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Medicine > Neuroanatomy > Flashcards

Neuroanatomy Flashcards

1
Q

Why is the nervous system most susceptible to insult during pre-natal development?

A

It takes a long time to develop

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2
Q

What are the 6 stages of formation of the neural tube?

A

1- Gastrulation produces the notochord
2- Notochord induces neurulation
3- Induction of neural plate
4- Elevation of lateral edges of neural plate
5- The depressed mid-region is the neural groove
6- Neural folds gradually approach each other in the midline and fuse, producing the neural tube

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3
Q

What is the Notochords responsibility in neurulation?

A

It is a solid rod of cells running in the midline with important signalling role

Notochord directs conversion of overlying ectoderm to neuroectoderm - the signalling is via diffusion and so only reaches a small area of space and also the responding tissues need to have the receptors fo these signals

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4
Q

How long does it take for the neural tube to form and during which days?

A

10 days to form

Starting day 18 and completing approximately day 28-32

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5
Q

How are neuropores related to the neural tube closure?

A

Have an anterior and posterior neuropore

The closing starts in the middle and then runs cranially and caudally leaving 2 areas that are not fused.

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6
Q

What does anencephaly mean?

A

Absence of brain and head structures due to the failure of the neural tube to close cranially

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7
Q

What is spina bifida in neurolodevelopmental terms?

A

Posterior closure defect

Can occur anywhere along the length but most commonly lumbosacral region

Not associated with cognitive delay

Hydrocephalus nearly always occurs

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8
Q

What is the difference between a meningocoele and mylomeningocoele?

A

Meningocoele = the nervous tissue doesn’t sit inside the cyst and remains within the space in the spinal column - the only thing affected is the vertebral arch

Mylomeningocoele = the spinal cord sits inside the cyst which is outside of the spinal column

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9
Q

What does rachischisis mean?

A

Failure of neural fold elevation

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10
Q

How do we screen for neural tube defects before the foetus is born?

A

Alpha-foetoprotein will be raised in the maternal serum = increased foetal proteins.

It is not diagnostic but indicates there is a problem

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11
Q

Up to which month is the spinal cord and the vertebral column the same length?

A

3rd month after which the vertebral column grows faster leading to the cauda equina

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12
Q

During neural fold formation 3 primary brain regions can be distinguished which are?

A

Forebrain - prosencephalon
Midbrain- Mesencephalon
Hindbrain- Rhombencephalon

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13
Q

During brain folding there are 5 secondary brain vesicles which lead to which 5 mature derivative structures?

A

Cerebral hemispheres, thalamus, midbrain, pons/ cerebellum, medulla oblongata

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14
Q

What is the difference between the alar plate and the basal plate in the early organisation of the neural tube?

A

Alar plate = sensory

Basal plate = motor

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15
Q

What are neural crest cells and what is their role?

A

Cells of the lateral border of the neuroectoderm tube

Become displaced and enter the mesoderm and undergo epithelial to mesenchymal transition

They will migrate from the dorsum to the ventral direction leaving behind cells that make the sympathetic ganglion, preaortic ganglia, enteric ganglia etc

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16
Q

Why can defects occur of the neural crest cells and their migration?

A

They migrate extensively and contribute to a wide range of structures

Because of the complex migratory pattern they are extremely vulnerable to environmental insult esp alcohol but can also be genetic

Defects can affect single components but also multiple components resulting in recognisable syndromes

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17
Q

Name 2 conditions that are caused by defects in the migration or morphogenesis of structure(s)

A

One structure affected= Hirschsprung’s disease (aganglionic megacolon)

Multiple structures=
DiGeorge syndrome (thyroid deficiency, immunodeficiency secondary to thymus defect, cardiac defects, abnormal faces.
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18
Q

What are the basic components of the CNS?

A

Cerebral hemispheres
Brainstem and cerebellum
Spinal cord

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19
Q

What are the basic components of the Parasympathetic NS?

A

Dorsal and ventral roots
Spinal nerves
Peripheral nerves

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20
Q

In a very basic sense which one of the following can regenerate: CNS or PNS?

A

PNS

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21
Q

What covers neurones in the CNS?

A

Oligodendrocytes

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22
Q

What covers neurones in the PNS?

A

Schwann cells

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23
Q

Describe 3 features of the grey matter

A

Comprised of cell bodies and dendrites
Highly vascular
Contains axons that communicate with the white matter

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24
Q

Describe 3 features of white matter

A

Composed of axons (with their supporting cells)
White due to the presence of fatty myelin compared to grey matter
Supported by oligodendrocytes

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25
Q

What is the equivalent of the grey matter in the PNS?

A

Ganglion (collection of cell bodies)

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26
Q

What is the equivalent of white matter in the PNS?

A

Peripheral nerves

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27
Q

How many spinal segments are there?

A

31

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28
Q

Each segment has 3 types of nerves/roots, what are they?

A

Spinal nerve = mixed
Dorsal = sensory
Ventral = motor root

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29
Q

What does funiculus mean?

A

A segment of white matter containing multiple distinct tracts. Impulses travel in multiple directions

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30
Q

What is a spinal tract?

A

Anatomically and functionally defined white matter pathway connecting two distinct regions of grey matter. Impulses travel in one direction e.g. cortico-spinal tract = cortex to spinal column 1 way

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31
Q

What does a fasciculus mean?

A

A subdivision of a tract supplying a distinct region of the body - important in sensory information

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32
Q

What is a nucleus?

A

A distinct population of motor neurones in the CNS that supply a given muscle but arise from multiple cord segments

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33
Q

What are the four fibre types in the CNS?

A

Association fibres = short and connect close regions in the same hemisphere

Cortex = folded area of the brain ~3mm deep

Commissural fibres = connect contralateral sides also in spinal cords

Projection fibres = brain down to spinal cord

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34
Q

What are colliculi?

A

Reflex centres in mid brain - rapid reflexes to auditory and visual stimuli

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35
Q

What is the midbrain, pons and medulla responsible for?

A

Mid brain - eye movements and reflex responses to sound and vision
Pons - Trigeminal nerves that responsible for feeding and sleeping
Medulla - homeostatic controls - cardiovascular and respiratory centres but contains a major motor pathway

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36
Q

What are the gyri and sulci?

A

Central sulcus- sitting in the coronal plane - key landmark separating frontal and parietal lobes
Pre-central gyrus - contains primary motor cortex
Post-central gyrus - contains primary sensory cortex
Lateral/Sylvian fissure- separates temporal from frontal/parietal lobes
Parieto-occipital sulcus - Separates from occipital lobe
Calcarine sulcus - primary visual cortex surrounds this

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37
Q

What are the key features of the brain - interior aspect

A
  • Optic chiasm = fibres in the visual system cross over
  • Uncus = part of the temporal lobe that can herniate compression the midbrain
  • Medullary pyramids = location of descending motor fibres - (each has around 1 million axons).
  • Parahippocampla gurys = Key cortical region for memory encoding
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38
Q

Name the structures on the midline of the brain and their functions

A

Corpus callosum - fibres connecting the two cerebral hemispheres
Thalamus - sensory relay station projecting to sensory cortex
Cingulate gyrus - cortical area important for emotion and memory
Hypothalamus - essential centre for homeostasis
Fornix - Major output pathway from the hippocampus
Tectum - dorsal part of the midbrain involved in involunatry responses to auditory and visual stimuli
Cerebellar tonsil- part of the cerebellum that can herniate and compress the medulla

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39
Q

What is the structure in the brain that produces CSF?

A

Choroid plexus

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40
Q

Name the 4 ventricles

A

I & II = lateral ventricles
III = squashed between the two thalami and make it flat - interventricular foramen
IV - at the position of the medulla

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41
Q

What two foramen are found in the 4th ventricle and what is their function?

A

Foramen of Lushka and sit lateral to the 4th ventricle

Foramen of Magendie sits in the midline and is a hole in the tube

Allow CSF to get into the subarachnoid space as there is a connection now

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42
Q

What ways are the cerebral ventricles connected?

A

3rd to the 4th ventricle = cerebral aqua duct

4th ventricle to the lower spinal column = central canal - very narrow though and v poor drainage therefore functionally small

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43
Q

Name the 3 types of glia

A

Astrocytes (several different types)

Oligodendrocytes

Microglia

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44
Q

What is the most basic function of the glial cells?

A

Astrocytes - most abundant type of glial cell and are the supporters

Oligodendrocytes - insulators

Microglia - immune response - brain has immune privilege anyway but these are the resident macrophages

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45
Q

What is the role of astrocytes?

A
  • Structural support
  • Provide nutrition for neurones - glucose-lactate shuttle
  • Remove neurotransmitters (uptake) - control concentration of neurotransmitters (especially important for glutamate (toxic)
  • Maintain ionic environment - K+ buffering
  • Help to form blood brain barrier
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46
Q

What is the need for glucose lactate shuttle?

A

Neurones do not store or produce glycogen

Therefore astrocytes produce lactate which is transferred to neurones and supplements their supply of glucose

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47
Q

Why and how do the astrocytes help to buffer K+ in brain ECF?

A

Why= high neuronal activity leads to rise in K+ ECF and astrocytes take up K+ to prevent this because this causes them to depolarise inappropriately.

Astrocytes are coupled to each other and so they can reduce ECF K+ quickly in a large space.

K+ entry quickly through potassium channels
Na/K ATPase - increased activity therefore more K+ mopped up from ECF, NKCC2 channels will also uptake K+ into the cell

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48
Q

What makes up/maintains the blood brain barrier?

A

Astrocytes surround the capillaries

Because the brain is so sensitive to external forces it is important to control the ECF environment

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49
Q

What glucose transporter is found in the brain?

A

GLUT3

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50
Q

What glucose transporter is found on the basal surface of epithelia?

A

GLUT1

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51
Q

What is allowed to pass through the BBB?

A

Glucose, amino acids, potassium, hydrogen etc

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52
Q

Why is the CNS immune privileged?

A

Rigid skull wont tolerate volume expansion which is what happens in inflammation (tumour).
T-cells can enter the CNS once antigen presentation has occurred by the microglia
T-cells response is inhibited to reduce the release of pro-inflammatory mediators which would cause cerebral oedema.

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53
Q

Where do the inhibitory neurones synapse onto the next neurone?

A

Directly onto the cell body

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54
Q

Where do excitatory neurones synapse onto the following neurones?

A

At the dendrites

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55
Q

What are 3 main broad categories of neurotransmitters?

A

Amino acids, biogenic amines, peptides

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56
Q

Give examples of amino acid neurotransmitters

A

Glutamate
GABA
Glycine

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57
Q

Give examples of biogenic amines as neurotransmitters

A 
Acetylcholine
Noradrenaline
Dopamine
Serotonin
Histamine
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58
Q

Gives examples of peptide neurotransmitters

A 
Dynorphin
Enkephalins
Substance P
Somatostatin
Cholecystokinin
Neuropeptide Y
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59
Q

Name one excitatory and 2 inhibitory amino acid neurotransmitters

A

Excitatory - Glutamate (70% of all CNS synapses are glutamatergic)

Inhibitory - GABA and Glycine

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60
Q

What do glutamate receptors mainly do and how do they work?

A

Ionotropic- AMPA receptors (Na/K channel), Kainate receptors (Na/K channel), NMDA receptors (Na/K and Ca channel)

Metabotropic- mGluR1-7
GPCR- linked to either changes in IP3 and Ca mobilisation or inhibition of adenylate cyclase and decreased cAMP levels

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61
Q

What are fast excitatory responses?

A

Excitatory neurotransmitters cause depolarisation of the postsynaptic cell by acting on ligand gated-ion channels

Excitatory postsynaptic potential (EPSP) depolarisation causes more action potentials

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62
Q

Describe the Glutamatergic synapse

A

They have both AMPA and NMDA receptors

AMPA receptors mediate the initial fast depolarisation

NMA receptors are permeable to calcium - they need glutamate to bind and the cell to be depolarised to allow ion flow through the channel - glycine acts as a co-agonist

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63
Q

How does the amount of calcium that enters the cell relate to function?

A

More calcium that enters the cell the more stronger the connection between 2 neurones and therefore the memory

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64
Q

What function does glutamate receptors have in learning and memory?

A

Activation of NMDA receptors (and mGluRs) can up-regulate AMPA receptors
Strong, high frequency stimulation causes long term potentiation
Calcium entry through NMDA receptors important for induction of long term potentiation
Too much Ca2+ entry through NMDA receptors causes excitotoxicity - therefore too much glutamate - excitotoxicity.

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65
Q

How do GABA and glycine receptors work?

A

GABA and glycine receptors have integral Cl- channels
Opening of the Cl- channels causes hyperpolarisation - inhibitory post-synaptic potential therefore decreased action potential firing

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66
Q

What two drug classes act on the GABA receptors?

A

Benzodiazepines and barbiturates

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67
Q

Where is glycine present in the highest concentration in the CNS?

A

Spinal cord and brainstem

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68
Q

What is the benefit of glycine being in high concentrations in the spinal cord and brain stem?

A

Glycine is an inhibitory neurotransmitter
This is important when wanting to inhibit a response for example in a monosynaptic reflex arc we want to activate one muscle group but inhibit the antagonistic muscle group to allow a movement to occur so glycine would inhibit the antagonistic muscle groups

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69
Q

What main areas are projected to by cholinergic pathways in the CNS?

A

Cortex and hippocampus

Also interneurones in the corpus striatum that are local cholinergic

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70
Q

What main functions do cholinergic pathways serve in the brain?

A

Arousal, learning, memory, motor control

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71
Q

Degeneration of cholinergic neurones in which part of the brain is associated with Alzheimer’s disease?

A

Nucleus basalis

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72
Q

What pathways are dopaminergic pathways in the CNS a part of?

A

Mesocortical pathway, mesolimbic pathway, nigrostriatal pathway

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73
Q

What does the nigrostriatal pathway do?

A

Motor control

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74
Q

What is the mesolimbic pathway involved in?

A

Mood, arousal and reward

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75
Q

What is the mesocortical pathway involved in?

A

Mood, arousal and reward

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76
Q

What are the two conditions associated with dopamine dysfunction?

A

Parkinson’s disease

Schizophrenia

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77
Q

What area of the brain has the substantia nigra?

A

Corpus striatum

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78
Q

What is the peripheral L-dopa enzyme that produces peripheral dopamine?

A

Aromatic amino acid decarboxylase

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79
Q

What receptors do noradrenaline work on in the CNS?

A

GPCR alpha and beta adrenoceptors are the same as in the periphery

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80
Q

Where are the cell bodies of NA containing neurones located?

A

Brainstem (pons and medulla)

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81
Q

What areas of the brain are responsive to NA?

A

Cortex
Hypothalamus
Amygdala
Cerebellum

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82
Q

What is the function of NA in behavioural arousal?

A

Most NA in brain comes from neurones in the locus ceruleus

LC neurones inactive during sleep but activity increases during behavioural arousal

There is a relationship between mood and state of arousal - depression maybe associated with a deficiency of NA

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83
Q

What is the distribution of serotonergic pathways in the CNS?

A

Similar to NA cortex, hypothalamus, amygdala, cerebellum and pons and medulla

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84
Q

What is the function of serotonin in the brain?

A

Sleep/wakefulness

Mood

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85
Q

In which part of the spinal column do sensory pathways go and in which direction?

A

Dorsal column and they are ascending tracts

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86
Q

In which part of the spinal column are motor tracts found and which direction of travel?

A

Motor tracts found in anterior horn through for example the medial longitudinal fasciculus, ventral corticospital tract, pontine reticulospinal tract etc

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87
Q

What are the 7 modalities of sensation?

A 
1- Temperature
2- Pain
3- Pressure
4- Fine touch
5- Vibration
6- Proprioception
7- 2-point discrimination
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88
Q

What modalities are running through the spinothalamic tract and where do they end up?

A

Pain, Crude touch (pressure), Temperature

End up in the somatosensory region of the thalamus

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89
Q

What modalities go through the dorsal column system?

A

Fine touch, Vibration, Proprioception, 2-point discrimination

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90
Q

What are the rapidly adapting receptors and their function?

A

They start with high frequency then over time will reduce to low frequency e.g. bum and sitting down

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91
Q

What are the slowly adapting receptors and their function?

A

Nociceptors remain high number of action potentials. They are important for harm and being able to do something about it

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92
Q

What is the receptive field in the sensory system?

A

Regions of skin that a nerve supplies e.g. dermatologist. Given area of skin e.g. 1cm squared.
Sensory acuity is inversely proportional to the receptive field size = smaller the sensory acuity the higher the receptive field size.
Acuity is proportional to the number of sensory neurones e.g. finger tip or tip of tongue where there are a lot of sensory neurones therefore there is a high level of acuity.

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93
Q

Where is the best place to test sensory acuity?

A

There would be overlap of the boundaries of the dermatomes and therefore the middle of the receptive field is the best place to clinically test for function

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94
Q

What are the basic principles of the 3 neurones between the receptor and primary sensory cortex?
(Location of cell body and the area of projection)

A

Primary neurone- aka the receptor
Cell body in sensory ganglion (dorsal root ganglion)
Projects into spinal cord on ipsilateral side

Secondary neurone -
Cell body in medulla or in dorsal horn
Decussates and projects onto the third order neurone

Tertiary neurone- aka. Third order neurone
Cell body in thalamus
Projects to primary sensory cortex via the internal capsule in post-central gyrus

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95
Q

What is the retina?

A

The area at the back of the eye which is responsible for vision

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96
Q

What is the blind spot the result of?

A

No photoreceptor cells at the optic disc where the central retinal artery and vein enter and exit the eye

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97
Q

What part of the eye gives the highest visual acuity?

A

The fovea centralis on the macula lutea

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98
Q

Why do albino people have photophobia/ sensitivity to bright lights?

A

No pigmented layer on the retina of the eye

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99
Q

What are the two layers of the retina?

A

Pigmented layer

Neural layer

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100
Q

What cell is responsible for black and white images?

A

Rods

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101
Q

What cell is responsible for colour vision?

A

Cone

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102
Q

What cell is responsible for visual acuity?

A

Cones

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103
Q

What is the function of the horizontal cells in the retina?

A

Inhibit cells lateral to the photoreceptor cell that has the most amount of light hitting it

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104
Q

What is the function of the bipolar cell of the retina?

A

Connect the rods and cones to the ganglion cells and transmit information directly or indirectly through to the ganglion cells

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105
Q

What does optical coherence tomography do?

A

Looks at layers of the retina for damage

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106
Q

What 2 fibres comprise the optic nerve?

A

Temporal and nasal fibres

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107
Q

How many segments is the visual field of one eye split into?

A

4-

Inferior and superior nasal and temporal

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108
Q

What is the difference between optic nerve and optic tract?

A

Optic nerve is all the fibres from one eye where as the optic tract is a combination of fibres from both eyes (temporal fibres on the ipsilateral side and the nasal fibres from the contralateral side)

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109
Q

From the optic chiasm where do the fibres go?

A

Lateral Geniculate Nucleus

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110
Q

The optic radiations start in which area and end in which area?

A

Start - lateral geniculate nucleus

End - Primary visual cortex in the occipital lobe

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111
Q

Where do the superior optic radiations go through and what is the visual field detected?

A

Parietal lobe

Superior quadrant fibres

Left parietal lobe will see left eye inferior nasal quadrant of view and right eye inferior temporal quadrant of view
Right parietal lobe will see right eye inferior temporal quadrant of view and left eye inferior nasal quadrant of view

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112
Q

Where do the inferior optic radiations go through and what is the visual field detected?

A

Temporal lobe

Inferior quadrants of vision

Left temporal lobe will see from the left eye superior temporal quadrant of view and right eye superior nasal quadrant of view
Right temporal lobe will see from the right eye superior nasal quadrant of view and left eye superior temporal quadrant of view

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113
Q

What is Baum’s loop?

A

The parietal lobe tracts

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114
Q

What is Meyer’s loop?

A

The temporal lobe tracts

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115
Q

What is an optic radiation?

A

The tracts after the fibres have passed through the LGN to the primary visual cortex

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116
Q

What fibres in the eye are responsible for temporal and nasal field of vision?

A

Nasal fibres responsible for temporal field of vision

Temporal fibres responsible for nasal field of vision

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117
Q

What is monocular blindness and what is it caused by?

A

When only can see through one eye and caused by damage to the optic nerve

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118
Q

What is and what causes bitemporal hemianopia?

A

Visual field where only the vision from the temporal fibres are seen and this would mean that there is a central field of view

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119
Q

What is homonomous hemianopia and what is the lesion?

A

Optic tract is affected therefore the visual field that can be seen is: contralateral nasal visual field and ipsilalateral temporal visual field.

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120
Q

What is a homonomous inferior quadrantanopia and what causes it?

A

Same sided inferior visual field quadrant affected

Damage to the optic radiations on parietal lobe affected therefore the lesion must result in left inferior visual field defect

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121
Q

What is a homonomous hemianopia and what is the cause?

A

Both fibres superior and inferior on one side are affected resulting in one whole sided visual field loss. Could be due to stroke.
Superior and inferior temporal fibres - ipsilateral visual field lost
Superior and inferior nasal fibres - contralateral visual field lost

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122
Q

What is a macula sparring visual field defect?

A

Occipital lobe has dual blood supply - PCA and MCA. PCA occlusion will still allow MCA to supply the occipital lobe and therefore the macula will be preserved. Central vision will be spared

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123
Q

What is the light reflex pathway?

A

Light stimulates the afferent nerve -optic nerve

Synapses in pretectal nucleus

Gives rise to neurones supplying Edinger Westphal nuclei bilaterally

Both occulomotor nerves are stimulated to cause direct and consensual pupillary constriction

Effect is to both direct and consensual pupillary constriction. The consensual reflex is mediated by the bilateral projections from the pretectal nucleus.

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124
Q

What is the accommodation reflex and what is the pathway?

A

Required for near vision

3 aspects (3C’s):
1- Convergence (medial rectus)
2- Pupillary Constriction (constrictor pupillae)
3- Convexity of the lens to increase refractive power (ciliary muscle)

Cerebral cortex involved because its relating to image analysis

The reflex follows the visual pathway via the LGN to the primary visual cortex. Neurones then synapse from the PVC to the Edinger Westphal nucleus and CN III causing Sphincter pupillae constriction with ciliary muscle relaxation and medial rectus activation for convergence respectively.

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125
Q

How many layers does the eye have and what are they?

A

3 layers

1- Outermost sclera (tough and continuous with dural sheath of the optic nerve

2- Uvea - pigmented vascular layer - choroid sitting just deep to sclera, ciliary body and iris sitting anteriorly

3- Retina (neural layer)

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126
Q

What are the layers of the retina?

A

Retinal pigment epithelium - prevents light from ‘bouncing around’ and causing glare in the eyeball

Photoreceptors

Bipolar cells (first order neurones receiving input from photoreceptors)

Ganglion cell layer - receives input from bipolar cells

Nerve fibre layer

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127
Q

From where does the brain get its blood supply?

A

Anterior circulation fed by internal carotid arteries and supplies most of the cerebral hemispheres

Posterior circulation fed by the vertebral arteries and supplies the brainstem, cerebellum some of the temporal lobe and the occipital lobe

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128
Q

What artery is a direct continuation of the internal carotid artery?

A

Middle cerebral artery

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129
Q

What does the MCA supply?

A

Cortical branches emerge from the lateral fissure to supply the lateral aspect of the cerebral hemisphere (cortex and underlying white matter) including lateral parts of the frontal and parietal lobes as well as the superior temporal lobe

Deep branches (the lenticulostriate arteries) supply deep grey matter structures including the lentiform nucleus, caudate as well as the internal capsule

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130
Q

What does the anterior cerebral artery supply?

A

Left and right anterior cerebral arteries anastomoses in the midline via the anterior communicating artery
The vessels loop over the corpus callosum and send branches to the adjacent cortex
Cortical branches supply the medial aspect of the frontal and parietal lobes

There are also branches to the corpus callosum itself

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131
Q

What is the name of the artery that is the confluence of the vertebral arteries in the midline?

A

Basilar artery

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132
Q

What does the basilar artery form?

A

Terminal bifurcation gives rise to the posterior cerebral artery

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133
Q

What does the posterior cerebral artery supply?

A

Occipital lobe, inferior temporal lobe and thalamus via thalamoperforator and thalamogeniculate branches

Supplies midbrain structures

Posterior communicating arteries branch from these to connect with the anterior circulation (internal carotid artery)

Superior cerebellar artery supplies the superior aspect of the cerebellum and midbrain

Pontine arteries supply the pons (including descending corticospinal fibres)

Anterior inferior cerebellar artery supplies the antero-inferior aspect of the cerebellum and lateral pons

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134
Q

What does the vertebral artery branch into that are important to the brain?

A

Anterior spinal arteries converge in the midline to supply the anterior 2/3 of the spinal cord

Posterior inferior cerebellar arteries supply the postero-inferior aspect of the cerebellum

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135
Q

Occlusion of or haemorrhage in which artery causes locked in syndrome?

A

Pontine arteries which supply the motor pathways anteriorly

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136
Q

What is the cause of Wallenberg syndrome?

A

Infarction in the lateral medulla part of the brain stem.

Infarction of the PCA or the posterior inferior cerebellar arteries

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137
Q

What are the signs and symptoms of Wallenberg Syndrome?

A

Contralateral sensory deficits of the trunk and extremities.
Ipsilateral sensory deficits of face and cranial nerves.
Specifically loss of pain and temperature sensation if the lateral spinothalamic tract is involved.
Ataxia (difficulty walking/ maintaining balance)
Dysphagia, dysarthria, dysphonia.
Horner syndrome - myosis, anhydrosis, partial ptosis

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138
Q

What are the 3 arteries that supply the cerebellum?

A

Superior cerebellar artery

Anterior inferior cerebellar artery

Posterior inferior cerebellar artery

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139
Q

What artery is most commonly involved in strokes?

A

MCA

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140
Q

Where are upper motor neurones found?

A

CNS - cell bodies in the primary motor cortex

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141
Q

Where are lower motor neurones found?

A

Ventral horn and brain stem

Cell bodies found in the CNS

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142
Q

What 2 areas of the brain are UMN not found in?

A

Cerebellum and basal ganglia

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143
Q

What is the basic difference between the areas of damage to the LMN and UMN?

A

LMN damage causes cell bodies to die/ damage to their axons

UMN damage affects the CNS entirely

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144
Q

What are the LMN signs of damage?

A

Hypotonia
Areflexia
Atrophy - myotonia innervated by the tract
Weakness - 1 cord segment = weakness >1 cord segment = paralysis
Fasciculations- uncoordinated muscle contractions
Fibrillation- uncoordinated electrical activity

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145
Q

Are UMN excitatory or inhibitory onto the LMN?

A

Excitatory

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146
Q

What is the problem with LMN damage in relation to excitation and inhibition?

A

Net excitation would cause a movement which would come from the UMN. However in this case as the LMN is damaged there is no response to cause contraction of the corresponding muscle.

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147
Q

What percentage of fibres go through the lateral corticospinal tract and ventral corticospinal tract?

A 
Lateral = 85%
Ventral = 15%
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148
Q

What is the internal capsule between?

A

Thalamus and lentiform nucleus

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149
Q

What musculature does the ventral corticospinal tract innervate?

A

Proximal muscles like posture spinal muscles/ gluteal muscles etc

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150
Q

What musculature does the lateral corticospinal tract innervate?

A

Distal muscle such as fingers

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151
Q

Which motor tract decussates in the medulla and which motor tract decussates at the spinal level?

A

Medullary decussation - Lateral corticospinal tract

Spinal level decussation -
Ventral corticospinal tract

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152
Q

What are the signs of UMN damage?

A

It is a loss of inhibition

Hypertonia- spasticity affecting all muscles equally
Upper limb-flexors win and limbs held in a flexed position
Lower limbs- Legs extended as against gravity
Hyperreflexia- easy in children
Clasp knife rigidity- hard to pull initially but after easy - Golgi tendon organs (sensory receptor organ that detects change in muscle stretch) have a high threshold
Weakness
Atrophy - dissuse atrophy - not loss of trophies factors
Babinski’s sign positive

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153
Q

What happens in an acute phase of UMN lesion?

A

Flaccid paralysis = could be for days to weeks which then converts to hypertonia

Spinal shock refers to hypotonia and areflexia

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154
Q

Internal capsule has motor tracts in which limb?

A

Posterior limb

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155
Q

In the posterior limb of the internal capsule in which orientation are the fibres?

A

Arm then trunk then leg after the genu

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156
Q

What 2 structures make up the lentiform nucleus?

A 
Globus pallidus (medial and lateral)
Putamen
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157
Q

What 4 structures is the internal capsule sandwiched between?

A

Thalamus posteriorly
Putamen and globus pallidus medially
Caudate nucleus anteriorly

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158
Q

What is the function of the putamen?

A

Regulate movements at various stages e.g. preparation and execution and influence various types of learning

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159
Q

What is the function of the caudate nucleus?

A

Brain learning, storming and processing of memories. Feedback processor - means it uses information from past experiences to influence future actions and decisions

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160
Q

What is the function of the globus pallidus?

A

Regulation of voluntary movement. Part of the basal ganglia - regulation of movement on a subconscious level

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161
Q

What is the basal ganglia responsible for?

A 
Control of voluntary motor movements
Procedural learning
Habit learning
Eye movement
Cognition
Emotion
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162
Q

What are the main parts of the basal ganglia?

A

Dorsal striatum - caudate nucleus and putamen
Ventral striatum - nucleus accumbens and olfactory tubercle
Globus pallidus
Ventral pallidum
Substantia nigra
Subthalamic nucleus

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163
Q

What is the function of the cerebellum?

A

Combines Proprioception with appropriate sequence to conduct the motor plan sent by the prefrontal cortex and then feedback’s onto the motor cortex

164
Q

What is the direct pathway of the motor cortex?

A

Excitatory pathway on the cortex with appropriate pathways where appropriate movements are wanted and carried out

It connects the basal ganglia to the motor cortex

165
Q

What is the indirect pathway of the motor cortex?

A

Connection between basal ganglia to the motor cortex but is inhibitory pathway onto the motor cortex

Inappropriate movements are inhibited.

166
Q

Where are D2 receptors and D1 receptors found in the brain (in relation to movement), and which are inhibitory or excitatory?

A

D2 receptors are inhibitory and found on the putamen in the indirect pathway

D1 receptors are excitatory and found on the putamen of the direct pathway

167
Q

How does deep brain stimulation work?

A

Target of the treatment is the subthalamic nucleus. By reducing the activation of it the indirect pathway is then affected and doesn’t excite the GPi. Reduced inhibition of the thalamus and so more excitation of the cortex which means more excitation of the putamen

168
Q

What is the mnemonic for cerebellar lesion effects and what does it stand for?

A

DANISH

Dysdiadochokinesis - difficulty in rapidly alternating movements
Ataxia - unsteady and wobbling - cant control limbs and thoracic movements
Nystagmus- flickering eyes
Intention tremor - finger nose test
Slurred speech - dysarthria
Hypotonia- patellar reflexes etc

169
Q

Occlusion of what vessels can also produce DANISH symptoms?

A

Cerebellar arteries

170
Q

What 3 ways can microorganisms gain entry into the CNS?

A

Direct spread - middle ear infection
Blood-bore - sepsis
Iatrogenic - V-P shunt

171
Q

Which layer of the covering of the brain are inflamed in meningitis?

A

Leptomeninges - Pia mater and arachnoid mater

172
Q

In Neonates which organism most commonly causes meningitis?

A

E. Coli

173
Q

In 2-5 year olds which organism most commonly causes meningitis?

A

H. Influenzae type B

174
Q

In 5-30 year olds which organism most commonly causes meningitis?

A

N. Meningitides

175
Q

In over 30 year olds which organism most commonly causes meningitis?

A

S. Pneumoniae

176
Q

What is a potential cause for chronic meningitis?

A

Mycobacterium tuberculosis

177
Q

Name 3 local complications of meningitis?

A

Death (swelling -> raised intracranial pressure)

Cerebral infarction -> neurological deficits

Subdural empyema- chronic inflammation

Epilepsy - particularly in paediatrics - abnormal brain parenchyma

Cerebral abcess

178
Q

What is encephalitis?

A

Classically a viral infection that causes a variety of symptoms that results in inflammation of the brain. Causes could be due to many factors

179
Q

Name 3 ways which cause encephalitis

A

Neuronal cell death by virus - inclusion bodies of virus

Temporal lobe - herpes virus therefore get epilepsy

Spinal cord motor neurones - polio

Brain stem - rabies in children commonly

Lymphocytic inflammation - ongoing infection in younger people which usually is self limiting but can cause raised intracranial pressure - epilepsy potentially death. It is usually a viral like illness which a LP can help diagnose

180
Q

What is a prion and how does it cause disease?

A

Prion protein (PrP)

Normal constituent of synapse with no known function

Mutated PrP can be sporadic, familial or ingested

Mutated PrP interacts with normal PrP to undergo a post translational conformational change. The proteins then aggregate inside the cell because it cant break it down causing the cell to undergo apoptosis.

Usually affects grey matter- cell bodies of neurones

181
Q

What is vCJD?

A

CJD caused by prions

Each case has a unique genetic prion sequence - mutated from the patients own prions

Strong evidence of causal association of vCJD with bovine spongiform encephalitis

It has a prolonged incubation of 15+ years.

182
Q

What are the differences and similarities between classical and variant CJD?
(Median age at death, median duration of illness, clinical signs and symptoms, periodic sharp waves on EEG, presence of florid plaques on neuropathology, immunohistochemical analysis of brain tissue shows accumulations, presence of agent in lymphoid tissue?)

A

VCJD - younger patients of death but longer duration of illness
Clinical signs and symptoms - dementia in cCJD but prominent psychiatric/ behavioural symptoms, delayed neurological signs in vCJD.

EEG - present sharp waves in cVJD but absent in vCJD

Florid plaques - rare in cCJD but present in large numbers in vCJD

Immunohistochemistry - variable accumulation in cCJD but marked accumulation of protease resistant PrP

Lymph’s- not readily detected in cCJD but readily detected in vCJD

183
Q

What is dementia?

A

Acquired global impairment of intellect, reason and personality without impairment of consciousness

184
Q

In its simplest sense what is different to dementia and delirium?

A

Dementia has consciousness whereas delirium doesn’t have consciousness

185
Q

Name the 4 subsets of dementia (we need to know)?

A

Alzheumer’s (50%) - sporadic/familial, early/late

Vascular dementia

Lewy body dementia

Picks diease

186
Q

What is Alzheimer’s disease in pathological terms?

A

Exaggerated aging process - ?Oxidative stress increase

Loss of cortical neurones - accelerated leading to decreased brain weight and cortical atrophy

Due to increased neuronal damage - neurofibrillary tangles or senile plaques

187
Q

What are neurofibrillary tangles in Alzheimer’s disease?

A

Intracellular twisted filaments of Tau protein

Tau normally binds and stabilises microtubules

Tau becomes hyperphosphorylated in AD making it unstable and dissolves out of solution

Staining techniques can show the tangles

188
Q

What is a senile plaque in Alzheimer’s disease?

A

Foci of enlarged axons synaptic terminals and dendrites - fusion

Amyloid deposition in vessels in centre of plaque - ischaemia and cell damage - cell loss

It is central to the pathogenesis

189
Q

What causes amyloid deposition in Alzheimer’s?

A

Mutations of 3 genes on chromosome 21

Amyloid precursor protein (APP) gene

Presenilin (PS) genes 1 and 2 code for components of secretase enzyme - normally breaks down amyloid protein

If the presenilin gene is defective then the APP has incomplete breakdown and amyloid is then deposited

190
Q

What is the normal intracranial pressure?

A

0-10mmHg

191
Q

What are 3 compensatory mechanisms to maintain normal ICP?

A

Reduced blood volume

Reduced CSF volume

Spatial - brain atrophy

Vascular mechanisms to maintain cerebral blood flow as long as ICP <60mmHg

192
Q

Name 2 space occupying lesions in the brain

A

Tumour

Haemorrhage

Oedema

193
Q

Name the 3 types of brain herniation

A

Subfalcine

Tentorial

Tonsilar

194
Q

What is a subfalcine brain herniation?

A

Same side as the mass

Cingulate gyrus pushed under the free edge of the falx cerebri

Ischaemia of medial parts of the frontal and parietal lobe, corpus callosum due to compression of anterior cerebral artery -> infarction

195
Q

What is a tentorial herniation?

A

Uncut/ medial part of the parahippocampal gyrus through the tentorial notch

Damage to the occulomotor nerve on the same side is a clinical sign

Occlusion of blood flow in posterior cerebral and superior cerebellar arteries

Frequently fatal because of secondary haemorrhage into the brain stem -> Duret haemorrhage

Common mode of death in those with large brain tumours and intracranial haemorrhage

196
Q

What is a tonsilar herniation?

A

Cerebellar tonsils pushed into the foramen magnum compressing the brainstem

197
Q

What is the Cushings reflex?

A

As the brain swells due to raised ICP the brainstem gets reduced blood and so thinks there is a reduced blood supply in general. Then causes vasoconstriction and therefore raises BP to try and improve blood supply to the brain but the brain then swells even more due to oedema causing the cycle to continue.

As a reflex - the general circulation is good to rest of the body and so the HR reduces as CO is meeting the demands of the rest of the body and also the rest of the body is getting enough Oxygen and so the resp rate starts to decrease.

Signs are Bradycardia, Hypertension and Bradyponea.

198
Q

Name 3 main tumours of the brain

A

Benign - meningioma - incidental finding usually.

Malignant - astrocytoma- mainly in paediatrics. Spread along nerve tracts and through subarachnoid space often presenting with a spinal secondary

Others - Neurofibroma, Ependymoma, Medulloblastoma, Lymphoma

199
Q

What is a stroke?

A

Sudden event producing a disturbance of CNS function due to vascular disease

200
Q

What are 2 broad categories of stroke?

A

Cerebral haemorrhage - 15%

Cerebral infarction - 85%

201
Q

What are the 2 types of infarct?

A

Regional - named by the cerebral artery causing it or the carotid

Lacuna - smaller infractions on the microcirculations. Less than 1cm. Associated with hypertension. Commonly affects the basal ganglia

202
Q

What is the pathogenesis of a subarachnoid haemorrhage?

A

Rupture of a berry aneurysm.

M>F
HTN and atheroma causes them

Sited at branching points in the Circle of Willis

203
Q

3 steps to death from SAH?

A

Sudden severe headache - thunderclap

Sentinel headache - small bleeds before headache therefore increased amounts of headaches

Loss of consciousness

Often instantly fatal

204
Q

Define consciousness

A

Difficult to define but something to do with awareness of both external world and internal states

205
Q

What is arousal?

A

The emotional state associated with some kind of goal or avoidance of something noxious

206
Q

How are the reticular formation and cortex connected in arousal?

A

Positive feedback reciprocal excitation

207
Q

What is the reticular formation?

A

Population of specialised interneurones in the brainstem.

208
Q

What are the inputs to regulate the level of arousal?

A

Sensory system and the cortex

209
Q

What are the outputs of the reticular formation?

A

Thalamus - sensory gating
Hypothalamus
Basal forebrain nuclei
Spinal cord (muscle tone)

210
Q

The 3 outputs from the reticular system release which neurotransmitters?

A

Basal forebrain nuclei - ACh - excitation on the cerebral cortex

Hypothalamus - Histamine - excitatory on cortex

Thalamus - glutamate - excitatory NT

211
Q

What structures make up the reticular activating system?

A

Thalamus, hypothalamus and the cerebral cortex (basal forebrain nuclei)

212
Q

How do we assess GCS?

A

EMV
Eyes, Motor, Verbal response
Eyes - spontaneous =4, Response to speech=3, To pain=2, no response=1

Motor- Obeys=6, Localises=5, Withdraws=4, Abnormal flexor response=3, Extensor response=2, No response=1

Verbal - Orientated=5, confused conversation=4, Inappropriate words=3 , incomprehensible sound=2, no response=1

213
Q

What are the EEG stages during sleep from awake to REM sleep?

A

Awake - beta waves - irregular and @ 50Hz

Eyes closed = alpha waves

Stage 1 sleep = Theta waves

Stage 2/3 = Sleep spindles and K complexes - background of alpha waves

Stage 4- Delta waves - very high amplitude, load of K-complexes, synchronicity

REM sleep - random, fast with sawtooth waves - similar to beta waves - dreaming - cortex own sensory inputs

214
Q

When going through the stages of sleep why does the EEG show decreasing frequency and increasing amplitude?

A

Neuronal populations in the cortex become synchronous

215
Q

What would prevent synchronicity in the sleep cycle?

A

Sensory inputs would prevent synchronicity and therefore wake the patient up

216
Q

What is the neural mechanism for sleep?

A

Deactivating the reticular activating system and hence the cortex and inhibiting the thalamus - to reduce sensory inputs coming through

Positive feedback loop between RAS and cortex is inhibited leading to decreased cortical activity

Inhibition of the positive feedback loop is assisted by removal of sensory inputs

217
Q

Why is muscle tone lost during sleep?

A

Descending inhibition of LMN’s by glycinergic fibres arising from the reticular formation and running down the reticulospinal tracts

Eye movements and some other cranial nerve functions are preserved

218
Q

What is insomnia?

A

Symptom of something else - mainly psychiatric cause - depression/ anxiety

219
Q

What is narcolepsy?

A

Rare - orexin is the sleep gene responsible for it. Sleeping at inappropriate times

220
Q

In brain death what would an EEG show?

A

Widespread cortical and brainstem damage would lead to a flat line on EEG tracing

221
Q

What is a coma in terms of consciousness?

A

Widespread brainstem and cortical damage with various (disordered) EEG patterns detectable. Unarousable and unresponsive to psychologically meaningful stimuli. No sleep-wake cycle detectable

222
Q

What is a persistent vegetative state?

A

Widespread brainstem and cortical damage with various (disordered) EEG patterns detectable. Like coma but with some spontaneous eye opening. Can even localise to stimuli via brainstem reflexes. Sleep-wake cycle detectable

223
Q

What is locked in syndrome?

A

Caused by basilar/pontine artery occlusion. Eye movements can be preserved, but all other somatic motor functions lost from the pons down

224
Q

What is the frontal lobe responsible for?

A

Motor cortex
Expression of speech (usually left hemisphere)
Behavioural regulation/Judgement
Cognition
Eye movements - occulomotor nuclei is controlled
Continence - UMN external urethral and anal sphincters

225
Q

What is the parietal lobe responsible for?

A

Sensory
Comprehension of speech (usually left hemisphere)
Body image (usually right hemisphere)
Awareness of external environment (attention) - hemisensory neglect
Calculation and writing

226
Q

What is the temporal lobe responsible for?

A

Hearing
Olfaction - uncut on medial temporal lobe
Memory - geographical map of the road, boundary cells - when near walls.
Emotion

227
Q

What is cerebral dominance?

A

Left hemisphere is dominant in 95% of people

The right hemisphere attends to both halves of space but the left hemisphere only attends to the right half of space.

228
Q

How would L brain or R brain damage affect cerebral dominance?

A

L damage = can still do both sides processing

R damage = cant do both side processing and inattention to L side

229
Q

What 2 areas of the brain are responsible for language?

A

Broca’s area - inferior lateral frontal lobe

Wernicke’s area - superior temporal lobe

230
Q

What connects the two areas of the brain that are responsible for language?

A

Arcuate fasiculus

231
Q

What is Broca’s area responsible for?

A

Talks to motor cortex

Correct sequence of motor movements in face/ mouth to make speech

232
Q

What is Wernicke’s area?

A

Understand speech - interpretation of language

233
Q

What is the pathway for repeating a heard word?

A

Wernicke’s area will understand the spoken word and integrates with the auditory information in the area. Sends the information via the arcuate fasciculus to Broca’s area which then sends information to the motor cortex to say the words.

234
Q

What is the pathway for speaking a written word?

A

Visual cortex sees the written word -> patterns of the lines, crosses and dots seen as language in Wernicke’s area -> Broca’s area -> primary motor cortex

235
Q

What is the pathway for speaking a thought?

A

Information comes from lots of different areas of the brain to Wernicke’s area -> Broca’s area -> Primary motor cortex

236
Q

What is Wernicke’s aphasia?

A

Fluent gibberish

Not understanding the question - comprehension is affected but speaking a lot

237
Q

What is Broca’s aphasia?

A

Trouble making words but understands and is visually distressed

Conscious of the fact she can’t speak - might be able to write it down

238
Q

What are the 2 main types of memory and what are they related to?

A

Declarative - explicit and facts

Non-declarative - implicit, motor skills and emotions

239
Q

How are memories stored?

A

Short term memory (seconds to minutes) -> Long term memory (up to a lifetime)

Consolidation causes short term memory to become long term memory

Consolidation depends on the following:

Emotional context - e.g. PTSD vivid flashbacks
Rehearsal
Association

240
Q

What part of the brain is crucial for consolidating declarative memories?

A

Hippocampus

241
Q

What is neuroplasticity?

A

Long term potentiation strengthens synaptic connections

242
Q

What is the main cause of confusion in the elderly?

A 
Dementia - impact on self/carers, impact on healthcare system
Delirium
Drugs
Depression
Metabolic (endocrine)
243
Q

What drugs can cause confusion in elderly patients?

A

Morphine, Cocaine, Alcohol - withdrawal, Zopiclone

244
Q

What are common metabolic causes of confusion in elderly patients?

A 
Hypothyroidism
Hypercalcaemia
Vitamin B12 deficiency
Normal pressure hydrocephalus
Hypo/Hypernatraemia
245
Q

What age is the cut off from early to late onset Alzheimer’s?

A

65 Years

246
Q

What are the subsections of mini mental state examination?

A

Orientation to where the patient is

Registration of 3 objects

Attention and calculation

Recall

Language

Copying

247
Q

What gene is affected in the late-onset Alzheimer’s?

A

Apolioprotein E gene

248
Q

Common presenting complaints of dementia?

A

Deterioration in memory

Deterioration in spatial navigation - cant retrace steps back home for example

Difficulty in executive functions:

  • Language
  • Visuspatial functioning
  • Calculation

Affecting activities of daily living

249
Q

What are the treatments for Alzheimer’s?

A

Wanting to increase ACh therefore inhibition of AChE.

Donepezil, Galantamine, Rivastigmine, Memantine (Glutamate)

250
Q

What are 3 core clinical features of Lewy body dementia?

A

Fluctuating cognition with variations in attention and alertness

Visual hallucinations

Features of Parkinsonism - shuffling gait, flexed posture (no rigidity or tremor complaint)

251
Q

What is the treatment for Lewy body dementia?

A

AChE inhibitor

Galantamine, Memantine, Donepezil, Rivastigmine

252
Q

What is fronto-temporal dementia?

A

Atrophy of frontal and temporal lobes

253
Q

What are symptoms based on tempero-frontal dementia?

A

Altered behaviour, personality, social conduct

Appear disinhibited and apathetic

Disorder of language - expressive dysphasia/ non-fluent aphasia

Primitive reflexes - Grasp reflex, Palmomental reflex

Short/long-term memory impairment

Disorder of language - receptive dysphasia/fluent aphasia - Wernicke’s area for understanding to speak after = hence talking jibberish.

254
Q

Why do HIV patients get AIDS-dementia complex?

A

HIV-infected macrophages will enter the brain and cause indirect damage to neurones

Insidious onset but once established - rapid progression

255
Q

What are common signs/ symptoms of AIDS-Dementia complex?

A

Global impairement and therefore non-specific symptoms

Cognitive impairement
Psychomotor retardation
Tremor
Ataxia
Dysarthria
Incontinence
256
Q

What are the two types of delirium?

A

Hyperactive

Hypoactive

257
Q

What is the difference between the two types of delirium?

A

Hypoactive

Hyperactive

Hyperactive - increased motor agitation and restlessness and sometimes aggressiveness

Hypoactive - underactive - sleepy and hard to respond, motor retardation, apathy, slowing of speech

258
Q

Mnemonic for delirium and meanings?

A

Drugs toxicity - withdrawal/ anticholinergics/ opiates etc.

Endocrine - hyper/hypothyroidism, Addison’s disease, cushings disease

Liver failure

Intracranial - stroke, haemorrhage, cerebral abscess, epilepsy

Renal failure

Infections - pneumonia, UTI, sepsis, meningitis

Urinary retention/ Faecal retention

Metabolic - electrolyte disturbances, hypoxia

259
Q

Difference between dementia and delirium clinically?

A

Dementia is slower on onset, steady decline, hallucination rare, speech often slow, normal GCS, clear consciousness

Delirium everything opposite to the above - rapid onset, fluctuating course, hallucinations, speech slow/ fast, reduced GCS, impaired consciouness

260
Q

What are the subsections of headache?

A

Primary (due to headache condition)

Secondary to another condition

261
Q

In terms of sight or life threatening which type of headache is likely to be both?

A

secondary headache

262
Q

Name 3 primary headache disorders

A

Tension headache
Migraine
Cluster headache

263
Q

Name a few causes of secondary headache

A

Life threatening:
Haemorrhage - SAH, subdural
Infection - meningitis, sepsis, abcess
Trauma
Space occupying lesion - generally headaches will be present but not acute headache
Sight threatening:
Giant cell arteritis - ischaemia of optic nerve
Acute glaucoma - closed angle
Medication related and medication-overuse
Systemic - HTN, pre-eclampsia

264
Q

Which type of headache is likely to present with clinical examination findings?

A

Secondary - may have clinical examination findings

265
Q

What is the mnemonic that helps catch potentially life threatening headaches?

A

SNOOP

Systemic signs and disorders - meningitis (fever, neck stiffness, ?HIV, Ca, Pregnancy)

Neurological symptoms - SOL, ICH, Glaucoma

Onset new or changed and patient >50 years old - malignancy, GCA

Onset in thunderclap presentation - Vascular haemorrhage

Papilloedema, pulsating tinnitus, positional provocation, precipitated by exercise - Raised ICP= coughing, leaning forward

266
Q

What is the common patient that presents with a tension type of headache?

A

Female
Young (teenagers and young adults)

First onset >50years is unusual

267
Q

What are the common PC of a tension type headache?

A

Generalised pain that has a predilection for frontal and occipital regions
Tight band like +/- neck radiations
Mild to moderate intensity
Worse at end of the day
Recurrent 30min-1hour
Stress, poor posture or lack of sleep aggregates it
Often responds to simple analgesics
Few associated symptoms - maybe slight nausea
Clinical examination - normal

268
Q

What is the common patient type to present with a migraine?

A

F>M (5:1)
Common 15/100
Presents early to mid-life (similar to tension headache)
Must have first attack <30years old

269
Q

What is the pathophysiology theory of migraines?

A

Vasodilation of meningeal blood vessels

270
Q

What is the common PC of a patient with migraine?

A

Unilateral, temporal or frontal
Throbbing, pulsating
Moderate-severe, often disabling
Prolonged headache - between 4-72 hours
Triggers= certain foods, menstrual cycle, stress, lack of sleep aggregates, often is a FH
Can respond to simple analgesics but may need triptans
Associated symptoms include - Aura, N+V, Visual defects, Neurological features, speech disturbances, photophobia, phonophobia, clinical examination is normal

271
Q

What is the common demographic to present with a cluster headache?

A

M > F
1 in 1000
Usually begins 30-40 years

272
Q

What is the theorised pathophysiology of a cluster headache?

A

Unknown but theorised to be hypothalamic activation with secondary trigeminal and autonomic involvement

Thought to be the worst headache that is enough to cause suicide

273
Q

How would a cluster headache present?

A

Unilateral, around or behind the eye
Sharp, stabbing, penetrating paid,
Severe and intense often disabling pain

15mins to 3 hours duration and as the name suggests they are in a cluster and so the clusters occur spaced between periods of remission (3m to 3 years)

Triggers - alcohol, cigarettes, volatile smells, warm temperature, lack of sleep

Treatment - high flow oxygen and triptans - regular analgesics wont work

Ipsilateral autonomic symptoms e.g. red watery eye, blocked runny nose, ptosis

During an attack there is evidence of autonomic eateries

274
Q

Space occupying lesions lead to headaches - how would they present?

A

Gradual and progressive course

Dull but usually progressive in severity

Mild in severity, worse in mornings

Early morning, on waking is when have symptoms usually

Worsening with leaning forward, cough or vassal a manoeuvre

Simple analgesics effective in early stages

N+V, focal lesion therefore focal symptoms/ signs - focal neurology or visual symptoms

OE - focal (unilateral) neurological signs, papilloedema

275
Q

What is the common cause of trigeminal neuralgia?

A

Compression of CN V due to loop of a blood vessel

5% due to tumours/ skull base abnormalities or arteriovenous malformations

276
Q

What demographic most commonly will present with trigeminal neuralgia?

A

F>M
25 in 100,000
50-60years first presentation peak incidence

277
Q

What are the signs and symptoms of trigeminal neuralgia and what is the history of them?

A

Unilateral, pain felt in divisions of CN V

Sharp stabbing electrical shock (sometimes burning)

Severe, lasting a few seconds - 2mins

Sudden onset

What makes it worse? Light touch to face/scalp, eating, cold wind, combing hair

Tx - simple analgesics not effective

Preceding symptoms - tingling, numbness, pain can radiate to areas within CN V distribution

OE - normal

278
Q

What is Temporal arteritis?

A

Superficial temporal artery commonly involved - worrying sign that other vessels also affected including the optic vessels and therefore sight threatening

279
Q

What is most significant about temporal arteritis aka Giant cell arteritis?

A

Sight threatening due to inflammation of the optic vessels

280
Q

What is the common demographic that will present with GCA?

A

F>M
>50 years (most common in >75 year olds)

Consider it in any >50 year old with abrupt onset of headache + visual disturbance or jaw claudication

281
Q

What are the signs and symptoms of GCA?

A 
Headache
Jaw claudication (pain on chewing)
Scalp tenderness
Loss of vision
Abnormalities of temporal artery
Fever
Night sweats
Weight loss
Proximal myalgia and neck/ shoulder/ pelvic girdle stiffness
282
Q

In non-traumatic SAH what is the most common cause?

A

Berry aneurysm rupture

283
Q

What are typical symptoms of spontaneous SAH?

A 
Headache (48%)
Dizziness
Orbital pain
Diplopia
Visual loss (aneurysms compressing any part of the visual pathway)
284
Q

Where in the vasculature would a berry aneurysm most commonly be found?

A

Anterior communicating artery in the circle of Willis (40%)

Middle cerebral artery distal branches - 34%

MCA proximal branches - 20%

The root of the basilar artery - 4%

285
Q

Apart from a berry aneurysm what is the other way of getting a spontaneous SAH?

A

Rupture of arteriovenous malformations - 10%

286
Q

What happens in 40% of SAH in the months preceding it?

A

Sentinel headaches in months preceding a SAH (40%)

Caused by minor leaks from the berry aneurysm which are spontaneous but then heal over

287
Q

What happens after a SAH with the brain and the surrounding tissues?

A

Microthrombi - occlude smaller distal arteries

Vasoconstriction (bleeding response) - from CSF irritant

Cerebral oedema - response to hypoxia and extravasation blood

Sympathetic activation - myocardial damage

Early rebleeding - common and often devastating

Acute hydrocephalus - blood in subarachnoid space may block normal drainage of CSF

Global cerebral ischaemia

288
Q

How to investigate a SAH?

A

CT scan - 93% sensitivity if done within 24 hours

LP if CT inconclusive - wait at least 6 hours (12+ is preferable). Measurement of bilirubin - need time for RBC lysis

CSF - high protein, WCC not raised and glucose normal

Angiography to localise aneurysm and treat it

289
Q

Treatment for a SAH?

A

A-E assessment

CCB - Nimodipine prevents vasospasm and secondary ischaemia

Operate who have good neurological status to prevent re-bleeding

Clipping - clamp neck of aneurysm

Coiling - insertion of wire into aneurysm sac which causes a local thrombus within it and prevents blood going into it

290
Q

Prognosis of a SAH?

A

10-15% die before getting to hospital

25% die within 24 hours

50% mortality within 6 months

40% mortality in first month

Rebleeding occurs in up to 30% within 2 weeks if unoperated on

Delayed ischaemia from cerebral vasospasm is commonest cause of death following aneurysmal SAH

291
Q

What is meningitis?

A

Infection of the meninges

292
Q

Infections of the CNS can be divided into 2 broad categories which are?

A

Encephalitis - focused on parenchyma

Meningitis - focused on the meninges
Inflammation of the dura
Inflammation of the leptomeninges (essential arachnoid tissue and subarachnoid space) more common

293
Q

What is the triad of meningism with a fever?

A

Headache
Neck stiffness
Photophobia

294
Q

What is the difference in onset of symptoms with bacterial and viral meningitis causes?

A

Bacterial is hours

Viral is days

295
Q

Apart from the triad of meningism what are the other symptoms of meningitis?

A

Flu like symptoms
Joint pains
Rash
Reduced GCS/ seizures

Babies-
Inconsolable crying
Reduced feeding
Floppy
Bulging fontanelle
296
Q

Why is a rash present in meningitis?

A

Most common with meningococcal meningitis

Bleeding into the skin or mucosa (microvascular thrombi)

Produces a non-blanching rash - blood is outside of blood vessels

Larger lesions called purpuric
Smaller lesions called petechial

297
Q

What are risk factors for meningitis?

A

Young and old the most affected
Crowding
Immune deficiency
Cochlear implants - physical pathway to meninges

298
Q

What 3 bacteria can cause meningitis?

A

Neiserria meningitides

Haemophilus influenza B

Streptococcus pneumonia

299
Q

What are a few complications of meningitis?

A

Septic shock due to bacteraemia

Disseminated intravascular coagulopathy

Seizures - irritation of brain parenchyma

300
Q

What is Kernig Sign?

A

Supine patient with thigh flexed to 90 degrees

Extension of knee is met with resistance

More common in children

301
Q

What is Brudzinski sign?

A

When neck is flexed and the child is in the supine position there is an involuntary flexion of knees and hips
More common in children

302
Q

How would you investigate bacterial meningitis and what would be found?

A

LP of CSF

Cloudy
Elevated protein - immune proteins
Low glucose - bacteria metabolise it
Positive gram staining

Blood cultures - be aware of previous antibiotic therapy as there may not be any bacteria in the blood

303
Q

How would you investigate viral meningitis and what would be found?

A

Clear or cloudy CSF
Normal or raised protein
Normal glucose

PCR - distinguishing bacterial from viral cause

304
Q

What is the treatment for meningitis?

A

Empirical antibiotics

Supportive therapy
Oxygen
Fluids
Intubation if altered consciousness

Dexamethasone to reduce cerebral oedema and prevent hearing loss

If viral - aciclovir for herpes

305
Q

What is normal CSF pressure?

A

10-15mmHg

306
Q

What is a non-invasive method of monitoring ICP?

A

Near-infrared spectroscopy - a probe put onto the forehead and then oxygen saturation’s are monitored as a proxy for blood flow to the brain

307
Q

Normally ICP does raise so what are the causes of the 3 physiological peaks in ICP?

A

P1 - arterial pulsation
P2 - brain tissue compliance
P3 - Dicrotic wave

308
Q

What happens to the peaks in raised ICP?

A

P2>P1

Compliance starts decreasing resulting in reversal of P1:P2

309
Q

What are the compensatory mechanism for raised ICP?

A

1- decrease in CSF
2- Reduced CSF production
3- Decrease in blood volume by squeezing the blood out of the sinuses

310
Q

What is the Monro-Kellie doctrine?

A

Volume-pressure relationship

As the volume increases the pressure usually increases slightly but then it gets to a point where the pressure rises exponentially

311
Q

Describe what happens in consciousness with extradural haemorrhage over a few days and why what happens when?

A

Sudden decrease in consciousness that gradually improves but then after a few days there is a sudden and sustained decrease in consciousness.

This middle period is called the ‘lucid interval’ that has an ongoing headache

Haematoma enlarges = ICP increases

312
Q

Name the 4 sites of brain herniation

A

Subfalcine
Trans tentorial
Uncal
Tonsilar

313
Q

What does a subdural haematoma look like on CT?

A

Lentiform - banana shape

314
Q

What does an extradural haemorrhage look like on CT?

A

Lemon shaped

315
Q

What is difference between a chronic and acute subdural haemorrhage on CT?

A

Chronic SDH has a much darker appearance in the location of the haemorrhage

316
Q

What is the pathophysiology of anoxic brain injury

A 
Decreased cerebral blood flow
Decreased Oxygen
Failure of ATP-driven ion pump
Effluent of K from cell
Influx of Na into cell
Depolarisation of neurones
Water flows Na into cell and causes oedema
Mitochondrial anoxia causes metabolic failure activating nitric oxide synthase producing NO
Toxic oxygen radicals also produced
317
Q

What reflexes can be tested to confirm brain death?

A 
Corneal reflex
Pupillary light reflex
Temperature
Gag reflex
Oculovestibular reflexes
Respiratory response
318
Q

What is the definition of a stroke?

A

Neurological deficit attributed to an acute focal injury of the CNS by a vascular cause including cerebral infarction, ICH and SAH

319
Q

What is a transient ischaemia attach?

A

Similarly clinical features of a stroke but completely resolve within 24 hours

320
Q

What is the difference between a mini stroke and a stroke?

A

Stroke symptoms last for >24 hours but in a TIA <24hours

321
Q

How would you acutely image for a stroke?

A

CT scan

322
Q

When would a CT head be better than an MRI for strokes?

A

Ischaemic strokes show better on an MRI

Haemorrhagic strokes - bleed will show up as a bright white area - maybe also see a mass effect

In a CT ischaemic areas of brain not visible early on (as infarct becomes more established the ischaemic area will become hypodense)

323
Q

What signs of weakness will be noticed in an anterior cerebral artery infarct?

A
  • Contralateral weakness in lower limb
  • Lower limb affected much worse than upper limb and face
  • Contralateral sensory changes in same pattern as moor deficits
  • Urinary incontinence due to paracentral lobules being affected - most medial part of the motor/sensory vortices and supply the perineal area
  • Apraxia is inability to complete motor planning (e.g. difficulty dressing oneself even when power is normal)
  • Dysarthria / aphasia - unusual sign in ACA infarcts compared with MCA - maybe related to frontal lobe damage
  • Split brain syndrome/ alien hand syndrome caused by involvement in corpus callosum which is normally supplied by the ACA
324
Q

What would the signs and symptoms of an MCA infarct be in these locations?

A

Proximal (main stem before the lenticulostriate arteries come off)

All branches of MCA will be affected including lenticulostriate and distal branches

  • Contralateral full hemispheres is (face, arm and leg affected) because internal capsule has been affected which carries fibres to face, arm and leg so even though the MCA supplies the face and arm area of the motor homonculus, this is irrelevant
  • Contralateral sensory loss - distribution of the primary sensory cortex supplied by the MCA (i.e. face and arm), but could involve larger areas if sensory fibres in internal capsule affected
  • Visual field defects - usually Contralateral homonomous hemianopia without macular sparing - due to destruction of both superior and inferior optic radiations as they run through superior (temporal and parietal lobes), More distal occlusion may affect one radiation causing quadrantanopias.
  • Aphasia global if dominant hemisphere affected therefore cannot understand or articulate words
  • Contralateral neglect - usually in lesions of right parietal lobe (can be caused by occlusion of more distal branches as well), issues with not acknowledging that visual side of space or even own body exists but visual fields normal
325
Q

What are the 3 branches of the MCA that are important in strokes?

A

Proximal branch
Lenticulostriate arteries
Distal branches

326
Q

What are the signs and symptoms of a lenticulostriate artery occlusion stroke?

A

Lacunar strokes
Cause destruction of small areas of internal capsule and basal ganglia
Essential distinguishing features from a proximal infarct is they don’t cause cortical features (neglect or aphasia)

There are subset of these strokes=

1- Pure motor - damage to motor fibres travelling through the internal capsule - occlusion to lenticulostriate arteries
2- Pure sensory - damage to sensory fibres travelling through internal capsule - occlusion of thalamoperforator arteries and maybe also lenticulostriate
3- Sensorimotor - mixed signs and symptoms as depends where at the boundary between sensory and motor fibres the infarct occurred

327
Q

What are the signs and symptoms of distal branches of the MCA occlusion?

A

MCA splits into superior and inferior division

Superior division essential supplies lateral frontal lobe=
Including primary motor cortex and Broca’s area
Occlusion will cause contralateral face and arm weakness expressive aphasia if left hemisphere affected

Inferior division essential supplies lateral parietal lobe and superior temporal lobe=
Including primary sensory cortex, Wernicke’s area and both optic radiations
Occlusion will cause contralateral sensory changes in face and arm, receptive aphasia if left hemisphere and contralateral visual field defect without macular sparing (often homonomous hemianopia as both radiations damaged)

328
Q

What are the signs and symptoms of a posterior cerebral artery occlusion?

A

Somatosensory and visual dysfunction

Contralateral homonymous hemianopia (with macular sparing due to collateral supply from MCA)

Contralateral sensory loss due to damage to thalamus

329
Q

What are the signs and symptoms of a cerebellar infarct?

A

N+V, headache, vertigo/ dizziness

Ipsilateral cerebellar signs - DANISH

Possible ipsilateral brainstem signs since cerebellar arteries supply brain stem as they loop around to the cerebellum

Possibly contralateral sensory deficit/ ipsilateral Horner’s (once again due to brainstem involvement)

330
Q

What are the signs and symptoms of a brainstem stroke?

A

Contralateral limb weakness is seen with ipsilateral cranial nerve signs
This can be explained by damage to corticospinal tracts (above deccusation of pyramids) and damage to cranial nerve nuclei on same side

331
Q

What are the signs and symptoms of a basilar artery occlusion?

A

Supplies brain stem - contains many vital centres - occlusion can sometimes cause sudden death

Occlusion of distal (superior basilar artery)=

  • Visual and oculomotor deficits (as basilar sends some branches to midbrain which contains oculomotor nuclei. Also occlusion at this site can prevent blood flowing into PCA’s affecting occipital lobes.
  • Behavioural abnormalities
  • Somnolence, hallucinations and dreamlike behaviour (as brain stem contains important centres for sleep regulation (reticular activating system)
  • Motor dysfunction often absent (if cerebral peduncle can get blood from PCAs which in turn are being filled by the Posterior communicating arteries.
332
Q

What are the signs and symptoms of a proximal basilar occlusion?

A

At level of pontine branches. Embolus in basilar artery can occlude pontine branches on each side

  • locked in syndrome
  • complete loss of movement of limbs however preserved ocular movement - eyes still move because midbrain is getting supply PCA’s via posterior communicating arteries
  • preserved consciousness (maybe because midbrain reticular formation is still intact)
333
Q

What does occlusion of the MCA supplying Wernicke’s area cause?

A

Comprehension problem

334
Q

What does occlusion of the MCA in Broca’s area cause?

A

Motor - articulation problem

335
Q

Stroke in which part of the brain leads to a macula sparing visual defect?

A

Posterior cerebral artery

336
Q

What does the Bamford stroke classification divide strokes into?

A

TACS - total anterior circulation stroke - Large cortical stroke in middle / anterior cerebral artery areas

PACS - partial anterior circulation syndrome - Cortical stroke in middle / anterior cerebral artery areas

POCS - posterior circulation syndrome

LACS - lacunar syndrome - Subcortical stroke de to small vessel disease. No evidence of higher cerebral dysfunction

337
Q

What is the rule of 4s for brainstem strokes?

A

Rule 1- 4 above the pons (midbrain), 4 in the pons and 4 in the medulla

Rule 2- CN 3, 4, 6 and 12 are all in the midline - all divide into 12

Rules 3- 4 midline M’s = Motor pathway (corticospinal tract), Medial Lemniscus (dorsal columns), Medial longitudinal fasciculus, Motor nuclei (only 3,4,6,12)

Rule 4- 4 side (lateral) Ss - Spinocerebellar pathway, spinothalamic pathway, sensory nucleus (mainly 5), sympathetic.

338
Q

What pathology does ipsilateral cranial nerve signs and contralateral sensory and motor tract deficits come from?

A

Brainstem pathology

339
Q

What is defined by anxiety?

A

Feeling of worry, nervousness, or unease about something with an uncertain outcome

340
Q

What are the symptoms of anxiety?

A 
Palpitations
Sweating
Trembling or shaking
Dry mouth
Difficulty breathing
Chest pain or discomfort
Nausea or abdominal distress
Feeling dizzy, unsteady, faint or light-headed
341
Q

What parts of the brain coordinate the stress response?

A

Limbic system

Limbic-hypothalamo-pituitary-adrenal axis

Cortex interacts with limbic structures which interacts with the hypothalamus which then interacts with two pathways motor regions and sympathetic nervous system

342
Q

What is the hippocampus involved in?

A

Memory and expressions of emotion

343
Q

What is the amygdala involved in?

A

Drives related behaviours and processing of associated emotions

344
Q

What are the inputs and outputs of the amygdala

A

Inputs of sensory information, brainstem, thalamus, cortex

Outputs to cortex, brainstem and hypothalamus

345
Q

What effects do the prefrontal cortex and anterior cingulate gyrus have on the hypothalamus?

A

Modulatory effect on the processes associated with the hypothalamus

346
Q

What are the 4 main anxiety disorders?

A

Social phobia

Specific phobia

Generalised anxiety disorder

Panic disorder

OCD

PTSD

347
Q

What neurotransmitters is decreased in which part of the brain in panic disorder?

A

GABA levels decreased in the CORTEX

348
Q

What medication and how do they basically work in panic disorder?

A

GABA level reduced

Benzodiazepines increase GABA transmission and so reduce anxiety

349
Q

Where does serotonin work in the brain and what are its uses in anxiety?

A

Increased levels of serotonin may stimulate serotonin receptors in the hippocampus

Leads to neuroprotection, neurogenesis and reduction of anxiety

350
Q

What are the main treatments of anxiety?

A

SSRI’s

Cognitive Behavioural Therapy

351
Q

What is CBT?

A

A method used by psychiatrists to help people overcome anxiety provoking situations.

People’s triggers and thoughts are connected with physical reactions and emotions which then lead to a particular type of behaviour. The idea of CBT is to break the cycle

352
Q

Define OCD

A

A thought that persists and dominates and individuals thinking despite their awareness that the thought is either entirely without purpose or has persisted and dominated their thinking beyond the point of relevance or usefulness.

Often causes great anxiety and guilt, particularly repugnant to individuals
Reflects changes in society

353
Q

What is a compulsion?

A

Obsessional motor acts.
(Aka a neutralising ritual) May result from an obsessional impulse that leads directly to the action, or they may be mediated by an obsessional mental image or fear

354
Q

What are the diagnostic criteria for OCD?

A

Obsessions/compulsions/ both present on most days for a period of at least 2 weeks

Obsessions and compulsions share all of the following features=

  • originate in the mind of the patient
  • repetitive and unpleasant
  • acknowledged as excessive or unreasonable
  • patient tries to resist, but at least one obsession/ compulsion is unsuccessfully resisted

Carrying out the obsessive thought or act is not in itself pleasurable

Obsessions/ compulsions must cause distress or interfere with the patients social or individuals functionining

355
Q

What are the 3 main theories of the pathophysiology of OCD?

A

Re-entry circuits in basal ganglia

Reduced serotonin

PANDAS

356
Q

What 4 areas make up Tourette’s?

A

Tics
OCD
ADHD
Behavioural problems, poor impulse control and other behavioural disorders

357
Q

What areas of the brain are the input, processing and outputs coming and going from in OCD?

A

Input - Cortical and subcortical areas

Processing - Caudate nucleus and putamen (striatum)

Output - Inhibitory projections from globus pallidus and substantia nigra to thalamus via GABA-ergot neurones

But in OCD there is an extra re-entry circuit from output to the processing

358
Q

How does PANDAS affect OCD?

A

Paediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infection

Sudden onset of OCD symptoms or tics after infection with Group-A- beta- haemolytic strep. Usually 3-12 years.
Usually a dramatic onset of psychiatric or behavioural problems

Antibodies cross react with neurones in basal ganglia causing symptoms
Responds to treatment with antibiotics and usual OCD management

359
Q

How do we treat OCD?

A 
CBT
Exposure response prevention - process of habituation/ extinction learning
High dose SSRI’s
Antipsychotics (TCA) - clomipramine
Deep brain stimulation
360
Q

How does deep brain stimulation work?

A

Excess excitation in the subthalamic nucleus which causes more glutamate release onto the globus pallidus interna and substantia nigra which then causes more GABA release onto the thalamus and so less glutamate release onto the cortex

361
Q

What is PTSD?

A

Within 6 months of a traumatic event of exceptional severity - usually life threatening the person has repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery or dreams.

Conspicuous emotional detachmen, numbing feeling and avoidance of stimuli that might arouse recollection of the trauma

Avoidance of triggers and chronic stress response ensues if they don’t deal with the memories

362
Q

What is the pathophysiology of PTSD?

A

Hyperactivity of the amygdala causing exaggerated response to perceived threat

Cortisol inhibits traumatic memory retrieval and controls sympathetic response
In PTSD there are lower than normal levels of cortisol

363
Q

How is PTSD treated?

A

Medical management - same as other anxiety disorders

CBT

Eye movement desensitisation and reprocessing

364
Q

Define disorder in psychiatry

A

A clinically recognisable set of symptoms or behaviour associated in most cases with distress and with interference with personal functions. Social deviance or conflict alone, without personal dysfunction, should not be included in mental disorder as defined here

365
Q

What are the general adaptation syndrome stages?

A

Stage 1 - The alarm reaction - release of adrenaline and cortisol as well as sympathetic activation

Stage 2 - Resistance - effect of adrenaline wears off and chronic stress response ensues, prolonged release of cortisol

Stage 3 - Exhaustion - chronic side effect of prolonged cortisol secretion start to occur

366
Q

What is psychosis?

A

Presence of hallucinations or delusions which describes symptoms and is not a diagnosis in itself

367
Q

What is a hallucination?

A

Perception without a stimulus
Can be in any sensory modality
Visual hallucinations are usually organic (caused by an actual problem with brain or eyes - e.g. space occupying lesion)

368
Q

What are the 2 normal hallucinations people can have?

A

Hypnogogic = going to sleep

Hypnopompic = waking up

369
Q

What is a delusion?

A

Fixed false belief which is unshakeable. Outside of cultural norms

370
Q

Define first rank symptom

A

A symptom that is diagnostic of schizophrenia

371
Q

What are the first rank symptoms?

A 
Auditory hallucinations
Passivity experiences
Thought withdrawal, broadcast or insertion
Delusional perceptions
Somatic hallucinations
372
Q

What is an auditory hallucination?

A

Thought echo - hearing thoughts aloud

Running commentary is normally what is heard - “he’s brushing his teeth” , “he’s sitting down”

In the third person voices

373
Q

What is a passivity experience?

A

Patient believes and action or feeling is caused by an external force

“MI5 have been moving my leg”

374
Q

What is a thought withdrawal?

A

Thoughts are being taken out of the mind

375
Q

What is a thought broadcast?

A

Everyone knows what the person is thinking

376
Q

What is a thought insertion?

A

Thoughts implanted by others

377
Q

What is a delusional perception?

A

Attribution of new meaning, usually in the sense of self-reference to a normal perceived object

New meaning cannot be understood as arising from patients affective state or previous attitudes

378
Q

What is a somatic hallucination?

A

Mimics feeling from inside the body - feel internal organs moving and is controlled by someone else

379
Q

What are positive and negative symptoms in schizophrenia?

A

Positive symptoms=

Delusions, hallucinations, thought disorder, lack of insight

These are added symptoms

Negative symptoms =

Under activity, low motivation, social withdrawal, emotional flattening, apathy, catatonia

Self neglect

Symptoms that take away from the patient

This is more difficult to treat

380
Q

What are the known pathophysiology reasons for schizophrenia?

A

Dopamine pathways
Brain changes
Limbic system

381
Q

What is the dopamine theory of schizophrenia?

A

Drugs which cause the release of dopamine induce psychotic symptoms

All medications that antagonise dopamine receptors help treat psychosis and those with the strongest affinity to D2 receptors are most clinically effective

382
Q

What are the 4 dopamine pathways in the brain?

A

Mesocortical pathway - from ventral tegmental area of the brain through the frontal cortex and cingulate cortex

Mesolimbic pathway - from ventral tegmental area to the nucleus accumbens and limbic structures

Nigrostriatal pathway - from ventral tegmental area to caudate nucleus and putamen

Tuberoinfundibular pathway - from hypothalamus to pituitary to ventral tegmental area to the spinal cord

383
Q

Of the 4 dopamine pathways in the brain which one is underactive and which one is overactive?

A

Overactive = mesolimbic pathway

Underactive = mesocortical pathway

384
Q

What are the brain changes associated with schizophrenia?

A

Enlarged ventricles

Reduced grey matter (with reduced brain weight)

Decreased temporal lobe volume

Reduced hippocampal formation, amygdala, parahippocampal gyrus and prefrontal cortex

Decreased pre-synaptic markers
Decreased oligodendroglia
Fewer thalamus neurones

385
Q

What is the treatment for schizophrenia?

A

Dopamine antagonism

Typical antipsychotics =
Block D2 receptors in all CNS dopaminergic pathways
Main action as antipsychotics is on mesolimbic and mesocortical pathways but side effects come from antagonising D2 receptors in other pathways

Atypical antipsychotics =
Lower affinity for D2 receptors
Milder side effects as dissociate rapidly from D2 receptors
BUT also block 5-HT2 receptors
S/e - less Parkinsonism and impaired glucose tolerance weight gain, hypercholesterolaemia, reduced cardiac conduction - prolonged QT

386
Q

What pathway in schizophrenia results in extrapyrimadal side effects as a result of treatment?

A

Nigrostriatal pathway

From the substantia nigra pars compacta

To the striatum (caudate nucleus and putamen)

Less dopamine reaching post-synaptic receptors leading to reduced movement

387
Q

Why do untreated patients in schizophrenia develop catatonia?

A

Less GABA binding so loss of inhibitory effect on the level of the basal ganglia in substantia nigra

388
Q

Why is hyperprolactinaemia common in antipsychotics?

A

Dopamine normally inhibits prolactin release from the pituitary

Dopamine antagonists lower Dopamine lead to loss of dopamines inhibitory function and therefore increased prolactin levels

389
Q

What are the mood disorders?

A

Depression

Bipolar type 1 and 2

390
Q

What are the features of depressive disorders?

A

Need to have symptoms continually for 2 weeks and consist of the following:

CORE SYMPTOMS=

  • low mood
  • lack of energy
  • lack of enjoyment and interest

Depressive thoughts - guilt, aversion to people etc

Somatic symptoms/ Biological symptoms - not sleeping, lose appetite and stop drinking too

In severe cases may have psychotic symptoms - beliefs and experiences that aren’t real

391
Q

What is the difference between a normal adjustment reaction and clinical depression?

A

Depression - symptoms develop gradually but are continuous lasting 2 weeks or more
The lack of interest and low energy can lead to loss of appetite and weight loss
Sleep disturbances usually have early morning wakefulness - so sleep poorly but wake up very early
Low self esteem and feelings of guilt and blame are typical

Adjustment reactions -
The onset is much quicker and typically after an event
Symptoms fluctuate unlike in depression. No pattern to sleep disturbance.
Appetite may be reduced but can also be increased.
Feelings of anger and frustration rather than guilt

392
Q

What is mania?

A

Exactly opposite to depression =

Elated mood, increased energy, pressure of speech, decreased need for sleep
Flight of ideas, normal social inhibitions are lost but attention cannot be sustained
Inflated even grandiose self esteem and possibly psychotic symptoms

393
Q

What is bipolar affective disorder?

A

Diagnosis is made following 2 episodes of a mood disorder at least one of which is mania or hypomania

Bipolar 1 - discrete episodes of mania only or mania and depression
Depression in bipolar 1 lasts much longer than the manic episode

Bipolar 2 - discrete episodes of hypomania or hypomania and depression - elevated mood only goes to hypomania

394
Q

What are the differentials to mania?

A

Iatrogenic - steroid induced

Hyperthyroidism

Delirium

Infection - encephalitis, HIV, syphyllis

Head injury

Intoxication with stimulants

395
Q

What are the differentials to depression?

A

Iron deficient anaemia

B12 deficiency

Chronic disease e.g. renal, CVS and liver failure

Hormone disturbances - thyroid function

Substance misuse - alcohol, cannabis and stimulants

Hypoactive delirium

396
Q

What is the main function of the basal ganglia?

A

Motor function- malfunction of the basal ganglia are implicated in neurological illnesses such as PD, Wilson’s disease, Huntington’s disease

Psychological function-
Emotion, Cognition, Behaviour

397
Q

What 3 abnormal brain circuits could account for symptoms in depression?

A

Prefrontal cortex - slowing of thought, executive dysfunction, altered emotional processing

Amygdala - abnormal emotional processing

Basal Ganglia - impaired incentive behaviours, psychomotor changes

398
Q

What two neurotransmitters are involved in mood disorders?

A

Serotonin

Noradrenaline

Both are monoamines

399
Q

Where is serotonin produced in the brain and where is it transported to?

A

Made - Brain stem in the Raphe Nuclei

Transported - cortical areas and limbic region

400
Q

What is the role of serotonin in mood disorders?

A

Serotonin low in depression

SSRI’s, SNRI’s, TCA’s, MAOI’s, treat depression

5HIAA (metabolite of serotonin) is low in the CSF of patients with depression

Tryptophan a precursor for serotonin depletion causes depression

401
Q

Where is noradrenaline produced and released in the CNS?

A

Locus coeruleus (pons) and projects to limbic system and the cortex

402
Q

What is the function of noradrenaline in the brain?

A

Mood

Suggests a role in behaviour - arousal and attention

Implicated in memory functions

403
Q

What is the treatment of depression?

A

Biological - SSRI’s then SNRI’s, TCA’s etc. Life threatening - ECT

Psychological - CBT

Social - help with isolation and social stressors

404
Q

How would you treat mania?

A

Biological - antipsychotics - dopamine antagonists
Alternatively - mood stabiliser

Psychological - acutely unlikely to be helpful longer term psychoeducation- triggers and signs of relapse. Improve sleep hygiene and length of sleep

Social - treatment in a place of safety

405
Q

What is the treatment of bipolar depression?

A

Biological - can use antidepressant - but only with mood stabiliser cover- ECT / Lithium

Psychological - CBT

Social - as for unipolar depression

406
Q

How would you maintain mood stability in bipolar depression?

A

Biological - mood stabiliser e.g. lithium or sodium valproate, antipsychotics - quetiapine

Psychological - psychoeducation / CBT

Social - consideration of BPAD on employment e.g. shift work and involvement of family

Medicine (15 decks)

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