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Phase3 Specialties - Imperial College London MBBS > MLA Neurology > Flashcards

MLA Neurology Flashcards

1
Q

Which dermatome is associated with a regimental badge distribution?

A

C5

Anterior shoulder dislocation can stretch and damage the axillary nerve which has the nerve root of C5. This supplies the sensation of the skin covering the inferior region of the deltoid muscle (regimental badge area), which is innervated by the superior lateral cutaneous nerve branch of the axillary nerve.

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2
Q

Which anomaly is commonly found in patients with neurogenic thoracic outlet syndrome?

A

Cervical rib

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3
Q

How long does a migraine without aura typically last for?

A

4-72 hours

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4
Q

What are the common visual auras in a migraine?

A

scotoma or fortification spectra

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5
Q

What is an episodic migraine x days/month?

A

<15 days/month

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6
Q

What is the minimum number of migraine attacks required under the ICHD-3 criteria to diagnose migraine?

A

At least 5 attacks

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7
Q

What are the headache characteristics associated with migraine?

A
  • Unilateral location (hemicranial pain)
  • Pulsating quality
  • Moderate or severe intensity
  • Aggravation by or causing avoidance of routine physical activity
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8
Q

What is the first line investigation indicated for a patient with a migraine?

A

A headache diary

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9
Q

What is the first line of management for migraines (symptomatic)?

A

Simple analgesia e.g., ibuprofen, aspirin or paracetamol

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10
Q

What is the first line acute symptomatic medical (post analgesia) for migraines?

A

Oral triptans

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11
Q

When should oral triptans be initiated during migraines?

A

At the start of the headache

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12
Q

Which anti-emetic is recommended for migraines?

A

metoclopramide 10 mg or prochlorperazine 10 mg

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13
Q

What are the serious adverse effects associated with metoclopramide?

A

Extrapyramidal symptoms

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14
Q

What are the three prophylactic medications for migraine?

A
  • Propranolol (80 – 160 mg daily, in divided doses).
  • Topiramate (50 – 100 mg daily, in divided doses); contraindicated in pregnancy.
  • Amitriptyline (25 – 75 mg at night).
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15
Q

What is the first line migraine prophylaxis in patients with no contraindications?

A

propranolol or topiramate

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16
Q

Which migraine prophylaxis is recommended as first in women?

A

propranolol

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17
Q

Which migraine prophylaxis is contraindicated in women due to teratogenicity?

A

Topiramate

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18
Q

What is the first line triptan indicated for patients with menstrual-related migraine?

A

frovatriptan (2.5 mg BDS) or zolmitriptan (2.5 mg BDS/TDS).

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19
Q

Which cerebral structure is postulated to be involved in cluster headache pathogenesis?

A

Hypothalamus

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20
Q

Which gender is most affected by cluster headache?

A

Male (5:1)

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21
Q

What is the typical duration of cluster headaches?

A

15 minutes to 3 hours

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22
Q

What is the characteristic location of cluster headaches?

A

unilateral orbital, supraorbital and/or temporal pain

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23
Q

What adjunctive symptoms associated with cluster headaches?

A
  • Autonomic symptoms:
  • Conjunctival injection or lacrimation
  • Nasal congestion or rhinorrhoea
  • Eyelid oedema or forehead/facial swelling
  • Facial flushing
  • Sensation of fullness in the ear
  • Miosis/ptosis (associated w/Horner Syndrome)
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24
Q

Horner syndrome is associated with which type of headache?

A

Cluster headache

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25
Q

Patients pacing or rocking i n place is associated with which type of headache?

A

Cluster headache

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26
Q

In patients with suspected cluster headache, what is the next line of management?

A

Refer to a neurologist specialist for specialist assessment and confirmation of diagnosis

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27
Q

What is the first line management for acute attacks of cluster headache?

A

Sumatriptan subcutaneous injection – 6 mg for one dose, followed by 6 mg >1 hour if a recurrent headache – maximum 12 mg/day.
- Intranasal spray (aged 18-65 years) – 10-20 mg initial dose; followed by 10-20 mg >2 hours – maximum 40 mg/day.

AND

Short-burst oxygen therapy (high flow oxygen 100%)

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28
Q

What is the prophylaxis for cluster headaches?

A

Verapamil

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29
Q

What investigation is indicated in patients on Verapamil?

A

ECG every 6 months

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30
Q

What is the duration of tension-type headache?

A

30 minutes to 7 days

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31
Q

What are the characteristic features and criteria for a diagnosis of tension type headache?

A
  • Bilateral localisation
  • Pressing or tightening, non-pulsatile quality is often described as a sensation akin to a tight band. Pain may originate from or radiate into the neck, and there is frequent pericranial tenderness on manual palpation.
  • Mild to moderate intensity
  • Not exacerbated by, nor does it lead to avoidance of, routine physical activity, such as walking or climbing stairs.
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32
Q

What is the mainstay of management for tension type headaches?

A

Patient reassurance with self-guided resources

Advise on the risk of medication overuse headache

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33
Q

What is the recommended investigation in patients with tension type headaches?

A

Headache diary for a minimum of 8 weeks

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34
Q

What is the management of choice for chronic tension-type headaches?

A

Acupuncture

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35
Q

What are the characteristic 3 features (Oxford Classification System) for a total anterior circulation stroke?

A
  1. Unilateral weakness or sensory loss of the face, arm and leg.
     Sensory: Paraesthesia or numbness
  2. Homonymous hemianopia
     Gaze paresis – horizontal and unidirectional.
     Diplopia
     Photophobia
  3. Higher cerebral dysfunction (e.g., dysphasia, visuospatial loss)
     Ataxia
     Dysphasia
     Dysarthria
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36
Q

DANISH symptoms?

A

Dysdiadochokinesis, ataxia, nystagmus, intention tremor, slurred speech, hypotonia/heel-shin test positive.

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37
Q

What type of stroke is associated with pure motor deficit?

A

Lacunar stroke

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38
Q

Lacunar strokes are associated with which structure?

A

Basal ganglia
Internal capsule

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39
Q

Duration of TIA?

A

<24 hours

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40
Q

What visual defect is typically associated with TIA?

A

Amaurosis fugax

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41
Q

Recurrent TIA suggests what underlying pathology?

A

Carotid artery stenosis - perform duplex carotid US

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42
Q

Which artery is most commonly affected by stroke?

A

Middle cerebral artery

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43
Q

What are the characteristic features of an anterior cerebral artery stroke?

A

Contralateral leg paresis, sensory loss, cognitive deficits (e.g., apathy, confusion, and poor judgement).

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44
Q

What are the characteristic features of MCA stroke?

A

Contralateral weakness and sensory loss of face and arm.
* Cortical sensory loss
* Contralateral homonymous hemianopia or quadrantanopia
* Left hemisphere (Dominant) – Aphasia.
* Right-hemisphere (Non-dominant) – Neglect + inattention.
* Eye deviation – Towards the side of the lesion and away from the weak side.

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45
Q

Which cranial nerves are involved in a posterior cerebral artery stroke (MIDBRAIN)?

A

CN III and IV palsy

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46
Q

An urgent carotid endarterectomy is indicated in symptomatic carotid stenosis >%?

A

50%

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47
Q

What is the first line investigation required for all patients with suspected stroke?

A

Non-contrast CT

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48
Q

What is the first line management for patients with ischaemic stroke?

A

300 mg aspirin

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49
Q

What is the first line management for ischaemic stroke <4.5 hours since symptom onset?

A

Thrombolysis (alteplase) and thrombectomy

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50
Q

What is the first line management for ischaemic stroke between 4.5 and 6 hours?

A

Thrombectomy

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51
Q

Blood pressure should be controlled to below what, for thrombolysis?

A

<185/110 mmHg

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52
Q

What investigation is used to assess salvageable brain tissue post-stroke?

A

Diffusion-weighted MRI/CT perfusion scan

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53
Q

What criteria is used to predict stroke?

A

NIHSS

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54
Q

What are the 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
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
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55
Q

What scale is used to assess for pre-stroke functional status?

A

Rankin scale

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56
Q

A thrombectomy is indicated in which National Institutes of Health Stroke Scale (NIHSS) score?

A

> 5

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57
Q

What is the first line anti-platelet therapy of choice post-stroke?

A

Clopidogrel 75 mg

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58
Q

Is clopidogrel is contraindicated, what is the preferred stroke prophylaxis?

A

Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily

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59
Q

If total cholesterol is >3.5 in stroke patents, what should be prescribed?

A
  • 20-80 mg atorvastatin (reduce non-HDL cholesterol by >40%)
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60
Q

What is the stroke prophylaxis indicated in patients post-stroke with AF?

A

Interim 300 mg aspirin for 14 days, followed by adjusted-dose warfarin or direct factor XA inhibitor

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61
Q

What is the DVLA advice for post-stroke?

A

Do not drive for 1 month - no need to notify the DVLA

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62
Q

What is the DVLA advice for recurrent TIAs?

A

Notify the DVLA, cease driving for 3 months

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63
Q

Which artery is implicated in lateral medullary syndrome?

A

Posterior inferior cerebellar artery

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64
Q

Ipsilateral ataxia, nystagmus, and dysphagia with contralateral hemisensory loss is suggestive of what diagnosis?

A

Lateral medullary syndrome

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65
Q

Which type of visual field defect is associated with posterior cerebral artery stroke?

A

Macular sparing homonymous hemianopia.

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66
Q

Which index is used to measure disability in patients post-stroke?

A

Barthel index

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67
Q

What are the causes of a CN3 palsy?

A
  • Vascular ischaemia
  • Diabetes mellitus, and hypertension.
  • Trauma
  • Intracranial neoplasm
  • Haemorrhage
  • Congenital
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68
Q

Which aneurysm is associated with a surgical third nerve palsy?

A

Posterior communicating artery aneurysm

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69
Q

What is the presentation of a surgical third cranial nerve palsy?

A

Dilated down and out pupil

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70
Q

Why does a posterior community artery aneurysm cause a surgical third cranial nerve palsy?

A

Compression of the outer parasympathetic fibres

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71
Q

What is the main cause of a pupil-sparing third nerve palsy?

A

diabetes mellitus or hypertension microangiography – affect the vaso vasorum

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72
Q

A down and out pupil is associated with what cranial nerve palsy?

A

Third cranial nerve (oculomotor)

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73
Q

Which two extra-ocular muscles are spared by CN3 palsy?

A

Lateral rectus (LR6)
Superior Oblique (SO4)

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74
Q

What investigation is indicated in patients with a surgical CN3 palsy?

A

CT angiography for suspected aneurysm

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75
Q

Which cranial nerve innervates the superior oblique?

A

Trochlear nerve (4)

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76
Q

Which cranial nerve palsy is associated with abnormal head position, vertical diplopia (noticed when reading a book)?

A

Fourth cranial nerve palsy

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77
Q

An up and rotated out pupil is associated with what CN palsy?

A

CN 4

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78
Q

The abducens nerve innervated which extra-ocular muscle?

A

Lateral rectus (responsible for ipsilateral eye abduction)

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79
Q

Impaired adduction of the eye and horizontal nystagmus in the contralateral eye suggests what?

A

Internuclear Ophthalmoplegia

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80
Q

Where is the lesion in Internuclear Ophthalmoplegia?

A

medial longitudinal fasciculus

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81
Q

ALS affects which type of cells and tracts?

A

Anterior horn cells and corticospinal tracts

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82
Q

Which mutations are associated with ALS?

A

SOD2

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83
Q

What is the most common type of MND?

A
  • Amyotrophic lateral sclerosis
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84
Q
  • Amyotrophic lateral sclerosis presents with what?
A
  • Constellation of LMN (in arms – flaccid paralysis) and UMN signs (in legs – spastic paralysis).
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85
Q

Which type of MDN is associated with the worst prognosis (due to loss of brainstem nuclei?

A
  • Progressive bulbar palsy:
  • Palsy of the tongue, muscles of mastication, dysphagia, dysphasia; due to loss of function of brainstem motor nuclei.
  • Worst prognosis.
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86
Q

Which type of MND is associated with UMN signs only?

A
  • Primary lateral sclerosis
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87
Q

Which type of MND is associated with lower motor neurone signs only?

A
  • Progressive muscular atrophy:
  • LMN signs only; affects distal muscles before proximal (best prognosis).
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88
Q

List LMN signs:

A
  • Weakness
  • Hypotonia
  • Muscle atrophy
  • Fasciculations
  • Hyporeflexia
  • Loss of deep tendon reflexes
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89
Q

List UMN signs:

A
  • Spasticity
  • Hyperreflexia
  • Clonus
  • Babinski sign
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90
Q

What is the first line disease modifying drug indicated for management of MND?

A

Riluzole

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91
Q

Which drug is indicated for the management of muscle cramps in MND?

A

Quinine

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92
Q

What is the first line medical management for MND spasticity?

A

Baclofen

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93
Q

What is the mechanism of action of baclofen?

A

GABA-B receptor agonist

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94
Q

In patients with respiratory impairment what is the first line management (MND)?

A

Non-invasive respiratory ventilation e.g., CPAP

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95
Q

What is the preferred first line management for patients with MND presenting with dysphagia?

A

percutaneous gastrostomy tube in at-risk patients

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96
Q

Which type of focal seizures are associated with deja vu, rising epigastric sensation and automatisms e.g., plucking, fidgeting?

A

Temporal lobe

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97
Q

What are the findings associated with temporal lobe focal seizures?

A
  • Aura:
  • Rising epigastric sensation
  • Psychic or experiential phenomena e.g., déjà vu, jamais vu
  • Hallucinations (auditory/gustatory/olfactory) – less common.
  • Automatisms (~60%): Repetitive, stereotyped movements e.g., picking, fidgeting, fumbling, chewing and lip-smacking.
  • Post-ictal confusion
  • EEG findings: Epileptiform sharp waves over the temporal region.
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98
Q

Which type of focal seizure is associated with a Jacksonian march?

A

Frontal lobe focal seizure

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99
Q

What are the findings associated with frontal lobe focal seizures?

A

Frontal Lobe (motor)
* Head/leg movements, posturing (fencing), post-ictal weakness, Jacksonian march.
* Bicycling automatisms e.g., pelvic thrusting and sexual automatisms
* Vocalisations
* The figure of four (localising contralateral to the extended arm)

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100
Q

What is the definition of epilepsy?

A

at least two unprovoked seizures occurring >24 hours apart

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101
Q

What is the most common type of generalised seizures?

A

Tonic-clonic

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102
Q

What neurocutaneous syndromes are associated with epilepsy?

A

Neurofibromatosis, tuberous sclerosis, and Sturge–Weber syndrome

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103
Q

Which type of seizure is associated with abrupt muscle contractions?

A
  • Myoclonic seizures
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104
Q

Which type of seizure is associated with a blank facial expression?

A

Absence seizure

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105
Q

Which type of seizure is associated with a sudden loss of muscle control?

A

Atonic seizure

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106
Q

When should an EEG be performed post-seizure?

A

Within 72 hours

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107
Q

Following a first episode seizure, what is the next most appropriate management step?

A

Urgent referral (within 2 weeks) for an assessment after a first suspected seizure (first fit clinic).

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108
Q

What is the first line drug for tonic-clonic seizures in males?

A
  • Sodium valproate
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109
Q

What is the first line of monotherapy for tonic-clonic seizures in women and girls with childbearing potential?

A
  • Lamotrigine or levetiracetam
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110
Q

What is the first line monotherapy for focal seizures?

A

Lamotrigine, levetiracetam

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111
Q

What is the preferred drug of choice in absence seizures?

A

Ethosuximide

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112
Q

Which anti-epileptic drug is not recommended in patients with absence seizures?

A

carbamazepine

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113
Q

Following a first unprovoked seizure, what is the minimum driving suspension period?

A

6 months

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114
Q

What is the DVLA advice for patients with epilepsy?

A

Suspension of driving license unless seizure-free for one year.

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115
Q

Sodium valproate is contraindicated in what disorder?

A

Acute porphyria

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116
Q

Status epileptics is defined as what?

A

Prolonged seizure >5 minutes or >2 within a 5 minute period without the patient returning to normal

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117
Q

What is the first-line drug indicated for patients with Status Epilepticus (without IV access)?

A

Buccal midazolam or rectal diazepam (10 mg)

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118
Q

What is the 1st line drug indicated for Status Epilepticus (with IV access)?

A

IV lorazepam (4 mg)

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119
Q

What is the 2nd line drug management for patients with Status Epilepticus ?

A

IV lorazepam within 5-10 minutes

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120
Q

What is the third medical management step for Status Epilepticus unresponsive to two doses of benzodiazepines?

A

IV levetiracetam, phenytoin or sodium valproate.

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121
Q

What is the mechanism of action of phenytoin?

A

Voltage-gated sodium channel blocker

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122
Q

What effect does phenytoin have on cytochrome p450?

A
  • Cytochrome P450 inducer
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123
Q

What are the acute adverse effects associated with phenytoin?

A
  • Syncope, diplopia, nystagmus, slurred speech, ataxia; confusion and seizures
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124
Q

What common chronic adverse effects are associated with phenytoin?

A

Gingival hyperplasia (secondary to increased expression of PDGF); hirsutism, coarsening of facial features, drowsiness

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125
Q

What haematological abnormality is associated with phenytoin?

A
  • Megaloblastic anaemia
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126
Q

What are the main risk factors associated with idiopathic intracranial hypertension?

A

Overweight women of childbearing age
Obesity
Pregnancy
Drugs e.g., steroids, COCP, retinoids, lithium

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127
Q

What is the characteristic headache presentation for IIH?

A

Throbbing/pulsatile

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128
Q

What precipitates the headache in IIH?

A
  • Precipitated by changes in position (e.g., standing, worse in the morning), Valsalva, bright light or eye movement.
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129
Q

What characteristic aural feature is associated with IIH?

A

Pulsatile tinnitus

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130
Q

What first line investigation is indicated for IIH?

A
  • Ophthalmoscopy – Optic disc oedema
  • Perimetry testing + visual acuity testing.
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131
Q

What is diagnostic of IIH?

A

Diagnostic lumbar puncture

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132
Q

What is the conservative management for IIH?

A

Weight loss

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133
Q

What is the first line drug indicated for IIH?

A

Acetazaolamide

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134
Q

What class of drug is acetazolamide and moa?

A
  • Carbonic anhydrase (acetazolamide) – decreases CSF production
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135
Q

What are the adverse effects associated with acetazolamide?

A

Hypokalaemia, paraesthesia of extremities

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136
Q

What are the two drugs recommended in the management of IIH?

A

acetazolamide

topiramate

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137
Q

What additional effect does topiramate confer in patients with IIH?

A

Weight loss

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138
Q

What is the surgical intervention recommended for patients with refractory IIH?

A
  • Optic nerve sheath defenestration
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139
Q

What type of hypersensitivity reaction is associated with MS?

A

Type IV hypersensitivity

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140
Q

Which modifiable factor adversely effects disease outcomes in MS?

A

Smoking and obesity

141
Q

T-cell mediated hypersensitivity reactions against what in MS?

A

Oligodendrocyte proteins e.g., basic myelin protein

142
Q

What is the most common type of multiple sclerosis?

A
  • Relapsing-remitting MS
143
Q

At what age does MS typically arise?

A

20-50 years

144
Q

Which visual symptom is commonly reported by patients with MS?

A

Optic neuritis

145
Q

Which term describes a transient recurrence of pre-existing neurological deficit due to small elevations in body temperature?

A
  • Uhthoff’s phenomenon
146
Q

Which pupillary defect is typically observed in patients with multiple sclerosis?

A

Relative afferent pupillary defect

147
Q

What corticospinal tract manifestation is associated with multiple sclerosis?

A

Transverse myelitits

148
Q

Which term/sign describes a shock-like sensation radiating down the spine?

A

Lhermitte’s phenomena

149
Q

What finding is observed in patients with MS on LP?

A

CSF-specific oligoclonal bands

150
Q

What is the diagnostic investigation for MS?

A
  • MRI (T2) with and without gadolinium contrast
151
Q

What is the first line acute management of multiple sclerosis?

A

High-dose corticosteroids (initiated within 14 days of symptom onset)

152
Q

What disease-modifying drug is indicated in the management of MS?

A
  • Natalizumab
153
Q

How is MS spasticity managed?

A

baclofen

154
Q

Which bacteria is commonly implicated in the pathogenesis of GBS?

A

campylobacter jejuni

155
Q

Which auto-antibodies are formed in patients with Guillain–Barre syndrome?

A

ganglioside antibodies

156
Q

What is the characteristic clinical presentation of GBS?

A

Ascending symmetrical muscle weakness

157
Q

What severe complication is associated with GBS?

A

Respiratory failure

158
Q

Which type of GBS is associated with ophthalmoplegia, areflexia, and ataxia (as descending paralysis)?

A

Miller Fischer Syndrome

159
Q

What finding on LP is associated with GBS?

A

albuminocytologic dissociation

160
Q

Which investigations are indicated for the diagnosis of GBS?

A

Lumbar puncture

Nerve conduction studies/Electromyography

161
Q

What abnormalities are detected on EMG for GBS?

A

Absent H-reflexes and prolonged distal latency

162
Q

What is the first line management of GBS?

A

IV immunoglobulins or plasma exchange

163
Q

What respiratory function should be measured in patients with GBS?

A

Forced vital capacity

164
Q

Which nerve roots form the median nerve?

A

C5-T1

165
Q

Which group of muscles are innervated by the median nerve (motor function)?

A

Thenar muscles and the lateral two lumbricals

166
Q

Which muscles are included in the thenar muscles? (3)

A

Flexor pollicis brevis, abductor pollicis brevis, opponens pollicis.

167
Q

What is the motor function of the median nerve?

A

Innervates the flexor and pronator muscles in the anterior compartment in the hand

168
Q

What is the sensory function of the median nerve?

A

Lateral 3 ½ fingers on the anterior surface of the hand.

169
Q

What nerve runs in the carpal tunnel?

A

Median nerve

170
Q

What are the two layers of the carpal tunnel?

A

Deep carpal arch and superficial flexor retinaculum

171
Q

What are the risk factors for carpal tunnel syndrome?

A
  • Repetitive wrist flexion or hand elevation
  • Obesity
  • Pregnancy
  • Osteoarthritis of the MCP joint of the thumb – compression of the median nerve by osteophytes
  • Inflammatory joint disease e.g., rheumatoid arthritis (due to synovitis in the carpal tunnel).
  • Ganglion cysts, tumour, scar tissue.
  • Hypothyroidism
  • Diabetes mellitus.
172
Q

What are the characteristic findings observed in carpal tunnel syndrome?

A
  • Intermittent paraesthesia, numbness or altered sensation, and burning or pain in the distribution of the median nerve (the thumb, index, middle finger and the radial half of the ring finger).
173
Q

What alleviates carpal tunnel syndrome pain?

A

Changing hand posture or shaking the wrist (‘the flick sign’).

174
Q

What hand weakness features are associated with carpal tunnel syndrome?

A
  • Loss of grip strength
  • Hand weakness
     Atrophy of the thenar muscles
     Trophic ulceration at the tips of the digits
     Weakness of thumb abduction and opposition
  • Reduced manual dexterity (doing up buttons, holding objects and opening jars).
175
Q

What sign denotes tapping the nerve in the carpal tunnel to elicit pain in the median nerve distribution?

A

Tinel’s sign

176
Q

What is Phalen’s manoeuvre?

A

Holding the wrist in flexion for 60 seconds to elicit numbness/pain in the median nerve distribution.

177
Q

What specialist assessment is used for the diagnosis of carpal tunnel syndrome?

A
  • Nerve conduction studies
178
Q

What is the fist line management for mild-moderate carpal tunnel syndrome?

A

Wrist splint for 6 weeks or single corticosteroid injection

179
Q

What is the definitive management for carpal tunnel syndrome?

A

Carpal tunnel surgery (decompression) – flexor retinaculum division.

180
Q

What is the gold-standard investigation to confirm degenerative cervical myelopathy?

A

MRI of the cervical spine

181
Q

What is the characteristic finding of degenerative cervical myelopathy?

A

Wide-based spastic gate, with clumsy upper extremity function due to compression of the lateral corticospinal tracts and spinocerebellar tracts

182
Q

What is the definitive management for degenerative cervical myelopathy?

A

Decompressive surgery

183
Q

Upper quadrant bitemporal hemianopia is caused by what?

A

Inferior chiasmal compression (pituitary tumour)

184
Q

What causes a lower quadrant bitemporal hemianopia?

A
  • Lower quadrant defect = Superior
185
Q

Superior homonymous quadrantopia is caused by what?

A

Lesion of the inferior optic radiations in the temporal lobe

186
Q

Inferior homonymous qudrantopia is caused by what?

A
  • Inferior: Lesion of the superior optic radiations in the parietal lobe
187
Q

Temporal arteritis is frequently associated with what?

A

polymyalgia rheumatica.

188
Q

Which visual defect is associated with GCA?

A
  • Anterior ischaemic optic neuropathy – Transient vision loss, amaurosis fugax and optic atrophy.

and optic neuritis

189
Q

What is the first line blood investigation for suspected GCA?

A

Seru ESR >50 mm/hour

190
Q

What is the diagnostic investigation to confirm GCA?

A

Temporal arterial biopsy

191
Q

What findings are observed in a temporal artery biopsy?

A

multinucleated giant cells or panarteritis (skip lesions).

192
Q

On duplex ultrasound, what is seen in temporal arteritis?

A

Halo sign

193
Q

What demographic is most affected by GCA?

A

> 50 years of age

194
Q

What is the first line management for temporal arteritis?

A

High dose corticosteroids e.g., prednisolone 40-60 mg/day

195
Q

What is the first line management for temporal arteritis with new visual loss or double vision?

A

urgent same-day ophthalmic assessment

and

500 mg - 1g of IV methylprednisolone

196
Q

Myasthenia Gravis affects what?

A

The neuromuscular junction

197
Q

Which autoantibodies are implicated in myasthenia Gravis?

A

Autoantibodies against postsynaptic membrane proteins (e.g., n-AChR, MuSK and LPR4)

198
Q

What typically precipitates myasthenia Gravis?

A

Infections, immunisations, surgeries, pregnancy and drugs e.g., aminoglycosides

199
Q

What is the paraneoplastic subtype of myasthenia Gravis?

A

Lambert–Eaton Myasthenic syndrome

200
Q

Which lung cancer is associated with Lambert–Eaton Myasthenic syndrome?

A

Small cell carcinoma

201
Q

What is the characteristic ocular finding observed in Myasthenia Gravis?

A
  • Extraocular muscle weakness (~85%)—diplopia and ptosis
202
Q

Which test can demonstrate amelioration of muscle weakness in myasthenia gravis?

A

ice-pack test

203
Q

What tests are indicated as first-line for patients with suspected myasthenia gravis?

A

Serology testing for anti-AChR and MuSK

204
Q

What is the most sensitive test for diagnosing myasthenia gravis?

A
  • Single-fibre electromyography (most sensitive): Mean jitter value is higher than normal.
205
Q

What is the first line management for myasthenia gravis?

A

Cholinesterase enzyme inhibitors e.g., long-acting pyridostigmine

206
Q

What neck procedure may be indicated in myasthenia gravis?

A

thymectomy

207
Q

What is the first line management for a myasthenic crisis?

A

IVIG or plasma exchange

208
Q

What parameter is used to monitor respiratory function during a myasthenic crisis?

A

Forced vital capacity (FVC)

209
Q

Which nerve is implicated in Bell’s palsy?

A

Facial nerve

210
Q

What is the characteristic presentation of Bell’s Palsy?

A

Unilateral non-forehead sparing facial weakness

211
Q

Why is Bell’s palsy non-forehead sparing?

A

Affects the lower motor neurones (whereas in stroke, there is innervation from the unilateral motor cortex)

212
Q

What are the common risk factors for Bell’s palsy?

A

Intranasal influenza vaccination

Pregnancy

Infection

213
Q

When do Bell’s palsy symptoms fully evolve?

A

Within 72 hours

214
Q

What scale is used to measure disease progression in patients with Bell’s palsy?

A

House–Brackmann scale

215
Q

What serology testing is indicated in certain patients with Bell’s palsy?

A
  • Borrelia burgdorferi
216
Q

Bell’s palsy with a vesicular rash in the auditory canal suggests whats?

A

Herpes zoster infection - Ramsay Hunt Syndrome

217
Q

What is the first line management for Bell’s palsy?

A

Prednisolone 50mg OD for 10 days

218
Q

What is the management for Ramsay Hunt Syndrome?

A

Oral prednisolone and acyclovir

219
Q

What conservative management is indicated in patients with Bell’s palsy?

A

Corneal protection with protective glasses or artificial tears

220
Q

What is a common acute complication associated with Bell’s palsy?

A

Keratoconjunctivitis sicca

221
Q

SAH typically concerns ruptures of saccular aneurysms where?

A

Circle of Willis

222
Q

What is the main contributing risk factor for a subarachnoid haemorrahge?

A

Hypertension

223
Q

Which conditions are associated with a subarachnoid haemorrhage?

A

Adult polycystic kidney disease, Marfan’s syndrome, pseudoxanthoma elasticum, Ehlers-Danlos Syndrome,

224
Q

What is the characteristic headache presentation for SAH?

A

Sudden-onset thunderclap headache in the occipital region associated with photophobia

225
Q

What is the emergency first line investigation for patients with suspected SAH?

A

Non-contrast CT within 6 hours

226
Q

What is revealed on a non-contrast CT in patient with a SAH?

A

Hyperdense areas in the basal regions of the skull

227
Q

When is a lumbar puncture indicated in a SAH?

A

> 12 hours of symptom onset

228
Q

What is revealed on lumbar puncture in patients with a SAH?

A

Xanthochromia

229
Q

Which investigation confirms the causative pathology for SAH?

A
  • CT intracranial angiogram
230
Q

Which ECG changes are typically observed in patients with a SAH?

A

ST-elevation

231
Q

What drug is indicated to reduce vasopasm in patients with SAH?

A
  • Nimodipine
232
Q

What is the definitive management of SAH?

A

Endovascular coiling

233
Q

How is hydrocephalus managed acutely?

A

External ventricular drain

234
Q

What is the common precipitating trigger for a subdural haemorrhage?

A

Shearing of bridging veins due to trauma e.g., shaken baby syndrome

235
Q

What is Cushing’s triad?

A

Bradycardia, hypertension and respiratory irregularities.

236
Q

On CT imaging, what finding is observed in a patient with a subdural haematoma?

A

Crescenteric in shape

Acute = hyperdense

Chronic = hypodense

237
Q

What i the surgical intervention for patients with subdural haematoma?

A

Burr-hole evacuation or craniotomy.

238
Q

Which vessel is commonly involved in an extradural haemorrhage?

A

Middle meningeal artery

239
Q

What is the initial presentation of an extradural haemorrhage?

A

Lucid interval: Initial episode of unconsciousness, followed by transient consciousness, reverting to complete unconsciousness

240
Q

A lentiform hyperdense collection on CT indicates what?

A

Extradural Haemorrhage

241
Q

What is the definitive management for an extradural haemorrhage?

A

craniotomy and evacuation of the haematoma.

242
Q

Which genetic disorder is associated with bilateral acoustic neuroma?

A
  • Neurofibromatosis type 2
243
Q

Which cranial nerve is implicated in acoustic neuroma?

A

vestibulocochlear nerve

244
Q

Where do acoustic neuromas typically reside?

A

cerebellopontine angle

245
Q

What type of hearing loss is associated with acoustic neuroma?

A

unilateral, high-frequency retro-cochlear sensorineural hearing loss

246
Q

What are the characteristic features associated with acoustic neuroma?

A

Unilateral sensorineural hearing loss
Vertigo
Headache
Tinnitus

247
Q

What is the first line audiological investigation for acoustic neuroma?

A

Pure tone audiometry

248
Q

What is the diagnostic investigation for acoustic neuroma?

A

Contrast-enhanced MRI

249
Q

What is the first line management for acoustic neuroma size 1.5 to 3 cm?

A

stereotactic radiotherapy

250
Q

What is the first line management for large acoustic neuroma (>3 cm)?

A

Surgical resection

251
Q

What monitoring is required during surgical resection of acoustic neuroma?

A

Intraoperative facial nerve monitory

252
Q

What disorder is associated with fluctuating sensorineural hearing loss, vertigo and tinnitus?

A

Meniere’s Disease

253
Q

What is the typical duration of Meniere’s Disease ?

A

20 minutes

254
Q

What is indicated for the symptomatic relief of Meniere’s Disease ?

A

prochlorperazine or an antihistamine

255
Q

What is the prophylactic management for Meniere’s Disease?

A

betahistine

256
Q

What is the typical duration of BPPV episode?

A

<60s

257
Q

Which semicircular canal is predominantly affected by BPPV?

A

Posterior semicircular canal

258
Q

Which manoeuvre is used to diagnose BPPV?

A

Dix–Hallpike manoeuvre

259
Q

What is the long term management for BPPV?

A

Epley and Sermont manoeuvres

260
Q

What are the risk factors associated with brain abscess?

A
  • Direct local spread:
  • Inferior temporal lobe: Otitis media, and mastoiditis
  • Frontal lobe: Dental infections, ethmoid sinuses
    N.B: Paranasal sinus infections account for ~30-50% of brain abscesses.
261
Q

What is the imaging study of choice for brain abscess?

A

CT scan

262
Q

What is observed on CT scan for brain abscess?

A

Ring-enhancing lesion

263
Q

What is the first line management for brain abscess?

A

IV 3rd generation cephalosporin (ceftriaxone) and metronidazole.

264
Q

What is the definitive management for brain abscess?

A

Craniotomy + abscess debridement

265
Q

Lisch nodules cafe au lait macules and optic pathway gliomas are associated with what genetic disorder?

A

Neurofibromatosis Type 1

266
Q

What is the inheritance pattern for Neurofibromatosis Type 1?

A

Autosomal dominant

267
Q

Which characteristic skin manifestation is observed in tuberous sclerosis?

A

Ash-leaf shaped white macules

Angiofibromas

Shagreen patach

268
Q

What is Vogt diagnostic triad for tuberous sclerosis?

A

seizures, intellectual disability and facial angiofibromas.

269
Q

What is the most common viral cause of encephalitis?

A

HSV-1

270
Q

HSV-1 typically affects which part of the brain?

A

Temporal and inferior frontal lobes

271
Q

What are the characteristic features observed in encephalitis?

A
  • Fever
  • Seizures
  • Vomiting
  • Headache
  • Behavioural changes/Mental state alteration – Confusion; deteriorating GCS.
  • Focal neurological symptoms: Dysphagia, hemiplegia, aphasia (Hallmark feature)
272
Q

What is the first line investigation for encephalitis?

A

CT

and Lumbar puncture

273
Q

What CT findings are consistent with a diagnosis of encephalitis?

A

medial temporal and inferior frontal lobe changes e.g., petechial haemorrhages

274
Q

What is the first line management for encephalitis?

A

IV acyclovir (10 mg/kg TDS); IV ceftriaxone

275
Q

Which artery is associated with trigeminal neuralgia?

A

superior cerebellar artery

276
Q

What is the investigation of choice for confirming trigeminal neuralgia?

A
  • MRI (if persistent): Evidence of compression of the trigeminal nerve by the superior cerebellar artery.
277
Q

What is the first line drug for trigeminal neuralgia?

A

Carbamazepine

278
Q

Unresponsive refractory trigeminal neuralgia can be managed with what?

A

microvascular decompression surgery of the trigeminal nerve (if evidenced arterial compression).

279
Q

What is the main characteristic feature for multisystem atrophy?

A
  • Dysautonomia
  • Urinary incontinence, anhidrosis and orthostatic hypotension.
  • Erectile dysfunction (early feature)
  • Atonic bladder
280
Q

What is the most common cause of meningitis in neonates?

A

Group B streptococcus

281
Q

What is the most common cause of bacterial meningitis in 10-19 year olds?

A

N. meningitis

282
Q

What is the most common cause of bacterial meningitis in adults?

A

Streptococcus pnuemoniae

283
Q

What is the most common cause of viral meningitis?

A

enterovirus (e.g., Coxsackie, echovirus)

284
Q

Which sign denotes resistance on full extension of the knee when the hip is flexed?

A

Kernig sign

285
Q

Which sign denotes the following:
Flexion of the patient’s neck causes the hips and knees to flex?

A
  • Brudzinski sign
286
Q

What are the first line investigations for suspected meningococcal disease?

A

Blood culture, white cell count, CRP, lactate levels, and whole-blood diagnostic PCR.

287
Q

What is the first line antibiotic therapy for bacterial meningitis?

A

Empirical antibiotic therapy (high-dose ceftriaxone) should promptly be initiated within 1 hour of presentation accompanied by immediate fluid resuscitation in septic patients.

288
Q

Primary care management for bacterial meningitis?

A

IM benzylpenicillin

289
Q

In confirmed non-meningococcal disease what is the management for meningitis?

A

V ceftriaxone and corticosteroids

290
Q

What are the two signs for a basal skull fracture?

A

Racoon eyes
Battle sign

291
Q

What is battle sign?

A

Basilar skull fracture – bruise over the mastoid process – takes 1 day to appear.

292
Q

What is the first line management for raised ICP?

A

Head elevation and IV mannitol

293
Q

Which genes are associated with early-onset Alzheimer’s disease?

A

presenilin 1 protein (PSEN1), PSEN2

294
Q

What genes are associated with late-onset Alzheimer’s disease?

A

APOE e4 allele increases risk

295
Q

What are the extracellular deposits in Alzheimer’s disease?

A

Beta-amyloid

296
Q

What are the intracellular deposits in Alzheimer’s disease?

A

neurofibrillatory tangles.

297
Q

What is the diagnostic cut off for diagnosis fo Alzheimer’s disease on a MoCa?

A

<26

298
Q

An AMTS <x is suggestive of cognitive impairment?

A

<7

299
Q

Rapidly progressing dementia is suggestive of what?

A

Creutzfeldt-Jakob disease

300
Q

What is the investigation of choice for Creutzfeldt-Jakob disease?

A

CSF examination

301
Q

What MRI findings are consistent with Alzheimer’s disease?

A
302
Q

What is the first line drug for Alzheimer’s disease?

A

Acetylcholinesterase (AChE) inhibitor monotherapy
e.g., Donepezil, galantamine, rivastigmine

303
Q

What is the first line management for severe Alzheimer’s disease?

A

Memantine

304
Q

What is the mechanism of action of memantine?

A

NMDA partial receptor agonist

305
Q

What is the pathological hallmark of Lewy-body dementia?

A

Eosinophilic intracytoplasmic inclusions (Lewy Bodies) – contain aggregated alpha-synuclein.

306
Q

What are the characteristic features of Lewy-body dementia?

A
  • Recurrent visual hallucinations
  • Well-formed and detailed – people, children or small animals.
  • Lilliputian hallucinations.
  • Fluctuating confusion with marked variations in alertness levels
    o Associated with lucid intervals.
  • Rapid eye movement (REM) sleep behaviour disorder
  • Parasomnia is characterised by dream enactment.
  • Motor features of Parkisonism:
  • Bradykinesia
  • Rest tremor
  • Anosmia – early sign of PD
  • Antipsychotic sensitivity
    o Antipsychotic drugs  Acute reactions – irreversible parkinsonism, and impaired consciousness.
  • Rigidity
  • Frequent falls
    o Supportive clinical features:
     Postural instability
     Autonomic dysfunction
     Syncope
     Delusions
     Non-visual hallucinations
     Apathy
     Anxiety
     Depression
307
Q

What is the management of choice for Sleep disturbance in Lewy body dementia?

A

Clonazepam

308
Q

What drug is indicated for the management of frontotemporal dementia?

A

Anti-depressants

309
Q

Which pathway is affected in Parkinson’s disease?

A

Nigrostriatal pathway

310
Q

What is the difference in tremor between drug-induced and idiopathic Parkinson’s?

A

Drug-induced = bilateral

311
Q

What is the first line management for Parkinson’s disease?

A

Levodopa

312
Q

What is co-prescribed with levodopa in Parkinson’s disease?

A

Levodopa, co-administered with a dopa decarboxylase inhibitor

313
Q

What are the common adverse effects associated with Parkinson’s disease manaegment?

A

postural hypotension, nausea, and vomiting.

314
Q

Which drug is indicated for motor symptoms in Parkinson’s disease?

A

Oral dopamine agonists e.g., ropinirole

315
Q

What are the adverse effects associated with oral dopamine agonists?

A

sleepiness, hallucinations, and impulse control disorders

316
Q

What is the management of dyskinesia in Parkinson’s disease?

A

amantadine

317
Q

What disorder is associated with a vertical supranuclear gaze palsy?

A

Progressive supranuclear palsy

318
Q

What is the clinical triad for Wernicke’s encephalopathy?

A

ophthalmoplegia, gait ataxia, and encephalopathy

319
Q

Which vitamin is deficient in Wernicke’s encephalopathy?

A

thiamine (Vitamin B1) deficiency

320
Q

What oculomotor dysfunction is associated with Wernicke’s encephalopathy?

A
  • Nystagmus
  • Lateral rectus palsy
  • Conjugate gaze palsies
321
Q

What is a complication of Wernicke’s encephalopathy characterised by confabulation?

A

Korsakoff’s syndrome

322
Q

What is Hakim’s clinical triad in NPH?

A

gait disturbance, cognitive deterioration, and urinary incontinence

323
Q

What is the preferred investigation for NPH?

A

MRI is the preferred confirmatory investigation for a definitive diagnosis of NPH

324
Q

What is the management for NPH?

A

ventriculoperitoneal shunting or endoscopic third ventriculostomy

325
Q

What is the presentation of essential tremor?

A
  • Bilateral action tremor:
  • Affecting the hands and arm
  • Exaggerated with posture holding (arms are held in a fixed posture against gravity) and with goal-directed limb movements.
326
Q

What is the first line management of essential tremor?

A

Propranolol

327
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal dominant

328
Q

What trinucleotide repeat is implicated in Huntington’s disease?

A

36 CAG trinucleotide

329
Q

What is this the management for chorea symptoms in Huntington’s disease?

A

VMAT inhibitors (e.g., tetrabenazine)

330
Q

Recreation use of which drug causes subacute degeneration of the spinal cord?

A

Nitric oxide

331
Q

Subacute degeneration of the spinal cord is associated with which type of vitamin deficiency?

A

Vitamin B12

332
Q

What should be measured in patients with nitrous oxide use presenting with subacute degeneration of the spinal cord?

A

measure homocysteine and methylmalonic acid

333
Q

The radial nerve innervates which muscle groups?

A

The triceps brachii and the extensor muscles in the forearm

334
Q

What are the nerve roots for the radial nerve?

A

C5 -T1

335
Q

What is the clinical manifestation of a radial nerve palsy?

A

Wrist drop

336
Q

What is the clinical manifestation of an ulnar nerve palsy?

A

Claw hand and sensory loss of the medial 1 1/2 fingers

337
Q

What is the first line drug indicated in patients with neuropathic pain?

A

Amitriptyline, duloxetine, gabapentin or pregabalin.

338
Q

What is the management for diabetic gastroparesis?

A

Small particle size diet and consideration of a prokinetic drug e.g., metoclopramide

339
Q

What distribution pattern is observed in patients with peripheral diabetic neuropathy?

A

stocking-glove distribution

340
Q

What are the autonomic dysfunction features associated with diabetic neuropathy?

A
  • Postural hypotension (defined as a drop in systolic blood pressure >30 mmHg when transitioning from a supine to a standing position).
  • Diabetic gastroparesis: Delayed gastric emptying, bloating, nausea and post-prandial vomiting.
     Advise: Small-particle-size diet (mashed or pureed food) for symptom relief + referral to a gastroenterologist for consideration of a prokinetic drug (e.g., metoclopramide, domperidone, or erythromycin).
  • Lower gastrointestinal involvement: Lower abdominal pain, unexplained diarrhoea, and faecal incontinence.
  • Unexplained urinary symptoms e.g., hesitancy, reduced frequency, inadequate bladder emptying and urinary retention.
341
Q

What is the rescue therapy for exacerbations of neuropathic pain?

A

Tramadol

342
Q

What is the most common cause of sciatica?

A

Intervertebral disc herniation

343
Q

Which nerve roots are involved in sciatica?

A

L4 - S1

344
Q

A positive straight leg test is indicative of what disorder?

A

Sciatica (Lumbar Radiculopathy)

345
Q

What is the first line management for sciatica?

A

Analgesia (e.g., paracetamol) to manage back pain – Low-dose NSAIDs.
* Group exercise programme
* Physiotherapist for manual therapy
* CBT

346
Q

What autoantibodies are associated with Lambert-Eaton syndrome?

A

presynaptic voltage-gated calcium channel antibodies

347
Q

What is the characteristic finding associated with Lamber-Eaton syndrome?

A

Weakness improves with activities

348
Q

What is the first line medical management for Lambert–eaton syndrome?

A

Phase3 Specialties - Imperial College London MBBS (14 decks)

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