Neurology AS Flashcards

1
Q

Gross anatomy of the spinal cord?

A
  • From Foramen magnum to L1
  • Terminates as conus medullaris
  • Spinal nerves continue inferiorly as corda equina
  • Denticulate ligament and filum terminale are pial extensions that suspend cord in subarachnoid space.
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2
Q

What is the blood supply of the spinal cord?

A

3 longitudinal vessels.

  • 2 posterior spinal arteries supply the dorsal 1/3
  • 1 anterior spinal artery supplies 2/3
  • Reinforced by segmental feeder arteries (artery of Adamkiewicz)
  • Longitudinal veins drain into extradural vertebral plexus.
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3
Q

What are the tracts of the spinal cord?

A

Dorsal Columns
Lateral spinothalamic tract
lateral corticiospinal tract
Thalamic nuclei

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4
Q

Where are the dorsal columns organised in the spinal cord?

A

Most posteriorly.

  • Composed of the fasciculus gracilis and cuneate fasciculus.
  • Cuneate is cervical + thoracic and is positioned less posteriorly than gracile (sacral and lumbar).
  • Sensory tracts moving info upwards.
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5
Q

What mode of information do the dorsal columns carry?

A
  • Fine touch
  • Vibration
  • Proprioception

Cell body in the dorsal root ganglion

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6
Q

Where is the decussation of the dorsal columns?

A

In the medulla forming medial lemniscus

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7
Q

Where is the lateral spinothalamic tract situated in the spinal cord?

A
  • Organised anterolaterally
    Cervical is medial, whilst sacral is lateral.
  • Also known as the anterior white commisure
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8
Q

What mode of information does the lateral spinothalamic tract carry?

A
  • Pain and temperature
  • Cell body in the DRG

Carrying information upwards

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9
Q

Where is the decussation of the lateral spinothalamic tract

A

In the cord, at the entry level.

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10
Q

Where is the lateral corticospinal tract situated in the spinal cord?

Motor Pyramidal tracts

A

These are the pyramidal tracts

- posterio-laterally but also anterior.

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11
Q

What mode of information does the lateral corticospinal tract carry?

A
  • Motor information

- Cell body in the primary motor cortex.

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12
Q

Where is the decussation of the lateral corticospinal tract?

A

Pyramidal decussation in the ventral medulla

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13
Q

Other motor tracts of the spinal cord?

A

Rubrospinal
Reticulospinal
Vestibulospinal
Olivospinal

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14
Q

Other sensory tracts?

A

Spinocerebellar

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15
Q

What are the thalamic nuclei?

A

VPL: Ventral posteriolateral nucleus
VPM: Ventral posteriomedial nucleus
LGN: Lateral Geniculate Nucleus
MGN: Medial Geniculate Nucleus

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16
Q

What is the role of the ventral posteriolateral nucleus?

A

Somatosensory body - Touch

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17
Q

What is the role of the ventral posteriomedial nucleus?

A

Somatosensory head - Touch

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18
Q

What is the role of the lateral geniculate nucleus?

A

Visual

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19
Q

What is the role of the medial geniculate nucleus?

A

Auditory

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20
Q

Role of the cerebellum and basal ganglia?

A
  • Output to cortex via thalamus

- Regulation of posture, locomotion, coordination and movement.

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21
Q

Role of internal capsule?

A

White matter carrying axonal fibres from motor cortex to pyramids of medulla

An infarction here –> Contralateral hemiparesis

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22
Q

Role of the frontal lobe?

A
  • Cognition and memory
  • Executive function
  • Motor cortex
  • Dominant hemisphere: motor speech (Broca’s Area).
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23
Q

Role of the parietal lobe?

What will a defect in this present as?

A

Sensory cortex

  • sensory inattention
  • apraxias
  • astereognosis (tactile agnosia)
  • inferior homonymous quadrantanopia
  • Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation

Apraxia is a disorder of the brain and nervous system in which a person is unable to perform tasks or movements when asked, even though: The request or command is understood. They are willing to perform the task.

Astereognosis is used to describe both the inability to discriminate shape and size by touch and the inability to recognize objects by touch. These are apperceptive and associative types of agnosia.

Body orientation - Visuospatial processing

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24
Q

Role of temporal lobe

A

Memory

Dominant hemisphere: receptive language (Wernicke’s - language comprehension).

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25
Q

Homunculus structure?

A

Medially, the feet, legs, then head.

Laterally, hand, nose, upper lip.

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26
Q

Anterior cerebral circulation?

A

Medial top band of brain.
Therefore occlusion = paralysis or weakness of foot and lef on the opposite side.

Cortical sensory loss in opposite foot and leg

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27
Q

Middle cerebral

A
  • Bulk of lateral surface of hemisphere
  • Superior division of Broca’s area = language expression (resulting aphasia) (anterior branch of MCA)
  • INferior devision supplies lateral temporal lobe (location of Wernicke’s areas - Language comprehension
    (posterior branch of MCA)

Lesion is located in the superior temporal gyrus.

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28
Q

Posterior cerebral artery

A

Supplies occipital lobe, cerebellum and brainstem.

Vertebral arteries

  • Basilar artery splits
  • Can get PICA (posterior inferior cerebellar artery) = Lateral medullary syndrome
  • Anterior inferior cerebellar artery
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29
Q

Long tracts of the motor pathway?

A
Descending motor pathway (UMN) 
- From motor cortex
            V
-  internal capsule
            V
- Midbrain
            V
- Pons
            V
- Medulla
            V
- Decussation of pyramids (cross over) 
            V
- Cervical cord 
- Thoracic cord 
etc
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30
Q

Long tracts of the dorsal column pathway? Sensory (proprioception, fine touch, vibration)

A
- Post-central gyrus
            V
-  Thalamus (VPL) 
            V
- Midbrain
            V
- Pons (becoming the medial lemniscus)
            V
- Medulla (cross over of medial lemniscus (becomes nucleus gracilis, nucleus cuneate)
            V
- Decussation of pyramids (cross over) 
            V
- Cervical cord 
- Thoracic cord 
etc
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31
Q

Long tracts of the spinothalamic pathway? Sensory (pain + temperature)

A
- Post-central gyrus
            V
-  Thalamus (VPL) 
            V
- Midbrain
            V
- Pons (becoming the medial lemniscus)
            V
- Medulla 
            V
- Cervical cord 
- Thoracic cord 
etc
- Lumbar 
            V
- CROSS OVER THEN
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32
Q

12 cranial nerves?

A
I - Olfactory
II - Optic
III - Oculomotor
IV - Trochlear
V - Trigeminal
VI - Abducens
VII - Facial
VIII - Vestibulocochlear
IX - Glossopharyngeal
X - Vagus
XI - Accessory
XII - Hypoglossal
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33
Q

Nuclei of the cranial nerves?

A

All cranial nerves have a nucleus that are present in the brainstem EXCEPT the optic and olfactory (I + II).

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34
Q

Mid-brain contains nuclei of which cranial nerves?

A

Mid- brain houses oculomotor nerve (III) and trochlear nerve (IV).

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35
Q

Pons contains nuclei of which cranial nerve?

A

Trigeminal (V) (M+S)
Abducens (VI)
Facial nerve (VII)
Vestibulocochlear (VIII)

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36
Q

Medulla contains nuclei of which cranial nerve?

A

Glossopharyngeal (XI)
Vagus (X)
Accessory (XI)
Hypoglossal (XII)

Rule of S + M

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37
Q

What is special about Trigeminal (V)

A

Sensory and motor nerve fibres from 4 nuclei

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38
Q

What is the structure of the NMJ + Stages of synaptic conduction?

A
  1. Presynaptic voltage-gated Ca2+ channels open –> Ca influx
  2. ACh vesicles released from presynaptic terminal
  3. Ach diffuses across cleft
  4. Ach binds to NICOTINIC receptors on post-synaptic terminal
  5. –> Na+ influx –> Depolarisation –> Ca2+ release from SR –> Muscle contraction
  6. Ach is degraded by acetylcholinesterase and choline is taken up into presynaptic terminal
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39
Q

What drug is used to block presynaptic choline uptake?

A

Hemicholinium

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40
Q

What drug blocks ACh vesicle fusion?

A

Botulinum

Lambert-Eaton Myasthenic Syndrome

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41
Q

Which drugs block nicotinic ACh receptors?

A

Antimuscarinic blocks muscarinic Ach
Antinicotonic block nicotonic receptors.

Non-depolarising: Atracurium, vecuronium

Depolarising: suxamethonium - paralysis therefore short-term paralysis as part of GA.

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42
Q

Antimuscarinic agents?

A
Antipsychotics (clozapine) 
Atropine
Tropicamide
Scopolamine
Atropine
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43
Q

Antinicotinic agents?

A

Bupropion

Hexamethonium

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44
Q

What are the dopamine pathways of the CNS?

A

Mesocorticolimbic
Nigrostriatal
Tuberoinfundibular

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45
Q

Role of Mesocorticolimbic in disease?

A

Schizophrenia

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46
Q

Role of Nigrostriatal in disease?

A

Parkinson

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47
Q

Role of tuberoinfundibular?

A

Hyperprolactinaemia

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48
Q

Sympathetic Nervous System structure?

A
  • Autonomic nervous system
  • Cell Bodies from T1-L2.
    Response to fight-flight or freeze.
  • Supplied form the spinal cord, to the left + right ganglia.
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49
Q

Where do general visceral efferent fibres synapes to in the sympathetic nervous system?

A
  • Paravertebral ganglia
  • Prevertebral ganglia
  • Chromaffin cells of adrenal medulla
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50
Q

How are preganglionic fibres different to postganglionic fibres?

A
Pre = Myelinated + release ACh @ nicotinic receptors
Post = Unmyelinated + release noradrenaline @ adrenergic receptors (except @ sweat glands where they reelase ACh for muscarinic receptor)
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51
Q

What are the parasympathetic nerve system cranial nerves?

A

Rest and digest/ Feed and Breed. Arousal, salivation, lacrimation, urination, digestion, defectation.

3 - Ciliary Ganglion for eye
7 -
- Pterygopalatine: mucus membranes of nose, palate + lacrimal gland
- Submandibular: submandibular and sublingual glands

9 - Otic: Parotid gland

10 - Vagus (thoracic and abdo viscera)

Sacral: Pelvic splanchnic nerves (S2-4) innervate pelvic viscera.

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52
Q

What is the difference between preganglionic and post ganglion parasympathetic fibres?

A
Pregang = ACh @ nicotinic receptors 
Postgang = ACh @ muscarinic receptors
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53
Q

All nuclei except 4 in Cranial nerves?

A

All except 4 innervate ipsilateral side.

Fibres from trochlear nucleus decussate in medulla + supply contralateral superior oblique muscle.

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54
Q

Vestibulo-ocular pathways?

A

Vestibulo-ocular reflex (VOR)

  • Axons from vestibular neurons project via MLF to abducens and oculomotor nuclei.
  • Head turns L –> Eyes turn R
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55
Q

Absent Doll’s Eye Sign

A

Brainstem death

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56
Q

Caloric Test physiology?

A

Warm –> Increasing firing of vestibular nerve –> eye turn to contralateral side with nystagmus to ipsilateral side.

  • Fast direction of nystagmus COWS
    Cold: opposite
    Warm: Same

Absence = brainstem damage on side being tested

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57
Q

Visual Field Defects? Central Scotoma?

A

Blind Spot or due to MS

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58
Q

Visual Field Defects? Monocular vision loss?

A

Damage of the optic nerve

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59
Q

Bitemporal hemianopia?

A

Damage at the optic chiasm

Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, from pituitary tumour

Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma. This may cause a diabetic insipidus.

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60
Q

Contralateral homonymous hemianopia

A

Therefore a left contralateral homonymous hemianopia means there is damage to the right hand side. Defect is on the left.

Due to damage at the optic tract. = Incongruous defect

Also due to damage at the whole of the optic radiation. = congrous defect.

Also due to damage of the entire calcarine fissure.

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61
Q

Contralateral superior quadrantanopia?

A
  • Damage at the right Meyer’s Loop in the right temporal radiation.
  • Temporal = Superior

Superior TEMPO

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62
Q

Contralateral inferior quadrantanopia

A
  • Damage at the calcarine fissure at the parietal lobe
    Inferior quadrantanopia
  • Remember left inferior quadrantanopia = right parietal lobe lesion.
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63
Q

Homonymous hemianopia with central macular sparing?

A

Lesion at occipital pole - Contralateral. Lesion of the occipital cortex

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64
Q

Pupillary light reflex? Optic nerve damage to left?

A

Left direct reflex is lost. When left eye is stimulated, neither pupil constrict.

Right consensual reflex is lost. When left eye is stimulated, right does not constrict.

Right direct reflex is intact. Right constricts when signs.

Left consensual is intact as it relies on the oculomotor nerve.

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65
Q

Schematic diagram for pupillary light reflex?

A
  • Retina on left and right
  • Travels down optic nerve either side.
  • Cross overs at retectal N to contralateral and ipsilateral Edinger-Westphal nuclei.
  • Then travels down CN3 (oculomotor) to the ciliary sphincter.
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66
Q

Oculomotor nerve damage on left?

A
  • Left direct is lost
  • Right consensual reflex is intact
  • Right direct reflex is intact.
  • Left consensual reflex is lost.
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67
Q

What is a Marcus Gunn Pupil

A
  • Person with abnormal left direct + abnormal right consensual reflex
  • Afferent pupillary defect.
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68
Q

Pattern of Motor Deficits

- Cortical Lesions?

A

Hyperreflexia proximally in arm or leg

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69
Q

Pattern of Motor Deficits

- Internal capsule and corticospinal lesions?

A
  • Contralateral hemiparesis with pyramidal distribution
  • Lesions with epilepsy, decrease cognition of homonymous hemianopia = In cerebral hemisphere
  • Lesion with contralateral CN palsy = brainstem lesion on the side of the palsy (e.g Milliard-Gubler syn)
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70
Q

Pattern of Motor Deficits

- Cord Lesions?

A

Quadriparesis/paraparesis

Motor and reflex level: LMN signs at level of lesion and UMN sign below

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71
Q

Pattern of Motor Deficits

- Peripheral Neuropathies?

A
  • Usually distal weakness
  • GBS weakness is proximal (root involvement)
  • Single nerve = Mononeuropathy: trauma or entrapment
  • Several nerves = mononeuritis multiplex: Vasculitis or DM.

Asymmetrical involvement of individual non-contiguous nerve trunks.

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72
Q

What is the UMN lesion pattern?

A
  • increased tone ± clonus
  • Hyperreflexia
  • Up-going plantars
  • pyramidal weakness:
    extensors in UL (weak extensor)
    flexors in LL (weak flexor)
  • No wasting

Motor cells in pre-central gyrus to anterior horn cells in the cord.

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73
Q

What is the LMN lesion pattern

A
  • Decreased tone/flaccidity
  • Hyporeflexia
  • Down-going plantars (normal
  • Wasting
  • Fasciculations

Anterior horn cells to peripheral nerves

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74
Q

Pattern of Motor Deficits

- Primary Muscle Lesions?

A
  • Symmetrical loss
  • reflexes lost later vs neuropathies
  • No sensory loss
  • Fatiguability in myasthenia
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75
Q

Patterns of sensory deficits

- Where do sensations travels in the cord?

A
  • Pain + temp travel along spinothalamic tracts

- Touch, joint and vibration travel in large fibres peripherally + dorsal column centrally.

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76
Q

Patterns of sensory deficits

- Distal sensory loss?

A

Neuropathy

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77
Q

Sensory level?

A

Hallmark of cord lesion

  • Hemi-cord lesion –> Brown-Sequard Syndrome
  • Ipsilateral loss of proprioception + vibration and UMN weakness with contralateral loss of pain + temp
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78
Q

Dissociated sensory loss cause?

A
  • Selective loss of pain and temp with conservation of proprioception and vibration
  • Occurs in cervical cord lesions e.g syringomyelia
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79
Q

What are the specific signs of cerebellar syndrome?

A

DANISH

  • Dydiadochokinesia
  • Dysmetria: past-pointing
  • Ataxia
  • Nystagmus
  • Intention Tremor
  • Speech: slurred, staccato, scanning dysarthria
  • Hypotonia

Head: head tremor (titubation) eye nystagmus and dysarthria (Speech - British Constitution)

Arms: rebound pehomenon, intention tremor, past pointing.

LEgs: heel-shin, ataxic gait, Romberg’s negative.

Cerebellar hemisphere - finger-nose ataxia.

Cerebellar vermis - Gait ataxia.

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80
Q

What are the common causes of cerebellar syndrome?

A

PASTRIES

  • Paraneoplastic: e.g from bronchial Ca
  • Alcohol: thiamine
  • Sclerosis
  • Tumour: e.g CPA lesion
  • Rare: MSA, Friedrich’s, Ataxia Telangiectasia
  • Iatrogenic: phenytoin
  • Endo: hypothyroidism
  • Stroke: vertebrobasilar
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81
Q

Anterior Cerebral Artery stroke?

A
  • Supplies frontal and medial part of cerebrum
  • Contralateral motor/sensory loss in the legs >arms
  • Face is spared
  • Abulia (pathological laziness)
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82
Q

Middle Cerebral Artery?

A
  • Supplies lateral and external part of hemisphere
  • Contralateral motor/sensory loss in face and arms > legs
  • Contralateral homonymous hemianopia due to involvement of optic radiation.
  • Cognitive changes
    Dominant (L): aphasia (Broca’s)
    Non-dominant (R): neglect, apraxia.
Broca's = inferior frontal gyrus. expressive. Comprehension is normal, but speech is non-lfuent, laboured and halting. 
Wernicke's = receptive aphasia - superior temporal gyrus. Sentences make no sense, speech remains fluient and comprehension is impaired. 

Dominant is normally left. Therefore the middle cerebral artery supplies both Wernicke’s and Broca’s area.

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83
Q

Posterior cerebral artery?

A

Supplies occipital lobe

Contralateral homonymous hemianopia with macula sparing

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84
Q

Vertebrobasilar Circulation

A
  • Supplies cerebellum, brainstem and occipital lobes.
  • Combination of symptoms
    : Visual: hemianopia, cortical blindness
  • Cerebellar: DANISH
  • CN Lesions
  • Hemi-/quadriplegia
  • Uni/bilateral sensory symptoms.
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85
Q

What is lateral medullary syndrome/Wallenberg’s syndrome?

A

PICA: Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

AICA: Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness

It is an important syndrome to be aware of as it is most often due to a stroke affecting the posterior inferior cerebellar artery (PICA). It is the most commonly survived stroke that affects the brainstem and is commonly used as an exam question scenario. Given her symptoms, this would be in keeping with a right-sided posterior inferior cerebellar artery infarct.

An anterior inferior cerebellar artery infarct would present in the same way but with the additional symptoms of a same-sided facial weakness and loss of hearing. A basilar artery infarct would result in a locked-in syndrome where the patient is unable to move or communicate but is fully conscious. Both of these are more likely to affect the autonomic centres in the medulla and are associated with a higher mortality.

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86
Q

Millard-Gubler Syndrome: Crossed hemiplegia

A
Pontine lesions (e.g infarc) 
Effects: 6th (can't look laterally) and 7th CN palsy + contralateral hemiplegia.
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87
Q

Locked in syndrome?

A
  • Pt is aware + cognitively intact but completely paralysed except for eye muscle

Causes
- Ventral pons infarction: basilar artery. Secondary to hypertension. Reduced GCS, quadriplegia, miosis, absent horizontal eye movement. Pinpoint pupils point to pons.

  • Central pontine myelinolysis: rapid correction of hyponatreamia
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88
Q

Cerebellopontine Angle Syndrome?

A

Causes: Acoustic neuroma, meningioma, cerebellar astrocytoma, metastasis

Leads to a ipsilateral CN5,6,7,8 + cerebellar signs

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89
Q

Subclavian Steal Syndrome?

A

Subclavian A stenossi proximal to origin of vertebral A may_-> blood being stolen from this vertebral artery by retrograde flow

  • Syncope/presyncope or focal neurology using the arm
  • BP difference of >20mmHg between arms.
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90
Q

What is anterior spinal artery/ Beck’s Syndrome

A
  • Infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord.
  • Causes: Aortic Aneurysm dissection or repair
  • Effects
    Para/Quadriparesis
    Impaired pain and temperature sensation
    Preserved touch and proprioception
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91
Q

What are the differentials for muscle weakness? Causes in the CNS?

A

Cerebrum

  • Vascular: infarct, haemorrhage
  • Inflammation: MS
  • SOL
  • Infection: Encephalitis, abscess

Cord

  • Vascular: Anterior spinal artery infarction
  • Inflammation: MS
  • Injury

Anterior Horn
- MND, polio

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92
Q

What are the differentials for muscle weakness? Causes in the PNS?

A
- Motor Nerves
Mononeuropathy: compression
Polyneuropathy: GBS, CMT
- NMJ 
GB, LEMS, Botulism
- Muscle
Toxins: steroids
Poly/dermatomyositis
Inherited: DMD, BMD, FSH
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93
Q

Gait Disturbance Differential (Motor) - Basal Ganglia: Shuffling gait

A

Basal:

  • PD
  • Parkinsonism: MSA, PSP, Lewy Body Dementia, CBD

Hypokinetic (parkinsons)
Hyperkinetic (Huntington’s)

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94
Q

Gait Disturbance Differential (Motor)

UMN Bilateral: Spastic, scissoring

A

Cord: Compression, trauma, hereditary spastic paraparesis, syringomyelia, transverse myelitis

Bihemispheric: CP, MS

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95
Q

Gait Disturbance Differential (Motor)

UMN Unilateral: Spastic circumducting

A

Hemisphere lesion: CVS, MS, SOL

Hemicord: MS, tumour

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96
Q

Gait Disturbance Differential (Motor)

LMN bilateral: bilateral foot drop

A

Polyneuropathy: CMT (charcot-marie tooth), GBS

Corda equina

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97
Q

Gait disturbance differential: (Motor) LMN Unilateral: foot drop –> high stepping gait.

A

Ant horn: Polio
Radicular: L5 root lesion
Sciatic/common peroneal nerve: trauma, DM.

Weakness of hip abduction is L5 radiculopathy.

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98
Q

Mixed UMN and LMN: MAST ?

A
  • Motor Neuron Disease
  • Friedrich’s ataxia - Same as SCD but with cerebellar ataxia.
  • Subacute combined degeneration of the cord =

First to go is the dorsal column with joint position and vibration.

bilateral spastic paresis (damage to lateral columns) bilateral loss of proprioception and vibration sensation (damage to posterior columns) leading to sensory ataxia and positive romberg’s test. Bilateral limb ataxia (damage to peripheral nerve) - absent ankle and knee jerk.

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99
Q

What are the differentials for hand wasting?

A

Cord

  • Anterior Horn: MND, polio
  • Syringomyelia

Roots
- Compression: spondylosis, neurofibroma

Brachial Plexus
-  Compression 
Cervical rib
Tumour: Pancoast's, breast
- Avulsion: Klumpke's palsy
Neuropathy 
- Generalised: Charcot Marie Tooth
- Mononeuritis multiplex: DM
- Compressive mononeuropathy 
Median: thenar wasting 
Ulnar: hypothenar and interossei wasting

Muscle

  • Disuse: RA
  • Compartment syndrome: Volkman’s ischaemia
  • Distal myopathy: myotonic dystrophy
  • Cachexia
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100
Q

Gait disturbance due to sensory impairment? Vestibular causes?

A

(all Romberg’s +ve)

Meniere’s
Viral Labyrinthitis
Brainstem Lesion

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101
Q

Gait disturbance due to sensory impairment? Cerebellar causes?

A

Ataxic

  • ETOH
  • Infarct

Wide-based gait, loss of heel to toe pattern and instability.

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102
Q

Gait disturbance due to sensory impairment? Proprioceptive loss (Romberg’ +ve)

A

Dorsal columns: B12 deficiency
Peripheral Neuropathy: DM, ETOH, Uraemia

Visual Loss

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103
Q

What are the cardiac causes of LOC?

A

Stokes-Adams Attack = collapse without warning and loss of consciousness.

  • Bradycardia: heart block, sick sinus, Long QT
  • Tachycardia: SVT, VT
  • Structural

Weak heart: LVF, tamponade
Block: AS, HOCM, PE, ACS

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104
Q

What are the reflex causes of LOC?

A

Vagal overactivity

  • Vasovagal syncope
  • Situational: cough, effort, micturition
  • Carotid sinus syncope

Sympathetic underactivity= postural hypotension
- Salt deficiency: hypovolaemia, Addison’s
- Toxins
Cardiac: ACEi, diuretics, nitrates, a-B
Neuro: TCAs, benzos, antipsychotics, L-DOPA
- Autonomic neuropathy: DM, Parkinson’s, GBS
Dialysis
Unwell: chronic bed-rest
Pooling, venous: varicose veins, prolonged standing (orthostatic hypotension) .

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105
Q

What are the arterial causes of LOC?

A

Vertebrobasilar insufficiency: migraine, TIA, CVA, Subclavian steal
Shock
HTN: phaeochromocytoma

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106
Q

What are the systemic causes of LOC?

A

Metabolic: decreased glucos
Resp: hypoxia, hypercapnoea
Blood: anaemia, hypervisocity

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107
Q

What are the head causes of LOC?

A

Epilepsy

Drop Attacks

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108
Q

Examination of LOC?

A
  • Postural HTN: difference of >20/10 after standing for 3 mins vs lying down - Orthostatic hypotension
  • Cardiovascular assessment
  • Neurological assessment
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109
Q

Investigations of LOC?

A
  • ECG ± 24hr ECG
  • U+E, FBC, Glucose
  • Tilt table (confirms dysautomomia for neuro)
  • EEG, Sleep EEG
  • Echo, CT, MRI brain
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110
Q

Presentation of cardiogenic syncope?

A

Trigger: Exertion, drug, unknown

Before: Palpitations, chest pain, dyspnoea

During: pale, slow/absent
pulse, clonic jerks may occur

After: Rapid recovery

IX: ECG, 24hr ECG, Echo

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111
Q

Presentation of vasovagal syncope?

A

Trigger: prolonged standing, heat, fatigue, stress, emotional upset
Before
- Gradual onset: sec–> mins
- Nausea, pallor, sweating, tunnel vision, tinnitus.
- Cannot occur lying down

During

  • Pale, grey, clammy, brady
  • Clonic jerks and incontinence can occur, but no tongue biting

After: rapid recovery

Ix: Tilt-table testing

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112
Q

Reflex: Postural hypotension presentation?

A

Prodrome of sweating, pallor and N+V before a transient LOC are suggestive of a reflex syncope.
Most common cause.

Defined as SBP fall of at least 20mmHg within 3 mins of standing.

Trigger: standing up
Before, during and after same as vagal above

Ix: Tilt-table testing

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113
Q

Presentations of Arterial causes of LOC?

A

Trigger: Arm elevation (Subclavian steal), migraine

Before, during and after same as vasovagal ± brainstem signs (diplopia, nausea, dysarthria

Ix: MRA, duplex vertebrobasilar circulation

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114
Q

Presentation of systemic causes of LOC?

A

Hypoglycaemia: tremor, hunger, sweating, light-headedness –> LOC

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115
Q

Epileptic presentation of LOC?

A

Trigger: flashing lights, fatigue, fasting

Before: aura in complex partial seizures - feeling strange, epigastric rising, deja/jamais vu, smells, lights, automatisms

During: tongue biting, incontinence, stiffness –> Jerking, eyes open, cyanosis, Decreased SpO2.

After: headache, confusion, sleeps, Todd’s palsy.

Ix: EEG, increased SE prolactin at 10-20mins (greater than 2x baseline indicates generalise tonic clonic seizure). Check glucose, WBC, electrolytes.

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116
Q

Drop attack? Distinct from syncope?

A

No trigger. No warning.
During: Sudden weakness of legs causes older woman to fall to ground.
No post-ictal phase.

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117
Q

What is the definition of vertigo?

A
  • The illusion of movement: usually rotatory
  • Of patients or surrounding
  • Worse on movement
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118
Q

What is not classified as vertigo?

A

Faintness
Light-headedness
Lost awareness

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119
Q

What is dizziness?

A

With impaired consciousness = blackout

Without impaired consciousness:

  • Vertigo: Vestibular in nature
  • Imbalance: vestibular, cerebellar, extrapyramidal
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120
Q

What are the causes of Vertigo? Infection?

A

IMBALANCE

Infection/Injury

  • Labyrinthitis: post-viral severe vertigo, n/v, hearing loss
  • Ramsay Hunt (shingles of facial nerve)
  • Trauma: to petrous temporal bone

Investigation with audiogram, Rinne’s and Weber’s test. Will show a sensorineural hearing loss. Previous viral infection.

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121
Q

What are the causes of Vertigo? Meniere’s

A
  • Recurrent vertigo (~20mins) ± n/v
  • Fluctuating SNHL (sensorineural hearing loss)
  • Tinnitis
  • Aural fullness (ear feeling full)
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122
Q

What are the causes of Vertigo? BPPV?

A

Sudden vertigo proved by head rotation. Short lived experience. Free-floating endolymph particles otoconia).
- Episodic vertigo.

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123
Q

Other causes of vertigo?

A

Aminoglycosides/Frusemide

Lymph, peri, fistula
Path: Connection between inner and middle ears
Causes: congenital, truama
PC: vertigo, SNHL
O/E: tulio’s phenomenon - nystagmus evoked by loud sound

Arterial

  • Migraine
  • TIA/Stroke

Nerve
- Acoustic Neuroma/Vestibular schwannoma

Central lesions
- Demyelination, tumour, infarction

Epilepsy
- Complex partial

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124
Q

Causes of hearing loss - Conductive?

A

WIDENING

  • Wax or foreign body
  • Infection: Otitis media, OME
  • Drum perforation
  • Extra: ossicle discntinuity - otosclerosis, trauma
  • Neoplasia: carcinoma
  • Injury: Barotrauma
  • Granulomatous: Wegener’s, Sarcoid
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125
Q

Causes of hearing loss: sensorineural? DIVINITY

A

Development

  • Genetic: Alport’s
  • Congenital: TORCH
  • Perinatal: Anoxia

Degenerative
- Presbyacusis

Infection

  • VZV, Measles, Mumps, Influenza
  • Meningitis

Vascular

  • Ischaemia: Interal Auditory Artery - sudden hearing loss and vertigo
  • Stroke

Inflammation

  • Vasculitis
  • Sarcoidosis

Neoplasia
- CPA tumours: acoustic neuroma (commonest cause of unilateral SNHL)

Injury

  • Noise
  • head trauma

Toxins

  • Gentamicin
  • Frusemide
  • Aspirin

Lymph

  • Endolymphatic hydrops = Meniere’s (abnormal fluctuation of the fluid in the ear).
  • Perilymphatic fistula: ruptured round window.
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126
Q

Abnormal Involuntary Movements - Dyskinesias.

Define Tremor

A

Regular, rhythmic oscillation

Asterixis = rhythmic myoclonus - tremor of the hand when stretched out

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127
Q

Types of Tremor? RAPID?

A

Resting
Action/Postural
Intention
Dystonic

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128
Q

What is a resting tremor?

A

Features

  • 4-6 Hz, pill rolling
  • Abolished on voluntary movement
  • increased with distraction (counting backwards)

Causes: Parkinsonism
Management: Dopamine agonists (levodopa, cabergoline, bromocriptine), antimuscarinic (procyclidine)

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129
Q

What is a postural/action tremor?

A

Features

  • 6-12Hz
  • Absent at rest
  • Worse with outstretched hands or movement (part of the essential tremors)
  • Equally bad at all stages of movement
  • Can also affect the vocal cords.

Cause

  • Benign essential tremor
  • Endo: thyrotoxicosis, decreased glucose, phaeo
  • Alcohol withdrawal (caffeine, opioids)
  • toxins, valproate, theophylline
  • Sympathetic: physiological tremor may be enhanced e.g in anxiety
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130
Q

What is an intention tremor?

A

Features

  • > 6Hz, irregular, large amplitude
  • worse at the end of movement
  • E.g past-pointing

Causes: cerebellar damage

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131
Q

What is a dystonic tremor

A

Variable presentations

Mostly idiopathic, as for dystonia

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132
Q

What is a benign essential tremor?

A
  • Autosomal dominant
  • Occurs with action and worse with anxiety, emotion, caffeine
  • Arms, neck, voice
  • Doesn’t occur during sleep
  • Better with ETOH.

Management: Propranolol
Primidone

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133
Q

What is myoclonus?

A

Sudden, involuntary jerks

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134
Q

What is myoclonus caused by?

A

Metabolic = asterixis (L, R, increased CO2)
Neurodegenerative disease
CJD
Myoclonic epilepsies (infantile spasms)

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135
Q

What is benign essential myoclonus?

A
  • AD
  • Childhood onset frequency generalised myoclonus without progression
  • May respond to valproate
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136
Q

What is dystonia?

A

Prolonged muscle contractures –> Unusual joint posture or repetitive movement

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137
Q

What is idiopathic generalised dystonia?

A

AD

Childhood onset: starts in one leg, spreads on that side of the body over 5-10 years.

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138
Q

What is idiopathic focal dystonia

A
  • Commonest form of dystonia
  • Confined to one part of the body
  • worsened by stress
  • Involves rigidity and writhing movements rather than twitching.

Types

  • Spasmodic torticolis
  • Blepharospasm (eyelids)
  • Oromandibular
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139
Q

What is acute dystonia?

A
  • Torticollis, trismus and or occulogyric crisis
  • Typically a drug reaction:
    Antipsychotics
    Metoclopramide
    L-Dopa
    Rx: Procyclidine (antimuscarinics).
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140
Q

Chorea?

A
  • Non-rhythmic, purposeless, jerky, flitting movements
  • Facial grimacing, extending the fingers
  • Huntington’s
  • Sydenham’s
  • Wilson’s
  • L-Dopa
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141
Q

Athetosis?

A

Slow, sinuous, writhing movements
- Causes
Cerebral palsy
Kernicterus

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142
Q

Tardive Syndromes?

A

Delayed onset following chronic exposure to Da agonists (antipsychotics, antiemetics, L-DOPA).

  • Dyskinesia: orobuccolingual, truncal
  • Dystonia: Sustained, sterotyped muscle spasms of twitching or turning
  • Akathisia: unpleasant sense of inner restlessness ± repetitive movements

Manage: Change to atypical or slowly withdraw drug
Dyskinesia: Da antagonist
Akathisia: B-Blockers.

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143
Q

Define Dementia?

A

Chronically impaired cognition that affects multiple domains: memory, attention, language

  • No impairment of consciousness
  • Acquired and progressive
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144
Q

What are the most common types of dementia?

A

Alzheimer’s
Vascular
Lewy Body
Frontotemporal Dementia (Pick’s)

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145
Q

Summary of Alzheimer’s?

A

Epi: 50%
Path: neurofibrillary tangles and B amyloid plaques
PC: Progressive, global cognitive decline. Memory loss, loss of recent memory first. Misplacing items, apathy, decline in activities, personality change. IADLs.
RF: ApoE4, presenillin 1/2 mutation, Down’s
Ix: MRI - medial temporal lobe atrophy. MMSE, metabolic panel
Rx: cholinesterase inhibitor (Donepezil, rivastigmine) if MMSE is 10-20.

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146
Q

Summary of Vascular Dementia?

A

Epi: 20%
Path: multiple infarcts
PC: sudden onset, stepwise deterioration, patchy deficits, vascular RFs.
Ix: MRI - extensive infarcts or small vessel disease
Rx: Manage predisposing factors

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147
Q

Summary of Lewy Body Dementia

A

Epi: 20%
Path: Lewy body in occipito-parital cortex.
PC: Fluctuating cognitive dysfunction, recurrent visual hallucinations, REM sleep behaviour disorder. MAy have a symptom of parkinson’s. Distinguished from parkinson’s in the onset of dementia first.
Rx: Minise antipsychotics, use cholinesterase inhibitors - donepezil/rivastigmine.

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148
Q

Summary of Frontotemporal Dementia (Pick’s)

A

<5%

  • Path: Pick bodies
  • PC: Disinhibition, personality change, early memory preservation, progressive aphasia
  • Ix: MRI - frontal or temporal atrophy
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149
Q

What are the ameliorable causes of dementia?

A

Infection

  • viral: HIV, HSV, PML
  • Helminth: cysticercosis, toxi

Vascular
- Chronic subdural haematoma

Inflammation

  • SLE
  • Sarcoid

Neoplasia

Nutrition

  • Thiamine deficiency
  • B12 and folate deficiency
  • Pellagra (B3/niacin deficiency)

Endocrinology

  • hypothyroidism
  • Hypoadrenalism
  • Hypocalcaemia
  • Hypocephalus (normal pressure)
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150
Q

What is the definition of delirium?

A

Globally impaired cognition and impaired consciousness

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151
Q

Features of delirium?

A
  • Disorientation of person, time and place
  • Reversal of sleep-wake cycle (hyperactive at night)
  • Labile mood
  • illusions, delusions and hallucinations
  • Cognitive impairment: memory, language, concentration
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152
Q

What are the causes of Delirium?

A

DELIRIUMS

  • Drugs : opiods, sedatives, L-DOPA
  • Eyes, ears and other sensory deficit
  • Low O2 states: MI, stroke, PE
  • Infection: UTI
  • Retention: stool or urine
  • Ictal
  • under-hydration/nutrition
  • Metabolic: DM, post-op, sodium, uraemia
  • Subdural haemorrhage or other intracranial pathology
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153
Q

Investigations for delirium

A
  • Bloods: FBC, U+E, LFTs, glucose, ABG
  • Urine Dip
  • Septic Screen
  • ECG, LP

Confusion screen = B12/folate, macrocytic anaemia and deficiencies worsen confusion.

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154
Q

Management of delirium

A

ID and Rx underlying cause
Surround with familiar people
Nurse in moderately lit, quiet room
Find glasses, hearing aids
Avoid sedatives if possible, but if disruptive:
- Haloperidol 0.5-2mg
- Chlorpromazine 50-100mg PO/IM (avoid in elderly)

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155
Q

What are the differentials for an acute headache?

A

Common

  • Acute sinusitis
  • Otitis media
  • Menstrual headache
  • Medication withdrawal/overuse
  • Migraine
  • Tension headache
  • Cerebrovascular incident
ACUTE: Vicious 
- Vascular 
Haemorrhage: SAH, intracranial, intracerebral, intraventricular
Infarction: esp. posterior circulation
Venous: Sinus/cortical thrombosis
- Infection/Inflammation
Meningitis
Encephalitis
Abscess
trigeminal neuralgia
  • Compression
    Obstructive hydrocephalus:tumour
    Pituitary enlargement: apoplexy

ICP
- Spontaneous intracranial hypotension
Acute dural CSF leak
Worse on standing initially

Ophthalmic
- Acute Glaucoma

Unknown

  • Situational: cough, exertion, coitus.
  • medication overuse/withdrawal
  • Dental caries/wisdom tooth

Systemic

  • HTN: Phaeo, PET
  • Infection: sinusitis, tonsillitis, atypical pneumonia
  • Toxins: CO
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156
Q

Chronic headache?

A
MCD TINGS 
- Migraine
- Cluster Headache 
- Drugs 
Analgesics
Caffeine 
Vasodilators: Ca2+ antagonists, nitrates

Tension headaches

ICP increased/decreased

  • Increased: tumour, aneurysm, AVM, benign intracranial HTn
  • Decreased: Spontaneous intracranial hypotension

Trigeminal Neuralgia

GCA

Systemic

  • HTN
  • Organ failure e.g uraemia
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157
Q

What are the investigations for headache?

A
  • Bloods
  • Urine
  • Micro
    Blood cultures
    Serology: enterovirus (common cause if viral meningitis), HSV, HIV, Syphilis, crypto
  • CSF
  • Radiology
  • Non-contrast CT
    SAH: blood in sulci, cisterns (white). 90% sensitivity in first 24hr
  • MRI: MRA - aneurysm
  • MRV: sinus thrombosis
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158
Q

CSF opening pressure for headaches?

A

Opening pressure (normal = 5-20cm H20):

  • increased: SAH, meningitis
  • decreased: spontaneous intracranial hypotension
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159
Q

What is xanthochromia?

A

Yellow appearance of CSF due to bilirubin. Detected by spectrophotometry. Can show evidence of a subarachnoid haemorrhage.

If no answer here then cerebral angiography.

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160
Q

Bacteria on CSF?

A
Appearance - Turbid 
Cells - PMN
Count - 100-1000
Glucose - decreased (<1/2 plasma) 
Protein - Increased x2 (>1.5)
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161
Q

TB on CSF?

A
Appearance - fibrin web
Cells - lympho/mononuc
Count - 10-1000
Glucose - Decreased (<1/2 plasma) 
Protein - Very very high (X3)
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162
Q

Viral of CSF?

A
Appearance - Clear
Cells - Lympho-mononuclear
Count - 50-1000
Glucose - >1/2 plasma
Protein - mild increased (<1)
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163
Q

Summary of subarachnoid headache?

A
  • Sudden onset, worse ever, occipital headache

- Meningism, focal signs, decreased consciousness

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164
Q

Summary of Venous sinus thrombosis?

A

Rapid onset of symptoms
Unilateral.
Can be septic or aseptic (trauma, prothrombotic feature)
Can have fever, ptosis, reduced corneal reflex, retinal-vein dilatation.

Sagittal: headache, vomiting, seizures, decreased vision, papilloedema

Transverse: headache ± mastoid pain, focal CNS signs, seizure, papilloedema

Need a contrast enhanced high res CT of head.
Contrast-enhanced MRI of head
Blood cultures
Factor V Leiden

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165
Q

Summary of Meningitis

A
  • Fever, photophobia, neck stiffness, Kernig’s +ve
  • Purpuric rash
  • Decreased consciousness
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166
Q

Summary of Encephalitis?

A
  • Fever
  • Odd behaviour/confused
  • fits
  • focal neurology (complicated by temporal lobe may give motionless stare or confusion)
  • Decreased consciousness

Investigation
CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz

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167
Q

Summary of acute glaucoma?

A
  • Constant unilateral eye pain, radiating to forehead
  • Decreased acuity, haloes, n/v
  • Red eye, cloudy cornea
  • Dilated non-responsive pupil
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168
Q

Summary of tension headache?

A
  • Bilateral/vertex-bitemporal

- Non-pulsatile, bandlike headache.

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169
Q

What is a cortical vein thrombosis?

A
  • Thunderclap headache
  • Stroke-like focal symptoms over days
  • Focal seizures are common
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170
Q

Migraine headache?

A

Prodrome –> aura –> headache

  • Unilateral, throbbing
  • n/v phono/photophobia
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171
Q

Cluster headache?

A

Alcohol may trigger an attack. Occurs in smokers.

  • Rapid onset very severe pain around/behind eye
  • Red, watery eye, nasal congestion
  • Miosis, ptosis
  • Attacks last 15mins -3hrs, 1-2x a day.
  • Mostly nocturnal
  • Clusters last 4-12 weeks, remission lasts 3months - 3yrs.

Management: 100% O2 via non-rebreathe mask, sumitriptan

Prevention: verapamil, topiramate, Li.

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172
Q

What is miosis?

A

Constriction of eye

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173
Q

What is ptosis

A

Dropping of eyelid

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174
Q

What is mydriasis

A

Dilation of the pupil of eye

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175
Q

What is trigeminal neuralgia?

A

Paroxysms of unilateral intense stabbing pain in trigeminal distribution (usually V2/V3).

  • triggers: washing area, shaving, eating ,talking
  • Male >50yrs (refer if less than 50)
  • 2ndry in 14%: compression of CNV, MS, Zoster, Chiari malformation
  • Exclude 2nd cause by MRI

Management: carbamazepine, lamotrigine, gabapentin

Management surgery: microvascular decompression

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176
Q

Analgesia overuse?

A
  • Episodic headache becomes daily chronic headache

- Use OTC analgesia on 6 days/month max

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177
Q

ICP headache?

A

Increased ICP: worse in AM, stooping, visual problems (papilloedema), obese women
decreased ICP: worse sitting or standing

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178
Q

Red flags for headache?

A
  • Worse on lying down
  • Pain wakes patient up
  • Present when waking up
  • Unexplained weight loss
  • Focal neurological deficit
  • N/V
  • Seizures
  • Vomiting more than once with no cause
  • New neurological deficit
  • Reduction in conscious level
  • Valsalva (coughing or sneezing headache)
  • Progressive headache with fever)

2 or more red flag are present an urgent CT should be performed as the likelihood of a serious intracranial pathology is high.

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179
Q

TMJ dysfunction headache?

A

Preauricular pain on chewing
Associated with crepitus
Earache, headache

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180
Q

Giant Cell arteritis (>60 yrs, ESR >60, pred 60mg)

A
  • Unilateral temple/scalp pain and tenderness
  • Thickened, pulseless temporal artery
  • Jaw claudication
  • amaurosis fugax,
  • sudden blindness
  • Associated with PMR in 50%

Ix: ESR very high, platelets raised, ALP raised, HB reduced, temporal artery biopsy

Management

  • High dose prednisolone (60mg) for 5-7 days
  • guideed by symptoms and ESR
  • Give PPI + bisphosphonates
  • Prognosis: 2yr course then complete remission
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181
Q

What are the risk factors for migraine?

A
Family history 
High caffeine intake
Obesity
Female
Stress life event 
Lack of sleep
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182
Q

What is the pathophysiology of migraine?

A

Vascular: cerebrovascular constriction –> aura, dilatation –> headache

Brain: spreading cortical depression

Inflammation: activation of CN V nerve terminals in meninges and cerebral vessels

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183
Q

What are the triggers for migraines?

A
Chocolate
Cheese
OCP - contraindicated due to increased risk of stroke. 
Caffeine
Alcohol 
Anxiety
Travel
Exercise
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184
Q

Symptoms of a migraine?

A

Headache- Aura lasting 15-30 mins then unilateral, throbbing headache

  • Phono/photophobia
  • N/V
  • Allodynia (pain in response to touch etc)
  • Often premenstrual
  • Prodrome: precedes migraine by hrs - days
    Yawning
    Food cravings
    Changes in sleep, appetite, mood.
  • Aura: precedes migraine by mins + may persist
    Visual: distortion, lines, dots, zig-zags, scotoma. Hemianiopic disturbance - spreading scintillating scotoma.

Are fully reversible, develop over at least 5 mins, lasts 5-60 minutes.

hemianopia
Sensory: Paraesthesia (Fingers –> Face)
Motor: dysarthria, ataxia, ophthalmoplegia. May have a hemiplegia.
Speech: Dysphasia, paraphasia

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185
Q

How do you classify migraine?

A

Migraine with aura (classical migraine) - 25% of patients

Migraine without aura (common migraine)

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186
Q

What is the diagnostic criteria for migraine?

A
  • Typical aura + headache or
  • > 5 headaches lasting 4-72hrs with either N/v or photo/phonophobia + >2:
  • Unilateral
  • Pulsating
  • Interferes with normal life
  • Worsened by routine activity

During headache at least one of the following:

    1. nausea and/or vomiting
    1. photophobia and phonophobia
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187
Q

What is the differential for a migraine?

A
  • Cluster/tension headache
  • Cervical spondylosis
  • HTN
  • Intracranial pathology
  • Epilepsy
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188
Q

Acute Management of migraine?

A

Acute episode
NICE = oral triptan + NSAID/paracetamol
(diclofenac/aspirin) + M/D

2nd: Paracetamol + metoclopramide/domperidone
(metoclopramide can cause extrapyramidal SE)
3rd: Rizatriptan (CI: IHD, Uncontrolled HTN, SSRI)

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189
Q

Prophylactic management of migraine?

A

Avoid triggers
1st line: Propranolol, topiramate. Propranolol instead of topiramate in child bearing age.
2ns line: Valproate, pizotifen (increased weight) gabapentin

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190
Q

Causes of subarachnoid haemorrhage?

A
  • Rupture of saccular aneurysms (80%)
  • AVMs
  • Anticoagulants
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191
Q

Risk factors for SAH?

A
  • Smoking
  • HTN
  • ETOH
  • Bleeding diathesis
  • Mycotic aneurysms (SBE)
  • FH (close relatives have 3-5x isk)
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192
Q

What are the sites of berry aneurysms?

A
  • Junction of the posterior communicating with internal carotid artery
  • Anterior communicating with anterior cerebral artery
  • Middle cerebral artery bifurcation
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193
Q

Associations of berry aneurysms with other diseases?

A

Adult Polycystic kidneys
CoA
Ehler’s Danlos

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194
Q

Symptoms of SAH?

A
  • Sudden, severe occipital headache
  • Collapse
  • Meningism: neck stiffness, n/v, photophobia
  • Seizures
  • Drowsiness –> coma
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195
Q

Signs of a SAH?

A
  • Kernig’s +ve (flex hips, and knee at 90 degree, extension of knee causes back pain)
  • Retinal or subhyaloid haemorrhage
  • Focal neuro
    @presentation suggests aneurysm location
    Later deficits suggests complications
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196
Q

Sentinal headache

A

Around 6% of patients experience sentinel headache from a small warning bleed

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197
Q

Differential for SAH?

A

In primary care, 25% of those with thunderclap headache have SAH

  • 50-60% no cause found
  • Rest: Meningitis, intracerebral bleed, cortical vein thrombosis
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198
Q

Investigations for SAH?

A

Hyponatraemia is very common in these patients and sodium levels are usually closely monitored in the acute period.

CT
- Detects >90% of SAH within first 48hrs
Hyperdense areas in the basal cisterns, sulci + major fissures.

50% of patients have an abnormal ECG

LP

  • If CT -ve and no CIs >12hr after start of headache.
  • Xanthochromia due to breakdown of bilirubin
  • May have normal or raised opening pressure.

On LP = straw coloured, protein.

Refer to Neurosurg as soon as SAH is confirmed

Then confirm SAH with intracranial angiogram +/- digital subtraction angiogram

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199
Q

What is the management of an SAH?

A
  • Frequent neuro obs: pupils, GCS, BP
  • Maintain CPP: Keep SBP >160
  • CCB vasospasm prophylaxis: Nimodipine 60mg orally every 4hrs for 21 days.
  • Endovascular coiling (preferable to surgical clipping)

If young unruptured aneurysms >7mm, young patients benefit from surgery.

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200
Q

Complications of SAH?

A
  • Rebleeding in 20%
  • Cerebral ischaemia - Due to vasospasm
  • Hydrocephalus
    Due to blockage of arachnoid granulations. Suddenly become unresponsive.

May require ventricular or lumbar drain

  • hyponatraemia: common and don’t manage with fluid restriction SIADH
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201
Q

Define stroke?

A

Rapid onset, focal neurological deficit due to a vascular lesion lasting >24hr

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202
Q

Pathogenesis for a stroke?

A

Infarction due to ischaemia (80%) or intracerebral haemorrhage (20%)

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203
Q

Causes of an ischaemic stroke?

A

Atheroma (80%)

  • Large (MCA
  • Small vessel perforators (lacunar)

Embolism

  • Cardiac (30%) of strokes: AF, endocarditis, MI
  • Atherothromboembolism: from carotids
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204
Q

Causes of a haemorrhagic stroke?

A
  • Increased BP
  • Trauma
  • Aneurysm rupture
  • Anticoagulation
  • Thrombolysis
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205
Q

What are the rarer causes of stroke?

A
  • Watershed stroke: sudden decreased in BP (e.g sepsis)
  • Carotid artery dissection
  • Vasculitis: PAN, HIV
  • Cerebral vasospasm: 2ndry to SAH
  • Venous sinus thrombosis
  • Antiphospholipid syndrome, thrombophilia
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206
Q

Risk factors for stroke?

A
Hypertension!!!
Smoking 
DM 
Increased lipids
FH
Cardiac: AF, valve disease
Peripheral vascular disease
Previous histroy 
Ethnicity: Increased in blacks and asians 
Increased PCV/Hct
OCP
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207
Q

Investigations for HTN induced stroke?

A

retinopathy
nephropathy
Big heart of CXR

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208
Q

Investigations for cardiac emboli

A
  • ECG± 24hr tape: AF
  • Echo: mural thrombus,
  • hypokinesis, valve lesions, ASD, VSD (paradoxical emboli)
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209
Q

Investigations for carotid artery stenosis?

A

Doppler US ± Angio

Endarterectomy beneficial if >70% symptomatic stenosis

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210
Q

Bleeding and thrombotic tendency investigations?

A

‘Young’ Stroke blood test include thrombophilia and autoimmune screening - performed in those under 55

  • ANA, APL, ACL, Lupus anticoagulant, coagulation factors, ESR, homocysteine, syphilis.

Thrombophilia screen
Autoimmune
Thrombocytopenia

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211
Q

What is the classification of Stroke?

A

Oxford/Bamford Classification
- Based on clinical localisation of infarct
S = Syndrome: prior to imaging
I = Infarct: after imaging when atheroembolic infarct confirmed

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212
Q

In the Oxford/Bamford classification - what is a TACS?

A

Total Anterior Circulation Stroke (TACS)

  • Highest mortality + poor independence
  • Large infarct in carotid/MCa, ACA territory.

Has all 3 of

1) Hemiparesis (contralateral) and or sensory deficit (>2 of face, arm and leg)
2) Homonyzmous hemianopia (contralateral)
3) Higher cortical dysfunction
(dysphagia)

  • Dominant (L usually) dysphasia
  • Non-dominant: hemispatial neglect
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213
Q

In the Oxford/Bamford classification - what is a PACS?

A

Partial Anterior Circulation Stroke (PACS)

  • Carotid, MCA and ACA territory. Smaller arteries of anterior circulation (upper/lower division of middle cerebral artery)
  • 2/3 TACS criteria, usually:
    1) Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)
    2) Higher cortical dysfunction
  • Dominant: dysphasia
  • Non-dom: neglect, constructional apraxia

Deficit is less dense or incomplete.

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214
Q

In the Oxford/Bamford classification - what is a Posterior Circulation Stroke?

A
  • Infarct in the vertebrobasilar territory?
  • Any of
    1. Cerebellar syndrome
    2. Brainstem syndrome
    3. Contralateral homonymous hemianopia (to the damage). Therefore homonymous hemianopia is on the same side as the paresis.

Lesion in the superior cerebellar artery, PICA or AICA.

Presetns with vertical nystagmus, and ataxia.

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215
Q

In the Oxford/Bamford classification - what is a LACS (lacunar infarct stroke)

A

Presents with

    1. Unilateral weakness of face and arm, arm and leg or all three
      1. pure sensory stroke
      2. ataxic hemiparesis
Small infarct around the basal ganglia, internal capsule, thalamus and pons. 
- Absence of
Higher cortical dysfunction
Homonymous hemianopia
Drowsiness
Brainstem signs
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216
Q

What are the 5 syndromes of a LACS?

A
  • Pure motor: Post. limb of internal capsule (commonest)
  • Pure sensory: Posterior thalamus (VPL)
  • Mix sensorimotor: internal capsule
  • Dysarthria/clumsy hand
  • Ataxic hemiparesis: ant. limb of internal capsule - weakness + dysmetria
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217
Q

Other signs of ischaemic stroke?

A

Carotid bruit
AF
Past TIA
IHD

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218
Q

Other signs of haemorrhagic stroke?

A

Meningism
Severe headache
Coma

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219
Q

Brainstem infarcts - what are the signs for a corticospinal tract damage?

A

Hemi/quadrparesis

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220
Q

Brainstem infarcts - what are the signs for oculomotor system damage

A

Conjugate gaze palsy (difficulty in moving eyes in the same direction)

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221
Q

Brainstem infarcts - what are the signs for a Sympathetic fibres?

A

Horner’s

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222
Q

Brainstem infarcts - what are the signs for a CN7 infarct?

A

Facial weakness

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223
Q

Brainstem infarcts - what are the signs for a CN8 infarct?

A

Nystagmus, Vertigo

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224
Q

Brainstem infarcts - what are the signs for CN 9 and 10 infarct?

A

Dysphagia, dysarthria

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225
Q

Brainstem infarcts - what are the signs for cerebellar damage?

A

Dysarthria, ataxia

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226
Q

What is the acute management of a stroke? Step 1 = Resuscitate

A

Assessment - ROSIER. Exclude hypoglycaemia.
LOC = -1
Seizure activity = -1

New acute onset

  • Asymmetric facial weakness
  • Asymmetric arm weakness
  • Asymmetric leg weakness
  • Speech disturbance
  • Visual field defect

Investigations = Non-contrast CT head scan is first line.

ABCDE

Ensure patent airway: consider NGT
NBM until swallowing assessment by SALT
Don’t overhydrate: risk of cerebral oedema

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227
Q

What is the acute management of a stroke? Step 2 = Monitor

A
  • Glucose: 4-11mM: sliding scale if DM
  • BP: <185/110 (for thrombolysis)
  • Rx of HTN can –> decreased cerebral perfusion
  • Neuro obs
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228
Q

What is the acute management of a stroke? Imaging Step 3

A

Urgent CT/MRI
Diffusion-weight MRI is most sensitive for acute infarct. T2 weighted

CT will exclude primary haemorrhage (contraindicatons = seizure at onset of stroke, cancer, GI haemorrhage, active bleeding, pregnancy, oesophageal varicies, uncontrolled HTN >200)

Carotid Dopplers (>70% stenosis) - don't treat it because it's done. 
ECG and ECho 

24hr tape to identify AF.

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229
Q

What is the acute management of a stroke? Step 4 = Medical Management

A
  • Consider thrombolysis if 18-80 yr and <4.5hr since onset of symptoms
  • Alteplase (tPA)

Thrombectomy - pre-stroke status of <3 on Rankin scale. >5 on NIHSS.

OFfer thrombectomy within 6hrs + IV thrombolysis IF acute ischaemic stroke + occlusion of the proximal anterior circulation on CTA.

Offer thrombectomy ASAP between 6-24hr if confirmed occlusion of proximal anterior circulation and if there is a potential to salvage brain tissue shown on DW MRI.

Consider thrombectomy + IV thrombolysis as soon as possible for people last known to be well up to 24hrs.

+ CT 24hr post-thromboylsis to look for haemorrhage

+ ASAP Aspirin 24hr (300mg) once haemorrhagic stroke excluded ± PPI. If outside of the window give aspirin (Clopi is a more chronic drug).

Clopidogrel if aspirin sensitive.

VTE prophylaxis - heparin 5000 units every 12hrs.

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230
Q

What is the acute management of a stroke? Step 5 = Neurosurgical opinion if intracranial haemorrhage

A

May coil bleeding aneurysm
Decompressive hemicraniectomy for some forms of MCA infarction.

Stroke Unit

  • Specialist nursing and physio
  • Early mobilisation
  • DVT prophylaxis

Secondary prevention
Rehab

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231
Q

What is the primary prevention management of stroke?

A
  • Control RFs: HTN, increased lipids, DM, smoking, cardiac disease. Consider statin is cholesterol >3.5.
  • Consider life-long anticoagulation in AF (use CHADS2)
  • Carotid endarterectomy if symptomatic 70% stenosis
  • Exercise
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232
Q

What is the secondary prevention management of stroke?

A

Risk factor control as above - Start on a statin

  • Aspirin/Clopi 300mg for 2 weeks after stroke then either
  • Clopi 75 OD (preferred)
  • Aspirin 75mg OD

Warfarin instead of aspirin/clopi if

Cardioembolic stroke or chronic AF

  • Starts 2 weeks post-stroke (INR 2-3)
  • Don’t use aspirin and warfarin together. Switch to NOAC.

Carotid endarterecotmy if good recovery + ipsilateral stenosis >70%

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233
Q

What is the rehabilitation for stroke patients?

A

MDT: Physio, SALT, Dietician, OT, specialist nurses, neurologist, family

Eating

  • Screen swallowing: refer to specialist (consider PEG/NG)
  • Screen for malnutrition

Neurorehab: physio and speech therapy (Botulinum can help)

DVT prophylaxis

Sores must be avoided.

Occupational therapy

  • Impairment
  • Disability
  • Handicap

Chronic Risk management

  • AF start anticoagulation 10-14 days after stroke
  • HTN
  • Diabetes
  • Smoking

Carotid artery stenosis> Don’t forget carotid dopplers in investigations.

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234
Q

What is a TIA?

A
  • Sudden onset focal neurology lasting <24hr due to temporary occlusion of part of the cerebral circulation
    ~15% of 1st strokes are preceded by a TIA.
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235
Q

Symptoms of TIA?

A
  • Symptoms usually brief
  • Global events (syncope, dizziness) are not typical
  • Signs mimic those of CVA in the same arterial territory
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236
Q

Signs of Causes of TIA?

A
  • Carotid bruits
  • Increased BP
  • Heart murmur
  • AF
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237
Q

Causes of TIA?

A

Atherothromboembolism from carotids is main cause
Cardioembolism: post-MI, AF, Valve disease
Hyperviscosity: poylcythaemia, SCD, myeloma

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238
Q

Differentials for a TIA

A

Vascular: CVA, migraine, GCA
Epilepsy
Hyperventilation
Hypoglycaemia

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239
Q

Investigations for a TIA?

A
Blood glucose: <3.3 = hypo
U+E - Na, K, High Ca
FBC: usually normal
ECG: look for AF
CXR
Carotid doppler ± angiography
Consider diffusion weight MRI
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240
Q

Management of TIA - Antiplatelet?

A

In last 7 days = Make urgent assessment within 24hrs by stroke physician.

More than a week = refer to specialist assessment as soon as possible within 7 days.

Time to intervention is crucial
- Avoid driving for 1 month

ACAS
- Antiplatelet therapy =
Aspirin/clopi 300mg/d for 2 weeks then 75mg/d
Add dipyridamole MR to aspirin

  • Warfarin if cardiac emboli: AF, MI, MS
    After 2 weeks

The Royal College of Physicians have published National Clinical Guidelines for Stroke that recommend Carotid endarterectomy for carotid stenosis 50-99% by NASCET criteria, for patients with TIA. The most appropriate initial treatment would therefore be antiplatelet therapy, and a statin would also be indicated.

The National Stroke Guidelines suggest patients with suspected TIA who are at high risk of stroke (e.g. an ABCD2 score of 4 or above) should receive aspirin or clopidogrel (each as a 300 mg loading dose and 75 mg thereafter) and a statin, e.g. simvastatin 40 mg started immediately after specialist assessment and investigation within 24 hours of onset of symptoms.

Therefore she could be given either aspirin or clopidogrel 300mg (as a one-off dose) then to continue on either aspirin or clopidogrel long-term.

Give clopidogrel as first line (aspirin acutely), then aspirin and dipyridamole for patients who cannot tolerate clopidogrel. Give it lifelong.

Don’t give aspirin if patient has bleeding disorder, taking an anticoagulant, patient is already taking low-dose aspirin regularly. Aspirin is contraindicated.

A single TIA patients can start driving if symptom free for 1 month and there is no need for them to inform the DVLA.

If multiple TIA 3 months off driving and inform DVLA.

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241
Q

Management TIA - Cardiac Risk factor control

A

BP, lipids, DM Smoking
Exercise
Diet: decreased salt

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242
Q

Management TIA - Assess risk of subsequent stroke

A

ABCD2

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243
Q

Specialist referral to TIA clinic in how long if ABCD >4?

A

Within 24hr

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244
Q

Specialist referral to TIA clinic in how long if ABCD <4?

A

Within 1 week

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245
Q

What does ABCD2 Score stand for?

A
  • Age >60
  • BP >140/90
  • Clinical Features
    1. Unilateral weakness (2 points)
    2. Speech distubances w/o weakness
  • Duration
    >1hr = 2 points
    10-59 mins
  • DM
    NB: 7 points max
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246
Q

What is a subdural haemorrhage?

A
  • Bleeding from bridging veins between cortex and sinuses
  • Haematoma between dura and arachnoid
  • Often due to minor trauma that occured a long time previously - especially deceleration injuries.

Acute subdural

  • Collection of fresh blood within the subdural space and is most commonly caused by high-impact trauma.
  • CT shows cresentic collection, not limited by suture lines. Appear hyperdense in comparison to brain.

Chronic subdural haematoma

  • Collection of blood in the subdural space that has been present for weeks to months.
  • Elderly and alcoholic patients are particularly at risk. Taught bridging veins.
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247
Q

Risk factors for a subdural haemorrhage?

A

Elderly: brain atrophy
Falls: Epileptics, alcoholics
Anticoagulation

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248
Q

Symptoms for subdural haemorrhage?

A
  • Headache
  • Fluctuating GCS, sleepiness that can last for days.
  • Nausea/Vomiting
  • Gradual physical or mental slowing
  • Unsteadiness

SUBDURAL cannot cause meningeal irritation.

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249
Q

Signs for a subdural haemorrhage?

A
  • Increased ICP (can lead to tentorial herniation)

- Localising signs occur late

250
Q

Imaging for a subdural haemorrhage?

A

CT-non contrast. Convexity

  • Crescentic haematoma over one hemisphere
  • Clot goes from white –> Grey over time (hyperdense to hypodense)
  • Mid-line shift
  • Does not respect the suture lines.
251
Q

What is the management of a subdural haemorrhage?

A

Try ICP lowering techniques = bed to 30 degrees - reverse Trendelenberg. Hyperosmolar with hypertonic saline? Osmotic diuretics mannitol.

1st line: irrigation/evacuation via burr-hole craniostomy. Two holes made, clot is irrigated using saline.

2nd line: craniotomy/hemicraniectomy + duraplasty.
Address causes of trauma

252
Q

Differential for Subdural haemorrhage?

A

Stroke
Dementia
SOL

253
Q

Extradural Haemorrhage? What is it?

A
  • Often due to fracture of the temporal or parietal bone –> - Laceration of the middle meningeal artery and vein.
  • Blood between bone and dura.
  • Suspect if after head injury GCS falls, is slow to improve or there is a lucid interval.
254
Q

Presentation of an extradural haemorrhage?

A

Lucid Interval!

  • Deterioration of GCSe after head injury that caused no LOC, or following initial improvement in GCS
  • Lucid Interval may be hrs or days.

ICP increased:

  • Headache
  • Vomiting
  • Confusion –> coma
  • Fits
  • Ipsilateral blown pupil (3rd nerve palsy)
  • ± hemiparesis with upgoing plantars and increased reflexes.

Brainstem Compression
- Deep irregular breathing (brainstem compression)

  • Cushing response in response to increased IC Pressure.
  • increased BP - brain meets perfusion needs by increasing BP.
  • decreased HR is late.
  • Irregular breathing (Cheyne Stokes)
  • Death by cardioresp arrest.
255
Q

What imaging do you use for a extradural haematoma?

A

CT - will see a lens-shaped haematoma.
Skull # (increased risk of extradural haemorrhage).
- Limited by suture lines

256
Q

Management of extradural haemorrhage?

A
  • Neuroprotective ventilation (O2 >100, CO2 35-40)
  • Consider mannitol (1g/kg IV via central line)
  • Craniectomy for clot evacuation and vessel ligation
257
Q

Dural venous sinus thrombosis - when do symptoms generally come on?

A

Gradually over days/weeks.
Sinus thrombosis may extended to cortical veins.

Thrombus formation within the cavernous sinus.

258
Q

Sagittal sinus Intracranial venous thrombosis?

A
  • 45% of IVT
  • Often co-exists if other sinuses are thrombosed
  • Headache, vomiting, seizures, decreased vision, papilloedema.
  • Cushing’s reflex
259
Q

Transverse sinus - Intracranial venous thrombosis?

A
  • 35% of IVT

- Headache + mastoid pain, focal neuro, seizures, papilloedema.

260
Q

Sigmoid sinus - intracranial venous thrombosis?

A

Cerebellar signs, lower CN palsy

261
Q

Inferior Petrosal sinus?

A

5-6th nerve palsies (Gradenigo’s syndrome?)

262
Q

Cavernous sinus syndrome

A
  • Spread from facial pustules or folliculitis
  • Headache, chemosis, eyelid oedema, proptosis, painful ophthalmoplegia, fever.
  • Mostly caused cavernous sinus such as a nasopharyngeal malignancy.

Lateral wall components

  • Oculomotor nerve
  • Trochlear nerve
  • Ophthalmic nerve
  • Maxillary nerve
263
Q

Cortical Vein thrombosis?

A

Often –> venous infarcts with stroke-like focal symptoms that evolve over days
Thunderclap headache
Focal-seizures

264
Q

Differential for intracranial venous thrombosis ?

A
SAH
Meningitis
Encephalitis
Intracranial abscess
Arterial Stroke
265
Q

What are the common causes of IVT?

A
Pregnancy/puerperium
OCP
Head injury
Dehydration
Intracranial/extracranial malignancy
Thrombophilia
266
Q

Investigations for IVT?

A
  • Exclude SAH and meningitis
  • CT/MRI venography: Absence of a sinus/Contrast CT may show an enlarged sinus.
    LP: increased pressure, may show RBCs and xanthochromia?
267
Q

Management of IVT?

A
  • LMWH –> warfarin (INR 2-3).
  • Fibrinolytic (streptokinase) can be used via selective catheterisation
  • Thrombophilia screen
268
Q

What are the meningitic features?

A

Meningitic
- Headache

  • Neck Stiffness
    Kernig’s: Straightening leg with hip @ 90
    Brudzinski’s: lifting head –> Lifting of legs
  • Photophobia
  • N/V
269
Q

What are the neurological features of meningitis?

A

Decreased GCS –> Coma
Seizures (20%)
Focal neuro (20% ): E.g CN palsies

270
Q

What are the septic features of meningitis?

A
Fever 
Decreased BP, increased HR
Increased CRT 
Purpuric rash
DIC
271
Q

Causes of Meningitis?

A
  • Neisseria meningitidis (gram negative diplococci)
  • Strep Pneumo (gram positive diplococci) = 6-60yrs.

Listeria Monocytogenes (gram positive rod)
Haemophilus influenza (gram negative coccobacilli)
Group B strep
TB
Cryptococcus
Virus: Enterovirus (Coxsackie, echovirus), HSV2

0-3 months = GBS, E.coli, Listeria

3months - 6 yrs = Neisseria, Strep pneumonia, Haemophilus

6 yrs - 60 yrs = Neisseria meningitidis, Strep Pneumonia

> 60 = Strep pneumonia, neisseria meningitidis, listeria monocytogenes.

272
Q

Investigations for meningitis?

A

LP: MCS, glucose, virology/PCR, lactate/Gram stain.

Bloods: FBC, U+E, Clotting, Glucose, ABG

BLood cultures

273
Q

Abx Management of meningitis?

A

Community: benpen 1.2g IV/IM
<50: ceftriaxone/cefotaxime 2g IV/IM BD + vancomycin
>50: cetriaxone/cefotaxime + ampicillin (cover listeria)

If viral suspected: aciclovir.

274
Q

What is the acute management of meningitis?

A

ABC

  • O2 15L - SpO2 94-98%
  • IVI fluid resus with crystalloid

If mainly septicaemic

  • Don’t attempt LP
  • Ceftriaxone 2g IVI
  • Consider ITU if shocked.

If mainly meningitic

  • If no shock or CIs do LP
  • Dexamethasone 0.15mg/kg IV QDS
  • Ceftriaxone 2g IVI post-LP

For TB treat for 12 months.

275
Q

What is the continuing management of meningitis?

A

Ceftriaxone 2g BD IVI

  • Meningococcus: 7d IV then review
  • Pneumococcus: 14 d IV then review

Maintenance fluids

  • UO 30ml/h
  • SBP >80mm Hg

Rifampicin prophylaxis for household contacts
If response poor, consider !± inotropic support.

276
Q

CIs to LPs: Try LP Unless contraindicated

A
  • Thrombocytopenia
  • Pressure (signs of raised ICP)
  • Unstable (Cardio+ resp systems)
  • Coagulation disorder
  • Infection at LP site
  • Neurology (focal neurological signs)
277
Q

Encephalitis presentation?

A
  • Infectious prodrome: fever, rash, LNs, cold sores, conjunctivitis, meningeal signs.
  • Bizarre behaviour or personality change
  • Confusion
  • Decreased GCS –> coma
  • Fever
  • Headache
  • Focal neuro
  • Seizures
  • Hx of travel or animal bite
278
Q

Viral Causes of encephalitis?

A

Usually viral

  • HSV 1/2
  • CMV, EBV, VZV
  • Arbovirusues
  • HIV
279
Q

What are the bacterial causes of encephalitis?

A

Same as meningitis (Strep Pneumo, Neisseria Meningitides, Haemophilus Infuenza, GBS

TB
Malaria
Lyme Disease

280
Q

Investigations of encephalitis?

A
  • Blood: Cultures, viral PCR, malaria film, U+E (rickettsial), LFTs (coxiella, burnetii, rickettsia, tick-borne disase, cytomegalovirus)
  • Contrast CT: focal bilateral temporal involvement suggests HSV
  • LP: increased CSF protein, lymphocytes, PCR
  • EEG: shows diffuse abnormalities, may confirm ddx
281
Q

Management of encephalitis?

A
  • Aciclovir STAT: 10mg.kg/8h IVI over 1h for 14/7.
  • Supportive measures in HDU/ITU
  • Phenytoin for seizures

If CMV = ganciclovir
EBV = aciclovir, ganciclovir, cidofovir

282
Q

Without fever consider encephalopathy due to -

A
hypoglycemia 
Hepatic
DKA
Drugs
SLE
Uraemia
Hypoxic brain injury
Beri-Beri
283
Q

What is a cerebral abscess and what factors predispose to it?

A

Suppurative collection of microbes within a gliotic capsule occuring within the brain parenchyma.

Infection: ear, sinus, dental or peridontal 
Skull fracture
Congenital heart disease
Endocarditis
Bronchiectasis
Immunosuppression
284
Q

What organisms cause a cerebral abscess?

A
  • Frontal sinus/teeth: Streptocuccus pyogenes, Strep Milleri, Staph A, oropharyngal anaerobes
  • Ear: Bacteriodes, other anaerobes
285
Q

Signs for cerebral abscess?

A
Seizures
Fever
Localising signs
Signs of ICP
Signs of infection elsewhere

Common complication of sinusitis = unilateral facial oedema, photophobia, proptosis, palsies of the cranial nerves which pass through it.

286
Q

Investigations of Cerebral abscess?

A

CT/MRI: ring-enhancing lesion

Increased WCC, increaseD ESR

287
Q

Management of Cerebral Abscess?

A

Neurosurgical referral
Abx: e.g ceftriaxone
Treat increased ICP.

288
Q

What is the definition of epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizure.

289
Q

What are the causes of epilepsy/ Seizures?

A

2/3 are idiopathic - 2/3.
Mutations in the sodium/potassium channels.

Congenital

  • NF
  • Tuberous Sclerosis
  • TORCH
  • Perinatal anoxia

Acquired

  • Vascular: CVA
  • Cortical scarring: trauma, infection.
  • SOL
  • Other: SLE, PAN, MS, sarcoidosis

Non-epileptic/provoked seizures?

  • Withdrawal: ETOH, opiates, benzos
  • Metabolic: glucose, Na, Ca, Urea, NH3
  • increased ICP: trauma, haemorrhage, encephalitis, cycticerosis, HIV
  • Eclampsia
  • Pseudoseizures (pelvic thrusting, family member with epilepsy, common in females, crying after seizure, don’t occur when alone, gradual onset).

Phenomenon that can mimic true seizures but generally have findings which are not consistent with a seizure. The ability to control location of symptoms is very typical of pseudoseizures and does not fit with any other option.

290
Q

What is a seizure prodrome?

A
  • Prodrome: Pt or others may notice change in mood or behaviour lasting hrs-days.
  • Not part of seizures.
291
Q

What is a seizure aura?

A

A simple partial seizure (usually temporal) which may precede other manifestations

  • Experienced as strange feeling:
  • Epigastric rising
  • Deja/jamais vu
  • Automatism
  • Smells, lights, sounds
292
Q

What is a partial (focal) seizure?

A

Isolated to one hemisphere

293
Q

What is a primary generalised seizure?

A

No warning/aura

Discharge is seen through the cortex and no ascertainable localising features.

294
Q

What is a simple seizure?

A

Awareness is unimpaired

295
Q

What is a complex seizure

A

Awareness is impaired

296
Q

What is a secondary generalised seizure?

A

Focal seizure moving to generalised

Such as an aura moving towards a tonic clonic.

297
Q

What are the diagnostic pointers to epilepsy?

A
  • Aura
  • Specific trigger e.g flashing lights
  • Lateral tongue biting (>incontinence)
  • Typical movements e.g tonic-clonic
  • Cyanosis
  • Post-ictal phase
298
Q

What are the presenting features associated with epilepsy? / Types of epilepsy?

A
Simple partial
Complex partial 
Absence (petit mal) 
Tonic-Clonic
Myoclonic seizure
Atonic 
West Syndrome/Infantile spasms
299
Q

What is a simple partial seizure?

A

Focal motor, sensory, autonomic or psychic symptoms.

Can present with 2 mins of involuntary twitching movements in their right hand.
- Stereotyped movements and quick recovery is consistent with focal aware seizure.

300
Q

What is a complex partial seizure/Focal seizures with impaired awareness.

A

5As

Aura
Autonomic: change in skin colour, temperature, palpitations
Awareness loss: Motor arrest, motionless stare.
Automatisms: lip smacking, fumbling, chewing, swallowing
Amnesia

Usually arise from temporal lobe.

Emotional disturbance and automatism are features of focal seizures.

301
Q

What is an absence seizure?

A
Abrupt onset and offset
Short: <10s 
Eyes: glazed, blank-stare
Normal: intelligence, examination, brain-scan
Clonus or automatisms may occur
EEG: 3Hz spike and wave

Stimulated by hyperventilation and photics.

Doesnt involve motor aspects.

302
Q

What is a tonic-clonic seizure (Grand Mal)

A
  • LOC
  • Tonic: limbs stiffen
  • Clonic: rhythmic jerking of limbs
    ± cyanosis, incontinence, - tongue biting
  • Post-ictal confusion and drowsiness. Normally lasts a while.
303
Q

What is a myoclonic seizure?

A

Sudden jerk of limb, face or trunk

304
Q

what is a atonic seizure?

A

Sudden loss of muscle tone – fall

No LOC

305
Q

What is West Syndrome?

A

Clusters of head nodding and arm jerks

EEG shows hysarrhythrimia

306
Q

What are the localising features of epilepsy? Temporal lobe?

A

Temporal

  • Automatisms: lip smacking, chewing, fumbling
  • Deja vu
  • Delusional behaviour
  • Abdominal; rising or n/v
  • Emotional disturbance: terror, panic, anger, elation
  • Tastes, smell
307
Q

What are the localising symptoms of frontal lobe epilepsy?

A

Frontal
- Motor features: arrest, Jacksonian march) is a phenomenon where a simple partial seizure spreads from the distal part of the limb toward the ipsilateral face , -

Todd’s palsy (weakness if part of the body after a seizure). One part of the body after means Todd’s Paresis.

  • Head/leg movement
308
Q

What are the parietal symptoms of epilepsy?

A

Sensory disturbance: tingling, numbness

309
Q

What are the occipital features of epilepsy?

A

Visual phenomena: spots, lines, flashes.

310
Q

What are the general management principles for epilepsy?

A
  • After any seizure advise against driving, swimming etc until a Dx is established.
  • Following first seizure, patients must be seizure free for 6 months before they may reapply to the DVLA for their license to be reissued.
  • Formal diagnosis means seizure free for 12 months before they apply to DVLA.
  • For bus drivers - if 2 seizures must be seizure free for 10 yrs.
  • Don’t diagnose epilepsy from a single seizure
  • Diagnosis should be made by a specialist
  • After Dx, cannot drive until seizure-free for ?1yr
    10yr for HGV (no meds)
311
Q

What are the investigations for epilepsy?

A

Top investigations - EEG

  • Used to support Dx (cannot exclude or prove)
  • helps classification and prognosis (may show a generalised epileptiform activity or focal, localising abnormality).
  • Use with hyperventilation and photic stimulation

Other investigations

  • FBC, U+E, glucose
  • Se increased prolactin 10mins after fit (relative to baseline) - indicated a GTCS.
  • Se AED levels
  • Urine toxicology
  • ECG
312
Q

What imaging is used for epilepsy?

A
  • Consider CT head for structural lesions or other process that have caused the seizure.
  • MRI not routine for idiopathic generalised epilepsy
  • Indications
    = Developed epilepsy as an adult
    or any evidence of focal onset
    -Seizures continue despite 1st line Rx.
313
Q

What is the management of a tonic-clonic seizure?

A

1st: Valproate (should not be prescribed to female children or aolescents).
2nd: Lamotrigine, carbamazepine

314
Q

What is the management of an absence seizure?

A

1st: Valproate/Ethosuximide
2nd: Lamotrigine

315
Q

What is the management of tonic, atonic or myoclonic seizure?

A

1st: Valproate
2nd: Levetiracetam

316
Q

What is the management of focal ± 2nd gen?

A

1st: Lamotrigine/Carbamazepine
2nd: Levetiracetam, sodium valproate, oxcarbazepine.

317
Q

What epilepsy drugs should be avoided in pregnancy?

A

Avoid valproate: take lamotrigine or CBZ.

  • Ensure you give 5mg folic acid daily if child-bearing age.
  • CBZ and PHE are enzyme inducers and decrease the effectiveness of the OCP.
318
Q

What other management is there of epilepsy?

A

Following a first seizure, antiepileptic drug treatment should only be started before specialist review in exceptional circumstances.

Only start medication if:

  1. Seizure activity observed on EEG
  2. Presence of a neurological deficit
  3. Presence of a structural brain abnormality
  4. Patient, parent or carer considers the risk of a further seizure to be unacceptable
  • Neurosurgical resection can be an option if single epileptogenic focus is identified
  • Vagal nerve stimulation can decreased seizure frequency and severity in ~33%.

Driving - patients must contact the DVLA

  • Can drive again after one year of being seizures-free
  • If a patient has only had a single seizure: Six months if investigations normal.

Contraception
Pregnancy: valproate. Women considering should take regular folate

Safety measures - patients should not bathe or swim

319
Q

Which epilepsy drugs are enzyme inducers?

A

Carbamazepine
Phenytoin
Barbiturates

320
Q

Which epilepsy drugs are enzyme inhibitors?

A

Valproate

321
Q

What are the side-effects of lamotrigine?

A
  • Skin rash –> SJS occurs within 8 weeks. Prodromal illness which resembles a viral URTI. Rapid onset of a painful red skin rash which starts on the trunks and extends abruptly onto the face and limbs. Does not affect scalp, palms or soles.
    Fluid replacement.
  • Rash may be associated with hypersensitivity –> fever, increased LFTs and DIC.
  • Diplopia, blurred vision
  • Levels affected by enzyme inhibitors/inducers
322
Q

What are the side-effects of valproate?

A

VALPROATE

Vomiting.
Alopecia.
Liver toxicity.
Pancreatitis/ Pancytopenia.
Retention of fats (weight gain)
Oedema (peripheral)
Anorexia.
Tremor
Enzyme Inhibitor
323
Q

What are the side-effects of carbamazepine?

A

Leukopenia
Skin reactions
Diplopia, blurred vision
SIADH –> hyponatraemia

324
Q

What are the side effects of phenytoin?

A
PHENYTOIN:
P: P-450 interactions
H: Hirsutism
E: Enlarged gums
N: Nystagmus
Y: Yellow-browning of skin
T: Teratogenicity
O: Osteomalacia
I: Interference with folic acid absorption (hence anemia)
N: Neuropathies: vertigo, ataxia, headache

Trough levels, immediately before dose should be checked if

  • adjustment of phenytoin dose
  • Suspected toxicity
  • Detection of non-adherence to prescribed medication.
325
Q

What is Status epilepticus?

A

Generalised convulsive and non-convulsive status epilepticus are neurological and medical emergencies defined as 5 or more minutes of either continuous seizure activity or repetitive seizures with no intervening recovery of consciousness.

326
Q

Investigations of Status epilepticus?

A

BM
Bloods: Glucose, ABG, U+E, FBC, Ca2+
ECG, EEG
Consider: AED levels, tox screen, LP, B-HCG, CT.

Rule out hypoxia and hypoglycaemia before thinking of other causes.
Use the ABCDE approach.

327
Q

What drugs are used in status epilepticus?

A
Lorazepam 
- 2-4mg IV bolus over 30s
- 2nd dose if no response within 2 mins
- Alternatives 
Diazepam 10mg IV/PR (2mg max) 
Midazolam 10mg buccal

If the following does not help

  • May need phenytoin
  • 20mg/kg IVI @ 50mg/min
  • 100mg/6-8hr maintenance
  • Monitor ECG and BP
  • CI: bradycardia or heart block
328
Q

Acute management of status epilepticus?

A

Airway - Oral/nasal airway, intubate/ Suction
Breathing: 100% oxygen
Check capillary glucose.

Gain IV access and take bloods

  • U+E, LFTs, FBC, Glucose, Ca2+
  • AED levels
  • Tox screen

Reverse potential causes

  • Thiamine 250mg IV if ETOH
  • 100ml 20% glucose unless glucose known to be normal

Then start slow IV bolus phase

  • Lorazepam IV
  • IM Midazolam/ Buccal (10mg)
  • Rectal Diazepam (10mg)

Second dose if no response within 2 mins

Then

  • Phenytoin 18mg/kg IV (then 100mg/6-8hr)
  • Diazepam 100mg in 500ml 5% dex IVI
  • Phenobarbital if already on regular phenytoin.

Remember to use cardiac monitoring when using phenytoin.

RSI phase - Rapid sequence induction of anaesthesia.

  • never spend >20 mins with someone in status w/o getting an anaesthetist.
  • Propofol/thiopental
329
Q

What is the initial management of a head injury? in the primary survey ?

A

Primary survey

  • A: Intubation, immobilisation, C-spine
  • B: 100% O2, RR
  • C: IV access, BP, HR
  • D: GCS, pupils

If patient has a GCS less than 8, need immediate review by anaesthetist due to risk of unsecure airway.

Treat seizures
Lorazepam 2-4mg IV
Phenytoin 18mg/kg IVI then 100mg/6-8hr.

E: exposure patient and look for other obvious injuries

330
Q

What is the secondary survey management of a patient with head injury?

A
Look for: 
Lacerations
- Obvious facial/skull deformity
- CSF leak from nose or eats
- Battle's sign, Racoon eyes
- Blood behind TM
- C-spine tenderness ± deformities 

To test for CSF - check glucose.

Gold standard for CSF is Beta-2-transferrin.

Head-to-toe examination for other injuries
Fundoscopy
Log roll

331
Q

What do you ask in a history of head injury?

A

How + when
GCS and other vitals immediately after injury
Headache, fits, vomiting, amnesia, ETOH.

332
Q

Investigations for head injury?

A

Bloods: FBC (for required blood products) , U+E, glucose, clotting (coagulopathy) , ETOH, ABG (if not breathing),
CT head + c-spine. Non-contrast CT - to detect midline shift, subarachnoid haemorrhage.

MRI if not clear - immediate CT indicated in all patients with TBI.

333
Q

Management of head injury?

A
  • Neurosurgical opinion if signs of increased ICP, CT evidence of intracranial bleed significant skull #.

Admit if

  • Abnormalities on imaging
  • Difficulty to assess: ETOH, post-ictal
  • Not returned to GCS 15 after imaging
  • CNS signs: vomiting, severe headache

Neuro-obs half-hrly until GCS 15

  • GCS
  • Pupils
  • HR/BP
  • RR/SpO2
  • Temperature
334
Q

What discharge advice do you give someone with a head injury?

A
- Stay with someone for first 48hr
Give advice card advising to return on: 
- Confusion, drowsiness, unconsciousness
- Visual problems
- Weakness
- Deafness
- V.painful headache that won't go away
- Vomiting 
- Fit
335
Q

When do you intubate someone with a head injury?

A
  • GCS <8
  • PaO2 <9kPA on air/ <13 kPA on O2 or PCOs >6
  • Spontaneous hyperventilation: PCO2 <4kPa
  • Respiratory irregularity
336
Q

CT head guidelines for head injury?

A

CT immediately

Break: Open, depressed or base of skull
Amnesia >30 mins retrograde
Neuro deficit or seizure
GCS: <13 @ any time or <15 2hr after injury
Sickness: vomited > once

Within 8hrs.

LOC or any amnesia and any of:

  • Dangerous mechanism: RTA, great height
  • Age >65
  • Coagulopathy (inc warfarin).
337
Q

Risk of intracranial haematoma in adults?

A

Fully conscious with no fracture = <1:1000

Confused with skull fracture = 1:4

338
Q

GCS score for eyes?

A

Out of 4

Eyes: 4
4 – Spontaneous eye opening 
3 – Open to voice
2 – Open to pain
1 – No opening
339
Q

GCS score for verbal?

A

Out of 5

Verbal: 5
5 – Orientated conversation 
4 – Confused conversation
3 – Inappropriate speech
2 – Incomprehensible sounds 
1 – No speech
340
Q

GCS score for motor?

A

Motor: 6

6 – Obeys commands
5 – Localises pain
4 – Withdraws to pain
3 – Decorticate posturing to pain (flexor)
2 – Decerebrate posturing to pain (extensor)
1 – No movement

341
Q

What is the presentation of a space occupying lesion?

A

Increased ICP

  • Headache: worse on walking, lying down, bending forward, coughing, straining
  • Vomiting
  • Papilloedema
  • decreased GCS

Seizure
- Exclude SOL in adult-onset seizures, especially with localising aura or post-ictal weakness (Todd’s).

Evolving focal neurology
- May be false-localising (esp. CN6 palsy)

Subtle personality change

342
Q

What are the causes of SOL?

A
  • Vascular: chronic subdural haematoma, AVM, Aneurysm
  • Infection: abscess, cyst (cysticercosis)
  • Neoplasm: primary or secondary
  • Granuloma: TB, sarcoid
343
Q

What types of tumour cause SOL?

A

30% are metastatic: breast, lung, melanoma, colorectal.

AStrocytoma

Glioblastoma multiforme
- Glioblastoma is the most common primary tumour in adults and is associated with a poor prognosis (~ 1yr).

  • On imaging they are solid tumours with central necrosis and a rim that enhances with contrast. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema.
  • Histology: Pleomorphic tumour cells border necrotic areas
  • Treatment is surgical with postoperative chemotherapy and/or radiotherapy. Dexamethasone is used to treat the oedema.
  • Ependymoma
  • Commonly seen in the 4th ventricle
  • May cause hydrocephalus
  • Histology: perivascular pseudorosettes

Meningioma

The second most common primary brain tumour in adults

  • Meningiomas are typically benign, extrinsic tumours of the central nervous system. They arise from the dura mater of the meninges and cause symptoms by compression rather than invasion.
  • They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base.
  • Histology: Spindle cells in concentric whorls and calcified psammoma bodies
  • Investigation is with CT (will show contrast enhancement) and MRI, and treatment will involve either observation, radiotherapy or surgical resection.

Cerebellar haemangioblastoma

Vascular tumour of the cerebellum
• Associated with von Hippel-Lindau syndrome
• Histology: foam cells and high vascularity

CNS lymphoma

344
Q

Investigations for SOL?

A
  • CT or MRI (for better post.cranial fossa)

- Consider biopsy

345
Q

What is idiopathic intracranial HTN?

A
  • A syndrome of reduced cerebrospinal fluid absorption

Risk factors = Obesity, female, pregnancy, drugs (OCP, steroids, tetracycline, Vit A, Lithium).

346
Q

Presentation of idiopathic intracranial hypertension?

A
Typically obese females
As if SOL 
- Increased ICP
- Headache
- Papilloedema

Visual

  • Blurred vision
  • 6th nerve palsy
  • Enlarged blind spot
347
Q

Investigations of IIH?

A

High opening pressure on Lumbar puncture

Visual field defects testing - looking for enlarged blind spot, inferonasal loss, other nerve fibre bundle.

348
Q

Management of IIH?

A
  • Weight loss
  • 1st line: Acetazolamide = carbonic anhydrase inhibitor
  • Topiramate
  • Lumbar-peritoneal shunt may be necessary if drugs fail and visual loss deteriorates.

NB - if it is cerebral oedema = give DEX.

349
Q

What are the types of cerebral oedema?

A
  1. Vasogenic (increased cap permeability): trauma, tumour, ischaemia, infection.
  2. Cytotoxic: from hypoxia
  3. Interstitial: e.g obstructive hydrocephalus, decreased Na.
350
Q

What are the causes of a raised ICP?

A
  • Haemorrhage
  • Tumours
  • Infection: meningitis, encephalitis, abscess
  • Hydrocephalus
  • Status
  • Cerebral oedema
351
Q

Signs and symptoms of raised ICP?

A
  • Headache
  • N/V
  • Seizures
  • Drowsiness –> coma
  • Cushing reflex –> increased HR, decreased BP, irregular breathing.
  • 6th CN palsy (may be false localising)
  • Cheyne-Stokes respiration (longer, deeper breathing, followed by apnoeic episodes).
  • Pupils: miosis –> mydriasis
  • Papilloedema, loss of venous - pulsation @ disc.
352
Q

Acute management of raised ICP?

A
ABC 
- Then treat seizure and correct HTN
- Elevate bed to 40 degrees
- Neuroprotective ventilation 
PaO2 >13 
PCO2 4.5 
Good sedation ± NM blockade
- Mannitol or hypertonic saline. Start first then give Burr Hole.
- Decreased ICP short-term but may lead to rebound increased ICP later. 
Mannitol 1g/kg (20% @ 5ml/kg).
353
Q

What are the herniation syndromes?

A

Tonsillar
Transtentorial
Subfalcine

354
Q

What is a tonsillar hernia (coning)

A

Increased pressure in posterior fossa –> displacement of cerebellar tonsils through foramen magnum
–> compression of brainstem and cardioresp centres in medulla
CN6 palsy, upgoing plantars –> irregular breathing –> apnoea

355
Q

Transtentorial/ Uncal Herniation syndrome?

A
  • Lateral supratentorial mass –> compression of ipsilateral inferomedial temporal lobe (uncas) against free margin of tentorium cerebelli.
  • Ipsilateral CN3 palsy: mydriasis (dilation) then down and out. Parasympathetic fibres of CN3 nerve are arranged around the outside, they are damaged first, leaving a tonic sympathetic input, creating a dilated and fixed pupil.
  • Ipsilateral corticospinal tract: contralateral hemiparesis
  • May –> compression of contralateral corticospinal tracts –> Ipsilateral hemiparesis.
356
Q

Subfalcine herniation?

A
  • Frontal mass
  • Displacement of cingulate gyrus (medial frontal lobe) under falx cerebri
  • Compression of ACA –> Stroke
  • Contralateral motor/sensory loss in legs>arms
    Abulia (pathological laziness)
357
Q

What are the causes of Parkinsonism?

A
  • Parkinson’s disease
  • Parkinson’s Plus syndrome (basal ganglia degeneration + other symptoms)
  • MSA/Shy Drager
  • Progressive supranuclear palsy
  • Corticobasilar degeneration
  • Lewy body dementia
358
Q

What other conditions can cause parkinsonism

A
Infection: Syphilis, HIV, CJD
Vascular: Multiple infarcts in SN
Drugs: Antipsychotics, metoclopramide
Trauma: Dementia pugilistica
Genetic: Wilson's

Drug induced parkinson’s = Symmetrical tremor is rarely caused by idiopathic Parkinson’s disease.

359
Q

What are the symptoms of MSA?

A
  • Autonomic dysfunction: postural hypotension, bladder dysfunction
  • Cerebellar + pyramidal signs
  • Unilateral symptoms
  • Rigidity > Tremor
  • Severe/early onset autonomic dysfunction (postural hypotension/erectile dysfunction)
360
Q

What are the symptoms of progressive supranuclear palsy?

A

Postural instability –> falls
Speech disturbance (+ dementia)
Palsy: vertical gaze

361
Q

What are the symptoms of corticobasilar degeneration?

A
  • Aphasia, dysarthria, apraxia
  • Akinetic rigidity in one limb
  • Asterognosis (cortical sensory loss)
  • Alien limb phenomenon
362
Q

Lewy body dementia:

A

Fluctuating cognition

Visual hallucinations

363
Q

General symptoms of parkinsonism?

A

Tremor

  • Worse at rest
  • Exacerbated by distraction
  • 4-6Hz, pill rolling
  • Unilateral resting tremor with bradykinesia.

Rigidity

  • Increased tone in all muscle groups: lead-pipe rigidity
  • Rigidity + tremor –> cogwheel rigidity

Bradykinesia

  • Slow initiation of movement with reduction of amplitude on repetition
  • Expressionless face
  • Monotonous voice
  • Micrographia

Gait

  • Decreased arm swing
  • Festinance (Shortened stride quickened gait)
  • Freezing (esp in doorways
364
Q

Parkinson’s Disease epidemiology?

A

Mean onset 65 yrs

2% prevalence

365
Q

Pathophysiology of Parkinson’s Disease?

A

Destruction of dopamingeric neurons in pars compacta of substantia nigra?

  • alpha synuclein
  • Lewy bodies
366
Q

What are the features of PD?

A

Asymmetric onst: side of onset remains worse

  • Resting Tremor: increased by stress, decreased by sleep.
  • Rigidity: lead-pipe, cogwheel
  • Bradykinesia: slow initiation, difficulty with repetitive movement, micrographia, monotonous voice, mask-like face.
  • Postural instability: stooped gait with festingation
  • Postural hypotension + Other autonomic dysfunction
  • Sleep disorder: insomnia, excessive daytime sleeping, OSA, RBD
  • Psychosis: esp visual hallucination
  • Depression/Dementia.
367
Q

What are the sleep disorders associated with PD?

A

Affects ~90% of PD patients

  • Insomnia + frequent waking –> excessive daytime sleeping. Inability to turn, restless legs, early morning dystonia, nocturia, OSA.
  • REM Behavior sleep disorder
    Loss of muscle atonia during REM sleep
    Violent enactment of dreams

Da SEs: insomnia, drowsiness, excessive daytime sleeping

368
Q

What are the autonomic dysfunctions associated with PD?

A
  • Combined effects of drugs and neurodegeneration
  • Postural hypotension
  • Constipation
  • Hypersalivation –> Dribbling (decreased ability to swallow saliva)
  • Urgency, frequency, nocturia
  • ED
  • Hyperhidrosis (excessive sweating)
369
Q

What are the side effects of L-Dopa?

A

DOPAMINE

  • Dyskinesia
  • On-Off phenomena = mototr fluctuations
  • Psychosis
  • Decreased ABP
  • Mouth dryness
  • Insomnia
  • N/V
  • EDS (excessive daytime sleeping)
370
Q

Motor fluctuations in Parkinson’s caused by?

A

End-of dose: deterioration as dose wears off with progressively shorter benefit

On-Off effect: unpredictable fluctuations in motor performance unrelated to timing of dose.

371
Q

Investigations for Parkinson’s Disease?

A
  • Dopaminergic agent trial
    Mainly diagnosis is made clinically.
  • Consider MRI brain (mostly normal. May show mild small vessel disease.
  • DaTscan
    Bins to dopamingeric neurons and allows visualisation of substantial nigra.
372
Q

General Management of Parkinson’s disease?

A

MDT: neurologist, PD nurse, physio, OT, social worker , GP and carers.
Assess disability
- UPDRS: unified Parkinson’s Disease Rating Scale. - FALLS assessment
- Physiotherapy: postural exercises
- Depression screening.

Medications

  • Ensure regular medication review to anticipate any difficulties, non-concordance, polypharmacy.
  • Risk of acute akinesia or neuroleptic malignant syndrome if medication is not taken/absorbed (gastroenteritis).
  • Advise against giving patients a drug holiday.
  • Avoid dopamine antagonist like Haloperidol.
  • Impulse control disorder more common with dopamine agonist therapy, history of previous impulsive behaviours.
  • Orthostatic hypotension - develops review potential causes. Use Midodrine.
  • Glycopyrronium bromide for drooling.
  • If nauseous - prescribe domperidone - does not cross BBB.
373
Q

What is the medical management of Parkinson’s Disease?

A

If GP suspects signs - refer urgently to neurology. Medications is handled by a specialist - and requires careful titration to maximise effect.

If young and motor symptoms affecting quality of life
1. Levodopa. If they cannot take levodopa orally, given a dopamine agonist patch to rescue and prevent acute dystonia.

If young motor symptoms not affecting quality of life
1. Da agonists: Ropinirole, pramipexole, or levodopa, monoamine oxidase B (MAO-B) inhibitor.

Drugs

  • Da agonist: ropinirole, pramipexole
  • MOA-B inhibitors: rasagiline, selegiline
  • L-Dopa: co-careldopa or co-beneldopa.

Complications

  • Falls, cognitive impairment, depression.
  • SE of medications.
374
Q

What are the special points to consider with Levodopa?

A

More improvement in motor symptoms. More improvement in ADLs.

BUT more motor complications

Fewer specified adverse events.

Usually combined with a decarboxylase inhibitor (carbidopa) to prevent peripheral metabolism of levodopa to dopamine (Sinemet, Medapar)

  • reduced effectiveness with time
  • Unwanted effects: dyskinesia, on-off effect, dry mouth, postural hypotension, psychosis. Normally at a higher dose.
  • No use in neuroleptic induced parkinsonism
  • It is important not to acutely stop levodopa. Can be given a dopamine agonist patch as rescue medication to prevent acute dystonia.
375
Q

Dopamine receptor agonists?

A

Less improvement in motor symptoms, less improvement in ADLs, fewer motor complications, and more specific adverse effects such as hallucinations.

Ropinirole, apomorphine (non-ergot)
Bromocriptine, cabergoline (ergot derived) associated with pulmonary, retroperitoneal and cardiac fibrosis.

Must do a echo, ESR, creatinine + chest x-ray. More likely than levodopa to cause hallucinations in older patients.

  • Can also cause nasal congestion + postural hypotension.
376
Q

What are the MAO-B inhibitors?

A

MAO-B = less improvement in motor symptoms, less improvement in ADLs, fewer motor complications, fewer adverse events.

  • Selegiline
  • Inhibits the breakdown of dopamine secreted by the dopaminergic neurons.
377
Q

What is amantadine in PD?

A

Mechanism not understood. Increases dopamine release + inhibits uptake from dopaminergic synapses.
- side effects include ataxia, slurred speech, confusion, dizziness, livido reticularis.

Management of drug induced dyskinesias

378
Q

COMT inhibitors in PD?

A

Entacapone, tolcapone

- COMT is an enzyme involved in the breakdown of dopamine + used as an adjunct to levodopa

379
Q

Antimuscarinics in PD?

A
  • Block cholinergic receptors
  • Now used more to treat drug-induced parkinsonism rather than idiopathic.

Help tremor and rigidity
- Procyclidine, benzotropine

380
Q

Differential for parkinson’s?

A
Parkinson's plus syndrome 
Multiple infarct
Drugs: neuroleptics
 Inherited: Wilsons 
Infection: HIV, Syphilis, CJD
Dementia pugilistica.
381
Q

What is multiple sclerosis?

A

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

382
Q

Epidemiology of MS?

A

Common: 1/1000
Age: Mean @ onset = 30 yrs
Sex: F>M = 3:1
Race: rare in blacks

383
Q

Aetiology of MS?

A

Genetic (HLA-DRB1), environmental, viral?

384
Q

What is the pathophysiology of MS?

A

CD4 cell-mediated destruction of oligodendrocytes –> Demyelination and eventual neuronal death

  • Initial viral inflammation primes humoral AB responses vs MBP
  • Plaques of demyelination are hallmark.
385
Q

Classification of MS?

A

Relapsing-remitting: 80% - acute attacks followed by periods of remission.

Secondary Progressive (RR patients who have deteriorated + developed neuro signs + symptoms).

Primary Progressive (progressive accumulation) : 10%

386
Q

Presentation of multiple sclerosis?

A

Female, catheterised, eye signs, cerebellar signs - ATAXIA (unable to heel-toe walk)

  • UMN signs - pyramidal weakness + brisk reflexes.
  • Tingling/burning
  • Eye: optic neuritis (decreased central vision + eye movement pain)
  • Ataxia + other cerebellar signs
  • Motor: usually spastic paraparesis (motor walking) - muscle stiffness.
387
Q

Sensory Clinical features of MS?

A
  • Dys/paraesthesia
  • Decreased vibrations sense
  • trigeminal neuralgia
388
Q

Motor clinical features of MS?

A

Spastic weakness
Transverse myelitis
Foot dragging
Fatigue

389
Q

Eye clinical features of MS?

A
  • Diplopia
  • Visual phenomena
  • Bilateral INO (internuclear ophthalmoplegia) - due to medial longitudinal fasciculus lesion.
  • Optic nerve damage - central scotoma, RAPD, colour and VA loss, optic atrophy.
  • Optic neuritis
390
Q

Cerebellum features of MS?

A
  • Trunk and limb ataxia
  • Scanning dysarthria (jerky, explosive speech)
  • Fall
  • Dorsal column disease - reduced vibration, proprioception, Romberg’s +ve.
391
Q

GI features of MS?

A

Swallowing disorders

Constipation

392
Q

Sexual/GU?

A

ED + anorgasmia
Retention
Incontinence

393
Q

What is Lhermitte’s Sign?

A

Neck Flexion –> electric shocks in trunk/limbs

394
Q

What is Optic Neuritis?

A
  • Pain on eye movement, rapid decrease in central vision
  • Uhthoff’s: vision decreased with heat: hot bath, hot meal, exercise.
  • O/E: decreased acuity, decreased colour vision, white disc, central scotoma, RAPD.
395
Q

What is an internuclear ophthalmoplegia?

A
  • Disruption of Medial Longitudinal Fasciculus connecting CN6 and CN3.
  • Weak adduction of ipsilateral eye.
  • Nystagmus of contralateral eye.
    Convergence preserved.
396
Q

What investigations are needed for MS?

A

MRI: Gd-enhancing or T2 hyper-intense plaques.
Gd-enhancing = active inflammation
MRI contrast. Shows dissemination in time and space.

-Typically located in periventricular white matter.
SAgitall FLAIR = periventricular white matter.

LP: IgG oligoclonal bands (not present in serum) - less used

Ab:
Anti-MBP,
NMO-IgG: highly specific for Devic’s syndrome (affects the optic nerves + spinal cord).

Evoked potentials: delayed auditory, visual, sensory.

Don’t forget hypothyroidism and B12.

397
Q

Diagnosis of MS?

A
  • Demonstration of lesions disseminated in time and space
  • May use McDonald’s Criteria.

Dissemination in space (DIS)
- One or more T2-hyperintense lesions in 2 or more of 4 areas of CNS: periventricular, cortical or juxtacortical, infratentorial and spinal cord.

Dissemintated in time

  • Asymptomatic Gd enhancing and non-enhancing lesions at any time
  • New T2 and/or Gd-enhancing lesion on follow-up MRI.
398
Q

What are the differentials for MS?

A

Cervical spondylosis - without the cerebellar signs
CNS sarcoidosis
SLE
Devic’s Neuromyelitis optica (NMO)
- MS variant with transverse myelitis and optic atrophy
- Distinguished by presence of NMO-IgG abs. Don’t get hemiplegia/spasticity

Transverse myelitis (entire width of spinal care) - acute or subacute development of motor weakness, sensory impairment and autonomic dysfunction. Seperate entity to MS - demyelination, autoimmune causes, infectio, 
Follows a pyramidal pattern. 
May develop sensory loss. 
Bladder symptoms 
Bowel symptoms 
Lhermitte sign
399
Q

General Management of MS?

A

MDT: Neurologist, radiologist, physio, OT, specialist nurse, GP, family.

400
Q

Medical management of an acute attack of MS?

A
  • Methylprednisolone 1000 mg OD for 3 days.
    Doesn’t influence long-term outcome
  • Decreased duration and severity of attack. Consider plasma exchange?
401
Q

Medical management to prevent relapse of MS?

A

DMARDS

  • IFN-B: decreased relapse by 30% in RR MS
  • Glatiramer: similar efficacy to IFN-B

-Natalizumab, ocrelizumab, cladribine and alemtuzumab are for more aggressive disease.

Biologicals
- Natalizumab: anti-VLA-4Ab 
decreases relapses by 2/3 in RRMS
- Alemtuzumab (Campath): anti-CD52 
2nd line RRMS
402
Q

What are the symptomatic treatments of MS?

A
  • Fatigue: amantadine, consider mindfulness training and CBT.
  • Depression: SSRI
  • Pain: amitryptylline, gabapentin
  • Spasticity: physio, baclofen, dantrolene, botulinum. Second line is diazepam, dantrolene, tizanidine.
  • Oscillopsia (visual fields appear to oscillate). Gabapentin is first-line.
  • Urgency/frequency: oxybutynin, tolterodine
  • ED: sildenafil
  • Tremor: clonazepam
403
Q

What are poor prognostic signs for MS?

A
Older
Male
Motor signs @onset
Many relapses early on
Many MRI lesions 
Axonal loss
404
Q

What are better prognostic signs

A
Female 
<25
Sensory signs @onset
Long interval between relapses
Few MRI lesions
405
Q

Cord compression - What are the symptoms?

A
  • Deep, local spinal pain
    Stabbing, radicular pain in a dermatomal distribution and LMN weakness @ lesion level.
  • Progressive UMN weakness and sensory loss below lesion
  • Bladder hesitancy, frequency –> painless retention.
  • Faecal incontinence or constipation.
406
Q

What are the signs of cord compression?

A
  • Look for motor, reflex and sensory level.
  • SHooting, radicular pain @ level, anaesthesia below
  • LMN signs @ level, UMN below level.
  • Tone and reflexes are usually reduced in acute cord compression.
407
Q

What are the causes of cord compression?

A
  • Trauma
  • Infection: epidural abscess, TB
  • 2ndry to malignancy: breasth, thyroid, bronchus, kidney, prostate.
  • Disc prolapse
  • Haematoma: warfarin
  • Intrinsic cord tumour
  • Myeloma
408
Q

What investigations would you do for cord compression?

A
  • CXR for primaries (Disc space height, loss of bony detail)
  • MRI is definitive modality
    Epidural enhancement, mass effect, T2 cord signal.
  • Gadolinum-enchanced MRI spine
409
Q

What is the management of cord compression?

A

This is a neurosurgical emergency
- Malignancy
Dexamethasone IV
Consider chemo radio, decompressive laminectomy
- Abscess: abx and surgical decompression.

410
Q

What are the differentials for cord compression?

A
  • Transverse myelitis
  • MS
  • Cord vasculitis
  • Spinal artery thrombosis
  • Aortic dissection
411
Q

What is cauda equina and conus medullaris lesions?

A
  • Spinal cord tapers to its end at L1

- Compared with lesions high up the cord, these lesions are - flaccid and areflecix (cf spastic and hyperreflexic)

412
Q

What is conus medullaris lesions?

A

At the cone itself

  • Mixed UMN/LMN weakness
  • Early constipation and retention
  • Back pain - mild pain
  • Sacral sensory disturbance
  • Erectile Dysfunction
413
Q

What is the cauda equina lesion?

A
  • Saddle anaesthesia
  • Back pain
  • Radicular pain down legs
  • Bilateral flaccid, areflexic lower limb weakness
  • Incontinence, retention of faeces, urine.
  • POOR anal tone.
414
Q

What is the management of cauda equina/conus medullaris?

A

As for cord compression

These are neurosurgical emergencies and require urgent imaging and surgical decompression

415
Q

What is spondylosis?

A
  • Degeneration due to trauma or ageing
  • IV disc/vertebral collapse
  • Osteophytes
  • May –> central (myelopathy) = cord itself and/or lateral (radiculopathy - nerve root)) pathology.
416
Q

What percentage of men and women are affected by cervical spondylosis? Also called degenerative cervical myelopathy

A

90% of men >60

Women >50

417
Q

What is cervical spondylosis?

A

Specific term for osteoarthritis of the spine, including spontaneous degeneration of either disc or facet joints.

418
Q

What is the presentation of cervical spondylosis?

A
  • Usually asymptomatic
  • Neck stiffness ± crepitus
  • Stabbing/dull arm pain (brachialgia)
  • Upper limb motor and sensory disturbances according to compression level (often C7).
  • Can –> Myelopathy with quadriparesis and sphincter dysfunction

Specific signs

  • Lhermitte’s sign: neck lexion –> tingling down spine
  • Hoffman reflex: flick to middle finger pulp –> brief pincer flexion of thumb and index finger
419
Q

What is the motor and sensory presentation of a C5 Root (C4/C5 disc) manifestation?

A

Motor weakness - Deltoid, Supraspinatus, decreased supinator jerk.

Sensory abnormality - Numb elbow

420
Q

What is the motor and sensory presentation of a C6 Root (C5/C6 disc) manifestation?

A

Motor weakness

  • Biceps (bicep reflex)
  • Brachioradialis (brachioradialis test)
  • Decreased biceps jerk

Sensory
- numb thumb and index finger

421
Q

What is the motor and sensory presentation of a C7 Root (C7/C8 disc) manifestation?

A

Motor weakness

  • Triceps (tricep test)
  • Finger extension
  • Decreased tricep jerk

Sensory
- Numb middle finger

422
Q

What is the motor and sensory presentation of a C8 Root (C7/C8 disc) manifestation?

A

Finger flexors
Intrinsic hand

Numbness ring and little finger and medial side of hand.

C8 exits the spine below the C7 vertebra, only nerve root below a vertebra.

423
Q

What are the investigations for cervical spondylosis?

A

MRI

Consider X-ray

424
Q

What is the management of cervical spondylosis?

A

Urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery).

Conservative: stiff collar, analgesia/physiotherapy
Medical: Consider NSAIDs, transforaminal steroid injection

Most effective treatment -
Surgical: decompression, laminectomy or laminoplasty

Postoperatively, patients with cervical myelopathy require ongoing follow-up as pathology can recur at adjacent spinal levels. Known as adjacent segment disease.

425
Q

Differential for cervical spondylosis?

A
  • MS
  • Nerve root neurofibroma
  • SACD (subacute combined degeneration of the spine) .
426
Q

What is lumbosacral spondylosis?

A

L5 and S1 roots most commonly compressed by prolapse of L4/L5, L5/S1 disc.

  • may present as severe pain on sneezing/ coughing a few days after low back strain.
  • Lumbago - low back pain
  • Sciatica - shooting radicular pain down buttocks and thigh.
427
Q

What are the signs of lumbosacral spondylosis?

A
  • Limited spinal flexion

- Pain on straight-leg raise

428
Q

What L4/L5 root compression present as?

A

Weak hallux extension ± foot drop.

  • In foot drop due to L5 radiculopathy, weak inversion (tibpost) helps distinguish from peroneal N. palsy.
  • Decreased sensation on inner dorsum of foot.

Conservative management - leg crossing, squatting and kneeling should be avoided.

Symptoms typically improve over 2-3 months.

429
Q

Wht is L5/S1 –> S1 root compression

A
  • Weak foot plantarflexion and eversion
  • Loss of ankle-jerk
  • Calf pain
  • Decreased sensation over sole of foot and back of calf
430
Q

Management of lumbosacral spondylosis?

A
  • MRI is definitive (emergency if cauda-equina syndrome)
431
Q

Management of lumbosacral spondylosis

A
  • Conservative: rest, analgesia, mobilisation
  • Medical: transforaminal steroid injection
  • Surgical: Discectomy or laminectomy may be considered in cauda-equina
432
Q

What is Bell’s Palsy?

A
  • Inflammatory oedema from entrapment of CN7 in narrow facial canal.
  • Probably of viral origin (HSV1)
    75% of facial palsy
  • Pregnant women are 3x more likely to develop Bell’s palsy.
433
Q

What are the features of Bell’s Palsy?

A
  • Sudden onset: eg overnight
    Complete, unilateral facial weakness in 24-72hrs
  • Failure of eye closure –> dryness
  • Bell’s Sign: eyeballs roll up on attempted closure
  • Smooth of nasolabial folds
  • Drooling, speech difficulty
  • Numbness or pain around ear
  • decreased taste (Ageusia)
  • Hyperacusis: stapedius palsy (sensitivity to sound)
  • involvement of all nerve branches

Examination
- Close eyes, raise eyebrows, frown

UMN/LMN - UMN spares the upper fae - presumed evolutionary bicortical innervation to protect eyes.

  • Loss of corneal reflex (efferent)
434
Q

Investigations for Bell’s palsy?

A
  • Mainly clinical
  • EMG (decreasd in amplitude in muscle action)
  • Serology for Borrelia Burgdoferi
  • Examination for Ears (Herpes Zoster Ramsey Hunt).
  • Must go to ENT - cholesteatoma
  • Consider MRI: (SOL, stroke, MS), consider LP
435
Q

What is the management of Bell’s Palsy?

A

Give prednisolone w/i 72hrs
- 60mg/d PO for 5/7 following by tapering

  • Valaciclovir if zoster is suspected: Otherwise antiviral don’t help
  • Protect glasses
    Dark glasses, artificial tears, tape closed at night.
  • Plastic surgery may help if no recovery.
436
Q

What is the prognosis of Bell’s Palsy?

A
  • Incomplete paralysis: recovers completely within weeks

- Complete paralysis: 80% get full recovery: remainder

437
Q

Complications of Bell’s Palsy?

A

Aberrant Neural Connections

  • Synkinesis: e.g blinking causing up-turning or mouth
  • Crocodile tears: eating stimulates unilateral lacrimation, not salivation
438
Q

What is Ramsey Hunt Syndrome?

A

Reactivation of VZV in geniculate ganglion of CNVII

439
Q

Features of Ramsay Hunt Syndrome?

A
  • Preceding ear pain or stiff neck
  • Vesicular rash in auditory canal ± TM, pinna, tongue, hard palate (no rash = zoster sine herpete)
  • Normal ear exam goes against RH.
  • Ipsilateral facial weakness, ageusia, hyeracusis
  • May affect CN8 –> vertigo, tinnitus, deafness
440
Q

Management of Ramsay Hunt Syndrome?

A

If Dx suspected give valaciclovir and prednisolone within first 72hrs

441
Q

Prognosis of Ramsay Hunt Syndrome?

A

Managed within 72hrs: 75% recovery

Otherwise: 1/3 full recovery, 1/3 partial, 1/3 poor.

442
Q

Other causes of facial nerve palsy apart from RH and Bell’s?

A

Bilateral symptoms: consider Lyme, GBS, Leukaemia, Sarcoid, MG.

UMN signs: Sparing of frontalis and orbicularis oculi
- Due to bilateral cortical representation
Other CN palsies
Limb weakness
Rashes

LMN 
- Bell's palsy
Ramsay-Hunt syndrome (due to herpes zoster)
acoustic neuroma
parotid tumours
HIV
multiple sclerosis*
diabetes mellitus
443
Q

Intracranial causes of facial palsy?

A

SOL, MS, Vascular.
- motor cortex –> UMN (assoicated with ipsilateral hemiplegia)
- Brainstem nuclei –> LMN
Usually associated with CN6 palsy + contralateral hemiplegia
- Cerebello-pontine angle: acoustic neuroma, meningioma
Both may be accompanied by 5th, 6th and 8th Cn palsies and cerebellar signs
- Loss of corneal reflex
- Sensorineural deafness, tinnitus, vertigo
- DANISH

444
Q

Intra-temporal Facial palsy? - Labrinth to mastoid

A
  • Cholesteatoma
  • Ramsay Hunt
  • Otitis Media
  • Trauma
445
Q

Infra-temporal facial palsy?

A

Parotid tumours

Trauma

446
Q

Systemic causes of facial palsy?

A

Peripheral neuropathy

  • Demyelinating: GBS
  • Axonal: DM, Lyme, HIV, Sarcoid
  • Pseudopalsy: MG, Botulism
447
Q

Types of Mononeuropathies?

A
Median 
Ulnar 
Radial 
Brachial Plexus
Phrenic 
Lat Cut N Thigh 
Sciatic
Common Peroneal
Tibial
448
Q

What is a mononeuropathy?

A
  • Lesions of individual peripheral or cranial nerves.
  • EMG helps define site of lesions
  • Mononeuritis multiplex: 2 or more peripheral nerves affects :
    Usually systemic cause: DM most commonly
  • Also WAARDS PLC
    Wegener’s
    AIDS
    Amyloid
    RA
    DM
    Sarcoidosis
    PAN
    Leprosy
    Carcinomatosis

Investigation = Blood (Autoimmune serology: ANA, ANCA, RF, dsDNA.

Imaging

  • XR elbow
  • US cubital tunnel

Special tests
- Nerve conduction studies

449
Q

Which dermatomes involved in median nerve palsy?

A

C6-T1

Wrist: carpal tunnel, trauma (amyloidosis)

450
Q

What are the features (motor + sensory of Median nerve palsy)

A

Motor features?

  • LLOAF muscles (lateral 2 lumbricals, Opponens Pollicis, Abductor Pollicis Brevis, Flexor Pollicis Brevis)
  • Thenar wasting
  • Sign of Benediction
  • Pronation of hand

Sensory Loss/Features
- Radial 3.5 fingers and palm.
- Aching pain in hand (decreased 2 point discrimination)
- Tinel’s and Phalen’s +ve.
Look for sensation over the thenar eminence
- If lost - cannot be carpal tunnel syndroe
- PCB arises proximal to the carpal tunnel

451
Q

What are the dermatomes of an ulnar palsy?

A
  • C8-T1
  • Mainly caused by Elbow Trauma (e.g supracondylar fracture).

BRanches
- Muscular branch = flexor carpi ulnaris, medial half of the flexor digitorum profundus.

  • Palmar cutaneous branch - medial part of the palm
  • Dorsal cutaneous branch - dorsal surface of medial part of hand.
452
Q

What are the motor and sensory loss features of ulnar palsy?

A

Motor weakness - most muscles except LOAF. Medial two lumbricals, aDductor pollicis, interossei, abductor digitia minimi, flexor digiti minimi .

  • Partial claw hand
  • Hypothenar wasting (first dorsal interosseus)
  • Can’t do good luck sign
  • Weakness and wasting of 1st dorsal interosseous
  • Froment’s +ve (finger pinch grip)
  • Loss of thumb adduction

Sensory Loss/Features

  • Ulnar 1.5 fingers
  • Loss of senation over hypothenar eminence means PCB affect - injury is above wrist.

Ulnar paradox - higher lesion causes lesser deforimit
- Lower lesions spares FDP - causes flexion at the DIP

453
Q

What are the dermatomes of radial nerve palsy?

A

If Low: wrist trauma
If high: humerus
if V high: axilla

Fracture of the shaft of the humerus.

454
Q

What are the motor features and sensory loss features of radial nerve palsy?

A

Motor:

Low: finger drop
High: wrist drop
V.high: triceps paralysis, wrist drop

Sensory:
Dorsal thumb root (snuff box)

455
Q

What are the presentations of a Brachial plexus injury?

A
  • Caused by Trauma
  • Radiotherapy (e.g breast)

High (C5-C6): Erb’s Palsy –> Waiter’s tip (Catching from behind). Loss of C5-C6 dermatome. Hand hanging loose, pronated and medially rotated.

Low (C8-T1) - Klumpke’s –> claw hand. Loss of C8-T1 dermatome. Horner’s syndrome. Weakness of hand intrinsic muscle.

Root which supplies the thumb adduction and finger abduction is T1. Medial epicondyle is the testing point for the T1 dermatome.

456
Q

Which nerve is at C3-C5?

A

Phrenic.

Damage caused by

  • Neoplastic: Lung Ca, Myeloma, Thymoma.
  • Mechanical: Cervical spondylosis, big left atrium.
  • Infective; C3-C5 zoster, HIV, lyme, TB.

Presents with orthopnoea + raised hemidiaphragm.

457
Q

Lateral Cutaneous Nerve Thigh: L2-L3

A

Entrapment under inguinal ligament.

Meralgia paraesthetica –> anterolateral burning thigh pain.

458
Q

Sciatic nerve L4-S3?

A

Causes of mononeuropathy

  • Pelvic tumours
  • Pelvic or femur #s.

Motor features

  • Hamstrings
  • All muscles below knees weakened.

Sensory
- Below knee laterally and foot

459
Q

Common peroneal nerve: l4-S1?

A

Fibular head: trauma, sitting cross legged.
Motor:
Foot drop: can’t walk on heels
Weak ankle dorsiflexion, eversion. NB: inversion intact!

Sensory loss/Features: Below knee laterally.

460
Q

Tibial damage L4-S3

A
  • Can’t plantar flex –> can’t stand on tiptoe
  • Foot inversion
  • Toe Flexion

Loss of sensation sole of foot.

461
Q

What are the features of polyneuropathies?

A
  • Generalised disorders of peripheral or cranial nerves.
  • Distribution is symmetrical and widespread
  • Distal weakness and sensory loss (Glove and stocking)
    Classification of polyneuropathies
  • Time-course: acute, chronc
  • Function: motor, sensory, autonomic, mixed
  • Path: Demyelination, axonal degeneration, both.
462
Q

What are the metabolic causes of polyneuropathies?

A

Mostly axonal

  • DM
  • Renal failure/uraemia
  • hypothyroidism
  • decreased B1/B12 (EToH)
463
Q

What are the vasculitic causes of polyneuropathies?

A

PAN (Polyarteritis Nodosa)
RA
Wegener’s

464
Q

What are the inflammatory causes of polyneuropathies /

A
  • GBS

- Sarcoidosis

465
Q

What are the infective causes of polyneuropathies?

A

HIV
Syphilis
Leprosy
Lyme

466
Q

What are the inherited causes of polyneuropathies?

A

Charcot Marie Tooth

Refsum’s syndrome

467
Q

What are the toxin causes of polyneuropathies?

A

Lead
Amyloid
Paraproteinemias

468
Q

What are the drug causes of polneuropathies

A

Isoniazid
ETOH
Phenytoin
Vincristine

469
Q

What to ask in a neuro history for polyneuropathy?

A
Time-course
Precise symptoms 
Associated event 
- D+V: GBS
- DecreaseD weight loss: Ca
- Arthralgia: connective tissue

Travel, ETOH, drugs.

470
Q

What investigations to do in a polyneuropathy station

A
  • LFTs, U+E, Glucose, ESR, B12
  • TFTs, B1, ANA, ANCA
  • Genetic tests: PMP22 in CMt
  • NErve conduction studies
  • EMG
471
Q

What are the main causes of a sensory neuropathy?

A
  • Alcohol
  • B12
  • Chronic Renal Failure and Ca (paraneoplastic)
  • DM
  • Every vasculitis
  • Hypothyroidism
  • HIV
472
Q

General features of a sensory neuropathy

A
  • Gloves and stocking distribution: length dependent
  • Deep tendon reflexes may be decreased or absent
    E.g Loss of ankle jerks in diabetic neuropathy
  • Signs of trauma or joint deformity (Charcot’s joints)
  • Diabetic and alcoholic neuropathies are painful
  • Some aetiologies favour loss of particular fibres.
473
Q

What are the features of large myelinated fibre damage?

A

Caused in B12

  • Loss of proprioception –> ataia
  • Pins and needles
474
Q

What are the features of small demyelinated fibre damage?

A

Caused in alcohol

  • Loss of pain and temperature sensation
  • Painful dysaethesia: e.g burning, hyperalgesia
475
Q

What are the main causes of a motor neuropathy?

A
  • Guillan Barre Syndrome
  • Charcot Marie Tooth, Hereditary Motor and Sensory Neuropathy
  • Paraneoplastic
  • Lead poisoning
476
Q

Features of Motor Neuropathy?

A

Weakness/clumsiness of hands, difficulty walking
LMN signs
CN: diplopia, Dysarthria, dysphagia
Involvement of respiratory muscles –> Decreased FVC.

477
Q

What are the causes of a autonomic neuropathy?

A
Diabetes
HIV
SLE
GBS 
LEMS
478
Q

Features of autonomic neuropathy?

A
  • Postural hypotension
  • Ejaculatory failure
  • Decreased sweating
  • Constipation
  • Retention
  • Horner’s
479
Q

Autonomic function tests?

A

BP: Postural drop >20mmHg
ECG: variation >10bpm with respiration

480
Q

Primary autonomic failure causes?

A

Idiopathic or part of MSA/PD.

481
Q

What is Guillain- Barre Syndrome Classification?

A

AIPD: acute autoimmune demyelinating polyneuropathy
AMAN: acute motor (+ sensory) axonal neuropathy
Miller-Fisher: (mainly japan) Ophthalmoplegia + ataxia + areflexia. Eyes are affected first.

482
Q

What is the aetiology of GBS?

A
  • 2/3 patients have had infections within 6 weeks of conditions, usually URTI .

Immune mediated attack on myelin sheath.

483
Q

Causes of GBS?

A

Abs cross-react to gangliosides
No precipitants found in 40%?
Bacteria: C.jejuni, mycoplasma

Viruses; CMV, EBV, HSV, HIV, Flu

Vaccines: esp rabies.

484
Q

What are the features and investigations for GBS?

A

GBS = AIDP = acute autoimmune demyelinating polyneuropathy

  • Presents with GBS (Diarrhoea then weakness).

Growing weakness
Breathing + bulbar problems
Back pain
- Sensory disturbances (paraesthesia in extremities + sensory ataxia in Miller-Fisher)
Autonomic neuropathy (arrhythmias, decreased HR, Labile BP, sweating, urinary retention)

485
Q

Growing weakness features of GBS?

A
  • Symmetrical, ascending flaccid weakness/paralysis
  • LMN sign: areflexia, fasciculations may occur
  • Proximal > distal (trunk, resp, CNS 7)
  • Progressive phase last <4 weeks.
486
Q

Investigations for GBS?

A
  • Immune - Serology for anti-ganglioside ABs. Evidence of infections - stool sample
  • Demyelinating nerve conduction studies - slow conduction velocities
  • isolated raised Protein in CSF - protein often >5.5 g/L. Normal WCC.
  • Spirometry - Vital Capacity + ABG on air for vent.
  • Swallow assessment
  • ECG for arrhythmia and BP for autonomic disturbance.
487
Q

Management of GBS?

A

Supportive

  • Airway/ventilation: ITU if FVC <1.5L
  • Analgesia: NSAIDS, gabapentin
  • Autonomic: may need inotropes, catheter
  • Antithrombotic: TEDs, LMWH

Immunosuppression

  • IVIG
  • Plasma exchange

Prognosis

  • 85% complete recovery
  • 10% unable to walk alone at 1yr
  • 5% mortality
488
Q

What is Charcot-Marie-Tooth Syndrome?

A
  • Peroneal muscular atrophy

- Hereditary motor and sensory neuropathy

489
Q

Types of CMT syndrome?

A

HMSN1/CMT1 - commonest form, demyelinating, AD mutation in the peripheral myelin protein 22 gene
HMSN2/CMT2 - second commonest form. Axonal degeneration (therefore near normal conduction studies)
CMT4 - AR

490
Q

What are the motor features of CMT?

A

Typically history of ankle sprains and scoliosis.
Motor and sensory loss (sensory milder).
- Antero-lateral compartments affected.
- Absent reflexes
- Pes cavus

Onset at puberty? 
- Nerve = thickened, enlarged nerves 
- Motor = 
Foot drop --> high stepping gait, 
weak ankle dorsiflexion and toe extension, 
- absent ankle jerks 
- symmetrical muscle atrophy: 
Peroneal muscles (loss of muscles) 
- champagne bottle 
Hand and arm muscles
- Claw hand
Pes Cavus (high-arched feet)

Papable lateral popliteral nerve - thickened nerves at medial malleolus.

491
Q

What are the sensory features of CMT?

A
  • Variable loss of sensation in a stocking distribution

- Neuropathic pain in some

492
Q

Investigations for CMT?

A

-Genetic tests: PMP22 gene mutations
- Nerve conduction studies: decreased conduction speed in CMT1
B12
DM
Alcohol
- Physio
- Walking aids
- Ankle and foot supports

493
Q

Management of CMT?

A
  • Supportive
    Physio
    Podiatry
    Orthoses e.g ankles braces
494
Q

Motor neuron Disease characteristics?

A
  • Cluster of degenerative diseases characterised by axonal degeneration of neurones in the motor cortex, CN nuclei, anterior horn cells.
  • UM and LN neurons affected (polyneuropathy)
  • No sensory loss or sphincter disturbances (cf. MS)
  • Never affects eye movements (compared to MG)
495
Q

Epidemiology of MND?

A

Prevalence: 6/100,000
Sex: M>F = 3:2
median age @ onset = 60yrs
Often fatal in 2-4 yrs

496
Q

Causes of MND?

A

Unknown

Types:
- ALS (Amyotrophic lateral sclerosis) = death of both UMN and LMN in motor cortex.
LMN signs = flaccid paralysis, weakness, wasting, fasiciultion.
UMN = Spastic paralysis, pyramidal weakness, hyper-reflexia, up-going plantars.

Primary lateral sclerosis
- UMN signs only

Progressive muscular atrophy

  • LMN signs only
  • Affects distal muscles before proximal
  • Carries best prognosis

Progressive bulbar palsy

  • Palsy of tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei.
  • Caries worst prognosis.
497
Q

Investigations for MND?

A

Primarily Clinical

Braincord MRI: exclude structural causes - cervical cord compression (myelopathy) or brainstem lesions).
LP: exclude inflammatory cause
EMG: shows acute denervation

Use Revised EI Escorial Diagnostic Criteria (presence of UMN + LMN of the cranial, cervical, thoracic and lumbosacral segments of neuroaxis.

498
Q

General Management of MND?

A

MDT: Neurologist, physio, OT, dietician, specialist nurse, GP, family
Discussion of end-of-life decision
- Advanced directive
- DNAR

499
Q

Specific management of MND?

A

Riluzole: antiglutamatergic that prolongs life by 3 months.

500
Q

What supportive management of MND?

A
Drooling: proantheline or amitriptyline
Dysphagia: NG or PEG feeding
Respiratory failure: NIV
Pain: analgesic ladder
Spasticity: Baclofen
501
Q

What are the classifications of MND?

A
  • ALS - Loss of Motor neurones in cortex and anterior horn (UMN + LMN + fasciculation)
  • Progressive Bulbar Palsy (only affects CN9-12 –> bulbar palsy)
  • Progressive Muscular Atrophy (Anterior horn cell lesions (LMN signs only), distal to proximal. Better prognosis vs ALS)

Primary Lateral Sclerosis

  • Loss of Betz cells in motor cortex –> mainly UMN signs
  • Marked spastic leg weakness and pseudobulbar palsy
  • No cognitive decline
502
Q

What is a bulbar palsy?

A
Disease of nuclei 9-12 in the medulla. 
- LMN lesions of tongue, talking and swallowing. 
- Signs 
Flaccid, fasciculating tongue
Speech: quiet or nasal (donald duck) 
Normal/absent jaw jerk
Loss of gag reflex

Causes

  • MND
  • GBS
  • MG
  • Central pontine myelinolysis
503
Q

What is a pseudobulbar/corticobulbar palsy?

A

Commoner than bulbar palsy
Bilateral lesions above mid-pons (corticobulbar tracts) –> UMN lesions of swallowing and talking.
CN motor nuclei have bilateral cortical representation except lower half of CN7.

Signs

  • Spastic tongue
  • Slow tongue movements with slow deliberate speech: Hot-potato speech
  • Brisk jaw jerk
  • Emotional incontinence

Causes

  • MS
  • MND
  • Stroke
  • CPM
504
Q

How can Polio cause a motor neuron disease?

A

RNA virus
Affects anterior horn cells
Fever, sore throat, myalgia.
- Asymmetric LMN paralysis
- No sensory involvement
- May be confined to upper or lower limbs or both
- Respiratory muscle paralysis can –> Death

505
Q

How is myopathy different to neuropathy? s for myopathies?

A

Myopathy

  • Gradual onset
  • Symmetrical, proximal weakness: Difficulty combing hair, climbing stairs, getting up from chairs
  • Dystrophies usually affect specific muscle groups
  • Preserved tendon reflexes.

Neuropathy

  • Distal weakness
  • Paraesthesia (tingling) , bladder problems.

Other pointers-

  • Rapid onset: neuropathy, or drug, toxic or metabolic myopathy
  • Fatigability: MG, LEMS
  • Spontaneous pain and tenderness @ rest: inflammatory myopathy
  • Pain on exercise: ischaemia or metabolic myopathy
  • Oddly firm muscles: pseudohypertrophy in muscular dystrophies
  • Fasciculations: anterior horn cell or root disease
506
Q

Investigation for myopathies?

A
  • ESR, CK, AST, LDH

- EMG

507
Q

what are the muscular dystrophies?

A

Group of genetic disease with progressive degeneration and weakness of specific muscle groups.

508
Q

Duchenne’s Muscular dystrophy?

A

3/1000 male births.
X-linked recessive –> non-functional dystrophin.

  • presents at 4 yrs old
  • Difficulty standing
  • Calf pseudohypertrophy
  • Resp failure
  • increasing lordosis
  • Diminished muscle tone + Deep tendon reflexes.

Investigations: increased CK
Some survive >20 yrs.

Can use steroids etc.

509
Q

Becker’s Muscular dystrophy?

A

X-linked recessive
Partially functioning dystrophin
Presents later is less severe and has better prognosis.

510
Q

Landouzy-Dejerine?

A
Almost as common as DMD
AD inheritence 
- Presents @12-14 yrs old 
Difficulty puffing cheeks and raising arms above heads. 
Signs 
- Weakness of face, shoulders, upper arms (asymmetric with deltoids spared) 
- winging of scapula 
- Foot drop
511
Q

Myotonic dystrophy?

A
  • AD Cl- channelopathy
  • Onset in 20s
  • Tonic muscle spasm (myotonia)

Lower Motor Neuron.

Presentation

Face

  • Myopathic face: Long, thin, expressionless
  • Wasting of facial muscles and SCM (guttering of the temporalis)
  • Bilateral Ptosis
  • Dysarthria: myotonia of tongue and pharynx.

Shake hand - squeeze my hand, and told for 3 seconds. try to let go. Percussion myotonia: hypothenar eminence depression visibly fills slowly after percussion.

Hands

  • Myotonia: slow relaxation so inability to release hand after shake.
  • Wasting and weakness of distal muscles + areflexia –> Wrist drop
  • Percussion myotonia: percuss thenar eminence –> involuntary thumb flexion.

Other signs

  • Frontal balding
  • Cataracts
  • DM
  • Cardiomyopathy, tachy/bradyarrythmias (pacemaker scar)
  • Dysphagia
  • Testicular atrophy

Assocations

  • Cataracts
  • Dysphagia
  • Cardiac - cardio + heart block (PPM)
  • DM
  • Hypogonasism

Invx

  • LFTs should be checked for NM rsp insufficient
  • ECG conduction block
  • Echo for CM
  • Fasting glucose DM
  • Slit lamp for cataracts
  • SALT
  • EMG: ‘ Dive bomber’ potentials.

How to present
- The gentleman has evidence of myopathic facies, frontotemporal hair loss with bilateral ptosis, wasting of the facial msucles and sternocleidomastoids.

There is also symmetrical wasting of the forearm muscles and small muscles of the hands bilaterally. There is a reduction in power distally in both arm in all muscle groups tested with normal sensation and coordination. The reflexes are reduced.

Mr X had difficulty in releasing my hand from a squeeze and opening his eyes when closed firmly - suggesting myotonia.

THis is likely to be myoptonic dystrophy> to complete my assessment I owuld like to exaomine the cardiovascular, check bloods, perform a full functional asssessment. Diagnosis can be confirmed with a family history, EMG and geentic testing.

512
Q

What is the management of Myotonic dystrophy?

A

No Rx for weakness
Phenytoin may improve myotonia
Caution with GA: high risk of anaesthetic complications.

513
Q

Acquired myopathies of late onset/

A

Part of systemic disease

  • Hyperthyroidism, Cushing’s increased or decreased Ca.
  • Drugs: Steroids, Statins, ETOH.
514
Q

What are the inflammatory myopathies?

A

Inclusion body myositis
Polymyositis
Dermatomyositis

515
Q

What is the pathophysiology of Myasthenia Gravis?

A

AI disease mediated by Abs vs nicotinic Ach receptors

- Interferes with NM transmission via deletion of working post-synaptic receptor sites.

516
Q

Presentation of MG?

A

Increasing muscle fatigue

  • Extra-ocular: Bilateral ptosis, diplopia
  • Bulbar: voice deteriorates on counting to 50
  • Face: myasthenic snarl on attempt to smile
  • Neck: head droop
  • Limb: asymmetric, prox weakness
  • Normal tendon reflexes
  • Weakness worsened by: pregnancy,
    infection,
    emotion,
    drugs (B-B, gent, opiates, tetracylines)
517
Q

Investigations for MG?

A

Tensilon Test

  • Give edrophonium IV
  • +ve if power improves within 1 min. Not commonly used due to risk of cardiac arrhythmia.

Anti-AChR Abs: Increases in 90%, MuSK abs

EMG: decreased response to a train of impulses

Respiratory function: Decreased FVC

Thymus CT

TFTs

518
Q

Differentials for Muscle Fatigability?

A

Polymyositis
SLE
Botulism

519
Q

MG associations?

A
  • <50yr MG is commoner in women and asssociated with other AI disease (DM, RA, Graves) and thymic hyperplasia
  • > 50 yrs MG is commoner in men and associated with thymic atrophy or thymic tumour
520
Q

Treatment of MG?

A

Symptom control:
Anticholinesterase: eg. pyridostigmine
- Cholingeric SEs= SLUDGEM

Immunosuppression

  • Rx relapse with pred
  • Steroid may be combined with azathioprine or methotrexate

Thymectomy

  • Consider if young onset and disease not control by anticholinesterases
  • Remission in 25%, benefit in further 50%.
521
Q

Complications of MG?

A

Myasthenic Crisis
- Weakness of resp muscles during relapse may be lethal
- Monitor FVC: vent support if <20ml/kg
- Plasmapheresis or IVIg
- Manage trigger for relapse (drugs, infection)
= Beta-blockers such as bisoprolol are common precipitants of myasthenic crises.

Penicillamine 
Quinidine, procainamide
Beta-blockers 
Lithium
Phenytoin
Antibitocs: gentamicin, macrolides, quinolones, tetracyclines. 

For surgery -

522
Q

What is the pathophysiology of Lambert-Eaton Syndrome?

A

Abs to VGCC decreased influx of Ca2+ during presynaptic excitation –> Decreased presynaptic ACh-vesicle fusion

523
Q

Causes of LEMS?

A

Paraneoplastic: Eg. SCLC

Autoimmune

524
Q

PResentation of LEMS?

A
Same as MG except: 
- LEMS 
LEgs weakness early (before eyes) 
- Extra: Autonomic and areflexia
- Movement improves symptoms 
- Small response to edrophonium
-Anti-VGC abs
525
Q

Management of LEMS?

A

3,4-diaminopyridine (amifampridine)
or IVIG
Do regular CXR/HRCTs as symptoms may precede Ca by 4 yrs

526
Q

What is Botulism

A
  • Botulinum toxin prevents Ach vesicles release
  • Descending flaccid paralysis with no sensory signs
    Anti-cholingeric effects: Mydriasis, cycloplegia, n/v, dry mouth.
  • Benpen + antiserum
527
Q

Neurofibromatosis 1 features

A
CAFE NOIR 
- Cafe au lait spots 
1st yr of life
Increase in size and no with age
Adults: >6, >15 mm across
  • Axillary Freckling
    Skin folds
  • Fibromas, neuro-
    1) Subcutaneous
    Small, gelantinous, violaceous nodules
    Appear at puberty
    May itch
    Increased with age

2) Plexiform
- Overgrowth of nerve trunk and overlyign tissue
- Large cutaneous mass

Complications
- Sarcomatous change, compression of nerve roots or GI bleeds.

  • Eye
    Lisch Nodules (brown/translucent iris hamartomas so use a slit lamp)
    Optic N. glioma.

Neoplasia

  • CNS (Meningioma, ependyoma, astrocytoma)
  • Phaemochromocytoma
  • Chronic or AML

Orthopaedic

  • Kyphoscoliosis
  • Sphenoid dysplasia

Decreased IQ and epilepsy

Renal - RAS –> Increased BP

528
Q

Management of NFT Type 1

A

MDT with GP
yearly BP + cutaneous review
Excise some neurofibromas
Genetic counselling

529
Q

Differential for Cafe Au Lait?

A

NF
Mccune-albright
Multiple Lentigenes
Urticaria Pigmentosa

530
Q

NF Type 2?

A

Rarer - AD Chromosome 22 but 50% are de novo.

531
Q

Features of NF type 2?

A

Cafe-au-Lait (Rare, fewer than NF1)
- Bilateral vestibular schwannaomas (Characteristic, symptomatic by 20yrs, SNHL is first sign, then tinnitus, vertgio).

  • Juvenile Posterior Subcapsular Lenticular Opacity
  • Form of cataract
  • Bilateral

Complications

  • Tender schwannomas of cranial and peripheral nerve and spinal nerve roots
  • Meningiomas, GLiomas.
532
Q

Management of NF Type 2

A

Hearing Test from puberty

MRI brain if abnormality detected

533
Q

What is Brown-Sequard SYndrome?

A
  • Hemi-cord lesion
  • Ipsilateral loss of proprioception sense and vibration
  • Ipsilateral UMN weakness
  • Contralateral loss of pain sensation
534
Q

What is Syringomyelia?

A
  • Syrinx: tubular cavity in central canal of the cervical cord. Downward displacement or herniation of the cerebellar tonsils through the foramen magnum. Malformation may be congentia.
  • Onset @ 30 yrs.
  • Symptoms may be static for years but then worsen fast.
    e. g on coughing, sneezing as pressure increased.
  • Commonly located in cervical cord
  • Syrinx expands ventrally affecting
  • Decussating spinothalamic neurons
  • Anterior horn cells
  • Corticospinal tracts
535
Q

Causes of Syringomyelia?

A
  • Blocked CSF circulation with decreased flow from posterior fossa
  • Arnold-Chiari malformation (cerebellum herniates through foramen magnum)
  • Masses

Spina bifida
2ndry to cord trauma, myelitis, cord tumours and AVM.

536
Q

What are the cardinal signs of Syringomyelia/

A
  • Dissociated Sensory Loss (absent pain + temp –> Scar from burns). = Cape sign.
  • Spastic weakness (upper limbs)
  • Paraesthesia
  • Neuropathic pain
  • Upgoing plantars, bowel and bladder dysfunction.

Preserved touch proprioception + vibration

Root distribution reflects syrinx location.
IN a cape distribution (upper limbs + chest).
- Wasting/weakness of hand± claw hand
- Loss of reflexes in upper limbs
- Charcot Joints: shoulder and elbow

Other signs

  • UMN weakness in lower limbs with upgoing plantars
  • Horner’s syndrome
  • Syringobulbia: cerebellar and lower CN signs
  • Kyphoscoliosis
537
Q

Investigations of Syringomyelia?

A

MRI spine

538
Q

Management of Syringomyelia?

A

Decompression at the foramen magnum for Chiari Mal.

Use Shunt.

539
Q

What is Friedrichs Ataxia?

A
  • AR progressive degeneration of DRGs, spinocerebrellar and corticospinal tracts and cerebrellar cells.

Mitochondrial disoder
Onset in teenage

Associated with HOCM and mild dementia

540
Q

What is the presentation of Friedrich’s Ataxia?

A
- Pes Cavus and scoliosis 
Bilateral cerebellar signs (age <25) 
- Ataxia 
- Dysarthria
- Nystagmus 

Leg wasting + areflexia but extensor plantar
Loss of lower limb proprioception and vibration sense
Optic atrophy (paleness of the disc)
HOCM –> ESM + 4th heart sound
DM –> Hyperglycaemia

20 yr old present with progressive difficulty in walking. Legs are stiff she has been complaining of tripping . UNcle has similar symptoms. Paternal grandfather, also had life long difficulties walking and died of an MI at 59. On examination, she is dysarthrtic. Pes Cavus bilaterall.y
Cerebellar signs

541
Q

What is hereditary spastic paraparesis?

A

Lower limb spasticity
Ataxia
Extrapyramidal signs

542
Q

HTLV-1?

A

Retrovirus in Japan and Caribbean?

Features 
- Adult T cell leukaemia/lymphoma
- Tropical spastic paraplegia
Slowly progressing spastic paraplegia
Sensory loss and paraesthesia
Bladder dysfunction
543
Q

How to present MS?

A

On inspection Mrs is well There is a right sided pronator drift and psuedoathetosis of the fingers (suggesting loss of proprioception). There is disuse atrophy of the muscles of the right arm. There are pyramidal signs as evidenced by rebound phenomenon and an intention tremor.

The combination of cerebellar, dorsal and pyramidal signs suggest a central pathology and the most likely diagnosis is demyelinating disease such as multiple sclerosis. Mrs X is currently using a wheelchair and there is a urinary catheter in place. She needs a full functional assessment.

I’d like to examine the fundi to complete my examination. The diagnosis can be confirmed on MRI looking for periventricular white matter lesion and VEPs. A full history would be beneficial to assess.

544
Q

Presenting INO

A

There is an ataxic nystagmus in the right eye as if fails to adduct. When the abducting eye is covered the other eye is able to adduct normally.

This is intranuclear ophthalmoplegia which is most likely related to MS due to lesion in the medial longitudinal fasciculus.

545
Q

Causes of demyelination

A
HIV
CIDP
Multiple Myeloma
MGUS
HMSN
546
Q

How to present CMT?

A

On inspection of MR X there is symmetrical wasting of the muscles of the lower limbs distally with evidence of hammer toes with relative preservation of the thigh muscles with pes cavus. THere is also wasting of the distal small muscles of the hands.

There is a LMN pattern of weakness in the extensor of the toes and feet and a loss of sensation to light touch in a stocking distribution in both legs. The ankle jerks are absent and the plantar reflexes show no response.

The gait is high-stepping.

There is a combined sensory and motor peripheral neuropathy - likely hereditary motor and sensory neuropathy.

Mr X is currently using foot splints as mobility aids. He needs a full functional assessment. The diagnosis can be confirmed with a family history, nerve conduction studies and genetic testing.

547
Q

Pes Cavus causes?

A

High Foot arch that does not flatten on weight bearing

  • Causes: bilateral: Friedrich’s ataxia, spinal cord tumours, syringomyelia.
  • Unilateral: polio, compartment syndrome, spinal trauma/tumour.
548
Q

PCAA

A

Posterior communicating artery aneurysms

Painful eye to move apart from laterally and downward. Pupil is enlarged and the eyelid drooping.

549
Q

How to present PD?

A

This gentleman has signs on inspection of a resting pill-rolling tremor, expressionless face and decreased blink rate.

The gait is stooped, slow to initiate, and the steps are shuffling with decreased arm swing.

On examination of the arms there are asymmetric: UMN signs including increased tone and lead-pipe rigidity in the left compared with right and some loss of muscle power in all groups tested.

There is bradykinesia to all movements. There is no sensory involvement.

This gentleman has signs consistent with Parkinsonism - he needs a full functional assessment and MMSE. He is currently limited in his mobility as he uses a walkign stick.

I would like to take a drug history, look for postural BP drop and examine the cranial nerves for limited upgaze.

550
Q

Incontinence + dementia + shuffling gait

A

Normal pressure hydrocephalus

  • Failure to absorb CSF in subarachnoid spcce
  • LP - Normal pressure
  • Shunt will treat 70%. - Ventriculoperitoneal shunting.

Wet, wobbly and whacky.

551
Q

72 yr old - acute onset dizziness, sensory loss over right side of his face and left arm and leg. On examination, his right pupil is smaller with a mild right ptosis. Which arterial territory is likely to be affected?

A

Right PICA (same side). Switches below that level.

552
Q

Ophthalmoplegia

A

Primary Position
Max diplopia (outer image)
3rd nerve pupil involvement

553
Q

3rd nerve palsy

A

On inspection there has a complete right sided ptosis

Globe down and out

Pupil dilatation
- if present means parasympathetic nerve damage, only in surgical causes like tumours/dissection/PCAA (classically painful)

  • Diabetes spares the pupil classically
554
Q

What muscle for ptosis?

A

LPS - levator palpebrae superioris

555
Q

Management of 3rd Nerve Palsy

A

Check the BP and the capillary glucose and examine for a 4th nerve palsy

Dilated pupil warrants CT scan + angiography

556
Q

Causes of Medical 3rd nerve palsy

A

Mononeuritis multiplex,
HTN + DM;
autoimmune, MS.

Additional cause include

  • Infections: lyme disease, syphillis
  • Autoimmune disease: SLE,RA, Small vessel vasculitidies
  • Malignancy: haematological malignancy

Consider mass lesion or compression along route of nerve.

  • Mid-brain
  • Cavernous sinus
  • Base of skull.
557
Q

Pupil involvement - 4th nerve palsy

A

Eye is held adducted and slightly elevated and the patient has a head tilt away from the affect eye.

Unable to depress eye in adduction - causes worse diplopia

Outer image disappears when the affected eye is covered.

558
Q

Causes of 4th nerve palsy

A

Vertical diplopia - reading books or climbing stairs
Trauma
MOnoneuritis mutliplex
Congenital

III, IV, V1, VI - Cavernous sinus
- Tumour, thrombosis, aneurysm

559
Q

6th Nerve palsy?

A

Longest intracranial nerve - false localising sign
May be raised ICP or Cancer.
Tumour till proven otherwise.

Examine the other cranial nerves; 7th and 8th nerve palsies and cerebellar system.

Fundoscopy: papilloedema
Palsy results in defective abduction –> Horizontal diplopia.

560
Q

DDx Sixth Nerve Palsy

A

ICP
Helps to be anatomical - so start at the nucleus
Nerve itself (infiltrated by heavy metal/sarcoid, demyelinate)
- Diabetic neuropathy
- Compression by tumour, arterial aneurysm
- CPA

561
Q

CPA - cerebello-pontine angle lesion

A
Petrous temporal bone, lateral pons, cerebellar 
First sign - loss of corneal reflex
- Failure of Abduct eye
- SNHL 
- Facial sensation loss
- Cerebellar sign

-Which nerves? 69 Nooooo try 58.

562
Q

Weber’s Syndrome

A

Midbrain: ipsilateral III CN and contralateral hemiparesis.

Involves the oculomotor nerve resulting in an ipsilateral CN III palsy.

563
Q

Rule of S+M

A

Lateral (Sensory + sympathetic + pain)

  • Pons = 5,7,8
  • MEdulla = 9,10,11

Medial (motor)

  • 3,4 (midbrain)
  • Pons (6)
  • Medulla (12)
564
Q

Causes of Bilateral Ptosis

A

MG
Myotonic dystrophy
Bilateral Horner’s and 3rd Nerve palsy
Congenital

565
Q

Dilated pupil?

A

Compressive 3rd nerve

Holmes Adie Pupil

566
Q

Compressed pupil?

A

Miosis

Argyll-Robertson,
Horner’s

567
Q

Holmes Adie Pupil

A

Mainly in women
Benign
Associated with Sjorgens
Sluggish pupil constriction to light, normal to accommodation.

May be associated with reduced/absent reflexes and autonomic neuropathy.

568
Q

Argyll- Robertson

A

Small, irregularly shaped pupils
Neurosyphillis
Diabetes

Accommodates but doesn;t react

569
Q

Wasting of hand muscle

A

Dorsal guttering - first to be affected in ulnar lesion.

570
Q

Presentation of stroke

A

This elderly lady is well on inspection and hold her right hand in a flexed position at the elbow with her right leg in extension. The gait is hemiplegic.

On examination of the legs a pyramidal pattern of weakness is evident with UMN sign on the right including increased tone, reduced power to at least grade 4 (with relatively greater weakness in the flexors) and brisk reflexes. Coordinations is intact but sensations is impaired to light touch with no clearly demonstrable sensory level or dermatome.

Those signs suggest a hemiparesis and the commonest cause of this would be a CVA.

The patient is currently wheelchair bound. This lady needs a full functional assessment.
To complete my exam i would like to fully examine the neurology in the arms and cranial nerves, look at an ECG for AF, the BP chart and dipstick the urine to aggressively control her secondary risk factors.

Image the brain with a stroke protocol MRI.

571
Q

Wernicke’s Encephalopathy

A

Thiamine Deficiency - chronic alcohol use or repeated vomiting

Triad: Delirium, ataxia and an eye movement disorder (most common nystagmus, could be 6th nerve or INO) . Can also have peripheral neuropathy. Bilateral lateral rectus palsy.

-

Mamillary bodies - classically involved on MRI.

IV thiamine for 2 days, then tablets.

Irreversible damage = amnesic syndrome (Korsakoff psychosis).

Addition of antero-retrograde amnesia and confabulation.

572
Q

Fundoscopy

A

Red reflex (loss in cataract, retinoblasta, vitreous haemorrhage)
Disc
Follow each vessel to periphery
Look at the light - macula

3 C of disc - Colour, cup and contour

573
Q

Sudden visual loss

A

Vitreous - DM
Retina (RA/RV occlusion, hemorrhagic macular degeneration)
Optic nerve (ischaemia)
Cortex

Headaches? GCA?

Unilateral

  • Compressive
  • Ischaemic
  • Demyelination

Bilateral

  • Inherited
  • Toxic
  • Nutritional - Vitamin A
574
Q

Retinitis Pigmentosa?

A

Blind Patient (white stick)
ABsent red reflex - associated cataract
Peripheral retina - bone spickle pigmentation

Optic atrophy (pale disc)

50% is sporadic
Friedrich’s ataxia
Deafness (hearing-ad/white stick with red stripes): Kearns-Sayre syndrome.

Discussion - blind by age 40, first sign - reduction in night vision
Retinal degeneration
Vitamin A - slow progression.

575
Q

Syndromes with RP?

A

Lawrence-Moon-Bardet- Diedl: polydactyl
Usher: deafness
Kearns-Sayre: ophthalmoplegia - can’t see.
Refsum: cerebellar ataxia

576
Q

Gradual Visual Loss

A

Cataract
ARMD
Diabetic maculopathy
Glaucoma

577
Q

Diabetic Retinopathy - Made worse with pregnancy

A

Retinopathy - Need photocoagulation (reduce rate of progression) - Tunnel vision (peripheral vision worse). Should have a full assessment.

  • Aneurysm
  • Hard exudates
  • Cotton wool spots

Maculopathy
- Symptomatic loss of central vision (treated with laser).

578
Q

Neuroleptic malignant syndrome?

A
  • Dopamine blockage by antipsychotics trigger massive glutamate release and subsequent neurotoxicity and muscle damage.
  • Presents with pyrexia, muscle rigidity, autonomic lability: HTN, Tachy, tachypnoea, agitated delirium with confusion.

CK present in most cases. AKI secondary to rhabdo may develop in severe cases - leading to deranged U+E.

Management

  • Stop antipsychotic
  • IV fluid s
  • Dantrolene in some cases.
  • Mainly dopamine agonist like bromocriptine.
579
Q

Motor, Sensory or both cranial nerves?

A

Some Say Marry Money But My Brother Says Big Brains Matter Most

580
Q

FLAIR MRI

A

Estimating onset of acute ischaemic stroke within 6 hours enabling more patients to receive thrombolytic therapy.

T2 is more sensitive than T1 weighted imaging in detecting ischaemic changes.

581
Q

Diffusion weighted MRI?

A

Early changes after stroke event and diagnose vascular strokes highlighting the early presence of hypoxic oedematous changes.

582
Q

CT head with contrast?

A

Detecting cerebral mets and abscesses.

583
Q

Tuberous sclerosis?

A

Genetic condition of autosomal dominant inheritance.

Neurocutaneous feature:

  • Depigmented ash-leaf spots which fluoresce under UV light.
  • Roughened patches of skin over lumbar spine.
  • Adenoma sebaceum (angiofibromas): butterfly distribution over nose.
  • Fibromata beneath nails
  • Cafe-au-lait spots may be seen.

Neurological features

  • Developmental delay
  • Epilepsy
  • Intellectual impairment

Also

  • Retinal hamartomas
  • Rhabodymoyomas
  • Gliomatous changes in brain
  • PKD
584
Q

Lennox-Gastaut syndrome

A

Severe, complex, childhood onset epilepsy.

Associated with West Syndrome

585
Q

Neuropathic pain management?

A

Damage to nervous system - often difficult to treat and responds poorly to standard analgesia.

Examples - diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, prolapsed intervertebral disc.

First line
- Amitriptyline, duloxetine, gabapentin or pregabalin

  • if the first-line drug treatment does not work try one of the other 3 drugs.
  • Tramadol may be used as rescue therapy for exacerbation.
    Topical capsaicin may be used for localised neuropathic pain
586
Q

Hoover sign

A

Push down with your right heel and lift left lef up against resistance.

Sign of leg paresis is a specific manouever to distinguish organic and non-organic paresis.

This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.

587
Q

Jendrassik Maneouvre

A

Compares a reflex with/without distraction.

588
Q

Hoffman’s sign

A

Reflex test to investigation corticospinal tract lesion.

This patient is likely to have degenerative cervical myelopathy [DCM], which is associated with upper motor neuron signs. Hoffmans sign is elicited by flicking the distal phalaynx of the middle finger to cause momentary flexion. A positive result is exaggerated flexion of the terminal phalanyx of the thumb. Patients with DCM often have subtle signs that are easily missed [1], but as a progressive condition, these are likely to get worse [2]. Whilst the sensitivity of signs is low (i.e. their absence does not rule out a problem), their specificity is high (i.e. there will be a problem). Therefore, in order to diagnose early DCM and improve patient outcomes, a high index of suspicion, alongside a comprehensive neurological examination and monitoring for progression is required.

589
Q

Psychogenic non-epilectic seizure

A

Remains conscious during whole-body convulsions, has no post-ictal state and can remember what happened.

Focal seizures do NOT involve whole-body convulsions.

590
Q

MRC grading?

A

Grade 0 = No movement
Grade 1 = Trace of contraction
Grad 2 = Movement at the joint with gravity eliminated
Grade 3 = Movement against gravity, but not against added resistance
Grade 4 = Movement against an external resistance with reduced strength
Grade 5 = Normal strength

591
Q

Brain abscess?

A

May result from a number of causes:

CNS abscesses may result from a number of causes including, extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis
The presenting symptoms will depend upon the site of the abscess (those in critical areas e.g.motor cortex) will present earlier. Abscesses have a considerable mass effect in the brain and raised intra cranial pressure is common.
Although fever, headache and focal neurology are highly suggestive of a brain abscess the absence of one or more of these does not exclude the diagnosis, fever may be absent and even if present, is usually not the swinging pyrexia seen with abscesses at other sites.
Assessment of the patient includes imaging with CT scanning.
Treatment is usually surgical, a craniotomy is performed and the abscess cavity debrided. The abscess may reform because the head is closed following abscess drainage.

592
Q

Intercostobrachial

A

Injured during axillary dissection. Armpit numbness.

593
Q

Cataplexy

A

Sudden and transient loss of muscular tone caused by strong emotion (laughter, being frightened). Around 2/3 patients with narcolepsy have cataplexy.

Ranges from buckling knees to collapse.

594
Q

5-HT3 antagonists

A

Antiemetics used in the management of chemotherapy related nausea.

Mainly act in the chemoreceptor trigger zone area of the medulla oblongata.

Examples - ondansetron, granisetron.

Constipation and prolonged QT interval are common SE.

595
Q

Reflexes?

A

Ankle - S1-S2 Button my shoe
Knee - L3-L4 Kick the door
Bicep - C5-C6 Pick up sticks
Tricep - C7-C8 open the gate

596
Q

Carbamazepine

A

Carbamazepine is chemically similar to the tricyclic antidepressant drugs. It is most commonly used in the treatment of epilepsy, particularly partial seizures, where carbamazepine remains a first-line medication. Other uses include
trigeminal neuralgia
bipolar disorder

Adverse effects
P450 enzyme inducer
dizziness and ataxia
drowsiness
headache
visual disturbances (especially diplopia)
Steven-Johnson syndrome
leucopenia and agranulocytosis
hyponatraemia secondary to syndrome of inappropriate ADH secretion
597
Q

What is autonomic dysreflexia.

A

Can only occur if the spinal cord injury occurs above the T6 level.

  • Combination of severe HTN, flushing, sweating without congruent response in HR in the context of spinal cord injury.
  • Indicates autonomic dysreflexia
  • Indicates a discontinuity between nocioreceptors on the visera and brainstem autonomic centres due to cord injury.

Afferent signals cause a sympathetic spina lreflex via thoracolumbar outflow. Usually centrally mediated, parasympathetic response is prevented by the cord lesion.

598
Q

What is a low pressure headache?

A

Commonly develops after a lumbar puncture

Caffeine and fluids used to treat low pressure headache. Small volume of cerebrospinal fluid is removed, which reduced pressure around the brain.

Second line: blood patch - small volume of the patients blood in to the epidural space a the site of the original lumbar puncture. The blood clots and in effect patches up the meningeal leak.

usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

Factors contributing to headache

  • Increased needle size
  • Direction of bevel
  • Not replacing the stylet
  • Increased number of LP attempts

Factors which do not contribute to headache

  • Increased volume of CSF removed
  • Bed rest following procedure
  • Increased fluid intake post procedure
  • Opening pressure of CSF
  • Position of patient
599
Q

Axillary nerve

A

Winds around the bone at the neck of the humerus. Also at risk during shoulder dislocation.

600
Q

Restless Leg syndrome?

A

Restless legs syndrome (RLS) is a syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia. It is extremely common, affecting between 2-10% of the general population. Males and females are equally affected and a family history may be present

Clinical features
uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)

Causes and associations

  • there is a positive family history in 50% of patients with - idiopathic RLS
  • iron deficiency anaemia
  • uraemia
  • diabetes mellitus
  • pregnancy

Mangement

simple measures: walking,stretching, massaging affected limbs
treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
benzodiazepines
gabapentin
Ropinirole

601
Q

Spontaneous intracranial hypotension

A

Spontaneous intracranial hypotension is a very rare cause of headaches that results from a CSF leak. The leak is typically from the thoracic nerve root sleeves.

Risk factors include connective tissue disorders such as Marfan’s syndrome.

Key features
strong postural relationship with the headache generally much worse when upright. Patients may, therefore, be bed-bound

Investigations
MRI with gadolinium: typically shows pachymeningeal enhancement

Management
usually conservative
if this fails an epidural blood patch may be tried

602
Q

Bacterial vaginosis?

A

Anaerobic organisms = Gardnerella vaginalis.

Fall in lactic acid - raised vaginal pH.

Fishy, offensive odour.

Amsel criteria

  • Thin, white homogenous discharge.
  • Clue cells on microscopy
  • Vaginal pH >4.5
  • positive whiff test.

Manage with oral metronidazole

603
Q

Epidural spinal abscess investigation for confirmation?

A

Full spine MRI to search for skip lesions.

SEA is commonly caused by Staph A. Due to IVDU or direct inoculation.

Presents with fever, back pain, focal neurological deficits.

604
Q

Pressure Sores?

A
Pressure ulcers develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel. The following factors predispose to the development of pressure ulcers:
malnourishment
incontinence
lack of mobility
pain (leads to a reduction in mobility)

Waterlow score used to screen for patients who are at risk of developing pressure area.

605
Q

Head injury ATLS - patient comes in with cerebral contusion what is the management?

A

Insert an intracranial pressure monitoring device.

For those with GCS 3-8 with normal CT.

Mandatory for patients with GCS 3-8 with abnormal CT can.

606
Q

Bilaterally dilated pupils?

A

Poor CNS Perfusion

607
Q

Unilaterally dilated pupils?

A

3rd nerve compression secondary to tentorial herniation

608
Q

Bilaterally constricted pupils?

A

Opiates
Pontine lesions
Metabolic encephalopathy

609
Q

Unilateral constricted pupils

A

Sympathetic pathway disruption

610
Q

Brain stem death?

A

Criteria for brain stem death testing

  • Deep coma of known aetiology
  • reversible cause excluded
  • No sedation
  • Normal electrolytes.
611
Q

Testing for brain death?

A
  • Fixed pupils which do not respond to sharp changes in the intensity of incident light
  • No corneal reflex
  • Absent oculo-vesibular reflex
  • No response to supraorbital pressure
  • No cough reflex to bronchial stimulation or gagging response
  • No observed respiratory effort in response to disconnection of ventilator.
612
Q

When is an urgent neurosurgical review warranted before CT?

A

GCS <8 or = 8 with open fracture and depressed skull fracture.

613
Q

When should a patient with a +ve Battle’s sign have a CT?

A

Within 1 hr.

614
Q

What are the clinical suspicions of cervical spine injury?

A

Age 65 and older
Danger mechanism of injury - fall from height, axial load to head like diving.
Focal peripheral neurological deficit
Paraesthesia in the upper or lower limbs
Provisional written radiology report should be made within 1hr of scan being performed.

615
Q

What is binocular vision post-facial trauma and pain on opening mouth suggest?

A

Depressed fracture of the zygoma.

616
Q

Infants presenting with hydrocephalus?

A

Present with increased head circumference, a bulging fontanelle and sunsetting of the eyes (pressure on the tectal plate)

617
Q

Hydrocephalus definition?

A

Hydrocephalus is defined as a condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption.

618
Q

Symptoms of hydrocephalus?

A

Headache (typically worse in the morning, when lying down and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)

619
Q

Types of hydrocephalus

A

Obstructive (‘non-communicating’) hydrocephalus - due to the structural pathology blocking the cerebrospinal fluid.

Non-obstructive (‘communicating’) hydrocephalus - increased production or failure of absorption - post-haemorrhagic.

620
Q

Normal pressure hydrocephalus triad?

A

Dementia
Incontinence
Disturbed gait

621
Q

Diffuse axonal injury?

A

Head is rapidly accelerated or decelerated.

Multiple haemorrhages
Diffuse axonal damage in white matter.