Basic neurosciences Flashcards

1
Q

Blood supply to the brain (overview)

A

The body supplies blood to the brain via:

  • the internal carotid arteries
  • the vertebral arteries

These vessels come together to form a ring called the circle of Willis. The function of the circle of Willis is to provide a shunt system should any of the vessels become damaged.

Arising from the circle are the three main vessels that supply the brain with blood:

  • the anterior cerebral artery
  • middle cerebral artery
  • the posterior cerebral artery.
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2
Q

Anterior cerebral artery (ACA) occlusion (associated defects)

A

Hemiparesis of the contralateral foot and leg (more severely than the arm)

Sensory loss of the contralateral foot and leg

Motor dysphasia

(If stroke occurs prior to the anterior communicating artery it is usually well tolerated secondary to collateral circulation)

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3
Q

Middle cerebral artery (MCA) occlusion (associated defects)

A

Hemiparesis of the contralateral face and limbs

Sensory loss of contralateral face and limbs

Dysphasia (when dominant hemisphere affected)

Contralateral neglect

Homonymous hemianopia or quadrantanopia

Dorsolateral prefrontal dysfunction

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4
Q

Posterior cerebral artery (PCA) occlusion (associated defects)

A

Alexia without agraphia (left PCA)

Contralateral loss of pain and temperature sensation

Contralateral hemianopia

Prosopagnosia

Ipsilateral cranial nerve defects (V, VIII, IX, X, & XI)

Horner’s syndrome

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5
Q

Frontal lobe and Parietal lobe are separated by … (aka)

A

The central sulcus

aka fissure of Rolando

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6
Q

Primary motor cortex (region, lobe and Brodmann area)

A

Pre-central gyrus, frontal lobe

Brodmann area 4

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7
Q

Subdivisions of the motor cortex, and their functions (3)

A

Primary motor cortex
- initiating motor movements

Premotor cortex
- planning and initiation of movements on the basis of past experience

Supplementary motor cortex
- regulation of posture

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8
Q

Broca’s area (function, location, and Brodmann areas)

A

Motor speech area

Located in the inferior frontal gyrus on the dominant (usually left) hemisphere

Brodmann areas 44+45

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9
Q

Frontal eye field (function, location, and Brodmann areas)

A

Voluntary saccadic eye movements

Located at the caudal ends of the superior frontal gyrus (Brodmann 8) and middle front gyrus (Brodmann 6)

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10
Q

Primary somatosensory cortex (region, lobe and Brodmann areas)

A

Postcentral gyrus, parietal lobe

Brodmann areas 1, 2, and 3

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11
Q

Primary auditory cortex (region, lobe and Brodmann area)

A

Heschl’s gyrus, aka transverse temporal gyrus, in the temporal lobe

Brodmann areas 41 + 42

It is entirely hidden within the Sylvian fissure (lateral sulcus), with the planum temporale and superior temporal gyrus located lateral to it.

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12
Q

Planum temporale (location and key fact)

A

A triangular region on the upper surface of the superior temporal gyrus (temporal lobe).

It is important for language processing.

The most notable feature is that it displays left-right asymmetry - the left PT is larger than the right in 65% of right-handed individuals.

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13
Q

Wernicke’s area (function, location, and Brodmann areas)

A

Comprehension of written and spoken language.

Superior temporal gyrus in the dominant hemisphere.

Brodmann area 22.

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14
Q

Lateralisation of brain function (summary)

A

Right-handed people

  • Left hemisphere dominant in 90%
  • Right hemisphere dominant in 10%

Left-handed people

  • Left hemisphere dominant in 64%
  • Right hemisphere dominant in 20%
  • Bilateral dominance in 16%
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15
Q

Primary visual cortex (region, lobe and Brodmann area)

A

Striate cortex (calcarine cortex) in the occipital lobe

Brodmann area 17

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16
Q

Which lobe?:

Motor movements
Executive function (e.g. planning, initiation, organisation, set-shifting, reasoning/judgement, abstract thinking)
Decision-making
Working memory; Attention
Language (motor expression of speech)
Inhibition
Personality/emotions/social conduct
Saccadic eye movements
A

Frontal lobe

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17
Q

Motor movements (specific region & lobe)

A

Motor cortex - frontal lobe

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18
Q

Brain region & lobe responsible for:

  • Executive function (e.g. planning, initiation, organisation, set-shifting, reasoning/judgement, abstract thinking)
  • Decision-making
  • Working memory; Attention
A

Premotor cortex - frontal lobe

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19
Q

Brain region + lobe responsible for:

  • Inhibition
  • Personality/emotions/social conduct
A

Orbitofrontal cortex - frontal lobe

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20
Q

Language - motor expression of speech (specific region & lobe)

A

Broca’s area - inferior frontal gyrus on the dominant (usually left) hemisphere; frontal lobe

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21
Q

Saccadic eye movements (specific region & lobe)

A

Frontal eye fields - frontal lobe

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22
Q
Gerstmann syndrome
(brain region deficit, key features)
A

Results from lesions in the left (/dominant) inferior parietal lobe

  • agraphia
  • acalculia
  • finger agnosia (inability to distinguish fingers in the hand)
  • left-right disorientation
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23
Q
Balint syndrome
(brain region deficit, key features)
A

Results from bilateral damage to the posterior parietal lobe

  • ocular apraxia (difficulty keeping the eyes still)
  • optic ataxia (difficulty moving the eyes to a specific position)
  • simultanagnosia (inability to simultaneously perceive the different aspects of a picture and appreciate it as a whole)
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24
Q

Which lobe?:

Perception and processing of sensory information
Visuospatial processing
Praxis
Somatognosia (awareness of one's body)
Calculation ability
Reading
Writing
Naming
Left-right orientation
Visual field processing
A

Parietal lobe

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25
Q

Which lobe?:

Memory
Deductive reasoning
Language comprehension
Auditory perception
Affective prosody
Music comprehension
Face recognition
Visual field processing (superior)
Olfactory perception
A

Temporal lobe

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26
Q

Kluver-Bucy Syndrome

brain region deficit, key features

A

Rare, neurobehavioural impairment resulting bilateral medial temporal lobe dysfunction (specifically the amygdala)

  • hyperorality (pica)
  • hypersexuality
  • placidity/docility (lack of anger)
  • visual agnosia
  • prosopagnosia
  • psychic blindness (emotional unresponsiveness)
  • hypermetamorphosis (tendency to react to every visual stimulus which could lead to easy distractibility - objects are repeatedly examined as they were novel)
  • memory loss
  • seizures
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27
Q

Anton-Babinski syndrome (essence)

A

Cortical blindness

Caused by injury to the occipital lobe

Features

  • Anosognosia - denial of blindness despite objective evidence of visual loss
  • Confabulation - to fill in the missing sensory input
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28
Q

Occipital lobe function

A

The occipital lobe is responsible for perception of visual sensation.

However, having a lesion on any other site in the course of the optic tract (which runs under the frontal lobe and through the temporal and parietal lobes) could also affect vision despite having an intact occipital lobe.

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29
Q

Structures in the visual pathway (7)

A
Eye
Optic nerve
Optic chiasm
Optic tract
Lateral geniculate nucleus
Optic radiation
Primary visual cortex
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30
Q

Limbic system (basic substructure (2) and functions)

A
  1. Structures in the cerebral cortex - collectively termed the limbic lobe
    - hippocampus
    - insular cortex
    - orbital frontal cortex
    - subcallosal gyrus
    - cingulate gyrus
    - parahippocampal gyrus
  2. Subcortical structures
    - olfactory bulb
    - hypothalamus
    - amygdala
    - septal nuclei
    - some thalamic nuclei

Functions:

  • Processing of emotions
  • Encoding and retrieval of memory
  • Autonomic functions
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31
Q

Limbic lobe (2 major components)

A

Cingulate gyrus

  • lies immediately above the corpus callosum
  • the posterior cingulate cortex has a central function in supporting autobiographical memories, planning for the future and focussing attention

Parahippocampal gyrus

  • lies in the medial temporal lobe and surrounds the hippocampal formation
  • active in general memory creation/recall, and specific recollection of visual scenes
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32
Q

Hippocampus - functions (3)

A

declarative memory (encoding, retrieval)
visuospatial orientation
regulation of the HPA axis

Impairment is one of the first things to occur in Alzheimer’s disease, often leading to confusion and memory loss

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33
Q

two almond-shaped clusters of nuclei located deep and medially within the temporal lobes of the brain

part of the limbic system

associated with processing of emotion and the acquisition and expression of fear conditioning

A

Amydala(e)

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34
Q

a set of structures that lie below the rostrum of the corpus callosum

part of the limbic system

they receive reciprocal connections from the olfactory bulb, hippocampus, amygdala, hypothalamus, midbrain, habenula, cingulate gyrus, and thalamus

A

Septal nuclei (medial olfactory area)

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35
Q

lies just below the septal nuclei, below the rostrum of the corpus collosum

plays a key role in reward and reinforcement, and hence things such as motivation and drug dependency

A

Nucleus accumbens

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36
Q

Diencephalon - subdivision (4)

A

The — is divided into 4 areas, which are interposed between the brain stem and cerebral hemispheres:

  • thalamus
  • hypothalamus
  • epithalamus
  • subthalamic nucleus
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37
Q

The — is like a switchboard regulating and relaying information to and from the brain. Almost all sensory input (with the exception of the olfactory system) goes through the — and motor output goes via the — to the rest of the body.

It also plays a role in regulating sleep and wakefulness, level of arousal and consciousness - damage can lead to permanent coma.

A

Thalamus

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38
Q
Links the nervous system to the endocrine system, through control of the pituitary gland, to release 8 major hormones
Temperature regulation
Management of food and water intake
Sexual behaviour and reproduction
Mediation of the emotional response
A

Hypothalamus

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39
Q

White matter (essence)

A

White matter is composed of myelinated axons, which run in bundles called white matter tracts - these tracts connect various grey matter areas of the brain to each other.

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40
Q

3 main types of white matter tracts

A

Commissural fibres
Association fibres
Projection fibres

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41
Q

The largest white matter tract

A

Corpus callosum

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42
Q

Commissural fibres (aka, function, examples)

A

aka transverse fibres

connect the corresponding areas between the two hemispheres of the brain

e.g.
transverse fibres of the corpus callosum
anterior commissure
posterior commisure
hippocampal commissure
habenular commissure
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43
Q

Which white matter tract?:

Transports nociceptive (pain) stimuli to the contralateral side of the brain in the lateral spinothalamic tracts

Also contains decussating fibres from the olfactory tracts and connects the two amygdala and other parts of the temporal lobe, thus contributing to olfaction, memory, emotion, speech, and hearing.

A

Anterior commissure

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44
Q

Which white matter tract?:

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

A

Posterior commissure

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45
Q

Association fibres (function, examples)

A

Connect regions of within the same hemisphere of the brain

e.g.
the cingulum
the superior longitudinal fasciculus and arcuate fasciculus
the inferior longitudinal fasciculus and uncinate fasciculus
the fornix of the hippocampi

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46
Q

Which white matter tract?:

Travels in a C-shape through the frontal, parietal and temporal lobes above the corpus callosum.

Hippocampal atrophy in Alzheimer’s disease has been linked to disruption of this tract.sy

A

The cingulum

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47
Q

The longest intrahemispheric white matter tract

A

The superior longitudinal fasciculus

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48
Q

Which white matter tract?:

  • an association tract
  • one of the subdivisions of the superior longitudinal fasciculus
  • connects Broca’s and Wernicke’s areas
  • plays a major role in language use and comprehension
  • damage results in conduction aphasia
A

The arcuate fasciculus

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49
Q

Projection fibres (function, key example)

A

— connect the cerebral cortex with the lower parts of the brain (brainstem) and the spinal cord, in both directions. These could be afferent to the cerebral cortex (corticopetal) or efferent from the cerebral cortex (corticofugal).

e.g. the internal capsule

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50
Q

Basal ganglia - components (4)

A

Striatum (caudate, putamen, nucleus accumbens)

Subthalamic nucleus

Substantia nigra (divided into pars compacta and pars reticulate)

Globus pallidus

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51
Q

The — enable practised motor acts, gating the voluntary movements initiated in the motor cortex and suppressing inappropriate motor commands.

They also play a role in cognitive function, especially certain forms of implicit memory tasks, through connections to the prefrontal association cortex and limbic cortex.

A

Basal Ganglia

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52
Q

Brainstem - key structures (3)

A

Medulla oblongata
Pons
Midbrain

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53
Q

Midbrain - 2 major structures

A

Red nucleus

Substantia nigra

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54
Q

Substantia nigra - subdivisions (2)

A

pars compacta
- contains mainly dopaminergic neurons

pars reticulata
- contains mainly GABAnergic neurons

Degeneration of dopaminergic neurons in the pars compacta is the main pathological feature of Parkinson’s disease, leading to depletion of dopamine in the nigrostriatal pathway

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55
Q
Olfactory nerve (I)
(fibres, function, test)
A

Sensory
- Smell

Test smell with clove or coffee

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56
Q
Optic nerve (II)
(fibres, function, test)
A

Sensory
- Vision

Tests:

  • snellen chart (acuity)
  • ischihara chart (colour vision)
  • pupillary reflexes - light and accommodation
  • visual fields
  • fundoscopy
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57
Q
Oculomotor nerve (III)
(fibres, function, test)
A
Motor
- Movement of eye muscles:
   - superior/inferior/medial rectus;
   - inferior oblique
   - levator palpabrae
Test - follow finger with head still

Parasympathetic
- Pupillary constriction
Test - accommodation reflex

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58
Q
Trochlear nerve (IV)
(fibres, function, test)
A

Motor
- Movement of eye muscle:
superior oblique
(downward and medial movement of eye)

Test - eye movements with head still

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59
Q
Trigeminal nerve (V)
(fibres, function, test)
A

Sensory
- general sensation of face, scalp, oral and nasal cavities; corneal reflex
Test - touch patient on each side of face

Motor
- muscles of mastication
Test - bite down and open mouth against resistance

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60
Q
Abducens nerve (VI)
(fibres, function, test)
A
Motor
- Movement of eye muscle:
   lateral rectus
   (lateral movement of eye)
Test - eye movements with head still
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61
Q
Facial nerve (VII)
(fibres, function, test)
A

Sensory
- Taste sensation to anterior 2/3 of tongue
Test - taste sensation

Motor
- Muscles of facial expression
Test - make various facial expressions

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62
Q

Vestibulo-cochlear nerve (VIII)

fibres, function, test

A

Sensory
- hearing
- proprioception of head and balance
Test - Rhinne and Weber tests

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63
Q

Glosso-pharyngeal nerve (IX)

fibres, function, test

A

Sensory

  • general sensation of middle ear and pharynx
  • taste of posterior 1/3 of the tongue

Motor
- swallowing

Parasympathetic
- salivation

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64
Q
Vagus nerve (X)
(fibres, function, test)
A

Sensory
- general sensations of pharynx, larynx, oesophagus, external ear and viscera

Motor
- speech and swallowing

Parasympathetic
- control of GI, cardiovascular and respiratory systems
Test - say ‘ahh’ and look at uvula

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65
Q
Accessory nerve (XI)
(fibres, function, test)
A

Motor
- trapezius and sternocleidomastoid muscles
Test - turn head and shrug shoulders against resistance

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66
Q
Hypoglossal nerve (XII)
(fibres, function, test)
A

Motor
- movement of tongue
Test - look for wasting/fasciculation. Stick out tongue and look for deviation.

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67
Q

How many nerve nuclei does the brainstem contain?

A

10

Olfactory and optic nerves come from the cerebrum

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68
Q

Which side of the body do cerebellar lesions affect?

A

Ipsilateral

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69
Q

Cerebellar dysfunction - clinical features

A
Dysdiadochokinesis / Dysmetria (lack of finger nose co-ordination
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia/Heel-shin test
Broad based gait

‘DANISH - B’

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70
Q

Which white matter tract?:

Connects the orbitofrontal cortex to the anterior temporal lobes. Plays an important role in social cognition and language.

A

Uncinate fasciculus

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71
Q

2 main types of cells in the nervous system

A

Neurons

Glial cells

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72
Q

From which primary germ layer do neurons originate?

A

Ectoderm

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73
Q

Neuron - basic components (3)

A

Cell body (soma) - the major site of metabolic activity

Dendrites - outward extensions of the cell body, receiving signals from other neurons

Axon - conducts nerve impulses (action potentials) away from the cell body

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74
Q

Functional classification of neurons (3)

A

Sensory
Motor
Interneurons (aka association neurons)

Interneurons are found entirely within the CNS - their function is to enable communication between the CNS and other neurons

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75
Q

Structural classification of neurons (3)

A

Unipolar
Bipolar
Multipolar

Most neurons are multipolar - one axon and one or more dendrites

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76
Q

Glial cell (essence)

A

They are not directly involved in electrical signalling, but rather provide a supportive function to help maintain the action of neurons

More numerous (10-50 times more) than neurons

Lack axons and dendrites

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77
Q

(cell)

  • derived from neural tube ectoderm
  • star shaped
  • the largest type of glial cell
  • aid formation of the blood-brain barrier
  • provide structural support and repair processes, regulating oxidised potassium concentration in the extracellular fluid
  • form a ‘glial scar’ in response to brain tissue damage (process called astrocytosis/gliosis)
A

Astrocyte

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78
Q

(cell)

Glial cell

  • derived from neural tube ectoderm
  • found mainly in white matter

-responsible for the formation and maintenance of the myelin sheath around an axon in the CNS

A

Oligodendrocyte

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79
Q

(cell)

  • small glial cells of mesenchymal origin
  • the primary immune cells of the CNS
A

Microglia

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80
Q

(cell)

  • type of glial cell
  • make up the lining of the ventricles of the brain and central canal of the spinal cord
  • they do this by forming the specialised choroid plexus epithelium that secretes CSF
A

Columnar epithelial cells

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81
Q

Glial cell

  • derived from the neural crest
  • only found in the peripheral nervous system

-responsible for the myelination of the PNS

A

Schwann cells

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82
Q

Glial cell in the PNS, derived from the neural crest

Provides a supportive role

A

Satellite cells

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83
Q

Cerebral cortex

essence, subdivisions

A

The outer covering of grey matter over the cerebral hemispheres

  • Neocortex (top layer)
  • Allocortex
    • Paleocortex
    • Archicortex
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84
Q

Paleocortex - subdivisions (2)

A

part of the cerebral cortex

includes the entorhinal cortex (in the medial temporal lobe) and piriform lobe (specialised for olfaction)

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85
Q

Archicortex (function)

A

consists of the hippocampus, dealing with memory and spatial function

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86
Q

Neocortex - layers (6)

A
I - Molecular (plexiform) layer
II - Outer granular
III - Outer pyramidal
IV - Inner granular
V - Inner pyramidal
VI - Multiform

Neocortex covers more than 90% of the cerebral cortex

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87
Q

Neocortex - 2 main cell types

A

Pyramidal cells

Stellate cells

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88
Q

Pyramidal cells (location)

A
  • make up 75% of cortical neurons

- the principal output neurons, found in layers II-V of the neocortex

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89
Q

Betz cells

A

Giant pyramidal cells located within layer V of the grey matter in the primary motor cortex.

They are the largest neurons in the nervous system

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90
Q

Stellate cells (aka, location, function)

A

aka Granular cells

small multipolar neurons with a star-like shape

  • spiny — cells (excitatory)
  • smooth — cells (inhibitory)

most prominent in layer IV of the neocortex

the main interneurons of the neocortex - their short axons do not leave the cortex

they are the most common cells in the cerebral cortex

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91
Q

Other cells in the neocortex (3)

A

Fusiform cells
Horizontal cells of Cajul
Cells or Martionotti

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92
Q

Cerebellar cortex - layers (3, +cells)

A

Molecular, outermost layer

Purkinje, middle layer

Granular, innermost layer

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93
Q

Molecular, outermost layer of the cerebellar cortex - cells (4)

A

Axons of granule cells

Dendrites of Purkinje cells

Stellate and Basket cells

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94
Q

Purkinje, middle layer of the cerebellar cortex - cells (1)

A

A single layer of Purkinje cell bodies

Their axons extend deep into the cerebellum, and their multiple dendrites extend into the molecular level

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95
Q

Granular, innermost layer of the cerebellar cortex - cells (2)

A

Granule cells - whose axons extend into the molecular layer

Golgi cells

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96
Q

Cell type?:

  • found uniquely in the cerebellum
  • only source of output from the cerebellar cortex
  • inhibitory (use GABA)
A

Purkinje cells

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97
Q

Cell type?:

  • most numerous type of cell in the cerebellum
  • excitatory (use glutamate)
  • excite the Purkinje cells via axonal branches called ‘mossy fibres’
A

Granule cells

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98
Q

Stellate, basket and Golgi cells (location, function)

A

inhibitory interneurons in the cerebellar cortex

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99
Q

Main cell type found in the hippocampus

A

Pyramidal cell

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100
Q

Main cell type found in the dentate gyrus (within the hippocampus)

A

Granule cell

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101
Q

Major neurotransmitters (6)

A
Dopamine
Noradrenaline
Serotonin
Acetylcholine
Histamine
Glutamate
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102
Q

Brian region involved in major neurochemical pathways

Lying within the striatum, this is associated with motivation, pleasure, and reward/reinforcement. Conditions affecting this area can cause delusions and hallucinations

A

Nucleus accumbens

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103
Q

Brian region involved in major neurochemical pathways

Associated with executive function (working memory, judgement, decision-making, reasoning, problem-solving, planning), emotional regulation, social behaviour, impulse control and motor control. Conditions affecting this area can cause obsessions and compulsions.

A

Prefrontal cortex

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104
Q

Brian regions involved in major neurochemical pathways

Regions involved in motor control (3)

A

Subtantia nigra (in the brainstem)
Striatum
Cerebellum

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105
Q

Brian region involved in major neurochemical pathways

Regions involved in appetite and hormone release (2)

A

Hypothalamus

Pituitary

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106
Q

Brian region involved in major neurochemical pathways

Associated with relaying sensory and motor signals to the cortex, as well as sleep and wakefulness

A

Thalamus

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107
Q

Brian region involved in major neurochemical pathways

… lies in the brainstem and is associated with sleep and respiratory function

A

Locus coeruleus

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108
Q

Brian region involved in major neurochemical pathways

Regions involved with memory (3)

A

Amygdala (fear and memory consolidation)
Hippocampus
Nucleus basalis of Meynert

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109
Q

Brian region involved in major neurochemical pathways

… lies in the brainstem and is involved with emotions and behaviour

A

Ventral tegmental area

==================
in the midbrain

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110
Q

Brian region involved in major neurochemical pathways

… lies in the brainstem and is associated with pain, sleep and wakefulness

A

Raphe nuclei

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111
Q

4 major dopamine pathways in the brain

A

Mesolimbic
Mesocortical
Nigrostriatal
Tuberoinfundibular

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112
Q

Mesolimbic pathway (dopamine) - brain regions

A

Projects from the ventral tegmental area (in the brainstem) to the nucleus accumbens (in the striatum) which is part of the limbic system

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113
Q

Mesolimbic pathway (dopamine) - clinical significance

A

Overactivity of this pathway (increased dopamine) mediates the positive symptoms of psychosis.

The pathway is also associated with motivation/pleasure/reward/reinforcement

  • this explain the worsening of negative symptoms after treatment with typical antipsychotics
  • it also has a role in the neurobiology of addiction
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114
Q

Mesocortical pathway (dopamine) - brain regions

A

Projects from the ventral tegmental area (in the brainstem) to the prefrontal cortex.

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115
Q

Mesocortical pathway (dopamine) - clinical significance

A

Hypoactivity of this pathway (e.g. by dopamine blockade) mediates the negative, cognitive and affective symptoms of schizophrenia (alogia, anhedonia, avolition, blunted affect)

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116
Q

Nigrostriatal pathway (dopamine) - brain regions

A

Projects from the substantia nigra (in the brainstem) to the striatum (caudate nucleus and putamen)

This pathway is part of the extrapyramidal system and is associated with motor control

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117
Q

Nigrostriatal pathway (dopamine) - clinical significance

A

Hypoactivity of this pathway (e.g. deficiency of dopamine in Parkinson’s disease, or antipsychotic dopamine receptor blockade)
-> EPSEs: parkinsonism (rigidity, tremor, bradykinesia), akathisia, dystonia

Chronic dopamine blockade in this pathway -> tardive dyskinesia

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118
Q

Tuberoinfundibular pathway (dopamine) - brain regions

A

Projects from the hypothalamus to the anterior pituitary gland

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119
Q

Tuberoinfundibular pathway (dopamine) - clinical significance

A

Dopamine in this pathway normally inhibits prolactin secretion.

Hypoactivity (caused by dopamine receptor blockade)-> hyperprolactinaemia

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120
Q

2 major noradrenaline pathways in the brain

A

Ascending noradrenaline pathway

Descending noradrenaline pathway

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121
Q

Ascending noradrenaline pathway

brain regions and functions

A

Projects from the locus coeruleus (in the brainstem) to multiple brain regions:

  • prefrontal cortex
  • thalamus + hypothalamus
  • amygdala + hippocampus
  • cerebellum

Regulates multiple functions:

  • mood
  • arousal
  • cognition
  • sexual behaviour
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122
Q

Descending noradrenaline pathway

brain regions and functions

A

Projects from the brainstem down the spinal cord

Regulates pain pathways

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123
Q

2 major serotonin pathways in the brain

A

Ascending serotonin pathway

Descending serotonin pathway

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124
Q

Ascending serotonin pathway

brain regions and functions

A

Projects from the raphe nuclei (in the brainstem) to multiple brain regions:

  • prefrontal cortex
  • thalamus + hypothalamus
  • amygdala + hippocampus
  • nucleus accumbens (in the striatum)
  • cerebellum

Regulates multiple functions:

  • mood, anxiety
  • sleep, wakefulness
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125
Q

Descending serotonin pathway

brain regions and functions

A

Projects from the brainstem down the spinal cord

Regulates pain pathways

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126
Q

2 major acetylcholine pathways in the brain

A

Acetylcholine pathway from the brainstem

Acetylcholine pathway from the basal forebrain

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127
Q

Acetylcholine pathway from the brainstem

brain regions and functions

A

Projects from the brainstem to multiple brain regions:

  • prefrontal cortex
  • thalamus + hypothalamus
  • amygdala + hippocampus

Regulates arousal, cognition and other functions

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128
Q

Acetylcholine pathway from the basal forebrain

brain regions and functions

A

Projects from the nucleus basalis of Meynert (in the basal forebrain) to:

  • prefrontal cortex
  • amygdala + hippocampus

It regulates memory and is implicated in the pathophysiology of Alzheimer’s disease

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129
Q

The major histamine pathway in the brain

brain regions and functions

A

Projects from the tuberomammiliary nucleus (in the hypothalamus) to multiple brain regions:

  • prefrontal cortex
  • thalamus
  • amygdala + hippocampus
  • striatum

Regulates arousal, sleep and wakefulness

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130
Q

5 major glutamate pathways in the brain

A

Cortical brainstem glutamate pathway

Corticostriatal glutamate pathway

Thalamocortical glutamate pathway

Corticothalamic glutamate pathway

Cortico-cortical glutamate pathway

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131
Q

Cortical brainstem glutamate pathway (brain regions)

A

A descending pathway projecting from the prefrontal cortex to the brainstem neurotransmitter centres:

  • substantia nigra
  • ventral tegmental area
  • locus coeruleus
  • raphe nucleus

This pathway communicates with the mesolimbic and mesocortical dopamine pathways

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132
Q

Cortical brainstem glutamate pathway (clinical significance)

A

The cortical brainstem glutamate pathway normally:

  1. acts a brake on the mesolimbic dopamine pathway (glutamate -> GABA release -> dopamine release inhibited)
    - Hypoactivity -> increased mesolimbic activity and therefore the positive symptoms of schizophrenia
  2. acts as an accelerator on the mesocortical dopamine pathway
    - Hypoactivity -> decreased mesocortical activity and therefore the negative symptoms of schizophrenia
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133
Q

Which white matter tract?

  • a major (association) frontotemporal tract
  • connects the orbitofrontal cortex to the anterior temporal lobes
  • plays an important role in social cognition and language
A

Uncinate fasciculus

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134
Q

Neuronal resting membrane potential (voltage + reason)

A

When a cell is not stimulated, it is in a resting state and the inside of the cell is negatively charged with respect to the outside.

The membrane potential of the resting state is -70mV.

  • This negative charge is due to a high concentration of Na+ outside compared to the K+ inside the cell.
  • This ionic gradient is maintained by the Na/K pump.
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135
Q

Action potential (process)

A
  • Neurotransmitter binds to the post-synaptic neuron -> ion channel opening
  • The membrane potential is raised from -70mV to -55mV (threshold potential)
  • This causes influx of Na+ -> depolarisation
  • Membrane potential reaches +40mV
  • Na+ channels close
  • Voltage-gated K+ channels open -> repolarisation
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136
Q

Synapse - definition + types (3)

A

A junction between two nerve cells

  1. Chemical synapses
    - excitatory (depolarisation of the postsynaptic neuron)
    - inhibitory (hypoerpolarisation of the postsynaptic neuron)
  2. Electrical synapses
    - abundant both in the retina and cerebral cortex
  3. Conjoint synapses (electrical and chemical properties)
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137
Q

The role of the hypothalamus in feeding behaviour (2)

A

Ventromedial hypothalamus - the satiety centre

Lateral hypothalamus - the feeding centre

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138
Q

Orexigenic hormones (hormones that increase appetite) - 2

A

Neuropeptide Y
- produced by the hypothalamus

Ghrelin
- produces in the gastric mucosa
(only orexigenic hormone produced outside the CNS)

[think ‘NG’ (tube) which is used for feeding]

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139
Q

Anorexigenic hormones (hormones that decrease appetite) - 2

A

Leptin
- produced by adipose tissue

Cholecystokinine (CCK)
- produced mainly by the gut

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140
Q

Primary afferent axons (4)

A

convey information about touch and pain from the surface of the body to the spinal cord and brain.

A-alpha (proprioception)
A-beta (touch)
A-delta (pain and temperature)
C (pain, temperature, and itch)

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141
Q

Which primary afferent axons are myelinated?

A

All of the A axons (alpha, beta, delta) are myelinated

C fibres are unmyelinated

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142
Q

Primary afferent axons involved in pain (2)

A

A-delta fibres are responsible for sharp initial pain

C fibres are responsible for slow, dull, longer lasting, second pain

(both carry pain sensations to the dorsal horn of the spinal cord)

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143
Q

Embryonic brain - divisions (3)

A

Forebrain (prosencephalon)

  • diencephalon
  • telencephalon

Midbrain (mesencephalon)

Hindbrain (rhombencephalon)

  • metencephalon
  • myelencephalon
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144
Q

Forebrain (prosencephalon) - subdivisions

A

Telencephalon (cerebrum)

  • cerebral cortex
  • underlying white matter
  • basal ganglia.

Diencephalon

  • prethalamus
  • thalamus
  • hypothalamus
  • subthalamus
  • epithalamus
  • pretectum
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145
Q

Midbrain (mesencephalon) - subdivisions

A

tectum (or corpora quadrigemina)
tegmentum
ventricular mesocoelia
cerebral peduncles

several nuclei and fasciculi.

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146
Q

Hindbrain (rhombencephalon) - subdivision

A

medulla, pons, and cerebellum

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147
Q

Neurotransmitter (definition)

A

A substance released from presynaptic nerve terminals which produces rapid inhibitory or excitatory effects on the post synaptic cell

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148
Q

Neurotrophic factor (definition)

A

A substance which influences gene expression and neuronal growth.

Predominantly released by glia.

Brain-derived neurotrophic factor (BDNF)
- increased in cortical areas
- decreased in the hippocampus
in patients with schizophrenia

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149
Q

Amino acid neurotransmitters (2 + 2)

A

GABA
Glutamate

(also Glycine and Aspartate, but these are less important to psychiatry)

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150
Q

Monoamine neurotransmitters (3 + 3)

A

Dopamine
Serotonin
Noradrenaline

Adrenaline
Melatonin
Histamine
(less important for psychiatry/less well understood)

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151
Q

Neurotransmitters - Other amine (1)

A

Acetylcholine

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152
Q

The major excitatory neurotransmitter in the CNS

A

Glutamate

======
also Aspartate

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153
Q

The major inhibitory neurotransmitter in the CNS

A

GABA

=======
also Glycine

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154
Q

Neurotransmitter release (process)

A
  • Action potential travels down the neuron (depolarising the membrane by sequential opening of Na channels)
  • > Influx of calcium through voltage dependent calcium selective ion channels
  • > Vesicles packed with neurotransmitters fuse with the synaptic membrane and release the neurotransmitter into the synaptic cleft (exocytosis)
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155
Q

Glutamate and GABA

precursors, degradation

A

Precursors:
both derived either from
- glucose (transported to the CSF from the peripher)
- glutamine (synthesised by glial cells)

“Glucose -> Glutamate -> GABA”

Termination:
They have their actions terminated mainly by being transported out of the synaptic terminal
- Glutamate - degraded by glutamine synthase
- GABA - degraded by GABA transaminase

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156
Q

Catecholamines (3)

A

Dopamine
Adrenaline
Noradrenaline

‘DAN’

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157
Q

Noradrenaline/Dopamine - synthesis pathway (4 molecules, 3 enzymes)

A
Tyrosine
   (Tyrosine hydroxylase) - *rate-limiting step*
Levodopa
   (DOPA decarboxylase)
Dopamine
   (Dopamine beta-hydroxylase)
Noradrenaline
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158
Q

Serotonin - synthesis pathway (3 molecules, 2 enzymes)

A

Tryptophan
(Tryptophan hydroxylase) - rate-limiting step
5-Hydroxytryptophan
(DOPA decarboxylase)*
5-Hydroxytryptamine (5-HT) i.e. Serotonin

========================
* aka L-aromatic amino acid decarboxylase

159
Q

Serotonin - location of synthesis

A
CNS in the raphe nuclei (in the brainstem)
GI tract (enterochromaffin cells)

It is synthesised from the amino acid L-tryptophan which is obtained from the diet. L-tryptophan can cross the blood brain barrier, whereas serotonin cannot

160
Q

Degradation of noradrenaline, dopamine, and serotonin (summary of enzymes involved)

A

COMT (catechol-O-methyltransferase) only breaks down the catecholamines (noradrenaline and dopamine)

Monamine oxidase A degrades all three (noradrenaline, dopamine, serotonin)

Monamine oxidase B degrades dopamine only
(hence use of MAO-Bi’s in parkinson’s)

Aldehyde dehydrogenase is involved in the degradation of serotonin’s breakdown product to 5-Hydroxyindoleacetic acid (5-HIAA).

161
Q

Cheese reaction (mechanism)

A
  • Tyramine is an amine in the diet which triggers release of noradrenaline
  • Usually this noradrenaline is degraded by MAO in the gut
  • If MAO is inhibited, then the excess noradrenaline leads to rise in blood pressure and hypertensive crisis
162
Q

Noradrenaline - degradation enzymes (2) and product

A

COMT (catechol-O-methyltransferase)
MAO-A
—————–
MHPG (3-methoxy-4-hydroxyphenylglycoll)

163
Q

Dopamine - degradation enzymes (3) and product

A
COMT (catechol-O-methyltransferase)
MAO-A
MAO-B
-------------------
HVA (homovanilic acid)
164
Q

Serotonin - degradation enzymes (2) and product

A
Serotonin
   (MAO-A)
Intermediary
   (Aldehyde dehydrogenase)
5-H1AA
165
Q

Acetylcholine - synthesis

A

Choline + acetyl coenzyme-A
(Choline acetyltransferase)
Acetylcholine

Choline is a nutrient present in a wide range of foods. It is taken up by neurons via specific transporters.

166
Q

Acetylcholine - degradation

A

Acetylcholine
(Acetylcholinesterase)
(Butyrylcholinesterase)
Choline and Acetate

Acetylcholinesterase is found predominantly at synapses
Butyrylcholinesterase is made by the liver and circulates in the blood. It is also found in the brain. Its role at synapses is unclear.

167
Q

Presynaptic processes occurring at the synapse (3)

A

Autoreceptors
Heteroreceptors
Reuptake transporter proteins

168
Q

Autoreceptors (essence)

A

Presynaptic receptors on the same neuron (e.g. serotonergic receptors on serotonergic terminals)

Inhibit further neurotransmitter release via negative feedback

169
Q

Heteroreceptors (essence)

A

Presynaptic receptors that respond to neurochemicals released from other neurons

170
Q

Reuptake transporter proteins (essence)

A

Proteins located on the presynaptic membrane that return the neurotransmitters to the axon terminal, where they are stored in a vesicle or degraded by catabolic enzymes

171
Q

Ionotropic receptors (essence)

A

Ligand-gated ion channels that open allowing an electrical current to pass through the cell membrane

172
Q

Metabotropic receptors (essence)

A

Receptors that are linked to membrane-bound G proteins which either open up ion channels or initiate a range of second messenger systems

173
Q

Ionotropic receptors - examples (5)

A
GABA-A
5HT-3
Nicotinic acetylcholine
NMDA (Glutaminergic)
Glycine
174
Q

Metabotropic receptors - examples (6)

A
GABA-B
Serotonin (except 5HT-3)
Muscarinic acetylcholine (M1-M3)
Noradrenaline (alpha and beta)
Mu Opioid
Dopamine (D1-D5)
175
Q

A drug or substance that acts at a cell receptor to produce a response, by activating the receptor

A

Agonist

176
Q

A drug or substance that blocks a receptor, preventing activation

A

Antagonist

177
Q

A drug that binds to a receptor and produces a submaximal response. May therefore prevent other agonists from producing their full response.

A

Partial agonist

178
Q

A drug or substance that has the opposite effect to the agonist at that receptor

A

Inverse agonist

179
Q

A drug that can cause neuroregulation of neuroreceptors, leading to down- or up-regulation

A

Chronic agonist

180
Q

Neuroreceptor up-regulation

A

Occurs when an increased concentration of neurotransmitters causes an increase in the number of postsynaptic receptors

181
Q

Neuroreceptor down-regulation

A

Occurs when there is a decrease in the number of receptors in response to a long-term increase in neurotransmission

182
Q

A sudden decrease in the effects produced by a drug or substance that may occur during continuous use or repeated administration. Increasing the dose of the drug may restore the original response.

A

Tachyphylaxis

183
Q

A reduction in the effect produced by a drug or substance over time.

A

Tolerance

184
Q

Dopamine receptors (classification)

A

D1-like receptors

  • D1
  • D5

D2-like receptors

  • D2
  • D3
  • D4

They are all metabotropic
D1-like receptors activate adenylyl cyclase
D2-like receptors inhibit adenylyl cyclase

185
Q

Noradrenaline receptors (classification)

A

alpha 1

  • postsynaptic
  • antagonism causes hypotension, sedation, and sexual dysfunction

alpha 2

  • pre and post synaptic
  • the presynaptic receptors act as autoreceptors (and are blocked by mirtazepine)
  • the postsynaptic receptors affect the release of growth hormone, arousal and blood pressure
  • linked with hypersalivation

beta 1

  • found mainly in neurons and heart
  • increases heart rate and cardiac contraction

beta 2
- dense in the cerebellum and found in glia and blood vessels

all are metabotropic

186
Q

Serotonin receptors (summary)

A

~14 5-HT receptor subtypes
All are metabotropic except 5-HT3 which is ionotropic

5-HT1A - presynaptic downregulation is thought to be responsible for the delayed action of SSRIs
5HT1D - stimulation causes anti-migraine action
5-HT2 - post-synaptic, the target of atypical antipsychotics. Stimulation causes anxiety, agitation, insomnia, sexual dysfunction
5-HT2C - post-synaptic, atypical antipsychotics are associated with weight gain
5-HT3 - stimulation causes nausea, diarrhoea, headache. Ondansetron is antagonist
5-HT7 - involved in circadian rhythm regulation

187
Q

Presynaptic downregulation of these receptors is thought to be responsible for the delayed action of SSRIs

A

5-HT1A

188
Q

Stimulation of these serotonin receptors has an anti-migraine effect

A

5-HT1D

189
Q

These serotonin receptors are the target of atypical antipsychotics.

Stimulation causes anxiety, agitation, insomnia, sexual dysfunction

A

5-HT2

190
Q

These serotonin receptors are associated with the propensity of atypical antipsychotics to cause weight gain

A

5-HT2C

191
Q

The only ionotropic serotonin receptor.

Stimulation (e.g. by SSRIs) causes nausea, diarrhoea, and headache. Ondansetron is an antagonist.

A

5-HT3

192
Q

This serotonin receptor is involved in circadian rhythm regulation.

A

5-HT7

193
Q

Acetylcholine receptors (classification)

A

Nicotinic receptors
- ionotropic

Muscarinic receptors (M1-M5)

  • metabotropic
  • mediate the effects of anticholinergic drugs
  • M1 (peripheral) - tachycardia
  • M4 - hypersalivation (in clozapine)
194
Q

GABA receptors (classification)

A

GABA-A

  • ionotropic
  • composed of 5 subunits
  • agonists: ethanol, benzodiazepines, z-drugs, barbiturates

GABA-B

  • metabotropic
  • agonists: baclofen, GHB

GABA-C
- mainly found in the retina

195
Q

Benzodiazepines (mechanism of action)

A

Bind to the alpha subunit of GABA-A

-> increases the frequency of chloride channel openings

196
Q

Dysfunction of which lobe?

Contralateral hemiplegia, impaired problem solving, disinhibition, lack of initiative, Broca’s aphasia and agraphia (dominant)

A

Frontal lobe

197
Q

Dysfunction of which lobe?

Wernicke’s aphasia (dominant), homonymous upper quadrantanopia, auditory agnosia (non-dominant)

A

Temporal lobe

198
Q

Dysfunction of which lobe?

anosognosia (lack of awareness of a disability or disease)
dressing apraxia (difficulty in getting dressed)
spatial neglect (lack of awareness of one side of the body)
constructional apraxia (inability to copy pictures or combine parts of something into a meaningful whole)
A

Parietal lobe (non-dominant)

199
Q

Dysfunction of which lobe?

finger agnosia (loss in ability to name or recognise specific fingers on the patient’s own or on others hands)
dyscalculia (an impaired ability to perform mental arithmetic)
dysgraphia (inability to write)
right-left disorientation (inability to carry out instructions that involve an appreciation of the right and left)

A

Parietal lobe (dominant)

this is known as Gerstmann’s syndrome

200
Q

Dysfunction of which lobe?

Visual agnosia, visual illusions, contralateral homonymous hemianopia

A

Occipital lobe

201
Q

Alexia without agraphia

essence and pathology

A

The patient cannot read but is able to write. Understanding spoken language and conversation are intact.

Usually due to a lesion destroying the left visual cortex, as well as the connections to the right visual cortex in the corpus callosum.

It is typically caused by an occlusion of a branch of the PCA.

202
Q

Aphasia - definition and classification (3)

A

inability to comprehend or formulate language because of damage to specific brain regions

  • Fluent (receptive) aphasia
  • Non-fluent (expressive aphasia)
  • Pure aphasia
203
Q

Fluent (receptive) aphasia - examples (4)

A

Wernicke’s aphasia
Anomic aphasia
Conduction aphasia
Transcortical sensory aphasia

204
Q

Non fluent (expressive) aphasia - examples (3)

A

Broca’s aphasia
Transcortical motor aphasia
Global aphasia

205
Q

Pure aphasia - example (3)

A

Pure alexia
pure agraphia
pure word deafness

206
Q

Dementia (essence)

A

an acquired syndrome of decline in memory and at least one other cognitive domain (e.g. Language, visuospatial or executive dysfunction) that is sufficient to interfere with social and occupational function in an alert person.

The ICD-10 requires the following for a diagnosis:-

  • Disturbed higher cortical function (memory, thinking, orientation)
  • Consciousness is not clouded (to differentiate from delirium)

It also adds that this may be accompanied by affective, motivational, emotional, perceptual, and motor changes.

207
Q

total population prevalence of dementia among over 65s

A

7.1%

208
Q

total population prevalence of dementia in the UK

A

1.3%

209
Q

Alzheimer’s disease (% of all dementia cases)

A

62%

210
Q

Vascular dementia (% of all dementia cases)

A

17%

211
Q

Mixed dementia (% of all dementia cases)

A

10%

212
Q

Dementia with Lewy bodies (% of all dementia cases)

A

4%

213
Q

Frontotemporal dementia (% of all dementia cases)

A

2%

214
Q

Parkinson’s dementia (% of all dementia cases)

A

2%

215
Q

Anatomical classification of dementia (3)

A

Cortical
Subcortical
Mixed

216
Q

Cortical dementia - areas affected (3)

A

Frontal lobes
Temporal lobes
Parietal lobes

217
Q

Cortical dementia - clinical features (4)

A

Amnesia (memory loss)

Aphasia (inability to understand/express language)

Apraxia (inability to coordinate skilled, purposeful motor tasks e.g. dressing/brushing teeth)

Agnosia (inability to recognise familiar people/objects)

218
Q

Cortical dementia - examples (4)

A

Alzheimer’s disease
Pick’s disease
Creutzfeldt-Jakob disease
Binswanger’s disease

219
Q

Subcortical dementia - areas affected (3)

A

Thalamus
Basal ganglia (caudate nucleus, substantia nigra)
Deep white matter

220
Q

Subcortical dementia - clinical features (3)

A

Bradyphrenia (slowing in cognition), frequently a/w perseveration

Frontal executive dysfunction (planning, organisation, problem-solving, multitasking, motivation, controlling emotion)

Personality/mood changes

221
Q

Subcortical dementia - examples (6)

A

Vascular dementia
Dementia associated Huntington’s disease
Dementia associated AIDS
Dementia associated with Parkinson’s disease
Dementia associated with Wilson’s disease
Dementia associated with progressive supranuclear palsy

222
Q

Mixed dementia - examples (3)

A

Multi-infarct dementia
Corticobasal degeneration
Frontotemporal dementia (amyotrophic form of motor neurone disease)

223
Q

Alzheimer’s disease - gross anatomical (macroscopic) features (3)

A

Generalised brain atrophy
(shrivelling of the cerebral cortex)

Focal atrophy of the medial temporal lobes

  • hippocampus
  • entorhinal cortex

Dilatation of the lateral ventricles
(aka hydrocephalus ex vacuo)

224
Q

Alzheimer’s disease - main histopathological lesions (2)

A

Senile plaques
(extracellular deposits of beta amyloid in the gray matter of the brain)

Neurofibrillary tangles
(intracellular structures made by the hyperphosphorylation of the microtubule-associated tau protein)
225
Q

Senile plaques (description)

A

extracellular deposits of beta amyloid in the gray matter of the brain

found in Alzheimer’s disease

226
Q

Neurofibrillary tangles (description)

A

intracellular structures made by the hyperphosphorylation of the microtubule-associated tau protein

found in Alzheimer’s disease

227
Q

In which disease are the following histopathological features seen?:

cerebral amyloid angiopathy (CAA)
granulovacuolar degeneration (GVD)
Hirano bodies

A

Alzheimer’s disease

228
Q

Alzheimer’s disease - biochemical pathology

A

deficit of acetylecholine from damage to an ascending forebrain projection

229
Q

Alzheimer’s disease - management (4 drugs)

A

NICE now recommend the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease

memantine (a NMDA receptor antagonist) is reserved for patients with moderate - severe Alzheimer’s

230
Q

Frontotemporal dementia - essence, subtypes (3)

A

FTD refers to a clinical syndrome, of which there are 3 types:

  • behavioural variant (BVFTD)
  • progressive non-fluent aphasia (PNFA)
  • semantic dementia (SD)
231
Q

Frontotemporal dementia - common features (4)

A

Onset before 65
Insidious onset
Personality change and social conduct problems
Relatively preserved memory and visuospatial skills

232
Q

Frontotemporal lobe degeneration (FTLD) - essence, subtypes (2)

A

FTLD refers to a pathological diagnosis, of which there are 2 types:

Tauopathies (FTLD-tau)

  • Pick’s disease
  • Corticobasal degeneration (CBD)
  • Progressive supranuclear palsy (PSP) - aka Steele-Richardson-Olszewski syndrome)
  • FTDP-17
  • Multisystem atrophy (MSA)

Ubiquitinopathies (FTLD-U)

  • FTLD-TDP
  • FTDP-17 (PGRN)
  • FTLD-FUS
233
Q

Frontotemporal lobe degeneration (gross anatomical features)

A

Atrophy of the frontal and temporal lobes

234
Q

Pick’s Disease - presentation

A

behavioural-variant frontotemporal dementia

personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.

235
Q

Pick’s Disease - gross anatomical features

A

‘knife-blade’ atrophy of the frontal and temporal lobes

236
Q

Pick’s Disease - histopathological features

A
Pick bodies (spherical aggregations of tau protein)
Pick cells
Gliosis
Neurofibrillary tangles
Senile plaques
237
Q

Lewy body disorders - classification

A

Parkinson’s disease without dementia (PD)

Lewy body dementia (LBD)

  • Dementia with Lewy Bodies (DLB)
  • Parkinson’s disease dementia (PDD)

DLB - PD symptoms develop >1yr after the onset of memory problems
PDD - PD symptoms develop within a year of memory problems; or PD symptoms develop first

238
Q

What drugs should be avoided in Lewy body dementia as patients?

A

Neuroleptics - patients can develop irreversible parkinsonism

239
Q

Lewy body dementia - macroscopic changes (2)

A
Pallor of the substantia nigra
Cerebral atrophy (but less marked than in Alzheimer's)
240
Q

Lewy body dementia - microscopic changes (3)

A

Lewy bodies

  • intracellular protein accumulations
  • made of alpha synuclein

Neurofibrillary tangles

Senile plaques

241
Q

Classic (sporadic) Creutzfeldt-Jakob disease (CJD)

  • age of onset
  • cause
  • duration to death
  • symptoms
  • MRI
  • EEG
A
Age 55-65
Caused by Genetic mutation
5 month duration to death
Early neurological signs and dementia
MRI - Bilateral anterior basal ganglia high signal
EEG - triphasic waves
242
Q

Variant Creutzfeldt-Jakob disease (vCJD)

  • age of onset
  • cause
  • duration to death
  • symptoms
  • MRI
  • EEG
A
Age 25-30
Caused by infected meat products
~1 year duration to death
psychological symptoms such as anxiety, withdrawal and dysphonia are the most common presenting features
MRI - pulvinar sign
EEG - generalised slowing
243
Q

Schizophrenia - macroscopic pathological changes (3)

A

Ventricular enlargement

Reduced brain volume (up to 5%)

Reduced left planum temporale gray matter, and reversed planum temporale surface area asymmetry (normally left larger than right in a right handed person)

244
Q

Schizophrenia - microscopic pathological changes (2)

A

reduction of the size of the dorsolateral prefrontal cortex

reduction of the size of the hippocampus

245
Q

Pure sensory cranial nerves (3)

A

Olfactory
Optic
Vestibulocochlear

1 - 2 - 8

246
Q

Pure motor cranial nerves (5)

A
Oculomotor
Trochlear
Abducens
Accessory
Hypoglossal

3 - 4 - 6 - 11 - 12

247
Q

Mixed (sensory and motor) cranial nerves (4)

A

Trigeminal
Facial
Glossopharyngeal
Vagus

5 - 7 - 9 - 10

248
Q

Neuronal cells (key characteristics)

  • Golgi type 1
  • Golgi type 2
  • Amacrine neurons
A
  • Golgi type 1 - Long axon;
  • Golgi type 2 - Short axon terminating near the parent cell;
  • Amacrine neurons - No axon.
249
Q
Angular gyrus
(location, function, Brodman area)
A

Inferior parietal lobe

Processing of auditory and visual input
Comprehension of language
Number processing

Brodmann area 39

250
Q

Dementia pugilistica

aka, common presentation

A

aka ‘punch drunk syndrome’

a form of dementia usually seen in people who experience repeated head injuries, such as boxers.

Symptoms may appear immediately after a single traumatic brain injury, but are typically described following the cessation of exposure to chronic brain injury.

251
Q

Which white matter tract + type

Efferent projection fibers that connect motor cortex to the brain stem and spinal cord (2)

A

Corticospinal
Corticobulbar

both are projection tracts

252
Q

Which white matter tract + type

Fibers to and from virtually all cortical areas fan out superolaterally from the internal capsule

A

Corona Radiata

Projection tract

253
Q

Which white matter tract + type

Major conduit of fibers to and from the cerebral cortex

A

Internal capsule

Projection tract

254
Q

Which white matter tract + type

Connects the lateral geniculate nucleus to occipital (primary visual) cortex

A

Geniculocalcarine Tract (optic radiation)

Projection tract

255
Q

Which white matter tract + type

The largest white matter fiber bundle, the corpus callosum is a massive accumulation of fibers connecting corresponding areas of cortex between the hemispheres

A

Corpus Callosum

Commissural tract

256
Q

Which white matter tract + type

— crosses through the lamina terminalis. Its anterior fibers connect the olfactory bulbs and nuclei; its posterior fibers connect middle and inferior temporal gyri

A

Anterior Commissure

Commissural tract

257
Q

Which white matter tract + type

Interconnects portions of the frontal, parietal, and temporal lobes

A

Cingulum

Association tract

258
Q

Which white matter tract + type

Connects occipital and frontal lobes (2)

A

Superior Occipitofrontal Fasciculus
Inferior Occipitofrontal Fasciculus

Association tracts

259
Q

Which white matter tract + type

Connects the orbital and inferior frontal gyri of the frontal lobe to the anterior temporal lobe

A

Uncinate Fasciculus

Association tract

260
Q

Which white matter tract + type

Connects the frontal lobe cortex to parietal, temporal, and occipital lobe cortices (the largest association bundle)

A

Superior Longitudinal Fasciculus

Association tract

261
Q

Which white matter tract + type

Connects temporal and occipital lobe cortices

A

Inferior Longitudinal (occipitotemporal) Fasciculus

262
Q

Cerebrospinal fluid

  • formed by which cells
  • where
  • how much
A

formed by ependymal cells in the choroid plexus of the lateral, third and fourth ventricles

approx 500ml/day
the fluid is constantly reabsorbed, so that only 100-160ml is present at any one time.

It occupies the space between the arachnoid and pia matter.

263
Q

Cerebrospinal fluid

  • transport
A

Lateral ventricles
(foramen of Munro)
Third ventricle
(aqueduct of Sylvius aka cerebral aqueduct)
Fourth ventricle
(foramen of Magendie + foramen of Lushka)
Subarachnoid space and spinal cord
(arachnoid villi)
Dural venous sinuses -> return to the vascular system

264
Q

CSF

composition compared with plasma

A

CSF has a composition identical to that of the brain ECF.
Major differences with plasma:

Reduced

  • protein content
  • glucose
  • cholesterol
  • pH
  • calcium
  • potassium

Unchanged
- sodium

Increased

  • chloride
  • magnesium
265
Q

Blood brain barrier

essence

A

a semi permeable membrane formed by the tight junctions of endothelial cells in the capillaries of the brain

separates the blood from the CSF

266
Q

Blood brain barrier

fenestrations - 6

A

At several areas the BBB is fenestrated to allow neurosecretory products to enter the blood. These areas are known as circumventricular organs and include:-

  • Pineal body
  • Posterior pituitary
  • Area postrema
  • Subfornical organ
  • Vascular organ of the lamina terminalis
  • Median eminence
267
Q

Blood brain barrier

permeability - key facts

A
  • Lipid soluble molecules pass through relatively easily whereas water soluble ones do not.
  • Large molecules do not pass through the BBB easily
  • Molecules that are highly charged struggle to pass through
  • The permeability of the BBB increases when it is inflamed
  • Nasally administered drugs can theoretically bypass the BBB
  • The BBB is fenestrated at the circumventricular organs (make an effort to remember the posterior pituitary and the area postrema)
268
Q

Hydrocephalus

essence, classification

A

an abnormal accumulation of CSF in the ventricles of the brain

COMMUNICATING - i.e. normal pressure hydocephalus
NON-COMMUNICATING

269
Q

Normal pressure hydrocephalus

  • cause
  • classic triad (aka)
A

impaired re-absorption of CSF by the arachnoid villi

The CSF pressure is typically high but still within the normal range, for this reason it does not present with features of high ICP such as headache and nausea

Hakim’s triad:

  • Incontinence
  • Gait ataxia
  • Dementia

(‘wet, wobbly, wacky’)

270
Q

Non-communicating hydrocephalus

  • cause
  • features (6)
A

obstruction to the flow of CSF in the third or fourth ventricle

signs of raised intracranial pressure:-

  • Headache
  • Vomiting
  • Hypertension
  • Bradycardia
  • Altered consciousness
  • Papilledema
271
Q

Anterior cranial fossa

  • bones (3)
  • contents (of the brain)
A

Frontal bones
Ethmoid bones
Lesser wing of sphenoid

Frontal lobes

272
Q

Middle cranial fossa

  • bones (3)
  • contents (of the brain)
A

Greater wing of the sphenoid
Sella turcica
Majority of temporal bones

Temporal lobes

273
Q

Posterior cranial fossa

  • bones
  • contents (of the brain) - 3
A

Occipital bone

occipital lobes
cerebellum
medulla

274
Q

Foramen spinosum

  • location (fossa)
  • allows passage of…
A

Middle fossa

Middle meningeal artery

275
Q

Foramen ovale

  • location (fossa)
  • allows passage of…
A

Middle fossa

Mandibular division of trigeminal nerve

276
Q

Foramen lacerum

  • location (fossa)
  • allows passage of…
A

Middle fossa

Internal carotid artery

277
Q

Foramen magnum

  • location (fossa)
  • allows passage of…
A

Posterior fossa

Spinal cord

278
Q

Jugular foramen

  • location (fossa)
  • allows passage of…
A

Posterior fossa

Cranial nerves IX, X, and XI

279
Q

Angular gyrus

  • location (lobe)
  • functions
A

Parietal lobe

Language, mathematics and cognition

280
Q

Cingulate gyrus

  • location
  • functions
A

Adjacent to the corpus callosum

Emotion, learning, and memory

281
Q

Fusiform gyrus

  • location (lobe)
  • functions
A

Temporal lobe

Face and body recognition (damage -> prosopagnosia)
word and number recognition (visual)

282
Q

Precentral gyrus

  • location (lobe)
  • functions
A

Frontal lobe

Voluntary movement control

283
Q

Postcentral gyrus

  • location (lobe)
  • functions
A

Parietal lobe

Touch

284
Q

Lingual gyrus

  • location (lobe)
  • functions
A

Occipital lobe

Dreaming, word recognition (visual)

285
Q

Superior frontal gyrus

  • location (lobe)
  • functions
A

Frontal lobe

Laughter and self awareness

286
Q

Superior temporal gyrus

  • location (lobe)
  • functions
A

Temporal lobe

Language (Wernicke’s area)
Sensation of sound

287
Q

Parahippocampal gyrus

  • location
  • functions
A

Surrounds the hippocampus

Memory
also asymmetry has been observed in schizophrenia

288
Q

Dentate gyrus

  • location
  • functions
A

Hippocampus

Formation of episodic memory

289
Q

Papp-Lantos bodies

  • associated condition
  • description
A

Multisystem atrophy

alpha-synuclein inclusions in oligodendrocytes found in the substantia nigra, cerebellum, and basal ganglia

290
Q

Pick bodies

  • associated condition
  • description
A

Frontotemporal dementia

Large, dark-staining aggregates of proteins in neurological tissue

291
Q

Lewy bodies

  • associated conditions (2)
  • description
A

Parkinson’s disease
Lewy Body dementia

Round, concentrically laminated, pale eosinophilic cytoplasmic inclusions (aggregates of alpha-synuclein)

292
Q

Asteroid bodies

  • associated conditions (2)
A

Sarcoidosis

Berylliosis

293
Q

Barr bodies

essence

A

Stains of inactivated X chromosomes

294
Q

Mallory bodies

  • associated conditions (4)
A

alcoholic hepatitis
alcoholic cirrhosis
Wilson’s disease
primary-biliary cirrhosis

295
Q

Schaumann bodies

  • associated conditions (2)
A

Sarcoidosis

Berylliosis

296
Q

Zebra bodies

  • associated conditions (3)
A

Niemann-Pick disease
Tay-Sachs disease
Any of the mucopolysaccharidoses

297
Q

LE bodies (AKA hematoxylin bodies)

  • associated condition
A

SLE (lupus)

298
Q

Hirano bodies

  • associated conditions (2)
  • description
A

Normal ageing
but more numerous in Alzheimers disease

Eosinophilic, football shaped inclusion seen in neurons of the brain

299
Q

Neurofibrillary Tangles

  • associated condition
  • description
A

Alzheimer’s disease

Microtubule-associated proteins and neurofilaments

300
Q

Kayser-Fleischer rings

  • associated condition
  • description
A

Wilson’s disease

Rings of discoloration on cornea

301
Q

Kuru plaques

  • associated condition
  • description
A

Kuru and Gerstmann-Sträussler syndrome
sometimes present in Creutzfeldt-Jakob disease (CJD)

composed partly of a host-encoded prion protein

302
Q

Papez circuit

essence

A

a neural pathway in the brain that mediates the process of emotion

it was one of the first descriptions of the limbic system

bilateral, symmetrical and located on the medial surface of the brain.

llinks the cortex to the hypothalamus

303
Q

Papez circuit - components (8)

A
Hippocampus
   fornix (its major output tract)
Mamillary bodies of the hypothalamus
   mamillothalamic tract
Anterior nucleus of the thalamus
Cingulate gyrus
Parahippocampal gyrus
Entorhinal cortex
   (-> returns to hippocampus)
304
Q

EEG Delta Waves

  • Frequency
  • Brain region
  • Normally seen in
A

1-4 Hz

Frontally in adults and posteriorly in children

Slow wave sleep and in babies.
If present when awake this strongly suggests pathology

305
Q

EEG Theta Waves

  • Frequency
  • Brain region
  • Normally seen in
A

4-8 Hz

Generalised

Young children,
drowsy and sleeping adults,
with certain medications,
meditation.

Small amount seen in awake adults, excessive amount when awake may indicate pathology

306
Q

EEG Alpha Waves

  • Frequency
  • Brain region
  • Normally seen in
A

8-12 Hz

Posteriorly

When relaxed and when the eyes are closed (whilst awake)

307
Q

EEG Beta Waves

  • Frequency
  • Brain region
  • Normally seen in
A

12-30 Hz

Frontally

When busy or concentrating

=================
‘Beta’ - B for ‘busy’

308
Q

EEG Sigma Waves (aka)

  • Frequency
  • Brain region
  • Normally seen in
A

(aka sleep spindles)

12-14 Hz

Frontal and central regions

Stage 2 sleep.

===================
Along with k-complexes they are the defining characteristic of stage 2 sleep

309
Q

EEG Gamma Waves

  • Frequency
  • Brain region
  • Normally seen in
A

30-100 Hz

No specific areas

Meditation

310
Q

sporadic CJD

  • EEG findings (2)
A

Early - non specific slowing

Later - periodic biphasic and triphasic synchronous sharp wave complexes, superimposed on a slow background rhythm

311
Q

Huntingdon’s disease

  • EEG findings
A

Low voltage EEG,

Flattened trace (in particular no alpha)

312
Q

Delirium

  • EEG findings (3)
A

Diffuse slowing

Decreased alpha

Increased theta and delta

313
Q

Delirium tremens

  • EEG findings
A

Hyperactive trace, fast

314
Q

Alzheimer’s disease

  • EEG findings (2)
A

Reduced alpha and beta

Increased delta and theta

315
Q

Petit mal epilepsy (absence seizure)

  • EEG findings
A

Generalised, bilateral, synchronous, 3Hz (3 waves per second) spike and wave pattern

316
Q

Generalised epilepsy

  • EEG findings
A

Sharp spikes, 25-30Hz

317
Q

Partial epilepsy

  • EEG findings
A

Focal spikes

318
Q

Myoclonic epilepsy

  • EEG findings
A

Generalised spike and wave activity

319
Q

Encephalopathy

  • EEG findings
A

Diffuse slowing

320
Q

Normal aging

  • EEG findings
A

Diffuse slowing, which can be focal or diffuse,

if focal most commonly seen in the left temporal region

321
Q

Typical antipsychotics

  • effect on EEG (2)
A

Decreased beta
Increased alpha and delta,

====================
haloperidol least effect

322
Q

Which atypical antipsychotic has most significant effect on the EEG?

A

Clozapine

323
Q

Antidepressants

  • effect on EEG (2)
A

Reduce beta

Increase in all other wave forms

324
Q

Anticonvulsants

  • effect on EEG
A

None

325
Q

Lithium

  • effect on EEG
A

Slowing

326
Q

Benzodiazepines

  • effect on EEG (2)
A

Increase beta

Decrease alpha

327
Q

Barbiturates

  • effect on EEG
A

Increase beta

328
Q

Stimulants (cocaine, nicotine)

  • effect on EEG
A

Increase alpha

329
Q

Depressants (alcohol, opioids)

  • effect on EEG
A

Decrease alpha

330
Q

Cannabis

  • effect on EEG
A

Increase alpha

331
Q

Which stage of sleep predominates in a neonate?

A

REM sleep

=========================
Newborns sleep about 16 hours a day. They spend more than 50% of sleep time in REM sleep. Sleep-onset REM is also seen in neonates.

332
Q

HPA axis (summary)

A
Hypothalamus
   (CRH)
Anterior pituitary
   (ACTH)
Adrenal cortex
   (Cortisol)
333
Q

HPA axis dysfunction in depression

A

Hypersecretion of CRH, ACTH, and Cortisol
Adrenocoritcal enlargement
CRH elevated in the CSF

About 50% of depressed inpatients do not show the normal suppression of cortisol on dexamethasone suppression test

334
Q

NREM Sleep Stage I

  • % of time spent in stage
  • EEG findings
A

5%

Theta waves

335
Q

NREM Sleep Stage II

  • % of time spent in stage
  • EEG findings
A

45%

Sleep spindles
K complexes

336
Q

NREM Sleep Stage III

  • % of time spent in stage
  • EEG findings
A

12%

<50% Delta waves

337
Q

NREM Sleep Stage IV

  • % of time spent in stage
  • EEG findings
A

13%

> 50% Delta waves

338
Q

Sleep latency

  • definition
  • average time
A

Time taken to fall asleep (onset of NREM Stage I)

15-20mins

339
Q

Mirror neuron

  • location
  • function
A

a particular class of visuomotor neurons, originally discovered in area F5 of the monkey PREMOTOR CORTEX

they discharge both when the monkey does a particular action and when it observes another individual (monkey or human) doing a similar action.

They offer a model for understanding imitation learning

340
Q

Wernicke and Korsakoff syndrome

  • specific brain region affected
A

Medial thalamus and mammillary bodies of the hypothalamus

341
Q

Hemiballism

  • specific brain region affected
A

Subthalamic nucleus of the basal ganglia

342
Q

Huntington chorea

  • specific brain region affected
A

Striatum (caudate nucleus) of the basal ganglia

343
Q

Parkinson’s disease

  • specific brain region affected
A

Substantia nigra of the basal ganglia

344
Q

Kluver-Bucy syndrome
(hypersexuality, hyperorality, hyperphagia, visual agnosia)

  • specific brain region affected
A

Amygdala

345
Q

Utilization behaviour

  • description
  • caused by dysfunction to which lobe?
A

reaching out and automatically using objects in the environment in an object-appropriate manner that is inappropriate for the particular context.

e.g. a patient may pick up a toothbrush and begin to brush his teeth, in response to a toothbrush being placed in front of him, but in a context or setting in which brushing teeth would not normally be expected or done, such as in an appointment with a doctor.

results from lesions of the orbitofrontal lobe whereby there is a loss of normal inhibitory control.

346
Q

Alien hand sign

A

the experience of bizarre hands movements for which the patient feels no sense of control

347
Q

Manual groping behaviour

  • description
A

refers to situations where the hand (and often the eyes as well) follow an object under examination, in a somewhat magnetic fashion.

Following tactile stimulation, automatic manual manipulation is observed. The patients may, for example, hold, rub, or manipulate objects placed in front of them or on their own person (e.g., buttons, the fabric of collars, etc.).

348
Q

Environmental Dependency Syndrome

A

the deficits in personal control of action and a striking overreliance on social and physical environmental stimuli for guiding ones behaviour in a more elaborate social context.

e.g. one patient, upon being told that the examiners office was an art gallery, began staring and commenting on pictures as if they were on display.

349
Q

Multisystem atrophy

  • essence
  • presentations/cardinal features (3)
A

one of the Parkinson plus syndromes, three presentations:

Triad of symptoms:

  • Cerebellar Ataxia
  • Autonomic failure
  • Parkinsonism
Shy-Drager Syndrome (mainly autonomic failure)
Striatonigral degeneration (mainly Parkinsonism)
Olivopontocerebellar atrophy (mainly cerebellar ataxia)
350
Q

Multisystem atrophy

  • macroscopic features (3)
  • microscopic features (1)
A

Macroscopic features

  • Pallor of substantia nigra
  • Greenish discolouration and atrophy of the putamen
  • Cerebellar atrophy

Micrscopic features:
- Papp-Lantos bodies
(alpha-synuclein inclusions in oligodendrocytes found in the substantia nigra, cerebellum, and basal ganglia)

351
Q

Cranial nerve reflexes:

Pupillary light reflex

  • Sensory component
  • Motor component
A

Sensory: Optic

Motor: Oculomotor

352
Q

Cranial nerve reflexes:

Accommodation reflex

  • Sensory component
  • Motor component
A

Sensory: Optic

Motor: Oculomotor

353
Q

Cranial nerve reflexes:

Jaw jerk

  • Sensory component
  • Motor component
A

Sensory: Trigeminal

Motor: Trigeminal

354
Q

Cranial nerve reflexes:

Corneal reflex

  • Sensory component
  • Motor component
A

Sensory: Trigeminal

Motor: Facial

355
Q

Cranial nerve reflexes:

Vestibulo-ocular reflex

  • Sensory component
  • Motor component
A

Sensory: Vestibulocochlear

Motor: Oculomotor, trochlear, abducent

356
Q

Cranial nerve reflexes:

Gag reflex

  • Sensory component
  • Motor component
A

Sensory: Glossopharyngeal

Motor: Vagus

357
Q

Apraxia

essence

A

a motor disorder caused by damage to the brain (specifically the posterior parietal cortex) in which the individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and the individual is willing to perform the task.

358
Q

an inability to make fine/delicate movements

A

Limb kinetic apraxia

359
Q

an inability to follow out learned tasks when given the necessary objects

e.g. if given a hairbrush they try to write with it

A

Ideomotor apraxia

360
Q

an inability to copy a picture or combine parts of something to form a whole

A

Constructional apraxia

361
Q

an inability to follow a sequence of actions in the correct order

e.g. Take a match out a box and strike it with your left hand

A

Ideational apraxia

362
Q

an inability to control eye movements

A

Oculomotor apraxia

363
Q

Homonymous hemianopia (location of lesions)

  • incongruous (asymmetrical)
  • congruous (symmetrical)
  • macula sparing
A
  • incongruous (asymmetrical) - optic tract
  • congruous (symmetrical) - optic radiation or occipital cortex
  • macula sparing - occipital cortex
364
Q

Homonymous quadrantanopia (location of lesions)

  • superior
  • inferior
A

superior: lesion of temporal lobe
inferior: lesion of parietal lobe

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

365
Q

Bitemporal hemianopia (location of lesions)

  • upper quadrant defect > lower quadrant defect
  • lower quadrant defect > upper quadrant defect
A

optic chiasm

upper quadrant defect > lower quadrant defect:

  • inferior chiasmal compression
  • commonly a pituitary tumour

lower quadrant defect > upper quadrant defect

  • superior chiasmal compression
  • commonly a craniopharyngioma
366
Q

Illicit drugs (mechanism of action)

  • drugs that interefere with ionotropic receptors or ion channels (4)
A

Alcohol
nicotine
benzodiazepines
ketamine

367
Q

Illicit drugs (mechanism of action)

  • Drugs which interfere with G coupled receptors (3)
A

Opioids
cannabinoids
y-hydroxybutyrate (GHB)

368
Q

Illicit drugs (mechanism of action)

Drugs that target monoamine transporters (3)

A

Amphetamine
ecstasy
cocaine

=====================
The main mechanism by which cocaine and amphetamine act is by increasing levels of dopamine in the synaptic cleft.
They do this however in slightly different ways.

369
Q

Wilson’s disease

  • aka
  • pathophysiology
  • brain regions affected
A

hepatolenticular degeneration

failure to excrete copper results in very high levels in the liver and brain

degeneration of the lenticular nucleus (putamen and globus pallidus)

370
Q

Wilson’s disease

  • biochemistry findings
  • clinical features
A

low levels of both ceruloplasmin and total serum copper.

The condition presents with movement disorders such as dystonia, parkinsonian tremor, and rigidity combined with behavioural problems and a degree of dementia is often seen.

A Kayser-Fleischer ring is the term given to the brown ring seen around the iris in people with Wilson’s disease.

371
Q

Which cranial nerves exit through the Cribiform plate?

A

Olfactory (I)

372
Q

Which cranial nerves exit through the Optic foramen?

A

Optic nerve (II)

373
Q

Which cranial nerves exit through the Superior orbital fissure?

A

Oculomotor (III)
Trochlear (IV)
Trigeminal (ophthalmic V1)
Abducens (VI)

374
Q

Which cranial nerves exit through the Round foramen?

A

Trigeminal (maxillary V2)

375
Q

Which cranial nerves exit through the Oval foramen (Foramen Ovale)?

A

Trigeminal (mandibular V3)

376
Q

Which cranial nerves exit through the Internal auditory canal?

A

Facial (VII)

Vestibulocochlear (VIII)

377
Q

Which cranial nerves exit through the Jugular foramen?

A

Glossopharyngeal (IX)
Vagus (X)
Accessory (XI)

378
Q

Which cranial nerves exit through the Hypoglossal canal?

A

Hypoglossal (XII)

379
Q

Autotopagnosia

A

Inability to orient parts of the body

380
Q

Phonagnosia

A

Inability to recognize familiar voices

381
Q

Astereoagnosia

A

Inability to recognize objects by touch

382
Q

Lentiform nucleus

  • components (2)
A

Putamen

Globus pallidus

383
Q

Hypothalamic nucleus responsible for:

Circadian rhythm

A

Suprachiasmatic

384
Q

Hypothalamic nucleus responsible for:

Secretes GnRH to stimulate LH and FSH in the anterior pituitary
Regulates body temperature

A

Preoptic

385
Q

Hypothalamic nucleus responsible for:

Synthesizes oxytocin

A

Paraventricular

386
Q

Hypothalamic nucleus responsible for:

Regulates parasympathetics to keep cool

A

Anterior

387
Q

Hypothalamic nucleus responsible for:

Regulates sympathetics to keep warm

A

Posterior

388
Q

Hypothalamic nucleus responsible for:

Synthesizes ADH

A

Supraoptic

389
Q

Hypothalamic nucleus responsible for:

Releases dopamine
GHRH to anterior pituitary
Hunger & satiety

A

Arcuate

390
Q

Hypothalamic nucleus responsible for:

Stimulate gastrointestinal system, hunger
Triggers shivering

A

Dorsomedial

391
Q

Hypothalamic nucleus responsible for:

Satiety

A

Ventromedial

392
Q

Hypothalamic nucleus responsible for:

Hunger and thirst

A

Lateral

393
Q

5-HIAA

  • what is it
  • association with depression
A

serotonin metabolite (5-hydroxyindoleacetic acid)

low CSF levels in a third of people with depression

low CSF levels also associated with:

  • higher likelihood of suicide
  • increased levels of aggression
394
Q

What brain region is responsible for executive functions such as planning, judgement, and decision-making?

A

Dorsolateral prefrontal cortex