deep within cerebral hemispheres
- Widely studied (including here at Sheffield)
- Role in motor control not fully understood- inhibitory
- Basal ganglia dysfunction implicated in many disorders

206
Q

What happens in the basal ganglia?

A

Receives excitatory input from many areas of cortex (Glutamate)
Output goes back to cortex via the thalamus
Output is mainly inhibitory (GABA)
Complex internal connectivity involving 5 principle nuclei

207
Q

What are the 5 principle nuclei of the basal ganglia?

A
208
Q

What is the selection problem?

A

Multiple command systems

Spatially distributed

Processing in parallel

All act through final common motor path

[Cannot do more then one thing (well) at a time]

How do you resolve the competition?

209
Q

work out how to word slide 24

A

dopamine drives disinhibitory effect

210
Q

Give an overview of the cerebellum

A

The cerebellum is a large brain structure that acts as a ‘parallel processor’, enabling smooth, co-ordinated movements. It may also be very important in a range of cognitive tasks
Like basal ganglia, no direct projection to the lower motor neurons – instead modulate activity of upper motor neurons

211
Q

Describe some key facts about the neurons and weight of cerebellum

A

Contains approx half total number of CNS neurons
Just 10% of total brain weight
Projects to almost all upper motor neurons

212
Q

What inputs into the cerebellum?

A

Cerebral cortex via pons
Vestibular system
spinal cord

213
Q

What is the output of the cerebellum

A

Via thalamus to motor cortex

214
Q

See slide 30

A
215
Q

Cerebellar function

A

-It knows what the current motor command is
-It knows about actual body position and movement
-It projects back to motor cortex
Computes motor error and adjusts cortical motor commands accordingly

216
Q

What are some debating thoughts about what the cerebellum does?

A

Not just motor control, but motor learning too, in collaboration with basal ganglia and cortical circuits.
Functional brain imaging studies have demonstrated that the cerebellum is involved in a wide variety of non-motor tasks

217
Q

How to bypass lower motor neurons?

A

Record brain activity
Decode
Specify desired movement sequence
Move limbs

218
Q

Phototransduction

A
219
Q

What are the 3 types of vision?

A

Emmetropia- normal vision
Myopia- short sightedness as refractive power is too high
Hypermetropia- long sightedness as refractive power is too low

220
Q

Hypermetropia

A

Underpowered to focus near objects on the retina
May be due to:
Corneal curvature too shallow
Lens not flexible enough
Axial length of eyeball too short

221
Q

Posterior segment

A

Vitreous humour
Avascular viscoestalic gel
Hyaluronic acid (GAG)
Collagen

222
Q

Adnexae (things near the eye)

A

Lids- protect the globe
Anterior skin
Eye lashes
Melbomian glands
Orbicularis oculi
Tarsal plate
Tarsal conjunctiva
Levator palpebrae superioris and sympathetic muscle
Conjunctiva- palpebral (tarsal) vs bulbar (ocular)
Limbal stem cells
Conjunctival fornix
Mucous membranes (goblet cells)
Lymphoid cells ( protective)
Tear film

223
Q

Lids

A

Anterior skin
Eye lashes
Melbomian glands
Orbicularis oculi
Tarsal plate
Tarsal conjunctiva
Levator palpebrae superioris and sympathetic muscle

224
Q

Conjunctiva

A

palpebral (tarsal) vs bulbar (ocular)
Limbal stem cells
Conjunctival fornix
Mucous membranes (goblet cells)
Lymphoid cells ( protective)

225
Q

Tear film

A

3 layers- anterior lipid, middle aqueous, posterior mucous
Protective
Nutrition for cornea

226
Q

Arterial supply of the eye

A
  • Internal carotid a. -> Ophthalmic a.
  • Branches of the ophthalmic a. (ocular group):
    • central retinal a.
    • Posterior ciliary a. -> long and short
    • muscular a. -> anterior ciliary a.
  • Branches of the ophthalmic artery (orbital group:
    - lacrimal a.
    - several other branches supply the face and lids
  • External carotid a. -> facial a. -> angular a.
227
Q

Allodynia

A

Pain due to a stimulus that does not normally provoke pain.

228
Q

Dysesthesia

A

An unpleasant abnormal sensation, whether spontaneous or evoked.

229
Q

Hyperalgesia

A

Increased pain from a stimulus that normally provokes pain.

230
Q

Hypoalgesia

A

Diminished pain in response to a normally painful stimulus.

231
Q

Pain pathway

A

Peripheral receptor
1st order neuron
2nd order neuron
3rd order neuron

232
Q

peripheral receptor

A

to detect the relevant stimulus

233
Q

1st order neuron

A
  • from the periphery to the ipsilateral spinal cord
234
Q

2nd order neuron

A

which crosses to the contralateral cord and ascends to the thalamus, the system’s integrative ‘relay station’

235
Q

3rd order neuron

A

rom thalamus to midbrain and higher cortical centers

236
Q

Function of nociceptors

A

Transduction

Physical stimulus  action potential

Most are poly-modal (thermal / chemical / mechanical)

237
Q

Describe primary afferent neurons

A

Nociceptors are the free nerve endings of primary afferent neurons
AΔ fibres
C fibres
found in any area of the body that can sense pain either externally or internally

External: skin / cornea / mucosa
Internal: viscera / joints / muscles / connective tissue

The cell bodies of these neurons reside in either
Dorsal root ganglion (body)
Trigeminal ganglion (face / head / neck)

238
Q

Dorsal root ganglion

A

Present on the dorsal root (sensory)
Composed of cell bodies of nerve fibres that are sensory (afferent)
First order neurons
Pseudo-unipolar neurons
Can be the source of pain pathology
Trigeminal ganglion is the equivalent for the face / head

239
Q

A- alpha nerve fibers

A

Info carried- proprioception
Myelin sheath?- yes
Diameter(micrometers)-13- 20
Conduction (m/s)- 80-120

240
Q

A- beta nerve fibres

A

Info carried- touch
Myelin sheath?- yes
Diameter (micrometers)- 6-12
Conduction- 35-90

241
Q

A- delta nerve fibre

A

Info carried- pain (mechanical and thermal)
Myelin sheath?- yes
Diameter 1-5
Conduction 5-40

242
Q

C

A
243
Q

Describe doral horn

A

On the posterior aspect of the SC the grey matter forms two horns called the dorsal horns. (the ones at the front are called the ventral horns)
Contains distal nerve endings from primary afferents, cell bodies of second order neurones as well as a complex network of other nerves such as excitatory and inhibitory interneurons (and projection neurones) that transmit somatosensory info from the SC to the brain
1952 Rexed subdivided the grey matter of the SC into 10 laminae. Lamina 1 5/6 correspond to the DH. Some of these rexed laminae have special names e.g. lamina II (2) is called substantia gelatinosa

244
Q
A

Aδ primary afferents synapse directly withsecondary afferentsthat will eventually carry the pain signal to the thalamus.
C fibres do not synapse directly with secondary afferents, but connect instead withinterneuronsthat carry the signal on to secondary afferents in laminae I or V. These interneurons are important in modulation of the pain signal
Visceral input differs in that fewer primary afferents activate a larger number of second order neurons, resulting in poorer localisation of pain. Visceral afferents also converge with somatic inputs, which may account for the phenomenon of referred pain

245
Q

Spinothalamic tract

A

Sensory pathway that carries pain, temperature and crude touch information from the body
2nd order neurons
Originate in the spinal cord (substantia gelatinosa and nucleus proprius)
Axons decussate at / few levels above the site of entry / spinal segment
Cross the midline in the anterior commissure
Then form the anterolateral tract
lateral STT (pain & temperature) and
anterior STT (crude touch)

Terminate in the thalamus
(ventral posterior lateral nucleus)

246
Q

Ascending tracts

A

Doral columns- fine touch, proprioception, vibration)
Lateral spinothalamic tract- pain and tgemperature
Ventral spinothalamic tract- light touch

247
Q

Describe the thalamus

A

Midline, paired symmetrical structure in the brain
Approx 6 X 3 cms long
All sensations (except olfactory) relay / pass through
Multiple nuclei
VPL
Medial group
Reciprocal connections to all parts of the cortex

248
Q

Insula

A

severity of pain and addiction

249
Q

Amygdala

A

emotional processing of pain

250
Q

Cingulate cortex

A

Emotional formation around pain

251
Q

Periaqueductal gray

A

Grey matter located around the cerebral aqueduct
Receives input from cortical and sub-cortical areas
Projects onto neurons in the dorsal horn
Modulate afferent noxious transmission
Neurons bear opioid receptors
Pathways also include noradrenergic and serotonergic neurones
Stimulus of the PAG can result in profound analgesia

252
Q

Bio-psycho-social model of pain

A

Pain affects all areas which then affects the pain

253
Q

Yellow flags

A

Beliefs and emotional response
pain behaviours- being told something about how you should cope with pain affects how you will cope with it and its duration

254
Q

Blue flags

A

Pain perception and relationship between work and health

255
Q

Black flags

A

System or contextual obstacles
e.g ongoing lawsuit

256
Q

Gate control theory

A

This schematic has drawn a gate to illustrate what inhibitory interneurons would do functionally
What you have to know about Melzack and Walls gate control theory is that it is the concept that onwards transmission of a nociceptive signal depends on the balance between inhibitory and excitatory inputs at points of integration along the path from transduction to perception.

257
Q

Drugs used in pain management

A

NSAID’S
Paracetamol
Opioids
LA’s
⍺2 agonists
NMDA receptor antagonists
TCA’s
gabapentinoids
SNRI’s

258
Q

Define pain

A

Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.

259
Q

Nociplastic pain

A

Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain.

260
Q

Neuropathic pain

A

Pain caused by a lesion or disease of the somatosensory nervous system

261
Q

Nociceptive pain

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.

262
Q

Acute vs chronic pain

A

Acute- physiological- Pain < 12 weeks duration

Chronic- pathological- Continuous pain lasting > 12 weeks
Pain that persist beyond the tissue healing time
classified into cancer and non-cancer pain

263
Q

Nociceptive pain pathways

A

Transduction in the periphery, through transmission to the dorsal horn of the spinal cord, then on to the brain

264
Q

What is nociception?

A

Describes the neural processes involved in producing the sensation of pain

265
Q

What is the purpose of persisting pain?

A

Later,persisting painencourages us to immobilize the injured area, giving damaged tissue the best chance to heal.

266
Q

What is the purpose of immediate pain?

A

Immediate painwarns of imminent tissue damage  withdraw from the source of injury

267
Q

What is depression

A

-Low mood, anhedonia, low energy
-“Biological” symptoms
◦ Poor sleep
◦ Poor appetite
◦ Reduced libido
◦ Poor concentration
-“Cognitive” symptoms
◦ Worthlessness (poor self esteem)
◦ Guilt
◦ Hopelessness
◦ Suicidal thought

268
Q

Describe how the Hypothalamus Pituitary Adrenal axis changes in depression

A
  • Increased CRH
  • Enlarged adrenals and pituitary
  • Reduced –ve feedback
  • Reduced GR expression in the brain
    ◦ “Glucocorticoid resistance”
269
Q

Describe the HPA axis

A

Hypothalamus –(CRH- corticotropin releasing hormone)—-> Anterior pituitary —(ACTH- adrenocorticotropic hormone)—> Adrenal cortex —(CORT)—-> Negative feedback to the hypothalamus

270
Q

Role of early adversity and parenting effect on depression

A

History of childhood maltreatment (with or
without current MDD) -> ↑ACTH release in
response to stress
 Offspring of “high licking” lab rats show high
GR expression (higher ACTH suppression)
◦ Even if swapped at birth
◦ Or even if brushed
by a research assistant!
◦ Blocked by 5HT antagonists
◦ Possibly oxytocin mediated

271
Q

Social rank effects on HPA function

A

Subordinate monkeys have:
◦ Heavier adrenal glands.
◦ Increased cortisol in hair
◦ Reduced dexamethasone suppression

272
Q

How does stress affect the brain?

A

Findings suggest that steroids are:
◦ Neurotoxic
◦ Cause neuro-vulnerability
◦ Affect dendrite formation
◦ Reduces neurogenesis
◦ Cause changes to the EEG.
 Particularly affects the frontal lobes and
hippocampus.

273
Q

Impact on stress on different parts of the frontal lobes

A

 Medial PFC
◦ Evaluating emotional state
◦ Social cognition
◦ Less volume loss
 Dorsolateral PFC
◦ Working memory
◦ Problem solving
◦ Large volume loss

274
Q

Impact of depression on the hippocampus

A

 Reduced in size in MDD
◦ Up to 20% volume loss
 A dose related effect
◦ Correlated with number of,
and length of previous episodes.
 Associates with learning based cognitive
deficits.
 Much of the volume loss is irreversible
◦ Is depression a neurodegenerative disease?

275
Q

What is neurogenesis

A

 Grow axons
and dendrites,
and integrate
into existing
networks
 6% of the total
dendate gyrus
population a
month!

276
Q

How does stress regulate neurogenesis

A

 Restraint and shock stress
causes reduced neurogenesis.
Particularly when learned
helplessness is induced.
 ‘Social dominance stress’
reduces the number of
surviving new cells (same
rate)

277
Q

How does stress affect dendrites

A

Mediated by reduced neurotrophins
 Eg. Brain derived neurotrophic factor (BDNF)

278
Q

Link between Brain Derived Neurotrophic Factor and depression

A

Stress -> ↓BDNF (animals).
◦ Reversed with antidepressants
 Low BDNF in unmedicated depressives
◦ Normal to high in medicated patients
 The lowest levels in post-mortems of
successful suicide victims

279
Q

How do antidepressants work?

A
  • Original observations about their
    pharmacology ->
    ◦ “The monoamine theory of depression”
  • The answer is “by affecting gene expression”
  • Antidepressants increase GR expression
    ◦ (regulating HPA activity)
  • Antidepressants increase neurogenesis
     They increase BDNF synthesis.
    ◦ ∴ improve connectivity and increase
    number of synapses.
280
Q

What is the function of the default mode network?

A

It’s what comes on when there’s nothing to
do (“resting state”)
- The brain’s ‘screen saver’
- Daydreaming, internal ‘flow’ of
consciousness.
- Autobiographical details
◦ The self’s place in time and space
◦ Projecting to other places in time and space
- Self reference
◦ Referring to traits or states
◦ Emotional and moral reasoning
- Thinking about others
◦ Theory of mind
◦ Social judgements/evaluations

281
Q

DMN in depression

A
  • Depressed people find it hard to
    appropriately switch off their DMN in
    response to a task.1
  • We already knew depressed people
    excessively ruminate.
  • Dinner party with a deadline.
282
Q

Relationship between the DMN and LSD

A
  • Carhart Harris used modern functional
    scanning techniques on people in the acute
    psychedelic state.
  • Positive symptoms -> ?surely increased
    activity
  • Reduced activity in the DMN
  • Reduced alpha power in PCC
283
Q

5 pillars of wellbeing

A
  • Physical activity
  • Connect with others
  • Learn something new
  • Practice mindfulness
  • Acts of generosity
284
Q

Differences between the somatic and autonomic nervous system

A

S:Conscious- A: unconscious
S: no synapse after CNS - A: fibres synapse at a ganglion after the CNS
S: SkM, stimulatory - A: SmM and CM stimulatory and inhibitory

285
Q

Parasympathetic

A

Cranial nerves to head, thorax + abdm
Sacral outflow to pelvic organs
The vagus nerve to thorax and abdm

286
Q

Sympathetic

A

Cranial nerves to eye
The sympathetic chain
Other ganglia
Post ganglionic fibres

287
Q

Where are the ganglion in the autonomic nerves?

A

In the middle of the motor neuron
Before it is myelinated after it is not
Usually uses acetyl choline or NE at the neuromuscular junction

288
Q

Functions of the autonomic nervous system

A

Thermoregulation, Exercise, Digestion, Competition, Sexual Function, Fight/flight

289
Q

Sympathetic stimulation

A

Heart rate and force of contraction increases
Blood vessel constriction
Bronchodilation]
Decreased motility in gut
Sphincter contraction
Decreased secretion in gut
Male ejaculation

290
Q

Parasympathetic stimulation

A

Heart rate and force of contraction decrease
Blood vessels can dilate
Bronchoconstriction
Increased gut motility
Sphincter relaxation
Increased secretions in gut

291
Q
A

Sympathetic chain running alongside spinal cord

292
Q
A

parasymp acetyl choline
symp adrenaline/noradrenaline

293
Q

Rami communicantes

A
294
Q

Which cranial nerves have parasympathetic fibres?

A

Oculomotor III
Facial nerve VII
Glossopharyngeal nerve IX
Vagus nerve X

295
Q

Main neurotransmitter in enteric nervous system

A

Serotonin

296
Q

Nicotinic receptos

A
297
Q

Muscarinic receptors

A

Only in parasympathetic

298
Q

Adrenergic receptors

A

Only in sympathetic

299
Q

Subtypes of noradrenaline

A

Alpha- alpha 1, alpha 2
Beta- beta 1,2,3

300
Q

ANS inputs carotid receptors

A

Carotid body in carotid bifurcation
Baroreceptors for BP
Chemoreceptors for O2
Afferents to the brainstem
Affect output of brainstem

301
Q

ANS inputs- ventricle receptor

A

Volume in ventricle

302
Q

Diving response

A
303
Q

Acute primary A.N.S disorders

A

Pan-dysautonomia with neurological features

304
Q

Chronic primary A.N.S. disorders

A

Pure autonomic failure
Multiple system atrophy (Shy-Drager syndrome)
Autonomic failure with Parkinson’s disease

305
Q

Secondary A.N.S. disorders- metabolic diseases

A

Diabetes mellitus
Chronic renal failure
Chronic liver disease
Alcohol induced

306
Q

Secondary ANS disorders

A

Inflammatory- Guillian-Barré syndrome
Infections- Bacterial: tetanus
Parasitic: Chagas’ disease
Viral: HIV
Neoplasmia- Brain tumours, especially of third ventricle or posterior fossa

307
Q

Cardiovascular disorders of the ANS

A

Postural hypoternsion
Supine hypertension
Liability of BP
Paroxysmal hypertension
Tachycardia
Bradycardia
Fainting

308
Q

Sexual disorders of the ANS

A

Erectile failure
Ejaculatory failure
Retrograde ejaculation
Priapism

309
Q

Sudomotor disorders

A

Hypo/anhidrosis
Hyperhidrosis
Gustatory sweating
hypothermia
Hyperpyrexia

310
Q

Ailementary disorders

A

Gastric stasis
Dumping syndrome
Constipation
Diarrhoea

311
Q

Disorders of the eyes

A

Pupillary abnormalities
Ptosis
Alachryma

312
Q

How can you measure the ANS cardiovascularly?

A

HR and BP- preferably beat by beat
-> can do it using the radial artery
Tilt test
Baro-reflex testing- By Phenylephrine test

313
Q

Non cardiovascular ANS measurement

A

Pupillometry
Sweat measurement
Skin blood flow, thermoregulation
Gastric acid secretion
Sexual function

314
Q

Outline fMRI

A
  • BOLD contrast reflects blood flow changes
    secondary to neuronal activation
  • Simple or complex tasks compared with a
    “rest” state
  • Statistical analysis of significant changes in
    BOLD contrast demonstrates areas of
    “activation” which are overlaid on anatomical
    images
315
Q

Outline auditory fMRI

A
  • Study the auditory pathway
    both in cortical & subcortical
    structures
  • 3T
    -HIGH Resolution 2x2x2 mm3
    -HIGH SENSE factor 2.5
    -“Silent gap” scanning
    -Binaural auditory stimulation
316
Q
A
317
Q

Define pain

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

318
Q

Important factors in understanding pain in the moment

A

Body/nervous system
Attention
Expectation
Past experience (incl. trauma)
Thoughts/words
Senses
Emotions
Feedback/response

319
Q

What is DIM and SIM

A

DIM- Danger
SIM- Safety

320
Q

Key features of long term pain

A
  • Sensitisation
  • catastrophic thinking - not only more likely to experience pain, but more likely to have an acute pain become chronic
  • situation where sustaining an injury would have high levels of consequence
  • more general psychological states of threat (e.g. abuse)
321
Q

What is sensitisation?

A
  • Neurons that fire together
    (path through the woods)
    (playing the pain song)
  • Nervous system
  • “Smudging” etc.
322
Q

Acute pain

A

A warning – (generally) helpful and protects you from further physical damage
Can usually be explained and treated
E.g. toothache, sprained ankle, broken bone
Others tend to understand and offer sympathy
Temporary - you can carry on as normal afterwards

323
Q

Chronic pain

A

Typically serves no useful warning purpose – a ‘nuisance’
Medical investigations may not provide a diagnosis or an explanation
Treatment is aimed at relieving pain, not curing it
Others might not understand
Ongoing and often has a negative and widespread effect on life

324
Q

What can chronic pain affect?

A

Ability to work
Activities (e.g. social and daily activities)
Satisfaction and enjoyment from activities
Contact with others
Relationships with family and friends
Self confidence
Sleeping patterns
Poor concentration
Mood
Sense of self -‘Not the person I used to be’
pre-occupation with pain
Uncertainty about the cause of pain and the future

325
Q

What are the 3 Ps

A
  • Pacing
  • Prioritising
  • Planning
326
Q

What is pacing?

A

Limiting the time spent on an activity to prevent marked increases in pain, and keeping to a regular amount of activity to prevent the problems of too much rest.
Planning activity rather than just doing things according to how you feel.
Taking frequent short breaks, breaking tasks or activities down to smaller tasks and changing position regularly.

327
Q

What is planning?

A

Involves thinking about when and how activities are going to be done.
Make sure that difficult activities are spread out
Balance essential with non-essential activities
Taking regular breaks

328
Q

What is prioritising?

A

Means making (difficult) choices about what is done

Try to balance what needs to be done with what is pleasurable or interesting.

329
Q

Why can learning to relax be helpful?

A

When we know something is going to hurt the natural and automatic response is for our muscles to tense up in anticipation to protect ourselves Pain leads to muscle tension
Egs: something being thrown at us, injections
Muscle tension can make the experience of pain worse

330
Q

Effects of prolonged muscle tension

A

cause aches, discomfort and tiredness
cause simple movements, e.g. walking or getting out of a chair, to become stiff and slow
become normal - maybe physically tense without being aware of it

331
Q

What can relaxation do?

A

Be beneficial to a person’s general health
Help to change their experience of pain
Help to manage pain and feel more in control
Be a useful means of distraction
Be helpful in dealing with stress

332
Q

Distraction

A

Pain is a powerful signal which gets your attention, but we can influence that attention
Awareness of pain is affected by mental activity
Distraction is a very valuable and practical approach to managing pain

333
Q

Tips for managing flare ups

A

Help patients Plan for flare ups
Remember the ‘box of tools’
Advise patients to talk to others about flare ups and how best they can help
Advise patients to focus on getting through the short period of time during a flare up.
Review medication use during and after a flare up.

334
Q

What are the different circuits in the basal ganglia?

A

-Motor circuit
-Limbic circuit
-Oculomotor circuit

335
Q

Motor disorders related to the basal ganglia

A

Parkinson’s Disease
Huntington’s Disease
Dystonia
Gilles de la Tourette syndrome

336
Q

What are some psychiatric disorders related to the basal ganglia?

A

Obsessive compulsive disorder
Attention Deficit Hyperactivity Disorder (ADHD)

337
Q

What are some diseases secondary to damage of the basal ganglia?

A

Cerebral Palsy
Wilson Disease

338
Q

Key points of parkinsons disease

A

Increased muscle tone
Reduced movements
Not enough dopamine

339
Q

Key points of huntington’s disease

A

-Decreased muscle tone
-Overshooting movements
-Too much dopamine

340
Q

How to synthesise dopamine?

A

-Tyrosine- amino acid
-L-DOPA
-Dopamine

341
Q

Key findings in the brain of someone with Parkinson’s

A

loss of dopaminergic receptors in the substantia nigra
Presence of lewy bodies

342
Q

What is the area of cell loss in Huntington’s disease?

A

Striatum

343
Q

Pathway of

A
344
Q

What is the dopamine antagonist in the brain?

A

GABA- produced in striatum

345
Q

WHere is dopamine produced?

A

Substantia nigra

346
Q

What happens biochemically in parkinsons?

A

Loss of substantia nigra means decreased dopamine and so more GABA and less movement

347
Q

What happens biochemically in Huntington’s?

A

Loss of striatum means loss of GABA so more dopamine and more movement

348
Q

Key features of Parkinson’s disease

A

Brady/Akinesia
Problems with doing up buttons, keyboard etc
Writing smaller
Walking deteriorated: Small steps, dragging one foot etc

Tremor
At rest
May be on one side only

Rigidity
Pain
Problems with turning in bed

349
Q

Drug treatment of Parkinson’s disease

A

Drugs mostly aim at correction of dopamine deficit

But:
More and more cells die

The drugs work shorter and shorter

The longer on treatment, the more likely are the patients to develop side effects, in particular dyskinesias

350
Q

Outline deep brain stimulation to treat Parkinson’s

A

Functional lesioning of the subthalamic
Nucleus leads to dramatic improvement of PD
It deactivates the break (subthalamic nucleus)

351
Q

Key clinical features of Huntington’s disease

A

Chorea
Dementia/psychiatric illness
Personality change

352
Q

Clinical genetics of Huntington’s disease

A

Autosomal dominant
Fully penetrant
Trinucleotide repeat expansion

353
Q
A

Trinucleotide repeat expansion

Phase 1 (22 decks)

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