Neuropsychology Flashcards
(197 cards)
1
Q
define behaviour
A
anything that a living creature does in reaction to some kind of environmental stimulation
2
Q
define neuroscience
A
study of nervous system
3
Q
What does the nervous system consist of?
A
brain, spinal chord, sensory/motor neurons
4
Q
what are the four approaches to behavioural neuroscience?
A
functional, developmental, anatomically, medical
5
Q
What is the Cardiocentric model and what time period was this theorised
A
during the heart vs head debate in the Egyptian times. the model says that the heart is the key organ of the body.
6
Q
What were the revelations from the 5th century BC Hippocratic revolution by Alcmaeon and by Hippocrates?
A
Alcmaeon- the brain as the site of sensation and thought
Hippocrates- the brain is the controlling organ of the body
7
Q
Explain the triune soul (Plate 428-348BC)
A
three parts to the soul which are the brain, the heart and the gut. The brain represents intellect, the heart represents anger and pride. The gut represents greed and desire. The intellectual soul was believed to be immortal.
8
Q
Describe Aristotle’s (348-322 BC) reasoning for the purpose of the brain
A
he stated that the brain is not responsible for any sensations at all. The brain exists as cooling system to cool down the heat of the heart in order to have more rational thoughts
9
Q
Why was Galen (130-200AD) known as the most influential physician of the roman empire?
A
his research relied on dissecting animals. He was the first to number cranial nerves and suggest them for motor and sensory functions. He deciphered the basic comments of intellect as being imagination/perception, cognition, and memory
10
Q
Explain the Ventricular Doctrine (390AD) by Bishop Doctrine
A
suggested ventricles as homes of three components. Anterior ventricle for perception, middle ventricles for cognition, and posterior ventricles for memory. This was supported by research where a damage to a specific region equates to a loss of that function.
11
Q
During what time period was the Ventricular Doctrine rejected?
A
the renaissance by Andreas Vesalius who was able to study human bodies in Padua.
12
Q
What is the localisation in the spinal chord?
A
the spinal chord has two types of nerves emerging. The dorsal carries sensory information to the spinal chord. The ventral carries motor signals to muscles in order to produce movement
13
Q
What is the Bell-Magendie Law (Bell and Magendie)
A
The anterior nerves contain only motor fibres. The posterior roots contain only sensory fibres.
14
Q
Describe the extreme theory of localization (Franz Gall, 1758-1828)
A
regions of the brain relate to specific functions and traits. The greater the skill, the larger area in the brain. Greater development in the brain is portrayed by a matching development in the skull
15
Q
What is the theory of phrenology?
A
the more spiritual the trait, the higher it is placed on the skull. e.g. destructiveness indicated by development above the ear, acquisitiveness indicated on the upper front of the squamous structure
16
Q
How is phrenology still present in modern days?
A
can be found in modern phrases e.g. highbrow vs lowbrow
17
Q
Describe Cortical equivalence (Marie-Jean-Pierre Flourens 1794-1867)
A
The cortex functions as a whole. All parts are responsible for intelligence, will, and perception. During animal studies subjects were able to recover abilities after destruction of cortical areas.
18
Q
In what case was there a shift towards localisation?
A
Paul Broca had patient Tan in 1861. The patient suffered damage to the left inferior frontal cortex. His language understanding remained functioning however his language production was impaired. This was used to then prove that the proposed site did not fit with phrenological theories
19
Q
What injury did Phineas Gage endure in 1848?
A
Phineas Gage was a railroad construction foreman who suffered a blasting accident in 1848. An iron rod shot through his skull and obliterated the greater part of the left frontal lobe.
20
Q
How did Phineas Gage’s personality change following his injury?
A
Pre injury he was described as responsible, intelligent, and social. Following his injury there were dramatic changes in his personality and he was described as unreliable, disrespectful, and irresponsible.
21
Q
What did the case of Phineas Gage provide evidence for?
A
The case provided evidence for localisation of function due to it being an index case for personality change due to frontal lobe damage.
22
Q
What is Cytoarchitecture?
A
cellular architecture of the brain (Theodor Meynert 1833-1892)
23
Q
What did the Nissl Method (Franz Nissl 1860-1919) allow scientists to do?
A
The Nissl Method involved staining cell bodies to highlight structures. This allowed for the examination of internal structures
24
Q
What did Camillo Golgi’s use of silver nitrate solution allow him to inspect?
A
visualisation of axon, dendrite, and length of neuron
25
Describe the Neuron Doctrine (Santiago Ramon y Cajal, 1852-1934)
nerve cells are individual structures with no physical connection between them. and later in 1906- the brain is made of individual units specialised depending on function. They are connected by synapses which each release one type of transmitter
26
What are the most recent beliefs regarding localisation?
brain regions can be related to specific behaviours however no part of the brain is isolated and there are vast interconnections between the regions and structures. no previous extreme views suit what we observe today
27
Name three recent biological psychology ideas:
lateralisation of functions, neuroplasticity, neuroethics
28
Describe what is meant by 'laterisation of functions'
localisations of certain functions to left or right hemisphere. language is to the left hemisphere and face recognition to the right. emotions are also localised to the right
29
What is the modern day conclusion to the left vs right brain debate?
'left vs right brained' is a myth. functions are not as strictly allocated and parts of the brain are interconnected
30
What are Tinbergen's four categories of explanations for behaviour?
Functional mechanism, physiological mechanism, ontogenetic mechanism, evolutionary mechanism
31
What question does the functional mechanism propose?
Why are they doing it now
32
What question does the physiological mechanism propose?
how are they doing it
33
What question does the ontogenetic mechanism propose?
how does this behaviour develop over the lifetime of an individual (Nature vs nurture)
34
What question does the evolutionary mechanism propose?
why did the behaviour originally develop
35
The key behavioural neuroscience question is:
what causes it to happen?
36
What evidence did Peleg et al 2006 provide for the genetic influence of facial expressions?
in his study he found similarity in facial expressions between sighted and congeniality blind family member
37
Explain Pavlov 1987 example of nurture using dogs?
Dogs respond with salivation to a food stimulus. Initially, a sound stimulus would not cause the dog to produce any salivation. Combining sound to mean food and therefore salivation, dogs were able to produce salivation in response to a sound stimulus.
38
When studying the rh-5HTTLPR gene among two groups of monkeys (Barr et al 2005)- monkeys raised by their mothers, and monkeys raised on their own- how did the groups of monkeys respond to a stressful situation?
there were different responses to stress hormone release within both groups.
39
What did Barr et al 2005 gene-environment interaction provide evidence towards?
this suggested that both a genetic predisposition to a disorder as well as the environment play a part in determining if one will have a disorder or not
40
Bluetits originally used their beaks to forage and find food. At a point, they begam to use the functions of their beaks to open milk cartons on doorsteps. What is this an example of?
This is a functional mechanism where behaviours lose their original purpose (food, shelter, reproductive stress) and can now be used for a different reason in a current environment (or are simply no longer useful)
41
What is an example of evolutionary mechanisms in humans?
goosebumps. goosebumps were originally produced in humans for defence and thermal radiation. humans now have no need for goosebumps however they still persist.
42
Analyse infant crying behaviour using Tinbergen's four questions:
-Physiological (how are they doing it): internal physiological regulation due to the CNS maturing
-Ontogenetic (how did it develop over the lifetime of an individual): initially due to internal changes as an infant grows. developed to become more directed e.g. when a caregiver is near
-Evolutionary (why did the behaviour originally develop): communication to caregivers which worked over distances and when visual light was low
-Functional (why are they doing it now): signalling to caregivers to indicate infants particular needs
43
the key behavioural psychology question is:
how does a certain behaviour relate to activity in the brain? the relationship between biological and psychological processes. we manipulate a biological process and see what effect it has on a psychological measure
44
What is the question proposed in neuropsychology?
which behaviours and mental processes change when a particular area has been damaged?
45
What is the question proposed in psychopharmacology?
which behaviour and mental processes are affected by drugs that change chemical processes in the brain?
46
What is the question proposed in psychophysiology?
what physiological changes (e.g. heart rate, blood pressure) occur when a behaviour/mental process is carried out?
47
What is the question proposed in neuroimaging?
which brain areas show changes in activity when a behaviour or mental process is carried out?
48
What are the three factors analysed in methods of neuroimaging?
temporal resolution (ability to record activity over time), spatial resolution (ability to indicate location of activity), and invasive/non-invasive
49
Explain the method of single cell recording and analyse the procedure:
a microelectrode is inserted into the brain to record changes in voltage or current in individual cells.
Temporal resolution: wide, ranging from ms to hours
Spatial resolution: limited to one cell
Invasive technique
50
Analyse the method of Electroencephalography (EEG):
EEG measures electrical activity at scalp surface, studies expose the brain to repeated stimulus to identify the responses to a particular stimulus. This is often used for studies of language. The procedure is non invasive with good temporal resolution. However, the spatial resolution is low. This can help to diagnose conditions such as epilepsy and sleep disorders.
51
Analyse the method of Magneto-encephalography (MEG):
MEG measures the magnetic fields produced by brain activity at the skull. The procedure is non invasive with excellent temporal resolution. Spatial resolutions are better compared to EEG because magnetic fields are not distorted by the skull. The procedure can be used to plan brain surgeries such as removing tumours.
52
Analyse the method of Positron Emission Tomography (PET):
PET detects regions of brain activities by tracking emissions from radioactive substances. The procedure has reasonable spatial resolution however it is an invasive procedure (via injection) and the temporal resolution is low as it can only record activities over 60 seconds. This can be used to detect cancer and brain conditions.
53
Analyse the method of Functional Magnetic Resonance Imaging:
FMRI detect functionally induced changes in blood flow oxygenation to the brain. This is indirect as it only looks at flood flow and not neural activity. The procedure is non invasive and has excellent spatial resolution, but poor temporal resolution as it tracks over several seconds. FMRI can effects of strokes and other diseases.
54
FMRI, PET, MEG, EEG, TMS and Single Cell Recordings are all techniques of what?
Functional neuroimaging. They compare brain activity in different conditions to a baseline condition.
55
How did dead salmon prove errors in functional neuroimaging techniques?
dead salmon from the Atlantic ocean were taken from the fishmongers. they were placed in a FMRI lab and made to observe emotional faces. The lab found reasons of activation. This showed a possibility for error in functional neuroimaging techniques.
56
Why has neuroimaging been referred to as 'the new phrenology'?
There is an assumption that the area that lights up is responsible for the function. This is untrue because imaging does not indicate a casual link. There is strong evidence for methodological convergence which cross references findings across methods.
57
Analyse the method of Transcranial Magnetic Stimulation (TMS):
TMS stimulates temporary lesions, the magnetic pulse of the current is used to temporarily inhibit processing in that area. This examines where inhibiting a region interferes with a particular task. The procedure has poor temporal resolution which is not fully known. The spatial resolution is poor because the area affected by TMS is fairly large. TMS therapy can be used to treat depression, OCD and other brain related conditions.
58
What do lesion studies observe?
Lesion studies observe patients following brain damage. They observe what tasks they are able and unable to do
59
Why is spatial resolution low in lesion studies?
Typically, lesions are widely spread and so spatial resolution is low because it is difficult to determine where boundaries are
60
Why is temporal resolution inconsistent across lesion studies?
Procedures allow for the assessment of long term damage however patients may have been able to develop coping strategies making it harder to determine the exact effects of the lesion.
61
Why are animals used in neuroscience studies?
animals are used to understand the basic processes underlying human behaviour which is similar to the processes underlying animal behaviour
62
What can animal studies hope to achieve?
methods to treat or prevent conditions such as Alzheimer's, AIDS, and Strokes
63
What are the 3R's and what do they advise in an attempt to find replacements to animal testing?
-Replacement: for example using chip skin to replicate organs, or using human volunteers
-Refinement: using less invasive techniques and providing better care and better living conditions for the animals.
-Reduction: improving experimental techniques and techniques of data analysis, and encouraging open science where researchers share their findings.
64
How do the presynaptic and postsynaptic neuron work together?
the presynaptic neuron sends the signal and the post synaptic neuron receives the signal.
65
What are the two communication types between neurons?
electrical and chemical
66
What is the process of electrical signalling?
The pre and post synapse are linked at a gap junction. There is a fast direct passive flow from one neuron to another. Ions diffuse through channels containing the action potential. The post synaptic neuron can start to signal within ms of receiving the input from the pre synaptic neuron
67
How does electrical signalling allow for synchronisation of signals?
brainstem neurons regulate breathing
68
What is the process of chemical signalling?
there is no link between neurons across synapses. neurotransmitters are released from the presynaptic cell and diffuse across the gap binding to receptors on the post synaptic cell membrane. the neurotransmitter either excites or inhibits the receiving neuron
69
What are the key differences between electrical and chemical signalling?
in chemical signalling there is no link between neurons across synapses, in electrical signalling the pre and post synapses are linked at a gap junction. Chemical signalling is a slower transmission and is far more common than electrical signalling.
70
what is required for a substance to be a neurotransmitter?
the substance must be in a pre synaptic terminal stored in a vesicle. it must be released in response to an action potential arriving at the terminal and receptors on the post synaptic cell must be able to bind to it
71
What are the key differences between Small molecule chemical processes, and neuropeptide chemical processes?
In the small molecules the enzymes are synthesised in the cell body. However, in the neuropeptides most processes happen in the cell body including enzyme synthesis and enzyme packaging into vesicles.
72
How do small molecules and neuropeptides differ in their response to frequency stimulations?
In high frequency stimuli there is more distributed release of Ca2+ and both types of neurotransmitters will release. In low frequency stimuli there is only a localised increase in Ca2+ and only the small molecule neurotransmitters will be released.
73
What is the release of neurotransmitters triggered by?
the release is triggered by the arrival of an action potential at the presynaptic terminal. vesicle packages merge with the synapse membrane and the contents are released into the cleft
74
How does the neurotransmitter bind to the post synaptic receptors in ionotropic signalling?
the neurotransmitter binds to the ion channel. the channel opens and the ions flow across to the post synaptic cell where an action potential is triggered
75
How does the neurotransmitter bind to post synaptic receptors in metabotropic signalling?
neurotransmitters bind to a receptor protein. The receptor activates the attached G-proteins which detaches and can dock onto an effector protein. The effector protein triggers the opening of an ion channel.
76
Out of ionotropic signalling and metabotropic signalling, which is quicker?
Ionotropic signalling is faster. Metabotropic signalling goes into effect 30ms after release.
77
what happens to neurotransmitters to end the signalling?
the neurotransmitter detaches from the receptor. It is transported back to the presynaptic neuron for reuptake or it is broken down by enzymes in the synaptic cleft where by-products are recycled.
78
What are the three stages of chemical signalling?
1) Synthesis and storage of the neurotransmitters
2)Binding of neurotransmitters to post synaptic receptors
3)Deactivation of neurotransmitters to end the signalling
79
What is the role of an agonist?
Agonists mimic or enhance the effects of naturally occurring neurotransmitters. They destroy enzymes that break down neurotransmitters and increase the amount released blocking auto receptors that limit neurotransmitter release. They bind to site causing channels to open
80
What is the role of an antagonist?
Antagonists block or reduce the effects of naturally occurring neurotransmitters. It decreases the amount of neurotransmitters made by breaking open the vesicles so that they are destroyed by enzymes. They also activate auto receptors to limit neurotransmitter release and bind to receptor sights to block them
81
What is the nature of nicotinic receptors?
nicotinic receptors are ionotropic. They are primarily in the CNS and are involved in learning, memory, arousal, motor control and alertness after waking.
82
What is the nature of muscarinic receptors?
Muscarinic receptors are metabotropic. They are primarily in the CNS and are involved in the control of physiological functions in the Parasympathetic nervous system. This slows heart rate and relaxes muscles.
83
How does nicotine react on ionotropic receptors?
nicotine acts s an agonist enhancing the effects of ACh in the CNS. Lower doses cause feeling of euphoria and relaxation. In high doses it causes nausea, vomiting, and confusion.
84
How does muscarine act on metabotropic muscarine receptors?
Muscarine acts as an agonist. This enhances parasympathetic functions such as reducing blood pressure, salivation increase, slowed heart rate, and nausea. This can lead to circulatory collapse, coma and death.
85
Explain the nature of a-bungarotoxin on nicotinic receptors?
a-bungarotoxin is a type of venom possessed by some snakes. This acts as an antagonist. Its effects block nicotine ACh receptors and are irreversible. This prevents skeletal muscle activation leading to paralysis.
86
Explain the nature of antagonists on the muscarinic receptor?
such as atropine and scopolamine (deadly nightshade and henbane). these reduce parasympathetic functions to increase heart rate. This can be used in surgeries to reduce saliva production.
87
Why is glutamate important?
Glutamate is important for normal brain function. Almost all excitatory neurons in the CNS are glutamatergic. Over half of the brains synapses are though to release this.
88
How is glutamate synthesised?
Glutamate does not cross the blood barrier and must be synthesised from local precursors.
89
What does ibotenic acid do as an agonist?
Ibotenic acid prolongs activation of the NDMA receptor that is linked to long term changed in the brain necessary for learning and memory (synaptic plasticity)
90
What happens to extended functions of the NDMA receptor?
extended functions lead to cell damage and death.
91
What is the effect of ketamine on glutamate?
Ketamine blocks the excitatory effect of glutamate. This can be a sedative or anaesthetic but if also used recreationally for hallucinatory processes.
92
What is excitotoxicity and when does it occur?
Excitotoxity is cell death due to enhanced activation. This occurs following damage due to injury or strokes.
93
Describe the process whereby glutamate leads to cell deaths:
damage > release of glutamate> glutamate activates post synaptic cells > cells die. an excess of glutamate results in cell damage/deaths.
94
explain neuroprotective therapy:
this would be where glutamate antagonists block receptors limiting the damage that could be caused by the excess glutamate
95
What are the two main reasons neuroprotective therapy might not work?
Signalling: glutamate receptors are widespread in the brain, other glutamate receptors can be blocked resulting in reduced signalling
Timing: a sharp increase is linked to destruction immediately after injury, increases are already milder following the injury.
96
Why do Ikonomidou and Turski (2002) disprove of glutamate antagonists?
glutamates normal role is to promote neuronal survival. initial increases in cell death are followed by an attempt to help maintain cell function, and antagonists inhibit this process.
97
What are six examples of biogenic amines?
dopamine, serotonin, histamine, adrenaline, norepinephrine, endocannabinoids
98
What kind of neurotransmitters are biogenic amines?
small molecule neurotransmitter
99
What is the distribution of serotonin signals?
90% to gut, 10% to brain
100
What is the function of serotonin?
regulation of mood, appetite, sleep, memory, learning
101
What is the significance of tryptophan and where do we get it from?
tryptophan is the critical precursor of serotonin and is taken in in our diets
102
Describe the symptoms of major depressive disorder:
intense persistent sadness, helplessness, hopelessness, tiredness, lack of energy, abnormal eating and sleeping habits, impairments in concentration and memory
103
How was depression initially linked to monoamines?
reserpine was a medication for hypertension. In 1960 it was noted that people taking this were reporting sides effects of major depression. it was determined to be an antagonist of monoamines. this suggested that monoamine levels were lower in patients with depression. (Michaels and Gibbon, 1963)
104
What does SSRI stand for?
selective serotonin reuptake inhibitor
104
Describe the effect of antidepressants on the enzyme MAO:
antidepressants block the enzyme (inhibitor) MAO which breaks down monoamines so that there is nothing to clear up the neurotransmitters that are there
105
What does SNRI stand for?
selective noradrenaline reuptake inhibitor
106
What do SSRIs do and what are the side effects?
SSRIs block channels that allow serotonin to be removed from the cleft. side effects include weight loss, nausea and diarrhoea
107
What is the nature of serotonin in depressed patients?
There is no strong evidence for lowered serotonin actions in depressed patients compared to controls (Moncrieff 2022 meta analysis). The Royal College of Psychiatrists said that antidepressants correcting a chemical imbalance is an over simplification (2019).
108
Summarise the findings of the timing of the effects of SSRIs:
In one study, significant improvements in mood were found from around 4 weeks after taking SSRIs despite an instant increase in levels. Another study found all the drugs more effective than an administered placebo (Cipriani et al 2018 meta analysis).
109
Describe the effect of SSRIs on cognitive mechanism of depression:
following a single dose, despite not reporting noticeable effects in mood at this point, depressed patients showed enhanced recognition of facial expressions particularly happiness, and increased recall of positive stimuli in word memory tasks
110
Explain cognitive mechanisms of depression:
Beck 1967 found cognitive mechanism as a cause of depression. This includes negative automatic thoughts, negative schema, and a negative information processing bias
111
How many dopamine pathways are there in the brain and what are they called?
four pathways; Tuberoinfundibular pathway, Nigrostriatal pathway, Mesocortical pathway, Mesolimbic pathway
112
Describe schizophrenia:
psychotic disorder involving disturbances of thought, emotions and behaviour. Including fragmented thinking, disconnection between person's subjective experiences and objective reality
113
What are the three categories of symptoms associated with schizophrenia?
positive symptoms- hallucinations, delusions, disorganised speech and behaviour (additions to behaviours)
negative symptoms- lack of emotion, apathy, anhedonia, social withdrawal and poverty of speech (reduction to behaviour)
cognitive symptoms- broad impairments to attention, working memory and executive functions
114
What is the dopamine hypothesis of schizophrenia?
psychosis (positive symptoms) are caused by excess levels of dopamine
115
What drugs are examples of dopamine agonists?
amphetamine and cocaine
116
Describe amphetamine psychosis:
chronic abuse of dopamine agonists can lead to schizophrenia like symptoms which is called amphetamine psychosis
117
What are the dangers of Parkinson's medication?
excessively high doses of L-dopa can lead to schizophrenia like symptoms
118
How do antipsychotics work?
antipsychotics block dopamine behaviours preventing their activation. these are used to treat positive symptoms such as hallucinations and delusions, and have little to no effect on negative symptoms
119
How can antipsychotics worsen negative symptoms?
negative symptoms reflect abnormal levels of dopamine and reduced brain activity in the prefrontal cortex
120
What is the theory of dopamine regulation in schizophrenia?
there is under activity of dopamine in the prefrontal cortex which is the primary deficit in schizophrenia. This leads to reduced inhibitory control over dopamine producing neurons based in basal forebrain areas. runaway dopamine is released into the basal forebrain areas leading to positive symptoms (Davis et al 1991)
121
What treatment is most likely to be effective for schizophrenia type symptoms?
antipsychotics can make delusions and hallucinations feel less important and distressing. psychotherapies such as CBT can help actually change delusional beliefs and are most likely to succeed in combination (Elis et al 2013)
122
What are side effects of dopamine treatments?
Agonists- hallucinations, psychosis, impulsive control disorders
Antagonists- Parkinson's like symptoms such as tremors and dystonia. unusual secretion of breast milk
123
What makes neurotransmitters unconventional?
there neurotransmitters are not stored in the pre synaptic terminal. they are not released by exocytosis and may not be released at all. these may be used in retrograde signalling
124
Describe Endocannabinoids:
these are produced on demand from cell membranes. retrograde signalling to control incoming traffic to the post synaptic cell reduces the release of conventional neurotransmitters for a short period of time. these are involved in memory, appetite regulation, and homeostasis
125
Describe THC:
THC is an agonist. It is the psychoactive component in marijuana. This has an effect on perception, motor behaviour, short term memory, and appetite
126
Why has THC been suggested as a medication for chemotherapy patients and those with multiple sclerosis?
THC contains emetic properties which are vomiting inhibiting. THC also eases symptoms such as muscle stiffness
127
What are the widely debated risks of using THC?
excessive use of THC may increase the risk of developing schizophrenia and slowing of cognitive functions
128
Describe CBD:
CBD is an antagonist which effects receptors in charge of perception, motor behaviour, short term memory, and appetite
129
What was Rimonabant originally used for and why was it withdrawn?
Originally, Rimonabant was used for weight loss as it reduced appetite. However, in 2008 it was withdrawn due to sever psychiatric side effects
130
Why is CBD not widely approved as a medical prescription ?
there has been interest in CBD as a treatment of psychosis and seizures. However, the interactions between CBD and other medications are currently unknown
131
Where are the premotor and primary motor cortex?
in the frontal lobes
132
Describe the organisation of the motor cortex:
contralateral (left hemisphere for right side of body, right hemisphere for left side of body), somatotopically organised (grouped by body part)
133
What is the motor cortex responsible for?
the motor cortex is responsible for planning movements and more precise control in voluntary movements
134
Explain the purpose of the Montreal Procedure (Wilder Penfield 1937):
the Montreal procedure was for motor mapping. This was a pioneering surgery for epilepsy. The map doesn't represent individual muscle/body parts but rather coordinated groups of muscles
135
How can motor mapping be carried out?
TMS Simulations (transcranial magnetic stimulation)
136
In humans, larger representations for left hand digits were mapped out in string players (Elbert et al 1995). what is this an example of?
Sensory Motor Talents where key motor areas have more representation in motor cortex e.g. whiskers in rats and mice
137
What is the purpose of the Basal Ganglia?
preparation for movement initiation and suppression of unwanted movement
138
What receptors are a key part of the basal ganglia region?
dopaminergic synapses and their receptors
139
Striatum, pallidum, thalamus, and subthalamic nucleus are all major structures of what?
the Basal Ganglia
140
What type of pathway is in the basal ganglia?
direct pathway
141
Determine the difference between tonic and transient regions:
tonic regions are constantly activated, transient regions are activated for a brief period of time
142
Why is correct regulation of the direct pathway in the basal ganglia important?
correct regulation is vital in allowing movements to begin
143
what is the process of the nigrostriatal pathway?
the nigrostriatal pathway links the subtantia nigra and striatum and provides additional excitatory impulses. it allows the frontal cortex to initiate movement
144
what is Parkinson's Disease including the symptoms and causes?
Parkinson's is a neurodegenerative progressive disorder first observed by Dr James Parkinson in 1817. the most recognised symptoms affect movement including tremors, slowness, rigidity and postural instability. the causes are unclear but thought to be a combination of genetics and environmental factors
145
What does Parkinson's disease do to the direct pathway?
death of dopaminergic neurons in nigrostriatal pathway. reduced activation of the striatum which cannot inhibit globus pallidus. the thalamus continues inhibited and movement cannot be easily initiated
146
What is the treatment of Parkinson's diease?
There is no distinct cure. L-dopa (artificial precursors of dopamine that cross the blood brain barrier) an antagonist of dopamine increases the concentration of dopamine in the synaptic cleft. as cells die this treatment becomes less effective and there are side effects due to increased dopamine in other pathways
147
how does the indirect pathway operate?
the indirect pathway stops unwanted movement by increasing the ability of the globus pallidus to inhibit the thalamus.
external segments inhibit internal segments preventing further inhibition of the thalamus which does not signal to cortex for movement
148
What is Huntington's Disease including causes and symptoms ?
Huntington's disease is a mutation of chromosome 4 where symptoms typically prevail in mid life (30-50s). Huntington's causes changes in mood/personality ( increased irritability, suspiciousness, eccentric behaviour, depression) and coordination problems. there is selective atrophy of caudate and putamen and motor symptoms include rapid, jerky movements with no purpose affecting a finger of whole extremity
149
What is a disorder of the basal ganglia that affects movement inhibition?
Huntington's Disease (George Huntington 1872)
150
What is the treatment for Huntington's Disease?
there is currently no cure and death is expected within 10 to 20 years. Tetrabenazine is used to treat involuntary movement but the side effects include Parkinsonism and depression.
151
What are the three types of muscle?
skeletal (movement of bones)
smooth (forms organs)
cardiac (contracts the heart)
152
Describe lower motor neurons:
muscles are arranged in antagonistic pairs. contractions of skeletal muscle are initiated by lower motor neurons
153
What forms the neuromuscular junction?
cell bodies found in spinal cord and brainstem
154
What is the difference between a motor neuron pool and a motor unit:
in a motor unit all fibres in a muscle are innervated by one neuron. in a motor neuron pool all the neurons innervate one muscle
155
What is at the neuromuscular junction?
motor neuron synapses with skeletal muscle fibres
156
what acts as an excitatory neurotransmitter as the motor neuron synapse?
ACh
157
what does the size of the motor unit relate to?
the size of the motor unit relates to the type of movement produced. when they innervate many fibres movements are coarser e.g. biceps. when only few are innovated by one axon, movements are more precise e.g. eye movements
158
describe the somatotopic organisation of the neuromuscular joint:
spinal cord neurons act on muscles of trunk located medially, neurons from arms and legs are more laterally
159
Explain Amyotrophic Lateral Sclerosis:
this is also known as motor neuron disease and dates back to 1824. it is a progressive degenerative disease of the upper and lower motor neurons. neurons in the brain and spinal cord die. It begins to weaken affected regions and gradually worsens as muscles waste. sensory and cognitive abilities are preserved
160
What can augmented/alternative communication help with?
the last muscular groups affected are eye movements. Systems can be used to help people with ALS
161
what is biopsychology?
the science of how the brain controls behaviour
162
explain the function of each of the following brain parts:
1- Pia mater
2- Arachnoid membrane
3- Dura mater
4- gryus
5- groove
6- Fissures
1- a very slight membrane directly on top of the brain, not visible
2- cushions the brain, subarachnoid fluid underneath filled with cerebrospinal fluid
3- flexible but unstretchable, keeps the brain in place and brings blood to brain via large blood vessels
4- 'bulge'
5- 'groove'
(^provide cushion against shock and allow more processing space to cram into brain)
6- very large grooves separating parts of brain from one another
163
What happens in the grey and the white matter?
grey matter- processing, typically the outer parts of the brain (cortex)
white matter- transfers info between cortical sights (can be visualised with DTI)
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How do the two hemispheres of the brain communicate?
via the corpus callosum
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what is the central sulcus?
separates the brain from front half to back
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what does the primary motor cortex do?
controls body movements, electrical currents can get movements from different parts of the body depending on where you stimulate
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How is the brain organised?
contralaterally and somatotopic
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what lies in front of the central sulcus?
the motor strip of brain -> primary motor cortex
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What are ventricles in the brain?
interconnected systems filled with cerebrospinal fluid. serves several functions including trauma protection, buoyancy, removal of waste products into blood, and hormone transport
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explain localisation of function:
different brain regions are physiologically different and so hypothetically should have different roles in cognitive processing
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what happened when the temporal lobe of monkeys was removed (1930)?
-monkeys could see and hear but no longer clearly understood the meanings of sights and sounds
-poor memory
-would observe things regardless of dangers e.g. fire and broken glass
-eat everything including faeces
-mate with everything including all sexes and inanimate objects
-became tame such as loss of fear and aggression towards humans
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What part of the brain does semantic dementia affect first?
temporal lobes
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what are the symptoms of semantic dementia?
-characterised by loss of semantic memory
-language symptoms which are obvious such as anomia
-problems with prosopagnosia and object agnosia
-personality changes and emotional difficulties
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What part of the brain are words given meaning?
the auditory cortex in the temporal lobe. auditory info is sent from the cortex to the Wernicke's area where words are recognised
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What problems arise as a result of lesions to the auditory cortex and the Wernicke's area?
impaired sound perception in general as result of lesions from auditory cortex. Wernicke's area lesions only impair speech perception
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Explain Associative Agnosia:
patients are unable to recognise objects. they can see whole form and shape of objects, as well as copy figures however there is disruption to object recognition between visual and meaning nodes. can be selective for different stimulus classes e.g. artifact vs natural kinds
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Could a patient with associative agnosia recognise an object through touch?
yes- there is a failure to link only vision to knowledge
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Explain Prosopagnosia:
problem with face recognition where patients are able to see a face but unable to link it to knowledge they have about the person. this is socially disruptive
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How can patients with Prosopagnosia develop coping strategies?
they can recognise people through their mannerisms, voice etc. Some parents have been known to colour code their children
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Give an example of pavlovian learning:
dogs learned to salivate at the sound of a bell because they learned that this was the sound that came before they were given food
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What is the amygdala suggested to be specialised in?
fear
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how does the amygdala elicit responses?
learns what happens when exposed to relevant stimuli and so when the stimulus is re encountered appropriate emotional responses are elicited
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What does the hypothalamus do?
receives info from all areas of the body and compares these to biological setpoints. acts on the endocrine and autonomous nervous systems to control blood sugar level, hormone levels, and temperatures
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What happened when Henry Molaison had his medial temporal lobe removed?
this was as a last resort to treat severe epileptic seizures. he lost his ability to form new memories
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How does Retrograde amnesia affect memory?
encoding new experiences into memory can take several years. however motor skills, working memory, long term planning and other memory remains in tact
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How does the temporal lobe contribute to efficient behaviour ?
identifies things, triggers emotional responses, and encodes them in memory. all together provides you with the meaning of things
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what is the homunculus?
an image of the body where the parts greater represented in the brain are enlarged
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what is somatotopic organisation?
parts of the body that we use more have more dedicated space in the cortex e.g. smaller for foot than hand as we don't have as many sensations in the foot
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what would result from lesions to the primary somatosensory cortex?
feeling things on parts of your body e.g. touch, pain
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how many types of skin receptors does the primary somatosensory lobe receive input from?
20 (touch, temperature, stretch etc.)
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In what three ways does the parietal lobe create links between the external world and the body?
where you can look, which visually guided actions you can perform with the objects around you, which learned actions you can perform with them
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What is Optic Ataxia and where are the lesions that cause this?
lesions of the superior parietal lobe.
unsteady and clumsy motions of limbs and poorly coordinated movements. the deficit occurs for movement under visual guidance even although primary vision is present. reaching objects from memory is better, and patients can perform well known gestures and pantomime using objects (disorder of visually guided movements)
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What happens as a result of lesions to the Left inferior parietal lobe?
disorders of learned actions. mostly actions using tools but can include gestures
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Explain Ideomotor Apraxia:
a result of lesions to the left inferior parietal lobe.
the loss of ability to execute learned, purposeful movements despite having the physical ability to perform them.
unable to use tools, pantomime use of imaginary tools, and recognise pantomimed actions.
can effectively grasp objects and touch parts on their own body
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What happens as a result of lesions to the right inferior parietal lobe?
disorders of attention and looking
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Explain Hemispatial Neglect:
patients forget one side of space. they show failure to orient towards, explore and respond to stimuli presented on the contralateral side. these patients often only talk to people on their right, and bump into objects on their left but are completely unaware of their deficit
