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Neuro ESA 4 > All content > Flashcards

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1
Q

Define Grey matter within the CNS.

A

Composed of cell bodies and dendrites

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2
Q

Define White matter within the CNS.

A

The axons of the cells, very fatty due to myelin sheaths

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3
Q

Describe the pattern of Grey and White matter within the brain, starting from the centre.

A

Grey matter in the centre, surrounded by white matter, with a grey matter layer around the outside.
Same in Spinal cord, without the extra grey matter layer.

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4
Q

Define the meaning of a “tract” within the spine

A

A white matter pathway between two grey matter regions. Sensory tracts ascend to the brain, motor descend from the brain.

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5
Q

Define a funiculus

A

A collection of white matter pathways (tracts)

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6
Q

What is the Cerebral Cortex?

A

A collection of grey matter structures found on the surface of the brain

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7
Q

What is a Commissural Fibre (Axon)?

A

A white matter axon that connects right and left hemispheres of the brain

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8
Q

What is a Projection Fibre (Axon)?

A

A white matter axon that connects the cerebral hemispheres to the spinal cord/brainstem

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9
Q

What is an Association Fibre (Axon)?

A

A white matter pathway that connects two cortical regions within the same hemisphere

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10
Q

Name the parts of the Brainstem in order

A

Midbrain, Pons, Medulla

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11
Q

What are the roles of the Midbrain?

A

Eye movements and responses to sound and vision

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12
Q

What are the roles of the Pons?

A

Feeding/Sleeping

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13
Q

What are the roles of the Medulla?

A

CVS and Resp centre management and major motor pathway location (medullary pyramids)

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14
Q

What is the Pre-central Gyrus?

A

Location of the Primary Motor Cortex

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15
Q

What is the Post-central Gyrus?

A

Location of the Primary Sensory Cortex

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16
Q

What is the Sylvian Fissure?

A

Separates the Frontal and Temporal lobes

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17
Q

What is the Calcarine sulcus?

A

Located within the occipital lobe, surrounded by the Primary Visual Cortex

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18
Q

What is the Optic Chiasm?

A

The location where the Optic nerves meet and visual systems cross over

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19
Q

What is the Uncus?

A

A part of the temporal lobe, located by the Optic Chiasm, which can herniate down through the foramen magnum and impinge on the brainstem, causing death. Important in olfaction.

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20
Q

What are the Medullary Pyramids?

A

Location of descending motor fibres

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21
Q

What is the Parahippocampal Gyrus?

A

Located right next to the Uncus, important for encoding long term memory in the hippocampus.

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22
Q

What is the Corpus Callosum?

A

The fibres connecting the two hemispheres of the brain

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23
Q

What is the Thalamus?

A

Relays sensory signals to the cerebral cortex and important in consciousness, sleep and alertness.

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24
Q

What is the Cingulate Gyrus?

A

The area of the brain around the Corpus Callosum, important for emotion and memory.

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25
Q

What is the Hypothalamus?

A

Centre for homeostasis (eg. Pituitary control), located in front of the thalamus.

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26
Q

What is the Hippocampus, where is it and what is its exit pathway called?

A

The Hippocampus is part of the Limbic system associated with new memory storage. Located below the Thalmus, with the exit pathway being the fornix.

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27
Q

What is the Tectum?

A

The dorsum of the midbrain, involved in response to sound/visuals.

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28
Q

What are the Cerebellar Tonsils?

A

Bottom of the Cerebellum that can herniate and compress the Medulla. Leads to “Coning” and death.

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29
Q

How much CSF is made per day and by what?

A

600ml, by the choroid plexus cells. Most is made in the lateral ventricles.

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30
Q

Name and describe the passage of the Ventricles.

A

Lateral Ventricles connect to the Third Ventricle in the centre via the interventricular foramen, which is in the midline. The third ventricle is connected to the Fourth Ventricle via the Cerebral Aqueduct. This then leads to the Subarachnoid Space.

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31
Q

What is on either side of the Third Ventricle?

A

The Thalamus.

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32
Q

Blockage of the Cerebral Aqueduct leads to what?

A

Hydrocephalus

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33
Q

How does the CSF leave the Fourth Ventricle to enter the Subarachnoid space?

A

Via the Foramens of Luschka and Magdendie. It enters the vertebrae via the Central Canal.

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34
Q

What week does Neurulation occur in?

A

Week 4

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35
Q

What is the role of the Notochord?

A

It causes conversion of overlying ectoderm into neuroectoderm, which forms the neural plate and folds into the neural tube.

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36
Q

What can failure of the neural tube to fuse lead to?

A

Anencephaly and Spina Bifida, depending on where the fusion failed to occur.

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37
Q

What does a Cranial neural tube fusion defect lead to?

A

Anencephaly

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38
Q

What does a Caudal neural tube fusion defect lead to?

A

Spina Bifida

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39
Q

What is Spina Bifida?

A

Failure of the neural tube to close caudally. Usually manifests in the lumbosacral region. Leads to neurological defects, no cognitive delay, always leads to hydrocephalus. A lump appears with CSF leaking from the spinal cord.

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40
Q

What does Spina Bifida lead to?

A

Neurological defects, no cognitive delay, always leads to hydrocephalus.

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41
Q

What are the types of Spine Bifida, in order of severity?

A

Occulta - least bad
Cystica:
- Meningocoele
- Myelomeningocoele - worst type, spinal cord exits the vertebrae

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42
Q

What is Anencephaly?

A

Failure of the neural tube to close cranially. Incompatible with life, will not have a brain.

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43
Q

How can a Neural Tube Defect (NTD) be detected?

A

Via raised Serum a-fetoprotein in the mother’s serum. Can also do a USS.

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44
Q

How can a Neural Tube Defect (NTD) be prevented?

A

Folic acid given pre-conceptually for 3 months and in first trimester.

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45
Q

What develops from the Cranial portion of the neural tube?

A

The brain - the 5 main components of the brain (cerebral hemispheres, thalamus, midbrain, pons/cerebellum, medulla oblongata)

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46
Q

What develops from the Caudal portion of the neural tube?

A

The spinal cord

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47
Q

What develops from the Lumen of the neural tube?

A

The ventricles of the brain (CSF)

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48
Q

What are the boundaries of the Cauda Equina?

A

L2-S5

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49
Q

Name the 3 Primary Brain Vesicles from the development of the Neural tube.

A

Forebrain - Prosencephalon
Midbrain - Mesencephalon
Hundbrain - Rhombencephalon

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50
Q

Name the 5 Secondary Brain Vesicles and their pre-decessors.

A

Prosencephalon -> Telencephalon and Diencephalon
Mesencephalon -> Mesencephalon
Rhombencephalon -> Metencephalon and Myencephalon

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51
Q

Name the 5 mature brain components that mature from the Secondary Brain Vesicles.

A 
Telencephalon - Cerebral hemispheres
Diencephelon - Thalamus
Mesencephalon - Midbrain
Metencephalon - Pons/Cerebellum
Myencephalon - Medulla Oblongata
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52
Q

Name the two flexures of the brain and where they are located.

A

Cervical flexure = at spinal cord attachment to brain

Cephalic flexure = at the midbrain

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53
Q

Name the main ventricular system abnormality, who it is most common in and how to treat it.

A

Hydrocephalus - most common in newborns, suffering from Spina Bifida and treatable with a shunt. Usually due to cerebral aqueduct blockage.

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54
Q

What do the Alar plate and Basal plate of the primitive neural tube associate with in an adult?

A

Alar plate = Sensory, therefore Dorsal (DS)

Basal plate = Motor, therefore Ventral

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55
Q

What are neural crest cells?

A

Cells of the lateral borders of the neuroectoderm tube that undergo epithelial to mesenchymal transition (become functional body components eg. Glial cells).

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56
Q

Name one reason for neural crest defects to occur.

A

Alcohol - very sensitive.

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57
Q

Name 2 conditions of neural crest cell migration failure.

A

Single structures: Hirschsprung’s disease - no nerves to muscles of colon
Multiple structures: DiGeorge - no thyroid gland, cardiac defects

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58
Q

What spinal cord levels mediate the knee jerk reflex?

A

L2-L4

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59
Q

Describe the process of the knee jerk reflex

A

Muscle spindles (normal stretch) and the Golgi organ (extreme stretch) detect the tendon hammer hit. These transfer this information the motor ventral horn via the sensory fibres. The motor fibres from the ventral horn go to the knee flexors.

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60
Q

What is the Jendrassik manoeuvre?

A

Hands are held together and teeth clenched to increase the reflex response.

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61
Q

Why do seizures always manifest in the hands first?

A

Hands have a disproportionate representation within the somaesthetic cortex, in terms of size (humunculus).

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62
Q

What is a meningioma?

A

Benign, white matter, non-glial tumour of the meninges

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63
Q

Describe the difference between a T1 and T2 MRI.

A

T1 - White matter (fat) bright

T2 - Water bright (H2O = mnemonic)

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64
Q

What does Gd being visible on a T1 MRI mean.

A

Gd is usually not permeable to the BBB. If it is present on a scan, the BBB has been breached.

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65
Q

What is the role of Astrocytes within the CNS? (5 marks)

A

Most common glial cell. They support the NS by:

  • Providing structural support
  • Providing nutrition via glucose-lactate shuttle (convert blood glucose to lactate for the neuronal cells) - neurones do not store glycogen
  • Removing neurotransmitters (uptake) eg. glutamate
  • Forming the BBB
  • Maintaining the ionic environment via K+ buffering (keep low by taking it in)
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66
Q

What is the role of Oligodendrocytes within the CNS?

A

Myelinate multiple axons at once - instead of Schwann cells in the PNS.

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67
Q

What is the role of Microglia within the CNS?

A

Immune cells of the CNS - can phagocytose foreign bodies and debris. Must be “activated” to become phagocytic.

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68
Q

Describe the makeup of the Blood Brain Barrier.

A

Endothelial cells with tight junctions and a basement membrane - astrocytes sen signals to endothelial cells to form tight junctions.

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69
Q

What must transported across the Blood Brain Barrier to control its concentration?

A

Glucose (glucose-lactate shuttle via Astrocytes/GLUT 1 channel) and Amino acids

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70
Q

Describe how the brain is immune privileged.

A

Will not get attacked. T cells can enter the BBB, but the T cell pro-inflammatory response is inhibited. Microglia act as antigen presenting cells.

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71
Q

Name the amino acid neurotransmitters.

A

Excitatory: Glutamate
Inhibitory: GABA, Glycine

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72
Q

Name the excitatory neurotransmitter/s of the CNS.

A

Glutamate.

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73
Q

Name the inhibitory neurotransmitter/s of the CNS.

A

GABA/Glycine

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74
Q

What are the two types of excitatory receptor for Glutamate?

A

AMPA and NMDA

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75
Q

Describe the MOA of excitatory receptors within the CNS.

A

AMPA = initial fast depolarisation (fast synaptic transmission) via Na+/K+
NMDA = allow ion flow through the channel after glutamate binding AND are permeable to Ca2+ (AMPA aren’t)
NMDA receptors up-regulate AMPA receptors

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76
Q

Describe the role of excitatory receptors within synaptic plasticity and excitotoxicity.

A

NMDA activation leads to up-regulation of AMPA receptors.
High frequency stimulation leads to long-term potentiation (learning).
Ca2+ entry through NMDA is important for this - however too much Ca2+ can lead to excitotoxicity (Ca2+ activates many processes within cells, destroying them).

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77
Q

What is the main inhibitory neurotransmitter within the brain?

A

GABA

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78
Q

What is the main inhibitory neurotransmitter within the spinal cord?

A

Glycine

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79
Q

What is the MOA of GABA and Glycine receptor channels in being inhibitory?

A

There receptor channels allow Cl- through. These lead to hyperpolarisation and decreased action potential firing - the inhibitory post-synaptic potential.

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80
Q

Name two drugs that target GABA receptors within the brain and their MOA.

A

Enhance the response of receptors to GABA:
Barbiturates - sedatives, risk of fatal overdose
Benzodiazepines - sedative/anxiolytic, treats anxiety, insomnia and epilespy

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81
Q

What do inhibitory interneurones within the spine release?

A

Glycine

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82
Q

Name the 4 main modulatory neurotransmitters within the CNS.

A

AcH
Dopamine
Noradrenaline
Serotonin (5-HT)

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83
Q

Describe the role of AcH as a modulatory neurotransmitter within the CNS.

A

Excitatory mainly. Acts on nicotinic and muscarinic neurotransmitters - these are mainly on pre-synaptic terminals to enhance the release of other neurotransmitters (eg. Glutamate).
Involved in memory, learning and motor.

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84
Q

How is Alzheimer’s disease linked to AcH. What is a treatment of Alzheimer’s that is based around this?

A

Degeneration of the cholinergic neurones in the nucleus basalis seen in Alzheimer’s - AcHesterase inhibitors are given to treat SYMPTOMS of Alzheimer’s.

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85
Q

What conditions are associated with Dopamine dysfunction and describe the basic pathophysiology.

A

Parkinson’s - loss of dopaminergic neurones in the substantia nigra - treated with Levodopa.
Schizophrenia - too much dopamine released - anti-psychotic drugs are dopamine antagonists of D2 receptors

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86
Q

What is the role of NA within the CNS and where is it primarily found?

A

Created mainly in the Locus Ceruleus (this area is inactive during sleep) - excitatory, leads to behaviour arousal.
Amphetamines increase NA release and increase wakefulness.

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87
Q

Define Somatic sensation.

A

Conscious body sensation.

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88
Q

Name the two somatosensory modalities.

A

“Spinothalamic” and “Dorsal Column Medial Lemniscus” system.

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89
Q

What can the Spinothalamic modality feel?

A
  • Temperature (thermoreceptors)
  • Pain (nociceptors)
  • Pressure/Crude touch (mechanoreceptors)
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90
Q

What can the Dorsal Column Medial Lemniscus modality feel?

A
  • Vibration
  • Proprioception (Joint position sense from Golgi tendon/ Muscle spindles)
  • Fine touch
  • Two point discrimination
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91
Q

What can the Spinothalamic modality feel?

A
  • Temperature (thermoreceptors)
  • Pain (nociceptors)
  • Pressure/Crude touch (mechanoreceptors)
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92
Q

What can the Dorsal Column Medial Lemniscus modality feel?

A
  • Vibration
  • Proprioception (Joint position sense from Golgi tendon/ Muscle spindles)
  • Fine touch
  • Two point discrimination
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93
Q

In the Spinothalamic System: What is a Primary (1st Order) Sensory Neurone and where is its cell body?

A

A primary sensory neurone transmits sensory information from a sensory receptor to their cell body in the Dorsal Root Ganglion (not Dorsal Horn), ipsilaterally.

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94
Q

Name the two sensory receptor types, give an example of each and describe them.

A

Rapidly adapting - eg. Mechanoreceptors - frequency of firing diminishes quickly after initial stimulus (explains why cannot feel clothes on skin)
Slowly adapting - eg. Nociceptors - do not change frequency of firing after initial stimulus (means pain can be persistent and not go away)

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95
Q

What is a “Receptive Field”?

A

An area of skin supplied by a single primary sensory neurone, connected to multiple sensory receptors.

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96
Q

Define the Acuity of a Receptive Field and its relationship with the size of the Receptive Field.

A

Acuity = how small a change/movement can be felt - two point discrimination
A larger receptive field = a lower acuity (inversely proportional)
Fields can overlap, leading to fuzzy dermatome boundaries

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97
Q

Give examples of a high and low acuity area of the body.

A

High acuity area = fingertip

Low acuity area = skin of the back

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98
Q

Describe the layout of the Homunculus in Primary Sensory Cortex in relation to the limbs, medial to lateral.

A

Medial: Lower limb
Lateral: Upper limb
Extra lateral: Hand
Extra-extra lateral: Face

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99
Q

How many neurones are there in the somatosensory neurone chain?

A

3 - Primary, Secondary, Tertiary

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100
Q

In the Spinothalamic System: What is a Secondary (2nd Order) Sensory Neurone and where is its cell body and where does it travel to?

A

From 1st order neurone, has cell body in dorsal horn and decussates in the Ventral White Commisure. Travels to the Thalamus via the Spinothalamic Tract.

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101
Q

In the Spinothalamic System: What is a Third (3rd Order) Sensory Neurone and where is its cell body and where does it travel to?

A

From Thalamus, cell body in the Thalamus. Projects to Primary Sensory Cortex in the post-central gyrus.
Inferior parts of the body: Medial
Superior part of the body: Lateral

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102
Q

Why is the hand disproportionately likely to be affected by a tumour?

A

Hand has a disproportionately large representation in the Homunculus of the Primary Sensory Cortex.

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103
Q

How does Somatotopy link to the Homunculus?

A

Every part of the body has a corresponding part of the brain within the Homunculus.

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104
Q

In the DCML System: What is a Primary (1st Order) Sensory Neurone and how/where does it ascend?

A

From Lower body: ascend through the Gracile Fasciculus to the Gracile Nucleus in the medulla
From Upper body: ascend through the Cuneate Fasciculus to the Cuneate Nucleus in the medulla

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105
Q

In the DCML System: What is a Secondary (2nd Order) Sensory Neurone and how/where does it ascend?

A

From Lower Body: Gracile Nucleus to contralateral Thalamus in the Medial Lemniscus.
From Upper Body: Cuneate Nucleus to contralateral Thalamus in the Medial Lemniscus.

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106
Q

In the DCML System: What is a Tertiary (3rd Order) Sensory Neurone and how/where does it ascend?

A

From Lower Body: Project to the Medial part of the Primary Sensory Cortex.
From Upper Body: Project to the Lateral part of the Primary Sensory Cortex.

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107
Q

In the DCML system: where do axons from the lower and upper body run up to the brain? (which is medial and which is lateral)

A

Lower body: Medial

Upper body: added Laterally

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108
Q

In the Spinothalamic system: where do axons from the lower and upper body run up to the brain? (which is medial and which is lateral)

A

Lower body: Laterally

Upper body: Medially - due to decussations

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109
Q

Describe Brown-Sequard syndrome.

A

Complete hemisection destruction of the spinal cord (destruction on one side) - dorsal and ventral horns and all white matter pathways destroyed.
Will lead to:
- Ipsilateral DCML modalities below the destroyed segment
- Contralateral Spinothalamic modalities below the destroyed segment
- Segmental anaesthesia ipsilaterally in a single dermatome

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110
Q

Describe the process of pain modulation, including the fibres involved.

A

A fibres = mechanoreceptors - when activated, inhibits C fibres via adrenaline mediated response
C fibres = carry pain

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111
Q

Describe B12 deficiency’s effect on the body.

A

B12 is only from meat.

Leads to demyelination of the spinal cord - will get loss of peripheral sensation, as well as megaloblastic anaemia.

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112
Q

List 2 causes for insensitivity to pain.

A
  • Drugs

- Diabetes

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113
Q

Describe how bilateral symptoms of pain can occur,

A

Central canal swelling will lead to:

  • Spinothalamic system Upper Limbs is fucked first, as Ventral White Commissure taken out first (decussating fibres lost)
  • Gracile Fasciculus lost next, so DCML lost
  • Finally Spinothalamic tracts of Lower Limbs (lateral) would be lost
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114
Q

What is the role of the Pigmented layer of the retina?

A

Prevents glare.

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115
Q

Why do people with albinism struggle to see in bright sunlight?

A

They do not have Melanin - the retinal pigment cells contain Melanin. Will not prevent glare.

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116
Q

What is Uveitis?

A

Inflammation of the Choroid layer of the eye.

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117
Q

What are Bipolar cells within the eye?

A

First Order Neurones of the eye - interact with retinal ganglion cells.

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118
Q

What is the process of viewing the retina of the eye?

A

A fundoscopy.

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119
Q

What is the white disc on a fundoscopy and how many photoreceptors does it have?

A

The Optic nerve and 0.

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120
Q

What is the dark circle on a fundoscopy? (2 things)

A

Macula and the Fovea. The fovea of the macula has the cones with the highest resolution

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121
Q

What is darker on a fundoscopy, an artery or a vein?

A

Vein

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122
Q

What is papilloedema?

A

Inflammation of the Optic nerve due to raised ICP.

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123
Q

Describe the optic pathway in words, from the eye, the journey of the optic nerve and where it ends up (including radiations and lobes)

A
  1. Optic nerve travels to optic chiasm.
  2. Nasal fibres decussate at chiasm, Temporal fibres do not.
  3. The optic fibres travel down the optic tract to the Lateral Geniculate Nucleus.
  4. From the Lateral Geniculate Nucleus, the fibres travel down the optic radiations to the Primary Visual Cortex in the Occipital Lobe.
    Via:
    - Superior radiations - Parietal (GB Adv SP)
    - Inferior radiations - Temporal
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124
Q

Name the two sides of Visual field.

A

Temporal - lateral, but seen by Nasal fibres

Nasal - medial, but seen by Temporal fibres

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125
Q

What fibres (Nasal or Temporal) are responsible for seeing the Temporal viewing field?

A

The Nasal (alternate)

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126
Q

Which fibres decussate at the Optic chiasm?

A

Nasal

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127
Q

Which fibres do not decussate at the Optic chiasm?

A

Temporal

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128
Q

From the Optic chiasm, where do the fibres go and via which tract?

A

The fibres travel from the Optic chiasm to the Lateral Geniculate Nucleus via the Optic Tracts.

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129
Q

Describe how Monocular Blindness can occur and what it is. Give a cause.

A

Loss of all fields in one eye only.
Must have compression or loss pre-Optic-chiasm.
Retinal detachment or occlusion of a retinal artery or vein.
CN 2 lesion is most likely.

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130
Q

Describe how Bitemporal Hemianopia can occur and what it is. Give a cause.

A

Loss of Temporal fields on both eyes.
This means Nasal fibres lost (to see Temporal visual field). Most likely at the Optic Chiasm, as this is where the Nasal Fibres decussate.
Cause: Pituitary Adenoma.

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131
Q

Describe how Homonymous Hemianopia can occur (no-radiations) and what it is. Give a cause.

A

Loss of Left or Right side of vision of both eyes (one Nasal, one Temporal lost).
Damage to the Optic Tract on one side, so loss of one Nasal (contralateral) and one Temporal (ipsilateral).
Named based on which side of vision is lost.
Caused by Stroke/Tumour.

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132
Q

What quadrant of vision are the Superior Radiations responsible for?

A

The inferior quadrant.

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133
Q

What quadrant of vision are the Inferior Radiations responsible for?

A

The superior quadrant.

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134
Q

What lobe do the Superior radiations travel through?

A

The Parietal lobe (SP)

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135
Q

What lobe do the Inferior radiations travel through?

A

The Temporal lobe

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136
Q

Where do the Optic Radiations all end up?

A

The Occipital lobe, Primary Visual Cortex.

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137
Q

Describe how a right-sided Homonymous Inferior Quadrantinopia can occur and what it is. Give a cause.

A

Lesion of the right Superior Optic Radiation (Parietal Lobe):
- Loss of ipsilateral (right) Temporal fibre, supplying Inferior Nasal visual field
- Loss of contralateral (left) Nasal fibre, supplying Inferior Temporal visual field
Overall: Lost inferior right nasal field, lost inferior left temporal field

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138
Q

Describe how a right-sided Homonymous Superior Quadrantinopia can occur and what it is. Give a cause.

A

Lesion of the right Inferior Optic Radiation (Temporal Lobe):
- Loss of ipsilateral (right) Temporal fibre, supplying Superior Nasal visual field
- Loss of contralateral (left) Nasal fibre, supplying Superior Temporal visual field
Overall: Lost superior right nasal field, lost superior left temporal field

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139
Q

Describe how a Right Homonymous Hemianopia can occur (radiations cause) and what it is. Give a cause.

A

Loss of both optic radiations on one side (Left)

Happens only in stroke.

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140
Q

Describe Macular Sparing.

A

Only relevant to vascular lesions.
The occipital lobe has a dual blood supply:
- PCA
- MCA - supplies occipital pole
If PCA stroke occurs, macula will be okay, as supplied by MCA

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141
Q

Describe the Pupillary Light Reflex.

A
  1. Light enters eye, travels down Optic nerve to Lateral Geniculate Nucleus.
  2. Also travels to Pretectal Nucleus, which feeds into Edinger Westphal Nucleus.
  3. This stimulates Direct and Consensual Light reflexes.
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142
Q

Describe the Accomodation Reflex.

A 
Required for near vision.
3 Cs:
- Convergence of the eyes to a point
- Constriction of the iris
- Contraction of the lens by the ciliary *muscle*
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143
Q

Describe the role of the Medial Longitudinal Fasciculus.

A

Lies in the brainstem - makes the nerves that supply motor to the eye communicate with eachother.

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144
Q

What supplies blood to the anterior portion of the brain?

A

Internal Carotid Artery

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145
Q

What supplies blood to the posterior portion of the brain?

A

Vertebral Arteries

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146
Q

What structure/s are supplied by the anterior circulation of the Circle of Willis?

A

The cerebral hemispheres.

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147
Q

What structures are supplied by the posterior circulation of the Circle of Willis?

A

The brainstem, cerebellum and some of the temporal and occipital lobes.

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148
Q

What does the anterior cerebral artery supply and what is it a branch of?

A

Frontal and Parietal lobes medially - can affect homunculi if blocked.
Branch of ICA.

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149
Q

Name the branches of the ICA within the Circle of Willis.

A

Ophthalmic artery, anterior choroidal artery, Middle Cerebral Artery, Anterior Cerebral Artery, Posterior Communicating Artery (not PCA)

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150
Q

What important structure does the Posterior cerebral artery supply?

A

Thalamus

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151
Q

What does a PCA occlusion lead to in the eyes?

A

Homomymous hemianopia - Macular Sparing

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152
Q

Name the Cerebellar arteries.

A

Superior Cerebellar
Anterior Inferior Cerebellar
Posterior Inferior Cerebellar (branch of vertebral arteries)

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153
Q

Describe what the Middle Cerebral Artery supplies.

A 
The *lateral* part of the cerebral hemispheres (eg. Parietal/Temporal)
Deep branches (lenticulostriate arteries) supply lentiform/caudate nuclei and the internal capsule
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154
Q

Describe what the Anterior Cerebral Artery supplies.

A

Medial aspect of Frontal and Parietal lobes.

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155
Q

Describe what the Basilar artery supplies (and its branches - from below posterior communicating artery).

A
  • Posterior Cerebral Artery - supplies Occipital Lobe, Temporal Lobe medially and Thalamus, as well as Midbrain (en-passant)
  • Superior Cerebellar Artery - superior Cerebellum and Midbrain (en-passant)
  • Potine arteries - Pons
  • Anterior Inferior Cerebellar Artery - anterior inferior Cerebellum and Pons (en-passant)
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156
Q

Describe the branches of the Vertebral arteries and what they supply.

A
  • Posterior Inferior Cerebellar - Posterior Inferior cerebellum
  • Spinal arteries - anterior 2/3 of the spinal cord
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157
Q

What occurs if the Pontine arteries of the Basilar artery are occluded?

A

Locked-in syndrome - all motor pathways lost, consciousness still there.

158
Q

Where do the Upper Motor Neurones (UMNs) of the body have their cell bodies?

A

In the Primary Motor Cortex (Pre-central Gyrus)

159
Q

Where do the Lower Motor Neurones (LMNs) of the body have their cell bodies?

A

Brainstem (Cranial nerve motor nuclei) and Ventral horn of the spinal cord

160
Q

What happens when a LMN is activated by a synapsing UMN?

A

Contraction of the muscle.

161
Q

What are the Lower Motor Neurone damage signs?

A
  • Weakness of muscles
  • Areflexia
  • Wasting (loss of trophic support from LMN)
  • Hypotonia
  • Fasciculation (nAChRs are upregulated, can lead to mini contractions)
162
Q

Does damage to the Basal Ganglia or the Cerebellum lead to UMN signs?

A

No.

163
Q

What is the general role of the UMN in relation to its synapse with LMNs?

A

Generally inhibit LMNs via inhibitory interneurones.

164
Q

Describe the path an UMN will take to descend to a LMN.

A
  1. Corona radiata
  2. Internal capsule (between thalamus and lentiform nucleus)
  3. Cerebral peduncles of midbrain
  4. Pons
  5. Medullary pyramids
  6. Decussation of the pyramids
  7. Lateral corticospinal tract
  8. Ventral horn
  9. Synapse (either directly or indirectly via inhibitory interneurones)
165
Q

What is the role of the Corticonuclear tract?

A

Allows UMNs to supply LMNs in the face - decussates

166
Q

Describe what is strange about the Facial Motor Nucleus. Explain why forehead sparing occurs in UMN lesions of the face eg. Stroke.

A

It is split into two halves - one that supplies the upper half of the face, one that supplies the lower half of the face.
The part of the facial motor nucleus receiving signals for the upper part of the face receives signals from both hemispheres - therefore is spared.

167
Q

What happens in a facial nerve lesion that happens at a point after leaving the brainstem? (eg. parotid cancer)

A

Bell’s Palsy - entire side of face affected, no forehead sparing.

168
Q

Define Pyramidal and Extra-pyramidal signs.

A 
Pyramidal = due to damage to lateral corticospinal tratc
Extra-pyramidal = due to damage to the Basal Ganglia or Cerebellum
169
Q

What are the Upper Motor Neurone damage signs?

A
  1. Weakness (due to loss of excitatory inputs from UMNs into LMNs)
  2. Hypertonia (loss of inhibition) -> clonus
  3. Hyperreflexia -> clasp knife reflex
  4. Extensor plantar reflexes (Babinski sign)
170
Q

Describe how to check for Hypertonia.

A

Clonus test

171
Q

Describe how to test for Hyperreflexia.

A

Clasp-knife reflex

172
Q

Describe the Spinal Shock Phenomenon.

A

Occurs a few days after an UMN lesion.
Will present as a LMN lesion due to shock.
Flaccid paralysis, areflexia -> eventually get hypertonia and hyperreflexia after.

173
Q

Name the components of the Striatum

A
  • Caudate nucleus

- Putamen

174
Q

Name the components of the Lentiform Nucleus

A

Putamen + Globus Pallidus (internus/externus)

175
Q

How does the Basal Ganglia communicate with the Motor Cortex?

A

Via the Thalamus.

176
Q

Name all of the components of the Basal ganglia

A
  • Substantia Nigra Pars Compacta (dopamine releaser)
  • Caudate Nucleus
  • Putamen
  • Globus Pallidus
  • Subthalamic Nucleus
177
Q

Describe the components of Mickey Mouse

A 
Top of ears - Corticospinal tracts
Bottom of ears - Substantia nigra
Eyes - Red nuclei
Tears - Reticular formation
Mouth - Cerebral aqueduct
Around mouth - Periaqueductal grey
178
Q

Describe the Basal Ganglia components cross-sectionally

A

At front - Caudate Nucleus
Insula = Putamen around outside, globus pallidus inside
Between Caudate Nucleus and Globus Pallidus/Thalamus = Internal Capsule
Thalamus is at the back

179
Q

Which Dopamine receptors act for which pathway? D1 or D2?

A 
D1 = direct pathway
D2 = indirect pathway
180
Q

What is the role of the Basal Ganglia?

A

Determines best movements to achieve goal - reinforces correct movements and removes inappropriate movements.

181
Q

Describe the Basal Ganglia effects of Parkinson’s disease.

A

Substantia Nigra Pars Compacta degeneration, leading to reduced Dopamine release.

182
Q

Describe the Basal Ganglia effects of Parkinson’s disease.

A

Substantia Nigra Pars Compacta degeneration, leading to reduced Dopamine release.
Affects contralateral side, as corticospinal tract will decussate.

183
Q

Describe the Basal Ganglia effects of Huntington’s Chorea.

A

Reduced inhibition by Putamen on Globus Pallidus (indirect pathway), leads to reduced STN activity and thus more Thalamus activity

184
Q

Describe the symptoms of Huntington’s Chorea.

A

Choreiform movements, dystonia and incoordination

185
Q

Describe the Basal Ganglia effects of Hemiballismus.

A

Subthalamic nucleus does not function - caused by sub-cortical stroke.

186
Q

What lies down the centre of the Third Ventricle?

A

Septum Pellucidum

187
Q

How does the Cerebellum communicate with the rest of the body?

A

Cerebellar peduncles (not CEREBRAL PEDUNCLES of the midbrain)

188
Q

What can a cerebellar lesion lead to in relation to the ventricles?

A

Hydrocephalus, can impinge on the cerebral aqueduct

189
Q

What is the role of the Cerebellum?

A

Works with the Basal Ganglia to co-ordinate movements - particularly the sequence of movements. Puts things in order.

190
Q

Why does a Cerebellar lesion lead to ipsilateral signs?

A

Cerebellum sends out motor neurones to the contralateral motor cortex. When these descend, they then decussate - leads to ipsilateral overall.

191
Q

What are the signs of Cerebellar disease?

A 
D - Dysdiadochokinesia
A - Ataxia (unsteady gait)
N - Nystagmus
I - Intention tremor
S - Slurred speech (dysarthria)
H - Hypotonia
192
Q

What is Ataxia?

A

Unsteady gait

193
Q

What is Dysarthria?

A

Slurred speech due to laryngeal and tongue muscle lack of co-ordination

194
Q

What is the Vermis of the Cerebellum?

A

Down the middle, supplies the trunk

195
Q

Name all of the components of the VITAMIN C mnemonic for cerebellar disease causes.

A 
V - Vascular
I - Infection
T - Trauma
A - Autoimmune
M - Metabolic
I - Iatrogenic
N - Neoplastic
C - Congenital
196
Q

Where is an epidural placed?

A

L3/L4 or L4/L5

197
Q

Where is an epidural placed?

A

L3/L4 or L4/L5

198
Q

How many “pops” would you feel when doing an epidural.? What is the needle passing through?

A 
2 pops
1. Skin
2. Ligamentum flavum
Enters epidural space
Epidural bathes nerve roots
DO NOT ENTER DURA
199
Q

How many “pops” would you feel when doing an Lumbar Puncture? What is the needle passing through?

A

3 pops

  1. Skin
  2. Ligamentum Flavum
  3. Dura
200
Q

Where is a Lumbar Puncture placed?

A

L1/L2

201
Q

What is the role of the Reticular Formation? (Tears on Mickey Mouse)

A

Maintain alertness and consciousness via cortical activation

202
Q

What does the Frontal Lobe contain?

A
  • Primary Motor Cortex
  • Left side has Broca’s area
  • Pre-frontal Cortex - behaviour and judgement/ cognition
  • Eye movement in same direction can be frontal lobe
  • Continence centre - paracentral lobules found in Frontal Lobe
203
Q

How does a Frontal Lobe lesion present?

A
  • Motor weakness - UMN lesion, contralateral
  • Expressive aphasia - Broca’s area damaged if left side lesion
  • Sexual inappropriateness/aggression
  • Problem solving issues
  • Continence issues
204
Q

What does the Parietal Lobe contain?

A
  • Primary Sensory Cortex
  • Wernicke’s Area on the left
  • Body image - ability to tell a side of the body exists
  • Calculation
  • Superior Radiations
205
Q

How does a Parietal Lobe lesion present?

A
  • Anaesthesia, contralateral, affects all modalities
  • Receptive aphasia (inability to understand speech) - left sided lesion
  • Loss of one side of body - no awareness
  • Loss of writing and calculation ability
  • Inferior homonymous quadrantinopia
206
Q

What does the Temporal Lobe contain?

A
  • Primary auditory cortex (near Wernicke’s)
  • Primary Olfactory centre
  • Memory centre - Hippocampus
  • Emotion - Limbic structures, such as Hippocampus and Amygdala
  • Inferior Optic Radiations
207
Q

How does a Temporal Lobe lesion present?

A
  • Loss of hearing
  • Loss of smell
  • Memory loss
  • Psychiatric disorders (rip Limbic system)
  • Superior Homonymous Quadrantinopia
208
Q

Cerebral Dominance: What is the Left Hemisphere better for?

A

Language/ Maths/ Logic

209
Q

Cerebral Dominance: What is the Right Hemisphere better for?

A 
Whole picture processing eg.
Body Image
Visuospatial awareness
Emotion
Music
210
Q

What Hemisphere leads to Hemispatial neglect when damaged? Why?

A

Right - in charge of whole body image processing.
Left can attend to both halves of space.
Will not be able to see things on the left side.

211
Q

Describe the effects of damage to the Corpus Callosum.

A
  • Alien hands syndrome
  • Cannot name things in Temporal visual field. Nasal fibres decussate fine to other side, but cannot pass back to left side of brain to Broca’s area.
212
Q

What does Broca’s area do and where is it located?

A

In the Frontal Lobe Left Hemisphere, close to Primary Motor Cortex.
Produces speech.
Damage leads to Expressive Aphasia.

213
Q

What does Wernicke’s area do and where is it located?

A

In the Parietal/Temporal Lobe.
Understands speech - sits next to Primary Auditory Centre in Temporal lobe.
Receptive Aphasia - fluent gibberish, cannot understand

214
Q

What connects Broca’s and Wernicke’s areas?

A

Arcuate Fasciculus

215
Q

What does damage to the Arcuate Fasciculus lead to?

A

Inability to speak hear words.

216
Q

Name the two types of memory and where they are stored.

A

Declarative - facts - stored in the cerebral cortex

Non-declarative - motor skills, emotions - stored in the cerebellum and basal ganglia

217
Q

What is the role of the Hippocampus and where does it sit in the brain?

A

In the Temporal lobe.
Important in the consolidation of declarative memories, dependent on emotional, association and rehearsal context. Short -> Long term memory.
Output: Fornix -> Thalamus -> Cerebral Cortex

218
Q

Describe basically how Long Term Potentiation occurs.

A

Glutamate receptors up-regulated in synapses, leading to synaptic strengthening and allowing new connections.

219
Q

What is the difference between arousal and consciousness?

A 
Arousal = emotional, has a goal
Consciousness = awareness
220
Q

What two components does consciousness require?

A

Cerebral Cortex - thoughts

Reticular Formation - keeps cortex awake with excitatory neurones

221
Q

What are the 3 relays used to transfer excitatory signals from the Reticular Formation to the Cerebral Cortex?

A
  • Basal forebrain nuclei -> AcH
  • Hypothalamus -> Histamine
  • Thalamus -> Glutamatergic
222
Q

Why can anticholinergics cause sedation?

A

They inhibit the Basal forebrain nuclei pathway from the Reticular Formation to the Cerebral Cortex

223
Q

Is the relationship between the Cerebral cortex and the Reticular Formation a positive or negative feedback loop?

A

Positive feedback

224
Q

What are the 3 components of the GCS?

A
  • Eye opening
  • Motor response (commands)
  • Verbal response
225
Q

What is an EEG, what does it measure and what is it useful for?

A

Measures electrical activity within the brain, useful for detecting neural synchrony and normal cerebral function

226
Q

How many stages of sleep are there? What happens to the frequency of waves as sleep gets deeper? How many cycles per night?

A 
4 stages, plus REM
Frequency of waves gets less
B-waves = awake
A-waves = sleep initiated
Theta-waves = more deep sleep
Stage 4 = delta waves - deep sleep
Random K complexes
REM looks like awake - dreaming occurs
6 cycles per night
227
Q

What happens during REM sleep?

A

B-waves, as if awake. Dreaming.

Loss of motor function, as LMNs inhibited, Thalamus inhibited.

228
Q

What is Narcolepsy?

A

Lack of Orexin.

Leads to random sleep, sleep paralysis, halluciations.

229
Q

What is sleep apnoea?

A

Excess neck fat causes compression of airways during sleep.
Daytime sleepiness.
Should lose weight, sleep propped up or use a device to hold the tongue forward (Mandibular advancement device).

230
Q

What is Meningitis, pathphysiologically?

A

Inflammation of the leptomeninges

231
Q

What are the main causative organisms of Meningitis in neonates, children, normal people, elderly?

A

Neonates - E. coli
Children - H. influenzae
Normal - N. meningitidis
Elderly - S. pneumoniae

232
Q

What is the causative organism of Chronic Meningitis?

A

M. tuberculosis

233
Q

Name 4 complications of Meningitis.

A
  • Death
  • Sepsis
  • Cerebral abscess
  • Epilepsy
234
Q

What is Encephalitis and what is it commonly caused by? What does the cell death lead to.

A

Inflammation of the brain parenchyma.
Commonly viral.
Eg. Spinal cord attacked by Polio, Temporal Lobe attacked by Herpes.
Cell death leads to Inclusion Bodies.

235
Q

Describe the process of Encephalopathy development.

A

PrP (prion protein) develops mutation to make it extra stable (PrPsc)
Aggregates in the brain, destroys neurones (grey matter)
Eg. BSE, CJD, vCJD

236
Q

Name the 4 types of Dementia in order of prevalence

A

Alzheimer’s
Vascular
Lewy Bodies
Picks

237
Q

Describe the pathophysiology of Alzheimer’s disease.

A

Increased neuronal damage and loss of cortical neurones due to:

  • Neurofibrilliary tangles - Tau protein twists, hyperphosphorylated
  • Senile plaques (amyloid deposition) - APP not broken down by Presenelin and so deposited
238
Q

Describe how Senile plaques are formed in Alzheimer’s

A

APP (amyloid precursor protein) not broken down by Presenelin and so deposited after converted by secretase to AB protein

239
Q

What is normal ICP?

A

0-10mmHg

240
Q

What compensation mechanisms are there for raised ICP?

A
  • Reduced blood pressure/ volume
  • Reduced CSF volume
  • Brain atrophy
241
Q

Name the 3 types of brain herniation.

A
  • Subfalcine
  • Tentorial
  • Tonsilar
242
Q

Describe Subfalcine herniation.

A

Cingulate gyrus is pushed under free edge of tentorium cerebelli.
Can compress the ACA and cause ischaemia of the Frontal and Parietal lobes and Corpus Callosum.

243
Q

What can Subfalcine herniation lead to?

A

Can compress the ACA and cause ischaemia of the Frontal and Parietal lobes and Corpus Callosum.

244
Q

Describe Tentorial herniation.

A

Medial Temporal lobe (Uncus) is pushed through the tentorial notch (free edge of tentorium cerebelli).
Can compress CN 3 and cerebral peduncle - causes ipsilateral UMN signs.

245
Q

Describe Tonsilar herniation.

A

Cerebellar tonsils pushed through foramen magnum (“Coning”), compressing the brainstem.

246
Q

Name 2 types of brain tumour

A

Benign: Meningioma
Malignant: Astrocytoma

247
Q

Name the two types of Stroke.

A
  1. Cerebral infarction - most common

2. Cerebral haemorrhage

248
Q

Name the two types of Cerebral infarction

A
  1. Regional

2. Lacunar - very small, associated with hypertension

249
Q

What is a Lacunar stroke?

A

Small stroke associated with hypertension that commonly affects the internal capsule/basal ganglia

250
Q

What are the two types of Cerebral haemorrhage?

A
  1. Intracerebral haemorrhage - age, hypertension cause - blood vessel rupture in parenchyma
  2. Subarachnoid haemorrhage - rupture of berry aneurysms at branch points in Circle of Willis
251
Q

What are the symptoms of a Subarachnoid haemorrhage?

A
  • Thunderclap headache
  • Sentinel headache = string headache before it happens
  • Loss of consciousness
  • Often fatal
252
Q

Name 4 cognitive symptoms of Dementia.

A
  • Memory impairment - Temporal
  • Poor judgement - Frontal
  • Learning capacity reduced - Frontal/Temporal
  • Poor Orientation - Parietal + Temporal
253
Q

Name 4 non-cognitive symptoms of Dementia.

A
  • Behavioural eg. lack of sexual inhibition - Frontal
  • Depression and anxiety
  • Psychotic symptoms eg. Hallucinations/ persecutory delusions/psychosis
  • Insomnia
254
Q

Describe the pathophysiology of Vascular Dementia.

A

Ischaemia due to haemorrhage or cerebrovascular disease

Leads to step-wise decline

255
Q

How is decline in Vascular Dementia described?

A

Step-wise - improvement, large deterioration and so on.

256
Q

Describe the pathophysiology of Dementia with Lewy Bodies.

A 
Aggregation of a-synuclein protein - deposited inside cells of:
SNpC
Temporal lobe
Frontal Lobe
Cingulate gyrus
257
Q

Describe the link between naming between Dementia with Lewy Bodies and Parkinson’s disease.

A

If movement disorder first, Parkinson’s

If dementia first, DLB

258
Q

What are the symptoms of Dementia with Lewy Bodies?

A
  • Vivid hallucinations
  • Parkinsonism
  • Fluctuating alertness
  • Shuffling gait
259
Q

Why should a patient with Dementia with Lewy Bodies not be given antipsychotics?

A

Can lead to Neuroleptic Malignant Syndrome -> sudden drop in dopamine

260
Q

What is the mnemonic for neuroleptic malignant syndrome?

A 
FEVER
F - fever
E - encephalopathy
V - vital signs fucked
E - elevated Creatine Phosphokinase
R - rigidity
261
Q

What happens in AIDS dementia complex?

A

HIV infected macrophages get into the brain and destroy.

262
Q

Name 2 treatments for Dementia symptoms.

A

AcHesterase inhibitors eg. Donepazil - more AcH

NMDA antagonists - reduces over-stimulation of glutamate, reduces agitation (eg. Memantine)

263
Q

What is Delirium?

A

Acute neuronal damage to the brain caused by hypoxia or inflammation.
Causes confused state, difficulty remembering, clouded consciousness etc.
Often reversible
Increases Dementia risk, mortality and stay in hospital

264
Q

Name the two types of Delirium and their symptoms.

A

Hyperactive - restless, agitated, aggressive (emotional) - worse at dawn and dusk
Hypoactive - withdrawn, quiet, sleepy

265
Q

Name 3 causes for Delirium.

A
  • Toxic insult to the brain eg. Alcohol
  • Infection eg. Sepsis from UTI
  • Vitamin Deficiency
266
Q

What are Delirium tremors?

A

Alcohol withdrawal due to less inhibition of NMDA receptors, but many still being made. Causes tactile hallucinations (spiders etc.).

267
Q

What is the difference between a primary headache and a secondary headache?

A 
Primary = sypmtoms due to a headache condition eg. Migraine, tension, cluster
Secondary = due to another condition eg. Meningitis, sinusitis
268
Q

Name the signs of a life-threatening headache.

A

Papilloedema
Thunderclap headache
Neurological signs

269
Q

Describe the epidemiology of Migraines.

A

Mainly female, 20s, gets better with age

270
Q

Describe the SQITARPS of a Migraine.

A

Site: Unilateral, front
Quality: Sudden
Intensity: Moderate
Time: 4-72 hours
Aggravating factors: Photophobia/Phonophobia
Relieving factors: Triptans/Sleep
Secondary symptoms: Aura, Nausea, Vomiting

271
Q

Name 3 triggers of Migraines.

A

Wine, cheese, stress

272
Q

Describe the epidemiology of Tension headaches.

A

Most common, female, young

273
Q

Describe the SQITARPS of a Tension headache.

A

Site: Bilateral, frontal, forehead, can radiate to neck
Quality: Constriction
Intensity: Mild
Timing: Worse at end of day
Aggravating factors: Stress, poor posture
Relieving factors: Analgesia

274
Q

Describe a Medication-overuse headache.

A

Codeine/ NSAID/ Paracetamol use more than 15 days/month - headache doesn’t improve with analgesia
Will get worse before it gets better (rebound headache) - takes 2 months to recover

275
Q

Describe the epidemiology of a Cluster headache.

A

Male, 20-40

276
Q

Describe the SQTARS of a Cluster headache.

A

Site: One eye
Quality: Sharp
Timing: Rapid onset, usually during sleep, lasts 15 mins - 3 hours
Aggravating factors: Head injury, alcohol, smoking

277
Q

Describe the secondary symptoms of a Cluster headache.

A

Red, watery eye, nasal congestion, ptosis

278
Q

Describe the epidemiology of Trigeminal Neuralgia.

A

50-60 years old, increases with age, women

279
Q

Describe the SQTARS of Trigeminal Neuralgia.

A

Site: Unilateral, over one eye
Quality: Electric shock
Intensity: Severe, lasts a few seconds, can’t bear to be touched

280
Q

What are the aggravating factors for Trigeminal Neuralgia?

A

Cold wind, eating, light touch to face, vibrations

281
Q

What should happen if a stroke is suspected?

A

CT head, check if within thombolysis window (4 hours)

282
Q

What are the terminal branches of the ICA?

A

Middle cerebral artery and Anterior cerebral artery.

283
Q

What joins the two Anterior Cerebral Arteries?

A

Anterior Communicating Artery.

284
Q

What are the Vertebral Arteries a branch off?

A

Subclavian artery

285
Q

Describe the symptoms of an Anterior Cerebral Artery infarct.

A
  • Limb weakness - Lower Limb affected far worse -Primary Motor Cortex affected
  • Expressive aphasia
  • Apraxia - inability to plan motor movements
  • Urinary Incontinence (paracentral lobules damaged)
  • Split brain syndrome - Corpus callosum is supplied by the ACA
286
Q

Describe the points at which the MCA can be occluded.

A
  • Proximal
  • Lenticulostriate
  • Distal
287
Q

Describe the symptoms of a Middle Cerebral Artery infarct PROXIMALLY.

A

Everything affected, as occludes all branches.

  • Contralateral full hemiparesis - internal capsule damaged
  • Contralateral sensory loss of Upper Limb and Face (lateral)
  • Contralateral homonymous hemianopia without macular sparing - both temporal and parietal lobes damaged - MCA supplies macula
  • If left sided, Aphasia, both Broca’s and Wernicke’s affected
  • if right sided, Hemispatial neglect (right parietal lobe)
288
Q

Describe the symptoms of a Middle Cerebral Artery infarct of the LENTICULOSTRIATE ARTERIES (lacunar stroke).

A
  • Motor and Sensory all lost - both motor and sensory fibres travel through the internal capsule
  • Could also get Basal Ganglia damage (Lentiform Nucleus - Putamen + Globus Pallidus) -> reduced Thalamus inhibition, therefore more movement if purely sensory loss
289
Q

Describe the symptoms of a Middle Cerebral Artery infarct DISTALLY.

A

MCA splits into superior and inferior divisions:

  • Superior - Lateral Frontal lobe loss - expressive aphasia, face and arm weakness (primary motor cortex)
  • Inferior - Lateral Parietal and Superior Temporal - Primary Sensory, Wernicke’s Optic radiations - sensory changes in face and arm (not legs, too lateral), receptive aphasia, homonymous hemianopia without macular sparing
290
Q

Describe the symptoms of a Posterior Cerebral Artery infarct.

A

Contralateral Homonymous Hemianopia with macular sparing (MCA supplies macular area)
Contralateral sensory loss due to Thalamus damage (supplied by PCA, all sensory channels move into it)

291
Q

How would you know if a Cerebellar Artery occlusion was proximal or distal?

A

If proximal, would also get brainstem signs, as it supplies that on the way to the Cerebellum.

292
Q

What extra symptoms would you get in the case of a proximal Cerebellar Artery infarct?

A

Nausea, vomiting, headache, vertigo (due to vestibulocochlear system link)
Due to brainstem loss of blood

293
Q

What are the ipsilateral cerebellar signs that would be seen in a Cerebellar Artery infarct?

A 
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech (dysarthria)
Heel-shin test positive
294
Q

Describe the effects of a DISTAL Basilar artery occlusion.

A

Supplies brainstem.
After pontine arteries, so pons not affected. No locked-in syndrome.
Only midbrain affected - oculomotor palsy. Sleep problems. Behaviour issues.

295
Q

Describe the effects of a PROXIMAL Basilar artery occlusion.

A

Supplies brainstem.
Causes locked-in syndrome, as pontine arteries occluded.
Eyes not affected as midbrain still supplied by PCA.

296
Q

Name the 4 classifications of the Bamford Stroke Classification.

A

TACS - total anterior
PACS - partial anterior
LACS - lacunar
POCS - posterior

297
Q

What does a TACS involve?

A 
Total anterior (ACA and MCA)
All 3 of:
- Unilateral weakness
- Homonymous hemianopia
- Higher vertebral dysfunction - aphasia, visuospatial
298
Q

What does a PACS involve?

A 
Partial anterior (ACA and MCA)
2 of:
- Unilateral weakness
- Homonymous hemianopia
- Higher vertebral dysfunction - aphasia, visuospatial
299
Q

What does a LACS involve?

A 
Lacunar
1 of:
- Pure sensory
- Pure motor
- Sensori-motor
- Ataxic hemiparesis
300
Q

What does a POCS involve?

A 
Posterior (PCA)
1 of:
- Cranial nerve palsy
- Eye movement disorder
- Cerebellar dysfunction
- Isolated homonymous hemianopia
301
Q

Describe the Monro-Kellie doctrine. Give an example in the brain.

A

Any increase in volume of any of the cranial constituents, must be compensated by a decrease in the volume of another.
Every time the heart beats, CSF also pumps out of the brain.

302
Q

Give 4 causes of raised ICP.

A
  • Too much blood - haemorrhage - extradural, subdural, subarachnoid
  • Too much CSF - hydrocephalus
  • Cerebral oedema
  • Tumour
303
Q

Give 3 causes of hydrocephalus.

A
  • Spina Bifida
  • Aqueductal stenosis
  • Increased CSF of production in meningitis
304
Q

What are the main symptoms of hydrocephalus in babies. How is it treated?

A 
Sunset eyes and enlarged forehead
Fontanelle tapping (extraventricular drain)
305
Q

What is an Extraventricular Drain used to treat?

A

Hydrocephalus - can lead to infection

306
Q

Describe how a “Omayya reservoir” is used to drain CSF from the brain.

A

One-way shunt into the peritoneum

307
Q

How many mls can the brain deal with in excess?

A

75ml

308
Q

What is the Cerebral Perfusion Pressure equation?

A

CPP = MAP - ICP

309
Q

How can a stroke cause raised CPP?

A

Increases MAP (CPP = MAP - ICP)

310
Q

What could cause reduced CPP?

A

MAP could fall if cardiac output falls. Would lead to reduced CPP.

311
Q

Describe Cushing’s Triad.

A
  1. Low CPP detected due to raised ICP. BP and heart rate raised in response by increased symapthetics -> increased MAP.
  2. Increased BP though leads to bradycardia due to baroreceptors increasing vagal activity - this also increases acid production, which can lead to Cushing’s Ulcer.
  3. Irregular breathing occurs due to brainstem being squashed by herniating brain (Tonsilar herniation)
    Can then progress to cardiac arrest.
312
Q

How is a Cushing’s Ulcer formed?

A
  1. Low CPP detected due to raised ICP. BP and heart rate raised in response by increased symapthetics -> increased MAP.
  2. Increased BP though leads to bradycardia due to baroreceptors increasing vagal activity - this also increases acid production, which can lead to Cushing’s Ulcer.
313
Q

What are the signs of raised ICP?

A
  • Headache
  • Nausea and vomiting
  • Confusion
  • Visual issues eg. Papilloedema
314
Q

Why should you do a CT before a lumbar puncture?

A

If risk of tumour, do CT to check before doing a lumbar puncture, as it could cause Tonsilar herniation of the brain. If just idiopathic intracranial hypertension, only fluid will leave.

315
Q

What is the sign of raised ICP on a lumbar puncture?

A

High opening pressure

316
Q

What is an ICP bolt?

A

Measure ICP continuously - must be done in ITU. Can also do brain oximetry.

317
Q

What is SCIWRA?

A

Spinal Cord Injury without Radiographic Abnormality - cannot pick up soft tissue injury to spine on the CT

318
Q

What are the protection measures for raised ICP?

A
  • Airway control
  • Circulatory support
  • Sedation
  • Head at 30 degrees
  • Reduce temperature to reduce meatbolic demand
319
Q

What are the treatments for raised ICP?

A
  • Mannitol - hypertonic, draws fluid out of brain and a diuretic
  • 3% hypertonic saline - either
  • Extraventricular drain
  • Decompressive craniectomy
320
Q

What are the risk factors for Subarachnoid Haemorrhage?

A
  • Hypertension
  • Smoking
  • Warfarin - haemorrhage risk
  • Marfan’s
321
Q

Give two common sites of Subarachnoid haemorrhage berry aneurysms.

A

Anterior Communicating Artery

Posterior Communicating Artery

322
Q

Describe the symptoms of a Subarachnoid haemorrhage.

A
  • Thunderclap headache
  • Loss of consciousness, confusion
  • Meningism
323
Q

What is Meningism?

A

Signs similar to Meningitis:

  • Stiff neck
  • Photophobia
  • Headache
324
Q

What is Xanthocromia of CSF?

A

Yellow CSF caused by haemoglobin bilirubin within the subarachnoid space.

325
Q

What is the treatment for Subarachnoid heamorrhage?

A

ABC approach:

  • Airway support
  • Breathing - give oxygen
  • Circulatory support - fluids
  • Give nimodipine
326
Q

Why is Nimodipine given to people post Subarachnoid haemorrhage?

A

Alleviates spasming, reducing permanent damage.

327
Q

What is a craniectomy?

A

Decompressive surgery

328
Q

What are the risk factors of Meningitis?

A
  • Crowded housing eg, students
  • Diabetes/ HIV - immunosuppression
  • Splenectomy
329
Q

What is “neck stiffness” in Meningitis?

A

Nuchal rigidity

330
Q

Describe the pathophysiology of Meningitis and how it can cause death.

A

Pathogen enters subarachnoid space, causes inflammation of the leptomeninges, can cause vasospasm and so infarct, and oedema, leading to raised ICP.

331
Q

What is the type of rash seen in meningococcal septicaemia?

A

Maculopapular rash - caused by microvascular thrombosis

332
Q

What investigations should be carried out in Meningitis?

A

Bloods

Lumbar puncture - cloudy CSF, low glucose if bacterial, clear if viral

333
Q

What is the treatment for Meningitis?

A

IV ceftriaxone

Dexamethosone - prevents hearing loss due to swelling of CN 8

334
Q

What is the difference between neurology and psychiatry?

A 
Neurology = nervous system disorders with established aetiologies
Psychiatry = disorders of mood with no physical signs
335
Q

Name the two categories of functional psychiatry.

A

Neurotic disorders - exaggerated normal reactions eg. depression, anxiety
Psychotic disorders - not normal experiences eg. bipolar, schizophrenia

336
Q

What is Organic Psychiatry?

A

Disorders of mood caused by physical pathology eg. Dementia/Huntington’s

337
Q

Define “disorder”.

A

A clinical set of symptoms that lead to personal interference

338
Q

Define anxiety.

A

A feeling of nervousness or worry about something with an uncertain outcome - caused by the stress response from the limbic system

339
Q

What is the role of the hippocampus? Where does it project to? What is its role in the acute stress response?

A

Adds emotional context to memories - projects to the Thalamus and Hypothalamus - this then creates the stress response via projections down to the adrenal medulla, causing adrenaline release.

340
Q

Where is the amygdala?

A

By the top of the hippocampus, in the roof of the third ventricle.

341
Q

Where does the amygdala project to and what is its role in the acute stress response?

A

Projects to Thalamus and so the cortex and also to the hypothalamus. This then creates the stress response via projections down to the adrenal medulla, causing adrenaline release.

342
Q

What is the role of the pre-frontal cortex?

A

Modulates emotional responses.

343
Q

What is the main hormone released as part of the “chronic” stress response?

A

Cortisol.

344
Q

Explain the steps of General Adaptation Syndrome to stress.

A
  1. Alarm reaction - immediate release of adrenaline and cortisol, as well as sympathetic innervation
  2. Resistance - Prolonged release of cortisol, adrenaline effects wear off
  3. Exhaustion - Side-effects of prolonged Cortisol
345
Q

What are the symptoms of Anxiety?

A
  • Palpitations
  • Sweating
  • Trembling
  • Dry mouth
  • Chest tightness
346
Q

Name all 6 types of anxiety disorder.

A
  • Social
  • Phobia
  • Generalised
  • Panic
  • OCD
  • PTSD
347
Q

Give 3 treatments of Anxiety disorders.

A
  • Benzodiazepines - short term
  • SSRIs
  • Cognitive behavioural therapy
348
Q

What is the MOA of benzodiazepines?

A

Increase GABA transmission, increasing cortex inhibition

349
Q

What is an Obsession?

A

Thoughts that dominate a person’s thinking despite knowledge that the thoughts are without purpose - must be unpleasant

350
Q

What is a Compulsion?

A

A motor act resulting from an obsession

351
Q

What is the ICD10 definition of OCD?

A

Obsessions and Compulsions on most days for 2 weeks
Obsessions must have the following features:
- Originate in the mind of the patient, be unpleasant, be acknowledged as excessive and be non-resistable

352
Q

Name some potential theories for OCD causes.

A
  • Basal Ganglia re-entrant loop - cortex -> basal ganglia -> cortex again. Caused by hyperactive Thalamus, which is why benzodiazepines work.
  • Reduced serotonin levels (hence SSRIs)
  • Cross-reactivity with streptococcus A antigens
353
Q

Name 3 treatments of OCD.

A
  • SSRIs +- antipsychotics
  • Deep brain stimulation
  • Cognitive behavioural therapy
354
Q

Describe the features of PTSD.

A

Repetitive recollection of a traumatic event within 6 months of a traumatic event. Emotional detachment, numbing of feeling.

355
Q

Name 3 treatments for PTSD.

A
  • SSRIs
  • Benzodiazepines
  • CBT
356
Q

What are the core symptoms for being diagnosed with a depressive disorder?

A

2 of 3:

  • Low mood
  • Lack of energy
  • Lack of enjoyment or interest
357
Q

What is there a deficiency of in depression?

A

Serotonin. If tryptophan is removed from the diet, depression is caused.

358
Q

What is the difference between an adjustment reaction and depression?

A

Adjustments are usually sudden, fluctuate and don’t lead to lack of energy or sleep disturbance.

359
Q

What is mania?

A
  • Elevated mood
  • Increased energy
  • Fast talking
  • Reduced sleep
  • Loss of social inhibitions
  • Grandiose delusions
  • Psychosis
360
Q

What is bipolar disorder?

A

2 episodes of mood disorder, at least one of which is mania (eg. mania to depression switch)
Bipolar 1 = mania episodes
Bipolar 2 = hypomania only, so no psychotic symptoms

361
Q

Name 3 causes of mood disorders.

A
  • Alcohol/drugs
  • Hormone disturbance eg. thyroid disorder
  • Kidney disease
362
Q

What brain structures are involved in mood disorders?

A
  • Frontal lobe
  • Limbic system
  • Basal Ganglia
363
Q

What are the main roles of NA in the brain?

A

Mood, behaviour, memory

364
Q

Where is Noradrenaline made in the brain?

A

Locus coerulus

365
Q

Name 2 Noradrenaline antidepressants.

A

Tricyclics, SNRIs

366
Q

What are the main roles of Serotonin in the brain?

A

Sleep, mood, appetite

367
Q

Where is Serotonin made in the brain?

A

Raphe nuclei

368
Q

Name 2 Serotonin antidepressants.

A

SSRIs, TCAs

369
Q

Name 4 medications for Depression.

A
  • SSRIs - sertaline
  • SNRIs - duloxetine
  • Lithium - mood stabiliser
  • Sodium valproate - mood stabiliser
370
Q

Name 2 medications for Bipolar disorder.

A

Mood stabilisers - Lithium and Sodium Valproate

Antipsychotics eg. Haloperidol

371
Q

Name an antipsychotic

A

Haloperidol

372
Q

What must not be given to someone with Bipolar disorder?

A

Antidepressants eg. SSRIs, SNRIs, TCAs

373
Q

What are the side effects of SSRIs?

A
  • Nausea
  • Dry mouth
  • Somnolescence
    Has anticholinergic effect
374
Q

What is the definition of Psychosis?

A

Presence of hallucinations or delusions - not a diagnosis.

375
Q

What is a Hallucination?

A

A perception without a stimulus.

376
Q

What is a Delusion?

A

An abnormal belief, unshakeable.

377
Q

Name 4 causes of Psychosis.

A

Delirium caused by infection
Delirium tremors
Drug/alcohol intoxication -> drug induced psychosis
Encephalitis

378
Q

What are the symptoms of Schizophrenia?

A
  • Auditory Hallucinations - hearing voices eg. running commentary
  • Passivity Experience - patient believes action is caused by external force
  • Thought withdrawal/broadcast/insertion
  • Delusional perceptions - think something terrible will happen
  • Somatic hallucination - mimics feeling something inside body
379
Q

Name the “Positive” symptoms of Schizophrenia

A

Symptoms added to the patient eg. Auditory hallucinations, passivity experience, thought withdrawal, delusional perceptions

380
Q

Name a “Negative” symptom of Schizophrenia

A

Symptoms taken from the paitent eg. Low mood, Low motivation, low energy

381
Q

What causes Schizophrenia?

A

Changes in the Mesolimbic and Mesocortical pathways:
Mesolimbic - overactive
Mesocortical - underactive
Have enlarged vesicles
D2 receptors are overstimulated due to excess of dopamine production

382
Q

What are the treatments for Schizophrenia?

A
  • Antipsychotics eg. Haloperidol
383
Q

How do antipsychotics work in Schizophrenia?

A

Block D2 receptors in mesolimbic and mesocortical pathways

384
Q

What are the side effects of antipsychotics?

A

Parkinsonian symptoms: Muscle rigidity, tremor, bradykinesia, sexual dysfunction due to raised prolactin

385
Q

What Dopamine receptors are mainly affected in Schizophrenia?

A

D2

386
Q

What happens to patients with Schizophrenia who are not treated?

A

Catatonia, rigidity, waxy flexibility (patient can be moved and adjusted as desired and will sit like that)

387
Q

What does CJD lead to?

A

Rapidly progressive dementia, memory loss, myoclonus (jerky movements)

388
Q

What is MS and what are its symptoms?

A 
Demyelination of the neurones in the CNS due to immune destruction or failure of myelin producing cells
Symptoms:
- Double vision
- Poor co-ordination
- Weakness
389
Q

What is Cerebral Palsy and what are the symptoms?

A

Permanent movement disorders caused by damage to parts of the brain that control movement and balance
Causes: Poor co-ordination, weak muscles, tremors, slow development

390
Q

What is the name for a wooshing sound?

A

Bruit

391
Q

What is an AVM? (arteriovenous malformation)

A

Abnormal connection between arteries and veins. Can lead to seizures, headaches, bleeding.

Neuro ESA 4 (1 decks)

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