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Pyschology > Biological Psychology > Flashcards

Biological Psychology Flashcards

1
Q

When did Rene Descartes live?

A

1596-1650

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2
Q

Where did Descartes believe was the connection between the ‘mental’ mind and the ‘physical’ brain?

A

The pineal gland

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3
Q

Who argued in 1949 that dualism was ‘Descarte’s Myth’?

A

Gilbert Ryle

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4
Q

Variants of monoism

A
  1. Materialism: everything that exists is material, the ultimate reality is physical matter
  2. Mentalism: the physical world could not exist unless some mind were aware of it
  3. The identity position: there is only one kind of substance that includes both material and mental aspects. Every mental experience is a brain activity
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5
Q

Who argued that ‘The mind is what the brain does’ (The identity position)?

A

Minsky, 1986

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6
Q

What is the operational definition of consciousness?

A

The person’s subjective experience of the world and the mind

Experiences that can be overtly reported

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7
Q

Benjamin Libet’s experiment studying consciousness and the result

A

1983
Subjects asked to move wrist at arbitrary time and report when they made the decision to move
Brain activity recorded
Brain activity started 350ms before the decision - conscious wish the outcome of unconscious activity

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8
Q

Who did the study on masked vs. unmasked priming?

A

Stan Dehaene

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9
Q

What kind of brain activity gives rise to consciousness?

A

A 50ms threshold for conscious access is associated with the time needed to establish sustained activity in recurrent cortical loops
Subliminal processing takes place in the occupito-temporal pathway
A late (>270ms) and highly distributed fronto-parieto-temporal activation correlates with conscious reportabikity

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10
Q

What is the blood-brain barrier (BBB)?

A
  • A semi-permeable barrier between the blood and the brain
  • Produced by tightly packed cells in the capillary walls of the brain
  • Protects and helps regulate the chemical balance of the brain
  • Excludes most viruses, bacteria and toxins
  • Nutrients cross the BBB passively and small, uncharged molecules such as oxygen and carbon dioxide diffuse across the cell membranes
  • Other molecules that dissolve in the fats of the membrane also enter brain cells
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11
Q

What was the neutron doctrine?

A

Santiago Ramón y Cajal (1852-1934) used newly developed staining techniques to show that neurones are separable - there is a small gap between the tips of one neurone’s fibres and the next neurone
The brain consists of individual neurones

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12
Q

Two main types of cells in the nervous system:

A
  1. Neurones

2. Glia

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13
Q

Numbers of neurones

A

70 billion in cerebellum
12-15 billion in cerebral cortex
1 billion in spinal cord

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14
Q

Numbers of glia:

A

Smaller than neurones but more numerous
76% oligodendrocytes
17% astrocytes
6% microglia

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15
Q

Functions of glia (6 functions)

A
  1. Provide structure - surround neurones and hold them in place
  2. Insulate nerve cells with myelin sheaths (oligodendrocytes in CNS, Schwann cells in PNS)
  3. Supply nutrients and oxygen to neurone (astrocytes)
  4. Removal of dead neuronal tissue and immune defence of the CNS (microglia)
  5. During development, glial cells provide scaffolds for neurones to migrate to their final destinations (radial glia)
  6. Modulate neurotransmission (astrocytes clear neurotransmitter from within the synaptic cleft, preventing buildup)
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16
Q

What increases as the ratio of astrocytes to neurones increases?

A

Behavioural complexity

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17
Q

What is Rett syndrome?

A

-Strikes young girls under 2 years
-Causes loss of speech, motor control and functional hand use, seizures, orthopaedic (skeletal system) and digestive problems, breathing, anxiety, etc.
Caused by mutations in the MeCP2 protein present in neurones and astrocytes
Re-expression of MeCP2 in neurones or astrocytes in mouse models dramatically reversed in Rett syndrome

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18
Q

3 types of neurone

A
  1. Sensory (afferent)
  2. Motor (efferent)
  3. Interneurons
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19
Q

Neurone structure

A
  • Soma (cell body): contains the cel nucleus and other cell machinery
  • Dendrites: branching fibres that get narrower at the end. They receive information from other neurones via synaptic receptors. The greater the surface area of a dendrite the more information it can receive
  • Axon: a thin fibre of constant diameter that extends away from the soma and transmits information from the soma to other neurones. In vertebrates usually covered by myelin sheath
  • The neurone’s edge, the membrane made of lipids and proteins, which is only permeable for small, uncharged molecules and some charged ions through specialised protein channels
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20
Q

Resting neurone

A
  • More K+ inside the neurone and higher concentration of Na+ and Cl- outside
  • Electrical gradient means both Na+ and K+ are dragged into cell due to negative charge inside
  • Concentration gradient drags Na+ into neurone
  • 3 Na+ ions pumped out for every 2 K+ pumped in
  • Resting potential is -70mV
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21
Q

Neurone stimulation definitions

A

Stimulation - change of the neurone’s membrane potential
Hyperpolarisation - increased polarisation of the membrane
Depolarisation - reduction of the neurone’s polarisation towards 0

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22
Q

What is the threshold of excitation and what is caused when it is crossed?

A

-55mV
If it is exceeded it produces a massive depolarisation of the membrane - an action potential. The potential shoots beyond the strength of the stimulus

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23
Q

What is an action potential independent of?

A

The amount of current which produced it - larger currents do not cause larger action potentials

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24
Q

What is the general amplitude of an action potential?

A

+40mV

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25
Q

How do action potentials move down a myelinated axon?

A
  • Via saltatory conduction
  • Action potentials hop along the axon, and recur at successive nodes of Ranvier, thus they travel faster
  • Myelination prevents any charge leakage
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26
Q

What is Multiple Sclerosis (MS)

A
  • Neurological condition
  • Affects 100,000 people in the UK
  • Diagnosed between 20-40
  • Cause is demyelination of axons in the brain and spinal cord
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27
Q

What is the length of a synaptic cleft?

A

20-30 nm wise

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28
Q

Who discovered the Synapse?

A

Charles Scott Sherrington (1857-1952)
Novel prize in 1932
Showed that reflexes are slower than conduction along the axon - delay in transmission due to synapses

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29
Q

Discovery of chemical transmission at synapses

A
  • Otto Loewi (1921)
  • Isolated two frog hearts: a donor heart and a recipient heart
  • Stimulated the vagus nerve of the donor heart. The heartbeat slowed down
  • Loewi collected the fluid from the donor heart and transferred it to the recipient heart. The recipient heart slowed down
  • The opposite effect came from experimenting with the accelerator nerve
  • He concluded that synaptic transmission is via chemical transmitters
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30
Q

How quickly do neurotransmitters cross the synaptic cleft?

A

0.01 ms

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31
Q

Why are the two types of receptor on the postsynaptic cell?

A
  • Ionotropic receptors

- Metabotropic receptors

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32
Q

What are ionotropic receptors?

A

Neurotransmitter directly opens the ion channels with these receptors. The effect is fast and short-lived (20ms)
Ionotropic receptors used for visual/hearing inputs and muscle activity

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33
Q

What are metabotropic receptors?

A

Neurotransmitter opens ion channels with these receptors indirectly and produces slower (after 30+ ms) but longer-lasting effects.
Metabotropic receptors are used for behaviours such as hunger, thirst, fear or anger

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34
Q

Three ways of terminating neurotransmitter action in the synapse

A
  1. Serotonin, dopamine and norepinephrine detach from receptor and are reabsorbed by presumptive neurone (re-uptake)
  2. Acetylcholine is broken down by acetylcholinesterase into acetate and choline (enzymatic degradation)
  3. Glial cells reabsorb transmitters at some synapses and influence synaptic activity by either reabsorbing or not reabsorbing a neurotransmitter
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35
Q

Purpose of acetylcholine and problems if neurones deteriorate

A 
Enables muscle action
Regulates attention
Learning
Memory
Sleeping and dreaming
Deterioration can cause Alzheimer’s disease
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36
Q

Purpose of dopamine and problems with low / high levels

A 
Influences movement
Motivation
Emotional pleasure and arousal
High levels linked to Schizophrenia
Low levels produce tremors and decreased mobility of Parkinson’s
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37
Q

Purpose of glutamate and problem with oversupply

A

A major excitatory neurotransmitter involved in learning and memory
Oversupply can overstimulate the brain producing migraines and seizures

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38
Q

Purpose of GABA (gamma-aminobutyric acid) and problem of undersupply

A

The primary inhibitory neurotransmitter

Undersupply linked with seizures, tremors and insomnia

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39
Q

Purpose of norepinephrine and problem with undersupply

A

Helps control mood and arousal

Undersupply can suppress mood

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40
Q

Purpose of serotonin and problems with undersupply

A

Regulates hunger, sleep, arousal and aggressive behaviour

Undersupply linked to depression. Prozac and some other antidepressant drugs raise serotonin levels

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41
Q

Purpose of endorphins and problem with undersupply

A

Act within the pain pathways and emotion centres of the brain. Lack of endorphins could lower pain threshold or reduce ability to self-soothe

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42
Q

What are the differences between species in neuron transmission?

A
  • All QUALITATIVE
  • Variations in the number of synapses
  • Variations in the amount of neurotransmitter released
  • Variations in the sensitivity of receptors on postsynaptic cells
  • These variations yield a rich variation in behaviour
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43
Q

What are agonist drugs?

A
  • Increase the production of neurotransmitters (L-dopa)
  • Increase the release of neurotransmitters (amphetamines)
  • Bind to autoreceptors and block their inhibitory effect
  • Block the deactivation or reuptake of neurotransmitters (Prozac, cocaine)
  • Increase neurotransmitter effect (nicotine)
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44
Q

What are antagonist drugs?

A
  • Block the production of neurotransmitters (AMPT)
  • Cause the depletion of neurotransmitters in vesicles
  • Block the release of neurotransmitters
  • Activate autoreceptors so that they inhibit release of neurotransmitters
  • Bind to postsynaptic receptors and block neurotransmitter binding
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45
Q

What is Myasthenia gravis?

A
  • An autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatiguability
  • Weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the stimulative effect of acetylcholine
  • To treat myasthenia gravis, the effect of acetylcholine must be increased
  • As acetylcholine is inactivated by enzymatic degradation, then acetylcholinesterase must be broken down so it cannot function. As a result, the acetylcholine stays for longer in the synapse and the effect is boosted
  • MG is therefore treated with acetylcholinesterase inhibitors
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46
Q

What are the two actions of recreational drugs?

A
  • Stimulants - increase physiological / nervous activity (e.g. cocaine, amphetamine)
  • Narcotics - dulls senses, relieves pain (e.g. morphine and other opiates)
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47
Q

How do most recreational drugs work?

A

By directly or indirectly stimulating the release of dopamine

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48
Q

How does cocaine work?

A

Blocks Na+ channels so interferes with the propagation of action potentials
Blocks the reuptake of dopamine and serotonin at synapses, potentiating their effect

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49
Q

What are the three dissecting planes of the human brain?

A
  • Coronal (frontal) section: the view of the brain from the front
  • Mid-sagittal (medial) section: the view from the side
  • Horizontal plane: the view from above
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50
Q

When comparing the brains of different species, more intelligence correlates with…

A
  1. More convolutions (coils or twists)

2. Proportionally larger cerebral hemispheres

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51
Q

What does the hindbrain control?

A

Reflex control of respiration, blood circulation and other basic tasks
In complex vertebrates, coordination of sensory input, motor dexterity and possible mental dexterity

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52
Q

Parts of the hindbrain

A

Medulla
Pons
Cerebellum

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53
Q

What is the medulla?

A

(An extension of the spinal cord)
Controls vital reflexes (heart rate, circulation, respiration, salivation, coughing, sneezing) via cranial nerves (VI-XII). These nerves control sensations from the head, muscle movements in the head and parasympathetic output to organs

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54
Q

What is the pons?

A

A major relay at which axonal projections cross sides, becoming contralateral (enter the side of the body which is the opposite to that where they originate). The pons contains centres related to sleep and arousal

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55
Q

What is the cerebellum?

A

Controls fine motor skills, coordination and balance. It plays a role in motor learning and cognitive functions of attention and language

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56
Q

What does the midbrain do?

A

Located at the top of the brain and contains structures that have secondary roles in vision, audition and movement

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57
Q

What are the parts of the midbrain?

A

Superior colliculi
Inferior colliculi
Substantia nigra

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58
Q

What are the superior colliculi?

A

A pair of structures which help guide eye movements and fixation of gaze

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59
Q

What are the inferior colliculi?

A

A pair of structures that help guide sound localisation

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60
Q

What is the substantia nigra?

A

Plays a role in reward and addiction, and projects to the basal ganglia to integrate movements

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61
Q

What parts of the brain make up the brainstem?

A

The midbrain and hindbrain

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62
Q

What does the forebrain do?

A

Receives and integrates sensory information from the nose, eyes and ears. In land-dwelling vertebrates, it contains the highest integrating centres

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63
Q

What are the two divisions of the forebrain?

A
  • Cerebrum (telencephalon), which is composed of the cerebral cortex, the limbic system and the basal ganglia
  • Diencephalon
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64
Q

What is in the diencephalon of the forebrain?

A

Thalamus
Hypothalamus
Mammillary bodies

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65
Q

What is the thalamus?

A

Relays and filters information from sensory organs (except olfaction) and transmits it to the cortex

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66
Q

What is the hypothalamus?

A

Regulates body temperature, hunger, thirst and sexual behaviour

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67
Q

What are mammillary bodies?

A

A relay for impulses coming from the amygdala and hippocampus

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68
Q

What is in the limbic system of the cerebrum (telencephalon) of the forebrain?

A

Hippocampus
Amygdala
Cingulate cortex

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69
Q

What is the hippocampus?

A

Involved in the creation of new memories and integration of new memories into stable knowledge

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70
Q

What is the amygdala?

A

Emotional behaviour and formation of emotional memories

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71
Q

What is the cingulate cortex?

A

Linking behavioural outcomes to motivation and learning (critical in depression and Schizophrenia)

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72
Q

What is in the basal ganglia of the cerebrum (telencephalon) of the forebrain?

A

Basal ganglia

Pituitary gland

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73
Q

What is the purpose of basal ganglia?

A
  • The caudate nucleus, putamen and globus pallidus
  • Participates in planning behaviour and emotional expression, abundant connections with prefrontal cortex
  • Produces direct intentional movements
  • Parkinson’s patients have an undersupply of dopamine in their basal ganglia
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74
Q

What is the pituitary gland?

A

Released hormones regulating many other glands in the body

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75
Q

What is in the cerebral cortex of the cerebrum (telencephalon) of the forebrain?

A

Consists of grey matter and white matter

1.5-4mm thick

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76
Q

What is grey matter?

A

Cell bodies, dendrites and glia. It covers the cerebral hemispheres and is wrinkled or convoluted, increasing the surface area

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77
Q

What is white matter?

A

A dense collection of myelinated axons

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78
Q

What are the cerebral hemispheres?

A
  • The brain is comprised of two roughly symmetrical halves: the left and right cerebral hemispheres
  • They are separated by a longitudinal fissure
  • The left and right cerebral cortices are joined by the corpus callosum, a dense band of fibres at the bottom of the longitudinal fissure
  • Incoming information is often directed at one hemisphere (eg visual information in the left visual field is processes by the right hemisphere
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79
Q

What is corpus callosotomy?

A
  • A surgical procedure that disconnects the cerebral hemispheres, resulting in a condition called ‘split-brain’
  • It was split brain patients who have informed the study of hemispheric specialisation
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80
Q

What is the left hemisphere more specialised for?

A

Language

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81
Q

What is the right hemisphere more specialised for?

A

Face recognition and spatial orientation

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82
Q

What are the 4 brain lobes?

A
  1. Frontal lobe (in front of the central sulcus and above the lateral fissure)
  2. Parietal lobe (behind the central sulcus)
  3. Occipital lobe (at the back of brain)
  4. Temporal lobe (on the sides of brain)
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83
Q

What is a gyrus (plural gyri)?

A

A ridge on the cortex

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84
Q

What is a sulcus (plural sulci)?

A

A groove on the brain surface

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85
Q

What are deep sulci called?

A

Fissures

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86
Q

What is the purpose of the frontal lobes?

A

The frontal lobes are important for movement and complex human capabilities, such as emotional expression, problem solving, memory, language and judgement

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87
Q

What is located in the frontal lobe?

A
  • The Broca’s area (important for speech production)
  • The primary motor cortex
  • The prefrontal cortex (plays a role in organising and planning, decision making and impulse control - the prefrontal cortex adjusts behaviour in response to rewards and punishments)
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88
Q

Result of prefrontal cortex damage

A
  • Impairs the ability to learn from consequences and decreases the ability to control impulses
  • In 1848 Phineas Gage, a 25 year old railroad construction worker survived an accident in which a large iron rod was driven completely through his left cheek and out of his skull
  • He was left with no speech, movement, intelligence or learning impairment
  • The injury changed his personality and behaviour
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89
Q

Frontal lobotomy

A
  • A surgical procedure that disconnects the prefrontal area from the rest of the brain
  • Used in US in 1940s and 1950s to calm agitated patients
  • Largely replaced by drug treatment
90
Q

What is a cortical homunculus?

A

A distorted representation of the human body based on a neurological map of the area and proportions of the brain dedicated to motor/sensory functions

91
Q

Features of parietal lobes

A
  • Important for body sensations and spatial localisation
  • The primary somatosensory cortex (postcentral gyrus) receives information about skin senses, body position and movements and maps these functions as a sensory homunculus
  • Parietal association areas combine information from body senses and vision. For example, they help identify objects by touch, determine the location of the limbs and locate objects in space
92
Q

Features of the occipital lobe

A
  • Hosts the primary visual cortex (striate cortex)
  • The primary visual cortex contains a map of visual space because adjacent receptors in the eye send information to adjacent points in the visual cortex, making a ‘retinotropic map’
  • Destruction in the striate cortex causes cortical blindness in the related part of the visual field
  • The occipital lobe has other visual areas that process individual components of a scene including colour, movement and form
93
Q

Temporal lobe features

A
  • Contain the auditory cortex, which receives information from the ear
  • Include language, auditory and visual association areas
  • Wernicke’s area is involved in language comprehension and production. Damage results in meaningless speech and poor comprehension of written and spoken communication
  • The inferior temporal cortex (part of the inferior temporal gyrus) is involved in visual identification. Damage caused difficulties in recognising objects and familiar faces (prosopagnosia)
94
Q

What is Broadmann’s area 41 & 42?

A

The posterior half of the inferior temporal gyrus (diving into the lateral sulcus as the transverse temporal gyri) - also known as the primary auditory cortex

95
Q

What is sound?

A

Periodic compressions of air, water or another medium

96
Q

What is the outer ear’s other name and what is its function?

A
  • Pinna

- The pinna captures sound and amplifies it by funnelling it into the smaller auditory canal

97
Q

What is the middle ear made up of?

A
  • The tympanic membrane (eardrum) collects the vibrations and transmits to the ossicles
  • The ossicles are 3 small bones: the hammer, anvil and stirrup. Their lever action transfers the vibration to the cochlea
98
Q

What is the inner ear made up of?

A
  • The cochlea is divided into three fluid-filled canals: the vestibular, tympanic and cochlear canal
  • The stirrup sends vibrations throughout the cochlea and to the organ of Corti
  • The organ of Corti has four rows of hair cells, opening potassium and calcium channels
  • This depolarises the cells and sets off signals in the neurons
  • The hair cells synaptically excite the cells of the auditory nerve
99
Q

How long does it take for a sound to travel from the eardrum to the auditory complex?

A

20ms

100
Q

Auditory pathway

A
  1. The impulse enters the brainstem
  2. The first relay - ipsilateral cochlear nuclei in the brainstem, which receive input from the auditory nerve. Some decoding of the signal duration, intensity and frequency occurs here
  3. The second relay - in the superior olivary nucleus. The majority of the auditory fibres are contralateral
  4. The third relay - in the inferior colliculus of the midbrain (mesencephalon)
  5. The final relay - in the thalamus (medial geniculate body)
  6. There is a neuronal projection from the thalamus to the auditory complex
101
Q

Sound properties

A
  • Intensity/amplitude: how much air fluctuation the sound creates - the energy of the sound
  • Sound wave pressure is in decibels (dB), and it is a logarithmic scale
  • A perceptual correlate of intensity is loudness
  • For all frequencies above 200 Hz, sound intensity is encoded via neuron firing rate - neurons fire more frequently as sound intensity grows
102
Q

What is frequency?

A

The number of air compressions per second that the object creates, measured in Hertz (Hz)

103
Q

What is the place code?

A

Encodes sound frequencies above 200 Hz
Different places along the cochlea respond to different sound frequencies because of differences in stiffness/elasticity of the cochlear membrane. This is called ‘tonotopic organisation’
Each frequency has a designated path from the cochlea to a specific part of the brain

104
Q

What’s the temporal code?

A

To encode frequencies below 200 Hz, the basilar membrane vibrates in synchrony with a sound, causing the auditory nerve axons to produce action potentials with the same frequency

105
Q

What are the three binaural cues to determine where the source of a sound is (sound localisation)?

A
  1. Difference in intensity between ears
  2. Difference in time of arrival at two ears
  3. Phase difference between ears
106
Q

Relative pitch

A

The distance of a musical note from a given reference point (eg. three octaves above C)

107
Q

Absolute pitch

A

The ability to name/ reproduce a musical note without an external reference
Quite rare

108
Q

Impaired auditory perception example: Amusia

A
  • Musical deafness
  • Congenital amusia is present from birth (4% of population)
  • Acquired amusia is the result of brain damage such as a lesion
  • Symptoms: inability to recognise familiar melodies, read musical notation or detect wrong / out of tune notes (receptive)
  • Sufferers may be unable to sing, write musical notation or play an instrument (expressive)
109
Q

Impaired auditory perception example: Conductive hearing loss

A
  • Results from damage to the eardrum or ossicles in the middle ear
  • Results in failure to transmit sound waves to the cochlea
  • It can be corrected by medication, surgery, sound amplification by hearing aids or using bond conduction
110
Q

Impaired auditory perception example: sensorineural hearing loss

A
  • ‘Nerve deafness’
  • Damage to the cochlea or hair cells in the inner ear
  • May be congenital, the result of a disease or due to repeated exposure
  • Can be corrected by cochlear implants - surgically implanted devices that receive a sound via a microphone and conduct it via thin wires to directly stimulate the auditory nerve
111
Q

Tinnitus

A
  • The perception of sound within the human ear in the absence of corresponding external sound
  • Due to inner ear damage caused by ageing, a medication side effect or as a result noise-induced hearing loss
  • The persisting sound comes from an enlarged sector in the auditory complex in which neurons are responding in a coordinated way in the absence of sound
112
Q

Two types of tinnitus

A
  1. Persistent ringing is dependent on abnormal patterns of activity that the damaged inner ear is feeding to the brain (cured by surgically severing the auditory nerve)
  2. Plastic changes in the brain to the extent that it can now sustain itself without ear input to generate the continuous ringing noises (not cured by severing the auditory nerve)
113
Q

Sound perception in Schizophrenia patients

A
  • Individuals with Schizophrenia show ventricular enlargement
  • During auditory hallucinations, the right inferior colliculus, the left and right insula, the left parahippocampal gyrus, the right superior temporal gyrus and the right thalamus are stimulated
114
Q

What is an emotion?

A

An internal process that modified the way an organism responds to certain kinds of external stimuli

115
Q

Emotion has 3 components:

A
  1. Cognitions ‘this is dangerous’
  2. Feelings ‘I feel frightened’
  3. Actions ‘run away’
116
Q

What two branches of the autonomic nervous system do emotional situations arouse?

A

The sympathetic nervous system - prepares body for brief, vigorous, flight of flight situations
The parasympathetic nervous system - increases digestion and other processes to save energy and prepare for later events

117
Q

What is the James-Lange theory?

A
  • He theorised that the emotional feeling is only experienced after the fight-or-flight action has occurred
  • This theory predicts that people with weak autonomic or skeletal responses well feel less emotion
  • It also suggests that causing or increasing someone’s action/ response should enhance an emotion
118
Q

Evidence supporting the James-Lange theory

A
  • People with paralysis through damage to the spinal cord are unable to instigate flight-or-flight behaviours. However, they report the same level of emotion as before their injury, but paralysis does not affect the autonomic nervous system
  • Pure autonomic failure (failure of output from the autonomic nervous system to the body) patients feel emotions less intensively
  • BOTOX is used to paralyse the muscles used for frowning to reduce wrinkles. It has been shown individuals take longer to ready unhappy sentences
  • Patients with locked-in syndrome are unable to make voluntary face movements and had problems recognising other people’s emotional expressions
119
Q

Evidence against the James-Lange theory

A
  • People with somatosensory cortex damage had normal autonomic physiological response to emotional music but little subjective experience
  • Patients with damage to prefrontal cortex had weak autonomic response but normal subjective response
120
Q

What is Mobius syndrome?

A

A rare congenital disorder, where the patient has problems feeding and exhibits a mask-like expression. Caused by palsies/paralysis of the VI and VII cranial nerves and skeletal defects. There are additional problems with eye movements in the horizontal plane. When patients were tested they found no impairment in recognising basic types of facial affect (anger, fear, sadness, happiness) although they did show mild impairment in face recognition

121
Q

What is the Cannon-Bard theory?

A
  • Suggests that an emotional stimulus simultaneously triggers an autonomic immune response and an emotional experience in the brain
  • The autonomic system responds too slow to account for the rapid onset of emotional experience
  • There are not enough unique patterns of autonomic activity to represent the array of emotional experiences we have
122
Q

What was Schacter and Singer’s conclusion in 1962?

A
  • James and Lange were right to equate emotion with bodily states
  • Cannon and Bard were right to note that there are not enough distinct bodily reactions to account for the variety of emotions we experience
  • Different emotions may reflect different interpretations of a single pattern of bodily activity - ‘undifferentiated bodily arousal’
123
Q

What area of the brain is disgust associated with?

A
  • Insular cortex and basal ganglia
  • The anterior insula is connected to the ventro-posterior-medial-thalamic nucleus, and has been identified as the gustatory cortex, containing neurones that respond to pleasant and unpleasant tastes
  • Calder (2000) reports a patient with damage to the left insula and left basal ganglia who was impaired at recognising disgust and in the ability to experience disgust himself
  • Adolphs (2002) report a patient with bi-lateral insula damage who was severely impaired at experiencing and recognising disgust from all types of stimuli
124
Q

Testosterone and emotion

A
  • Testosterone is linked with social dominance and aggression
  • Higher levels of testosterone are found in criminals who have committed violent crimes
  • It has been shown that testosterone delays conscious recognition of facial threat signals
125
Q

Serotonin and emotion

A
  • Low serotonin levels are linked to aggressive behaviour
  • Serotonin production is lower in juvenile rats than adults, and their aggression levels are higher
  • Low serotonin is linked to violent crime or suicide, and can be used as a predictor of further convictions upon release from prison
  • Diet can alter serotonin levels. Serotonin is synthesised from the amino acid tryptophan. It crosses the blood-brain barrier through channels also used by phenylalanine and other amino acids
  • Therefore, a higher concentration of those other amino acids reduces the amount of tryptophan that can get through, inspiring the brain’s ability to make serotonin
126
Q

What brain area affects fear and anxiety?

A
  • The amygdala
  • It receives input from pain, vision and hearing centres, and establishes conditioned responses
  • Some cells respond to reward and others to punishment
  • The amygdala projects to the hypothalamus which controls autonomic responses, the prefrontal cortex which modulates behaviour and to the midbrain regions that link to the pons which generates startle behaviour
127
Q

How is the function of the amygdala tested?

A
  • An animal is presented with a loud noise and a startle response is recorded
  • A light is then paired with the shock repeatedly
  • Finally, the light precedes the noise and increases the startle response
  • In rats with amygdala damage there is still a startle reflex but no increase from the light stimulus - amygdala damage causes difficulties in interpreting signals with emotional consequences
128
Q

What is toxoplasma gondii?

A

The animal which hosts the parasite excretes it’s eggs and these are then released into the ground. They infect burrowing animals like rats. The parasite attacks and damages the amygdala such that they show no fear when approaching cats. The cats then eat the rats and the parasite can complete its life cycle within a cat

129
Q

What is Kluver-Bucy syndrome?

A

Monkeys with amygdala damage attempt to pick up lighted matches and other objects they would normally avoid. They are also less fearful of snakes and more dominant monkeys

130
Q

What did Whalen et al argue in 2001?

A

The pattern of activation found for the amygdala may not reflect the processing of negative emotions per se, but more about detecting ambiguity in the face and how that relates to predictability of the persons actions. A fearful face conveys more ambiguity than an angry face, even though both perceive threat

131
Q

What is Urbach-Weithe disease?

A

Individuals with this disease accumulate calcium in the amygdala and it atrophies. Patients who are affected show lack of fear, which could be a risk for them. They also fail to recognise fear when expressed by others

132
Q

What is sensation?

A

Physical stimulation of a sense organ

133
Q

What is transduction?

A

Conversion of physical signals from the environment into neural signals carried by sensory neurons into the central nervous system

134
Q

3 different views of the relationship between our senses and the physical world

A
  • Objectivist view: our senses accurately reflect the physical world
  • Subjectivist view: our senses select and organise, thereby creating a world
  • Synthetic view: our senses capture some aspects of the world quite accurately
135
Q

Who was the Arab mathematician who was the first to explain that vision occurs when light bounces off an object and is then directed into a person’s eye?

A

Ibn al-Haytham

136
Q

What happens to light in the human eye?

A
  • Light enters the eye through the pupil and is then focused by the cornea (not adjustable) and lens (adjustable)
  • Focused light is projected on rear surface of the eye, the retina
  • Light from above strikes the bottom half of the retina, and light from below strikes the top half
  • The retina is lined with visual receptors
137
Q

A the retina:

A
  • Light originally passes through ganglion and bipolar cells en route to photoreceptors (they are transparent)
  • Ganglion cells axons join together to form the optic nerve that travels to the brain
  • The point where the optic nerve leaves the eye has no receptors (‘blind spot’)
  • People vary in the number of axons from the retina to their brain
  • Illnesses such as multiple sclerosis cause loss of axons so lower visual acuity
138
Q

What is a receptive field?

A

A region of the sensory surface in the retina that causes a change in the firing rate of a ganglion cell when stimulated in a specific matter. Changes in the firing rate can be excitatory or inhibitory.

  • If light detected by a particular spot on the retina excites a ganglion cell, then this location is part of the cells excitatory receptive field
  • If light detected by a particular spot on the retina inhibits a ganglion cell, then this location is part of the cells inhibitory receptive field
139
Q

Types of receptive field

A
  • Often organised in a centre-surround fashion
  • Version A: light in the centre excited the cell, light in the surround inhibits the cell
  • Version B: light in the centre inhibits the cell, light in the surround excites the cell
140
Q

How much do rods outnumber cones by?

A

20:1

141
Q

What % of the brains input do cones provide?

A

90% - due to different convergence rates

142
Q

What is the colour constancy challenge?

A
  • Light reflected into the eye from an object depends on both the intrinsic reflectance properties of the object and on surrounding illumination spectrum
  • A specific wavelength of light can appear as different colours depending on illumination
  • Reflected wavelength is not the same as perceived colour
  • Colour constancy is the ability to recognise colours despite changes in lighting, as the human brain tries to factor out the effects of illumination
143
Q

What is the Retinex Theory?

A

Land (1983)

The cortex compares information from various parts of the retina to determine colour

144
Q

Where is the visual cortex located?

A

Mainly in the occipital lobe but extends to temporal and parietal lobes

145
Q

From the eyes to V1 (the primary visual cortex)

A
  • Optic nerves from the two eyes meet at the optic chiasm (where the optic nerves cross)
  • At the optic chiasm, half of the axons from each eye cross to the opposite side of the brain
  • The minority of ganglion axons go to the superior colliculus
  • The majority of ganglion axons go to the lateral geniculate nucleus (LGN) in the thalamus
  • The lateral geniculate nucleus sends axons to other parts of the thalamus and the primary visual cortex
146
Q

Receptive fields in the primary visual cortex

A
  • As the information gets passed through the processing stream, the cells receptive fields increase in complexity
  • The cells of the lateral geniculate nucleus have receptive fields that resemble those of ganglion cells
  • However, the receptive fields in the primary visual cortex (V1) can be more complicated
  • Their size/organisation depends on the connections they receive (the combination of the receptive fields of several ganglion cells)
147
Q

What did Hubel and Wiesel achieve in 1959?

A

A landmark study where they recorded the activity from cells in cats’ and monkeys’ visual cortex while shining light patterns on the retina (via microelectrode recordings)

148
Q

Discovery of simple cells at V1

A
  • Receptive fields of relatively small size
  • Receptive field is usually bar-shaped
  • Fixed excitatory and inhibitory zones (the more light shines in an excitatory zone, the more the cell fires)
  • The light must therefore be moving in a specific direction to stimulate a specific cell
149
Q

Discovery of complex cells at V1 (striate complex)

A
  • Receptive field of medium size
  • Bar-shaped but without fixed excitatory or inhibitory zones
  • Cells respond to moving light patterns
150
Q

Discovery of hyper complex cells at V1 (striate cortex)

A
  • Receptive field of large size
  • Bar-/edge-shaped
  • Strong inhibitory area on one end
151
Q

The functional significance of V1

A
  • Contains many cells tuned to bars in different positions of the visual field
  • Based on the combination of many neurons with simple, complex and hypercomplex receptive fields we are able to detect edges in images
152
Q

Organisation of V1

A
  • Cells of similar properties are grouped together in columns (cells with similar receptive fields and/or coding information from the same eye)
  • Columns follow topographic organisation: adjacent neurons process adjacent portions of the visual field
  • Damage to small regions of V1 degrades vision generally within the corresponding portion of the visual field
153
Q

From V1 to V2 to V3

A
  • V1 has reciprocal connections with the secondary visual cortex (V2) and V2 has connections with the tertiary visual cortex (V3)
  • In V2 and V3 there are many complex and hypercomplex cells, but also cells that respond to even more complex patterns such as circles or lines that meet at a right angle
  • Visual information is passed from V2 to V3 to several additional regions across the occipital cortex
  • These regions analyse additional attributes such as colour, motion, shape and location
154
Q

Colour processing in V4

A
  • Damage to V4 results in cerebral achromatopsia
  • Patients have intact colour naming from memory but impaired colour naming for objects in their environment
  • Patients describe their surroundings as being darkly-coloured, as in an unlit room at twilight
  • Patients have intact shape and motion processing and intact achromatic discrimination (they can tell the difference between different levels of grey)
  • Responses to V4 correspond to the perceived colour of an object, not just the wavelength of light reflected from the object
155
Q

Motion processing in V5

A
  • Damage to V5 results in cerebral akinetopsia

- Patient loses ability to detect movement in three dimensions. They see movements as separate frozen images

156
Q

Two major visual processing streams

A
  1. Processing along the temporal cortex (ventral stream) is known as the WHAT pathway
  2. Processing along the parietal cortex (dorsal stream) is known as the WHERE/HOW pathway
    - Both pathways exchange information
157
Q

Ventral processing stream I

A
  • Detailed analysis of shape - involved in recognising / identifying objects
  • Cells in this processing stream respond to identifiable, familiar objects
  • High-level, abstract representations: cells respond consistently regardless of object size, position and angle
158
Q

Ventral processing stream II

A
  • Responsive cells bundled in certain locations

- Some entities of particular importance

159
Q

Ventral processing stream III

A
  • Damage in the ventral processing stream leads to visual form agnosia (inability to recognise objects by sight despite otherwise satisfactory vision)
  • Patients can recognise objects through their other senses
  • They are also not impaired in understanding where things are - they can go for walks without bumping into things and show normal eye movement
160
Q

Dorsal processing stream

A
  • Detailed analysis of the location and motion of an object and spatial relations (WHERE)
  • Processing in this stream guides human movements such as aiming, reaching, tracking with the eyes and grabbing (HOW)
  • Damage to this stream does not usually impair identification of objects, but it does impair understanding of where things are - patients have trouble grabbing thinks and walk into objects etc.
  • These are the common consequences of superior parietal lobe damage
  • Optic ataxia - inability to guide reaching movements using visual information
  • Balint’s syndrome - optic ataxia, gaze shift impairments, simultanagnosia (inability to see more than one object at once)
161
Q

What is the binding problem?

A
  • The visual system processes different visual properties/features (eg colour, shape, motion, location) in different brain regions
  • Making an accurate perception requires putting the right features together
  • The binding problem is the question of how various brain regions create a coherent/unified perceptual experience
162
Q

Feature integration theory (Treisman et al., 1980)

A
  • Visual features are initially processed separately and pre-attentively
  • Information gets forwarded to a ‘master map’
  • Attention on the master map binds features
163
Q

Fusiform face area

A

Study published in 1997 by Nancy Kanwisher and colleagues
Identified specific region in the ventral visual processing stream that showed consistently more activity to faces than other objects
This is the fusiform face area, and it is located in the fusiform gyrus

164
Q

Three regions associated with facial recognition

A
  1. Occipital face area (OFA)
  2. Fusiform face area (FFA)
  3. Posterior superior temporal sulcus (pSTS)
165
Q

What does the occipital face area do?

A

Feature-based processing - good at detecting changes in features

166
Q

What does the fusiform face area do?

A

Holistic processes and can recognise even a Mooney face

167
Q

What does the posterior superior temporal sulcus do?

A

Processes dynamic information such as facial movement

168
Q

Which hemisphere is stronger for face specific neural activity?

A

Right hemisphere

169
Q

What is the functional contribution of these modules?

A
  • Face perception involves specialised visual processing
  • Faces are highly homogenous
  • They must be differentiated based on very subtle differences
  • Humans process faces holistically - they combine various facial features into a unique whole
170
Q

What is the face composite effect?

A

Humans habitually fuse the upper and lower parts of the face to form a holistic impression, due to this they lose the ability to recognise the constituent parts of a face

171
Q

What is the face detection effect?

A

Holistic face processing is so good that we are often able to detect faces based on extremely impoverished visual information

172
Q

Face inversion effect

A

Holistic face processing breaks down when faces are inverted, and suddenly odd configurations are not easily detected

173
Q

What happens when the network gets damaged/disturbed?

A 
Face blindness (Prosopagnosia)
Alternative routes must be used to identify a person
174
Q

What is used in a 1-back detection task?

A

Faces/bodies as stimuli, compared to objects and scrambled control images
Comparison of the response of the brain to images of bodies compared to objects or scrambled images

175
Q

Three areas identified in recognising bodies

A
  1. Extrastriate body area (EBA)
  2. Fusiform body area (FBA)
  3. Posterior superior temporal sulcus (pSTS)
176
Q

What is learning?

A

A relatively permanent change in behaviour as a consequence of experience

177
Q

What are the two types of learning?

A
  • Classical (Pavlovian) conditioning - stimulus paired with reward
  • Instrumental (Operant) conditioning - action leads to reward
178
Q

Classical conditioning (Pavlov example)

A
  • An unconditioned stimulus (eg. food) will give way to an unconditioned reaction (eg. dog sits and wags tail)
  • If the unconditioned stimulus (food) is paired with a stimulus that must be conditioned (bell ringing), it will cause a conditioned response (dog expects food and sits/wags tail when it hears bell ringing)
  • The dog’s response to food is innate
  • The dog’s response to the bell is learned
  • Classical conditioning can occur in both humans and non-humans. It has been demonstrated on a range of species
  • It can be further subdivided into appetitive and aversive conditioning
179
Q

Appetitive conditioning

A
  • An instinctive physical desire, especially for food and drink
  • Largely positive
  • The dog example by Pavlov was an example
180
Q

Aversive conditioning

A
  • Pair an unconditioned stimulus that causes an aversive response with a conditioned stimulus
  • It only takes one experience to establish a conditioned response and the aversive response can last a lifetime
  • The space between the stimulus and response is longer is Pavlov’s origins demonstration
181
Q

What did Lloyd C. Morgan argue and when?

A
  • 1894
  • Suggested that animals learn about contingencies through mental representations which connect events through associations
  • He argued that neural centres represent certain events, and when these events happen in close temporal proximity, the representations are activated and a connection is formed
182
Q

Neural changes during Pavlovian conditioning (Carew, Hawkins and Kandel, 1983)

A
  • Studied sea slug nervous system
  • Found that when siphon or mantle shelf were stimulated, there was a full withdrawal reflex
  • The gill withdrawal was larger when followed by a shock
  • They began stimulating the siphon and pairing it with a shock, leading to a conditioned response of withdrawing the gills
  • They also stimulated the mantle shelf, but with no shock added, which led to a smaller conditioned reaction
  • They then measured the level of gill withdrawal when stimulating the siphon or mantle with no paired shock
  • The results were that there was a bigger gill withdrawal reflex when the siphon was stimulated than the mantle shelf
  • There was also a much greater change in motor neuron activity when the siphon was stimulated than the mantle shelf
  • The basis of associative learning seems to be related to the ease with which one neuron can excite another (change in effectiveness of connections between sensory and motor neurons)
183
Q

Eyeblink conditioning

A
  • Logan and Graton (1995): pairing a conditioned stimulus with an air puff to the eye. A PET scan shows activity increases in the cerebellum
  • Gerwig et al. (2005): people who have damage to the cerebellum have weaker conditioned eye blinks, and the eyeblinks are poorly timed
184
Q

Gottfried, O’Doherty and Dolan (2002)

A
  • Found more activation in the orbitofrontal cortex (OFC) and ventral striatum following the appetitive conditioned stimulus compared to the aversive conditioned stimulus
  • The OFC is thought to be involved in sending positive olfactory information to the visual system
  • The ventral striatum is thought to be involved in the conditioned response elicited by the appetitive conditioned stimulus
185
Q

Kumar et al. (2008)

A
  • Thirsty patients rewarded with water following a visual conditioned stimulus
  • Healthy participants (but not depressed patients) showed greater activation in the ventral striatum to the appetitive conditioned stimulus than patients with major depressive disorder
  • Thus the stimulus is not as rewarding to those suffering from depression
186
Q

Symptoms of major depressive disorder (MDD) (mood disorder)

A
  • Sleep problems
  • Change in weight or appetite
  • Fatigue/loss of energy
  • Psychomotor retardation / agitation
  • Difficulty concentrating / indecisiveness
  • Guilt / low self esteem
  • Recurrent thoughts of death or suicide
187
Q

Prevalence of MDD in UK

A

3.3%

188
Q

When does depression become more prevalent in females?

A

At age 14

189
Q

Genetics of MDD

A
  • Studies with twins and adopted twins suggest moderate degree of heritability
  • No single gene shows strong link to depression, genetic link may be masked by different onset types
  • Early onset and late onset
  • Serotonin uptake transporter gene comes in both long and short forms. Researchers asked 847 young adults about the number of stressful events they experienced over 5 years, then explored whether this gene and the environment were linked to depression
  • For people with two long forms of the gene, the environment had a minor impact
  • Short form individuals showed a marked environmental effect on the probability of developing depression
  • However, others have been unable to replicate this effect, it could be a false positive. It is also harder to measure stress than depression - frequency of stressful events does not account for the severity of stress
190
Q

Early onset MDD

A
  • Before 30 years
  • High probability (40-50%) if other relatives with depression, anxiety disorders, attention-deficit order, OCD, bulimia, migraine headaches, alcohol or drug abuse and irritable bowel syndrome
191
Q

Late onset MDD

A
  • Post 45 years

- High probability of relatives with circulatory problems

192
Q

Hormones contributing to the onset of MDD

A
  • Cortisol is linked to stress and in turn stress is linked to depression
  • Stress hormones reach a peak in late pregnancy and ovarian hormones change dramatically at the time of delivery. 20% of women report some degree of depression after childbirth
  • A drug-induced drop in estradiol and progesterone (hormones associated with pregnancy) linked to new depressive episodes in women with a history of post-partum depression
  • Decline in testosterone in older men also linked to increase probability of depression
  • No causal link between depression and hormones has been established
193
Q

Hemispheric factors contributing to the onset of MDD

A
  • Positive mood associated with activation of the left prefrontal cortex in the normal population
  • People suffering from depression have decreased activity in the left prefrontal cortex and increased activity in the right prefrontal cortex. This imbalance remains stable over time despite changes in symptom severity, which may reflect a biological disposition rather than a predictive factor
194
Q

4 types of antidepressants

A
  1. Tricyclics
  2. Selective serotonin reuptake inhibitors
  3. Monoamine oxidase inhibitors
  4. Atypical antidepressants
195
Q

Tricyclics

A

Block transporter proteins that reabsorb serotonin, dopamine and epinephrine (noradrenaline). Prolongs the presence of these neurotransmitters in the synaptic cleft. However, they also block histamine and acetylcholine receptors and some sodium channels. These have side effects such as drowsiness, dry mouth and heart irregularities respectively so are not suitable for long-term use

196
Q

Selective serotonin reuptake inhibitors (SSRIs)

A

Similar to tricyclics but specific to serotonin. Milder side effects but similar treatment outcomes. Prozac is one

197
Q

Monoamine oxidase inhibitors (MAOIs)

A

Block the enzyme monoamine oxidase (MAO). This enzyme metabolises catecholamine and serotonin and renders them inactive. By blocking this enzyme there is more of the neurotransmitter available for release

198
Q

Atypical antidepressants

A

Dopamine and Norepinephrine Reuptake Inhibitors sometimes used. St. John’s Wort is a non-prescription drug that has been argued to have similar properties to antidepressant prescription drugs. However, it promotes the production of a liver enzyme that breaks down toxins but also breaks down medication so renders other anti-depressant medication inactive

199
Q

When do antidepressant medications have a significant effect?

A

When MDD is already very severe

200
Q

Electroconvulsive therapy for MDD

A
  • Electrically induces seizures
  • Used in severe cases of depression when drug treatments have failed
  • Not clear exactly how it works to relieve depression, but does seem to alter expression of genes in the hippocampus and frontal lobes
  • Similar treatment of transcranial magnetic stimulation (TMS) often used now - stimulates axons near the surface of the brain, but not clear exactly how this relieves depression
201
Q

Bipolar I disorder

A

People with severe episodes of mania

202
Q

Bipolar II disorder

A

People with milder episodes of mania (hypomania)

203
Q

In addition to mood problems, what other issues do people with bipolar disorder have?

A
  • Attention problems
  • Poor self-control
  • Problems with verbal memory
204
Q

Genetics of bipolar disorder

A
  • Genetic predisposition supported by twin studies and adoption studies
  • Two genes have been identified that appear to increase the probability of bipolar II disorder
  • Genetic link between major depression and bipolar disorder
205
Q

Treatment of bipolar disorder: medication

A
  • Three mediation’s appear to reduce the number of AMPA type glutamate receptors in the hippocampus - linked with mania
    1. Lithium salts: stabilise mood preventing a relapse into mania or severe depression. Toxic in high doses but ineffective in low doses
    2. and 3. Valproate and Carbamazeprine: also prescribed. Sometimes supplemented with antidepressants or antipsychotic drugs (normally prescribed for schizophrenia)
  • These medications also block the synthesis of arachidonic acid that is produced when the brain is inflamed. Bipolar patients show increased gene expression associated with inflammation
206
Q

Bipolar treatment: sleep

A
  • Circadian rhythm affected in the depressed phase - patients spend long periods in bed
  • In the manic cycle they get very little sleep
  • The intensity of mood swings can be reduced by encouraging a healthy sleep cycle in a quiet, dark room
207
Q

Symptoms of schizophrenia

A
  • Delusions
  • Hallucinations
  • Disorganised speech
  • Abnormal psychomotor behaviour, including catatonia
  • Negative symptoms
  • Lower level of functioning in school/work/interpersonal relations/self-care
208
Q

How long must continuous signs of disturbance be noticed for to diagnose schizophrenia?

A

6 months, with at least 1 month including the symptoms above in full and active form

209
Q

What are the positive symptoms of schizophrenia?

A

Present but should be absent
Hallucinations
Delusions

210
Q

What are the negative symptoms of schizophrenia?

A

Absent but should be present

Diminished emotional expression or abolition (the motivation to perform self-directed purposeful activities)

211
Q

Disorganised symptoms

A

Speech

Catatonia

212
Q

Cognitive symptoms

A

Not part of diagnostic criteria

Tend to have lower IQ and deficits in attention and working memory

213
Q

What % of people worldwide suffer from schizophrenia?

A

1%

214
Q

Male:female ratio of schizophrenia sufferers

A

7:5

215
Q

Which gender has earlier onset and more severe schizophrenia?

A

Male

216
Q

Genetics contributing to onset of schizophrenia

A
  • As the genetic link decreases so does the probability of developing schizophrenia
  • Monozygotic (identical) twins have 50% concordance, could be linked to a gene active in one and not the other, or to environmental factors
  • Dizygotic (non-identical) twins have the same genetic resemblance as siblings but have a higher probability of both being affected by schizophrenia
  • Schizophrenia is more common in a twin’s biological family than their adopted one (if they are children)
  • Suggestion of genetic basis, but may also be accounted for by prenatal environmental influences
  • Schizophrenic mothers are more likely to drink, smoke and eat a poor diet during pregnancy, and also have a disproportionate risk of complications during pregnancy
  • There is a higher incidence of schizophrenia in adopted children with biological parents that had schizophrenia and disordered adoptive family
217
Q

Prenatal and neonatal environmental factors contributing to the onset of schizophrenia. Risk is elevated by:

A
  • Poor nutritional intake of mother during pregnancy
  • Premature birth
  • Low birth rate
  • Complications during pregnancy
  • Exposure if mother to extreme stress
  • Head injuries in early childhood
  • If an Rh-negative mother has an Rh-positive baby, the baby’s blood factor may trigger an immunological rejection by the mother. This response is weak in first births but exacerbated in later births leading to hearing defects, mental retardation and a higher probability of schizophrenia
  • Season of birth may affect onset of schizophrenia - 5-8% more likely if born in winter
  • Increased evidence of influenza virus in mothers whose children eventually developed schizophrenia
  • Schziophrenia rates also higher in mothers who had German measles, herpes and other infections during pregnancy
218
Q

Toxoplasma gondii and schizophrenia

A
  • Parasite carried by domestic cats
  • Infected infants have impaired brain development. Impairs memory and leads to hallucinations/delusions
  • Adults with diagnosis of schizophrenia are more likely to have had a pet cat in childhood
  • Blood tests also show higher concentration of toxoplasma antibodies in schizophrenics than in the general population
219
Q

Brain abnormalities and schizophrenia

A
  • Schizophrenia is associated with larger than average brain ventricles
  • Less than average grey matter and white matter in the brain. The largest difference is in the temporal and prefrontal areas of the brain
  • There are weaker connections between the prefrontal cortex and other brain areas
  • Thalamus is smaller
  • Schizophrenics show deficits in prefrontal cortex functions (attention and memory)
220
Q

Treatments of schizophrenia

A
  • Antipsychotic and neuroleptic drugs Clopromazine (Thorazine) and Haloperidol are used to treat schizophrenia
  • Each of the drugs block dopamine synapses (elevated dopamine is a key symptom in the first episodes of schizophrenia)
  • Lower than normal release of glutamate and fewer than normal number of receptors in prefrontal cortex and hippocampus
  • Narcotics such as PCP inhibit glutamate receptors and in high doses mirror schizophrenic symptoms

Pyschology (3 decks)

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