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MRCP Neurology > MRCP2 > Flashcards

MRCP2 Flashcards

1
Q

What are the side effects of 5HT3 antagonists?

A

prolonged QT interval
constipation is common

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2
Q

Where does ondansetron act?

A

Medulla oblongata - chemoreceptors

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3
Q

What is the other name for petit mal seizure?

A

Abscence

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4
Q

EEG: bilateral, symmetrical 3Hz spike and wave pattern~?

A

Abscence seizure ?

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5
Q

Features of abscence seizure?

A

absences last a few seconds and are associated with a quick recovery
seizures may be provoked by hyperventilation or stress
the child is usually unaware of the seizure
they may occur many times a day
EEG: bilateral, symmetrical 3Hz spike and wave pattern

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6
Q

Management of abscence seizure?

A

Sodium valoprate
Ethuoxomide

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7
Q

Risk factors of acute angle closure glaucoma?

A

hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

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8
Q

Features of acute angle closure glaucoma?

A

Severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain

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9
Q

Investigations of acvute angle closure glaucoma?

A
  1. Tonometry
  2. Gonioscopy - looks at the angle
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10
Q

Management of acute angle closure glaucoma?

A

Combination of eye drops:
- Pilocarpine
- Beta blocker
- Alpha 2 agonist

In addition:
- Acetazolamide

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11
Q

Definitive management of acute angle closure glaucoma?

A

laser peripheral iridotomy

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12
Q

Glaucoma: How does pilocarpine work?

A

Stimulates parasympathetic

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13
Q

Glaucoma: How does beta blocker work?

A

Descreases aqueous humour

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14
Q

Glaucoma: How does alpha 2 agonist work?

A

Decreases aqueous humour
+
Increases outflow

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15
Q

What is acute disseminated myelitis ?

A

autoimmune demyelinating disease of the central nervous system

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16
Q

Management of acute sinusitis?

A
  1. Analgesia
  2. Intranasal decongestants if present for 10 days
  3. Phenoxymethapenicillin if very unwell
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17
Q

What is double sickening in acute sinusitis?

A

‘double-sickening’ may sometimes be seen, where an initial viral sinusitis worsens due to secondary bacterial infection

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18
Q

What is an acute stress reaction?

A

First 4 weeks post traumatic event

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19
Q

Features of acute stress reaction?

A

intrusive thoughts e.g. flashbacks, nightmares
dissociation e.g. ‘being in a daze’, time slowing
negative mood
avoidance
arousal e.g. hypervigilance, sleep disturbance

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20
Q

Management for acute stress reaction?

A

trauma-focused cognitive-behavioural therapy (CBT)
BZD

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21
Q

Features of dry macular degeneraiton?

A

characterised by drusen - yellow round spots in Bruch’s membrane

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22
Q

Features of wet macular degeneration?

A

exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis

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23
Q

Features of macular degeneration?

A

reduction in visual acuity, particularly for near field objects
- gradual in dry ARMD
- subacute in wet ARMD

difficulties in dark adaptation. Worsening night vision
photopsia, (a perception of flickering or flashing lights), and glare around objects

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24
Q

Signs of macular degeneration?

A

distortion of line perception may be noted on Amsler grid testing

fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.

in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

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25
Q

Investigations for maccular degneration

A
  1. Slit lamp – chekc pigments / haemorrhages
  2. fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy.
  3. Ocular coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone.
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26
Q

Management of maccular degeneration?

A

combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third

  1. vascular endothelial growth factor (VEGF) (preferred)
  2. laser photocoagulation does slow progression of ARMD - but risk of sight loss
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27
Q

What is agoraphobia?

A

Agoraphobia is primarily describes a fear of open spaces but also includes related aspects, e.g. the presence of crowds or the difficulty of escaping to a safe place

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28
Q

Alcohol withdrawl symptoms?

A

symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety

peak incidence of seizures at 36 hours

peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

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29
Q

Management of alcohol withdrawl?

A
  1. Chlordiazepoxide / diazepam
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30
Q

WHat BZD is preferred in hepatic dysfunction in alcohol withdrawl?

A

Lorazepam

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31
Q

What antiepileptic can be used in alcohol withdrawl?

A

Carbamazepine - for siezures

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32
Q

What is alcohol hallucinosis?

A

Alcohol related psychosis - not the same of wernicke’s

Features:
1. A psychosis of less than 6 months duration
2. auditory hallucinations, often of persecutory or derogatory nature
3. occurs in clear consciousness

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33
Q

What is the other name of iritis?

A

Anterior uveitis

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34
Q

What is inflammaed in anterior uvieitis?

A

Anterior uvea
Iris and ciliary body.

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35
Q

Features of anterior uveitis?

A

acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired

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36
Q

Association conditions of anterior uveitis?

A

ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

associated with HLA B 27

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37
Q

Management of anterior uveitis?

A
  1. cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
  2. Steroid drops
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38
Q

What is anti NMDA encephaltis?

A

Anti-NMDA receptor encephalitis is a paraneoplastic syndrome, presenting as prominent psychiatric features

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39
Q

What cancer is associcated with NMDA encephaltis?

A

Ovarian teratomas

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40
Q

Autoantibody seen in anti NMDA encephalitis?

A

Ant-MuSK

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41
Q

Mechanism of typical antipsychotics?

A

D2 antagonist
blocking dopaminergic transmission in the mesolimbic pathways

e.g. Haloperidol
Chlopromazine

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42
Q

Mechanism of atypical antipsychotics?

A

Act on a variety of receptors (D2, D3, D4, 5-HT)

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43
Q

Side effect of typical vs atypical?

A

Typical:
Extrapyramidal side-effects and hyperprolactinaemia common

Atypical:
Extrapyramidal side-effects and hyperprolactinaemia less common
Metabolic effects

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44
Q

What extrapyramidal side effects are in antipsychotics?

A

Parkinsonism
Acute dystonia
Akasthsia
Tardive dyskinesia

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45
Q

What type of antipsycotic reduces seizure threshold?

A

Atypicals

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46
Q

What antipsychoatic increased QT?

A

Halperiodl
But a lot of them

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47
Q

Where is wernicke’s area?

A

superior temporal gyrus. It is typically supplied by the inferior division of the left MCA

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48
Q

Where is the broca area?

A

“expressive aphasia”
inferior frontal gyrus.
Comprehension not impaired

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49
Q

What is wernicke aphasia?

A

“Receptive aphasia”
Fluent nonsensical speach
Comprehension impaired

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50
Q

Where is the lesion in a conductive aphasia

A

Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area

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51
Q

Features of conductive aphasia?

A

Speech is fluent but repetition is poor. Aware of the errors they are making
Comprehension is normal

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52
Q

What is global aphasia?

A

Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia

May still be able to communicate using gestures

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53
Q
A

/

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54
Q

Small irregular pupil + No response to light + Accomodation relfex intact

A

Argyl robertson pupil intact

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55
Q

Causes of argyl robertson pupil?

A

Diabetes
Syphilus

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56
Q

What is arnold chiari malformation?

A

downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum

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57
Q

Features of arnold chiari malformation?

A

non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia

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58
Q

Features of ataxia telengectasia?

A

Telengectasia / spide angioma
IgA deficiencies
Increased leukaemia / lymphomarisk
Onset at 1 year - 5 years

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59
Q

Features of Friedrich’s ataxia

A

Trinucleotide nucleotide repeat disorder
Kyphoscliosis
Optic atrophy
HOCM
Diabetes mellituts
Onset 10-15

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60
Q

What is the inheritance pattern for friedrichs ataxia and ataxia telengectasia?

A

Autosmal recessive

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61
Q

Adverse effects of atypical antipsychotics/

A

weight gain
clozapine is associated with agranulocytosis (see below)
hyperprolactinaemia

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62
Q

Adverse effects of clozapine?

A

agranulocytosis (1%), neutropaenia (3%)
reduced seizure threshold - can induce seizures in up to 3% of patients
constipation
myocarditis: a baseline ECG should be taken before starting treatment
hypersalivation

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63
Q

What is autnomic dysreflexia?

A

extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.

Occurs in indivudals with injury above T6

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64
Q

Management of autonomic dysreflexia?

A

Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

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65
Q

Features of vertigo?

A

vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre, indicated by:
patient experiences vertigo
rotatory nystagmus

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66
Q

Management of vertigo?

A

Epley manoeuvre
Betahistine

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67
Q

Mechanism of BZD?

A

increase number of chloride channels

GABAA drugs
benzodiazipines increase the frequency of chloride channels
barbiturates increase the duration of chloride channel opening

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68
Q

Erb’s palsy?

A

damage to C5,6 roots
winged scapula
may be caused by a breech

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69
Q

Klumpe’s palsy?

A

damage to T1
loss of intrinsic hand muscles
due to traction

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70
Q

Features of brain abscess?

A

Headache
Fever - not swinging
Focal neurology

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71
Q

Management of brain abscess/

A

Surgery - craniotomy for decompression

IV antibiotics: IV 3rd-generation cephalosporin + metronidazole

intracranial pressure management: e.g. dexamethasone

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72
Q

What does subfalcine herniation mean?

A

Displacement of the cingulate gyrus under the falx cerebri

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73
Q

What does central herniation mean?

A

Downwards displacement of the brain

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74
Q

What for transtentorial herniation mean?

A

Displacement of the uncus of the temporal lobe under the tentorium cerebelli.

Clinical consequences include an ipsilateral fixed, dilated pupil (due to parasympathetic compression of the third cranial nerve) + contralateral paralysis (due to compression of the cerebral peduncle)

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75
Q

What does tonsillar herniation mean?

A

Displacement of the cerebellar tonsils through the foramen magnum. This is called ‘coning’. In raised ICP this causes compression of the cardiorespiratory centre. In Chiari 1 malformation, tonsillar herniation is seen without raised ICP

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76
Q

Feature of parietal lobe lesion?

A

sensory inattention
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia

Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation

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77
Q

Feature of occiptal lobe lesion?

A

homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia

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78
Q

Feature of temporal lobe lesion

A

Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent

superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)

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79
Q

feature of frontal love lesion?

A

expressive (Broca’s) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
disinhibition
perseveration
anosmia
inability to generate a list

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80
Q

feature of cerebral lesion?

A

midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus

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81
Q

Area affected in wernickes / Korsakoff?

A

Medial thalamus and mammillary bodies of the hypothalamus

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82
Q

Area affected in hemibalismis?

A

Subthalamic nucleus of the basal ganglia

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83
Q

Area affected in Huntington disease?

A

Striatum (caudate nucleus) of the basal ganglia

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84
Q

Area affected in Parkinson disease?

A

Substantia nigra of the basal ganglia

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85
Q

Area affected in Kluver-Bucy syndrome

A

amydala

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86
Q

Most common metastasis to the brain?

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

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87
Q

Brain tumour: Pleomorphic tumour cells border necrotic areas

A

Glioblastoma multiformi

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88
Q

Treatment for glioblastoma multiform?

A

Treatment is surgical with postoperative chemotherapy and/or radiotherapy.

Dexamethasone is used to treat the oedema.

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89
Q

Brain tumour: central necrosis and a rim that enhances with contrast

A

Glioblastoma multiforme

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90
Q

Most common primary brain tumour?

A

Glioblastoma multiforme

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91
Q

Second most common primary brain tumour?

A

Meningioma

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92
Q

Brain tumour: : Spindle cells in concentric whorls and calcified psammoma bodies

A

Meningioma

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93
Q

What condition is associated with vestibular schwaoma?

A

Neurofibromatosis type 2 is associated with bilateral vestibular schwannomas.

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94
Q

Where is vestibular schwannoma found?

A

benign tumour arising from the eighth cranial nerve (vestibulocochlear nerve).
Often seen in the cerebellopontine angle

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95
Q

Rosenthal fibres (corkscrew eosinophilic bundle)

A

Pilocytic astrocytoma

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96
Q

Small, blue cells. Rosette pattern of cells with many mitotic figures

A

Medulloblastoma

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97
Q

When is ependyma commonly located?

A

4th ventricle

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98
Q
  • Histology: perivascular pseudorosettes
A

Ependymoma

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99
Q

Calcifications with ‘fried-egg’ appearance

A

Oligodendroma

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100
Q

What brain tumour is associated with Hippel-Lindau syndrome

A

Haemangioblastoma

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101
Q

Brain tumour Histology: foam cells and high vascularity

A

Haemangioblastoma

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102
Q

Features of craniopharygioma?

A

hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.

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103
Q

What is capragas syndrome?

A

Capgras syndrome refers to a disorder in which a person holds a delusion that a friend or partner has been replaced by an identical-looking impostor.

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104
Q

Mechanism of carbamazepine?

A

binds to sodium channels increases their refractory period

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105
Q

Features of carbamazepine?

A

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

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106
Q

Cataplexy?

A

sudden and transient loss of muscular tone caused by strong emotion

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107
Q

Feature of central retinal artery occlusion?

A

sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina

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108
Q

Management of central rental vein occlusion?

A

macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents

retinal neovascularization - laser photocoagulation

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109
Q

Normal pressure in CSF

A

pressure = 60-150 mm (patient recumbent)

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110
Q

Protein in CSF?

A

protein = 0.2-0.4 g/l

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111
Q

Glucose in CSF

A

glucose = > 2/3 blood glucose

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112
Q

CSF + raised lymphocytes?

A

viral meningitis/encephalitis
TB meningitis
partially treated bacterial meningitis
Lyme disease
Behcet’s, SLE
lymphoma, leukaemia

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113
Q

Features of Charcot Marie tooth?

A

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

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114
Q

Wernicke encephalopathy?

A

Confusion, gait ataxia, nystagmus + ophthalmoplegia are features of Wernicke’s encephalopathy

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115
Q

Korsakoff syndrome?

A

amnesia, deficits in explicit memory, and confabulation.

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116
Q

Treatment for central retinal artery occlusion?

A

Treatment of underlying condition –> intravenous steroids for temporal arteritis

Acute: Intraarterial thrombolysis

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117
Q

Features of chronic demyelinating polyneuropathy?

A

Cause of peripheral neuropathy

Guillain-Barre syndrome (GBS), with motor features predominating

High protein CSF

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118
Q

Management of chronic demyelinating polyneuropathy?

A

Steroids + immunosuppression

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119
Q

Features of cluster headache?

A

-intense sharp, stabbing pain around one eye
pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
the patient is restless and agitated during an attack due to the severity
clusters typically last 4-12 weeks
accompanied by redness, lacrimation, lid swelling
nasal stuffiness
miosis and ptosis in a minority

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120
Q

Management of cluster headache?

A

acute
100% oxygen (80% response rate within 15 minutes)
subcutaneous triptan (75% response rate within 15 minutes)

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121
Q

Prophylaxis in cluster headache?

A

prophylaxis
verapamil is the drug of choice
there is also some evidence to support a tapering dose of prednisolone

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122
Q

Imaging in cluster headache and why?

A

Can be presenting of tumour

MRI with gadolinium contrast is the investigation of choice

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123
Q

Common perineal nerve lesion

A

weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles

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124
Q

EEG findings in CJD?

A

EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)

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125
Q

CSF in CJD§

A

Normal

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126
Q

MRI findings in CJD?

A

MRI: hyperintense signals in the basal ganglia and thalamus

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127
Q

Features of new variant CJD?

A

Age. onset - 25
psychological symptoms such as anxiety, withdrawal and dysphonia are the most common presenting features
the ‘prion protein’ is encoded on chromosome 20 - it’s role is not yet understood
methionine homozygosity at codon 129 of the prion protein is a risk factor for developing CJD - all patients who have so far died have had this
median survival = 13 months

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128
Q

Main features of CJD?

A

Myoclonus
Dementia

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129
Q

Most common cause of blindness 35-65?

A

Diabetic retinopathy

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130
Q

Mild Non proliferative diabetic retinopathy?

A

1 or more microaneurysm

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131
Q

Moderate nonproliferatie diabetic retinopathy?

A

microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

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132
Q

Severe non proliferative diabetic retinopathy?

A

blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant

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133
Q

Features of proliferative diabetic retinopathy?

A

retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years

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134
Q

What is maculopathy (diabetics) ?

A

based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM

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135
Q

Management of maculopathy?

A

Optimise glycaemic control

Maculopathy:
1. Anti-vegf inhibitors

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136
Q

Management of non-proliferative retinopathy?

A

if severe/very severe consider panretinal laser photocoagulation

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137
Q

Management of proliferative retinopathy?

A

Panretinal laser photocoagulation

Anti-VEGF

if severe or vitreous haemorrhage: vitreoretinal surgery

138
Q

What VEGF inhibitor is used in proliferative retinopathy?

A

ranibizumab

139
Q

Drugs that cause peripheral neuropathy?

A

amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

140
Q

List of patients who cannot drive and must call DVLA?

A

first unprovoked/isolated seizure: 6 months off - if no cause found then 12 months

established epilepsy or those with multiple unprovoked seizures
- qualify for a driving licence if they have been free from any seizure for 12 months
- no seizures for 5 years (with medication if necessary) a ’til 70 licence is usually restored

If withdrawing from antiepelpetic medication

141
Q

Restricitons in driving for 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

142
Q

DVLA: Stroke or TIA?

A

1 month off

143
Q

DVLA: Multiple TIA?

A

3 months off driving and inform DVLA

144
Q

DVLA: Craniotomy for meningioma

A

1 year off driving

145
Q

DVLA: craniotomy for pituitary tumour?

A

6 months

Transphenoidal surgery can drive

146
Q

DVLA: Narcolepsy / catoplexy

A

Cease driving at diagnosis

147
Q

For all psychiatric DVLA stuff?

A

may be able to drive but must inform the DVLA

Unless severe anxiety / suicidal: Must not drive

148
Q

Inheritance of the dystrophinopathies?

A

X linked recessive
- Duchenne
- Beckers

149
Q

Where is the mutation cause dystrophinopathies?

A

Xp21

150
Q

What is the absolute contrainidcation to ECT?

A

Raised intracranial pressure

151
Q

Short term side effect of electroconvulsion therapy?

A

headache
nausea
short term memory impairment
memory loss of events prior to ECT
cardiac arrhythmia

152
Q

What is most likely causative organism of encephalitis?

A

HSV - 1

153
Q

Management of encephalitis?

A

intravenous aciclovir should be started in all cases of suspected encephalitis

154
Q

Findings on CSF for encephalitis?

A

lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses

155
Q

EEG: lateralised periodic discharges at 2 Hz

A

Encephalitis

156
Q

Types of focal seizure?

A

Focal impaired awareness
FOcal aware

157
Q

Types of generalised seizure?

A

tonic-clonic (grand mal)
tonic
clonic
typical absence (petit mal)
atonic

158
Q

What is a focal to bilateral seizure?

A

starts on one side of the brain in a specific area before spreading to both lobes
previously termed secondary generalized seizures

159
Q

Pregnancy + sodium valporate

A

Neural tube defect

160
Q

Pregnancy + phenytoin?

A

Cleft lip

161
Q

Are anti-epileptic safe in pregnany ?

A

Yes - except phenobarbital

162
Q

Generalised tonic clonic management?

A

Males: Sodium valporate

Females: lamotrigine or levetiracetam

163
Q

Focal seizure management?

A

Lamotrigene or leveitacetam

164
Q

Abscence seizure management?

A

first line: ethosuximide

second line:
male: sodium valproate
female: lamotrigine or levetiracetam

165
Q

What treatment may exacerbate abscence seizures?

A

Carbamazepine

166
Q

Myoclonic seizure management?

A

males: sodium valproate
females: levetiracetam

167
Q

Tonic or atonic seizure management?

A

males: sodium valproate
females: lamotrigine

168
Q

What conditions see episcerlitis associated?

A

IBD
Rheumatoid arthritis

169
Q

Features of episcleritis?

A

Classically not painful
watering and mild photophobia may be present

170
Q

How to differentiated between scleritis and episcerlitis?

A

phenylephrine drops

phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels
if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made

171
Q

Inheritance of benign essential tremor ?

A

autosomal dominant condition

172
Q

Features of benign essential tremor?

A

postural tremor: worse if arms outstretched
improved by alcohol and rest
most common cause of titubation (head tremor)

173
Q

Management of benign essential tremor?

A

propranolol is first-line
primidone is sometimes used

174
Q

Causes of bilateral facial nerve palsy?

A

sarcoidosis
Guillain-Barre syndrome
Lyme disease
bilateral acoustic neuromas (as in neurofibromatosis type 2)

as Bell’s palsy is relatively common it accounts for up to 25% of cases f bilateral palsy, but this represents only 1% of total Bell’s palsy cases

175
Q

Facial nerve: LMN vs UMN?

A

upper motor neuron lesion ‘spares’ upper face i.e. forehead

lower motor neuron lesion affects all facial muscles

176
Q

Supply of facial nerve?

A

Supply - ‘face, ear, taste, tear’
face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands

177
Q

Inheritance of fasciohumeral dystrophy?

A

Autosomal dominant

it typically affects the face, scapula and upper arms first.

Average onset 20 years

178
Q

Features of fasciohumeral dystrophy?

A

facial muscles are involved first - difficulty closing eyes, smiling, blowing etc
weakness of the shoulder and upper arm muscles
abnormal prominence of the borders of the shoulder blades - ‘winging’
lower limb: hip girdle weakness, foot drop

179
Q

Features of foster keneddy syndrome?

A

optic atrophy in the ipsilateral eye
papilloedema in the contralateral eye
central scotoma in the ipsilateral eye
anosmia

180
Q

Genetics of friedrick’s ataxia?

A

autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat in the X25 gene on chromosome 9 (frataxin)

181
Q

Phenotype of friedrick’s ataxia?

A

absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration

absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration

182
Q

Management of GAD?

A

step 1: education about GAD + active monitoring
step 2: low-intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups)
step 3: high-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment. See drug treatment below for more information
step 4: highly specialist input e.g. Multi agency teams

183
Q

Drug treatment in GAD?

A
  1. Sertraline
  2. Offer an alternative SSRI or a serotonin–noradrenaline reuptake inhibitor (SNRI)
    examples of SNRIs include duloxetine and venlafaxine
184
Q

After 12 weeks of treatment with sertraline for GAD - no effect, how to manage?

A

imipramine or clomipramine should be offered

185
Q

What infection classically trigger guillain barre?

A

Camplobacter

186
Q

Antibodies in guillain barre?

A

anti-ganglioside antibody (e.g. anti-GM1)

187
Q

What is miller fisher syndrome?

A

variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first
usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
anti-GQ1b antibodies are present in 90% of cases

188
Q

What are the features of guillain barre syndrome?

A

classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

there may be a history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement
diplopia
bilateral facial nerve palsy
oropharyngeal weakness is common
autonomic involvement
urinary retention
diarrhoea

189
Q

CSF in guillain barre syndrome?

A

rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

190
Q

Nerve conduction studies for guillain barre?

A

decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency

191
Q

Management of guillain barre

A

IVIG first line

Plasma exchange

FVC regularly for monitoring respiratory function

192
Q

Where is the bleed in a extradural bleed?

A

Bleeding into the space between the dura mater and the skull.

Features of increase cranial pressure
Often has lucid level

193
Q

Head injury: fluctuating confusion/consciousness

A

Subdural

194
Q

Features of migraine?

A

Recurrent, severe headache which is usually unilateral and throbbing in nature
May be be associated with aura, nausea and photosensitivity
Aggravated by, or causes avoidance of, routine activities of daily living. Patients often describe ‘going to bed’.
In women may be associated with menstruation

195
Q

Tension headache?

A

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

196
Q

Features of cluster headache?

A

Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers

197
Q

Features of temporal arteritis?

A

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR

198
Q

Features of medication overuse headache?

A

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

199
Q

Treatment for paroxysmal hemicrania?

A

Indomethacin

200
Q

Where does HSV1 encephalitis usually affect?

A

Temporal lobes

201
Q

Features of HSV encephalitis?

A

meningitis
encephalitis
subarachnoid haemorrhage
head injury
sinusitis
glaucoma (acute closed-angle)
tropical illness e.g. Malaria

202
Q

Investigation findings for HSV encephalitis?

A

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

203
Q

Management of HSV encephalitis?

A

Aciclovir

204
Q

Features of herpes keratitis?

A

red, painful eye
photophobia
epiphora
visual acuity may be decreased

fluorescein staining may show an epithelial ulcer

205
Q

Management of herpes keratitis?

A

immediate referral to an ophthalmologist
topical aciclovir

206
Q

What causes herpes zoster opthalmicus?

A

Varicella zoster

207
Q

VZ: What is hutchinson sign?

A

Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

208
Q

Management of herpes zoster ophthalmicus?

A

Oral antivral for 7-10 days
topical antiviral treatment is not given in HZO

209
Q

Complications of herpes zodter ophthalmicus?

A

ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

210
Q

Holms tremor?

A

Red nucleus

211
Q

What is a holms addie pupil?

A

dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light

212
Q

What is holms addie syndrome?

A

association of Holmes-Adie pupil with absent ankle/knee reflexes

213
Q

Features of horners syndrome?

A

miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)

214
Q

Horners syndrome lesion according to anhidrosis?

A

Central lesion: Anhidrosis of the face, arm and trunk
Preganglionic: Anhidrosis of the face
Post ganglionic: NO anhidrosis

215
Q

Central causes of horners syndrome?

A

Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis

216
Q

Preganglionic causes of horner’s syndrome?

A

Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis

217
Q

Post ganglionic causes of horner’s syndromes?

A

Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

218
Q

What is Hereditary sensorimotor neuropathy (HSMN) called?

A

Charcot marie tooth disease

219
Q

Mechanism of HSMN type 1?

A

HSMN type I: primarily due to demyelinating pathology

220
Q

Mechanism of HSMN type 2?

A

HSMN type II: primarily due to axonal pathology

221
Q

Features of HSMN?

A

autosomal dominant
due to defect in PMP-22 gene (which codes for myelin)
features often start at puberty
motor symptoms predominate
distal muscle wasting, pes cavus, clawed toes
foot drop, leg weakness often first features

222
Q

Features of huntington disease?

A

chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements

223
Q

Gene problem in huntington’s disease?

A

Chromome - trinucleotide repeat disorder CAG

224
Q

Stage 1: Hypertensive retinopathy?

A

Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring

225
Q

Stage 2: Hypertensive retinopathy?

A

Arteriovenous nipping

226
Q

Stage 3: Hypertensive retinopathy?

A

Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’

227
Q

Stage 4: Hypertensive retinopathy?

A

Papilloedema

228
Q

Hypotension strokes - causes damage where?

A

Watershed areas

229
Q

Risk factors of idiopathic cranial hypertension?

A

obesity
female sex
pregnancy
Drugs

230
Q

What drugs cause idiopathic cranial hypertension ?

A

obesity
female sex
pregnancy

231
Q

Drug causes of idopathic intracranial hypertension?

A

combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium

232
Q

Features of idiopathic intracranial hypertension

A

headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present

233
Q

Management of idopathic intracranial hypertension?

A

Weight loss

diuretics e.g. acetazolamide

topiramate is also used,

repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management

surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.

234
Q

Features of inclusion body myositis?

A

typically affects older males
can affect both proximal and distal muscles
characteristically affects quadriceps and finger/wrist flexors are usually more severely affected than extensor counterparts

235
Q

cytoplasmic inclusions on muscle biopsy

A

Inclusion body myositis

236
Q

Goldstand imaging for intracranial venous thrombosis?

A

MRI venography is the gold standard
CT venography is an alternative

non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated

237
Q

Saggital sinus syndrome?

A

seizures and hemiplegia

parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen

‘empty delta sign’ seen on venography

238
Q

Cavernous sinus thrombosis?

A

periorbital oedema
ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
Trigeminal nerve involvement

central retinal vein thrombosis

239
Q

Lateral sinus thrombosis?

A

6th and 7th cranial nerve palsies

240
Q

What cancer is associated with lambert eaton syndrome?

A

Small cell lung cancer
Breast
Ovarian

241
Q

Antibody if lambert eaton syndrome?

A

antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.

242
Q

Features of lambert eaton syndrome?>

A

repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)

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)

243
Q

Treatment for lambert eaton syndrome?

A

immunosuppression, for example with prednisolone and/or azathioprine

intravenous immunoglobulin therapy and plasma exchange may be beneficial

244
Q

What artery is affected in lateral medullary syndrome?

A

Posterior inferior cerebellar artery.

245
Q

Features of lateral medullary syndrome?

A

Cerebellar features
ataxia
nystagmus

Brainstem features
ipsilateral: dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

246
Q

What is MELAS?

A

m.3243A>G mutation
Mitochondrial

247
Q

Features of MELAS?

A

MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like symptoms)

248
Q

Features of MELAS?

A

MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like symptoms)

249
Q

Features of MELAS

A

Diabetes
Sensorineural hearing loss
Stroke-like symptoms
Retinal dystrophy
Proximal myopathy
Cardiomyopathy, arrhythmias
End stage renal failure - most often FSGS pattern on biopsy
Short stature, low BMI

250
Q

Feature of medication overuse headache?

A

present for 15 days or more per month
developed or worsened whilst taking regular symptomatic medication
patients using opioids and triptans are at most risk
may be psychiatric co-morbidity

251
Q

Management of medication overuse headache?

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn

252
Q

Features of menieres disease?

A

recurrent episodes of vertigo, tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom
a sensation of aural fullness or pressure is now recognised as being common
other features include nystagmus and a positive Romberg test
episodes last minutes to hours
typically symptoms are unilateral but bilateral symptoms may develop after a number of years

253
Q

Clinical course of menieres disease ?

A

symptoms resolve in the majority of patients after 5-10 years
the majority of patients will be left with a degree of hearing loss
psychological distress is common

254
Q

Management of mernieres?

A

Inform DVLA

acute attacks: buccal or intramuscular prochlorperazine.

prevention: betahistine and vestibular rehabilitation exercises

255
Q

Most common cause of meningitis in adults ?

A

Strep pneumoniae
may follow on from an episode of otitis media

256
Q

Most common cause of menignits in elderly/ immunocompromised?

A

Listeria

257
Q

Acute management of migraine?

A

First-line: offer combination therapy with
an oral triptan and an NSAID, or
an oral triptan and paracetamol

Second line:
offer a non-oral preparation of metoclopramide or prochlorperazine and consider adding a non-oral NSAID or triptan

258
Q

Prophylaxis in migraines?

A

propranolol

topiramate: should be avoided in women of childbearing age as it may be teratogenic and it can reduce the effectiveness of hormonal

contraceptives

amitriptyline

259
Q

Vitamin advice in migraines?

A

400mg riboflavin (B2) per day

260
Q

Migraines related to menstruation?

A

frovatriptan (2.5 mg twice a day) or zolmitriptan (2.5 mg twice or three times a day)

261
Q

Other prophylaxis in migraines not liscenced yet? - but neurology can prescribe?

A

candesartan: recommended by the British Association for the Study of Headache guidelines

monoclonal antibodies directed against the calcitonin gene-related peptide (CGRP) receptor: examples include erenumab

262
Q

muscle biopsy classically shows ‘red, ragged fibres

A

Mitochondrial

263
Q

Features of mitochondrial disroders?

A

Leber’s optic atrophy

MELAS syndrome: mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes

MERRF syndrome: myoclonus epilepsy with ragged-red fibres

Kearns-Sayre syndrome: onset in patients < 20 years old, external ophthalmoplegia, retinitis pigmentosa. Ptosis may be seen

sensorineural hearing loss

264
Q

Features of motor neurone disease?

A

asymmetric limb weakness is the most common presentation of ALS
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations

265
Q

What does motor neurone disease not affect?

A

doesn’t affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction

266
Q

Management of motor neurone disease ?

A

Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months

Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months

Nutrition
percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition and has been associated with prolonged survival

267
Q

Neurological weakness + Anti- GM1 ?

A

Multifocal motor neuropathy

268
Q

Features of multiple sclerosis ?

A

Visual
optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia

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: more often seen during an acute relapse than as a presenting symptom
tremor

Others
urinary incontinence
sexual dysfunction
intellectual deterioration

269
Q

Investigation fidnings of MS?

A

MRI:
high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

CSF:
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG

Visual evoked potentials
delayed, but well preserved waveform

270
Q

Treatment of acute flare MS?

A

IV Methylprednisolone

271
Q

When to start DMARD therapy in relapsing remitting MS?

A

relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided

272
Q

When to start DMARD therapy in secondary progressive disease?

A

secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

273
Q

MS: natalizumab

A

antagonises alpha-4 beta-1-integrin found on the surface of leucocytes
inhibit migration of leucocytes across the endothelium across the blood-brain barrier

Used first line

274
Q

MS: Ocrelizumab?

A

humanized anti-CD20 monoclonal antibody

Used first line

275
Q

Management of spastisity in MS?

A

baclofen and gabapentin are first-line

276
Q

Bladder management in MS>?

A

if significant residual volume → intermittent self-catheterisation

if no significant residual volume → anticholinergics may improve urinary frequency

277
Q

MS:
Oscillopsia (visual fields appear to oscillate)

A

gabapentin is first-line

278
Q

Good prognosis MS?

A

female sex
age: young age of onset (i.e. 20s or 30s)
relapsing-remitting disease
sensory symptoms only
long interval between first two relapses
complete recovery between relapses

the typical patient carries a better prognosis than an atypical presentation

279
Q

Types of multi system atrophy?

A

1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features

280
Q

Features of multi system atrophy?

A

parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs

281
Q

Types of multi system atrophy?

A

1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features

282
Q

Features of myasthenia gravis?

A

extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

283
Q

Features of myasthenia gravis?

A

extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

284
Q

Associations of myasthenia gravis?

A

thymomas in 15%
autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
thymic hyperplasia in 50-70%

285
Q

Management of myasthenia gravis?

A

long-acting acetylcholinesterase inhibitors
pyridostigmine is first-line

Additional:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy

286
Q

Management of myasthenic crisis?

A

plasmapheresis
intravenous immunoglobulins

287
Q

Features of multi system atrophy?

A

parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs

1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features

288
Q

Exacerbating factors of myasthenia gravis?

A

penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

289
Q

Features of mytonic dystrophy?

A

myotonic facies (long, ‘haggard’ appearance)
frontal balding
bilateral ptosis
cataracts
dysarthria

myotonia (tonic spasm of muscle)
weakness of arms and legs (distal initially)
mild mental impairment
diabetes mellitus
testicular atrophy
cardiac involvement: heart block, cardiomyopathy
dysphagia

290
Q

Genetics of myotonic dystrophy?

A

autosomal dominant
a trinucleotide repeat disorder

DM1 is caused by a CTG repeat at the end of the DMPK (Dystrophia Myotonica-Protein Kinase) gene on chromosome 19

DM2 is caused by a repeat expansion of the ZNF9 gene on chromosome 3

291
Q

Difference between DM1 and DM2 myotonic dystrophy?

A

DM1:
Distal weakness more common

DM2 :
Proximal weakness more common

292
Q

Features of branchial cyst?

A

oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx

failure of obliteration of the second branchial cleft in embryonic development

293
Q

Nerve conduction study: Axonal damage?

A

normal conduction velocity
reduced amplitude

294
Q

Nerve conduction study: Demyelinating damage?

A

reduced conduction velocity
normal amplitude

295
Q

Features of NF 1?

A

Phaecrhomcytoma

Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis

296
Q

Features of NF 2?

A

Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

297
Q

Features of neuromyelitis optica?

A

Relapsing remitting CNS disorder

  1. Spinal cord lesion involving 3 or more spinal levels
  2. Initially normal MRI brain
  3. Aquaporin 4 positive serum antibody
298
Q

Aquaporin 4 positive serum antibody

A

Neuromyelitis optica

299
Q

Management of neuromyeltis otpica?

A

immunosuppressant e.g. with anti-CD20 agent rituximab)

300
Q

Treatment of normal pressure hydrocephalus?

A

urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson’s disease)

301
Q

Wernicke’s is caused by thiamine deficiency

A

Wernicke is caused by thiamine deficiency

302
Q

Middle cerebral artery lesion?

A

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

303
Q

Anterior cerebral artery lesion?

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

304
Q

Posterior cerebral artery lesion?

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

305
Q

Weber syndrome?

A

Posterior cerebral arttery supply to midbrain
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

306
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

307
Q

Anterior inferior cerebellar artery (lateral pontine syndrome)?

A

Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Ipsilateral: facial paralysis and deafness

308
Q

Lyme disease CSF?

A

results are similar to the ‘typical’ bacterial picture with low glucose and high protein, however in Lyme disease we would expect a lymphocytic pleocytosis

If see first degree heart block + focal neurological defects think lyme

309
Q

Absolute Contraindications for thrombolysis?

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • Lumbar puncture in preceding 7 days
  • Gastrointestinal haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
310
Q

Relative contraindications for thrombolysis?

A
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
311
Q

Anterior inferior cerebellar artery (lateral pontine syndrome)?

A

Symptoms are similar to Wallenberg’s (see above), but:

Ipsilateral: facial paralysis and deafness`

312
Q

MS and pregnancy?

A

Relapse is less common in pregnancy
Increase 3-6 months post partum
Then return to normal rates

313
Q

When can candesartan be considered for migraine prophlaxis

A

If others are contraindicated

314
Q

Management of haemorrhagic transofrmation stroke?

A

Thrombosis + haemorrhage

Manage with IV heparin
If haemorrhage dose occur, can be as easily reversed as possible

315
Q

Migraine prophylaxis - avoid in young women?

A

Topiramate

316
Q

Adenoma sebaceum?

A

Tuberous sclerosis

317
Q

Starting SSRI in young person, when should you review again?

A

Within one week

318
Q

Maccular star pattern?

A

Hypertensive retinopathy

319
Q

Continued seizure after lorazepam, and phenobarbitol?

A

Anaesthesia with thipentate

320
Q

Urgent management acute glaucoma?

A

IV analgesia and antiemetics, lie patient supine.
Topical beta blockers and steroids.
IV acetazolamide.
After initial treatment, pilocarpine will induce meiosis and open the angle. This is initially ineffective due to pressure induced ischaemic paralysis of the iris.
Iridotomy 24-48 hours after intra-ocular pressure is controlled to prevent recurrence.

321
Q

Headache + St Elevation?

A

Subarachnoid haemorrhage

322
Q

Increase intracranial pressure + sensory symptoms ?

A

Think cerebral venous thrombosis

323
Q

IN non-traumatic SAH, what must be done to identify source?

A

CT angiogram - to look for anneurysm

324
Q

What is malignant MCA syndrome?

A

occurs in younger patients who have suffered an extensive ischaemic stroke

. After infarction the brain swells. As younger brains are likely to have less atrophy, there is less room for expansion. Subsequently, intracranial hypertension develops. This typically presents 48 hours after onset of stroke with reduced conscious level.

325
Q

How is malignant MCA syndrome managed?

A

Decompressive carniotomy

326
Q

meningeal enhancement, thickening and shallow subdural haematoma

A

Features from low pressure headahce
e.g. lumbar puncture headache

327
Q

Grossly abnormal amonia + antiepileptic?

A

valproate-associated hyperammonaemic encephalopathy (VHE).

328
Q

Management of adenoma sebaceum (angiofibromas):

A

Sirolimus

329
Q

Features of superficial siderosis?

A

sensorineural hearing loss
ataxia
dementia
anosmia
anisocoria ( unequal pupils)

330
Q

How to investigate superfical siderosis?

A

MRI

331
Q

MS + new multiple confluent lesions in the parietooccipital and right motor white matter areas as well as the left occipital area, with no mass effect or enhancement

A

JC virus serology

Causes PML

332
Q

Difference between paroxysmal hemicrania and cluster headache?

A

Chronic paroxysmal hemicrania is characterised by multiple (5+) short (5-30 min) headaches centered around the eye. CPH headaches are shorter and more frequent than cluster headaches

Clust headahce last 1-3 hours

333
Q

Basilar migraine?

A

four episodes of loss of consciousness within the past 4 weeks. She denies palpitations or chest pain but reports sudden onset binocular black dots in visual fields, occasional flashing lights, dysarthria and hearing loss, all of which resolves after about 60 minutes. She is unsure about the relevance of an occipital headache, onset with frequency of about three times per week for the past year. She denies any limb weakness, altered sensation or facial droop. She has no past medical history or family history of epilepsy. Your neurological examination, including fundoscopy is unremarkable. An EEG is unremarkable.

334
Q

Guillain barre + eye stuff ?

A

Miller Fisher syndrome
Anti GQ1b

335
Q

Falling kidney function + dopamine agonist

A

Retroperitoneal fibrosis

336
Q

sensory loss in her upper limbs at the level of C5-C7. She has spastic paraparesis, Romberg +ve indicating loss of proprioception in her lower limbs.

A

Cervical myelopathy

337
Q

Causes of cervical myelopathy?

A

Cervical cord tumours
ossification of the posterior longitudinal ligament
Trauma
Cervical degenerative changes (spondylosis)
Cervical degenerative disc disease

338
Q

Motor deltoid?

A

C5, C6

339
Q

Motor bicep

A

C5 C6

340
Q

Motor serratus anterior

A

C5, 6, 7

MRCP Neurology (2 decks)

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