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RCPsych Paper A > NEUROSCIENCES > Flashcards

NEUROSCIENCES Flashcards

1
Q

Where is the prion gene located and what is is called?

A

Chromosome 20, called PrPc

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2
Q

What is the cellular prion protein?

A

Expressed in CNS
Has 0, 1 or 2 glycosyl residues (unglycosylated, mono or diglycosylated)
Expressed to lesser extent in lymphoid system, peripheral nerves and muscles

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3
Q

Function/roles of prion proteins (4)

A

Copper binding
Cell signalling
Promoting neuronal growth and survival
Regulating synapses, receptors, and circadian rhythms

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4
Q

What is the pathological prion protein?

A

PrPSc
Formed by conformational conversion of normal prion protein
Contains fewer alpha-helices and more beta-sheets
Can be endogenous or from environment
Can self-propagate
Aggregate into large extracellular deposits
Deposits trigger neurodegeneration
Resistant to breakdown by proteases

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5
Q

Histological features of prion disease (4)

A

Vaculoation in all grey matter areas - spongiform encephalopathy
Synaptic dysfunction
Loss of dendrites
Atypical brain inflammation

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6
Q

Advanced pathology of prion disease (3)

A

Neuronal loss
Gliosis
Severe brain atrophy

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7
Q

Histological changes in variant CJD

A

Visible spongiform changes
Multiple amyloid plaques (cluster plaques) surrounded by small vacuoles - ‘florid plaque’
Stellate astrocytes

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8
Q

Histological changes in sporadic CJD

A

Fine spongiform changes
Fine, disseminated vacuoles
Diffuse prior protein deposition
Occasional aggregates of dense coarse microplaques

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9
Q

Mechanism of pathogenesis of sporadic CJD

A

somatic mutation or spontaneous conversion of PrPc to PrPSc

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10
Q

Mechanism of pathogenesis of sporadic fatal insomnia

A

somatic mutation or spontaneous conversion of PrPc to PrPSc

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11
Q

Mechanism of pathogenesis of familial CJD

A

Germline mutations in C-terminal PRNP (Codon 200)

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12
Q

Somatic human prion diseases

A

sporadic CJD
Sporadic fatal insomnia

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13
Q

Heritable human prior diseases

A

Familial CJD

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14
Q

Infective human prion diseases (3)

A

KURU
Iatrogenic CJD
Variant CJD

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15
Q

Infective animal prion diseases (5)

A

Scrapie - affects sheep
Bovine spongiform encephalopathy (BSE)
Transmissible mink encephalopathy (TME)
Chronic wasting disease (CWD) - deer, elk, moose
Feline spongiform encephalopathy (FSE)

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16
Q

Mechanism of pathogenesis of kuru

A

Infection through ritualistic cannibalism

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17
Q

Mechanism of pathogenesis of iatrogenic CJD

A

Infection from dura mater transplants, prion-contaminated human growth hormone, contaminated medical equipment and other medical procedures

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18
Q

Mechanism of pathogenesis of variant CJD

A

transmission of bovine prions through the food chain

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19
Q

Mechanism of pathogenesis of scrapie

A

infection, possible vertical

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20
Q

Mechanism of pathogenesis of BSE

A

infection or sporadic

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21
Q

Mechanism of pathogenesis of TME

A

infection with prions from sheep or cattle

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22
Q

Mechanism of pathogenesis of CWD

A

infection

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23
Q

Mechanism of pathogenesis of FSE

A

infection with prion-contaminated bovine tissues or MBM

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24
Q

sporadic CJD

A

Divided into cognitive and ataxic subtypes
Cognitive - MM1 and MV1 are most common (cog impairment, cortical visual disturbance, ataxia, myoclonus)
Ataxic - VV2 and MV2 approx 1/3 of sCJD (primary symptom is ataxia, but cog imp often evident
For both, dementia and death within months

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25
Q

Presenting features of sCJD and fCJD (4)

A

Cognitive impairment and psych changes (80-83%)
Cerebellar signs (43-55%)
Visual signs (19%)
Myoclonic jerks (12%)

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26
Q

Late developing signs sCJD and fCJD (4)

A

Dementia (100%)
Myoclonus (73%)
Cerebellar signs (79%)
Seizures (40%)

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27
Q

Distinguishing signs between sCJD and fCJD

A

Peripheral neuropathy frequent in E200K-129M phenotype, but rare in sporadic CJD MM1

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28
Q

Sporadic fatal insomnia features

A

Rarest sporadic prion disease
Average age of onset is middle of 4th decade
Features mimic familial form
- Marked sleep disturbance
- Progressive reduction in hours of sleep
- Sympathetic over-activity
- Cognitive impairment
- Ataxia

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29
Q

Sporadic fatal insomnia histology

A

Distinct atrophy of the thalamus, often with mild and localised cortical degeneration

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30
Q

Main types of inherited prion disease (3)

A

Familial CJD
Gerstmann-Straussler-Scheinker (GSS) syndrome
Fatal familial insomnia (FFI)

MOST cases are autosomal dominant

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31
Q

Familial CJD

A

Usually between 45-75 years (mean 60y)
Rapid progression, average duration 5 months

Spongiform changes, astrogliosis, variable neuronal loss WITHOUT amyloid plaques

Lesions preferentially involve the cerebral cortex, striatum, medial thalamus and cerebellum

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32
Q

Gersman-Straussler-Scheinker (GSS) syndrome

A

Most common PRNP mutation are P102L and G131V
Typically present in 3rd or 4th decade
Chronic cerebellar ataxia and pyramidal features
Longer course than CJD
Dementia develops later
Average duration 5 years

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33
Q

Fatal familial insomnia mutation

A

Mutation in PRNP at codon 178, and another variant at position 129 (methionine codon)

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34
Q

variant CJD

A

Average age of onset 28 years
Slower progression than sCJD
Average 14 months duration

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35
Q

Investigations for prion disease (6)

A

EEG
CSF 14-3-3 examination
MRI
Tonsil biopsy
Genetic testing
Histology

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36
Q

HIV-1 vs HIV-2

A

HIV-1 more virulent and infectious
HIV-2 less readily transmitted and slower progression

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37
Q

How does HIV work

A

Uses CD4 receptors on T cells
Uses chemokine receptors to help the virus attach to the cell
Membrane of virus and host cell fuse, allowing viral material in
Host cell produces dsDNA from the HIV RNA, allowing viral component parts to be assembles

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38
Q

What do CD4 cells do

A

Helper T cells have a CD4 glycoprotein on their surface
Assist other WBCs and in activation of cytotoxic T cells and macrophages

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39
Q

What do CD8 cells do?

A

Cytotoxic T cells have a CD8 glycoprotein on their surface, fighting off invaders by destroying infected and cancerous cells.
Identify targets by binding to antigens.

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40
Q

HIV seroconversion syndrome

A

Represents exponential increase in viral load and inflammatory response
Fever, lymphadenopathy, sore throat, rash, much and joint pain, headaches

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41
Q

Viral set point in HIV

A

Where viral replication and host immune response reach equilibrium
When the immune system has develops specific T cells to fight against the virus, and viral load stops increasing
Lasts few weeks to 3 months
Symptoms often mild and short lived, similar to flu

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42
Q

AIDS

A

CD4 cell count below 200 (normal is 500-1600)
Development of >1 characteristics or ‘AIDS-defining’ infections

Without antiretroviral therapy, survival is around 3 years

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43
Q

HIV clinical latency stage

A

No/only mild symptoms
Low level viral reproduction
Can last several decades
Risk of transmission reduced but not absent

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44
Q

CNS effects of HIV

A

Depression
Short term memory impairment
Poor concentration
Behaviour/personality changes

Leg weakness, slow hand movement, gait changes

HAND - HIV-associated neurocognitive disorder

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45
Q

How does HIV get into the brain

A

Tight junctions in BBB dysregulated
Perijunctional proteins lost
BBB more permeable

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46
Q

Histological signs of brain HIV infection

A

Multinucleated giant cells (thought to be infected monocytes that have differentiated into macrophages, or infected microglia that have fused)

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47
Q

Complications of HIV-induced neuroinflammation (6)

A

Axonal damage
Atrophy of dendrites
Reduced neurogenesis
Impaired potentiation
Cognitive - memory and executive function
Behave/physiological - sustained sickness, depression, exaggerated weight loss

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48
Q

Risk factors for HANDs in HIV (8)

A

Comorbid Hep C infection
Parenteral illicit substance use
Low CD4 count
Female
Increasing age
High viral set point early in course of infection
Anaomia
Low BMI

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49
Q

HAND (HIV) investigations

A

CSF analysis
Neuroimaging - MRI or CT

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50
Q

Cerebral cortex

A

Surface of cerebrum

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51
Q

Cerebellar cortex

A

Surface of cerebellum

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52
Q

Within the brainstem (4)

A

Substantia nigra
Red nucleus
Olivary nuclei
Cranial nerve nuclei

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53
Q

Primary motor cortex

A

Precentral sulcus
Initiating motor movements

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54
Q

Anterior to primary motor cortex

A

Premotor cortex (lateral)
Supplementary motor cortex (medial)

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55
Q

Premotor cortex

A

Planning and initiation of movements on the basis of past experience

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56
Q

Supplementary motor cortex

A

Regulation of posture by communicating the best position for each movement to the motor cortex

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57
Q

Frontal gyrus

A

Dominant (usually left) - Broca’s area (Brodmann 44 and 45)

Superior frontal gyrus has role in working memory

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58
Q

Parietal lobe - association somatosensory area (Brodmann 5 and 7)

A

Involved in recognising objected by touch.
Damage: tactile agnosia or asterognosis

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59
Q

Parietal lobe - right posterior non-dominant inferior parietal lobe

A

RIGHT: Distribution of attention to both sides of the body - esp angular gyrus
LEFT: seems to only pay attention to right side of the world

Damage: hemineglect

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60
Q

Parietal lobe - angular gyrus

A

Brodmann 39
Semantic processing
Number processing, work reading and comprehension
Memory retrieval, attention and spatial cognition
Reasoning and social cognitionS

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61
Q

Parietal lobe - supramarginal gyrus

A

Brodmann 40
Phonological processing

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62
Q

Parietal lobe - precuneus

A

Integrated tasks
Visuospatial mental imagery
Deliberate shifts of attention
Recollection of past episodes
Self-processing operations eg reflection

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63
Q

Superior temporal gyrus

A

Processing sound through primary auditory area in transverse temporal gyri (Heschl’s gyri), within lateral sulcus

Social cognition

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64
Q

Superior frontal gyrus

A

Picks up spatial arrangement of sounds of different frequencies from medial geniculate nucleus

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65
Q

Middle and inferior temporal gyri

A

Visual perception (inferior)
Language and semantic memory processing (middle)
Multisensory integration

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66
Q

Fusiform gyrus

A

In temporal lobe
Colour information
Face and body recognition
Word recognition
Number recognition
Within-category identification

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67
Q

Left fusiform gyrus lesion

A

word finding difficulty
semantic paraphrasias

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68
Q

Right or left fusiform lesion

A

Prosopagnosia

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69
Q

Primary visual cortex formed of

A

cortical aspects of cuneate and lingual gyri on each bank of calcarine fissure, known collectively as the striate cortex/calcarine cortex

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70
Q

Frontal eye fields located in

A

Precentral sulcus at caudal end of superior frontal gyrus and middle frontal gyrus

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71
Q

Frontal eye fields are responsible for

A

Voluntary saccadic eye movements

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72
Q

Primary auditory area located in

A

Heschl’s gyrus

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73
Q

Frontal lobe functions (10)

A

Motor movement
Executive function
Decision making
Working memory
Attention/concentration
Language (motor expression)
Inhibition
Personality/emotions
Social appropriateness
Saccadic eye movements

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74
Q

Gerstmann’s Syndrome

A

Lesions in left inferior parietal lobe around angular gyrus
- agraphia
- acalculia
- finger agnosia
- left right disorientation

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75
Q

Balint Syndrome

A

Bilateral damage to posterior parietal lobe
- optic ataxia
- ocular apraxia
-simultanagnosia

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76
Q

Parietal lobe functions (10)

A

Perception and processing of sensory information
Visuospatial processing
Praxis (dressing, constructional, ideomotor)
Somatognosia (awareness of own body)
Calculation ability
Reading
Writing
Naming
Left right orientation
Visual field

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77
Q

Temporal lobe functions (9)

A

Memory (working memory, encoding, retrieval, selective attention)
Deductive reasoning
Language comprehension
Auditory perception
Affective prosody
Music comprehension
Face recognition
Visual field processing (superior)
Olfactory perception

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78
Q

Kluver-Bucy Syndrome

A

Bilateral lesions of anterior temporal lobe, including amygdaloid nucleus.

Hyperorality
Placidity
Visual agnosia
Prosopagnosia
Psychic blindness
Indiscriminate hypersexuality
Hypermetamorphosis
Memory loss
Seizures

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79
Q

Occipital lobe functions

A

Perception of visual sensation

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80
Q

Anton-Babinski Syndrome

A

Injury of occipital lobe from stroke or brain injury

Denial of blindness (anosognosia) despite objective evidence of visual loss
Confabulation to fill in missing sensory input

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81
Q

Optic nerve lesions

A

Monocular visual loss

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82
Q

Optic chiasm lesion

A

Bitemporal hemianopia

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83
Q

Optic tract lesion

A

Homonymous hemianopia

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84
Q

LEFT Upper/lower Optic radiation lesion

A

Upper/lower (superior/inferior) left homonymous quadrantonopia (vice versa for right lesion)

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85
Q

Lesion of both optic radiations on one side

A

Homonymous hemianopia with central sparing

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86
Q

Functions of limbic system

A

Emotion processing
Encoding and retrieval of memory
Autonomic functions
Role in reward and addiction

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87
Q

Areas included in limbic system

A

CEREBRAL CORTEX: hippocampus, insular cortex, orbital frontal cortex, subcallosal gyrus, cingulate gyrus, parahippocampal gyrus (collectively the limbic lobe)

SUBCORTICAL STRUCTURES: olfactory bulb, hypothalamus, amygdala, septal nuclei, some thalamic nuclei including anterior nucleus and possibly the dorsomedial nucleus

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88
Q

Cingulate gyrus

A

Part of limbic system
Role in sensory, motor, visceral, emotional, motivation, memory and cognitive adaptability.

Posterior cingulate cortex: supporting autobiographical memories, future planning, focusing attention

Abnormalities seen in depression, schizophrenia, autism, ADHD, Alzheimers and ageing.

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89
Q

Parahippocampal gyrus

A

Part of limbic system.
General memory creation and recall, specific recollection of visual scenes.

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90
Q

Anterior part of parahippocampal gyrus includes

A

Perihinal and entorhinal cortices

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91
Q

Functions of hippocampus (3)

A

Declarative memory (encoding, retrieval)
Visuospatial orientation
Regulation of the hypothalamo-pituitary-adrenal axis

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92
Q

Amygdala functions

A

processing of emotions
acquisition and expression of fear conditioning

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93
Q

Nucleus accumbens

A

With ventral tegmental area, central link in reward circuit

Amount of dopamine in Na increases on frequent drug use, explaining drive to seek more

Over stimulation of its neurons leads to decreased number of dopamine receptors

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94
Q

4 subdivisions of the diencephalon

A

hypothalamus
subthalamic nucleus
epithalamus (habenula, habenular commissure, stria medullaris, pineal body)
thalamus

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95
Q

Role of the thalamus

A

Switchboard regulating and relaying the information to and from the brain

almost all sensory input and motor output goes via thalamus

plays a role in regulating sleep and wakefulness

spatial memory and spatial sensory data, crucial for episodic memory

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96
Q

Symptoms following thalamus lesions

A

Contralateral hemianesthesia
Hyperalgesia and causalgia
Contralateral homonymous hemianopia
Movement disorders

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97
Q

Wernicke-Korsakoff’s syndrome

A

Caused by thiamine deficiency
Malnutrition, alcohol dependence, prolonged diarrhoea

Acute: nystagmus, opthalmoplegia, mental confusion, ataxia

reversible if treated quickly, otherwise progresses into chronic Korsakoff’s syndrome - profound anterograde amnesia. may also be retrograde amnesia. confabulation.

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98
Q

Functions of hypothalamus (5)

A

Control of pituitary hormone release
Temperature regulation
Management of food and water intake
Sexual behaviour and reproduction
Mediation of the emotional response

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99
Q

3 main groups of white matter tracts

A

commissural fibres
association fibres
projection fibres

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100
Q

white matter tracts function

A

role in learning, cognition and psychiatric diseases

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101
Q

what is myelin

A

mixture of proteins and phospholipids that insulates the neuronal fibres

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102
Q

What do commissural / transverse fibres do

A

Connect the corresponding areas between two brain hemispheres

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103
Q

Examples of commissural/transverse fibres (5)

A

Transverse fibres of corpus callosum
Anterior commissure
Posterior commissure
Hippocampal commissure or commissure of fornix
Habenular commissure

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104
Q

Corpus callosum

A

Connects cortices of the 2 hemispheres
Divided into the rostrum, genu, body/trunk and splenium
Mainly myelinated axons

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105
Q

Course of the corpus callosum

A

Fibres of genu cure into frontal lobe: FORCEPS MINOR

Fibres of body and some of splenium extend laterlly as the RADIATION OF THE CORPUS CALLOSUM. Running across these are the INTERDIGITATE FIBRES OF CORONA RADIATA.

Fibres from the splenium run backwards into the occipital lobe forming the FORCEPS MAJOR.

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106
Q

Marchiafava-Bignami disease

A

Rare condition in chronic alcoholism
Demyelinating processes affecting the corpus callosum
Radiological diagnosis - clinical features variable and non-specific

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107
Q

Anterior commissure

A

In anterior wall of third ventricle at upper end of the lamina terminalis.

Key role in nociceptive sensation to contralateral side of brain in lateral spinothalamic tracts.

Contains decussating fibres form the olfactory tracts and connects tow amygdala and other parts of temporal lobe contributing to olfaction, memory, emotion, speech and hearing.

Implicated in sexual orientation.

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108
Q

Posterior commissure

A

Interconnects the pretectal nuclei, which in turn receive the afferents from the optic tract, mediating the consensual pupillary light reflect and taking the fibres to the Edinger Westphal nuclei of the occulomotor nerve

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109
Q

Association fibres

A

Connect regions within same hemisphere of the brain

Bundles include:
the cingulum
the superior longitudinal fasciculus and arcuate fasciculus
inferior longitudinal fasciculus
inferior frontooccipital fasciculus and uncinate fasciculus
fornix of the hippocampi

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110
Q

The cingulum

A

Forms the core of the cingulate gyrus
Connects regions of the frontal lobe, precuneus, posterior cingulate cortex, parahippocampal gyrus and the uncus of the temporal lobe

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111
Q

Superior longitudinal fasciculus

A

longest interhemispheric fibre tract
connects the frontal, parietal, temporal and occipital lobes

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112
Q

Arcuate fasciculus

A

most notable subdivision of superiod longitudinal fasciculus
Connects the caudal temporal cortex and inferior parietal cortex to locations in the frontal lobe and plays a major role in language use and comprehension

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113
Q

Uncinate fasciculus

A

Component of the inferior frontoccipital fasciculus connecting the middle, inferior and orbital frontal gyri to the anterior temporal pole and curving around the lateral sulcus

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114
Q

abnormalities in uncinate fasciculus

A

social anxiety
alzheimers
bipolar disorder
violent behaviour

affected in Phineas Gage

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115
Q

Projection fibres

A

connect the cerebral cortex with brainstem and spinal cord
both afferent and efferent

internal capsule is a concentration of projection fibres

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116
Q

internal capsule lesions - anterior limb

A

movement disorders (corticospinal or corticonuclear motor tracts)

somatosensory losses (thalamocortical projections)

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117
Q

internal capsule lesions - THE GENU

A

UMN deficits of cranial nerves especially VII and XII (corticobulbar tracts)

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118
Q

internal capsule lesions - POSTERIOR LIMB

A

contralateral hemiplegia affecting upper and lower extremities

hemianesthesia on same side as the weakness

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119
Q

GABAergic inhibitory parts of basal ganglia

A

striatopallidal -between striatum and globus pallidum

striatonigral - between striatum and SNr

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120
Q

dopaminergic mixed effect areas of basal ganglia

A

nigrostriatal - between substantia nigra and striatum

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121
Q

Role of basal ganglia

A

Enable practiced motor acts, gating the voluntary movements initiate din motor cortex and suppressing inappropriate motor commands.

Role in cognitive function, implicit memory tasks, executive and emotional programmes.

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122
Q

Psychiatric disorders with basal ganglia involvement

A

OCD - overactive caudate nucleus
ADHD - underactive caudate
Tourette syndrome - putamen
Athymhormic syndrome or PAP syndrome - cortico-striatal complex (lack of motivation and urgency)

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123
Q

Motor disorders affecting basal ganglia

A

Huntington’s disease and parkinsonism

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124
Q

Huntington’s disease

A

Hereditory, progressive neurodegenerative disorder
CAG expansion repeat - malformationof huntingtin protein

Neurophysical and neuropsychiatric disturbances

Personality and behaviour changes, mood changes, psychosis.

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125
Q

Parts of the brain stem

A

Medulla oblongata
Pons
Midbrain

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126
Q

Brain stem function

A

Regulates cardiac and respiratory functions
Key role in sleep cycle regulation
Maintaining consciousness
Assist with reticular formation

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127
Q

Midbrain - inferior colliculus

A

Received auditory impulses from the cochlear nuclei

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128
Q

Midbrain - superior colliculi

A

Received visual information from teh retina and the visual cortex, directing the movements of the eyes toward a visual, auditory or tactile signal

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129
Q

The red ucleus

A

High iron content, very vascular
Part of extrapyramidal system

Relays superior cerebral peduncle fibres
Transmits descending motor information from the cortex to spinal cord via corticorubrospinal tract and cranial nerves to coordinate muscle tone and body position

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130
Q

Substantia nigra

A

darker in colour - presence of melanin (by-product of dopamine)

Two parts:
- pars compacta - mainly dopaminergic neurons
- pars reticulata - maining GABAergic neurons

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131
Q

Cause of parkinson symptoms

A

Degeneration of the dopamine cells in the pars compacta of the substantia nigra, leading to depletion of dopamine in the nigrostriatal pathway

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132
Q

Pars divided into

A

Pontine tegmentum - dorsally
Basilar pons - ventrally

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133
Q

Reticular formation

A

Area in the brain stem

Regulates sleep wake cycle / consciousness
Filtering incoming information to differential irrelevant background stimuli

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134
Q

medulla oblongata roles (5)

A

Respiration - chemoreceptors
Heart function - sympathetic and parasympathetic
Vasomotor centres - baroreceptors
Digestion
Reflex centres of vomiting, coughing, sneezing, swallowing

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135
Q

Olfactory nerve

A

CN I
Smell

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136
Q

Optic nerve

A

CN II
Vision

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137
Q

Oculomotor nerve

A

CN III
Eye movements
sup/inf/med recture
inf oblique
levator palpabrae
pupillary constriction

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138
Q

Trochlear nerve

A

CN IV
Downward and medial movement of eye - sup oblique

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139
Q

Trigeminal nerve

A

CN V
General sensory sensation of face, scalp, oral and nasal cavity
Corneal reflex
Muscles of mastication

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140
Q

Abducens nerve

A

CN VI
Lateral movement of eyeball

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141
Q

Facial nerve

A

CN VII
Taste sensation of anterior 2/3 of tongue
Muscles of facial expression

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142
Q

Auditory / vistibulo

A

CN VIII
Hearing and proprioception of head and balance

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143
Q

Glosso-pharyngeal nerve

A

CN IX
General sensation of middle ear, pharynx and taste of posterior third of the tongue
Swallowing

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144
Q

Vagus nerve

A

CN X
General sensations of pharynx, larynx, oesophagus, external ear and viscera
Speech and swallowing
Control of GI, CVS and resp systems

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145
Q

Accessory nerve

A

CN XI
Movement of head and shoulders through trapezius and sternocleidomastoid muscle

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146
Q

Hypoglossal nerve

A

CN XII
Movement of tongue

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147
Q

Cerebellum

A

Fibre bundles: superior, middle and inferior cerebellar peduncles

Acts as a quality controlled, correcting errors - esp motor
Received info regarding proprioception and balance
Connections to and from the rest of the cortex

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148
Q

Anterior lobe of cerebellum

A

Receives proprioception information from muscles and joints about our position in space, information on muscle tone is relayed in the spinocerebellar tract

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149
Q

Posterior lobe of cerebellum

A

Received motor information from the cortex, which is processed and streamlined in the posterior lobe. it is then conveyed back to the thalamus and cerebral cortex

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150
Q

Flocculonodular lobe of cerebellum

A

receives information from the vestibular nuclei and coordinates balance

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151
Q

Vermis of cerebellum

A

Coordinates truncal musculature stability

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152
Q

Cerebellar symptoms

A

Dysmetria
Dysdiadokinesia
Hypotonia
Intention tremor
Scanning and staccato speech
Nystagmus
Ataxia
Pendular knee-jerk

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153
Q

Spinal cord functions (4)

A

Receiving multimodal sensory afferents from the body
Relaying descending motor efferents to the trunk and limbs
Integrating autonomic functions for most of the viscera, including bladder and bowel functions
Plays a vital role in maintaining muscle tone and initiating reflex movements

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154
Q

Spinal meninges layers (6)

A

Pia mater - innermost layer
Subarachnoid space - CSF here
Arachnoid mater - surrounds cord like a sheath
Subdural space - potential space between arachnoid and dura mater
Dura mater - outermost covering, tough and fibrous
Epidural space - separates dura mater from bone wall of vertebrae, contains fat, lymphatics and vasculature

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155
Q

Ascending spinal tracts

A

Carry info on pain, heat, touch and proprioception
Some reaches consciousness, some unconscious

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156
Q

Dorsal columns function

A

Proprioception, fine touch and vibration
IPSILATERAL

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157
Q

Spinothalamic tracts function

A

Pain, temperature, deep touch and pressure
CONTRALATERAL

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158
Q

Spinocerebellar tracts

A

Control of posture and coordination of movement
IPSILATERAL

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159
Q

Spino-olivary tract function

A

Unconscious proprioception and is involved in balance
CONTRALATERAL

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160
Q

Types of descending spinal tracts (5)

A

corticospinal
rubrospinal
tectospinal
vestivulospinal
reticulospinal

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161
Q

Corticospinal tracts function

A

voluntary, discrete, skilled movements

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162
Q

Rubrospinal tracts function

A

Affects the tone of the limb and fine hand movements
CONTRALATERAL

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163
Q

Tectospinal tracts function

A

Mediates movement of the head in response to visual stimuli
CONTRALATERAL

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164
Q

Vestibulospinal tract function

A

Control extensor muscle tone in the anti-gravity position
IPSILATERAL

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165
Q

Reticulospinal tract function

A

Influence voluntary movement, reflex activity and muscle tone
IPSILATERAL

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166
Q

5 parts of basal ganglia

A

caudate
putamen
globus pallidus
subthalamic nucleus
substantia nigra

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167
Q

is basal ganglia grey or white matter

A

grey

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168
Q

ventral division of basal ganglia

A

emotional behaviours
substantia innominata, nucleus accumbens, olfactory tubercle

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169
Q

dorsal division of basal ganglia

A

motor function
globus pallidus, caudate nucleus and putamen

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170
Q

Globus pallidus

A

Forms part of the lentiform nucleus with the putamen

two segments: medial (internal) and lateral (external)

Both segments contain ‘tonically active’ GABAergic inhibitory neurons, that can be decreased by striatum signals. This is part of the direct pathway of the basal ganglia.

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171
Q

subthalamus strokes/tumours

A

contralateral hemiballismus
continuous, repetitive involuntary movements
can cause significant disability
lack of muscle tone in affected limbs

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172
Q

how do antipsychotics cause EPSEs

A

block D2 receptors
substantia nigra

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173
Q

nucleus accumbens

A

‘limbic motor interface’ - flow of information from various limbic structures to areas associated with motor processing

part of reward system, linked with dopamine

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174
Q

Nucleus basalis of Meynert (nbM)

A

‘open’ nucleus with no distinct boundaries
contains large amounts of acetylcholine and choline acetyltransferase
deficiency of cholinergic neurons - dementia symptoms in Alz and PD

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175
Q

ventral tegmental area

A

part of reward circuit - high percentage of dopamine
within midbrain
parallel functions to the pars compacta of substantia nigra

implicated in influencing newly learned behaviour through a rewards process

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176
Q

skeletomotor circuit of basal ganglia

A

most strongly linked with motor dysfunctions
movement is expedited via the direct pathway when neurons from the ventrolateral thalamus are disinhibited

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177
Q

Three common attributes displayed by cerebral cortical neurons affected by the basal ganglia

A
  • receive +++ sensory input
  • react to motivational stimuli
  • part of premovement activities

Lesions in these cortical areas result in attentional deficits and defective movements

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178
Q

eye movement control

A

oculomotor circuit
superior colliculus - closely linked with basal ganglia

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179
Q

3 behavioural circuits linked with prefrontal cortex

A

executive dysfunction - dorsolateral prefrontal circuit

apathy - anterior cingulate circuit

disinhibition - orbitofrontal circuit

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180
Q

dorsolateral prefrontal circuit

A

EXECUTIVE DYSFUNCTION

> dorsolateral prefrontal
caudate nucleus
globus pallidus, substantia nigra
thalamus

PROBLEMS:
dysexecutive syndrome
unable to recall memories
lack of verbal and non-verbal fluency

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181
Q

anterior cingulate circuit

A

APATHY / MOTIVATION
> medial frontal cortex
> nucleus accumbens
> globus pallidus, substantia nigra
> thalamus

PROBLEMS:
extreme state of apathy - akinetic mutism
lack of mental or physical initiative
unresponsiveness

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182
Q

orbitofrontal circuit

A

DISINHIBITION
> orbitofrontal cortex
> caudate nucleus
> globus pallidus, substantia nigra
> thalamus

PROBLEMS:
Huntington’s disease
behavioural disinhibition
general irritability

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183
Q

conditions related to dorsolateral prefrontal cortex dysfunction

A

parkinsons
huntingtons
PSP
wilsons
neuroacanthocytosis

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184
Q

what does the limbic striatum ventral striatum consist of?

A

ventral putamen
ventromedial caudate
olfactory tubercle
nucleus accumbens

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185
Q

side effects of DBS for parkinsons (7)

A

cognitive defects - including verbal fluency
profound hypersexuality
mental confusion
extreme tiredness
loss of visual fields
memory damage

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186
Q

psychiatric manifestations of parkinsons disease (6)

A

cognitive impairment and dementia
depression
psychosis
impulsivity
pathological gambling

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187
Q

atypical parkinsonism (5)

A

tendency to fall over backwards
difficulty looking downwards or blurring/double vision
dystonia in torso and neck
dysarthria
cognitive impairment

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188
Q

PSP

A

usually starts in 50s
rapid deterioration
death within 5-10 years

apathy and disinhibition
bradykinesia
depression
personality and behaviour change
emotional lability
impaired judgement
deficits in learning ability

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189
Q

huntingtons disease pathology

A

neurodegenerative, AD disorder
CAG repeat expansion >35
deterioration and loss of function in caudate nucleus and striatum
further decline in frontal cortex and selective loss of GABAergic neurons

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190
Q

huntingtons features

A

onset usually between 35-50y
chorea
dystonia - rigidity and contracture
slow or abnormal eye movements
impaired gait, posture, balance
difficulty with speech or swallowing

plus psychiatric and personality changes

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191
Q

PANDAS

A

paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections

appears between 3y - puberty

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192
Q

OCD brain changes

A

hyperactivity of orbitofrontal cortex - increase projections from caudate nucleus
lowers thalamus inhibition, makes it hyperactive
this further intensifies orbitofrontal cortex hyperactivity

imbalance within the direct/indirect pathways - my be underlying cause for development of OCD

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193
Q

brain areas relevant to the dopamine pathways (8)

A

ventral tegmental area
nucleus accumbens
prefrontal cortex
substantia nigra
striatum
hypothalamus
pituitary
thalamus

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194
Q

brain areas relevant to serotonin pathways (9)

A

raphe nuclei
prefrontal cortex
thalamus
hypothalamus
amygdala
hippocampus
striatum
nucleus accumbens
cerebellum

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195
Q

brain areas relevant to the acetylcholine pathways (7)

A

brainstem
nucleus basalis of meynert
prefrontal cortex
thalamus
hypothalamus
amygdala
hippocampus

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196
Q

brain areas relevant to the histamine pathways (6)

A

tuberomammillary nucleus (in hypothalamus)
prefrontal cortex
thalamus
amygdala
hippocampus
striatum

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197
Q

brain areas relevant to the glutamate pathways (5)

A

prefrontal cortex
brainstem
striatum
nucleus accumbens
thalamus

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198
Q

brain area associated with compulsions

A

prefrontal cortex

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199
Q

4 major dopamine pathways

A

mesolimbic
mesocortical
nigrostriatal
tuberoinfundibular

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200
Q

mesolimbic dopamine pathway

A

VTE to NA
overactivity - psychosis
associated with motivation, pleasure, reward - addiction

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201
Q

mesocortical dopamine pathway

A

VTE to prefrontal cortex
hypoactivity - negative symptoms of Scz
cognition, executive function - dorsolateral prefrontal cortex
emotion and affect - ventromedial prefrontal cortex

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202
Q

nigrostriatal dopamine pathway

A

substantia nigra to striatum
hypoactivity - parkinsonism, akathisia, dystonia
overactivity - chorea, dyskinesias, ticks

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203
Q

tuberoinfundibular dopamine pathway

A

hypothalamus to anterior pituitary gland
hypoactivity - hyperprolactinaemia

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204
Q

thalamic dopamine pathway

A

from multiple brain regions to the thalamus

function unclear
?sleep and arousal

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205
Q

2 major noradrenaline pathways

A

ASCENDING: locus coeruleus to hypothalamus, thalamus, hypothalamus, amygdala, hippocampus and cerebellum
> regulates mood, arousal, cognition, sexual behaviour

DESCENDING: from brainstem down spinal cord
> regulates pain pathways

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206
Q

two major serotonin pathways

A

ASCENDING: raphe nuclei to, prefrontal cortex, thalamus, hypothalamus, amygdala, hippocampus, striatum, nucleus accumbens, cerebellum
> mood, anxiety, sleep, wakefulness

DESCENDING: brainstem down spinal cord
> pain pathways

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207
Q

two major acetylcholine pathways

A
  • pathway from the brainstem: arousal cognition, otehr functions
  • pathway from the basal forebrain: memory, implicated in Alzheimers
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208
Q

histamine pathway

A

from tuberomammillary nucleus to prefrontal cortex, thalamus, amygdala, hippocampus, striatum

regulates arousal, sleep, wakefulness

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209
Q

5 key glutamate pathways

A
  • cortical brainstem glutamate pathway: hypoactive in scz
  • corticostriatal glutamate pathway: emotion, impulsivity, compulsivity, motor
  • thalamocortical pathway: fails in scz and info goes back to cortex causing positive and neg sx
  • corticothalamic pathway: some sensory info to thalamus
  • cortico-cortical pathway: dysregulation in negative sx scz
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210
Q

dopamine pathway associated with positive sx of scz

A

mesolimbic

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211
Q

structure associated with alz

A

nucleus basalis of meynert

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212
Q

glutamate pathway that acts as a brake on mesolimbic dopamine pathway

A

cortical brainstem pathway

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213
Q

parts of a neuron

A

cell body/’soma’
dendrites
axon

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214
Q

what is the axon hillock

A

initial segment of the axon as it moves down from the soma

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215
Q

role of golgi apparatus in neuron

A

modifies, sorts and packages proteins (including neurotransmitters) for secretion

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216
Q

role of nissl substance in neuron

A

contains RER and ribosomes
site of protein synthesis

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217
Q

role of lysosomes in neuron

A

contain enzymes that break down cellular debris

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218
Q

role of microfilaments and tubules in neuron

A

provide structural support and transportation within the cell

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219
Q

how can neurons be classified

A

functional classification: sensory, motor or interneurons

structural classification: unipolar, bipolar or multipolar

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220
Q

sensory/afferent neurons

A

conduct nerve impulses to CNS
uni and bipolar neurons are sensory in function

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221
Q

motor/efferent neurons

A

convey impulses outwards from the brain
these are the largest neurons

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222
Q

interneurons / association neurons

A

found entirely within the CNS
enable communication between CNS and other neurons

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223
Q

glial cells

A

provide a supportive function in maintaining the action of neurons

smaller than neurons, lack axons and dendritesa

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224
Q

astrocytes (7)

A

derived from neural tube ectoderm
star shaped
largest of glial cells
aid BBB formation
structural support
repair processes
regulate oxidised K+ conc in extracellular fluid

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225
Q

gliosis/astrocytosis

A

when brain tissue is damaged, astrocytes proliferate and fill the gap by forming a dense network termed a glial scar

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226
Q

oligodendrocytes

A

derived from neural tube ectoderm
responsible for formation and maintenance of myelin sheath in CNS
mainly found in white matter

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227
Q

microglia

A

mesenchymal origin
primary immune cells of CNS
scavengers of the nervous system
aid phagocytosis

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228
Q

ependymal cell derived from…

A

neural tube ectoderm

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229
Q

columnar epithelial cells

A

line ventricles of brain and central canal of spinal cord
form specialised choroid plexus epithelium that secretes the CSF

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230
Q

schwann cells

A

from neural crest
myelination of PNS

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231
Q

satellite cells

A

from neural crest
provide supportive role

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232
Q

allocortex consists of

A

paleocortex: includes entorhinal cortex and piriform lobe

archicortex: consists of hippocampus

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233
Q

neocortex

A

more than 90% of cerebral cortex

two main cell types: pyramidal cells and stellate cells

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234
Q

fusiform cells

A

spindle shaped cells places at right angles to surface in deep layer of cortex

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235
Q

horizontal cells of Cajal

A

spindle shaped cells orientated horizontally in cortex

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236
Q

cells of Martinotti

A

small multipolar cells found in layers 3-6 of cortex
in almost all layers of the cortex

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237
Q

6 layers of the neocortex

A
  1. plexiform / molecular level
  2. outer granular level
  3. outer pyramidal level
  4. inner granular level
  5. inner granular level
  6. multiform cell level
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238
Q

pyramidal cells

A

75% of cortical neurons
principal output neurons
layers 2-5 of neocortex
largest pyramidal cells and Betz cells

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239
Q

Betz cells

A

largest pyramidal cells
in layer 5 of motor cortex

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240
Q

stellate cells

A

aka granular cells
star shaped, small, multipolar neurons
prominent in layer 6
main interneurons in neocortex - pass on signals between cells of the same region
short axons do not leave the cortex

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241
Q

spiny vs smooth stellate cells

A

spiny: excitatory
smooth: inhibitory

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242
Q

molecular / outermost layer of cortex

A

axons of granule cells
dendrites of Purkinje cells
stellate and basket cells

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243
Q

purkinje / middle layer of cortex

A

single layer or cell bodies of Purkinje cells
large neurons with a single axon extending deep into the cerebellum and multiple dendrites extending into the molecular level

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244
Q

granular / innermost layer of the cortex

A

contains granule cells, small neurons whose axons extend into the molecular layer, and golgi cells, types of interneurons

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245
Q

purkinje cells

A

uniquely found in cerebellum
only source of output from cerebellar cortex
type of inhibitory neuron, use GABA

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246
Q

granule cells

A

most numerous type of neuron in the cerebellum
only excitatory neurons in the cerebellum (use glutamate)
excite the purkinje cells via axonal branches called ‘mossy fibres’

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247
Q

inhibitory interneurons

A

stellate, basket and golgi cells

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248
Q

hippocampus layers

A

polymorphic layer - contains nerve fibres and small cell bodies of interneurons

pyramidal layer - contains hippocampal pyramidal cells

molecular layer - contains dendrites of the pyramidal cells

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249
Q

principle cells of the hippocampus

A

pyramidal cells

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250
Q

most abundant cell in the nervous system

A

glial cells

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251
Q

ependymal cells

A

epithelial cells that line the ventricles and cover the choroid plexus.
contribute to production and directional flow of CSF

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252
Q

nodes of ranvier

A

small gaps between sections of myelin sheath which allow passage of ions, so propagating the electrical signal

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253
Q

resting membrane potential

A

-60 to -75 mV

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254
Q

how is resting membrane potential sustained

A

selective permeability of cell membrane to K+ ions

at rest, K+ allowed to leak out of the neuron, leaving negative charge on inner surface of the membrane

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255
Q

how does depolarisation happen

A

Na channels open briefly in response to excitators NTs

lots of small depolarisations raise membrane potential by around 10mV - beyond AP

Na rushes in making more +ve charged up to 100mV, Na channels then close

triggers opening of L+ channels, allowing K+ out - this is repolarisation

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256
Q

refractory period

A

immediately after an AP, open K+ channels cause membrane potential to repolarise and briefly drop below resting potential to about -80mV

K+ then close, returning membrane to its resting potential

limits the rate at which neurons can fire, and prevents AP being propagated in the wrong direction

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257
Q

saltatory conduction

A

speed of AP propagation usually related to size of axon
bigger diameter, faster transmission

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258
Q

3 types of synapses

A

chemical
electrical
conjoint

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259
Q

chemical synapses

A

NT diffuses across synaptic cleft and binds to post-synaptic receptors
leads to change in permeability of the membrane

reuptake by active transport

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260
Q

electrical synapses

A

direct membranous contact between neurons
neuron directly influenced by voltage changes in the other

areas: retina, vestibular nucleus, nucleus of 5th cranial nurse

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261
Q

conjoint synapses

A

properties in common with chemical and electrical synapses
rarer

found in lateral vestibular nucleus

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262
Q

gap junctions

A

collections of protein channels in cell membranes allowing intercellular connections

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263
Q

enhaptic transmission

A

form of communication between cells in nervous system, different to electrical synapses

when electrical activity of one neuron alters the excitability of nearby neurons

retinal photoreceptors, olfactory system, between cardiac cells

264
Q

excitatory NTs (7)

A

acetylcholine
aspartate
dopamine
histamine
noradrenaline
adrenaline
glutamate

265
Q

inhibitory NTs (3)

A

GABA
serotonin
glycine

266
Q

monoamines

A

serotonin, dopamine, noradrenaline, adrenaline

267
Q

acetylcholine derived from

A

choline

268
Q

serotonin derived from

A

tryptophan

269
Q

dopamine derived from

A

tyrosine

270
Q

noradrenaline derived from

A

tyrosine

271
Q

adrenaline derived from

A

tyrosine

272
Q

GABA derived from

A

glutamate

273
Q

glutamate derived from

A

dietary

274
Q

histamine derived from

A

histadine

275
Q

ionotropic receptors mechanism

A

act immediately
last around 10-20ms
open transmembrane channel allowing passage of ions

276
Q

ionotropic receptor examples (5)

A

glutamate rec
NMDA rec
GABAa rec
5-HT3 rec
nicotinic rec

277
Q

metabotropic receptors mechanism

A

take up to 30ms to start
last up to around 1s
initiation of a metabolic change by stimulating the membrane bound G proteins via series of reaction, initiating the change in the cell

278
Q

metabotropic receptor examples (3)

A

dopamine D1-D5 rec
serotonin rec (except 5-HT3)
muscarinic M1-M3 rec

279
Q

D1 group of dopamine receptors

A

D1 and D5
GPCR
increase intracellular conc of cAMP

280
Q

D2 group dopamine recptors

A

D2, 3 and 4
GPCR
decreases intracellular conc of cAMP

281
Q

which of the serotonin recptors if NOT GPCR

A

5-HT3 - this is ligand gated ion channel receptor

282
Q

2 types of noradrenaline receptors

A

alpha (1 and 2)
beta (1 and 2)

all are GPCR

a1 and b1 are excitatory
a2 and b2 are inhibitory

283
Q

divisions of acetylcholine receptors

A

muscarinic - GPCR
nicotinic - ion channel rec

284
Q

neuromodulator

A

acts some distance from site of release, and/or has long lasting effects, and/or is released by glia

285
Q

neurotrophic factor

A

substance which promotes neuronal differentiation and survival

286
Q

amino acid examples (4)

A

glutamate
GABA
glycine
aspartate

287
Q

monoamine examples (6)

A

noradrenaline
adrenaline
dopamine
serotonin
melatonin
histamine

288
Q

Purine examples (2)

A

adenosine
ATP

289
Q

neuropeptide examples (2)

A

cholecystokinin
endorphins

290
Q

what ion causes NT release

A

calcium

291
Q

pregabalin MOA

A

inhibits some types of voltage gated calcium channels, reducing release of many types of NT

292
Q

gabapentin MOA

A

inhibits some types of voltage gated calcium channels, reducing release of many types of NT

293
Q

amphetamine MOA

A

displaces noradrenaline from vesicles. causes noradrenaline’s conc in nerve terminal to increase, causing its transporter to operate in reverse, allowing it out into the synaptic cleft

294
Q

enzyme involved in glutamate to GABA

A

glutamic acid decarboxylase

295
Q

levodopa MOA

A

increases the availability of precursors for dopamine synthesis

296
Q

moclobemide MOA

A

reversibly inhibits a key enzyme for the degradation of noradrenaline, dopamine and serotonin

297
Q

selegiline MOA

A

irreversibly inhibits a key enzyme for the degradation of dopamine

298
Q

MAOI cheese reaction

A

tyramine is a dietary amine
can trigger the release of noradrenaline

299
Q

enzyme for choline to acetylcholine

A

choline acetyltransferase

300
Q

enzyme that degrades acetylcholine to choline and acetate

A

acetylcholinesterase or butytylcholinesterase

301
Q

donepezil MOA

A

inhibits acetylcholinesterase only

302
Q

rivastigmine MOA

A

inhibits acetylcholinesterase and butyrylcholinesterase

303
Q

galantamine MOA

A

inhibits acetylcholinesterase and allosterically modulates nicotinic cholinergic receptors

304
Q

autoreceptors

A

presynaptic receptors on the same neuron that inhibit further NT release via negative feedback

305
Q

heteroreceptors

A

located on presynaptic receptor terminals and respond to neurochemicals released from other neurons

306
Q

tachyphylaxis

A

sudden decrease in the effects produced by a drug or substance that may occur during continuous use or continuous repeated administration

307
Q

noradrenaline metabolism

A

metabolised by MAO-A and COMT to VMA and MPHG

308
Q

serotonin metabolism

A

degraded by MAO-A to 5HIAA

309
Q

which serotonin receptor can have antimigraine effect when stimulated

A

5-HT1D

310
Q

which serotonin receptor can cause anxiety, agitation, insomnia and sexual dysfunction when stimulated?

A

5-HT2

311
Q

which serotonin receptor is associated with antipsychotic weight gain

A

5-HT2C

312
Q

which serotonin receptor when stimulated can cause nausea, diarrhoea and headache

A

5-HT3
ondansetron is a 5-HT3 antagonist

313
Q

which serotonin receptor is involve din circadian rhythm regulation

A

5-HT7

314
Q

nicotinic receptors

A

ionotropic
fast acting
excitatory
thalamus and cortex

315
Q

muscarinic (M1-M5) receptors

A

metabotropic
G-protein mediated
inhibitory or excitatory
medicate the anticholinergic effect of drugs

316
Q

GABA-A ion channel

A

5 subunits shaped like a rosette

binding sites for:
GABA
benzos
barbiturates
neurosteroids

317
Q

AMPA receptors

A

glutamate receptor subtype
mainly postsynaptic
ionotropic
fast excitatory neurotransmission

318
Q

kainate receptors

A

glutamate receptor subtype
ionotropic
mainly presynaptic
regulate release of glutamate
mainly found in hippocampus

319
Q

principle site of noradrenaline synthesis

A

locus coerulus

320
Q

principle site of serotonin release

A

raphe nucleus

321
Q

4 dopamine pathways

A

nigrostriatal
mesolimbic
mesocortical
tuberoinfundibular

322
Q

where does acetylcholine arise form in the brain

A

nucelus basalis of Meynert

323
Q

2 inhibitors NTs

A

GABA
glycine

324
Q

CRH

A

released in hypothalamus
stimulates noradrenergic activity
controlled by glucocorticoid and ACTH levels
reduced appetite and sexual drive
excess - depression, anxiety, addictions

325
Q

CCK

A

gut peptide also found in brain
implicated in anxiety and pain
may inhibit feeding

326
Q

substance P

A

found in sensory neurons, spinal cord and brain
associated with pain
implicated in depression

327
Q

3 opioid receptor subtypes

A

mu - analgesia, addiction, resp depression
kappa - dysphoria
delta - reinforcement

328
Q

corticosteroids secreted from

A

adrenal glands

329
Q

corticosteroid subdivisions

A

glucocorticoids
mineralocorticoids
sex hormones

330
Q

neuropeptide Y

A

involved in feeding behaviour and anxiety

331
Q

vasopressin

A

role in memory

332
Q

typical antipsychotic receptor action

A

antagonism of postsynaptic D2 receptors

333
Q

atypical antipsychotics receptor action

A

block D2 and 5HT2 receptors

334
Q

clozapine receptor action

A

higher affinity for D4 and D1 rec

335
Q

aripiprazole mechanism

A

5HT2A antagonist and partial 5HT1A receptor

336
Q

memantine mechanism

A

specific uncompetitive NMDA antagonist

337
Q

phencyclidine mechanism

A

NMDA antagonist

338
Q

acamprosate mechanism

A

GABA analogue, stimulates GABA inhibiting transmission

339
Q

what is white matter composed of

A

glial cells and myelinated axons

340
Q

imaging - DTI

A

form of MRI that uses diffusion of water molecules alone the length of the nerve bundles

facilitates the measurement, orientation and location of the white matter pathways

341
Q

functions of white matter pathways

A

higher aspects of motor functioning
visual perception and related functions
auditory information and related functions
language funtions
pain perception

342
Q

white matter pathways - association tracts

A

connect cortical areas within the same hemisphere

343
Q

white matter pathways - commissural tracts

A

connect cortical regions between the two hemispheres

344
Q

white matter pathways - projection tracts

A

bidirectional pathways arising the the cortex and terminating in the sub-cortical centres

345
Q

long association fibres

A

bidirectional connections through deep white matter

346
Q

short association fibres

A

for connections with nearby gyri
subcortical, referred to as ‘u fibres’

347
Q

largest white matter tract in the limbic system

A

cingulum

348
Q

corpus callosum function

A

integrates perceptual information both early and higher level cognitive processing

coordinates bimanual tasks and bilateral axial movements during learning stages

role in lateralisation or asymmetry of the brain

inhibitory and excitatory role over both hemispheres

349
Q

corpus callosum stroke

A

Left ideomotor apraxia
left hand anomia and left colour anomia
associative visual agnosia
left visual field dyslexia
left hand agraphia
right hand constructional apraxia
left hemispatial neglect
left motor neglect
callosal alien hand syndrome
delay in visuomotor responses
optic ataxia

350
Q

lateral pain system

A

S1 and S2
arising from lateral thalamus
discriminates the location and intensity of painful stimuli

351
Q

medial pain system (ACC)

A

arises from medial thalamus
mediated affective cognitive-evaluative (psychological) component of the stimulus

352
Q

ascending pain pathway

A

pain signals travel via contralateral spinothalamic tract to medulla and brainstem

353
Q

type 1 delta fibres

A

fast adapting
high threshold for activity

354
Q

type 2 delta fibres

A

slow adapting
low threshold for activity

355
Q

C pain fibres

A

unmyelinated
slow conducting
burning sensation

356
Q

descending pain pathways

A

limbic cortical areas plus autonomic information from the brainstem

357
Q

most common dementia

A

alzheimers 62%

358
Q

cortical dementia 4 A’s

A

amnesia
aphasia
apraxia
agnosia

359
Q

subcortical dementia sx

A

bradyphrenia
frontal executive dysfunction
personality/mood changes

360
Q

tauopathies (5)

A

picks disease
corticobasal degeneration (CBD)
PSP
MAPT
multiple system atrophy (MSA)

361
Q

synucleinopathies (4)

A

lewy body dementia
parkinsons dementia
pure autonomic failure (PDD)
pure autonomic failure (PAF)
various subtypes of MSA

361
Q

ubiquitinopathies (3)

A

FTLD-TDP
FTDP-17 (PGRN)
PTLD-FUS

362
Q

gross anatomical features of alzheimers

A

generalised brain atrophy
focal atrophy of medial temporal lobe
dilatation of lateral ventricles

363
Q

stains for senile plaques

A

silver
congo red
thioflavin S

363
Q

histopathological features of alzheimers

A

senile/neuritic plaques - beta amyloid

neurofibrillary tangles - hyperphosphorylated tau

364
Q

what is amyloid precursor protein (APP) cleaved by

A

initially - beta secretase
then - gamma secretase

365
Q

hirano bodies seen in

A

alzheimers
FTLD
CJD

366
Q

3 stages of alzheimers NIA-AA criteria

A

preclinical
mild cognitive impairment
dementia

367
Q

what does CERAD criteria for Alz use

A

neuropathological and clinical components
uses senile plaques
definite/probable/possible/normal

368
Q

braak and braak staging system of Alz

A

purely neuropathological criterion

369
Q

multi infarct dementia

A

series of tiny strokes

370
Q

SVD with dementia

A

pathology in small arteries, arterioles, capillaries, venules

371
Q

strategic infarct dementia

A

single ischaemic lesion affecting parts of the brain invovled in cognition and behaviour

372
Q

Binswanger’s disease

A

subcortical arteriosclerotic leukoencephalopathy
deep white matter damaged due to arteriosclerosis

373
Q

cerebral amyloid angiopathy (CAA)

A

presence of beta amyloid in middle and outer layers of small and medium arteries in the brain

373
Q

CADASIL

A

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

most common genetic form for vascular dementia

AD mutations of notch 3 gene on Ch 19

374
Q

hypoperfusive dementia

A

ischaemic hypoxic dementia
hypotension and hypoperdusion

watershed zones, wedge shaped

related to COPD and surgical procedures

375
Q

haemorrhagic dementia

A

bleed in the brain
SAH, subdural

376
Q

common causes of CVD

A

atherosclerosis
arteriosclerosis
hypertensive arteriopathy
CAA

377
Q

histopathology of FTLD

A

tauopathies
ubiquitinopathies

378
Q

gross anatomical features of FTLD

A

atrophy of frontal and temporal lobes

379
Q

FTLD tauopathies (5)

A

Picks disease
corticobasal degeneration (CBD)
PSP
FTDP-17 (MAPT)
MSA

380
Q

FTLD ubiquitinopathies (3)

A

FTLD-TDP
FTDP-17 (PGRN)
FTLD-FUS

381
Q

picks disease gross anatomical features

A

knife blade atrophy

382
Q

histopathological features of picks disease (5)

A

pick bodies
pick cells

neuronal loss
gliosis
microvacuolation

383
Q

pick bodies

A

cytoplasmic neuronal inclusions
contain tau

384
Q

histopathological features of lewy body dementia

A

lewy neurites
cortical senile plaques
gliosis
loss of neurons in substantia nigra - depigmentation

385
Q

pick cells

A

swollen neurons with eccentrically displaced nuclei
‘ballooned’ neurons

386
Q

EEQ delta wave

A

<4 Hz
prominent during sleep, not waking adults
frontal - adults
posterior - children

387
Q

EEG theta wave

A

4-8 Hz
any age, usually during sleep
common in children to age 13
abnormal in waking adults

388
Q

EEG alpha wave

A

8-13 Hz
all ages, most commonly adults
diminish with concentration/focus

389
Q

EEG beta wave

A

14-40 Hz
all ages
usually anterior
drugs - barbituates, benzos

390
Q

EEG gamma wave

A

> 40 Hz
disappear during anaesthesia

391
Q

EEG - evoked responses/potentials

A

measure the electrophysiological response to various stimuli

  • visual evoked potential
  • brainstem auditory evoked potential
  • somatosensory evoked potential
392
Q

West syndrome

A

infantile spasms
developmental retardation
hypsarrhythmia
typically presents between 6-18 months

393
Q

childhood absence epilepsy - EEG

A

3Hz generalised spike and wave discharged with normal background for age

394
Q

Lennox Gestaut Syndrome

A

childhood epileptic encephalopathy
onset 3-5 y
atonic, tonic and atypical absense seizures
LD
slow background activity and diffuse slow spike and wave <2.5Hz

395
Q

encephalopathies EEG

A

diffuse generalised abnormal patterns

396
Q

hepatic encephalopathy EEG

A

bifrontal triphasic waves
positive sharp waves followed by negative waves with relatively low amplitude

397
Q

subacute sclerosing panencephalitis (SSPE) EEG

A

periodic complexes appear bilaterally symmetrical and synchronous between hemispheres
high voltage polyphasic stereotyped delta waves

398
Q

herpes encephalitis EEG

A

generalised slowing
fronto temporal predominance
discharges high amplitude

399
Q

HIV EEG

A

mild EEG slowing

400
Q

CJD EEG

A

predominantly anterior
frequency 0.5-2/sec
stop in sleep
low voltage slowing

401
Q

REM sleep EEG

A

fast, low voltage activity

402
Q

NREM sleep EEG

A

Stage 1 - mixed frequencies
Stage 2 - sleep spindles, K complexed, reduced prominence of slow waves
Stage 3 - delta, frontal predominence, sleep spindles, vertex waves, k complexes
Stage 4 - slow delta, frontal predominance

403
Q

narcolepsy

A

shortened REM latency

404
Q

lewy body EEG

A

significant slowing

405
Q

EEG schizophrenia

A

70% normal
abnormalities in catatonic scz

406
Q

EEG affective disorders

A

mostly normal
bipolar - generalised increased delta and theta, decreased alpha

407
Q

EEG anxiety disorders

A

low voltages
diminished alpha
increased beta

408
Q

EEG personality disorders

A

increased cortical slow activity in violent offenders / antisocial

409
Q

EEG lithium

A

may produce marked slow wave changes even at therapeutic levels

410
Q

Sylvian fissure

A

separates temporal lobe from frontal and parietal lobes
aka lateral sulcus

411
Q

Insula

A

cerebral cortex covering the sylvian fissure
role in production of speech, processing social emotions, pain, temp, taste, olfaction, auditory, vestibular and visceral perceptions

role in additction

receives afferent fibres from sensory thalamic nuclei

link with schizophrenia, FTD

412
Q

fusiform gyrus

A

on inferior surface of temporal and occipital lobes

facial recognition - impairment causes prosopagnosia

413
Q

parahippocampal gyrus

A

anterior part includes entorhinal and perihinal cortices

role in encoding and retrieving memories

414
Q

anterior cingulate cortex (ACC)

A

surrounds anterior corpus callosum
role in regulation of emotions, impulse control, motivation, decision making and reward anticipation
regulatory role in autonomic functions eg BP and HR

dorsal - cognitive
central - emotional

415
Q

error detection in the brain

A

ACC plays a role
directs attention to task related stimuli
responsible for managing responses to conflicting stimuli

ACC function tested by stroop test

affected in depression, and schizophrenia, OCD, social anxiety

extreme damage to ACC - akinetic mutism

416
Q

spindle neurons / von economo neurons

A

in frontal insula, anterior cingulate cortex and dorsolateral prefrontal cortex

process of transforming feelings into actions

faster than other types of neurons
social emotions across the whole brain

begin to form at 4m, but work in 2nd year of life (shame, anger, guilt)

417
Q

area of ACC in neuromodulatory treatment in treatment resistant depression

A

anterior subgenual cingulate area (Cg25)

overactive in treatment resistant depression
DBS can target this area

418
Q

role of hippocampus

A

encoding, storing and retrieving memories
declarative memory

damage - anterograde amnesia and recent retrograde amnesia

418
Q

entorhinal cortex

A

primary olfactory cortex
4 cellular layers

role in formation of declarative and spatial memories
memory consolidation and optimisation take place during sleep here

one of first structures affected by alzheimers - loss of volume
degeneration seen in temporal lobe epilepsy

418
Q

subiculum role

A

retrieval of newly learned information

role in initiation and maintenance of temporal lobe seizures

418
Q

uncus

A

covered with olfactory cortex
link with temporal love epilepsy - olfactory and gustatory hallucinations preceding seizures

can get uncal herniation due to mass effect - emergency decompression

418
Q

third cranial nerve palsy

A

eye down and out
part of uncal herniation

419
Q

dentate gyrus

A

neurogenesis takes place
role in formation of new memories, spatial orientation and addiction

420
Q

role of limbic system

A

fear, motivation, anger, memory, pleasure
‘old brain’ - functions for survival
impact on endocrine and PNS

421
Q

amygdala

A

integrative role between emotions and motivation
combine external and internal stimuli

modulates reactions to events that are essential for survival
related to fear and fear conditioning

422
Q

Urbach-Wiethe

A

gradual destruction of amygdala from early life due to calcium deposition

absence of fear, but other emotions (anger, sadness, happiness, disgust) are present

lose ability to recognise facial expressions of fear

423
Q

short fear pathway

A

thalamus-amygdala with omission of the cortex
instantaneous
value for survival
response even to subliminally perceived threat
results in secretion of norepinephrine, acetylcholine, dopamine and serotonin in the brain, and adrenalin and cortisol in the body
autonomic changes for flight/fight

424
Q

long fear pathway

A

thalamus-cortex-amygdala
guides perceptual search of environment to establish the cause of the aroused state

425
Q

mammillary bodies

A

round structures at end of anterior fornix pillars
role in autobiographical memories
damaged by thiamine deficiency - Korsakoffs

426
Q

left sided temporal lobe lesions

A

impaired repetition of words
impaired recognition of words and loss of comprehension
impaired memory of verbal material

426
Q

components of papez circuit

A

hippocampal formation
mammillary bodies
anterior thalamus
cingulate cortex
parahippocampal gyrus
hippocampal formation

426
Q

right sided temporal lobe lesions

A

decreased recognition of tonal sequences and musical abilities
loss of inhibition when talking
impaired recall of non-verbal material such as much or drawings

427
Q

8 principles of functional impairment in temporal lobe lesions

A

auditory sensation and perception
visual perception
selective attention
catergorisation of verbal material
language comprehension
long and short term memory
personality changes
altered sexual behaviour

428
Q

complex partial temporal lobe lesions

A

focal seizures - absence attacks
automatism - purposeless behaviour
olfactory and complex visual and auditory hallucinations
disturbances of mood and memory - deja vu

429
Q

presentation of limbic encephalitis

A

headache, low grade fever, flu sx
agitation, disinhibition
auditory and visual hallucinations
STM loss, concentration difficulties
epileptic seizures or dyskinesia
autonomic instability
association with neoplastic illness, eg ovarian teratomas

430
Q

Kluver-Bucy syndrome

A

hyperorality
sexual disinhibition
visual agnosia
loss of fear
apathy
amnesia
aphasia

431
Q

hippocampus changes early stages of psychosis

A

volume decrease

432
Q

unmedicated depression amygdala change

A

volume loss

433
Q

tests to assess temporal lobe

A

semantic memory
short term memory
visual function
visual fields
auditory functions
language functions

stroop effect test
rey-osterrieth complex figure test
mooney closure test
wechsler memore scale

434
Q

when does brain development start

A

week 3 in utero

435
Q

endoderm

A

gastro and resp systems

436
Q

ectoderm

A

epidermal ectoderm - skin, nails, sweat glands
neuroectoderm - brain, CNS

437
Q

prosencephalon

A

forebrain

gives rise to telencephalon (cerebral hemisphere) and diencephalon (thalamic structures)

438
Q

mesencephalon

A

midbrain

439
Q

rhombencephalon

A

hindbrain

440
Q

3 main modes of neuronal migration

A

radial migration
tangential migration
multipolar migration

441
Q

when does myelination start and finish

A

begins 5m in utero
complete around 20y

442
Q

optimum language learning for phonemes

A

6-12 m

443
Q

factors that influence brain plasticity (8)

A

genetic predisposition
experience (pre and post natal)
hormones
psychoactive drugs
dietary factors
aging
stress
brain injury or disease

444
Q

Bucharest early intervention project

A

studied impact of institutionalisation
- institutionalised form birth
- institutionalised at birth then foster
- never institutionalised

significant effect on brain development
ADHD, ODD
foster care helped with emotional difficulties

445
Q

anencephaly

A

neural tube fails to close
breakdown in tissue
incomplete skulls, large parts of brain missing
rise from Zika virus

446
Q

encephalocele

A

part of brain and membranes herniate through opening in skull, usually at back of neck

447
Q

lissencephaly

A

smooth brain
limited/absent sulci and gyri
causes - infection, ischarmia, chromosome abnormalities

448
Q

heterotopias

A

clumps of grey matter in wrong part of brain
cause seizures

449
Q

schizencephaly

A

abnormal neuronal migration results in clefts in the brain, lined with grey matter and filled with CSF

450
Q

complex neurodevelopmental disrders

A

due to combination of genetic, environmental and epigenetic factors

eg autism, schizophrenia, ADHD, epilepsy

451
Q

schizophrenia risk factors

A

genetic vulnerability
environmental
maternal - diabetes, preeclampsia
prenatal - rhesus, maternal malnutrition, infectious exposure
obstetric - hypoxia, low birth wt, pre-term, brain injury
childhood - drugs, trauma
other - urban birth, winter birth, migration, older paternal age

452
Q

Schizophrenia genetic factors

A

COMT
Dysbindin
Neuregulin

453
Q

schizophrenia structural brain changes

A

reduced cerebral volume
increased ventricle size
reduced amygdala and hippocampal volume

454
Q

anterolateral / spinothalamic tract

A

crude touch
pain and temperature

455
Q

ASD characterised by impairment in… (3)

A

receptive or expressive language as used in social communication
development of selective or reciprocal social interaction
functional or symbolic play

456
Q

brain areas involved in ASD

A

fusiform gyrus - hypoactivation
amygdala
insula - hypoactivation right AI
frontoinsular and cingulate cortex - von economo neurons
prefrontal cortex
cerebellum

456
Q

dorsal / posterior column tract

A

vibration
tactile discrimination / fine touch
proprioception

457
Q

ipsilateral spinocerebellar tracts

A

muscle and tendon positions

457
Q

alpha beta fibres - pain

A

large diameter
highly myelinated
fast conduction
low activation threshold
light touch, non-noxious

458
Q

c fibres - pain

A

smallest diameter
unmyelinated
slower conduction
high activation threshold
slow, diffuse, dull pain
temperature

release combination of glutamate and substance P

458
Q

alpha delta fibres - pain

A

small diameter
thinly myelinated
medium conduction velocity
high and low activation thresholds
rapid, sharp, localised pain

release glutamate

459
Q

pyramidal / corticospinal tract

A

control of voluntary movement

460
Q

extrapyramidal tracts

A

involuntary reflects, movement and coordination

461
Q

reticulospinal tract

A

controls somatic and visceral motor function

462
Q

extrapyramidal tracts

A

reticulospinal, vestibulospinal, rubrospinal, tectospinal
control of involuntary movements and reflexes
coordination
indirect innervation of motor neurons

462
Q

Brown-Sequard syndrome

A

hemi section injury to the spinal cord
loss of ipsilateral proprioception and 2 point discrimination
loss of contralateral temp and pain sensation
ipsilateral pyramidal signs causing spastic paralysis below lesion and abnormal reflexes

463
Q

pyramidal tracts

A

corticospinal and corticobulbar
voluntary postural and fine movement
direct innervation of motor neurons

463
Q

subacute combined degeneration of the spinal cord

A

vit B12 deficiency
absent ankle jerk and upgoing planters
muscle weakness that could become spastic
clumsiness, unsteady gait, depression, psychosis and progression to dementia if untreated

464
Q

parts of basal ganglia (6)

A

corpus striatum
claustrum
nucleus accumbens
septi and olfactory tubercle
substantia nigra
subthalamic nucleus

465
Q

where is melanin produced

A

pineal gland

466
Q

UMN deficits (4)

A

hypertonia
spastic paralysis
hyper-reflexia
extensor (Babinski sign) plantar reflexes

467
Q

LMN deficit (7)

A

hypotonia
flaccid paralysis
hypo-reflexia
flexor plantar reflexes
muscle wasting
fasciculation
fibrillation

468
Q

role of limbic system (4)

A

memory
emotional and behavioural expression
motivation
olfaction

469
Q

dorsolateral prefrontal cortex function

A

allows the organisation of information to facilitate response in major executive fuctions

470
Q

anterior cingulate function

A

has a role in motivating behaviour

471
Q

orbitofrontal lobe function

A

integration of limbic and emotional information into behavioural responses

472
Q

features of damage to dorsolateral prefrontal cortex (6)

A

poor planning
impaired concentration/attention, affecting working memory
perseveration and impersistence
deficits in set shifting
motor programming disturbances
concrete thinking and poor judgement

473
Q

bilateral medial temporal lobe lesions

A

profound global amnesia
problems with learning verbal material when lesions on dominant side
problems with learning non-verbal material when lesions on non-dominant side

474
Q

satiety centre

A

ventromedial hypothalamus

475
Q

circadian pacemaker

A

suprachiasmatic nucleus (SCN)

476
Q

ghrelin

A

fast acting orexigenic hormone
helps us start a meal
secreted mainly peripherally by the gut

477
Q

leptin

A

secreted by adipose tissue
long acting anorexigenic
suppress appetite

477
Q

cholecystokinin

A

induce satiety in combination with pancreatic glucagon and the hypothalamus

478
Q

mirror neurons

A

discovered by rizzolatti
prefrontal cortex
activated when performing a task and when observing others doing it
may mirror physical actions as well as emotions

479
Q

amygdala - aggression and placidity

A

stimulation - aggression
destroyed - placidity

480
Q

ASD and amygdala

A

hypoactivation of amygdala while attempting to make social inferences

481
Q

postpartum mood disorder treatment options

A

antidepressants eg fluoxetine, sertraline, nortriptyline
CBT
interpersonal therapy

481
Q

PMS treatment

A

SSRIs - either regular or anticipated and stopped several days into menstrual flow

482
Q

postpartum psychosis onset

A

abrupt onset usually within 2 weeks of delivery

482
Q

differentiating postpartum depression from baby blues

A

later onset (several weeks postpartum)
longer duration (months)
absence of labile mood
patients with postpartum blues can go on to develop postpartum depression

483
Q

where is TRH released from

A

hypothalamus

483
Q

hyperthyroidism treatment

A

anti-thyroid drugs
occasionally psychotropic medication may be needed

483
Q

Graves disease

A

Hyperthyroidism:
irritability
sweating
anxiety
exophthalmos
ophthalmoplefia
goitre
tachycardia
AF
thirst
D+V
tremor
stiffness
palmar erythema
proximal muscle wasting
heat intolerance
fatigue
weight loss
oligomenorrhoea

484
Q

anterior pituitary hormones (6)

A

TSH
ACTH
LH
FSH
GH
prolactin

485
Q

primary hypothyroidism causes

A

90% hashimotos thyroiditis
medication - lithium, amiodarone

486
Q

secondary hypothyroidism causes

A

tumours or infarction of the pituitary gland

487
Q

tertiary hypothyroidism causes

A

tumours or infarctions of the hypothalamus
carbamazepine

488
Q

hypothyroidism features

A

slow reflexes
dry skin
cold hands
bradycardia
depression
tired
feel cold
weight gain
menorrhagia
constipation
impaired memory

489
Q

congenital hypothyroidism

A

1:2000-4000 births
commonest cause is iodine deficiency
heel prick test after birth
untreated - learning disability

490
Q

adrenal cortex hormones (4)

A

steroid hormones
glucocorticoid (cortisol)
mineralocorticoid (aldosterone)
sex steroids (androgens)

491
Q

hormones secreted by adrenal medulla (3)

A

catecholamines
adrenaline
noradrenaline

492
Q

changes to HPA function in depression

A

increased CRH in CSF
failure to suppress cortisol in response to dexamethasone
increased adrenal size and sensitivity to corticotropin or ACTH
blunted ACTH response to CRH

492
Q

causes of cushings syndrome

A

exogenous steroid exposure
long term steroid use
endogenous over production of steroids (pituitary adenomas, adrenal adenoma/carcinoma, ectopic ACTH production, SCLC or bronchial tumours)

493
Q

Cushing’s syndrome

A

S+S occur due to sustained hypercortisolaemia of any cause

493
Q

Cushing’s disease

A

hypercortisolaemia occurs due to ACTH-secreting pituitary adenoma

494
Q

Cushing’s syndrome symptoms

A

facial fullness
hirsuitism
acne
buffalo hump
cardiac hypertrophy
hypertension
purple striae
central obesity
skin atrophy
peripheral oedema
osteoporosis
anxiety withdrawal
fatigue
mania and psychosis

495
Q

Tests for cushings syndrome

A

24 hour urinary free cortisol
overnight low dose dex supp test
salivary cortisol measurement

496
Q

cushings syndrome treatment

A

depends on cause
reduce steroid dose if taking
tumour resection
symptomatic treatment

497
Q

Addison’s disease

A

primary adrenal insufficiency
deficiency in cortisol, aldosterone and adrenal androgens

autoimmune commonest cause in western countries

autoantibodies directed against 21-hydroxylase enzyme

498
Q

features of hypoadrenalism

A

weight loss
vitiligo
hyperpigmentation of palmar creases and buccal mucosa
orthostatic hypotension
low body temp
weakness and fatigue
GI symptoms
anorexia
muscle, joint, abdo pain
postural dizziness
salt craving
intolerance to cold
loss of libido
dry skin
loss of axillary and pubic hair
depression
memory impairment
psychosis (rare)

499
Q

acute primary adrenal failure / adrenal crisis features

A

orthostatic hypotension
confusion
fever
hypoglycaemia
circulatory collapse

500
Q

diagnostic test for addisons

A

synacthen test

501
Q

treatment for adrenal insufficiency

A

large volume NaCl and 5% dextrose
replace glucocorticoids with parenteral hydrocortisone or dexamethasone

502
Q

pineal gland functions

A

sleep wake cycle
feeding
body temp

503
Q

suprachiasmatic nucleus

A

‘internal clock’

504
Q

circadian rhythm sleep disorder

A

mismatch between requirements for sleep and bodys internal clock
eg social demands not synchronised with circadian rhythm, eg jet lag, shift work
change in circadian rhythm eg delayed sleep phase syndrome

synthetic melatonin helps reset biological clock

505
Q

seasonal affective disorder

A

clear seasonal pattern
NICE - treatment same as depression
?preventative antidepressants
limited evidence on light therapy

506
Q

Klinefelter presentation

A

47 XXY

tall stature
mild-mod LD
reduced facial hair
gynaecomastic
obesity
small testes
erectile dysfunction
osteoporosis

507
Q

Turner Syndrome

A

45 X or XO

short stature
low set ears
micrognathia
webbed neck
high arched palate
coarctation of aorta
primary hypothyroidism
shield chest
widely spaced nipples
congenital renal abnormalities
peripheral lymhpoedema
cubitus valgus

508
Q

hyperprolactinaemia

A

sulpride, risperidone, typical antipsychotics

reduced libido
amenorrhoea
galactorrhoea
gynaecomastia

509
Q

long term effects of hyperprolactinaemia

A

reduced bone density
possible increased risk of thromboembolism
possible increase in risk of breast cancer

510
Q

CATIE

A

examined effectiveness of different antipsychotic medications in over 1400 pts with Scz and included physical health indicators

metabolic syndrome in >40% of pts
diabetes in 11%

510
Q

GH deficiency symptoms

A

weakness and fatigue
sensitivity to cold
loss of libido
decreased bone density
increased fracture risk
loss of pubic and axillary hair
amenorrhoea - females
impotence - males

depression with irritability
anergia, dullness, drowsiness
apathy
self neglect
memory impairment

511
Q

strategies to improve memory encoding

A

chunking
mnemonics
imagery
primacy-recency effects

512
Q

length of iconic memory

A

0.5 seconds

512
Q

length of echoic memory

A

2 seconds

513
Q

STM capacity

A

7 +/- 2 digit span

514
Q

what is chunking

A

combining units of information into chunks

515
Q

what is the brown peterson technique?

A

overcomes maintenance rehearsal
hear groups of 3 letters eg S-T-B
asked to repeat what they just heard, then count backwards

recall better with short delays in comparison to longer delays - STM without rehearsal is short lived

516
Q

what is non-declarative memory

A

cant be accessed consciously

517
Q

modes of retrieval

A

recognition - navigating familiar routes
recall - actively searching memory stores
reintegration/reconstruction - however in this mode become distorted, elaborated on, falsified

518
Q

memory - central executive

A

responsible for higher cognitive processes
eg planning, problem solving

DORSOLATERAL PREFRONTAL LOBE

capacity limited but modality free
important for dual task performance
part of attention system
‘in charge’ of slave systems - phonological loop and VSSP

519
Q

4 main components of working memory

A

central executive - represents attention
phonological loop - speech based info held
visuospatial sketchpad - codes visual and spatial info
episodic buffer - holds and integrates info from phonologicla loops, visuospatial sketchpad and LTM

520
Q

what brain area is phonological loop associated with?

A

dominant parieto-occipital hemisphere

521
Q

about phonological loop

A

codes acoustically (sounds)
verbal rehearsal loop
composed of phonological store and articulatory control process that feed back into the store (silent rehearsal)
causes memory traces to fade after about 2 seconds

522
Q

which brain area is visuospatial sketch pad associated with?

A

non-dominant parieto-occipital regions

523
Q

about visuospatial sketchpad

A

eg map reading and navigation

spatial component and visual component

524
Q

episodic buffer - memory

A

acts as backup store, communicating with components of WM and LTM
multimodal store of limited capacity

thought to use chunking

525
Q

how to assess working memory

A

digit span

526
Q

causes of working memory deficit / reduced digit span

A

phonological loop damage - injury to left hemisphere leads to difficulties with word and sentence repetition and reduced digit span

dorsolateral PFC injury - lesser degree

527
Q

recency effect and primacy effect

A

recency: words at end of list recalled first

primacy: words at beginning recalled better than middle

528
Q

episodic memory

A

autobiographical in nature
details about time and place
includes flashbulb memories
bilateral limbic system and temporal lobe

529
Q

semantic memory

A

factual knowledge
derived from episodic memory
SM stored conceptually, without reference to time and context in which info was acquired
expands throughout our lives

530
Q

examples of non-declarative memory

A

complex motor skills - surfing
priming
classical conditioning

531
Q

schema theory

A

Bartlett proposed that memory is determined by
- material presented with previous experience
- knowledge an individual may already have

theory argues that previous knowledge is stored as schemas, and the schemas play a role in how we represent and organise new knowledge in memory

532
Q

schema theory: accretion

A

a new example of a pre-existing schema is recorded, and added to the relevant schema in LTM

533
Q

schema theory: tuning

A

new information allows for changes to existing schema if they are not sufficient

534
Q

schema theory: restructuring

A

a new schema is formed, using information from a pre-existing schema

535
Q

forgetting curve

A

ebbinhaus curve

sharp drop over first 9 hours, rate of forgetting then slows and declines little thereafter

536
Q

forgetting: decay theory

A

structural change occurs in the brain when something is learned and remembered. with time, the engram is destroyed by metabolic process, though with repetition and rehearsal it can be preserved.

passage of time responsible for forgetting. a study disproved this showing that recall improved with sleep.

537
Q

forgetting: displacement theory

A

based on experimental evidence showing that once a memory system has reached capacity, old information is displaced by new information.

it explains forgetting in a limited-capacity system such as STM

538
Q

forgetting: interference theory

A

events that occur before and after learning are thought to influence forgetting

retroactive interference = recall of earlier learning affected by later learning

proactive interference = recall of later learning affected by earlier learning

strong evidence for these theories exists from laboratory studies but there is less ‘real world’ evidence

538
Q

forgetting: motivated forgetting (repression)

A

‘unconscious forgetting of painful memories in order to protect the psyche’ - Casey et al, 2009

539
Q

cure-dependent forgetting

A

Tulving’s encoding-specificity principle states that recall is improved if the recall environment is the same as the learning environment

cue dependent forgetting refers to both context and state dependent forgetting.
context dependent forgetting occurs when related contextual or environmental clues are not present
state dependent forgetting occur when physiological cues are not available

540
Q

forgetting: retrieval failure

A

theory is best illustrated by ‘tip of the tongue’ moments. it proposes that memories can not be retrieved because the correct cues are not available

540
Q

features of memory loss in amnesic syndromes

A

intact STM
anterograde amnesia
retrograde amnesia
unchanged intellectual abilities
unchanged implicit memory

541
Q

medial temporal lobe amnesia

A

bilateral damage to medial temporal lobe and hippocampal system
limited RA
no confabulation

542
Q

diencephalic amnesia

A

bilateral damage to the medial thalamic area, mammillary bodies and hypothalamic areas
typically marked RA
patients fill gaps with confabulation
distinctly poor insight

eg Korsakoff’s syndrome

543
Q

post traumatic amnesia (PTA)

A

time between initial injury and memory recovery:
PTA <1 hour - mild head injury
PTA 1-24 hours - mod head injury
PTA >24 hours - severe head injury

in PTA, patients are unable to transfer information from STM to LTM

544
Q

Ribot’s law

A

in retrograde amnesia following brain damage, more recently formed memories are more impaired compared to older memories

545
Q

transient global amnesia (TGA)

A

can last several hours
unable to make new memories so cant recall the TGA after
commonly in middle aged men
cause thought to be temporary loss of function of the limbic hippocampal circuits

546
Q

transient epileptic amnesia (TEA)

A

rare by possibly underdiagnosed
brief, recurring episodes of amnesia caused by underlying temporal lobe epilepsy

547
Q

psychogenic amnesia

A

dissociative or hysterical amnesia
occurs when an individual undergoes extreme trauma

loss of personal identity
loss of recollection of personal events
preservation of personality and social skills
no loss of the ability to kaperform complex behaviours

548
Q

katathymic amnesia aka motivated forgetting/dissociative amnesia

A

forgetting that can occur after traumatic events
first described by Freud 1895

if conscious - suppression
if unconscious - repression

549
Q

retrospective falsificaiton

A

unintentional distortion of memory that occurs due to an individuals altered mental state
feeling low in mood can paint a negative picture of past experiences

550
Q

false memory

A

when an individual remembers an event that did not happen, despite their belief that it did

551
Q

screen memory

A

when a memory in its entirety is too painful to recall, so it is remembered part truthfully and part falsely. an individual may recollect an event with different details in order to avoid a painful fact

552
Q

confabulation

A

falsification of memory in clear consciousness due to an organic pathology

553
Q

spontaneous confabulation

A

unprovoked expression of inaccurate memories
these can be bizarre, yet held with firm conviction and preoccupying

commonly linked with frontal lobe pathology

554
Q

provoked confabulation

A

associated with fleeting intrusion errors or distortions made in response to a challenge to memory such as a memory test
not a conscious attempt to fill in memory gaps and can occur in healthy patients

555
Q

pseudologica fantastica

A

pathological lying
occurs without brain pathology, usually in those with certain personality types eg antisocial or hysterical

556
Q

vorbeireden

A

‘approximate answers’
patient may understand the question but avoid the correct answer

556
Q

munchausen’s syndrome

A

pathological lying where an individual presents with false illness
can also be by proxy, usually parent and child

557
Q

cryptamnesia

A

occurs when a forgotten memory returns without being recognised as a memory, so the individual believes it to be an original thought, eg a ‘new joke’ that has been heard multiple times before

558
Q

perception

A

how we make sense of sensory information reaching our brain

558
Q

retrospective delusions

A

precede the start of psychosis
eg individual may state that their mother ‘has always been the Queen’

558
Q

hyperamnesia

A

exaggerated registration, retention and recall
flashbulb memories
PTSD flashbacks

558
Q

Phi phenomenon

A

animated light appearing to move but no motion

559
Q

figure ground differentiation

A

eg figure is words and ground is paper
illusion pictures eg faces kissing vs vase
cant hold both at the same time (multistable perception)
cocktail part effect is auditory equivalent

559
Q

Gestalt laws of perception (6)

A

similarity
proximity
closure
common fate
symmetry
continuity

‘some psychiatrists can frighten small children’

559
Q

top down processing

A

conceptually driven processing
our perceptions are the end result of ‘higher up’ processes, making inferences about what things are like

559
Q

bottom up processing

A

stimulus driven
involved processing information in a more ‘direct manner’, essentially determined only by the information presented to our sensory receptors

560
Q

components of perceptual constancy

A

size constancy
shape constancy
colour constancy
location constancy

560
Q

perceptual constancy

A

‘the ability to perceive an object as unchanging, despite changes in the sensory information that reaches our eye’

561
Q

visual cues associated with depth perception

A

retinal disparity
stereopsis
convergence
accommodation
motion parallax
light and shadow
angular declination
object overlap

561
Q

the gestault psychologists

A

koffka
wertheimer
kohler

562
Q

who described the perceptual set

A

allport

563
Q

structure involved in the visual pathway

A

superior colliculus
lateral geniculate nucleus

‘See Light’

564
Q

simultagnosia

A

inability to recognise more than one object at once

564
Q

cerebral akinetopsia

A

inability to see movement, patient sees life as a series of ‘stills’ - rare

564
Q

capgras syndrome

A

delusional belief that someone close to the sufferer has been replaced by an imposter

564
Q

structures involved with the auditory pathway

A

Inferior colliculus
Medial geniculate nucleus (MGN)

‘Interpret Music’

565
Q

amblyopia

A

reduced vision resulting from monocular deprivation

566
Q

when does visual depth perception develop

A

around 6 months
cliff test

567
Q

by what age is myelination of optic nerve completed

A

by 2 years

568
Q

charles bonnet syndrome

A

vivid visual hallucinations, which typically affect older people with visual loss and no other psychological symptoms

569
Q

NTs in auditory hallucinations

A

dopamine - high in limbic system
acetylcholine - low
glutamate - reduced NMDA receptor function
serotonin - hallucinations possible SE of SSRIs, 5HT2A agonist activity
GABA-A - reduced GABAA binding

569
Q

functional imaging of auditory hllucinations

A

brocas area
anterior cingulate
left temporal cortices

570
Q

signal detection theory (SDT)

A

state that all information recognition takes place in the presence of some uncertainty and that processing relied on both pattern recognition and biases in responding

hallucinations - difficulty deciphering which sensory inputs are real and which are not

570
Q

cho and wu - spontaneous activation model of hallucinations

A

auditory hallucinations arise from spontaneous activity in auditory and associated memory areas

more of a bottom up approach

570
Q

source monitoring theory of hallucinations

A

failure of a system that normally distinguishes between internal and external events

570
Q

self monitoring theory of hallucinations

A

when there is failure of the normal predictive processes that identify actions/language as ones own

an ‘inner voice’ is then taken to be ‘non self’

571
Q

waters et al - series of steps to hallucinations

A

early traumatic insult leading to aberrant activation of the auditory network
combination of hypersalient auditory signals and emotional modulation with highly personal experiences such as depression/anxiety/past memories, along with delusional ideas and reduced insight, is proposed to lead to hallucinatory beliefs

572
Q

changes in the body during sleep (6)

A

increased GH secretion
changes in melatonin secretion at different points
increased renal phosphate excretion
skin and tissue repair
maintenance of normal activity levels of CNS
sympathetic activity and muscle tone increases with sleep deprivation

573
Q

five key brain areas involved in sleep

A

sleep centres
reticular activating system
locus coeruleus
tuberomammilllary nucleus
ventrolateral preoptic nucleus

574
Q

neuromodulators involved in sleep (7)

A

noradrenaline
acetylcholine
serotonin
histamine
galanin
GABA
orexin

575
Q

locus coeruleus

A

within posterior area of rostral pons

role in physiological reactions to panic and stress

noradrenaline

576
Q

orexin

A

regulates appetite
arousal and wakefulness

produced in lateral hypothalamic area

also a role in emotion, reward and motivation

576
Q

locus coeruleus functions (7)

A

emotions and psychological stress
arousal and sleep wake cycle
behavioural flexibility and behavioural inhibition
neuroplasticity
balance and posture
attention and memory
cognitive control

577
Q

orexin deficiency

A

narcolepsy (plus cataplexy)

577
Q

ventrolateral preoptic nucleus

A

mainly active during sleep
neurons reposnible for onset of sleep by obstructing wake promoting systems
‘sleep neurons’ have sudden increase at point of sleep onset

578
Q

inhibitory NTs released by ventrolateral preoptic nucleus

A

GABA
galanin

579
Q

increasing frequency of EEG waves

A

Delta - <4 Hz
Theta - 408 Hz
Mu - 7-11 Hz
Alpha - 8-13 Hz
SMR - 12-15 Hz
Beta - 14-40 Hz
Gamma - >40 Hz

579
Q

wake promoting neurons

A

orexin
serotonin
histamine
acetylcholine
noradrenaline

579
Q

orexin action

A

increases food craving and promotes wakefulness

579
Q

stage 2 NREM EEG

A

sleep spindles
k complexes

580
Q

stage 1 NREM EEG

A

alpha waves decrease in amplitude
theta waves appear with frequency 4-7 Hz

580
Q

sleep spindles on EEG

A

waxing and waning 10-16Hz oscillations lasting 0.5-2s

580
Q

stage 3 NREM EEG

A

delta / slow wave sleep

581
Q

REM proportion of sleep

A

20-25% of total sleep time
approx 4-6 episodes in cycles of 90-120 minutes
REM episodes increase in length throughout the cycles

babies more REM than elderly etc

581
Q

areas of brain most active in dreaming

A

extrastriate visual areas
limbic system including hippocampus and amygdala
anterior cingulate gyrus
pons

582
Q

freud theory of dreaming

A

manifestation of subconscious mind’s interpretation of our deepest desires and fantasies

583
Q

drugs likely to affect dreaming (4)

A

dopamine increasing drugs eg levodopa
reserpine analogues
various blockers
centrally acting cholinergic drugs

584
Q

activation synthesis model of dreaming (Hobson and McCarley)

A

neurophysiology of dreaming genetically programmed to promote the construction and testing of neurons, circuits and pathways

automatically activated forebrain synthesizes the dream by comparing information generated in specific brain stem circuits with information stored in memory

585
Q

reverse learning model of dreaming - Crick and Michison

A

unwanted or ‘parasitic’ models of behaviour which exist in the cerebral cortex and associated subcortical areas of the brain

suggest that a reverse learning mechanisms is activated during RME sleep to get rid of these modes

done by modifying individual synapses through strengthening or weakening them

585
Q

how much time in adults spent in stage 1 NREM

A

10-15%

586
Q

who found REM linked with dreaming

A

Kleitman and Aserinsky

587
Q

area of brain most active during dreaming

A

pons

588
Q

suprachiasmatic nucleus

A

main circadian pacemaker
‘body clock’
group of cells in hypothalamus
reset daily by light input from retina

589
Q

where is melatonin secreted from

A

pineal gland

590
Q

drugs with insomnia as a side effect

A

SSRIs
SNRIs
beta blockers
cholinesterase inhibitors
some antipsychotics
mood stablisers

591
Q

antidepressants - hypnotic effect

A

melatonin secretion increased by SSRIs
suppression of REM sleep - this can help with mood lifting

592
Q

where is GABA found in the brain (6)

A

substantia nigra
globus pallidus
hippocampus
hypothalamus
cortex
spinal grey matter

593
Q

hayflicks limits - ageing

A

cells in culture will divide about 50 times then stop
due to shortening telomeres at each replication

594
Q

free radical theories of ageing

A

aerobic cellular respiration leads to the production of free radicals (eg superoxide, hydroxyl)
leads to protein damage due to inappropriate oxidation and damages DNA
damage is cumulative
results in ageing

595
Q

genes that control ageing

A

account for approx 25% in variation of ageing between individuals
generally genes associated with GH and receptors

596
Q

disposable some theory of ageing

A

animals have finite resources which can be put into maintaining the integrity of their body systems or reproduction
repair mechanisms not perfect
comprise on soma repair may have improved reproductive fitness
the population that sacrifices some repair in favour of reproduction will be more likeyl to be naturally selected

597
Q

reduction in brain weight in normal ageing

A

20% reduction

598
Q

vision changes with age

A

13% of >75y are visually impaired
less periorbital fat
iris weaker
pupil smaller and less reactive
lenses less elastic
less rhodopsin so deterioration in light reflexes

599
Q

hearing and balance changes in ageing

A

25% develop hearing loss
prescyacusis 28-43% of men and 17-20% women between 60-69y
increased risk of BPPV and dizziness
70% of over 70s have hearing loss that should be considered for a hearing aid

600
Q

GI changes in ageing

A

taste may change
tooth decay more common
salivation production reduced
reduced hepatic mass and blood flow
lives enzymes as effective, but reduced blood flow and mass can affect drug pharmacokinetics
constipation more common

600
Q

renal changes in ageing

A

general decline from 40y
GFR declines by 10% a decade after 40y and worsened by HTN and/or diabetes
reduced ability to concentrate urine

600
Q

memantine excretion

A

renal

601
Q

type of memory not affected by age

A

working memory

601
Q

prevalence of depression in older adults

A

10-17%

601
Q

as per ONS which are group has highest levels of life satisfaction

A

65-69y

602
Q

5 stages of grief

A

denial
anger
bargaining
depression
acceptance

RCPsych Paper A (3 decks)

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