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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the normal pressure hydrocephalus triad?

A
  1. Urinary incontinence
  2. Dementia and bradyphrenia
  3. Gait abnormality (similar to Parkinson’s)
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2
Q

How does a pontine haemorrhage usually present?

A

Reduced GCS
Paralysis
Pinpoint pupils

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3
Q

How does an anterior cerebral artery lesion present?

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

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4
Q

How does a middle cerebral artery lesion present?

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

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5
Q

How does a posterior cerebral artery lesion present?

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

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6
Q

How does Weber’s syndrome (lesion of branches of posterior cerebral artery that suppies the midbrain) present?

A

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

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7
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome) lesion symptoms?

A

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

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8
Q

Anterior inferior cerebellar artery (lateral pontine syndrome) lesion symptoms?

A

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

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9
Q

Retinal/ophthalmic artery lesion symptoms?

A

Amaurosis fugax

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10
Q

Basilar artery lesion symptoms?

A

‘Locked-in’ syndrome

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11
Q

How do lacunar stroke present?

A

Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
Strong association with hypertension
Common sites include the basal ganglia, thalamus and internal capsule

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12
Q

Clinical signs CN3?

A

Palsy results in
ptosis
‘down and out’ eye
dilated, fixed pupil

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13
Q

Clinical signs CN4?

A

Palsy results in defective downward gaze → vertical diplopia

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14
Q

Clinical signs CN5?

A

Lesions may cause:
trigeminal neuralgia
loss of corneal reflex (afferent)
loss of facial sensation
paralysis of mastication muscles
deviation of jaw to weak side

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15
Q

Clinical signs CN6?

A

Palsy results in defective abduction → horizontal diplopia

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16
Q

Clinical signs CN7?

A

Lesions may result in:
flaccid paralysis of upper + lower face
loss of corneal reflex (efferent)
loss of taste
hyperacusis

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17
Q

Clinical signs CN8?

A

Hearing loss
Vertigo, nystagmus
Acoustic neuromas are Schwann cell tumours of the cochlear nerve

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18
Q

Clinical signs CN9?

A

Lesions may result in;
hypersensitive carotid sinus reflex
loss of gag reflex (afferent)

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19
Q

Clinical signs CN10?

A

Lesions may result in;
uvula deviates away from site of lesion
loss of gag reflex (efferent)

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20
Q

Clinical signs CN11?

A

Lesions may result in;
weakness turning head to contralateral side

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21
Q

Clinical signs CN12?

A

Tongue deviates towards side of lesion

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22
Q

What is the diagnostic test for MS?

A

MRI with contrast

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23
Q

What are the three features of Wernicke’s (receptive) aphasia?

A

Speech Fluent
Comprehension abnormal
Repetition impaired

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24
Q

What is the difference between aphasia and dysarthria?

A

Aphasia- language comprehension and production problems
Dysarthria- Motor speech disorder

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25
Q

Where is Wernicke’s area located?

A

Superior temporal gyrus

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26
Q

Where is Broca’s area located?

A

Inferior frontal gyrus

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27
Q

What are the features of Broca’s (expressive) aphasia

A

Speech in non-fluent, laboured and halting
Repetition impaired
Comprehension normal

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28
Q

Is Bell’s palsy upper or lower motor neurone

A

Lower motor neurone and meaning the forehead is affected (UMN spares upper face)

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29
Q

What are the symptoms of Bell’s palsy

A

Lower motor neurone facial nerve palsy (forehead affected)
Post-auricular pain (may precede paralysis)
Altered taste
Dry eyes
Hyperacusis

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30
Q

Management of Bell’s palsy

A
  1. Corticosteroids- prednisolone
    (Potentially antiviral aciclovir)
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31
Q

What are the key features of MND?

A

Asymmetric limb weakness
Mixtures of lower and upper motor neurone signs
Wasting of small muscles in hand
Fasciculations
Absence of sensory signs/symptoms

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32
Q

What is conduction dysphasia?

A

A stroke affecting the arcuate fasciculus in the dominant hemisphere (connection between Wernicke’s and Broca’s area)

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33
Q

What are the features of conduction dysphasia?

A

Speech fluent but repetition poor
Comprehension relatively intact

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34
Q

What is first line for spasticity in MS?

A

Baclofen or Gabapentin

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35
Q

What is first line in an acute relapse of MS?

A

High dose steroids (methylprednisolone)

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36
Q

What is the investigation for narcolepsy?

A

Multiple sleep latency EEG

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37
Q

What is a focal aware seizure?

A

Sudden short-lived change is senses (smell, taste, tactile, visual). No post ictal. Accompanied by sweating, twitching or gaze deviation.

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38
Q

What is a complex focal seizure?

A

A focal impaired awareness seizure

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39
Q

Do all patients lose conciousness in generalised seizures?

A

Yes

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40
Q

What are the types of generalised seizure?

A

Tonic-clonic
Tonic
Clonic
Atonic
Absence

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41
Q

What is a focal to bilateral seizure? (secondary generalised)

A

Starts in one side and area of the brain before spreading to both lobes

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42
Q

Difference between tibial nerve palsy and peroneal nerve palsy

A

TIPPED
Tibial- inversion, plantarflexion
Peroneal- eversion, dorsiflexion

Opposite one spared wheras in L5 radiculopathy all knocked out and weakness of hip abduction

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43
Q

How to manage bladder dysfunction in MS?

A

May be (urgency, incontinence, overflow)
Get ultrasound to assess bladder emptying (anticholinergics may worsen problem in some)
If significant residual volume → intermittent self-catheterisation
If no significant residual volume → anticholinergics may improve urinary frequency

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44
Q

What are the features of autonomic dysreflexia?

A

Hypertension, flushing and sweating above the level of the lesion
Paleness below region

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45
Q

What type of Parkinson’s does asymmetrical tremor (symptoms) suggest?

A

Idiopathic Parkinson’s

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46
Q

What is the triad of Parkinson’s

A

Bradykinesia, tremor and rigidity

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47
Q

What type of tremor is seen in Parkinson’s

A

Unilateral that improves with voluntary movement

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48
Q

What is the key investigation for encephalitis?

A

Cerebrospinal fluid PCR

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49
Q

What is the management of encephalitis?

A

Intravenous aciclovir in all cases of suspected encephalitis

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50
Q

What are the features of progressive supranuclear palsy?

A

Postural instability, impairment of vertical gaze, Parkinsonism and frontal lobe dysfunction

Parkinson’s with visual problems and poor response to l-dopa

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51
Q

What is the acute management of a cluster headache?

A

100% oxygen
Subcutaneous triptan

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52
Q

What is the prophylactic treatment for a cluster headache?

A

Verapamil
(Tapering dose of prednisolone)

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53
Q

What condition is Lambert-Eaton syndrome also associated with?

A

Small cell lug caner

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54
Q

Myasthensia gravis and Lambert-Eaton difference?

A

MG worse with exercise, LE gets better with exercise

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55
Q

Features of Lambert-Eaton syndrome?

A

Repeated muscle contractions lead to increased muscle strength
Limb-girdle weakness (manifesting as a waddling gait)
Hyporeflexia
Autonomic symptoms: dry mouth, impotence, difficulty micturating
(No eye problems like in MG)

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56
Q

Lambert-Eaton syndrome management

A

Treat underlying cancer
Immunosupression (prednisolone and/or azathioprine)
Intravenous immunoglobulin therapy may be helpful

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57
Q

What is Guillain-Barre syndrome?

A

Immune mediated demyelination of the peripheral nervous system often triggered by an infection

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58
Q

What is often the initial symptom of GB

A

Back/leg pain

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59
Q

What are the characteristic features of GB?

A

Progressive, symmetrical weakness of all the limbs
Weakness typically ascending with legs affected first
Reflexes reduced or absent
Sensory symptoms mild
(History gastroenteritis common)

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60
Q

What are the GB investigations?

A

Lumbar puncture- High protein, normal WCC
Nerve conduction studies

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61
Q

Multiple sclerosis features

A

Lethargy

Visual:
Optic neuritis
Optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature

Sensory:
Pins and needles
Numbness
Trigeminal neuralgia

Motor:
Spastic weakness

Cerebellar:
Ataxia
Tremor

Urinary incontinence
Sexual dysfunction
Intellectual deterioration

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62
Q

How to remember GCS?

A

Motor (6 points) Verbal (5 points) Eye opening (4 points). Can remember as ‘654…MoVE’

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63
Q

What are the break downs for GCS?

A

Motor response
6. Obeys commands
5. Localises to pain
4. Normal flexion
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None
Verbal response
5. Orientated
4. Confused
3. Words
2. Sounds
1. None
Eye opening
4. Spontaneous
3. To speech
2. To pain
1. None

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64
Q

What are the features of a stroke?

A

Motor weakness
Speech problems (dysphasia)
Swallowing problems
Visual field defects (homonymous hemianopia)
Balance problems

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65
Q

What are the criteria for offering thrombolysis?

A

Patient presents within 4.5 hours of onset of symptoms
Patient has not has a previous intracranial haemorrhage, uncontrolled hypertension, pregnant etc

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66
Q

What should be done as soon as haemorrhagic stroke excluded?

A

Given 300mg of aspirin and anti platelet therapy continued

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67
Q

TIA management?

A

Give 300mg aspirin immediately unless contraindicated

If TIA in last 7 days- assessment by stoke physician within 24 hours

If TIA over 1 week ago- refer to specialist within 7 days

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68
Q

What is the management for haemorrhagic strokes?

A

Supportive

Stop/reverse anticoagulation/ antithrombotic

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69
Q

CN Motor, Sensory or Both

A

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

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70
Q

What does a defective CN IV cause?

A

Defective downward gaze- vertical diplopia

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71
Q

What are the three classifications of subdural hematoma?

A

Acute

Subacute

Chronic

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72
Q

What is the presentation of acute subdural hematoma on a CT?

A

Crescent shaped collection, not limited by suture lines

Hyperdense (bright)

If large may cause midline shift or herniation

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73
Q

Who is most at risk of subdural haematomas?

A

Elderly or alcoholic patients

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74
Q

What is the presentation of a chronic subdural haematoma?

A

Several weeks to month progressive confusion, reduced conciousness or neurological defecit

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75
Q

What is the difference between chronic and acute subdural on CT scans?

A

Acute- hyperdense (bright)

Chronic- hypodense (dark)

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76
Q

What is the treatment for an essential tremor?

A

Propanolol

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77
Q

What are the features of essential tremor?

A

Postural tremor- worse if arms outstretched

Improved by alcohol and rest

Most common cause of titubation (head tremor)

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78
Q

What are the common features of MND?

A

Asymmetric limb weakness most common presentation of ALS

Mixture of LMN and UMN signs

Wasting of small hand muscles/ tibialis anterior is common

Fasciculations

Absence of sensory signs

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79
Q

CN3 clinical presentation?

A

Palsy:
Ptosis
Down and out eye
Dilated, fixed pupil

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80
Q

CN4 clinical presentation?

A

Defective downwards gaze- vertical diplopia

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81
Q

CN5 clinical presentation?

A

Trigeminal neuralgia

Loss of corneal reflex

Loss of facial sensation

Paralysis of mastication muscles

Deviation of jaw to weak side

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82
Q

CN6 clinical presentation?

A

Defective abduction- horizontal diplopia

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83
Q

CN7 clinical presentation?

A

Flaccid paralysis of upper + lower face
Loss of conreal reflex (efferent)
Loss of taste
Hyperacusis

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84
Q

CN8 clinical presentation?

A

Hearing loss
Verigo, nystagmus
Acoustic neuromas are Schwann cell tumours of the cochlear nerve

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85
Q

CN9 clinical presentation?

A

Hypersensitive carotid sinus reflex
Loss of gag reflex (afferent)

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86
Q

CN10 clinical presentation?

A

Uvula deviates away from the site of lesion
Loss of gag reflex (efferent)

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87
Q

CN11 clinical presentation?

A

Weakness turning head to contralateral side

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88
Q

CN12 clinical presentation?

A

Tongue deviates towards side of lesion

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89
Q

What are the features of MS?

A

Lethargy

Visual- optic neuritis, optic atrophy, Uhthoff’s phenomenon- worsening of vision following rise in body temperature, internuclear opthalmoplegia

Sensory- Pins/needles, numbness, trigeminal neuralgia, Lhermitte’s syndrome- paraesthesiae in limbs on neck flexion

Motor- spastic weakness- most commonly seen in the legs

Cerebellar- ataxia- seen during acute relapse, tremor

Others:
Urinary incontinence
Sexual dysfuntion
Intellectual deterioration

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90
Q

Presentation of acute narrow angle glaucoma?

A

Severe pain around eye, nausea, redness, misty vision and semi dilated pupil

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91
Q

Anterior cerebral artery lesion?

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

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92
Q

Middle cerebral artery lesion?

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

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93
Q

Posterior cerebral artery lesion?

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

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94
Q

Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain) lesion?

A

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

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95
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome) lesion?

A

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

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96
Q

Anterior inferior cerebellar artery (lateral pontine syndrome) lesion?

A

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

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97
Q

Retinal/ophthalmic artery lesion?

A

Amaurosis fugax

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98
Q

Basilar artery lesion?

A

‘Locked-in’ syndrome

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99
Q

Lacunar stroke presentation?

A

Isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
Strong association with hypertension
Common sites include basal ganglia, thalamus and internal capsule

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100
Q

Parietal lobe lesions presenation?

A

Sensory inattention
Apraxias
Astereognosis
Inferior homonymous quadrantanopia
Gerstmann’s syndrome

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101
Q

Occipital lobe lesions?

A

Homonymous hemianopia (macular sparing)
Cortial blindness
Visual agnosia

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102
Q

Temporal lobe lesion?

A

Wernicke’s aphasia- (forms speech)- speech remains fluent but word substitutions and neologisms
Superior homonymous quadrantanopia
Auditory agnosia
Prosopagnosia

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103
Q

Frontal lobe lesions?

A

Expressive Broca’s aphasia- speech non-fluent, laboured and halting
Disinhibition
Perseveration
Anosmia
Inability to generate a list

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104
Q

Cerebellum lesions?

A

Midline lesions- gait and truncal ataxia
Hemisphere lesions- intention tremor, past pointing, dysdiadokinesis, nystagmus

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105
Q

Amygdala problem?

A

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

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106
Q

Substantia nigra of basal ganglia?

A

Parkinson’s disease

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107
Q

Striatum (caudate nucleus) of the basal ganglia damage?

A

Huntington chorea

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108
Q

Subthalamic nucleus of basal ganglia?

A

Hemiballism

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109
Q

Medial thalamus and mammillary bodies of the hypothalamus?

A

Wernicke and Korsakoff syndrome

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110
Q

What is the presentation of a vestibular schwannoma (acoustic neuroma)?

A

Vertigo, hearing loss, tinnitus and an absent corneal reflex

Affected CN
8- vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
5- Absent corneal reflex
7- Facial palsy

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111
Q

Epilepsy treatment summary?

A

Generalised tonic clonic- M-sodium valproate
F- Lam/leve
F under 10 may get SV

Focal
1st- Lam/leve
2nd- Carbamazepine

Absence-
1st- Ethosuximide
2nd- M- SV, F- lam/leve
Carbamazepine makes them worse

Myoclonic seizures
M- SV
F- Leve

Tonic or atonic
M- SV
F- Lam

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112
Q

Tonic or atonic treatment in female?

A

Lamotrigine

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113
Q

Myoclonic treatment in female?

A

Levetiracetam

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114
Q

What are the adverse effects of sodium valproate?

A

Teratogenic
P450 inhibitor
GI- nausea
Increased appetite and weight gain
Alopecia
Ataxia
Tremor
Hepatotoxicity
Pancreatitis
Thrombocytopaenia
Hyponatraemia
Hyperammonemic encephalopathy

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115
Q

What is the treaetment for focal seizures?

A

Lamotrigine or levetiracetam

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116
Q

What is the aphasia classifications?

A

Speech non fluent

Comprehension intact- Broca’s aphasia
Comprehension impaired- global aphasia

Speech fluent
Comprehension relatively intact- conduction aphasia
Comprehension impaired- Wernicke’s aphasia

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117
Q

What are the side effects of levodopa?

A

Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis

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118
Q

Migraine prophylaxis?

A

1st- Propanolol or topiramate M or F not of child bearing age
2nd- Amitriptyline

Topiramate is teratogenic so not in women of child bearing age

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119
Q

What is the acute treatment of a migraine

A

1st- combination therapy-
Oral triptan + NSAID or
Oral triptan + paracetamol

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120
Q

Classic triad in Parkinson’s?

A

Bradykinesia, tremor and rigidity. Characteristically asymmetrical

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121
Q

Carbamazepine adverse effects?

A

P450 enzyme inducer
Dizziness and ataxia
Drowsiness
Headache
Visual disturbances
Steven-Johnson syndrome
Leucopenia and agranulocytosis
Hyponatreamia secondary to SIADH

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122
Q

What is given pre hospital for status epilepticus?

A

Rectal diazepam or buccal midazolam

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123
Q

What is first line in hospital for status epilepticus?

A

IV Lorazepam

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124
Q

What is the management of status epilepticus?

A

ABC
(Pre hospital rectal diazepam or buccal midazolam)
In hospital IV lorazepam (another after 5 mins)
If ongoing add levetiracetam, phenytoin or sodium valproate
If over 45 mins general anaesthesia or phenobarbital

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125
Q

Status management?

A

Oh My Lord Phone the Anaesthetist
Oxygen, midazolam, lorazepam, phenytoin, general anaesthetic

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126
Q

What is the wernicke’s encephalopathy traid?

A

Opthalmoplegia/nystagmus
Ataxia
Encephalopathy

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127
Q

Features of wernicke’s encephalopathy?

A

Oculomotor dysfunction- nystagmus, opthalmoplegia
Gait ataia
Encephalopathy- confusion, disorientation, indifference and inattentiveness
Peripheral sensory neuropathy

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128
Q

Treatment for wernicke’s encephalopathy?

A

Urgent replacement of thiamine

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129
Q

When does wernicke’s syndrome become wernicke-korsakoff’s syndrome

A

When there is an onset of antero and retrograde amnesia and confabulation

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130
Q

Myasthenia gravis management?

A

1st- Pyridostigmine- long acting acetylcholinerase inhibitors
Add- prednisolone initally or azathioprine, cyclosporine
Thymectomy

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131
Q

What is Creutzfeldt-Jakob disease?

A

Rapidly progressing neurological condition-
Rapid onset demetntia
Myoclonus

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132
Q

Which hemisphere is usually dominant?

A

Left- 90% in RH, 60% in LH

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133
Q

What are the features of a common peroneal lesion?

A

Most characteristic feature is foot drop

Other features:
Weakness in dorsiflexion of the foot
Weakness of foot eversion
Wasting of the anterior tibial and peroneal muscles

134
Q

What should you not do in headaches linked to Valsalva manoeuvere?

A

LP

Raised ICP until proven otherwise

135
Q

What are the features of myasthenia gravis?

A

Muscle fatigue- progressive weakness improved with rest

Extraocular muscle weakness: diplopia
Proximal muscle weakness: face, neck, limb girdle
Ptosis
Dysphagia

136
Q

What is the definition of status epilepticus?

A

A single seizure lasting over 5 mins

2 seizure within 5 mins without the person returning to normal between them

137
Q

What is the management of status epilepticus?

A

ABC

Prehospital- PR diazepam or buccal midazolam

In hospital IV lorazepam. Repeat after 5-10 mins

Start second line such levetiracetam, phenytoin or sodium valproate

If no response within 45 mins from onset, induction of general anaesthesia or phenobarbital

138
Q

What are the features of cluster headaches?

A

Intense sharp stabbing pain around one eye

Occurs once or twice a day, each episode 15mins to 2 hours
Patient agitated and restless during attack

Clusters typically last 4-12 weeks
Redness, lacrimation, lid swelling
Nasal stuffiness
Miosis and ptosis in minority

139
Q

Investigations for cluster headaches?

A

Neuroimaging

MRI with gadolinium contrast is the investigation of choice

140
Q

Management of cluster headaches?

A

Advice from specialist

Acute
100% oxygen
Subcut triptan

Prophylaxis
Verapamil
Some evidence for tapering dose of prednisolone

141
Q

What is raised GGT a sign of?

A

Excessive alcohol consumption

142
Q

Peripheral neuropathy causes that are motor loss?

A

Guillain-Barre syndrome

Porphyria

Lead poisoning

Hereditary sensorimotor neuropathies (HSMN) -

Charcot-Marie-Tooth

Chronic inflammatory demyelinating polyneuropathy (CIDP)

Diphtheria

143
Q

Peripheral neuropathy causing mainly sensory loss?

A

Diabetes

Uraemia

Leprosy

Alcoholism

Vitamin B12 deficiency

Amyloidosis

144
Q

What is alcoholic neuropathy?

A

Sensory loss prior to motor loss

From alcohol and the loss of B vitamins

145
Q

Learn dermatomes

A

N

146
Q

When is neuroleptic malignant syndrome most commonly seen?

A

In patients who have just started treatement with antipsychotics

Can also occur with levodopa if drug is suddenly stopped

147
Q

What is a good way to remember neuroleptic malignant syndrome?

A

FEVER

Fever
Encephalopathy
Vitals dysregulation- increase in HR, RR, Fever
Enzyme- CK increase
Rigidity

148
Q

What are the features of neuroleptic malignant syndrome?

A

Within hours to days of starting antipsychotics

Pyrexia
Muscle rigidity
Autonomic lability- hypertension, tachycardia and tachypnoea
Agitated delirium with cofusion

Raised creatine kinase present in most cases, AKI secondary to rhabdmyolysis may occur

Leukocytosis may also be seen

149
Q

What is the management of neuroleptic malignant syndrome?

A

Stop antipsychotic

Patients transferred to medical ward if they on psychiatric ward

IV fluids to prevent renal failure

Dantrolene may be useful in some cases

Bromocriptine may also be used

150
Q

What to do if GCS is below 8?

A

Review by an anaesthetist

Intubation and ventilation

151
Q

What are the features of seizures in the temporal lobe?

A

With or without impairment of consciousness

Aura occurs in most patients- rising epigastric sensation
Pssychic phenomena such as deja vu
Less commonly hallucinations- olfactory, auditory

Seizures typically last around 1 minute- automatisms- lip smacking, grabbing, plucking

152
Q

What are the features of seizures in the frontal lobe?

A

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

153
Q

What are the features of parietal lobe seizures?

A

Paraesthesia

154
Q

What are the features of occipital lobe seizures?

A

Floaters/ flashes

155
Q

Who is idiopathic intracranial hypertension seen in?

A

Classically young, overweight females

156
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Obesity

Female

Pregnancy

Drugs:
COCP
Steroids
Tetracyclines
Retinoids/Vit A
Lithium

157
Q

What are the features of idiopathic intracranial hypertension?

A

Headache
Blurred vision
Papilloedema
Enlarged blind spot
CN6 nerve palsy may be present

158
Q

What is the management of idiopathic intracranial hypertension?

A

Weight loss

Carbonic anhydrase inhibitors- acetazolamide

Topiramate also used, added benefit of causing weight loss

LP can be use as temporary measure

Surgery- optic nerve decompression may be needed
Lumboperitoneal shunt to reduce intracranial pressure

159
Q

What are the features of trigeminal neuralgia

A

Unilateral brief electric shock pains, abrupt in onset and termination

Pain commonly evoked by light touch- washing, talking, brushing teeth etc

Pain remits for variable periods

160
Q

What are the red flag symptoms of trigeminal neuralgia?

A

Sensory changes

Deafness

Skin or oral lesions

Only opthalmic pain

Optic neuritis

FH MS

Onset before 40

161
Q

Trigeminal neuralgia management?

A

Carbamazepine

Failure to respond to treaetment or less than 50 should prompt referral to neurology

162
Q

How to remember arm injuries?

A

A- Top of arm (humeral head dislocation)- axillary nerve injury

R- Middle of arm- radial nerve injury

M- Supracondylar- median nerve injury

163
Q

What do the different nerve roots do?

A

C4 shoulder shrugs
C5 shoulder abduction and external rotation; elbow flexion
C6 wrist extension
C7 elbow extension and wrist flexion
C8 thumb extension and finger flexion
T1 finger abduction
L2 hip flexion
L3 knee extension
L4 ankle dorsiflexion
L5 great toe extension
S1 ankle plantarflexion
S4 bladder and rectum motor supply

C5,6 pick up sticks (biceps reflex)
C7,8 lay them straight (triceps reflex)
S1,S2 buckle my shoe (ankle reflex)
L3,L4 kick the door (patellar reflex)

164
Q

What is palsy of the radial nerve associated with?

A

Wrist drop

165
Q

What are the first line treatments for Parkinson’s disease?

A

If motor symptoms affecting the patient’s quality of life- Levodopa

If motor symptoms not affecting the patient’s quality of life- dopamine agonist, levodopa or MAO-B inhibitor

166
Q

Parkinson’s management?

A

Levodopa

If not worked add in either a dopamine agonist (ropinirole, cabergoline), MAO-B inhibitor (selegiline), COMT inhibitor (entacapone), amantidine

167
Q

When should thrombolysis with alteplase be done?

A

Within 4.5 hours of onset of stroke symptoms

A haemorrhage has definitely been excluded (imaging performed)

168
Q

What can cause parkinsonism?

A

Parkinson’s disease

Drug induced- antipsychotics, metoclopramide

Progressive supranuclear palsy

Multiple system atrophy

Wilson’s disease

Post-encephalitis

Dementia pugilistica (secondary to chronic head trauma)

Toxins- carbon monoxide, MPTP

169
Q

Which anti emetic to use in Parkinsonism?

A

Donperidone as does not cross blood brain barrier

170
Q

What is degenerative cervical myelopathy?

A

Pain (neck, upper or lower limbs)

Loss of motor function (dexterity)

Loss of sensory function (numbness)

Loss of autonomic function (urinary, faecal incontinence, impotence)

Hoffman’s sign (flicking one finger they all react)

171
Q

What are the causes of raised intracranial pressure?

A

Idiopathic intracranial hypertension

Traumatic head injuries

Infection- meningitis

Tumours

Hydrocephalus

172
Q

What are the features of raised intracranial pressure?

A

Headache

Vomiting

Reduced levels of consciousness

Papillodema

Cushing’s triad- widening pulse pressure, bradycardia, irregular breathing

173
Q

What investigations and monitoring for raised intracranial pressure?

A

Neuroimaging- CT/MRI- investigate underlying cause

Invasive ICP monitoring- catheter placed into lateral ventricles of brain to measure the pressure

174
Q

What is the management of raised intracranial pressure?

A

Investigate and treat underlying cause

Head elevation to 30 degrees

IV mannitol may be used as osmotic diuretic

Controlled hyperventilation- aims to reduce pCO2, temporary lowering of ICP

Removal of CSF-
Drain from intraventricular monitor
Repeated LP
Ventriculoperitoneal shunt (for hydrocephalus)

175
Q

Which conditions could have Hoffman’s sign?

A

MS

Degenerative cervical myelopathy (DCM)

Flick one finger all twitch

176
Q

Where is the damage for a subdural haemorrhage?

A

Bridging vein between cortex and venous sinuses

177
Q

Where is the bleeding for an extradural haematoma?

A

Middle meningeal artery

178
Q

Where is the bleeding for a subarachnoid haemorrhage?

A

Berry aneurysm

179
Q

What are first line for spasticity in MS?

A

Baclofen and gabapentin

180
Q

What is subacute degeneration of the spinal cord?

A

Vitamin B12 deficiency resulting in impairment of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts

181
Q

What are the features of subacute degeneration of the spinal cord?

A

Dorsal column involvement- distal tingling/burning/sensory loss-impaired proprioception and vibration loss

Lateral corticospinal tract involvement- muscle weakness, hyperreflexia, spasticity, UMN signs in the legs, brisk knee jerk, absent ankle jerk, extensor plantars

Spinocerebellar tract involvement- sensory ataxia–> gait abnormalities
Positive Romberg’s sign

182
Q

What is a sudden onset headache reaching its maxiumum intensity within 5 minutes indicative of?

A

Subarachnoid haemorrhage

183
Q

What is the investigation for SAH?

A

Non-contrast CT head as quicker

184
Q

What is a rare but serious complication of carbamazepine?

A

Carbemazepine can be used for trigeminal neuralgia

Steven Johnson syndrome

185
Q

What are the features of Steven-Johnson syndrome?

A

Rash typically maculopapular with target lesions being characteristic
may develop into vesicles or bullae

Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently

Mucosal involvement

Systemic symptoms: fever, arthralgia

186
Q

What drugs can cause Steven-Johnson syndrome?

A

Penicillin

Sulphonamides

Lamotrigine, carbamazepine, phenytoin

Allopurinol

NSAIDs

Oral contraceptive pill

187
Q

Hoffman’s vs Hoover’s sign?

A

HoFFman - Finger Flick (to see reflex of index finger Exaggerated or not- if exaggerated reflex then UMN lesion)
hOOver - Organic vs non Organic

188
Q

What can Hoffman’s sign differentiate between?

A

Organic and non-organic leg problems

If patient making an effort other leg presses down- organic

If patient not making effort other leg doesn’t press down- conversion disorder

189
Q

Which organism commonly causes Guillain-Barre syndrome?

A

Campylobacter jejuni

190
Q

Absent corneal reflex think which condition?

A

Acoustic neuroma

191
Q

Which cancers most commonly spread to the brain?

A

Metastatic most common type of brain tumour

Lung (most common)
Breast
Bowel
Skin
Kidney

192
Q

Glioblastoma multiforme features?

A

Poor prognosis

Associated with oedema

Surgical treatment with post operative chemotherapy

Dexamethosone for oedema

193
Q

Features of meningioma?

A

Second most common

Typically benign causing compression symptoms

Investigation- CT with contrast

Treatment- observation, radiotherapy or surgical resection

194
Q

What is the treatment for atrophic vaginitis?

A

Older post menopausal women- vaginal dryness, dyspareunia and occasional spotting

Vagianal lubricants and moisturisers, topical oestrogen cream can be used

195
Q

What happens when you give folate to a patient who is deficient in vitamin B12?

A

It can precipitate subacute degeneration of the spinal cord

Damage to the posterior columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).
Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).
Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).

Dorsal column involvement
distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
impaired proprioception and vibration sense
Lateral corticospinal tract involvement
muscle weakness, hyperreflexia, and spasticity
upper motor neuron signs typically develop in the legs first
brisk knee reflexes
absent ankle jerks
extensor plantars
Spinocerebellar tract involvement
sensory ataxia → gait abnormalities
positive Romberg’s sign

196
Q

Learn spinal cord problems

A

NJDSAf

197
Q

What does clozapine cause most dangerous?

A

Agranulocytosis, neutropaenia

198
Q

Phenytoin adverse effects?

A

Acute- dizziness, diplopia, nystagmus, slurred speech, ataxia. Later: confusion, seizures

Chronic- Gingival hyperplasia, megaloblastic anaemia, peripheral neuropathy, dyskinesia, lymphadenopathy,

Idiosyncratic- fever, rashes, hepatitis, Dupytren’s, aplastic anaemia, drug-induced lupus

Teratogenic- cleft palate and CHD

199
Q

Do phenytoin levels need to be monitored?

A

No, although trough levels immediately before dose if-

Adjustment of phenytoin dose

Suspected toxicity

Detection of non-adherence to the prescribed medication

200
Q

When should anti-D prophylaxis be given in termination of pregnancy?

A

Anti-D prophylaxis should be given to women who are rhesus D negative and are having an abortion after 10+0 weeks’ gestation

201
Q

What to do if gestation diabetes if diagnosed at over 7 when fasting?

A

Start insulin immediately

202
Q

What type of insulin is used to treat gestational diabetes?

A

Short-acting

203
Q

What is the management of endometrial hyperplasia?

A

Simple endometrial hyperplasia without atypia- high dose progestogens and repeat sampling in 3-4 months- levonorgestrel intra-uterine system may be useed

Atypia- hysterectomy usually advised

204
Q

Nerve damages on fractures?

A

The nerves damaged in humeral fractures from proximal to distal
ARM- Axillary (neck), Radial (shaft), Median (supracondylar)

205
Q

Do triptans increase the risk of serotonin syndrome?

A

Yes, sumatriptan so don’t use SSRI and triptan together

Think migraine

206
Q

What are the types of multiple sclerosis?

A

Relapsing-remitting- acute attacks followed by periods of remission

Secondary progressive disease- relapsing-remitting patients who have deteriorated and developed neurological signs and symptoms between relapses

Primary progressive disease- progressive deterioration from the onset

207
Q

What is intracranial venous thrombosis (venous sinus thrombosis)?

A

Clot in veins of brain

Can cause cerebral infarction but much less common than arterial causes

(Get signs ICP from venous occlusion)

208
Q

What are the features of intracranial venous thrombosis?

A

Headache (may be sudden onset but commonly gradual)

Nausea and vomiting

Reduced conciousness

Usually have some risk factors such as COCP, family history VTE

209
Q

Investigations for intracranial venous thrombosis?

A

MRI venography is gold standard (MR venogram)

D-dimer may be elevated

210
Q

What is the management of intracranial venous thrombosis?

A

Anticoagulation - LMWH

211
Q

What is syringomelia?

A

Collection of cerebrospinal fluid in the spinal cord

212
Q

What are the causes of syringomelia?

A

A Chiari malformation

Trauma

Tumours

Idiopathic

213
Q

What are the features of syringomyelia?

A

Cape like (neck, shoulders and arms)- loss of sensation.. continue

214
Q

Stoke management?

A

Within 4.5 hours: Thrombolysis with Alteplase, followed 24 hours later by aspirin 300mg

After 4.5 hours: No thrombolysis; just give Aspirin 300mg

215
Q

Triad for normal pressure hydocephalus remember tool?

A

Wet, wobbly and weird

Urinary incontinence, gait ataxia and dementia

216
Q

What is the definition of a TIA?

A

Now tissue based not time based

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

217
Q

What are the clinical features of a TIA?

A

The clinical features are similar to those of a stroke, i.e. sudden onset, focal neurological deficit but, rather than persisting, the features resolve, typically within 1 hour.

Possible features include:

Unilateral weakness or sensory loss

Aphasia or dysarthria

Ataxia, vertigo, or loss of balance

Visual problems

Sudden transient loss of vision in one eye (amaurosis fugax)

Diplopia

Homonymous hemianopia

218
Q

What is the assessment and referral criteria for TIAs?

A

ABCD2 no longer used

Immediate antithrombotic therapy:

Aspirin 300mg immediately unless:
1. Bleeding disorder or taking anticoagulant
2. Already taking aspirin- continue dose
3. Aspirin contraindicated

More than 1 TIA- discuss admission

Within last 7 days- 24 hour referral to specialist

Over 7 days ago- referral within a week to specialist

Don’t drive until seen by specialist

219
Q

What are the investigations of TIAs?

A

No CT unless clinical suspicion different diagnosis CT could detect

MRI- diffusion weighted- to assess territory of ischaemia

Carotid imaging- atherosclerosis in carotids can be source of emboli so- urgent carotid doppler- unless not elegible for carotid endarterectomy

220
Q

What is the further management of TIAs?

A

Secondary prevention

Antiplatelet to follow on from aspirin therapy- 1st-Clopidogrel
2nd- aspirin and dipyridamole if clopidogrel not tolerated

Lipid modification- High intensity statin- atorvastatin

Carotid artery endarterectomy- stroke or TIA and not severely disabled

Only considered if- carotid stenosis >70%

221
Q

What are the features of a brain abscess?

A

Mass effect in the brain- raised ICP common

Headache- dull

Fever

Focal neurology- oculomotor/abducens nerve palsy

Other features consistent with raised ICP- nausea, papilloedema, seizures

222
Q

Investigations of brain abscess?

A

CT scan

223
Q

Management of brain abscess?

A

Surgery- craniotomy performed

IV antibiotics- cephalosporin + metronidazole

Intracranial pressure management- dexamethasone

224
Q

What is the minimum length of time seizure free before driving a car?

A

12 months completely

After 5 years normal licence restored

225
Q

Driving rules if epilepsy?

A

All patients must not drive and must inform the DVLA

First unprovoked/isolated seizure: 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG. If these conditions are not met then this is increased to 12 months

Established epilepsy- qualify if seizure free for 12 months
No seizures for 5 years means licence restored

Should not drive while anti-epilepsy medication being withdrawn and for 6 months after the last dose

226
Q

Driving rules around syncope?

A

Simple faint: no restriction

Single episode, explained and treated: 4 weeks off

Single episode, unexplained: 6 months off

Two or more episodes: 12 months off

227
Q

Driving rules miscellaneous conditions?

A

Stroke or TIA: 1 month off driving, may not need to inform DVLA if no residual neurological deficit

Multiple TIAs over short period of times: 3 months off driving and inform DVLA

Craniotomy e.g. For meningioma: 1 year off driving*

Pituitary tumour: craniotomy: 6 months; trans-sphenoidal surgery ‘can drive when there is no debarring residual impairment likely to affect safe driving’

Narcolepsy/cataplexy: cease driving on diagnosis, can restart once ‘satisfactory control of symptoms’

Chronic neurological disorders e.g. multiple sclerosis, motor neuron disease: DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

228
Q

Acute management of cluster headaches?

A

High flow oxygen and subcutaneous sumatriptan

229
Q

What to do for a haemorrhagic transformation?

A

Stop anticoagulants such as aspirin and control BP

230
Q

What is the Cushing’s reflex?

A

Physiological nervous system response to increased intracranial pressure that results in hypertension and bradycardia

As the ICP raised to keep cerebral perfusion have to raise blood pressure but this causes counter reflex that lowers the heart rate- bradycardia

231
Q

What might a fall in CPP indicate?

A

Cerebral perfusion pressure

A cerebral ischaemia

Calculated using:

CPP= mean arterial pressure- intracranial pressure

232
Q

What is Lhermitte’s sign?

A

Electric shock sensation that extends down your spine

233
Q

What are the features of transient tachypnoea of the newborn?

A

Rapid breathing, grunting, mild intercostal recesssion

Caesarean is risk factor, maternal DM

O2 sats normal or mildly reduced

Resolves in 24-48 hours

234
Q

Features of medication overuse headache?

A

Features
Present for 15 days or more per month
Developed or worsened while taking regular symptomatic medication
Patients using opioids and triptans are most at risk
May be psychiatric co-morbiditiy

Management
Simple analgesics and triptans can be withdrawn abruptly (may initially worsen headaches)
Opioid analgesics should be gradually withdrawn

Withdrawal symptoms such as vomiting, hypotension, tachycardia, restlessness, sleep disturbances and anxiety may occur when medication is stopped

235
Q

What treatment can be helpful for severe eczema?

A

Wet wrapping

Management:

Avoid irritants
Simple emolients
Topical steroids
Wet wrapping
In severe cases, oral ciclosporin may be used

236
Q

TempORAL seizures features?

A

Oral- lip smacking, grabbing, plucking

Post ictal dysphasia

Epigastric sensation

Deja vu

Hallucinations

237
Q

What is thoracic outlet syndrome?

A

Thoracic outlet syndrome (TOS) is a disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet

238
Q

Features of thoracic outlet syndrome?

A

Painless wasting of hand muscles, patients complain of weakness

Sensory symptoms such as numbness

Cold hands, blanching or swelling

239
Q

Is the forehead affected in Bell’s palsy?

A

Yes as LMN signs

240
Q

What are the mot common triggers of autonomic dysreflexia?

A

Urinary retention and faecal impaction

241
Q

Why should topiramate be avoided in women of child bearing age?

A

Teratogenic and can reduce the effectiveness of hormonal contraceptives

242
Q

When can pre eclampsia and gestational hypertension be diagnosed in pregnancy?

A

Only after 20 weeks

243
Q

Meningitis complications?

A

Neurological sequalae

Sensorineural hearing loss (most common)

Seizures

Focal neurological deficit
infective

Sepsis

Intracerebral abscess
pressure

Brain herniation

Hydrocephalus

244
Q

Brown-Sequard syndrome?

A

Caused by lateral hemisection of the spinal cord

Features:
Ipsilateral weakness below lesion

Ipsilateral loss of proprioception and vibration sensation

Contralateral loss of pain and temperature sensation

245
Q

Management after a stoke?

A

300mg aspirin for first 14 days then clopidogrel long term

Any other secondary prevention measures (statins, BP)

246
Q

Which Parkinson’s medications can cause impulse control disorders?

A

Dopamine receptor agonists (bromocriptine, ropinirole, cabergoline, apomorphine)

247
Q

What is the Barthel index?

A

Measures disability or dependence in ADLs after a stroke

248
Q

Cerebellar lesion symptoms from which parts?

A

Cerebellar hemisphere- peripheral finger nose ataxia

Cerebellar vermis- gait ataxia

249
Q

Which antibiotics raise the risk of idiopathic intracranial hypertension?

A

Tetracyclines- doxycycline

250
Q

What is a classical history for multi system atrophy?

A

Poor response to levadopa, impotence, urinary retention and age group

Can have postural hypotension

251
Q

Drugs to prevent relapse in MS patients?

A

Natalizumab

Beta-interferon

252
Q

What is second line after clopidogrel for secondary stroke prevention?

A

Aspirin with modified release dipyridamole

253
Q

What investigations should all TIA patients get after imaging?

A

Urgent carotid doppler if eligible for a carotid endocardectomy

254
Q

Which lobes for quadrantanopias?

A

PITS
Parietal - Inferior quadrantanopia
Temporal - Superior quadrantanopia

255
Q

Visual field defects summary?

A

Visual field defects:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tract
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
incongruous defects = optic tract lesion; congruous defects= optic radiation lesion or occipital cortex

256
Q

Remember propanolol

A

Not to be used in asthmatics- for migraine

In women on of child bearing age- past menopause- use topiramate

257
Q

What do the power grades mean?

A

Grade 0 No muscle movement
Grade 1 Trace of contraction
Grade 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

258
Q

Reflex routes?

A

S1-S2 buckle my shoe- ankle
L3-L4 kick the door- knee
C5-C6 pick up sticks- bicep
C7-C8 open the gate- tricep

259
Q

Investigation for acoustic neuroma?

A

MRI of the cerebellopontine angle

260
Q

MS investigation?

A

MRI with contrast

261
Q

Subacute combined degeneration of the spinal cord (lack of vit B12) symptoms?

A

Loss of proprioception and vibration sense, muscle weakness and hyperrefelxia

262
Q

Is the entire face affected in Bell’s Palsy?

A

Yes, cannot move forehead all paralysed as LMN lesion

263
Q

GCS?

A

Motor response
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None
Verbal response 5. Orientated
4. Confused
3. Words
2. Sounds
1. None
Eye opening 4. Spontaneous
3. To speech
2. To pain
1. None

264
Q

Neuro eye problems?

A

Homonymous quadrantopia
- PITS- parietal inferior, temporal superior

Bitemporal hemianopia
- lesion of optic chiasm
upper quadrant>lower= pituitary tumour

lower quadrant>upper= craniopharyngioma

265
Q

Difference between vertical nystagmus and horizontal nystagmus when acute onset?

A

Vertical nystagmus- cerebellar stroke

Horizontal nystagmus- viral labyrinthitis

266
Q

What are the features mentioned in the Oxford Stroke Classification?

A

The following criteria should be assessed:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

267
Q

Myasthenia gravis is associated with which type of malignancy?

A

Thymoma

268
Q

Underlying pathology of myasthenia gravis?

A

Autoimmune disorder with antibodies to acetylcholine receptors

Extraocular muscle weakness: diplopia
Proximal muscle weakness: face, neck, limb girdle
Ptosis
Dysphagia

269
Q

Investigations for myasthenia gravis?

A

Single fibre electromyography: high sensitivity (92-100%)

CT thorax to exclude thymoma

CK normal

Antibodies to acetylcholine receptors
positive in around 85-90% of patients
n the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies

Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used any more due to the risk of cardiac arrhythmia

270
Q

Management of myasthenia gravis?

A

1st- long-acting acetylcholinesterase inhibitors- pyridostigmine

2nd- immunosuppression- prednisolone initially and then azathioprine

271
Q

Management of myasthenic crisis?

A

Plasmapheresis

Intravenous immunoglobulin

272
Q

What nerve may be damaged by a Colle’s fracture (fall on outstretched hand)?

A

Median nerve

Inability to abduct thumb

273
Q

Painful third nerve palsy?

A

Posterior communicating artery

274
Q

What to do with ovarian cyst in pregnancy?

A

Nothing- they should go by themselves

275
Q

HNPCC/Lynch syndrome is associated with which cancers?

A

Endometrial and ovarian

276
Q

Is tamoxifen associated with endometrial cancer?

A

Yes

277
Q

Temporal arteritis (GCA) features?

A

Overlap with polymyalgia rheumatica

Typically over 60 years old
Rapid onset
Headache
Jaw claudication
Vision testing a key investigation

Raised inflammatory markers- raised ESR
Temporal artery biopsy

Urgent high dose glucocorticoids before the temporal biopsy
High dose prednisolone if no visual loss
High dose methylprednisolone if visual loss

278
Q

Trigeminal neuralgia features?

A

Electric shock like pain down side of face- unilateral
Caused by light touch

Red flags- sensory changes, deafness, optic neuritis, FH MS, onset before 40

Carbamazepine first line, atypical features refer to neurology

279
Q

Tuberous sclerosis vs neurofibromatosis?

A

Look it up

Tuberous sclerosis- depigmented ash leaf spots

Neurofibromatosis- cafe au lait spots

280
Q

What can raised ICP and brain herniation due to bleeding in the brain acuse?

A

Third nerve palsy

Down and out of the eye

281
Q

What are the complications of meningitis?

A

Sensorineural hearing loss (most common)

Seizures

Focal neurological deficit

Infective
sepsis
intracerebral abscess

Pressure
brain herniation
hydrocephalus

282
Q

Meningitis CSF analysis overview?

A

Bacterial

Cloudy
Glucose low
Protein high
White cells- 10-5000 polymorphs

Viral

Clear
Normal glucose
Protein- normal
White cells- 15-1000 lymphocytes

TB same as bacterial but lymphocytes

283
Q

What are the features of encephalititis?

A

fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis

cerebrospinal fluid
lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses

neuroimaging
medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
normal in one-third of patients
MRI is better

EEG
lateralised periodic discharges at 2 Hz

IV aciclovir to all patients with suspected encephalitis

284
Q

Seizure vs vasovagal post ictal?

A

Seizure post-ictal lasts around 15 mins

Vasovagal lasts 2-3 mins

285
Q

Should beta blockers be avoided in MG?

A

Yes

286
Q

Which Parkinson’s medication is most associated with poor impulse control?

A

Dopamine receptor antagonists

287
Q

Differentiate between total and partial anterior circulation infarcts?

A

Total involves all 3 criteria

Partial involves 2 criteria

The following criteria should be assessed:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

288
Q

Difference between 3rd nerve palsy and Horner’s?

A

Ptosis and dilated pupil= third nerve palsy

Ptosis and constricted pupil= Horner’s (and anhidrosis loss of sweating on one side)

289
Q

Features of Charcot-Marie-Tooth

A

Features:
There may be a history of frequently sprained ankles
Foot drop
High-arched feet (pes cavus)
Hammer toes
Distal muscle weakness
Distal muscle atrophy
Hyporeflexia
Stork leg deformity

290
Q

Arteries vs nerves on MRI?

A

Approximate

Arteries- CT without contrast

Nerves- CT with contrast

291
Q

Four main features of neuroleptic malignant syndrome?

A

Rigidity, hyperthermia, autonomic instability (hypertension/tachycardia) and altered mental status (confusion)

Known cause of AKI so can cause deranged U+Es

292
Q

Bacterial meningitis on LP?

A

Turbid, high polymorphs, high protein, low glucose

293
Q

Migraine causes?

A

CHOCOLATE- Chocolate, hangover, orgasm, cheese, oral
contraceptive, lie in, alcohol, tumult, exercise

294
Q

Benign rolandic epilepsy?

A

Seizures at night parasthesia affecting the face but can also go to generalised tonic clonic

Good prognosis- resolve by adolescence

295
Q

Criteria for a CT head in under 1 hour head injury?

A

CT head within 1 hour
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

296
Q

Criteria for a CT head in under 8 hours head injury?

A

CT head scan within 8 hours of the head injury - for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
age 65 years or older
any history of bleeding or clotting disorders including anticogulants
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury

297
Q

Causes of spontaneous SAH

A

intracranial aneurysm (saccular ‘berry’ aneurysms)
accounts for around 85% of cases
conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
arteriovenous malformation
pituitary apoplexy
mycotic (infective) aneurysms

298
Q

Classic features of SAH?

A

Classical presenting features include:

Headache

Usually of sudden-onset (‘thunderclap’ or ‘hit with a baseball bat’)
severe (‘worst of my life’)

Occipital

typically peaking in intensity within 1 to 5 minutes

nausea and vomiting

meningism (photophobia, neck stiffness)

Coma

Seizures

ECG changes including ST elevation may be seen

299
Q

SAH investigation?

A

non-contrast CT head is the first-line investigation of choice

if CT head is done within 6 hours of symptom onset and is normal
new guidelines suggest not doing a lumbar puncture
consider an alternative diagnosis

if CT head is done more than 6 hours after symptom onset and is normal
do a lumber puncture (LP)
timing wise the LP should be performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).
xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
as well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure

if the CT shows evidence of a SAH
referral to neurosurgery to be made as soon as SAH is confirmed

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)

300
Q

Management of confirmed SAH?

A

Management of a confirmed aneurysmal subarachnoid haemorrhage
supportive

vasospasm is prevented using a course of oral nimodipine

intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours

most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon

301
Q

Complications of SAH?

A

Rebleeding

Hydrocephalus

Vasospasm

Hyponatraemia

Seizures

302
Q

Presentation of hydrocephalus?

A

Headache (typically worse in the morning, when lying down and during valsalva)

Nausea and vomiting

Papilloedema

Coma (in severe cases)

Infants can have increase in head size, bulging fontanelles and failure of upward gaze

303
Q

Neuropathic pain drugs?

A

Don’t get pain again

Duloxetine

Gabapentin

Pregabalin

Amitriptyline

304
Q

Can Parkinson’s cause postural hypertension?

A

Yes

Causes autonomic dysfunction

305
Q

What are the three things that occur in juvenile myoclonic epilepsy?

A

Absence seizures

Single limb jerking in the morning following sleep deprivation

Generalised tonic-clonic

306
Q

If a Bell’s palsy shows no signs of improvement, after how long should you refer urgently to ENT?

A

3 weeks

307
Q

Parkinson’s disease with more falls, ED, postural hypertension?

A

Potentially multiple system atrophy

308
Q

DANISH?

A

DANISH: dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred speech, and hypotonia

309
Q

Triptans?

A

Adverse effects
‘triptan sensations’ - tingling, heat, tightness (e.g. throat and chest), heaviness, pressure

Contraindications
patients with a history of, or significant risk factors for, ischaemic heart disease or cerebrovascular disease

310
Q

LP findings in MS?

A

Oligoclonal bands in CSF

311
Q

What score assesses stroke in an emergency setting?

A

ROSIER

312
Q

Triad for brain abscess?

A

Fever, headaches, focal neurology

313
Q

Should someone on warfarin/doac get a head CT after TIA?

A

Yes

314
Q

What is pituitary apoplexy?

A

Sudden enlargement of pituitary tumour due to haemorrhage

Sudden onset headache
Visual field defects
Vomiting
Neck stiffness

Urgent steroid replacement

315
Q

What triggers cluster headaches?

A

Smoking, alcohol, nocturnal sleep

316
Q

Chronic subdural management?

A

Asymptomatic- conservative

Symptomatic- burr hole evacuation

317
Q

Where does herpes simplex encephalitis affect?

A

The temporal lobes

318
Q

Lesion of the optic chiasm?

A

Pituitary adenoma- bitemporal hemianopia upper quadrant>lower quadrant

Craniopharyngioma- bitemporal hemianopia lower quadrant>upper quadrant

319
Q

Stopping antiepileptics?

A

Seizure free over 2 years, drugs stopped over 2-3 months

320
Q

What scale used to measure disability after a stroke?

A

Barthel index

321
Q

What antibody is involved in Lambert-Eaton syndrome?

A

An antibody directed against presynaptic voltage-gated calcium channel

Features of Lambert-Eaton

Features
repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
in reality, this is seen in only 50% of patients and following prolonged muscle use muscle strength will eventually decrease
limb-girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficulty micturating
ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)

322
Q

When to give aspirin after thrombectomy?

A

24 hours after

323
Q

Remember symptoms of stroke on the other side

A

If left symptoms, need a right carotid endarterectomy

324
Q

Todd’s paresis?

A

Occurs after a frontal lobe seizure

Post-ictal weakness

325
Q

Does multiple system atrophy present with significant cognitive dysfunction?

A

No, differentiates it from Lewy body dementia

326
Q

Charcot-Marie-Tooth

A

Long term demyelinating

High arched feet- CMT

(Muscle weakness, power reduction in limbs, sprained ankle)

327
Q

Difference between miosis and myadriasis?

A

Miosis- small pupil

Myadriasis- large pupil

328
Q

Spasticity in MS?

A

Baclofen and gabapentin are first line

329
Q

Differentiate between cavernous sinus syndrome or posterior communicating artery aneurysm?

A

Posterior communicating artery aneurysm (pupil dilated)
= Think: 3rd nerve palsy = ptosis + dilated pupil

Cavernous sinus thrombosis
= absent corneal reflex + proptosis

330
Q

Check for asthma when prescribing propanolol?

A

YEES

331
Q

Progressive supranuclear palsy?

A

PSP-Problems seeing planes

Features
postural instability and falls
patients tend to have a stiff, broad-based gait
impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
parkinsonism
bradykinesia is prominent
cognitive impairment
primarily frontal lobe dysfunction

Poor response to l-dopa

332
Q

Multiple system atrophy?

A

Parkinson’s with cerebellar signs and autonomic disturbance (ED, atonic bladder, postural hypotension)

Phase 3a (17 decks)

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