Clinical Neuroscience Flashcards
(132 cards)
1
Q
What is clinical neuroscience?
A
A neuroscientific approach to disorders of the brain and central nervous system.
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.
3
Q
Where does the parietal cortex receive input from?
A
V1
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
5
Q
What kind of disorder is Hemispatial neglect?
A
A disorder of space-based attention
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.
7
Q
What does hemispatial neglect impact?
A
Perception and mental imagery.
8
Q
How do we assess hemispatial neglect?
A
Through eye-tracking.
Piazza del Duomo, Milan study
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.
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
11
Q
How do patients with hemispatial neglect recover?
A
- Slow recovery
12
Q
What kind of disorder is Balint’s Syndrome?
A
A disorder of object-based attention
13
Q
What is Balint’s Syndrome?
A
- Bilateral damage to parietal and occipital lobes
- Three distinct impairments
14
Q
What are the 3 distinct impairments in Balint’s Syndrome?
A
- Simultanagnosia
- Optic Ataxia
- Oculomotor Apraxia
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.
16
Q
What is Optic Ataxia?
A
- disorder of reaching and grasping
- orientation errors
- position errors
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)
18
Q
What type of disorder is Dyscalculia?
A
A disorder of magnitude processing.
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
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
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.
22
Q
Lesions or atypicalities in the parietal lobe can lead to syndromes like…
A
- Hemispatial Neglect
- Balint’s Syndrome
- Dyscalculia
23
Q
What is MDD?
A
Major Depressive Disorder
24
Q
What is Anhedonia?
A
Reduced interest in pleasure
25
What is DBS?
Deep brain stimulation
26
What is VNS?
Vagal Nerve Stimulation
27
What is TMS?
Transmagnetic Stimulation
28
What is the main pharmacological intervention for depression?
SSRI's - have been relatively unchanged for 50 years.
29
In Beck's cognitive model of depression, individuals with depression are said to be prone to... (5)
- 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)
30
What are the elements of depression?
- Biased attention
- Biased processing
- Biased thought and rumination
- Biased Memory
- Negative schemas
31
Explain biased attention in depression.
- 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
32
Explain biased processing in depression.
- 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.
33
Explain biased memory in depression.
- 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.
34
What is the neurotrophic hypothesis of depression?
- 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
35
What is BDNF?
Brain Derived Neurotrophic Factor (chemical)
| - important for neuroplasticity and neurogenesis
36
Summarise depression in the brain.
- increased amygdala activity
- decreased activity in right VLPFC and right DLPFC and superior parietal cortex
- atypical frontostriatal activity
37
What are the 3 elements in the neurochemistry of depression?
- Glutocorticoids (mainly cortisol)
- Brain derived neurotrophic factor (BDNF)
- Monoamines
38
What is cortisol and what does it do?
A steroid hormone:
increases blood sugar, suppresses immune system, increases metabolism.
Increased cortisol raises performance during stress.
39
What is BDNF and what does it do?
- Maintains and supports the growth of neurons/synapses
| - expressed in many brain areas but especially related to memory formation in the hippocampus
40
How do cortisol and BDNF affect each other?
Increased cortisol, reduces BDNF.
| That means connections between brain areas don't develop when supposed to.
41
What are monoamines?
Neurotransmitters - they are released by neurons to send signals to other neurons.
42
What 3 monoamines affect depression?
Dopamine
Serotonin
Noradrenaline
43
What is the role of dopamine?
Reward and motivation, supports approach and consummatory behaviours.
Released from Ventral tegmental area to forebrain networks.
44
What is the role of serotonin?
It is the happiness molecule but also many other complex behaviours e.g. dominance.
Released from Dorsal Raphe to forebrain networks.
45
What is the role of Noradrenaline?
Fight or Flight molecule that prepares the body for action.
| Released to organs all over the body.
46
What are the symptoms of monoamine treatments of depression?
- Have to overcome homeostatic feedback (2-4 weeks)
- Many different side affects e.g. insomnia, aggression, nausea.
- Effects can wash out over time
47
How do monoamine treatments of MDD work?
They block the reuptake of serotonin by presynaptic neurones. It then stops releasing serotonin - less serotonin being reduced.
48
What was the aim of the CoBalT study?
To test the efficiency of CBT
| - showed improvement in 46% of PPs in intervention group vs 22% in usual care.
49
Explain the basic genetics of MDD. (3)
- 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
50
What are polygenic risk scores used for in depression?
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.
51
Why does gene SLC6A4 (aka 5-HTT) affect depression?
It regulates the expression and transportation of serotonin in the brain.
52
What did Capsi et al 2003 find about gene 5-HTT and depression?
- 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.
53
What method is used to measure gray matter volume of the 5HTT gene?
VBM - voxel-based morphometry
54
How is DLPFC affected by MDD?
DLPFC is hypoactive - problems with top-down regulation
55
How is the amygdala affected by MDD?
Amygdala is hyperactive - problems with processing negative stimuli
56
What is a stressor event?
Trauma
57
What are the criteria for PTSD diagnosis?
- Stressor
- Alterations in arousal and reactivity
- Intrusion symptoms
- Negative alterations in cognition/mood
- Avoidance
- Symptoms must last for more than 1 month
58
What is hypervigilance?
Elevated state of constantly assessing potential threats
59
What are the brain regions implicated in PTSD?
- Prefrontal Cortex
- Cingulate cortex
- Limbic regions
- Neuroendocrine system - the HPA
60
What is the HPA?
Hypothalamic Pituitary Adrenal Axis
61
What areas does the limbic region consist of?
- Thalamus
- Amygdala
- Hippocampus
62
How are the amygdala and HPA related?
The amygdala stimulates the HPA.
63
What did Gilbertson et al 2002 find about the amygdala in PTSD?
PTSD patients showed heightened responses in the amygdala to emotional stimuli.
64
What is the role of the cingulate cortex?
- 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
What was the aim of Etkin et al 2019 in PTSD?
To search for subtypes within PTSD.
66
What did Etkin et al 2019 find in PTSD?
The patients who has weak connectivity in the Ventral Attention Network (VAN) responded poorer to treatment.
67
What is the role of the thalamus?
- 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
What is the role of the Dorsolateral Prefrontal Cortex?
- Part of the frontoparietal attention network
- Greater BOLD activity when controlling cognitive response
- Part of the frontostriatal network
69
What is the role of the orbitofrontal cortex?
- AKA Ventromedial prefrontal cortex
- Decision making and future planning
- Task switching and evaluation
- On the pathway between the DLPFC and Amygdala
70
What is the insula?
Another area near the ACC
71
What is the role of the hippocampus?
- Memory processing
| - Attenuates the HPA axis
72
What is the relationship between the hippocampus and PTSD?
Smaller hippocampus = increased chance of PTSD.
| It is a risk factor for PTSD, not a result of trauma.
73
What is the role of the HPA axis?
- Coordinates neuroendocrine stress response systems.
| - Chain of neurochemical reactions that end in cortisol being released.
74
Which brain pathways modulate the HPA axis activity?
- Hippocampus and prefrontal cortex inhibit the HPA
| - Amygdala stimulates neurons in the hypothalamus
75
What are the final outputs of the HPA on the brain?
- 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
What is Plenadren?
Brand name for a common Hydrocortisone used to treat cortisol-related disorders like Addison's disease, a rarer disorder of the adrenal glands.
77
Explain the treatment of PTSD using cortisol?
Suggestion that hydrocortisone helps as a preventative after trauma against developing PTSD, but does very little if given after PTSD has been developed.
78
What is the current recommended treatment for PTSD and why?
SSRI - reduce PTSD symptoms but it is a small-moderate effect and not universal.
79
How is extinction beneficial in PTSD?
- the fear response can be inhibited
80
Which parts of the brain affect extinction of a fear response?
- 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
What is EMDR?
Eye movement desensitisation and reprogramming.
82
What does EMDR involve?
Patient follows moving stimulus with their eyes while holding different aspects of traumatic event in mind.
83
What are the neurobiological hypotheses behind EMDR?
- 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
What kind of drugs are commonly used to treat PTSD?
Antidepressants
85
What is Acquired Brain Injury?
Refers to damage to the brain that a child was not born with - the result of an accident/event that happened later
86
Define Traumatic Brain Injury
Caused by something happening outside the body e.g. a head injury
87
Define Non-traumatic Brain Injury
Caused by something going on inside the body e.g. a stroke
88
What are the 2 different types of traumatic brain injury?
Closed - when the dura layer has not been damaged (e.g. rapid deceleration)
Penetrating - damage to the dura (e.g. gunshot wound)
89
What are primary injuries?
Occur at the moment of damage.
90
What are secondary injuries?
Result from altered blood flow or inflammation of the brain.
91
How are traumatic brain injuries categorised?
Mild, moderate, severe.
92
For children aged 0-14, what is the most common cause of TBI?
Falls
93
For ages 15-25, what is the most common cause of TBI?
Contact sports and motor vehicle accidents?
94
How is working memory impaired in children with TBI?
- Inpaired inhibition
- Long-term problems in executive function
- Affects family functioning.
95
Why are orthopaedic controls used when studying TBI?
They want a control group that has also sustained injury, but there is no risk that the brain has been affected.
96
What affects the social impairment of children with TBI?
- Young age of injury
- Frontal regions and corpus callosum affected
- Environmental factors like social disadvantage and family dysfunction
97
What social impairments did Hanten et al 2011 find in children with TBI?
Problem solving difficulties like describing the problem, generating solutions, selecting appropriate responses, and evaluating outcomes.
98
What is Shaken Baby Syndrome?
Abusive head injury - when infants have been violently shaken.
99
What is a diffuse injury?
More widespread injury rather than damage to a very specific area partly because their skull has not finished developing.
100
What does the triad classification of SBS involve?
Subdural haematoma
Retinal haemorrhages
Encephalopathy
101
What is subdural haeematoma?
Bleeding in the dura layer
102
What are retinal haemorrhages?
Bleeding in the retina
103
What is encephalopathy?
Signs of brain disease e.g. seizures, sloppiness, vomitting.
104
How are outcomes of SBS correlated?
There is a correlation between age at admission and outcome - younger age correlated with poorer outcomes.
105
What is the most common predictor of SBS?
Crying - we need to think more about the impact of infants crying on parents
106
What is a stroke?
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
What is a ischemic stroke?
When arteries to the brain become blocked/narrowed, causing severely reduced blood flow.
108
What is a haemorrhagic stroke?
When blood vessels in the brain leak/rupture.
109
What is the prevalence of strokes in children?
1.2 to 13 cases per 100,000 children under the age of 18.
110
Why are children's strokes more underdiagnosed than adults?
Delay to diagnosis or a misdiagnosis is more likely.
111
What are the risk factors of strokes in children?
- Cardiac problems, especially congenital heart disease, or following surgery to the heart.
- Sickle cell disease
- Serious infections
112
What are the risk factors of strokes in adults?
- Hardening of the arteries
- Diabetes
- High blood pressure
113
What are signs of a stroke in infants?
- Seizures
- Extreme sleepiness
- Tendency to use only one side of the body
114
What are signs of a stoke in children/teens?
- Severe headaches
- Vomitting
- Sleepiness
- Diziness
- Loss of balance/coordination
115
What long-term outcomes of strokes did Christerson & Stromberg 2012 find?
- Neurological deficits
- School activity deficits
- Hemiparesis (weakness in one side of the body)
116
What is Feotal Alcohol Syndrome?
Alcohol-related birth disorders, and alcohol-related neurodevelopmental disorder caused by effect of alcohol on a developing foetus.
117
What physical characteristics are associated with FAS?
- Poor growth
- Distinctive facial features
- Health problems related to organs
118
What neurological characteristics are associated with FAS?
- Microencephaly
- Epilepsy/seziures
- Abnormal development of corpus collosum
119
What cognitive characteristics are associated with FAS?
- Learning difficulties
| - Attention and behavioural problems
120
How often are physical features presented in FAS?
25%
121
What is Partial Foetal Alcohol Syndrome (pFAS)?
- 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
What is Neurobehavioural Disorder associated with Prenatal Alcohol Exposure (ND-PAE)?
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
Why could you argue that FAS is an example of ABI?
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
Why could you argue that FAS is not an example of ABI?
ABI is normally defined as an event that happens post-birth
125
What causes FAS?
- 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
What social problems do children with FAS experience?
- exessively friendly
- do not discriminate between familiar and unfamiliar people
- they are at increased risk of exploitation and abuse
127
What are the two key theories about why recovery of ABI can occur?
- Restitution - injured system heals itseld
| - Substitution - neural function is transmitted from the injured to a non-injured site
128
What is the Kennard Principle?
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
Does age at injury predict better recover in FAS?
the outcome of alcohol seems very vaiable - we have a spectrum of outcomes.
130
Does age at injury predict better recovery in strokes?
Christerson & Stromberg 2010 found no effect of age at stroke but Anderson et al 3012 found that young children showed better improvements socially.
131
Does age at injury predict better recover in Shaken Baby Syndrome?
Younger age at hospitalisation predicted poorer outcome
132
How may hidden deficits emerge over time after ABI?
- As toddlers become children become adolescents, the demands made environmentally increase
- Expected to manage their own work
- Social lives become increasingly complex
