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Clinical Neuroscience Flashcards

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1
Q

What is clinical neuroscience?

A

A neuroscientific approach to disorders of the brain and central nervous system.

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2
Q

What is the ventral dorsal stream dichotomy?

A

Information processing can go by two pathways.
Dorsal - WHERE things are happening, preparing us to act and do actions based on things that are happening.
Ventral - WHAT objects are and who people are but doesn’t guided us to act on them.

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3
Q

Where does the parietal cortex receive input from?

A

V1

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4
Q

What are the functions of the parietal cortex? (5)

A
  • Space-based attention
  • Object-based attention
  • Reaching and grasping
  • Magnitude processing
  • Feature-based attention
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5
Q

What kind of disorder is Hemispatial neglect?

A

A disorder of space-based attention

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6
Q

What is Hemispatial Neglect?

A
  • Damage to the right parietal lobe
  • Patients don’t attend to the left side of space
  • But they can attend when objects are pointed out to them
  • Have trouble imagining the left visual field
  • NOT a problem in the visual cortex.
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7
Q

What does hemispatial neglect impact?

A

Perception and mental imagery.

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8
Q

How do we assess hemispatial neglect?

A

Through eye-tracking.

Piazza del Duomo, Milan study

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9
Q

Why is neglect more common in the right than left hemisphere?

A
  • RH dominant for visuo-spatial attention
  • RH represents contralateral and ipsilateral space
  • LH represents contralateral space only.
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10
Q

How does hemispatial neglect affect audio?

A
  • May respond to voices/sounds originating from the affected hemispace as if they occurred in the ipsilesional side
  • Poorer audio location compared to patients with right brain damage without neglect
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11
Q

How do patients with hemispatial neglect recover?

A
  • Slow recovery
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12
Q

What kind of disorder is Balint’s Syndrome?

A

A disorder of object-based attention

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13
Q

What is Balint’s Syndrome?

A
  • Bilateral damage to parietal and occipital lobes

- Three distinct impairments

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14
Q

What are the 3 distinct impairments in Balint’s Syndrome?

A
  • Simultanagnosia
  • Optic Ataxia
  • Oculomotor Apraxia
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15
Q

What is sumultanagnosia?

A

If two or more objects are presented, the patient can only see one at a time.
If the unseen object is jiggled then the patient will see it but lose perception of the first object.

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16
Q

What is Optic Ataxia?

A
  • disorder of reaching and grasping
  • orientation errors
  • position errors
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17
Q

What is Oculomotor Apraxia?

A
  • Problem making planned and purposeful eye movements
  • Have problems with saccade initiation and accuracy, and smooth visual persuit
  • May happen in Balint’s Syndrome due to deficit in a circuit between the parietal lobe and the frontal eye fields (FEF)
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18
Q

What type of disorder is Dyscalculia?

A

A disorder of magnitude processing.

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19
Q

What is Dyscalculia?

A
  • Developmental disorder
  • Patients have problems understanding and manipulating numbers
  • Prevalence estimates 3-6%
  • Neuroimaging studies suggest that the deficit may be localised in the right inferior parietal lobule
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20
Q

What is the numerical distance effect?

A

easier to identify the larger of two numbers when there is a greater numerical distance between them

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21
Q

Explain A theory of Magnitude (ATOM).

A
  • Time, Space, and Number all require us to compare size or magnitude
  • They share a common neural origin in the right intraparietal sulcus.
  • All bits of planning are relying on magnitude in order to plan the day.
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22
Q

Lesions or atypicalities in the parietal lobe can lead to syndromes like…

A
  • Hemispatial Neglect
  • Balint’s Syndrome
  • Dyscalculia
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23
Q

What is MDD?

A

Major Depressive Disorder

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24
Q

What is Anhedonia?

A

Reduced interest in pleasure

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25
Q

What is DBS?

A

Deep brain stimulation

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26
Q

What is VNS?

A

Vagal Nerve Stimulation

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27
Q

What is TMS?

A

Transmagnetic Stimulation

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28
Q

What is the main pharmacological intervention for depression?

A

SSRI’s - have been relatively unchanged for 50 years.

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29
Q

In Beck’s cognitive model of depression, individuals with depression are said to be prone to… (5)

A
  • selectively attend to negative stimuli (biased attention)
  • greater perception for negative stimuli (biased processing)
  • ruminate about depressive ideas (biased thought and rumination)
  • recall depressive episodes with more frequency (biased memory)
  • possess negative internal reps about the self and environment (negative schemas)
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30
Q

What are the elements of depression?

A
  • Biased attention
  • Biased processing
  • Biased thought and rumination
  • Biased Memory
  • Negative schemas
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31
Q

Explain biased attention in depression.

A
  • Healthy people’s attention is normally biased towards positive stimuli but individuals with depression show a bias for negative stimuli.
  • Problems could contribute to dysphoria
  • Brain regions involved are parts of the parietal cortex, and prefrontal cortex including VLPFC and DLPFC
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32
Q

Explain biased processing in depression.

A
  • Reward processing affected in depression
  • Reward is supported by a frontostriatal network and nucleus accumbens (NAcc)
  • Disruptions in this network has been argued to be the basis for anhedonia.
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33
Q

Explain biased memory in depression.

A
  • Activity in the amygdala facilitates the encoding and retrieval of emotional stimuli in healthy individuals by modulating brain regions associated with memory.
  • Biased memory in depression is associated with amygdala hyperactivity, which is positively correlated with activity in the hippocampus, caudate, and putamen.
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34
Q

What is the neurotrophic hypothesis of depression?

A
  • Decreased BDNF in hippocampus
  • Impairs memory encoding
  • Demonstrated neuroplasticity at a very specific anatomical level
  • Not clear if this is a cause or result of depression
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35
Q

What is BDNF?

A

Brain Derived Neurotrophic Factor (chemical)

- important for neuroplasticity and neurogenesis

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36
Q

Summarise depression in the brain.

A
  • increased amygdala activity
  • decreased activity in right VLPFC and right DLPFC and superior parietal cortex
  • atypical frontostriatal activity
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37
Q

What are the 3 elements in the neurochemistry of depression?

A
  • Glutocorticoids (mainly cortisol)
  • Brain derived neurotrophic factor (BDNF)
  • Monoamines
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38
Q

What is cortisol and what does it do?

A

A steroid hormone:
increases blood sugar, suppresses immune system, increases metabolism.
Increased cortisol raises performance during stress.

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39
Q

What is BDNF and what does it do?

A
  • Maintains and supports the growth of neurons/synapses

- expressed in many brain areas but especially related to memory formation in the hippocampus

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40
Q

How do cortisol and BDNF affect each other?

A

Increased cortisol, reduces BDNF.

That means connections between brain areas don’t develop when supposed to.

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41
Q

What are monoamines?

A

Neurotransmitters - they are released by neurons to send signals to other neurons.

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42
Q

What 3 monoamines affect depression?

A

Dopamine
Serotonin
Noradrenaline

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43
Q

What is the role of dopamine?

A

Reward and motivation, supports approach and consummatory behaviours.
Released from Ventral tegmental area to forebrain networks.

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44
Q

What is the role of serotonin?

A

It is the happiness molecule but also many other complex behaviours e.g. dominance.
Released from Dorsal Raphe to forebrain networks.

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45
Q

What is the role of Noradrenaline?

A

Fight or Flight molecule that prepares the body for action.

Released to organs all over the body.

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46
Q

What are the symptoms of monoamine treatments of depression?

A
  • Have to overcome homeostatic feedback (2-4 weeks)
  • Many different side affects e.g. insomnia, aggression, nausea.
  • Effects can wash out over time
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47
Q

How do monoamine treatments of MDD work?

A

They block the reuptake of serotonin by presynaptic neurones. It then stops releasing serotonin - less serotonin being reduced.

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48
Q

What was the aim of the CoBalT study?

A

To test the efficiency of CBT

- showed improvement in 46% of PPs in intervention group vs 22% in usual care.

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49
Q

Explain the basic genetics of MDD. (3)

A
  • Highly heritable (50% chance if parent diagnosed)
  • More heritable in women than men
  • We ALL have at least some of the genes that correlate with MDD
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50
Q

What are polygenic risk scores used for in depression?

A

To identify the likelihood of developing depression using polygenomic sequencing to compare an individual’s DNA to the roadmap.
Also used to see what covaries with depression.

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51
Q

Why does gene SLC6A4 (aka 5-HTT) affect depression?

A

It regulates the expression and transportation of serotonin in the brain.

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52
Q

What did Capsi et al 2003 find about gene 5-HTT and depression?

A
  • The 5HTT s/s homozygote allele is not enough to cause MDD
  • A combination of the 5HTT s/s variant and multiple early life stress events will increase the chances of MDD
  • risk of MDD is an output of both genetic predisposition and environment.
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53
Q

What method is used to measure gray matter volume of the 5HTT gene?

A

VBM - voxel-based morphometry

54
Q

How is DLPFC affected by MDD?

A

DLPFC is hypoactive - problems with top-down regulation

55
Q

How is the amygdala affected by MDD?

A

Amygdala is hyperactive - problems with processing negative stimuli

56
Q

What is a stressor event?

A

Trauma

57
Q

What are the criteria for PTSD diagnosis?

A
  • Stressor
  • Alterations in arousal and reactivity
  • Intrusion symptoms
  • Negative alterations in cognition/mood
  • Avoidance
  • Symptoms must last for more than 1 month
58
Q

What is hypervigilance?

A

Elevated state of constantly assessing potential threats

59
Q

What are the brain regions implicated in PTSD?

A
  • Prefrontal Cortex
  • Cingulate cortex
  • Limbic regions
  • Neuroendocrine system - the HPA
60
Q

What is the HPA?

A

Hypothalamic Pituitary Adrenal Axis

61
Q

What areas does the limbic region consist of?

A
  • Thalamus
  • Amygdala
  • Hippocampus
62
Q

How are the amygdala and HPA related?

A

The amygdala stimulates the HPA.

63
Q

What did Gilbertson et al 2002 find about the amygdala in PTSD?

A

PTSD patients showed heightened responses in the amygdala to emotional stimuli.

64
Q

What is the role of the cingulate cortex?

A
  • Involved in attention, reward, decision making and emotion
  • Part of the frontostriatal network
  • Also part of the salience network involved in alerting attention to threats
65
Q

What was the aim of Etkin et al 2019 in PTSD?

A

To search for subtypes within PTSD.

66
Q

What did Etkin et al 2019 find in PTSD?

A

The patients who has weak connectivity in the Ventral Attention Network (VAN) responded poorer to treatment.

67
Q

What is the role of the thalamus?

A
  • Relay station for sensory information
  • Important visual areas
  • Responds to bottom-up and top-down input
  • The hypothalamus forms a key part of the HPA.
68
Q

What is the role of the Dorsolateral Prefrontal Cortex?

A
  • Part of the frontoparietal attention network
  • Greater BOLD activity when controlling cognitive response
  • Part of the frontostriatal network
69
Q

What is the role of the orbitofrontal cortex?

A
  • AKA Ventromedial prefrontal cortex
  • Decision making and future planning
  • Task switching and evaluation
  • On the pathway between the DLPFC and Amygdala
70
Q

What is the insula?

A

Another area near the ACC

71
Q

What is the role of the hippocampus?

A
  • Memory processing

- Attenuates the HPA axis

72
Q

What is the relationship between the hippocampus and PTSD?

A

Smaller hippocampus = increased chance of PTSD.

It is a risk factor for PTSD, not a result of trauma.

73
Q

What is the role of the HPA axis?

A
  • Coordinates neuroendocrine stress response systems.

- Chain of neurochemical reactions that end in cortisol being released.

74
Q

Which brain pathways modulate the HPA axis activity?

A
  • Hippocampus and prefrontal cortex inhibit the HPA

- Amygdala stimulates neurons in the hypothalamus

75
Q

What are the final outputs of the HPA on the brain?

A
  • Glucocorticoids exert negative feedback control of the HPA axis by regulating hippocampal and PVN neurons.
  • Sustained glucocorticoid exposure has adverse effects on hippocampal neurons
76
Q

What is Plenadren?

A

Brand name for a common Hydrocortisone used to treat cortisol-related disorders like Addison’s disease, a rarer disorder of the adrenal glands.

77
Q

Explain the treatment of PTSD using cortisol?

A

Suggestion that hydrocortisone helps as a preventative after trauma against developing PTSD, but does very little if given after PTSD has been developed.

78
Q

What is the current recommended treatment for PTSD and why?

A

SSRI - reduce PTSD symptoms but it is a small-moderate effect and not universal.

79
Q

How is extinction beneficial in PTSD?

A
  • the fear response can be inhibited
80
Q

Which parts of the brain affect extinction of a fear response?

A
  • vmPFC - greater extinction learning
  • daCC - negatively correlated with extinction
  • cmPFC signals amygdala to reduce and control fear response
  • high connectivity between vmPFC and daCC leads to stronger extinction.
81
Q

What is EMDR?

A

Eye movement desensitisation and reprogramming.

82
Q

What does EMDR involve?

A

Patient follows moving stimulus with their eyes while holding different aspects of traumatic event in mind.

83
Q

What are the neurobiological hypotheses behind EMDR?

A
  • PTSD could be considered a consequence of failed memory processing
  • REM sleep argued to be important for memory consolidation
  • EMDR - induces a physiological state similar to that contoured in REM sleep
84
Q

What kind of drugs are commonly used to treat PTSD?

A

Antidepressants

85
Q

What is Acquired Brain Injury?

A

Refers to damage to the brain that a child was not born with - the result of an accident/event that happened later

86
Q

Define Traumatic Brain Injury

A

Caused by something happening outside the body e.g. a head injury

87
Q

Define Non-traumatic Brain Injury

A

Caused by something going on inside the body e.g. a stroke

88
Q

What are the 2 different types of traumatic brain injury?

A

Closed - when the dura layer has not been damaged (e.g. rapid deceleration)
Penetrating - damage to the dura (e.g. gunshot wound)

89
Q

What are primary injuries?

A

Occur at the moment of damage.

90
Q

What are secondary injuries?

A

Result from altered blood flow or inflammation of the brain.

91
Q

How are traumatic brain injuries categorised?

A

Mild, moderate, severe.

92
Q

For children aged 0-14, what is the most common cause of TBI?

A

Falls

93
Q

For ages 15-25, what is the most common cause of TBI?

A

Contact sports and motor vehicle accidents?

94
Q

How is working memory impaired in children with TBI?

A
  • Inpaired inhibition
  • Long-term problems in executive function
  • Affects family functioning.
95
Q

Why are orthopaedic controls used when studying TBI?

A

They want a control group that has also sustained injury, but there is no risk that the brain has been affected.

96
Q

What affects the social impairment of children with TBI?

A
  • Young age of injury
  • Frontal regions and corpus callosum affected
  • Environmental factors like social disadvantage and family dysfunction
97
Q

What social impairments did Hanten et al 2011 find in children with TBI?

A

Problem solving difficulties like describing the problem, generating solutions, selecting appropriate responses, and evaluating outcomes.

98
Q

What is Shaken Baby Syndrome?

A

Abusive head injury - when infants have been violently shaken.

99
Q

What is a diffuse injury?

A

More widespread injury rather than damage to a very specific area partly because their skull has not finished developing.

100
Q

What does the triad classification of SBS involve?

A

Subdural haematoma
Retinal haemorrhages
Encephalopathy

101
Q

What is subdural haeematoma?

A

Bleeding in the dura layer

102
Q

What are retinal haemorrhages?

A

Bleeding in the retina

103
Q

What is encephalopathy?

A

Signs of brain disease e.g. seizures, sloppiness, vomitting.

104
Q

How are outcomes of SBS correlated?

A

There is a correlation between age at admission and outcome - younger age correlated with poorer outcomes.

105
Q

What is the most common predictor of SBS?

A

Crying - we need to think more about the impact of infants crying on parents

106
Q

What is a stroke?

A

Occurs when blood flow to an area of the brain is cut off.

When these brain cells are deprived of oxygen, they lead to cell death.

107
Q

What is a ischemic stroke?

A

When arteries to the brain become blocked/narrowed, causing severely reduced blood flow.

108
Q

What is a haemorrhagic stroke?

A

When blood vessels in the brain leak/rupture.

109
Q

What is the prevalence of strokes in children?

A

1.2 to 13 cases per 100,000 children under the age of 18.

110
Q

Why are children’s strokes more underdiagnosed than adults?

A

Delay to diagnosis or a misdiagnosis is more likely.

111
Q

What are the risk factors of strokes in children?

A
  • Cardiac problems, especially congenital heart disease, or following surgery to the heart.
  • Sickle cell disease
  • Serious infections
112
Q

What are the risk factors of strokes in adults?

A
  • Hardening of the arteries
  • Diabetes
  • High blood pressure
113
Q

What are signs of a stroke in infants?

A
  • Seizures
  • Extreme sleepiness
  • Tendency to use only one side of the body
114
Q

What are signs of a stoke in children/teens?

A
  • Severe headaches
  • Vomitting
  • Sleepiness
  • Diziness
  • Loss of balance/coordination
115
Q

What long-term outcomes of strokes did Christerson & Stromberg 2012 find?

A
  • Neurological deficits
  • School activity deficits
  • Hemiparesis (weakness in one side of the body)
116
Q

What is Feotal Alcohol Syndrome?

A

Alcohol-related birth disorders, and alcohol-related neurodevelopmental disorder caused by effect of alcohol on a developing foetus.

117
Q

What physical characteristics are associated with FAS?

A
  • Poor growth
  • Distinctive facial features
  • Health problems related to organs
118
Q

What neurological characteristics are associated with FAS?

A
  • Microencephaly
  • Epilepsy/seziures
  • Abnormal development of corpus collosum
119
Q

What cognitive characteristics are associated with FAS?

A
  • Learning difficulties

- Attention and behavioural problems

120
Q

How often are physical features presented in FAS?

A

25%

121
Q

What is Partial Foetal Alcohol Syndrome (pFAS)?

A
  • confirmed history of prenatal alcohol exposure
  • CNS abnormalities same level as FAS
  • Might not have growth deficiency or one or more of the facial abnormalities
122
Q

What is Neurobehavioural Disorder associated with Prenatal Alcohol Exposure (ND-PAE)?

A

Think there might have been alcohol exposure but you don’t necessarily know.
They may not have the full physical and facial profile of FAS but have a lot of the behavioural and functional problems associated.

123
Q

Why could you argue that FAS is an example of ABI?

A

It is a result of something that has happened to the developing brain - there is nothing inherent within the foetus that meant it was going to have FAS so it is an environmental effect on the developing brain.

124
Q

Why could you argue that FAS is not an example of ABI?

A

ABI is normally defined as an event that happens post-birth

125
Q

What causes FAS?

A
  • Alcohol passes through the placenta to the baby
  • Foetus cannot process alcohol the same way so exposure leads to abnormal CNS development
  • Some foetuses will not survive
126
Q

What social problems do children with FAS experience?

A
  • exessively friendly
  • do not discriminate between familiar and unfamiliar people
  • they are at increased risk of exploitation and abuse
127
Q

What are the two key theories about why recovery of ABI can occur?

A
  • Restitution - injured system heals itseld

- Substitution - neural function is transmitted from the injured to a non-injured site

128
Q

What is the Kennard Principle?

A

Concept that the immature brain is more resilient to injury compared to more mature brain - a younger brain can reorganise better to preserve function.

129
Q

Does age at injury predict better recover in FAS?

A

the outcome of alcohol seems very vaiable - we have a spectrum of outcomes.

130
Q

Does age at injury predict better recovery in strokes?

A

Christerson & Stromberg 2010 found no effect of age at stroke but Anderson et al 3012 found that young children showed better improvements socially.

131
Q

Does age at injury predict better recover in Shaken Baby Syndrome?

A

Younger age at hospitalisation predicted poorer outcome

132
Q

How may hidden deficits emerge over time after ABI?

A
  • As toddlers become children become adolescents, the demands made environmentally increase
  • Expected to manage their own work
  • Social lives become increasingly complex

Brain and Behaviour (5 decks)

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