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PHASE 2A > Neuro > Flashcards

Neuro Flashcards

1
Q

What do oligodendrocytes myelinate?

A

Brain

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2
Q

What do Schwann cells myelinate?

A

Peripheral Nervous System (PNS)

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3
Q

Define nuclei

A

Collection of nerve cell bodies within the CNS

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4
Q

Define ganglia

A

Collection of nerve cell bodies outside the CNS and some in the CNS (in a capsule)

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5
Q

What sort of information is carried on afferent fibres?

A

Sensory fibres towards the CNS

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6
Q

What sort of information is carried on efferent fibres?

A

Motor fibres away from the CNS

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7
Q

What is the function of the frontal lobe?

A

Voluntary movement on opposite side of the body
Dominant frontal lobe control speech (Broca’s area) and writing
Intellectual functioning, thought processes, reasoning and memory

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8
Q

What is the function of the parietal lobe?

A

Receives and interprets sensations - pain, touch, pressure, proprioception

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9
Q

What is the function of the temporal lobe?

A

Understanding spoken word (Wernicke’s area)

Memory and emotion

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10
Q

What is the function of the occipital lobe?

A

Understanding visual images and meaning of written word

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11
Q

What are the components of the basal ganglia?

A

Striatum (Caudate nucleus + Putamen)
Globus pallidus
Subthalamic nucleus
Substantia nigra

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12
Q

What are the components of the striatum?

A

Caudate nucleus

Putamen

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13
Q

What are the components of the lentiform nucleus?

A

Globus Pallidus

Putamen

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14
Q

What is the function of the cerebellum?

A

Co-ordinates movement and balance

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15
Q

Describe the function of the hippocampus

A

Episodic memory
Construction of mental images
Short term memory
Spatial memory and navigation

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16
Q

How many axons can oligodendrocytes myelinate?

A

Multiple

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17
Q

How many axons can Schwann cells myelinate?

A

One

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18
Q

What is the function of ependymal cells?

A

Line ventricles of the brain and regulate the production and flow of CSF

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19
Q

Which cells make up the blood-brain-barrier?

A

Endothelial cells, pericytes and astrocytes

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20
Q

What are the features of the BBB?

A

Endothelial tight junctions
Astrocyte end feet
Pericytes
Continuous basement membrane

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21
Q

What is the name given to areas of the brain that lack a BBB?

A

Circumventricular organs

E.g. Posterior pituitary

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22
Q

Where does the CSF circulate?

A

Subarachnoid space

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23
Q

What is the volume of CSF?

A

120 mls

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24
Q

What is found in the CSF?

A

Protein, urea, glucose and salts

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25
Q

Where is CSF produced?

A

By ependymal cells in the choroid plexus (mainly in lateral ventricles)

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26
Q

How is CSF reabsorbed?

A

Via arachnoid granulations (villi) into the superior sagittal sinus

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27
Q

Describe the passage of CSF

A

Produced by ependymal cells in choroid plexuses of lateral ventricles –> 3rd ventricle via interventricular foramen –> 4th ventricle via the cerebral aqueduct –> subarachnoid space vis the median foramen of Magendie and 2 lateral foramen’s of Luschka –> absorbed via arachnoid granulations (vili) into superior sagittal sinus

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28
Q

Describe what happens in hydrocephalus

A

Abnormal accumulation of CSF in the brain which leads to a build-up of pressure often due to a blocked cerebral aqueduct

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29
Q

What are the 5 processes of synaptic transmission?

A
  1. Manufacture (intracellular biochemical processes)
  2. Storage - vesicles
  3. Release - AP
  4. Interaction with post synaptic receptors
  5. Inactivation
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30
Q

What are the 2 main acethylcholine receptors?

A
  1. Muscarinic

2. Nicotinic

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31
Q

Which enzymes is responsible for the breakdown of ACh in the synaptic cleft?

A

Acetylcholinesterase

ACh –> Choline + acetate

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32
Q

What functional area of the brain surrounds the primary auditory cortex?

A

Wernicke’s area (processes language)

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33
Q

Inferior colliculus and medial geniculate body are important for what sense?

A

Hearing

I’M Auditory

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34
Q

The superior colliculus and lateral geniculate body are important for what sense?

A

Vision

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35
Q

Which part of the eye is involved in the accommodation reflex?

A

Ciliary muscle

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36
Q

What does the iris do?

A

Controls the size of the pupil (which lets light into the eye)

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37
Q

What does the dilator papillae muscle do?

A

Dilates the pupil (sympathetic)

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38
Q

What does the sphincter papillae do?

A

Constricts the pupil (parasympathetic)

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39
Q

What fibres cross at the optic chiasm?

A

Nasal portions of the retina carrying the temporal visual field

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40
Q

Where in the thalamus do the optic tracts join to?

A

Lateral geniculate body

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41
Q

Outline the order of the visual pathway from the eye to visual cortex

A

Eye –> optic nerve –> optic chiasm –> optic tract –> lateral geniculate body (thalamus) –> optic radiation –> visual cortex

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42
Q

What is the name of the optic radiation that passes through the parietal lobe and what information does it carry?

A

Baum’s loop - information from the superior retina (so inferior visual fields)

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43
Q

What is the name of the optic radiation that passes through the temporal lobe and what information does it carry?

A

Meyer’s loop - information from inferior retina (so superior visual fields)

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44
Q

What is the effect of a lesion on the left optic nerve?

A

Left anopia = no vision in left eye

right lesion = right eye blindness

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45
Q

What is the effect of a lesion at the optic chiasm?

A

Loss of temporal visual fields = bilateral hemianopia

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46
Q

What is the effect of a lesion on the right optic tract?

A

Loss of vision of temporal field of the left eye
Loss of nasal field of the right eye
= right homonymous hemianopia

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47
Q

What is the effect of a lesion on the left Meyer’s loop?

A

Carries information from inferior retina and thus the superior visual field so:

  • Loss of vision in the superior nasal field of the left eye
  • Loss of vision in the superior temporal field of the right eye
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48
Q

What is the effect of a lesion on the left Baum’s loop?

A

Carries information from the superior retina and thus the inferior visual field so:

  • Loss of vision in the inferior temporal field of the right eye
  • Loss of vision in the inferior nasal field of the left eye
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49
Q

What is the name given to internal rotation of the eye (towards midline)?

A

Intorsion

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50
Q

What is the name given to external rotation of the eye (away form midline)?

A

Extorsion

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51
Q

What are the 6 ocular eye muscles?

A
  1. Superior rectus
  2. Inferior rectus
  3. Lateral rectus
  4. Medial rectus
  5. Superior oblique
  6. Inferior oblique
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52
Q

Which muscles of the eye are supplied by the oculomotor nerve (CN III) and what are their functions?

A

Superior rectus = medial rotation, elevation and adduction
Inferior rectus = lateral rotation, depression and adduction
Medial rectus = Adduction
Inferior oblique = extorsion, elevates and abducts

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53
Q

Which muscles of the eye are supplied by the abducens nerve (CN VI) and what are the functions?

A

Lateral rectus = abduction

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54
Q

Which muscles of the eye are supplied by the trochlear nerve (CN IV)?

A

Superior Oblique = intorsion, depresses and abducts

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55
Q

What does the somatic nervous system innervate?

A

Skeletal muscle

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56
Q

Do neurones of the somatic nervous system synapse before the skeletal muscle?

A

No

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57
Q

What is the only neurotransmitter involved in the somatic nervous system?

A

Acetylcholine

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58
Q

What does the autonomic nervous system innervate?

A

Smooth and cardiac muscle, glands, neurones in the GIT

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59
Q

Where is the first synapse of an autonomic nerve?

A

Synapses outside the CNS in the autonomic ganglion

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60
Q

What’s the name of the autonomic nerve between the CNS and the ganglia?

A

Preganglionic fibres

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61
Q

What’s the name of the autonomic nerve between the ganglion and the effect cells??

A

Postganglionic fibres

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62
Q

What are the 2 division of the autonomic nervous system?

A
  1. Sympathetic

2. Parasympathetic

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63
Q

Where do the sympathetic nerves leave the spinal cord?

A

Between T1 and L2

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64
Q

Where do the ganglia of the sympathetic neurones lie?

A

Close to the spinal cord = sympathetic chain

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65
Q

What neurotransmitter is used by the preganglionic sympathetic fibres?

A

Acethylcholine acts at nicotinic receptors

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66
Q

What neurotransmitter is used at the effector cell synapse in sympathetic fibres?

A

Noradrenaline acts at adrenergic receptors

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67
Q

What are the effects of the sympathetic nervous system?

A 
Increased HR (+ve chronotropic)
Increased force of contraction (=ve inotropic) 
Vasoconstriction 
Bronchodilation 
Reduced gastric secretion 
Reduced gastric motility 
Sphincter contraction
Male ejaculation
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68
Q

Where do parasympathetic nerves leave the spinal cord?

A

Brainstem and sacral regions of the spinal cord

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69
Q

Which cranial nerves are parasympathetic?

A

CN 3, 7, 9 and 10 (1973)

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70
Q

Where do the ganglia of parasympathetic nerves lie?

A

Close to the organs that the postganglionic fibres innervate

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71
Q

What is the neurotransmitter used by preganglionic parasympathetic fibres?

A

Acetylcholine at nicotinic receptors

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72
Q

What is the neurotransmitter used by postganglionic parasympathetic fibres?

A

Acetylcholine at muscarinic receptors

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73
Q

What are the effects of the parasympathetic nervous system?

A 
Decreased heart rate (-ve chronotropic)
Decreased force of contraction (-ve inotropic)
Vasodilation 
Bronchoconstrition 
Increased gastric motility 
Increased gastric secretion 
Sphincter relaxation
Male erection
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74
Q

Define CNS

A

Consists of the brain and spinal cord

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75
Q

Define PNS

A

Nerves and ganglia outside the brain and spinal cord

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76
Q

How many vertebrae are there?

A

Total = 33

  • 7 cervical
  • 12 thoracic
  • 5 lumbar
  • 5 sacral
  • 4 coccyx
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77
Q

How many spinal nerves are there?

A

31 pairs of spinal nerves

  • Cervical = 8 nerves (1 higher than the corresponding vertebrae and an extra below C8)
  • 12 thoracic nerves (1-2 vertebra below corresponding vertebra)
  • 5 lumbar nerves (3-4 vertebra below)
  • 5 sacral (5 vertebrae below)
  • 1 coccyx nerve
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78
Q

Define dermatome

A

Area of skin supplied by a single spinal nerve

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79
Q

Define myotome

A

A volume of muscle supplied by a single spinal nerve

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80
Q

What are the 2 division of the descending motor pathways?

A

Pyramidal and extrapyramidal

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81
Q

Describe the corticospinal pathway

A

Controls voluntary muscles
Originates in the cortex –> internal capsule –> crura cerebri
- 85% decussate in medulla through anterior white commissure = lateral –> limb muscles
- 15% ipsilateral = anterior –> axial muscles

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82
Q

Describe the extrapyramidal pathways

A

Originate in the brainstem and carry motor fibres to the spinal cord
Responsible for the involuntary autonomic control of all musculature

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83
Q

What are the extrapyramidal tracts?

A 
Rubrospinal 
 - Facilitates flexors and inhibits extensors (fine hand movements)
 - Originates in red nucelus 
 - Decussate in midbrain (contralateral)
Tectospinal 
 - Head turning in response to visual stimuli 
 - Originates from tectum - superior colliculus 
 - Decussate in midbrain
Vestibulospinal 
 - Muscle tone, balance and posture
 - Originates at vestibular nucleus 
 - Non-decussating (Ipsilateral)
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84
Q

What are the ascending sensory tracts?

A
  1. Dorsal/medial lemniscus columns
  2. Spinothalmic tract
  3. Spinocerebellar tract
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85
Q

Dorsal/medial lemniscus column consists of what and carries what sensations?

A

Fasciculus cuneatus and gracilis
Ascend to medulla and decussate to become the medial lemniscus –> thalamus –> somatosensory cortex
Proprioception, vibration and fine touch

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86
Q

What does the fasciculus cuneatus carry?

A

It is lateral and carries information from the UPPER body to the cuneate tubercle in the medulla

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87
Q

What does the fasciculus gracilis carry?

A

It is medial and carried information from the LOWER body to the gracile tubercle in the medulla

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88
Q

Describe the spinothalamic tract

A

Lateral = pain and temperature
Medial/anterior = Crude touch
Ascend on same side then decussate before ascending to thalamus

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89
Q

Describe the spinocerebellar tract

A 
Posterior = carries proprioception to ipsilateral inferior cerebellar peduncle 
Anterior = carries proprioception to the contralateral superior cerebellar peduncle
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90
Q

Describe Brown Sequard Syndrome

A

Hemi-section of the spinal cord

  • Ipsilateral weakness below the lesions due to damage to the ipsilateral descending motor corticspinal tract (decussated at the medulla)
  • Ipsilateral loss of vibrations and proprioceptive sensation due to damage to dorsal column
  • Contralateral loss of pain and temperature below the lesion due to spinothalamic damage (decussate within spinal cord)
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91
Q

What is the basal ganglia?

A

Group of nuclei lying deep within the cerebral hemispheres

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92
Q

What are the main functions of the basal ganglia?

A

Purposeful behaviour and movement
Inhibits unwanted movements
Controls posture and movement
Facilitation, integration and fine tuning of movements

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93
Q

What are the 3 coverings of the spinal cord form outermost to innermost?

A
  1. Dura
  2. Subarachnoid
  3. Pia
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94
Q

What are the 2 enlargements of the spinal cord?

A

Cervical (C3-T1) = uper limbs

Lumbar (L1-S3) = lower limbs

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95
Q

Describe the anatomy of the spinal cord after it ends at L1/2

A

Tapers into a cone (conus medullaris) and ends in a strand of tissue called filum terminale

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96
Q

What information does the lateral spinothalamic tract carry?

A

Pain and temperature

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97
Q

What does the medial spinothalamic tract carry?

A

Crude touch

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98
Q

What is the somatic motor function of the facial nerve?

A

Muscle of facial expression

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99
Q

What is the visceral motor function of the facial nerve?

A

Lacrimal glands

Submandibular and sublingual glands

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100
Q

What are the functions of the facial nerve?

A 
Motor to facial movements 
Salivation (submandibular and sublingual)
Lacrimination
Sensation from external ear 
Taste from anterior 2/3 of tongue
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101
Q

What are the 2 motor functions of the glossopharyngeal nerve?

A

Elevate the pharynx by supplying the stylopharyngeus

Secretion of the parotid gland (parasympathetic)

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102
Q

What are the sensory functions of the glossopharyngeal nerve?

A 
Sensation to external ear 
Posterior 1/3 of tongue 
Pharynx
Eustachian tube 
Carotid sinus, baro and chemoreceptors
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103
Q

What are the functions of the vagus nerve?

A

Taste - posterior pharynx
Swallowing - muscle of pharynx and larynx except stylopharyngeus
CV and GI regulation (parasympathetic)

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104
Q

What does the accessory nerve supply?

A

Sternocleidomastoid

Trapezius

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105
Q

What does the hypoglossal nerve supply?

A

Intrinsic and extrinsic muscles of the tongue

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106
Q

What is the sensory and taste innervation of the posterior 1/3 of the tongue?

A

Glossopharyngeal nerve

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107
Q

What is the sensory sensation of the anterior 2/3 tongue?

A

Lingual branch of the V3 from trigeminal (mandibular branch)

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108
Q

What is the taste sensation for the anterior 2/3 of tongue?

A

Chorda tympani branch of the facial nerve carried by lingual branch

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109
Q

What passes through the cavernous sinus?

A 
O TOM CAT:
Oculomotor (CN III)
Trigeminal (CN V)
Ophthalmic trigeminal (CN Va)
Maxillary trigeminal (CN Vb)
Carotid (internal) 
Abducens (CN VI)
Trochlear (CN IV)
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110
Q

Damage to Broca’s area results in what sort of aphasia?

A

Expressive aphasia

Understand what is being said and know what they want to say but can’t express it in meaningful words

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111
Q

Damage to Wernicke’s area results in what sort of aphasia?

A

Comprehension aphasia
Difficulty understanding written or spoken language but hearing and vision not impaired
Have fluent speech but may scramble words

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112
Q

What is the most common artery for a berry aneurysm to occur?

A

Anterior cerebral artery

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113
Q

What are the functions of the ophthalmic division of the trigeminal nerve?

A

Sensation to the anterior head and face (superior 1/3) including scalp, forehead, cornea and tip of nose

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114
Q

What are the functions of the maxillary division fo the trigeminal nerve?

A

Sensation to middle 1/3 of face including cheek, nose, upper lip, upper teeth and palate

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115
Q

What are the functions of the mandibular division of the trigeminal nerve?

A

Sensation to inferior 1/3 of face including lower lip, lower teeth, chin, jaw and anterior 2/3 of tongue
Motor to muscles of mastication and tensor tympani muscle

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116
Q

What is cerebellar syndrome?

A

Ataxia = loss of full control of body movements
Nystagmus = rapid eye movements
Deficit on IPSILATERAL side as cerebellar lesion

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117
Q

What is the criteria for brainstem death?

A 
Pupils 
Corneal reflex 
Caloric vestibular reflex 
Cough reflex 
Gag reflex 
Respirations 
Response to pain
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118
Q

Name 3 types of primary headache

A

No underlying cause

  1. Migraine
  2. Tension headache
  3. Cluster headache
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119
Q

Name 2 types of secondary headache

A

Underlying cause

  1. Meningitis
  2. Subarachnoid haemorrhage
  3. Giant cell arteritis
  4. Idiopathic intracranial hypertension
  5. Medication overuse headache
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120
Q

Give an example of a tertiary headache

A

Trigeminal neuralgia

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121
Q

Give 6 questions that are important to ask when taking a history of headache

A
  1. Time = onset, duration, frequency, pattern
  2. Pain = severity, quality, site, spread
  3. Associated symptoms - n/v, photophobia, phonophobia
  4. Triggers/aggravating/relieving factors
  5. Response to attack = is medication useful?
  6. What are the symptoms like between attacks?
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122
Q

Give 5 red flags for suspected brain tumour in a patient presenting with a headache

A
  1. New onset headache and history of cancer
  2. Cluster headache
  3. Seizure
  4. Significantly altered consciousness, memory, confusion
  5. Papilloedema
  6. Other abnormal neurological exam
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123
Q

How long do migraine attacks tend to last for?

A

Between 4-72 hours

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124
Q

Briefly describe the pathophysiology of migraines

A

Cerebrovascular contstriction –> aura, dilation –> headache
Spreading of cortical depression
Activation of CN V nerve terminals in meninges and cerebral vessels

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125
Q

Name 3 triggers of migraines

A
  1. Chocolate
  2. Cheese
  3. Excessive/not enough sleep
  4. Hangovers
  5. Orgasms
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126
Q

Describe the pain of a migraine

A

A symptoms:

  1. Unilateral
  2. Throbbing
  3. Moderate/severe pain
  4. Aggravated by physical activity
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127
Q

What other symptoms may a patient with a migraine experience other than pain?

A

B symptoms:

  1. Nausea
  2. Photophobia
  3. Phonophobia
  4. Aura
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128
Q

What is a prodrome?

A

Precedes migraine by hours-days

  • yawning
  • food cravings
  • changes in sleep, appetite or mood
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129
Q

What would a patient experiencing a migraine with aura complain of?

A

Visual = fortification spectra (zig-zags), hemianopia, scotoma
Paraesthesia
Dysphagia
Ataxia

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130
Q

Name 3 differential diagnoses for a migraine

A
  1. Other headache type
  2. Hypertension
  3. TIA
  4. Meningitis
  5. Subarachnoid haemorrhage
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131
Q

What is the diagnostic criteria for a migraine?

A

4-72 hour attack +
2 A symptoms (unilateral, throbbing, moderate/severe pain, aggravated by physical activity) +
1 B symptom (nausea, photophobia, phonophobia)
With or without aura

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132
Q

How can migraines be subdivided?

A
  1. Episodic with (20%)/without (80%) aura

2. Chronic migraine

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133
Q

Describe the treatment for migraines

A
  1. Lifestyle modification and trigger management
  2. Psychological and behavioural treatment
  3. Preventative treatment = propranolol (BB)/topiramate, amitriptyline, acupuncture
  4. Oral triptan + NSAID/paracetamol
  5. Botox
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134
Q

How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

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135
Q

How long do tension headaches usually last for?

A

From 30 minutes to 7 days

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136
Q

Describe the pain of a tension headache?

A

Bilateral
Pressing/tight band like pain
Mild to moderate pain
Not aggravated by physical activity

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137
Q

Would a patient with a tension headache experience any other symptoms other than pain?

A

NO

Nausea, photophobia and photophobia would NOT be associated

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138
Q

How do you treat a tension headache?

A

Regular exercise and stress relief

Symptomatic treatment = aspirin, paracetamol, NSAIDs, tricyclic antidepressant (amitriptyline)

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139
Q

Describe the pain of a cluster headache

A
  1. UNILATERAL
  2. Rapid onset severe orbital pain
  3. Severe/very severe pain
  4. Accompanied by lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis +/- ptosis
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140
Q

How can cluster headaches be subdivided?

A 
Episodic = >2 cluster periods lasting 7 days - 1 year separated by pain free periods lasting >1 month 
Chronic = attack occur for >1 year without remission or remission lasting <1 month
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141
Q

How long do cluster headaches tend to last?

A

Between 15 minutes and 3 hours

Mostly nocturnal

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142
Q

How do you treat cluster headaches?

A 
Attack = 100% oxygen, sumatriptan (selective serotonin (5HT) agonist) 
Prevention = avoid triggers, short term corticosteroids (prednisolone), verapamil, lithium
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143
Q

What is the most common type of secondary headache?

A

Medication overuse headache - episodic headache becomes daily chronic headache

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144
Q

What types of medications can cause drug overuse headaches?

A

Opioids, mixed analgesics, ergotamine, triptans

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145
Q

What is the diagnostic criteria for a medication overuse headache?

A
  1. Headache present for >15 days/month
  2. Regular use for >3 months of >1 symptomatic treatment drugs
  3. Headache has developed or markedly worsened during drug use
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146
Q

Describe the pain of trigeminal neuralgia

A
  1. Unilateral face pain
  2. Severe intensity
  3. Electric shock like, shooting, stabbing or sharp
  4. No radiation beyond the trigeminal distribution
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147
Q

Describe the epidemiology of trigeminal neuralgia

A

Peak age = 50-60 years

Women > men

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148
Q

Give 3 causes of trigeminal neuralgia

A
  1. Compression of tirgeminal nerve by a loop of vein or artery
  2. Aneurysms
  3. Meningeal inflammation
  4. Tumours
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149
Q

How long does the pain associated with trigeminal neuralgia usually last for?

A

A few seconds

Maximum 2 minutes

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150
Q

What is the treatment for trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin
Surgery = microvascular decompression

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151
Q

What features might be present in the hostly of a headache that make you suspect meningitis?

A
  1. Pyrexia
  2. Photophobia
  3. Neck stiffness
  4. Non-blanching purpura rash
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152
Q

Name 3 symptoms of giant cell arteritis

A
  1. Unilateral temple/scalp pain and tenderness
  2. Jaw claudication
  3. Visual symptoms - amaurosis fugax
  4. Associated with PMR
  5. Raised ESR and CRP
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153
Q

What is the treatment for giant cell arteritis?

A

High dose Prednisolone, guided by ESR and symptoms

PPI and bisphosphonate also given

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154
Q

At what level is a lumbar puncture done and why is an LP done?

A

L3/4 or L4/5

To obtain a CSF sample

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155
Q

What main regions of the brain does the anterior cerebral artery supply?

A

Motor cortex and top of brain

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156
Q

What main regions of the brain does the middle cerebral artery supply?

A

Majority of the outer surface of the brain

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157
Q

What main regions of the brain does the posterior cerebral artery supply?

A

Supplies peripheral vision

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158
Q

Where does the circle of willis lie?

A

In the subarachnoid space

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159
Q

Where do the meningeal vessels lie?

A

In the extradural space

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160
Q

What does a small response on an nerve conduction study suggest?

A

There is axon loss

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161
Q

What does a slow response on an nerve conduction study suggest?

A

There is myelin loss

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162
Q

What are the main arteries that come off the aortic arch?

A
  1. Brachiocepahlic trunk
    a) right common carotid artery
    b) right subclavian artery
  2. Left common carotid artery
  3. Lef subclavian artery
  4. Left vertebral artery (<1%)
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163
Q

At what level does the common carotid artery bifurcate?

A

C3/4 into the internal and external carotid artery

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164
Q

What 2 arteries does the internal carotid artery terminate in to?

A

Middle cerebral artery and anterior cerebral artery

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165
Q

Name the 4 segments of the internal carotid artery

A
  1. Cervical
  2. Petrous
  3. Cavernous
  4. Supraclinoid (intramural)
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166
Q

What branches does the supraclinoid segment of the internal carotid artery have?

A
  1. Ophthalmic artery
  2. Superior hypophyseal arteries/trunk
  3. Posterior communicating artery
  4. Anterior choroidal artery
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167
Q

Where do the vertebral arteries arise from?

A

Subclavian arteries

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168
Q

Give an example of a branch of the extracranial vertebral arteries

A 
Neck muscles
Spinal meninges (cervical spine)
Spinal cord (cervical cord)
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169
Q

Give an example of a branch of the intracranial vertebral arteries

A

Anterior spinal artery
Small medullary perforators
Posterior inferior cerebellar artery (PICA)

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170
Q

What areas of the brain does the posterior inferior cerebellar artery supply?

A

Medulla and inferior cerebellum

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171
Q

What forms the basilar artery?

A

The vertebral arteries unite to form the basilar artery

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172
Q

What are the branches of the basilar artery?

A
  1. Multiple perforating arteries to brainstem - pontine arteries
  2. Bilateral anterior inferior cerebellar arteries (supply cerebellum, CN VII and CN VIII)
  3. Bilateral superior cerebellar arteries
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173
Q

What are the terminal branches of the basilar artery?

A

Posterior cerebral arteries arise from terminal bifurcation of the basilar artery

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174
Q

Define encephalopathy

A

Reduced level of consciousness/diffuse disease of brain substance

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175
Q

Define neuropathy

A

Damage to one or more peripheral nerve, usually causing weakness and/or numbness

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176
Q

Define myelitis

A

Inflammation of the spinal cord

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177
Q

Define meningitis

A

Infection and inflammation of the meninges

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178
Q

Name 3 bacterial organisms that cause meningitis in adults

A
  1. N. meningitidis
  2. S. pneumoniae
  3. H. influenzae
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179
Q

Name 2 bacterial organisms that cause meningitis in neonates

A
  1. E.coli

2. Group B strep

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180
Q

Name 3 viruses that can cause meningitis

A
  1. Enterovirus (most common viral)
  2. HSV
  3. CMV
  4. Varicella zoster virus
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181
Q

Name 2 organisms that can cause meningitis in immunocompromised patients

A
  1. Listeria monocytogenes
  2. Cryptococcus
  3. TB
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182
Q

Give the main triad of symptoms of meningitis

A

Headache + neck stiffness + fever

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183
Q

Give 5 symptoms of meningitis

A
  1. Neck stiffness
  2. Photophobia
  3. Papilloedema (due to increased ICP)
  4. Petechial non-blanching rash
  5. Headache
  6. Fever
  7. Decreased GCS
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184
Q

Give 2 signs of meningitis

A

Kernig’s sign = unable to straighten left treated than 135 degrees without pain
Brudzinski’s sign = severe neck stiffness cause hip and knees to flex when neck is flexed

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185
Q

How would you describe the rash associated with meningococcal sepsis?

A

Petechial non-blanching rash

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186
Q

What investigations might you do in someone you suspect has meningitis?

A
  1. Blood cultures (pre LP)
  2. Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
  3. Lumbar puncture
  4. CT head
  5. Throat swabs - bacterial and viral
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187
Q

What is the treatment of bacterial meningitis?

A

Cefotaxime
+ amoxicillin
+ dexamethasone

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188
Q

What is the treatment of viral meningitis?

A

Watch and wait

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189
Q

What is the treatment for meningococcal septicaemia?

A

Immediate IV cefotaxime or IV benzylpenicillin

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190
Q

What can be given as prophylaxis against meningitis?

A

Ciprofloxacin

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191
Q

For which bacteria is meningitis prophylaxis effective against?

A

N. meningitidis

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192
Q

When is a child vaccinated against Meningitis B?

A

At 8 weeks, 16 weeks and a booster at 1 year

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193
Q

When is a child vaccinated against Meningitis C?

A

At 1 year

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194
Q

When is a child vaccinated against Meningitis ACWY?

A

At age 14

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195
Q

Give 4 potential adverse effect of a lumbar puncture

A
  1. Headache
  2. Paraesthesia
  3. CSF leak
  4. Damage to spinal cord
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196
Q

What investigations would you do on a CSF sample?

A

Protein and glucose levels
MCS
Bacterial and viral PCR

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197
Q

When would you do a CT before an LP?

A 
>60
Immunocompromised
History of CNS disease
New onset/recent seizures
Decreased GCS
Focal neurological signs 
Papilloedema
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198
Q

What is the colour of the CSF in someone with a bacterial infection?

A

Cloudy (normally it is clear)

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199
Q

Give 4 reasons why a LP might be contraindicated

A
  1. Thrombocytopenia
  2. Delay in Abx admin
  3. Signs of raised ICP
  4. Unstable cardio or resp systems
  5. Coagulation disorder
  6. Infections at LP site
  7. Focal neurological signs
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200
Q

Define encephalitis

A

Infection and inflammation of the brain parenchyma

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201
Q

In what group of people is encephalitis common?

A

Immunocompromised

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202
Q

What area of the brain does encephalitis mainly affect?

A

Frontal and temporal lobes

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203
Q

Give 4 viral causes of encephalitis

A
  1. HSV (most common)
  2. CMV
  3. EBV
  4. VZV
  5. HIV
  6. MMR
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204
Q

Name 2 non-viral causes of encephalitis

A
  1. Bacterial meningitis
  2. TB
  3. Malaria
  4. Lyme’s disease
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205
Q

Name the main triad of symptoms of encephalitis

A

Fever + headache + altered mental state

206
Q

Give 5 signs and symptoms of encephalitis

A
  1. Headache
  2. Fever
  3. Lethargy
  4. Change in behaviour
  5. Seizures
  6. Focal neurological signs - hemiparesis, dysphagia
  7. Decreased GCS
  8. Travel or animal history
207
Q

What would the LP show from someone with encephalitis?

A

Lymphocytosis
Raised protein
Normal glucose

208
Q

What investigations might you do on someone with encephalitis?

A

Bloods - culture, serum viral PCR, malaria film
Contrast CT head
LP
EEG

209
Q

What is the treatment for encephalitis?

A

Acyclovir

Primidone = anti-seizure medication if needed

210
Q

Briefly describe the pathophysiology of rabies

A

RNA virus, transmitted by saliva in mammals
Spreads to CNS via peripheral nerves
Prevented by a vaccine

211
Q

Give 3 symptoms of rabies

A
  1. Fever
  2. Anxiety
  3. Confusion
  4. Hydrophobia
  5. Hyperactivity
  6. Hallucinations
212
Q

Name the organism responsible for causing tetanus

A

Clostridium tetani

It infects via dirty wounds

213
Q

Give 3 symptoms of tetnaus

A
  1. Trismus (lockjaw)
  2. Sustained muscle contraction
  3. Facial muscle involvement
214
Q

How does herpes zoster occur?

A

Reactivation of varicella zoster virus

215
Q

Give 4 symptoms of herpes zoster

A
  1. Pain and paraesthesia in dermatomal distribution priced rash for days
  2. Malaise
  3. Myalgia
  4. Headache and fever
216
Q

Describe the rash associated with herpes zoster

A

Papules and vesicles

  • neuritis pain
  • crust formation and drying occurs
  • infectious until lesions are dried
217
Q

Describe the treatment for herpes zoster

A

Antiviral therapy within 72 hours of rash onset - acyclovir, valavivlovir, famciclovir
Analgesia

218
Q

Briefly describe the pathophysiology of herpes zoster

A

Latent virus is reactivated in dorsal root ganglia –> travels down affected nerve via sensory root in dermatomal distribution –> perineural and intramural inflammation

219
Q

What dermatome is herpes zoster most likely to affect?

A

Thoracic nerves

Then ophthalmic division of trigeminal

220
Q

Give 2 complications of herpes zoster

A
  1. Ophthalmic branch of trigmeinal = damages sight

2. Post herpetic neuralgia - pain lasts >4 months after

221
Q

What is MS?

A

A chronic autoimmune inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in space and time

222
Q

Briefly describe the pathophysiology of MS

A

AI inflammation –> CD4 mediated destruction of oligodendrocytes –> demyelination of CNS neurones –> myelination with short thin nodes or neuronal death

223
Q

What is MS characterised by?

A

Disseminated in space and time
Hypercellular plaque formation
BBB disruption

224
Q

Name 2 types of MS

A
  1. Relapsing remitting (80%) = random attacks –> disabilities accumulate, between attacks no disease progression
  2. Chronic progressive = steady neurological decline
225
Q

Describe the aetiology of MS

A

Unknown

Environment and genetic components

226
Q

Describe the epidemiology of MS

A

Presenting between 20-40 y/o
Females > Males
More common in white populations

227
Q

Give 3 eye signs associated with MS

A
  1. Optic neuritis - impaired vision and movement pain
  2. Nystagmus
  3. Double vision
228
Q

Give 5 signs of MS other than problems with the eyes

A
  1. Spastic weakness
  2. Paraesthesia
  3. Lhermitte’s sign (electric spine)
  4. Bladder, GI and sexual dysfunction
  5. Fatigue
  6. Vertigo
  7. Cognitive problems and depression
229
Q

What can exacerbate the symptoms of MS?

A

Heat (e.g. a warm shower)

230
Q

Name 3 differential diagnosis’s of MS

A
  1. SLE
  2. Sjogren’s
  3. AIDS
  4. Syphilis
231
Q

What investigations might you do in someone to see if they have MS?

A 
MRI = plague detection 
LP = oligoclonal IgG bands = CNS inflammation
Electrophysiology = delayed nerve conduction suggests demyelination
232
Q

What is the diagnostic criteria for MS?

A

> 2 CNS lesions disseminated in time and space (>2 attack affected different parts of the CNS)

233
Q

Describe the non-pharmacological treatment for MS

A

Regular exercise, smoking and alcohol cessation, low stress lifestyle
Psychological therapies
Speech therapists
Physio and OR

234
Q

Describe the pharmacological treatment for MS

A
  1. Disease modifying drugs - dimethyl fumarate
  2. Biologics - natalizumab
  3. Beta interferon s/c
235
Q

What symptomatic treatments can you give to those with MS?

A 
Spasticity = baclofen 
Depression = SSRI (citalopram)
Fatigue = modafinial
Pain = amitryptilline, gabapentin
236
Q

What medication might you give to someone to reduce the relapse severity of MS?

A

Short course steroids - methylprednisolone

237
Q

Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

238
Q

Define epileptic seizure

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excess, hypersynchronous neuronal discharge in the brain

239
Q

Give 5 causes of epilepsy

A
  1. Idiopathic
  2. Old head injury
  3. Stroke
  4. Tumour
  5. Alcohol withdrawal
  6. CNS infection
  7. Flashing lights
240
Q

What 2 categories can epileptic seizures be broadly divided into?

A
  1. Focal epilepsy - only one portion of the brain is involved
  2. Generalised epilepsy - whole brain is affected
241
Q

Give 2 examples of focal epileptic seizures

A
  1. Simple partial seizures

2. Complex partial seizures

242
Q

Give 3 examples of generalised epileptic seizures

A
  1. Absence seizures (petit mal)
  2. Tonic-clonic seizure (grand mal)
  3. Myoclonic seizure
  4. Atonic seizure
243
Q

Give 3 major characteristics of an epileptic seizure

A

30-120 seconds long
Positive ictal symptoms
Post ictal symptoms

244
Q

Describe a generalised tonic clonic seizure

A

Sudden onset rigid tonic phase followed by a convulsive clonic phase
LOC, tongue biting, urine incontinence and drowsiness/coma also associated

245
Q

Give 2 features of absence seizures

A
  1. Commonly present in childhood

2. Ceases activity and stares for few seconds

246
Q

Describe a myoclonic seizure

A

Sudden jerk of limb, face or trunk

Often fall backwards

247
Q

Describe a atonic seizure

A

Sudden loss of muscle tone –> fall forwards

248
Q

What is aura?

A

A sensation perceived which precedes a condition affecting the brain

249
Q

If a patient experienced epilepsy with aura, what other symptoms would they get?

A

Strange feeling in gut
Deja vu
Strange smells
Flashing lights

250
Q

Name 3 post-ictal symptoms

A
  1. Headache
  2. Confusion
  3. Myalgia
  4. Temporary weakness (focal seizure)
251
Q

What is the diagnostic criteria for epilepsy?

A

At least 2 or more unprovoked seizures occurring >24 hours apart

252
Q

What is the treatment for focal epileptic seizures?

A 
Lamotrigine = 1st line
Carbamazepine = 2nd line
253
Q

How do lamotrigine and Carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

254
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valproate = 1st line

Lamotrigine = 2nd line

255
Q

How does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

256
Q

What medication can control seizures?

A

Diazepam or lorazepam

257
Q

What possible surgery could you do to treat epilepsy?

A

Vagal nerve stimulation

Resection of affected area

258
Q

Give 4 potential side effects of anti-epileptic drugs (AED’s)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
259
Q

Give 4 differential diagnosis’s of epilepsy

A
  1. Syncope
  2. Non-epileptic seizure
  3. Migraine
  4. Hyperventilation
  5. TIA
260
Q

Define syncope

A

Insufficient blood or oxygen supply to the brains causes paroxysmal changes in behaviour, sensation and cognitive processes
Caused by sitting/standing
5-30 seconds duration

261
Q

Define non-epileptic seizure

A

Mental processes associated with psychological distress causes paroxysmal changes in behaviour, sensation and cognitive processes
1-20 minute duration
Closed eyes and mouth

262
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?

A

A non-epileptic seizure

263
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

An epileptic seizure

264
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

This is likely to be due to a blood circulation problem e.g. syncope

265
Q

What can be the affect of a non-missile trauma to the scalp?

A

Contusions and lacerations

266
Q

What can be the affect of a non-missile trauma to the skull?

267
Q

Give 2 risk associated with a skull fracture

A
  1. Haematoma

2. Infection

268
Q

What can be the affect of a non-missile trauma to the meninges?

A

Haemorrhage and infection (due to skull fracture)

269
Q

What can be the affect of a non-missile trauma to the brain?

A

Contusions
Lacerations
Haemorrhage
Infection

270
Q

Describe the pathophysiology of a diffuse traumatic axonal injury

A

Acceleration/deceleration –> shearing rotational forces –> axons tear

271
Q

Give a sign of diffuse vascular injury due to non-missile trauma

A

Multiple petechial haemorrhages throughout the brain

272
Q

What is more severe: diffuse traumatic axonal injury to diffuse vascular injury?

A

Diffuse vascular injury - usually results in near immediate death

273
Q

Describe the mechanism behind acceleration/deceleration damage

A

A force to the head can cause differential brain movements –> shearing, traction and compressive stresses –> risk of axon tear and blood vessel damage

274
Q

What is a contusion?

A

Superficial ‘bruises’ of the brain

275
Q

What is a laceration?

A

When a contusion is severe enough to tear the Pia mater

276
Q

What is the cause of chronic traumatic encephalopathy?

A

Often seen 8-10 years after repetitive mild traumatic brain injury

277
Q

Give 3 initial symptoms of chronic traumatic encephalopathy

A
  1. Irritability
  2. Impulsivity
  3. Aggression
  4. Depression
278
Q

Give 3 later symptoms of chronic traumatic encephalopathy

A
  1. Dementia
  2. Gait and speech problems
  3. Parkinsonism
279
Q

Give 3 signs of chronic traumatic encephalopathy

A
  1. Atrophy of deep brain structures
  2. Enlarges ventricles
  3. Tau neurofibrillary tangles deposited in sulci
280
Q

Give 3 types of missile head injuries

A
  1. Depressed = don’t penetrate skull
  2. Penetrating
  3. Perforating = missile enters and exits the skull, passing through the brain
281
Q

Name 3 intra-cranial haemorrhages

A
  1. Sub-arachnoid haemorrhage
  2. Sub-dural haemorrhage
  3. Extra-dural haemorrhage
282
Q

What can cause a subarachnoid haemorrhage?

A
  1. Rupture of berry aneurysm (80%)
  2. Atriovenous malformation (10%)
  3. Trauma
283
Q

Give 3 risk factors for a subarachnoid haemorrhage

A
  1. Previous berry aneurysm
  2. Smoking
  3. Alcohol
  4. Hypertension
  5. Family history
284
Q

Briefly describe the pathophysiology of a subarachnoid haemorrhage

A

Ruptured aneurysm –> tissue ischaemia and rapid raised ICP –> pressure on the brain

285
Q

Name 3 symptoms of a subarachnoid haemorrhage

A
  1. Sudden onset ‘thunderclap’ headache
  2. Neck stiffness
  3. Vomiting
  4. Photophobia
  5. Drowsiness –> coma
286
Q

Name 3 signs of a subarachnoid haemorrhage

A
  1. Kernig’s sign (can’t straighten leg past 135 degrees)
  2. Reduced GCS
  3. Papilloedema
287
Q

What investigations might you do to see if someone has a subarachnoid haemorrhage?

A
  1. Head CT = star pattern (diagnositic)

2. LP = bloody or xanthochromic

288
Q

Describe the treatment for a subarachnoid haemorrhage

A
  • Hydration, bed rest and BP control and frequent neurological obs
  • Nimodipine (CCB) = reduced vasospasm
  • CT angiography for aneurysm identification – coiling/clipping
289
Q

Give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
290
Q

What can cause a subdural haemorrhage?

A

Head injury –> vein rupture

291
Q

Describe the pathophysiology of a subdural haemorrhage

A

Rupture of bridging veins between hemispheres and sagittal sinus
Accumulating haematoma –> raised ICP –> tentorial herniation/coning

292
Q

What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?

A

Clot starts to break down and there is massive increase in oncotic pressure –> water is sucked up by osmosis into the haematoma

293
Q

Give 3 risk factors of a subdural haemorrhage

A
  1. Elderly - brain atrophy
  2. Frequent falls - epileptics, alcoholics
  3. Anticoagulants
294
Q

Give 4 signs and symptoms of a subdural haemorrhage

A
  1. Fluctuating GCS
  2. Headache
  3. Confusion
  4. Drowsiness
  5. Raised ICP –> seizures
295
Q

Name 3 differential diagnosis’s of a subdural haemorrhage

A
  1. Stroke
  2. Dementia
  3. CNS masses (tumour vs abscess)
296
Q

What would you see on a CT or MRI of a subdural haemorrhage?

A

Unilateral crescent shaped blood collection
Blood clot
Midline shift

297
Q

What is the treatment for a subdural haemorrhage?

A

Surgical evacuation of the clot
Treat cause
Mannitol = decreases ICP

298
Q

What can cause an extradural haemorrhage?

A

Traumatic head injury resulting in a skull fracture (often temporal bone) –> middle meningeal artery rupture –> bleed

299
Q

Describe the disease pattern of a extradural haemorrhage

A

Head injury –> unconscious –> lucid interval –> worse symptoms
Occurring over hours

300
Q

Give 4 symptoms of an extradural haemorrhage

A
  1. Reduced GCS
  2. Severe headache
  3. Confusion
  4. Seizures
  5. Hemiparesis
  6. Ipsilateral pupil dilation
  7. Coma
301
Q

What investigations might you do to see if someone has an extradural haemorrhage?

A

CT = lens shaped haematoma

LP is CONTRAINDICATED

302
Q

What do the ventricles do to prolong survival in someone with an extradural haemorrhage?

A

Get rid of CSF to prevent rise in ICP

303
Q

What is the treatment for an extradural haemorrhage?

A

Immediate clot evacuation

Mannitol to decrease ICP

304
Q

Give 3 differences in the presentation of a patient with a subdural haemorrhage in comparison to an extradural haemorrhage

A
  1. Time frame: extra-dural symptoms are more acute
  2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma
  3. CT: extra-dural haematoma will have a lens appearance whereas subdural will have a crescent shaped haematoma
305
Q

Define weakness

A

Impaired ability to move a body part in response to will

306
Q

Define paralysis

A

Ability to move a body part in response to will is completely lost

307
Q

Define ataxia

A

Willed movements are clumsy, ill-direction or uncontrolled

308
Q

Define involuntary movements

A

Spontaneous movement independent of will

309
Q

Define apraxia

A

Disorder of conscious organised pattern of movement or impaired ability to recall acquired motor skills

310
Q

Give 3 things that modulate LMN action potential transmission to effectors

A
  1. Cerebellum
  2. Basal ganglia
  3. Sensory feedback
311
Q

What is a Lower motor neurone?

A

A neurone that carries signals to effectors

Cell body is located in the brainstem (CN nuclei) or spinal cord

312
Q

Give 5 potential sites of damage along the ‘final common pathway’

A
  1. Cranial nerve nuclei
  2. Motor neurones
  3. Spinal ventral roots
  4. Peripheral nerves
  5. NMJ
  6. Muscles
313
Q

Give 3 disease that are associated with motor neurone damage

A
  1. Motor neurone disease
  2. Spinal atrophy
  3. Poliomyelitis
  4. Spinal cord compression
314
Q

Give 3 pathologies that are associated with ventral spinal root damage

A
  1. Prolapsed intervertebral disc
  2. Tumours
  3. Cervical or lumbar spondylosis
315
Q

Name a disease associated with NMJ damage

A

Myasthenia Gravis

316
Q

What are muscle spindles innervated by?

A

Gamma motor neurones

innervate the stretch receptors in muscle spindles

317
Q

What is the function of muscle spindles?

A

Control muscle tone and tell you how much a muscle is stretched

318
Q

Describe the pyramidal pattern of weakness in the upper limbs

A

Flexors are stronger than extensors

319
Q

Describe the pyramidal pattern of weakness in the lower limbs

A

Extensors are stronger than flexors

320
Q

What is a UMN?

A

A neurone that is located entirely in the CNS

Its cell body is located in the primary motor cortex

321
Q

Give 3 causes of UMN weakness

A
  1. MS
  2. Brain tumour
  3. Stroke
  4. MND
322
Q

Give 4 sites of UMN damage

A
  1. Motor cortex lesions
  2. Internal capsule
  3. Brainstem
  4. Spinal cord
323
Q

Give 4 signs of UMN weakness

A
  1. Spasticity
  2. Increased muscle tone (hypertonia)
  3. Hyper-reflexia
  4. Positive babinski’s reflex
324
Q

Give 4 signs of LMN weakness

A
  1. Flaccid
  2. Hypotonia
  3. Hypo-reflexia
  4. Muscle atrophy
  5. Fasciculation’s
325
Q

Define motor neurone disease

A

Cluster of major degenerative diseases characterised by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells

326
Q

Does MND affect UMN or LMN?

A

Both UMN and LMN are affected

327
Q

Does MND affect eye movements?

A

Never affects eye movements (cf of myasthenia gravis)

328
Q

Does MND cause sensory loss or sphincter disturbance?

A

No (cf of MS)

329
Q

Name 4 types of MND

A
  1. Amyotrophic lateral sclerosis (ALS) = motor cortex and anterior horns affected = LMN + UMN
  2. Progressive bulbar palsy = destruction of CN 9-12 = LMN
  3. Progressive muscular atrophy = anterior horn destruction = LMN
  4. Primary lateral sclerosis = betz cell loss in motor cortex = UMN
330
Q

What symptoms might present in someone with progressive bulbar palsy form of MND?

A

Dysarthria (slurred speech)
Dysphagia
Wasting and fasciculations of tongue

331
Q

What investigations might you do in someone you suspect to have MND?

A 
Head/spine MRI
Blood tests = muscle enzymes, autoantibodies 
Nerve conduction studies 
EMG
LP
332
Q

What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

333
Q

What is the treatment for MND?

A

Disease modifying drugs = riluzole - inhibits glutamates release (Na channel blocker) - slow down disease progression
Excess saliva = propantheline/amitriptyline
Anti-spasticity = baclofen
Dysphagia = NG/PEG feeding
Palliation

334
Q

Give 3 limb onset symptoms of MND

A
  1. Weakness
  2. Clumsiness
  3. Wasting of muscles
  4. Foot drop
  5. Tripping
335
Q

Give 3 respiratory onset symptoms of MND

A
  1. Dyspnoea
  2. Orthopnoea
  3. Poor sleep
336
Q

Would you do a LP in a patient that has a raised ICP?

A

NO

LP is contraindicated if they have a raised ICP due to the risk of coning

337
Q

Give 4 signs of raised ICP

A
  1. Papilloedema
  2. Focal neurological signs
  3. Loss of consciousness
  4. New onset seizures
338
Q

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol

339
Q

Explain the ICP/volume curve

A

Volume increase –> ICP plateau (compensate) –> rapid ICP increase

340
Q

What are the 3 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP –> headache, decrease GCS, n+v, papilloedema
  2. Progressive neurological deficit –> deficit of all major functions (motor, sensory, auditory, visual) + personality change
  3. Epilepsy
341
Q

You ask a patient with a brain tumour about any facts that aggravate their headache, what might they say?

A
  1. Worse first thing in the morning

2. Worse when coughing, straining or bending forward

342
Q

Name 2 differential diagnosis’s for a brain tumour

A
  1. Aneurysm
  2. Abscess
  3. Cyst
  4. Haemorrhage
  5. Idiopathic intracranial hypertension
343
Q

What investigations might you do in someone you suspect to have a brain tumour?

A

CT/MRI head and neck
Biopsy
LP = CONTRAINDICATED (high ICP)

344
Q

Where might secondary brain tumours arise from?

A
  1. LUNG
  2. Breast
  3. Melanoma
  4. Renal
  5. GI
  6. Thyroid
  7. Prostate
345
Q

Describe the treatment for secondary brain tumours

A
  1. Surgery and adjuvant radiotherapy
  2. Chemotherapy
  3. Supportive care
346
Q

From what cells to primary brain tumours originate?

A

Glial cells (gliomas)
- Astrocytoma (85-90%)
- Oligodendroglioma
Other primary = meningioma, schwannoma, medulloblastoma

347
Q

Describe the WHO glioma grading

A

Grade 1 = benign paediatric tumour
Grade 2 = Pre-malignant tumour (benign)
Grade 3 = ‘Anaplastic astrocytoma’ (cancer)
Grade 4 = Glioblastoma multiforme (GBM) - malignant

348
Q

Describe the epidemiology of grade 2 gliomas

A

Disease of young adults

349
Q

Give 3 causes of grade 2 glioma deterioration

A
  1. Tumour transformation to a malignant phenotype
  2. Progressive mass effect due to slow tumour growth
  3. Progressive neurological deficit form functional brain destruction by tumour
350
Q

Describe the common pathway to a GBM (grade 4 brain tumour)

A

Initial genetic error of glucose glycolysis –> Isocitrate Dehydrogenase 1 mutation –> excessive build up of 2-hydroxyglutarate –> genetic instability of glial cells –> grade II-IV glioma transform into glioblastoma

351
Q

Give 5 good prognostic factors for GBM

A
  1. <45 y/o
  2. Aggressive surgical therapy
  3. Good performance post-surgery
  4. Tumour that has transformed from previous lower grade tumour
  5. MGMT mutant - will respond will to chemo
352
Q

Describe the treatment for GBM

A
  1. Resective surgery
  2. Adjuvant chemotherapy with Temozolomide
  3. Dexamethasone - reduces tumour infalmamtion/oedema
  4. Palliative care
353
Q

How does Temozolomide work in treatment for GBM?

A

Methylates guanine in DNA making replication impossible

MGMT gene reverses it = tumour resistance

354
Q

Define dementia

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language
There is a progressive decline in cognitive function

355
Q

Describe the epidemiology of dementia

A

Rare <55
10% of people >65
20% of people >80

356
Q

Give 3 causes of dementia

A
  1. Alzheimer’s disease (50%)
  2. Vascular dementia (25%)
  3. Lewy body dementia (15%)
  4. Fronto-temporal (Pick’s)
  5. Huntington’s
  6. Liver failure
  7. Vitamin deficiency - B12 or folate
357
Q

Give 3 risk factors of dementia

A
  1. Family history
  2. Age
  3. Down’s syndrome
  4. Alcohol use, obesity, HTN, hyperlipidaemia, DM
  5. Depression
358
Q

Describe the pathophysiology of Alzheimer’s disease

A

Degeneration of temporal lobe and cerebral cortex, with cortical atrophy
Accumulation fo beta-amyloid peptide –> progressive neuronal damage, neurofibrillary tangles, increase in number of amyloid places and loss of ACh

359
Q

Give 4 symptoms of AD

A
  1. Short term memory loss
  2. Slow disintegration fo personality and intellect
  3. Language impairments - difficulty aiming and understand
  4. Apraxia
  5. Visuopatial impairments
  6. Agnosia
360
Q

Give 2 histological signs of AD

A
  1. Plagues of amyloid

2. Neuronal reduction

361
Q

25% of all patients with AD will develop what?

A

Parkinsons

362
Q

What does vascular dementia often present with?

A

Signs of vascular pathology = raised BP, past strokes and focal CNS signs
Stepwise deterioation

363
Q

Describe the pathophysiology of Lewy body dementia

A

Deposition of abnormal protein (levy bodies) within neurones of the occipito-parietal cortex

364
Q

Give 4 signs of Lewy body dementia

A
  1. Fluctuating cognition
  2. Prominent or persistent memory loss
  3. Impairment of attention, frontal, subcortical and visuospatial ability
  4. Depression and sleep disorders
  5. Visual hallucination
  6. Parkinsons
  7. Loss of inhibitions
365
Q

Frontal lobe atrophy is seen on an MRI, what kind of dementia is this patient likely to have?

A

Fronto-temporal

= frontal and temporal lobe atrophy

366
Q

Give 3 symptoms of Fronto-temporal dementia

A
  1. Behaviour variants - personality and behavioural change
  2. Language variants - progressive aphasia
  3. Lowers inhibitions and emotional unconcern
  4. Early memory preservation
  5. Association with MND
367
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in absence of an organic cause

368
Q

How could you determine whether someone has functional memory dysfunction or a degenerative disease?

A

When asked the question ‘when was the last time your memory let you down?’, someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer

369
Q

What investigations can you do in primary care to determine whether someone might have dementia?

A
  1. Good history of symptoms
  2. 6 item cognitive impairment test (6CIT)
  3. Blood tests - FBC, liver biochemistry, TFTs, vitamin B12 and folate
  4. Mini mental state examination = screening
370
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
  3. Give an address with 5 parts
  4. Count backwards from 20
  5. Say the months of the year in reverse
  6. Repeat the address
371
Q

What secondary care investigation can you do to investigate a dementia diagnosis?

A

Brain MRI - where and extent of atrophy
Brain function tests = PET, SPECT and functional MRI
Brain CT
Myeloid and tau histopathology

372
Q

Name the staging system that classifies the degree of pathology in AD

A

Braak staging
Stage 5/6 = high likelihood of AD
Stage 3/4 = intermediate likelihood
Stage 1/2 = low likelihood

373
Q

Give 3 ways in which dementia can be prevented

A
  1. Smoking cessation
  2. Healthy diet
  3. Regular exercise
  4. Low alcohol
  5. Engaging in leisure activités
374
Q

What support should be offered to patients with dementia?

A

Social suport
Cognitive support
Specialist memory service

375
Q

What medications might you use in someone with dementia?

A 
Acetylcholinesterase inhibitors - increase ACh = donepezil, rivastigmine
Control BP (ACEi) to reduce further vascular damage
376
Q

Define myasthenia gravis

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction

377
Q

Describe the pathophysiology behind myasthenia gravis

A

Autoantibodies (IgG) attach to ACh receptor and destroy them –> fewer action potentials fire –> muscle weakness and fatigue

378
Q

Describe the aetiology and associations of myasthenia gravis

A

If <50 = associated with other AI conditions (pernicious anaemia, SLE, RA) and more common in women
If >50 = associated with thymic atrophy or thymic tumour and more common in men

379
Q

Give 4 symptoms of myasthenia gravis

A
  1. Muscle weakness
  2. Increasing muscular fatigue
  3. Ptosis
  4. Diplopia
  5. Myasthenic snarl
  6. Tendon reflexes normal but fatigable
380
Q

What muscle groups are affected in myasthenia gravis?

A

Extra-ocular –> bulbar –> face –> neck –> trunk

381
Q

What can weakness due to myasthenia gravis be worsened by?

A 
Pregnancy
Hypokalaemia
Infection 
Emotion
Exercise 
Drugs (opiates, BB, gentamicin, tetracycline)
382
Q

What investigations might you do to see if someone has myasthenia gravis?

A
  • Serum anti-ACh receptors or muscle specific tyrosine kinase (muSK) antibodies
  • EMG and NCS = EMG detect MG
  • CT thymus
  • Tensilon test = IV edrophonium (short acting anti-cholinesterase) given –> muscle power increases within seconds
383
Q

Give 3 possible differential diagnosis’s for myasthenia gravis

A
  1. MS
  2. Hyperthyroidism
  3. Acute Guillain-Barre syndrome
  4. Lamert-Eaton myasthenia syndrome
384
Q

What is treatment for myasthenia gravis?

A

Anti-cholinesterase (more Ach in NMK) = pyridostigmine
Immunosuppression = prednisolone
Steroids can be combined with azathioprine or methotrexate
Thymectomy

385
Q

When is a thymectomy considered as a treatment for myasthenia gravis?

A

Onset <50 y/o and it is poorly controlled

386
Q

Give a complication of myasthenia gravis

A

Myasthenic crisis
Weakness of respiratory muscle during relapse
Treatment = plasmapheresis and IV immunoglobulin

387
Q

What is Lamert-Eaton myasthenia syndrome?

A

Paraneoplastic condition where there is defective ACh release at NMJ resulting in proximal limb weakness with some absent reflexes

388
Q

What is the function of the cerebellum?

A

Responsible for precise control, fine adjustment and coordination of morose activist based on continual sensory feedback

389
Q

What is the cerebellums output?

A

Purkinje cells only

390
Q

What does cerebellar dysfunction mean?

A

Cerebellar ataxia

391
Q

How can cerebellar ataxia be classified?

A
  1. Inherited
    a) autosomal recessive
    b) autosomal dominant
  2. Acquired
392
Q

Give an example of an AR inherited cerebellar ataxia

A

Friedrichs ataxia = motor and sensory problems, presenting in childhood

393
Q

Give an example of an AD inherited cerebellar ataxia

A

Spinocerebellar ataxia 6

Episodic ataxia

394
Q

Give 3 causes of acquired cerebellar ataxia

A
  1. Toxic - alcohol, lithium
  2. Idiopathic
  3. Neurodegenerative
  4. Immune mediated
395
Q

Give 2 examples of immune mediated cerebellar ataxia

A
  1. Post infection cerebellitus
  2. Gluten ataxia
  3. Paraneoplastic cerebellar degeneration
  4. Primary autoimmune cerebellar ataxia
396
Q

How can the severity of ataxia be classified?

A

Mild = mobilising independently or with 1 walking aid
Moderate = mobilising with 2 walking aids or walking frame
Severe = predominantly wheelchair dependent
Scale for the Assessment and Rating of Ataxia (SARA) can also be used - looks at gait, stance, sitting and speech

397
Q

Give 4 symptoms of cerebellar dysfunction

A
  1. Slurred speech
  2. Swallowing difficulties
  3. Clumsiness (arms and legs)
  4. Loss of precision of fine movement/motor skills
  5. Stumbles and falls
  6. Cognitive problems
398
Q

Give 4 signs of cerebellar dysfunction

A
  1. Nystagmus
  2. Action tremor
  3. Dysdiadochokinaesia - inability to perform rapid, alternating movements
  4. Truncal ataxia
  5. Limb ataxia
  6. Gait ataxia
399
Q

What investigations might you do in someone who is presenting with signs of cerebellar ataxia?

A

MRI = cerebellar atrophy and will exclude other causes (CV, tumour, hydrocephalus)

400
Q

Define Parkinson’s disease

A

Degenerative movement disorder caused by a reduction in dopamine in the pars compacta of the substantia nigra

401
Q

What is dopamine produced from?

A

Tyrosine –> L-dopa –> Dopamine

402
Q

Describe the pathophysiology of Parkinson’s disease

A

Death of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms
Lewy body formation in basal ganglia

403
Q

What is the 3 cardinal symptoms for Parkinsonism?

A

Tremor + Rigidity + Bradykinesia

404
Q

Describe the symptoms of Parkinson’s disease

A
  1. Resting tremor
  2. Rigidity - cogwheel
  3. Bradykinesia - slow movements and initiation, repetition = decreased amplitude, small steps/shuffling gait
  4. Constipation and urinary frequency
  5. Psychiatric issues (depression, anxiety, dementia)
405
Q

Would you describer the symptoms of Parkinson’s disease as symmetrical or asymmetrical?

A

Asymmetrical = One side is always worse than the other

406
Q

You ask a patient who you suspect to have Parkinson’s disease to walk up and down the corridor to assess their gait, what features would be suggestive of PD?

A

Stopped posture
Asymmetrical arm swing
Small steps
Shuffling

407
Q

Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra

2. Lewy bodies

408
Q

What investigations might you do in someone you suspect to have PD?

A

Functional neuroimaging - PET

Can confirm by reaction to levodopa

409
Q

Describe the pharmacological treatment for Parkinson’s disease

A 
Compensate for loss of dopamine 
- L-dopa (levodopa)
- Dopamine agonists 
- COMT inhibitors 
- MAO-B inhibitors 
Anticholinergics 
SSRIs (citalopram) for depression
410
Q

How does L-dopa work in the treatment of PD?

A

Precursor to dopamine and can cross the BBB (unlike dopamine)

411
Q

How do dopamine agonists work in the treatment of PD and give an example of one?

A

Reduced risk of dyskinesia
First line in patient <60
Ropinirole, pramipexole

412
Q

How do MAO-B inhibitors work in the treatment of PD and give an example of one?

A

Inhibit MAO-B enzymes which breakdown dopamine

Rasagiline, selegiline

413
Q

How do COMT inhibitors work in the treatment of PD and give an example of one?

A

Inhibit COMT enzymes which breakdown dopamine

Entacapone, tolcapone

414
Q

What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

415
Q

Describe an essential tremor

A

Action tremor, no rest tremor

416
Q

What is the treatment for an essential tremor?

A

Beta blockers
Primidone (anticonvulsant)
Gabapentin

417
Q

Define Huntington’s disease

A

Neurodegenerative disorder characterised by the lack of inhibitory neurotransmitter GABA

418
Q

Define chorea

A

Continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another

419
Q

Describe the inheritance pattern seen in Huntington’s disease

A

Autosomal dominant inheritance

420
Q

What triplet code is repeated in Huntington’s disease?

A

Cagoules triplet repeat
Adult onset = 36-55 repeats
Early onset = >60 repeats

421
Q

Briefly describe the pathophysiology of Huntington’s disease

A

Progressive cerebral atrophy with marked loss of neurones in caudate nucleus and putamen - specifically loss of corpus striatum GABA-nergic and cholinergic neurones
GABA = main inhibitory neurotransmitter –> decreased inhibition of dopamine release –> excessive thalamus stimulation –> excessive movements

422
Q

Name the 3 cardinal features of Huntington’s disease

A
  1. Chorea
  2. Dementia
  3. Psychiatric problems - personality change, depression, psychosis
423
Q

Name 3 other signs of Huntington’s disease

A
  1. Abnormal eye movements
  2. Dysarthria
  3. Dysphagia
  4. Rigidity
  5. Ataxia
424
Q

What investigations might you do in someone you suspect to have Huntington’s disease?

A

Genetic testing - CAG repeats (extensive counselling)

CT/MRI = caudate nucleus atrophy and increase size of frontal horns of lateral ventricles

425
Q

Describe the treatment of Huntington’s disease

A

Chorea
- Benzodiazepines
- Sulpiride (neuroleptic - depresses nerve function)
- Tetrabenazine - dopamine depleting agent
Depression = SSRIs (seroxate)
Psychosis = haloperidol
Agression = risperidone

426
Q

Define mononeuropathy

A

Lesions of individual peripheral or cranial nerves

427
Q

Define mononeuritis multiplex

A

2 or more individual nerves affected

428
Q

Give 3 causes of mononeuritis multiplex

A

WARDS PLC

  1. Wegner’s grnaulomatosis
  2. ADIS/amyloidosis
  3. RA
  4. DM
  5. Sarcoidosis
  6. Polyarteritis nodosa
  7. Leprosy
  8. Carcinoma
429
Q

What investigation can help you identify the site of a mononeuropathy lesion?

A

Electromyography (EMG)

430
Q

What nerve is affected in carpal tunnel syndrome?

A

The median nerve (C6-T1)

431
Q

Give 3 risk factors of carpal tunnel syndrome

A
  1. Pregnancy
  2. Obesity
  3. RA
  4. DM
  5. Hypothyroidism
  6. Acromegaly
432
Q

Describe the symptoms of carpal tunnel syndrome

A
  • Intermittent and gradual onset
  • Pain and paraesthesia = LLOAF muscles affected and thenar wasting
  • Sensory loss - radial 3.5 fingers and play
  • Worse at night, relieved by shaking
433
Q

What investigations might you do in someone who you suspect to have carpal tunnel syndrome?

A

EMG = slowing conduction velocity in median sensory nerves
Phalen’s test = 1 min maximal wrist flexion –> symptoms
Tinel’s test = tapping over nerve at wrist –> tingling

434
Q

What is the treatment for carpal tunnel syndrome?

A

Splinting
Local steroid injection
Decompression surgery

435
Q

Define polyneuropathy

A

Generalised disorders of peripheral and cranial nerves

436
Q

Describer the distribution of polyneuropathies

A

Symmetrical and widespread

Distal weakness and sensory loss

437
Q

How can polyneuropathies be classified?

A
  1. Time-course = Acute, chronic
  2. Function = motor, sensory, autonomic, mixed
  3. Pathology = demyelination, axonal degeneration, mixed
438
Q

Give 3 causes of sensory neuropathy

A
  1. DM
  2. CKD
  3. Alcohol
  4. Vasculitis
  5. Leprosy
439
Q

Give 3 signs of sensory neuropathy

A

Glove and stocking distribution of numbness and paraesthesia
Deep tendon reflexes may be decreased or absent
Signs of trauma - finger burns due to sensory loss

440
Q

Are large sensory fibres myelinated or unmyelinated and name the types of fibre?

A

Myelinated
A-alpha
A-beta

441
Q

Are small sensory fibres myelinated or unmyelinated and name the types of fibre?

A 
A-gamma = myelinated
C-fibres = unmyelinated
442
Q

What do A-alpha sensory fibres sense?

A

Proprioception

443
Q

What do A-beta sensory fibres sense?

A

Light touch, pressure and vibration

444
Q

What do A-gamma sensory fibres sense?

A

Pain and cold sensation

445
Q

What do C fibres sensory fibres sense?

A

Pain and hot sensation

446
Q

Give 3 cause of motor neuropathy

A
  1. Gullian-Barre syndrome
  2. Charcot-Marie-Tooth syndrome
  3. Lead poisoning
  4. Paraneoplastic
447
Q

Give 3 signs of motor neuroapthies

A
  1. Weakness/clumsiness of hands
  2. Difficulty walking
  3. LMN signs - hypotonia, hyporeflexia, fasciculations
  4. Involvement of respiratory muscles –> decreased FVC
448
Q

Give 3 causes of autonomic neuropathy

A
  1. DM
  2. HIV
  3. SLE
  4. Gullian-Barre syndrome
449
Q

Give 3 signs of autonomic neuropathy

A
  1. Postural hypotension
  2. ED
  3. Decreased sweating
  4. Constipation/nocturnal diarrhoea
  5. Urinary retention
450
Q

Name 3 types of axonal neuropathy presentation

A
  1. Symmetrical sensorimotor
  2. Sensory ganglionopathies (asymmetrical sensory)
  3. Asymmetrical sensorimotor
451
Q

Describe symmetrical sensorimotor neuropathy

A

Long fibres affected first (toes and fingers) = length dependent
Initially sensory but eventually sensorimotor

452
Q

Describe sensory ganglionopathies (asymmetrical sensory)

A

Patchy distribution of symptoms

Dorsal root ganglia are affected

453
Q

Describe asymmetrical sensorimotor

A

Mononeuritis multiplex

Randomly affect any nerve

454
Q

What investigations might you do in someone with a polyneuropathy?

A
  1. Clinical exam - reduced/absent tendon reflexes, sensory deficit, weakness
  2. NCS
  3. EMG
455
Q

Give an example of an acute polyneuropathy

A

Guillain-Barre syndrome

456
Q

What is autoimmune Guillain-Barre syndrome?

A

Acute inflammatory demyelinated ascending polyneuropathy affecting the PNS following an URTI or GI infection

457
Q

What can cause Guillain-Barre syndrome?

A 
Bacteria 
- Camplylobacter jejuni
- Mycoplasma 
Viruses 
- CMV
- EBV
- HIV
- Herpes zoster
458
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Same antigens on infectious organisms as Schwann cells –> autoantibody mediated nerve cell damage
Schwann cell damage –> demyelination –> reduction in peripheral nerve conduction –> acute polyneuropathy

459
Q

Give 4 signs of Guillain-Barre syndrome

A
  1. Ascending symmetrical muscle weakness (proximal muscles most affected - trunk, respiratory, CN)
  2. Pain
  3. Paraesthesia
  4. Reflexes lost
  5. Autonomic features = sweating, tachycardia, BP changes, arrhythmias
460
Q

What investigations might you do in someone you suspect has Guillain-Barre syndrome?

A

NCS = slowing of conduction, prolonged distal motor latency +/- conduction block
LP at L4 = raised protein and normal WCC
Spirometry = respiratory involvement

461
Q

Describe the treatment for Guillain-Barre syndrome

A

If FVC <1.5L/80% = ventilate and ITU monitoring
IV immunoglobulin for 5 days = decrease duration and severity of paralysis
Plasma exchange
Low molecular weight heparin
Analgesia

462
Q

When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?

A

If a patient has IgA deficiency

463
Q

Define stroke

A

Rapid onset of neurological deficit due to a vascular lesion lasting >24 hours and associated with infarction of central nervous tissue

464
Q

How can strokes be classified?

A
  1. Ischaemic (80%)

2. Haemorrhagic (20%)

465
Q

Give 2 causes of an ischaemic stroke

A

Occlusion of brain vasculature

  1. Atheroma
  2. Embolism –> AF, Infective endocarditis, carotid artherothromboembolism
466
Q

Give 2 causes of an haemorrhagic stroke

A

Bleeding from the Brian vasculature

  1. Hypertension
  2. Trauma
  3. Aneurysm rupture
  4. Sub-arachnoid haemorrhage
467
Q

Give 4 risk factors for stroke

A
  1. Hypertension
  2. DM
  3. Smoking
  4. PVD
  5. Hyperlipidaemia
  6. Heart disease
468
Q

Give 3 signs of an ACA stroke

A
  1. Leg weakness
  2. Sensory disturbance in legs
  3. Gait apraxia
  4. Incontinence
  5. Drowsiness
  6. Akinetic mutism - decrease in spontaneous speech
469
Q

Give 3 signs of a MCA stroke

A
  1. Contralateral arm and leg weakness and sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
470
Q

Give 3 signs of a PCA stroke

A
  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
471
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information

472
Q

What is prosopagnosia?

A

Inability to recognise a familiar face

473
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

Middle cerebral artery

474
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

Anterior cerebral artery

475
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

Posterior cerebral artery

476
Q

Give 3 differential diagnosis’s for a stroke

A
  1. Hypoglycaemia
  2. Intracranial tumour
  3. Head injury +/- haemorrhage
477
Q

What investigation could you do to determine whether someone has had a haemorrhagic or ischaemic stroke?

A

Head CT scan (before treatment)

478
Q

What is the treatment for an ischaemic stroke?

A

Thrombolysis - 4.5. hour limit = alteplase

Thrombolectomy

479
Q

How does alteplase work?

A

Converts plasminogen –> plasmin

So promotes breakdown of fibrin clot

480
Q

When can you do thrombolysis in someone with an ischaemic stroke?

A

Up to 4.5. hours post onset of symptoms

481
Q

What is primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
482
Q

What is secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

483
Q

What non-pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units
  2. Swallowing and feeding help
  3. Phsyio and OT
  4. Neurorehab - physio + speech therapy
484
Q

What is a TIA?

A

Sudden onset focal neurology lasting <24 hours due to temporal occlusion of part of the cerebral circulation

485
Q

Give 3 causes of a TIA

A
  1. Artherothromboembolism of the carotid
  2. Cardioembolism
  3. Hyperviscosity
  4. Vasculitis
486
Q

Describe the pathophysiology of a TIA

A

Cerebral ischaemia due to lack of O2 and nutrients –> cerebral dysfunction

487
Q

Give 3 signs of a carotid TIA

A
  1. Amaurosis fugax = retinal artery occlusion –> vision loss
  2. Asphasia
  3. Hemiparesis
  4. Hemisensory loss
488
Q

Give 3 signs of a vertebrobasilar TIA

A
  1. Double vision
  2. Choking
  3. Ataxia
  4. Hemisensory loss
  5. Vomiting
489
Q

Name 3 differential diagnosis’s for a TIA

A
  1. Migraine
  2. Epilepsy
  3. Hypoglycaemia
  4. Hyperventilation
490
Q

What investigations would you do in someone who you suspect to have a TIA?

A

Bloods

CT imaging

491
Q

What is it essential to do in someone who has had a TIA?

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

492
Q

What is the ABCD2 score?

A 
Assesses risk of stoke in the next 7 days for those who have had a TIA 
- Age > 60 (1 point)
- BP > 140/90mmHg (1 point)
- Clinical features
a) Unilateral weakness (2 points)
b) Speech disturbance (1 point)
- Duration
a) >60 minutes (2 points) 
b) <60 minutes (1 point) 
- Diabetes (1 point) 
Score >6 predicts stroke 
Score >4 assessed within 24 hours
493
Q

What classifies as a high risk stroke patient?

A

ABCD2 score >4
AF
>1 TIA in a week

494
Q

Within how long should someone with a suspected TIA been seen by a specialist?

A

Within 7 days

495
Q

What is treatment for a TIA?

A

2 weeks aspirin and dipyridamole
Long term clopidogrel
Control CV risk factors - antihypertensives, statins, anticoagulants

496
Q

Define myelopathy

A

Spinal cord disease - UMN problem

497
Q

Define radiculopathy

A

Spinal nerve root disease - LMN problem

498
Q

Give 3 causes of spinal cord compression

A
  1. Vertebral tumour (metastases from lung, breast, kidney, prostate, myeloma)
  2. Disc herniation
  3. Disc prolapse
  4. Trauma
  5. Infection
499
Q

Give 3 signs and symptoms of spinal cord compression

A
  1. Back pain
  2. Progressive spastic leg weakness
  3. UMN symptoms below lesion - hypertonia, hyper-reflexia
  4. LMN weakness and signs at level of lesion
  5. Sensory loss below lesion
  6. Bladder sphincter problems –> hesitancy, frequency, painless retention
500
Q

What investigations might you do in someone with suspected spinal cord compression?

A

Urgent MRI/CT scan

501
Q

What is the treatment for spinal cord compression?

A

Decompressive surgery

Dexamethasone and radiotherapy - if malignancy

502
Q

Briefly describe the pathophysiology of cauda equina syndrome

A

Spinal compression at or distal to L1 –> disrupts sensation and movement

503
Q

Give 3 causes of cauda equina syndrome

A
  1. Lumbar disc herniation
  2. Tumour
  3. Trauma
  4. Infection
504
Q

Give 4 signs of cauda equina syndrome

A
  1. Flaccid and areflexic leg weakness
  2. Back pain –> alternating/bilateral sciatica
  3. Saddle anaesthesia
  4. Loss of sphincter tone –> bladder/bowel dysfunction
  5. Erectile dysfunction
505
Q

What investigations might you do to see if someone has cauda equina syndrome?

A
  1. MRI/CT of spine
  2. CRE = reduced anal tone
  3. Reflex tests
506
Q

How do you treat cauda equina syndrome?

A
  1. Immediate surgical decompression

2. Treat cause

507
Q

What is treatment for sciatica without neurological signs?

A

Conservative management - physio and NSAIDs

508
Q

Define spondyloisthesis

A

Slippage of vertebra over the one below

509
Q

Define spondylosis

A

Degenerative disc disease

510
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs
  2. Aura
  3. Ictal
  4. Post-ictal - often drowsy and confused
511
Q

Give 3 activities that can trigger trigeminal neuralgia

A
  1. Washing your face
  2. Eating
  3. Shaving
  4. Talking
512
Q

How long do you wait for before doing a lumbar puncture in someone with a suspected subarachnoid haemorrhage?

A

At least 12 hours
You need to wait or the Hb to break down and then CSF will become yellow - sign that there is a bleeding in subarachnoid space (xanthochromia)

PHASE 2A (16 decks)

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