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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What triad is seen in Horner’s syndrome?

A

Anhydrosis

Ptosis

Miosis (pupil constriction)

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2
Q

Define Temporal Arteritis

A

Describes inflammatory vasculitis affecting large vessels of the scalp, neck and arms.

Most commonly affects the extracranial branches of the carotid artery.

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3
Q

What is the most common risk factor for temporal arteritis?

A

Polymylagia Rheumatica (proximal weakness - may have difficulty getting out of chair)

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4
Q

Give 4 clinical features of Temporal Arteritis

A

Rapid onset (<1 month)

Superficial, unilateral pounding headache

Scalp tenderness (when brushing hair)

Visual disturbance (diplopia, blurring, amaurosis fugax - transient loss of vision)

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5
Q

Give 1 complication of Temporal Arteritis

A

Irreversible loss of vision in affected eye

Occurs due to carotid claudication (vasculitis can extend to 1st branch of internal carotid artery (ophthalmic artery)

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6
Q

How is Temporal Arteritis managed? (2)

A

High dose glucocorticoids

No visual loss - Prednisolone

Visual loss - Methylprednisolone followed by prednisolone

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7
Q

What is the most common type of headache?

A

Tension headache

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8
Q

How may a tension headache present?

A

Slowly progressive
Bilateral
Tight “band like” headache.

May originate from the neck

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9
Q

Give 2 triggers of tension headache

A

Stress

Dehydration

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10
Q

What medications are used in the acute management of Tension Headaches? (3)

A

Aspirin, Paracetamol or NSAIDs

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11
Q

What is used as prophylaxis against tension headaches?

A

Acupuncture (up to 10 sessions over 5-8 weeks)

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12
Q

Describe a Cluster Headache

A

Describes excruciating, stabbing pain located unilaterally behind the eye.

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13
Q

Describe the duration of Cluster Headaches

A

Occur in series (clusters) lasting for weeks/months separated by periods of remission.

Attacks tend to be brief - lasting 15-180 minutes

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14
Q

Give 3 causes of Cluster Headaches

A

Smoking

Alcohol

Nocturnal sleep (late bedtime)

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15
Q

Give 2 clinical features of cluster headaches

A

Unilateral peri-orbital pain (severe stabbing pain around/behind one eye)

Ptosis, Miosis, Conjunctivitis, Eyelid oedema

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16
Q

Describe the acute management of cluster headaches (2)

A

100% inhaled oxygen

Subcutaneous sumatriptan

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17
Q

When may sumatriptan be contraindicated?

A

Cardiac disease - IHD, Coronary Vasospasm, Angina, Hypertension

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18
Q

Describe the prophylactic management of Cluster Headaches (2)

A

1st line - Verapamil

2nd line - Lithium, Topiramate, Gabapentin

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19
Q

Describe migraine

A

Severe, unilateral, throbbing/pulsating headache (aggravated by movement)

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20
Q

Give 3 clinical features of migraine

A

Nausea and Vomiting

Photophobia and/or Phonophobia

Aura (scintillating scotoma - waves of light/lines/spots)

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21
Q

Give 1 complication of migraine

A

Hemiplegic migraine - Temporary paralysis on 1 side of the body

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22
Q

Describe 2 types of migraine

A

Episodic - Occurs <15 days per month

Chronic - Occurs on at least 15 days per month for >3 months

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23
Q

Give 5 triggers of migraine

A

Lack of sleep

Irregular/missed meals

Excessive caffeine intake

Lack of exercise/physical exertion

Menstruation (occurring around the time of periods)

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24
Q

What is the MOA for triptans?

A

5-HT receptor agonists

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25
Q

Give 2 contraindications for triptan use

A

Ischemic heart disease

Cerebrovascular disease

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26
Q

Give 1 side effect of triptans

A

Throat and chest tightness

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27
Q

What is the 1st and 2nd line for acute management of migraine?

A

1st line - Oral triptan + NSAID or Oral triptan + Paracetamol.

Nasal > oral triptan in patients aged 12-17

2nd line - Metoclopramide or Prochlorperazine (+/- NSAID)

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28
Q

When should migraine prophylaxis be offered?

A

Give to patients experiencing 2 or more attacks per month

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29
Q

What is the 1st line prophylactic management of migraine? (3)

A

Propranolol or Topiramate

propranolol contraindicated in asthma

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30
Q

When should propranolol be favoured over topiramate for migraine prophylaxis?

A

In women of child bearing age (as topiramate is teratogenic and can reduce effectiveness of hormonal contraceptives)

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31
Q

What should be offered to women with predictable menstrual migraine?

A

Frovatriptan or Zlomitriptan

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32
Q

Describe trigeminal neuralgia

A

Sudden, excruciating, sharp, “lightning-like” unilateral facial pain occuring in the V2 (maxillary)nd V3 (mandibular) nerve branch distributions

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33
Q

What may trigeminal neuralgia be indicative of? (2)

A

Multiple sclerosis

Brain stem tumour

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34
Q

What is the 1st line treatment for trigeminal neuralgia?

A

Carbamazepine (as long as there are no red flag symptoms)

Others; Phenytoin, Gabapentin, Baclofen

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35
Q

What is the MOA of phenytoin?

A

Anti-convulsant (sodium channel blocker)

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36
Q

What is the MOA of gabapetin

A

Increases GABA concentrations in the brain

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37
Q

What is the moa for Baclofen?

A

Antispasmodic - GABA analogue

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38
Q

Describe idiopathic intracranial hypertension

A

Neurological condition caused by an increase in intracranial pressure in the absence of a tumour

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39
Q

How may idiopathic intracranial hypertension present?

A

Presents in young obese women

Recurrent (daily) throbbing morning headaches

Papilloedema (optic disc swelling)

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40
Q

Give 4 risk factors for idiopathic intracranial hypertension

A

Obesity

Female

Pregnancy

Drugs (vitamin A and COCP)

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41
Q

Why must CT/MRI be conducted before lumbar puncture in patients presenting with features of raised ICP?

A

To rule out tumour.

LP in the presence of a tumour can cause a sudden decrease in ICP, resulting in brain herniation.

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42
Q

How is idiopathic intracranial hypertension managed? (3)

A

Weight loss

Diuretics - Acetazolamide (Carbonic anhydrase inhibitor)

Repeated lumbar puncture

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43
Q

Name 2 types of stroke. Which is most common?

A

Ischemic (most common)

Haemorrhagic

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44
Q

Give 3 causes of ischemic stroke. Which is the most common?

A

Embolism (most common) - Atrial fibrillation, Infective endocarditis, MI

Atheroma (from carotid arteries)

Systemic hypoperfusion (watershed stroke - Sepsis)

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45
Q

What classification is used to classify strokes?

A

Oxford Stroke Classification (aka Bamford Classification)

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46
Q

What criteria are assessed in the Oxford Stroke Classification? (3)

A

Unilateral hemiparesis and/or hemisensory loss of the fact, arm and leg

Homonymous hemianopia

Higher cognitive dysfunction (e.g dysphasia)

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47
Q

What types of stroke are included in the Oxford Stroke Classification? (4)

A

Total Anterior Circulation Stroke (TACS)

Partial Anterior Circulation Stroke (PACS)

Posterior Circulation Stroke (POCS)

Lacunar Stroke (LACS)

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48
Q

Describe a Total Anterior Circulation Stroke (TACS) and state what factors must be present for diagnosis

A

Large cortical stroke affecting areas of the brain supplied by both the anterior and middle cerebral arteries.

All 3 must be present for diagnosis;

Hemiparesis (contralateral) and/or sensory deficit

Homonymous hemianopia (contralateral)

Higher cognitive dysfunction (i.e dysphasia)

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49
Q

Describe Partial Anterior Circulation Stroke (PACS) and state what factors must be present for diagnosis

A

Describes less severe form of TACS, in which only part of the anterior circulation has been compromised.

Requires only 2 of the following;

Hemiparesis (contralateral) and/or sensory deficit

Homonymous hemianopia (contralateral)

Higher cognitive dysfunction (i.e dysphasia)

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50
Q

Describe Posterior Circulation Stroke (POCS) and state what factors must be present for diagnosis

A

Describes damage to the area of the brain supplied by the posterior circulation (vertebrobasilar territory), particularly the brainstem and cerebellum.

One of the following must be present for diagnosis;

Cerebellar/Brainstem syndromes (ataxia, nystagmus, vertigo, cranial nerve palsy)

Loss of consciousness

Isolated contralateral homonymous hemianopia

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51
Q

What investigation is used to diagnose stroke? What does it help you identify?

A

Non-contrast CT head

Helps identify is stroke is ischemic or haemorrhagic

(Non contrast as contrast would appear hyperdense, just like blood)

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52
Q

What additional tests should be performed in patients <55 presenting with stroke symptoms (with no obvious cause)

A

Autoimmune and thrombophilia screening

Screen for;
Antinuclear antibodies (ANA)
Antiphospholipid antibodies (APL)
Anticardiolipin antibodies (ACL)
Lupus anticoagulant (LA)
Coagulation factors
ESR
Homocysteine and syphilis serology

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53
Q

Describe the acute management of stroke (2)

A

Oxygen (if hypoxic <92%)

Insulin and glucose

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54
Q

Describe management of ischemic stroke, once haemorrhagic stroke has been excluded.

A

Aspirin

Thrombolysis (alteplase) - Administered within 4.5 hours of onset of stroke symptoms

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55
Q

Give 5 contraindications for thrombolysis

A

Previous intracranial haemorrhage

Seizure at onset of stroke

Traumatic brain injury/stroke in last 3 months

Active bleeding/GI haemorrhage

Pregnancy

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56
Q

Describe the secondary prevention of strokes (2)

A

1st line - Clopidogrel

2nd line - Aspirin + Modified Release Dipyridamole (if clopidogrel contraindicated)

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57
Q

Give 1 contraindication for clopidogrel use

A

Active bleeding

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58
Q

What is the moa of clopidogrel

A

P2Y12 antagonist (inhibits activation of platelets)

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59
Q

Concurrent use of what medication can reduce the effectiveness of clopidogrel?

A

Proton Pump Inhibitors (PPIs - Omeprazole, Lansoprazole ect)

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60
Q

What is the MOA for Dipyridamole?

A

Anti-platelet - Inhibits function of phosphodiesterase and adenosine deaminase

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61
Q

How is TIA now defined?

A

A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction.

Symptoms typically resolve within an hour

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62
Q

What prognostic score is used to assess TIA risk? What factors does it use?

A

ABCD2

Age >60
BP - >140/90
Clinical features of TIA (unilateral weakness, Speech disturbance)
Duration of symptoms
History of diabetes

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63
Q

Describe the immediate antithrombotic management of TIA

A

Aspirin immediately

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64
Q

What neuroimaging is recommended by NICE following TIA?

A

MRI - Preferred as can determine territory of ischemia

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65
Q

What is the pattern of inheritance in Huntington’s disease?

A

Autosomal Dominant

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66
Q

Describe Huntington’s disease

A

Autosomal dominant, slowly progressive neurodegenerative disease characterised by chorea, cognitive decline, loss of coordination and personality changes.

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67
Q

Describe the pathophysiology of Huntington’s disease

A

Repeat expansion of CAG triplet encoding Huntingtin protein on chromosome 4.

The longer the repeat, the earlier symptoms tend to present.

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68
Q

Where in the brain is particularly affected in Huntington’s disease?

A

Caudate and Putamen (striatum - Basal ganglia)

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69
Q

What biochemical changes occur in the striatum in Huntington’s Disease? (3)

A

Decreased GABA

Decreased Acetyl Choline

Increased Dopamine

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70
Q

Give 5 clinical features of Huntington’s disease

A

Positive family history

Chorea (Jerky, unwanted movements)

Dysarthria (slurred speech)/Mutism (muteness)

Loss of coordination

Personality changes/Mutism

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71
Q

What medication can be used to treat chorea in huntingtons? (2)

A

Sulpiride (anti-psychotic - Dopamine antagonist)

Tetrabenazine (inhibits MAO-B re-uptake, MAO-B breaks down dopamine)

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72
Q

What is given to treat nausea caused by careldopa treatment? Why?

A

Domperidone

As cyclazine/prochlorperazine (anti-histamines) can exacerbate Parkinson’s disease

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73
Q

What medication can be used to treat bradykinesia/rigidity in Huntington’s?

A

Carel-dopa (dopamine agonist)

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74
Q

What is the function of the Caudate and Putamen? (2)

A

Areas of the basal ganglia involved in;

Facilitating desired movement

Inhibiting unwanted movement

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75
Q

What trinucleotide repeat is present in abundance in Huntingtons?

A

CAG repeat in chromosome 4

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76
Q

Describe Parkinsons disease

A

Parkinson’s disease is a degenerative movement disorder (motor disease) characterized by the progressive degeneration of dopaminergic neurons in the pars compacta of the substantia nigra in the midbrain.

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77
Q

What pathological structure is seen in Parkinson’ disease?

A

Lewy Bodies (protein deposits of synuclein) in the basal ganglia, brainstem and cortex

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78
Q

What triad of symptoms is typically seen in Parkinsons?

A

Bradykinesia (slow to execute movements - reduced arm swing, shuffling gait, expressionless face)

Resting tremor (pill-rolling)

Rigidity (hypertonia - lead-pipe or cogwheel)

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79
Q

Give 8 clinical features of parkinsons

A

TRAPPS PD

T - Tremor
R - Rigidity
A - Akinesia (slow initiation, difficulty with repetitive movement)
P - Postural instability (stooped gait, shuffling steps, reduced arm swing)
P - Postural hypotension
S - Sleep disorders 9insomndia, Excessive Daytime Sleepiness, Obstructive Sleep Apnoea)
P - Psychosis (visual hallucinations)
D - Depression/Dementia/Drug side effects

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80
Q

What are the 1st line treatments for Parkinson’s disease?

A

Motor symptoms - Levodopa

No motor symptoms - Dopamine agonist OR levodopa OR MAO-B inhibitor

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81
Q

Diagnosis of Parkinsons is made clinically, but if there is an unclear clinical diagnosis, what tests can be performed? (4)

A

Dopaminergic agent trial (monitor patient’s response to levodopa)

MRI

Dopamine transporter imaging (FP-CIT or beta CIT SPECT or Flurodopa PET)

Histology (post mortem, shows Lewy Bodies)

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82
Q

Name 2 dopamine agonists and give 3 side effects

A

Ropinirole or Pramipexole

S/E - Hallucinations, Compulsive Behaviour (gambling/hypersexuality), Drowsiness

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83
Q

Name 2 MAO-B inhibitors (monoamine Oxidase B inhibitors) and give 2 side effects

A

Selegiline and Rasagiline

S/E - Postural Hypotension and Atrial Fibrillation

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84
Q

Name 2 Anticholinergics and give 3 side effects

A

Procyclidine and Benzhexol

S/E - Dry mouth, Urinary retention and Blurred Vision

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85
Q

Describe Multiple System Atrophy

A

Aka Shy-Drager Syndrome

Presents similar to Parkinson’s but affects the autonomic nervous system

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86
Q

Give 5 clinical features of Multiple System Atrophy

A

Parkinsons symptoms (Bradykinesia, Tremor, Rigidity)

Ataxia (loss of coordination - Unsteady walking)

Postural hypotension

Urinary incontinence (atonic bladder - unable to spontaneously urinate)

Rectal incontinence

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87
Q

Do patients with Multiple System Atrophy respond to levodopa?

A

No. Poor response to levodopa

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88
Q

How does Progressive Supranuclear Palsy present? (4)

A

Presents similar to Parkinsons but with additional features affecting the eyes;

Slow eye movements

Impairment of vertical gaze (may have difficulty reading or walking down stairs)

Frontal lobe dysfunction (alterations to mood/behaviour)

No tremor

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89
Q

Define Alzheimers

A

Alzheimer’s disease is the most common type of dementia characterised by the degeneration of the cerebral cortex with cortical atrophy

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90
Q

Describe the pathophysiology of Alzheimer’s disease

A

Accumulation of;

Abnormal extracellular beta amyloid plaques

and

Intracellular neurofibrillary tangles of tau protein

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91
Q

Where in the brain does Alzheimer’s first present?

A

Hippocampus

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92
Q

Early onset Alzheimer’s is associated with mutations in what genes? (3)

A

Amyloid precursor protein (chromosome 21)

Presenilin 1 (most common cause of early onset)

Presenilin 2

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93
Q

Give 5 clinical features of Alzheimer’s disease

A

Decreased visuo-spatial skill (i.e using a map)

Decreased executive function

Nominal dysphasia (unable to name objects)

Apraxia (impaired ability to carry out motor tasks)

Agnosia (failure to recognise objects)

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94
Q

What would be seen on a CT of a patient with Alzheimer’s disease

A

Increased sulci depth (due to atrophy)

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95
Q

What are the 1st and 2nd line pharmaceutical treatments for Alzheimers?

A

1st line - Acetylcholinesterase inhibitors (Rivastigmine, Donepezil, Galantamine)

2nd line - Memantine (NMDA receptor antagonist)

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96
Q

Give 1 contraindication and 1 side effect of Donepezil

A

Contraindication - Bradycardia

Side effect - Insomnia

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97
Q

How is Status Epilepticus managed in a pre-hospital setting? (2

A

PR diazepam

or

Buccal Midazolam

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98
Q

What immediate non-medical management should be conducted in status epilepticus? (4)

A

ABC

Airway adjunct

Oxygen

Check blood glucose

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99
Q

Define status epilepticus

A

A single seizure lasting >5 minutes

Or

> =2 seizures within a 5 minute period without the person returning to normal between them

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100
Q

What are the 2 most important causes of status epilepticus to rule out first?

A

Hypoxia and Hypoglycemia

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101
Q

Describe the hospital management of status epilepticus (1st line and 2nd line)

A

1st line - IV lorazepam (may be repeated once after 10-20 minutes)

2nd line - Phenytoin or Phenobarbital infusion

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102
Q

When starting a phenytoin infusion, what investigation should also be performed?

A

Cardiac monitoring (as phenytoin has pro-arrythmogenic effects)

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103
Q

If there is no response to 1st and 2nd line treatments in Status Epilepticus within 45 minutes of onset, what is the next stage of management?

A

General anaesthesia

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104
Q

How may Bells palsy present? (4)

A

Acute onset, unilateral facial weakness (with NO forehead sparing - LMN palsy)

ear pain (may precede paralysis)

Hyperacusis

Altered taste and dry eyes/mouth

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105
Q

How is Bells’ palsy managed? (1)

A

Oral Prednisolone (10 days)

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106
Q

Define Multiple Sclerosis (pathologically)

A

MS is a chronic autoimmune disease of the CNS, characterised by T cell (CD4+) mediated inflammation and demyelination

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107
Q

What cell type drives MS?

A

T-cell (CD4+)

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108
Q

What cell type is targeted in MS?

A

Oligodendrocytes (CNS)

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109
Q

What cell type drives the PNS?

A

Schwann cells

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110
Q

How is MS defined clinically?

A

Defined as two episodes of neurological dysfunction that are separated by in time and space.

I.e patient must exhibit symptoms of MS in two separate CNS areas (brain, spinal cord, optic nerves) at two different times

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111
Q

A mutation in what is linked to MS?

A

HLA-DR2

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112
Q

Give 2 environmental factors that are linked to developing MS

A

Epstein Barr Virus (EBV)

Vitamin D Deficiency

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113
Q

What are the 4 patterns of MS? Which is most common?

A

Relapsing-Remitting MS (80%)

Secondary progressive MS

Primary progressive MS

Progressive Relapsing MS

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114
Q

Describe relapsing remitting MS

A

Characterised by acute attacks followed by episodes of remission

Some remyelination occurs but is often inefficient, resulting in some residual disability post attack

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115
Q

Describe secondary progressive MS

A

65% of relapsing remitting patients go on to develop secondary progressive MS within 15 years of diagnosis

Characterised by a constant immune attack causing a steady progression of disability

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116
Q

Describe progressive MS

A

More common in elderly

Characterised by a constant immune attack on myelin resulting in a steady progression of disability from the start.

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117
Q

Describe progressive relapsing MS

A

Characterised by constant immune attack on myelin with superimposed acute episodes of exaggerated immune attack.

Patients tend to deteriorate and develop significant symptoms much quicker.

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118
Q

Give 4 sensory symptoms of MS

A

Dysaesthesia (peculiar sensory phenomena - odd patches of wetness/burning)

Paraesthesia (pins and needles)

Trigeminal neuralgia (severe facial pain)

Uhthoff’s phenomenon (symptoms worsen with heat)

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119
Q

Give 4 motor symptoms of MS

A

Unilateral optic neuritis (blurring/graying of vision in one eye, may have pain moving eye)

Urinary frequency/bowel dysfunction (increases UTI risk)

Spastic weakness

Lhermitte’s sign (sudden sensation of electric shocks down spine after neck flexion)

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120
Q

Describe Uhthoff’s Phenomenon and Lhermitte’s sign

A

Both features of MS

Uhthoff’s phenomenon - Symptoms worsen with heat.

Lhermitte’s sign - Sudden sensation of electric shocks down spine after neck flexion.

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121
Q

What condition is often mistaken for MS. How is it differentially diagnosed?

A

Devic’s syndrome (aka neuromyelitis optica)

Characterised by immune attacks on the optic nerves and spinal cord.

DDx from MS achieved through presence of NMO antibody.

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122
Q

Describe a neurological history/exam for MS

A

History of transient motor, cerebellar, sensory, gait or visual dysfunction lasting over 48 hours and NOT accompanied by fever.

Symptoms often asymmetrical

Fundoscopy to view optic disc

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123
Q

What may be seen in a Lumbar Puncture in a patient with MS? (1)

A

CSF containing IgG oligoclonal bands (suggests inflammation of CNS)

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124
Q

What is the gold standard diagnostic test for identifying demyelinating lesions in MS?

A

MRI with contrast

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125
Q

What may be seen on an MRI of a patient with MS? (2)

A

Periventricular lesions (white matter near cerebral ventricles)

Multiple scattered plaques

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126
Q

How is an acute relapse of MS managed?

A

High dose steroids (IV methylprednisolone) given for 5 days.

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127
Q

Give 2 indications for use of disease-modifying drugs in MS patients

A

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

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

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128
Q

Name 3 disease modifying drugs used in MS treatment (give their MOA)

A

Dimethyl Fumarate (enhances Nrf2 pathway)

Alemtuzumab (CD52 MAB - targets and destroys T cells)

Natalizumab (Inhibits VLA-4 receptors to allow immune cells to cross BBB)

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129
Q

What drugs can be used to manage spasticity (stiff/tight muscles) in MS? (2)

A

Baclofen

Gabapentin

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130
Q

What drug can be used to manage tremor in MS?

A

Botulinum toxin

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131
Q

What can be used to manage fatigue in MS? (2)

A

Amantadine

CBT therapy

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132
Q

Give 1 side effect of Alemtuzumab (MS management)

A

Can increase risk of infection and triggering autoimmune disease

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133
Q

Define Guillain Barre Syndrome. What is it typically triggered by?

A

Describes an acute inflammatory peripheral neuropathy (PNS)

Triggered by infection

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134
Q

What cell type is affected (attacked) in GBS?

A

Schwann cells (PNS)

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135
Q

What are the most common triggers of GBS? (4)

A

Campylobacter Jejuni (most common)

CMV

EBV

Mycoplasma pneumoniae

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136
Q

Give 3 ways GBS can be differentiated from MND

A

Absent deep tendon reflexes (knee, bicep, triceps, patellar ect)

Increased CSF protein

Sensory features (Dysesthesia) (not seen in MND)

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137
Q

What triad of symptoms is classically seen in GBS

A

Ophthalmoplegia

Areflexia

Ataxia

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138
Q

Give 5 clinical features of GBS

A

Global symmetrical weakness of proximal and distal limbs (follows ascending pattern - starts in legs)

Respiratory distress (dyspnoea on exertion/SoB)

Back/leg pain (in early stages)

Dysphasia

Absent tendon reflexes

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139
Q

Give 2 diagnostic tests for GBS (and results)

A

Nerve conduction studies (showing decreased motor nerve conduction velocities)

Lumbar puncture (shows elevated CSF protein)

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140
Q

How is GBS managed?

A

Plasmapheresis (plasma exchange) + Intravenous Immunoglobulin (IgG)

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141
Q

Name 1 variant of GBS and it’s associated symptoms

A

Miller Fisher Syndrome

Associated with;

Opthalmoplegia
Areflexia
Ataxia

Usually presents with descending paralysis (rather than ascending seen in GBS)

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142
Q

What antibodies are seen in Miller Fisher syndrome? (variant of GBS)

A

Anti-GQ1b antibodies

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143
Q

Name 2 pyramidal tracts

A

Corticobulbar tract

Corticospinal tract

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144
Q

What is the function of the pyramidal tracts? What are they composed of?

A

Innervate skeletal muscle, facilitating voluntary movements

Composed of upper motor neurones that innervate lower motor neurones at the anterior horn of the spinal cord.

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145
Q

What is the function of extrapyramidal tracts? What are they composed of?

A

Function to coordinate muscle movement by indirectly activating or inhibiting groups of lower motor neurones, through interneurones

Do not directly innervate lower motor neurones.

Usually innervate multiple muscles that share the same function (i.e flexion, extension ect)

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146
Q

What cranial nerves are found at the terminus of the corticobulbar tracts? (4)

A

V - Trigeminal (pons)

VII - Facial (pons)

XI - Accessory (medulla)

XII - Hypoglossal (medulla)

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147
Q

What extrapyramidal tract facilitates posture?

A

Pontine (medial) Reticulospinal Tract

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148
Q

What extrapyramidal tract controls walking movements and breathing?

A

Medullary (lateral) Reticulospinal tract

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149
Q

What extrapyramidal tract is involved in coordinating balance?

A

Lateral vestibulospinal tract

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150
Q

What extrapyramidal tract is involved in coordinating the speed of movement?

A

Rubrospinal Tract

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151
Q

What extrapyramidal tract relays information regarding proprioception, stretch, vibration and fine touch?

A

DCML

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152
Q

How does the DCML detect touch? (3)

A

Through use of mechanoreceptors in the skin.

Meissner’s corpuscles and Merkel’s disks - Fine touch

Pacinian Corpuscles - Vibration

Ruffini Corpuscles - Stretch

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153
Q

Where does the DCML decussate?

A

Brainstem

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154
Q

Where does the spinothalamic tract decussate?

A

Spinal cord (before reaching the brainstem)

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155
Q

What does the spinalthalamic tract sense?

A

Pain and Temperature (lateral)

Crude touch (Anterior)

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156
Q

Describe a lower motor neurone

A

Describes a neurone which connects an UMN to skeletal muscle

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157
Q

Where do LMNs typically lie?

A

Within the ventral horn of the spinal cord

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158
Q

What motor neurones are responsible for coordinating muscle contraction? How is this achieved?

A

Alpha motor neurones (LMNs)

Achieved through the myostatic stretch reflex.

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159
Q

What is the myostatic stretch reflex?

A

Describes a reflex in which a muscle contracts when passively stretched (i.e patellar tendon tap)

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160
Q

How is Brown-Sequard Syndrome characterised?

A

Characterised by damage (lesion) to the spinal cord, resulting in;

Ispilateral loss of; Proprioception, motor and fine touch (DCML + Corticospinal)

Contralateral loss of; Pain and Temperature (Spinothalamic)

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161
Q

Define upper motor neurone

A

Describes a neurone whose cell body originates in the cerebral cortex (or brainstem) and terminates within the brainstem or spinal cord

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162
Q

Give 5 signs/symptoms of an Upper Motor Neurone Lesion

A

Hypertonia (too much muscle tone)

Hyper-reflexia (brisk reflexes and twitching)

Spasticity (Clasp Knife Pnenomenon - rigidity)

Positive Babinski Reflex

Minimal muscle atrophy

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163
Q

Give 5 signs/symptoms of Lower Motor Neurone Lesions

A

Muscle atrophy

Hyporeflexia (absent tendon reflexes)

Hypotonia

Flaccid muscle weakness or paralysis

Fasciculations (muscle twitch)

164
Q

Describe motor neurone disease

A

Describes a cluster of neurodegenerative diseases characterised by progressive degeneration of motor neurones, cranial nerve nuclei and anterior horn cells

165
Q

Name 4 types of MND

A

Amyotrophic Lateral Sclerosis (ALS) (most common)

Progressive Bulbar Palsy (PBP)

Progressive Muscular Atrophy (PMA)

Primary Lateral Sclerosis (PLS)

166
Q

How can MND be differentiated from other diseases affecting the nervous system?

A

MND has no sensory loss or sphincter disturbance (distinguishing from MS and polyneuropathies)

Also never affects eye movements (distinguishing from myasthenia)

167
Q

What gene mutation is associated with MND

A

SOD1 gene mutation

168
Q

What drugs can be used to manage drooling in MND?

A

Propantheline (anti-cholinergic)

Amitriptyline (tricyclic antidepressant)

169
Q

What motor neurones are affected in ALS?

A

Upper and Lower Motor Neurones

170
Q

What disease is ALS closely linked to?

A

Frontotemporal dementia

171
Q

What motor neurones are affected in PBP?

A

Lower Motor Neurones Only

172
Q

What cranial nerves are affected in PBP?

A

Glossopharyngeal (9)

Vagus (10)

Accessory (11)

Hypoglossal (12)

173
Q

Give 5 clinical features of PBP

A

Dysphagia (difficulty swallowing)

Dysarthria (difficulty speaking)

Flaccid fasciculating tongue

Nasal regurgitation

Choking (due to paralysis of glottis)

174
Q

What motor neurones are affected in PMA?

A

Lower Motor Neurones Only (anterior horn cell lesions)

175
Q

What motor neurones are affected in PLS? How is it characterised?

A

Upper motor neurones only.

Characterised by loss of Betz Cells (pyramidal cells in motor cortex)

176
Q

Describe Bells’ Palsy

A

Describes an acute, unilateral, lower motor neurone facial nerve paralysis

177
Q

What virus is linked to Bells’ palsy?

A

Herpes Simplex Virus

178
Q

What motor neurone is affected in Bells’ palsy?

A

Lower Motor Neurone (of facial nerve)

179
Q

How does Bells’ palsy typically present? (3)

A

Unilateral facial paralysis with NO forehead sparing

Inability to close eye

Hyperacusis (due to paralysis of stapedius muscle)

180
Q

How is Bells’ palsy managed? (2)

A

Oral prednisolone within 72 hours of onset

Eye care (artificial tears) - To prevent exposure keratopathy

181
Q

What is the prognosis for Bells’ palsy?

A

Most people make a full recovery after 3-4 months

182
Q

Describe the long term pharmacological treatment of ischemic stroke

A

Clopidogrel + Atorvastatin

If clopidogrel is contraindicated, offer;

Aspirin + Dipyridamole

183
Q

NICE recommend thrombectomy for stroke patients who; (3)

A

Last known to be well up to 24 hours previously

Who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (demonstrated on CTA or MRA)

If there is potential to salvage brain tissue shown by CT perfusion or MRI (showing limited infarct core volume)

184
Q

Define Wernicke’s encephalopathy

A

Describes a neuropsychiatric disorder caused by thiamine deficiency, most commonly seen in alcoholics.

Is acute and reversible

185
Q

Wernicke’s encephalopathy is characterised by a deficiency in what?

A

Thiamine (vitamin B1)

186
Q

Give 4 causes of Wernicke’s encephalopathy

A

Alcoholics (most common)

Persistent vomiting (i.e hyperemesis gravidarum)

Stomach cancer

Dietary deficiency

187
Q

What classic triad is seen in Wernicke’s encephalopathy?

A

Opthalmoplegia/nystagmus

Ataxia (Gait)

Confusion (altered GCS)

188
Q

How is Wernicke’s encephalopathy managed? (3)

A

Immediate IV thiamine/vitamin B1 (must be given before IV glucose infusion as can worsen symptoms)

Long term oral replacement of vitamin B1, B6, B12 and folic acid

Abstinence from alcohol

189
Q

What investigation result would be seen in Wernicke’s encephalopathy?

A

Decreased red cell transketolase (indicates thiamine deficiency)

190
Q

Define Korsakoff syndrome

A

Describes a condition occuring in patients with persistent thiamine deficiency (due to chronic alcohol use)

Chronic and irreversible

191
Q

Give 5 clinical features of Korsakoff Syndrome (5)

A

Similar to Wernicke’s encephalopathy;

Opthalmoplegia/nystagmus, Ataxia (Gait) and Confusion (altered GCS)

With;
Anterograde and Retrograde amnesia

Confabulation (producing fabricated memories)

Personality changes (apathy, decrease executive function ect)

Disorientation/Hallucinations

192
Q

What nerve innervates the skin on the palmar aspect of the hand?

A

Median nerve

193
Q

What nerve innervates the nail bed of the index finger?

A

Median nerve

194
Q

What nerve innervates the skin overlying the medial aspect of the hand?

A

Ulnar nerve

195
Q

From which vertebrae does the Brachial Plexus originate?

A

Anterior rami of C5-T1

196
Q

Give 4 causes of brain abscesses

A

Sepsis extending from middle ear or sinuses (i.e sinusitis)

Trauma

Surgery to scalp

Embolic events from endocarditis

197
Q

Give 4 clinical features of brain abscess

A

Headache

Fever

Focal neurology (i.e CN III, VI palsy)

Raised ICP (nausea, papilloedema, vomiting, seizures)

198
Q

How are brain abscesses managed? (2)

A

IV cephalosporin (ceftriaxone) + Metronidazole

Intracranial pressure management - Dexamethasone

199
Q

Give 4 symptoms of uncal herniation

A

Recent onset of loss of consciousness

New onset horizontal diplopia

CNIII palsy (unequal pupil size - anisocoria)

Cheyne-Stokes respiration

200
Q

What is the 1st line drug treatment for generalised tonic clonic seizures in males and females?

A

Males; Sodium Valporate

Females; Lamotrigine or levetriacetam

201
Q

Define epilepsy

A

Describes a recurrent tendency of spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures.

Convulsions are the motor signs of electrical discharges.

202
Q

What are the 1st and 2nd line treatments for focal seizures?

A

1st line - Lamotrigine or levetriacetam

2nd line - Carbamazepine, oxycarbazepine or zonisamide

203
Q

Define seizure

A

Defined as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.

204
Q

Give 8 causes of seizures

A

VITAMINS;

V - Vascular (ischaemic/haemorrhagic stroke)
I - Infection (meningitis, encephalitis, abscess)
T - Trauma or toxins
A - Autoimmune (CNS vasculitis or lupus)
M - Metabolic (hyponatraemia, hypocalcemia, hypoglycemia)
I - Idiopathic (epilepsy)
N - Neoplasm
S - Syncope/Psychogenic seizures

205
Q

What are the 1st and 2nd line treatments for absence seizures?

A

1st line - Ethosuximide

2nd line;
Males - Sodium Valoprate
Females - Lamotragine or levetriacetam

206
Q

What drug can exacerbate absence seizures?

A

Carbamazepine

207
Q

What is the 1st line treatment for myoclonic seizures in males and females?

A

Males - Sodium valporate
Females - levetriacetam

208
Q

What is the 1st line treatment for males and females with tonic/atonic seizures?

A

Males - Sodium valoprate
Females - lamotrigine

209
Q

Define focal seizures

A

Most common type of seizure

Characterised by abnormal neural activity localised to one area of the cerebral hemisphere

210
Q

What symptoms are seen in a focal seizure located to the temporal lobe? (5)

A

Automatisms - Lip smacking, chewing

Deja vu/Jamais vu

Delisions

Tastes +smells

Abdominal rising/nausea/vomiting

211
Q

What symptoms would be seen in a focal seizure localised to the frontal lobe? (motor cortex) (3)

A

Motor features;

Arrest

Jacksonian March (twitching)

Todd’s palsy (post-ictal weakness of limbs)

212
Q

What symptoms would be seen in a focal seizure localised to the parietal lobe?

A

Sensory disturbances (tingling, numbness ect)

213
Q

Describe myoclonic seizures

A

Sudden jerk of limb, face or trunk

214
Q

Describe atonic seizures

A

Sudden loss of muscle tone (causing patient to fall to the ground)

216
Q

How should a patient with a seizure be managed?

A

Specialist referral and investigation in <2 weeks

217
Q

What is the MOA for ethosuzimide

A

Blocks T-type calcium channels in thalamic neurones

218
Q

What is the MOA for lamotrigine. Give 3 side effects

A

Inhibits voltage gated sodium channels and inhibits glutamate release

S/E - Skin rash, Diplopia, Blurred vision

219
Q

Give 4 side effects of Sodium Valoprate

A

Increased appetite

Liver failure

Oedema

Ataxia

220
Q

What effect do phenytoin and carbamazepine have on the COCP? why?

A

Reduce it’s effectiveness

As are enzyme inducers

221
Q

What is the MOA for phenytoin and give 3 side effects.

A

Inhibits voltage gated sodium channels

S/E - Gingival hypertrophy, Hirsutism, Cerebellar symptoms (ataxia, nystagmus, dysarthria)

222
Q

Define febrile seizures

A

Describes seizures accompanied by fever in infants aged 6 months to 6 years old

223
Q

Name 2 types of febrile seizure

A

Simple febrile seizure

Complex febrile seizure

224
Q

How are simple febrile seizures defined? (3)

A

Generalized (tonic clonic - involving both cerebral hemispheres)

Lasts <15 minutes

Doesn’t occur again in 24 hours

225
Q

How are complex febrile seizures defined? (3)

A

Focal seizures (limited to one side of the body/limb)

Lasts >15 minutes

Recurrence in 24 hours

226
Q

What virus has a high association with febrile seizures?

A

Human Herpes Virus 6 (HHV-6)

(Associated with Roseola Infantum in children - Fever first, Rash later)

227
Q

Define status epilepticus (2)

A

A single seizure

228
Q

What medication should be avoided in patients with Lewy Body Dementia? (2)

A

Risperidone
Haloperidol (neuroleptics)

229
Q

What is the 1st line treatment for cognitive impairment and behavioural symptoms in Lewy Body Dementia?

A

Donepezil (acetyl cholinesterase inhibitor)

230
Q

What is the 1st line treatment for motor symptoms in Lewy Body Dementia?

A

Carbidopa/Levodopa

231
Q

What is used to treat REM sleep disturbances in Lewy Body Dementia?

A

Clonazepam

232
Q

What is the preferred antidepressant to treat depression in Lewy Body dementia?

A

Sertraline (SSRI)`

233
Q

What drugs are associated with increased mortality in dementia patients?

A

Antipsychotics (i.e olanzapine)

234
Q

Give 5 risk factors associated with a worse prognosis in MS

A

Older
Male
Motor signs at onset
Early relapses
Many MRI lesions

235
Q

What laboratory results would you expect to see in Wilson’s disease? (3)

A

Low Serum Copper

Low Serum Caeruloplasmin

High Urinary Copper

236
Q

Wilson’s disease occurs due to a defect in what?

A

Defective ATP9B protein.

Results in impaired copper metabolism resulting in copper build up in tissues.

237
Q

How may encephalitis present? (4)

A

Absence of neck stiffness

High fever

Altered mental status

Seizures

238
Q

What is the most common cause of encephalitis?

A

Herpes simplex virus

239
Q

How is encephalitis treated?

A

IV acyclovir

240
Q

Name 4 drugs that are contraindicated in myasthenia gravis (exacerbate symptoms)

A

Beta blockers (Propranolol)

Calcium channel blockers (Verapamil)

Lithium

Antibiotics (Ciprofloxacin)

241
Q

Define lateral medullary syndrome

A

Syndrome caused by lesion in the posterior inferior cerebellar artery

242
Q

Lateral medullary syndrome is characterised by a lesion in which artery?

A

Posterior inferior cerebellar artery

243
Q

What symptoms would be seen in lateral medullary syndrome? (4)

A

Cerebellar signs (ataxia, nystagmus)

Ispilateral facial numbness

Horner’s syndrome (ptosis, miosis, anhidrosis)

Contralateral sensory loss

(if damage is on the right, the right side is affected)

244
Q

How is Cerebral Perfusion Pressure Calculated?

A

CPP = Mean arterial pressure (MAP) - Intracranial Pressure (IP)

245
Q

Describe Cushing reflex

A

Describes a response to increased intracranial pressure that results in hypertension and bradycardia.

May be seen in extradural haemorrhages (injury, loss of consciousness, lucid interval)

246
Q

Give 4 clinical signs of of Cushing’s reflex

A

Widening pulse pressure

Bradycardia

Hypertension

Irregular breathing (sign of impending brian herniation)

247
Q

How may Meniere’s disease present?

A

Recurrent episodes of;

Vertigo, tinnitus and hearing loss (sensorineural)

Aural fullness/pressure

Episodes lasting minutes to hours

248
Q

How are acute attacks of Meniere’s disease managed?

A

Buccal or IM Prochlorperazine

249
Q

What neurological condition are vegans more susceptible to? Why?

A

Sub-acute combined degeneration of the cord

Occurs due to vitamin B12 deficiency

250
Q

How may subacute combined degeneration of the cord present?

A

Positive Romberg’s sign (balance problems in the shower)

Brisk knee jerk and up-going plantars

Absent ankle jerks

251
Q

What is seen on CT for extradural haemorrhage?

A

Biconcave disk/lens shaped bleed

252
Q

What is seen on CT for subdural haemorrhage?

A

Crescent shaped haemorrhage

253
Q

How may Ramsey Hunt Syndrome present?

A

Auricular pain (first feature)

Facial Nerve Palsy

Vesicular Rash around ear

Vertigo/tinnitus

254
Q

What pathogen causes Ramsey Hunt Syndrome?

A

Herpes Zoster (reactivation of varicella zoster)

255
Q

Where does Varicella Zoster reactivate in Ramsey Hunt Syndrome?

A

Geniculate ganglion of CN VII

256
Q

Describe the management of Ramsey Hunt Syndrome

A

Oral aciclovir and corticosteroids

257
Q

What is the most common cause of subarachnoid haemorrhage?

A

Ruptured berry aneurysms

258
Q

Where are the most common sites for berry aneurysms to form?

A

Junctions of;
Posterior communicating artery and internal carotid

Anterior cerebral artery and anterior communicating artery

Bifurcation of middle cerebral artery

259
Q

Name 3 diseases that predispose to berry aneurysms

A

Polycystic kidney disease

Ehlers Danlos syndrome

Coarctation of the aorta

260
Q

Give 5 clinical features of subarachnoid haemorrhage

A

Sudden onset Thunder-clap headache

Vomiting

Collapse

Photophobia

Depressed/loss of consciousness

261
Q

Give 5 risk factors for subarachnoid haemorrhages

A

Smoking

Hypertension

Mycotic aneurysms

Diseases that predispose to berry aneurysms (Polycystic kidney disease, Ehlers-Danlos syndrome, Coarctation of the aorta)

History of previous subarachnoid haemorrhages

262
Q

What 2 clinical signs are likely to be positive in subarachnoid haemorrhage?

A

Positive Kernig’s sign (Pain felt on leg extension)

Positive Brudzinski’s sign (involuntary hip/knee flexion on neck flexion)

Both indicate meningeal irritation

263
Q

What tests are used to diagnose subarachnoid haemorrhage? (1st and 2nd line)

A

1st line - Non-contrast CT head

2nd line - Lumbar puncture (if CT is negative but symptoms suggest SAH - shows xanthochromic CSF)

264
Q

What pupil changes may be seen in subarachnoid haemorrhages?

A

Fixed dilated pupil

III nerve palsy due to rupture of posterior communicating artery aneurysm.

265
Q

What is used to identify ruptured aneurysms in patients with confirmed SAH?

A

CT angiography

266
Q

What surgical technique is used to treat SAH?

A

Endovascular coiling

267
Q

What medical treatment may be used in the acute management of subarachnoid haemorrhage?

A

Calcium channel blocker - Nimodipine (reduce vasospasm)

268
Q

Give 3 complications of subarachnoid haemorrhage

A

Rebleeding

Cerebran ischemia

Hyponatremia

269
Q

Describe subdural haematoma

A

Describes collection of blood between the dura and arachnoid meningeal layers

Bleeding occurs from bridging veins between cortex and venous sinuses.

270
Q

Give 5 symptoms of subdural haematoma

A

Fluctuating level of consciousness

Nausea/vomiting (due to increased ICP)

Headache

Gradual physical/intellectual slowing

Unsteadiness

271
Q

How is subdural haematoma diagnosed?

A

Non - Contrast CT showing crescent shaped collection of blood

272
Q

Describe extradural haematoma

A

Commonly occurs perforation of middle meningeal artery.

Describes collection of blood between the bone and the dura.

273
Q

Give 3 symptoms of extradural haemorrhage

A

Lucid interval (may last hours/days)

Decreasing level of consciousness

Nausea and vomiting

274
Q

How is extradural haematoma diagnosed?

A

Non-contrast CT - Lens Shaped Haematoma

275
Q

What may be used to lower ICP in extradural haemorrhage?

276
Q

What does a positive Romberg’s test suggest?

A

Sensory ataxia

277
Q

Give 3 symptoms of encephalitis

A

Altered mental status

High fever, tachycardia, tachypnoea

New onset seizures

278
Q

Where in the brain does encephalitis commonly affect?

A

Temporal lobe

279
Q

What investigation results are likely seen in encephalitis?

A

Raised CRP and lymphocytes (raised in viral infection)

LP - Raised lymphocytes and CSF protein

280
Q

What is the most common cause of encephalitis?

A

Herpes Simplex Virus 1

281
Q

How is encephalitis treated?

A

IV Ceftriaxone + Oral Acicloviry

282
Q

Give 3 side effects of acyclovir

A

Generalised fatigue/malaise

GI disturbance

Photosensitivity and urticarial rash

283
Q

Describe the driving law (car) for epilepsy

A

One off seizure - Inform DVLA and don’t drive for 6 months

> 1 seizure - Inform DVLA and don’t drive for 1 year

Seizure following change in epileptic medication - Reapply to drive if seizure was >6 months ago or if back on previous medication for 6 months

284
Q

Describe the driving law (HGV) for epilepsy

A

One off seizure - Inform DVLA and don’t drive for 5 years (unless haven’t taken medications for 5 years)

> 1 seizure - Inform DVLA and don’t drive for 10 years.

285
Q

Describe MRC grading for power

A

Grade 0 - No muscle involvement

Grade 1 - Trace of contraction

Grade 2 - Movement at the joint with gravity eliminated

Grade 3 - Movement against gravity, but not against added resistance

Grade 4 - Movement against external resistance with reduced strength

Grade 5 - Normal strength

286
Q

Describe essential tremor

A

Describes autosomal dominant condition, usually affecting both upper limbs

287
Q

Give 3 features of essential tremor

A

Postural tremor - Worse if arms are outstretched

Symptoms improve with alcohol and rest

Most common cause of titubation (head tremor)

288
Q

How is essential tremor managed?

A

Propranolol

Primidone (barbituate) sometimes used

289
Q

What is used in the management of chemotherapy-related nausea?

A

Ondansetron (5-HT3 receptor antagonist) + Dexamethasone

290
Q

What is a common cause of third nerve palsy?

A

Posterior communicating artery aneurysm

291
Q

What clinical findings would likely be seen in a patient with cavernous sinus thrombosis?

A

Third nerve palsy

Ptosis
Dilated Pupil (unable to constrict)
Down and out position of eye.

Pupil is dilated as CNIII carries efferent fibres controlling light reflex

292
Q

Give 1 risk factor for cavernous sinus thrombosis

A

Anti-phospholipid syndrome

293
Q

How may Horner’s syndrome present?

A

Ptosis

Pupil constriction

Intact light reflex

294
Q

What are the 1st and 2nd line treatments for focal seizures?

A

1st - Lamotrigine or carbamazepine

2nd - Levetriacetam

295
Q

What are the 1st and 2nd line treatments for generalized tonic clonic seizures?

A

1st - Sodium valporate (males)

2nd - Lamotrigine (women of child bearing age)

296
Q

What are the 1st and 2nd line treatments for absence seizures?

A

1st line - Ethosuximide (women) or sodium valoprate (males)

2nd line - Lamotrigine

297
Q

What are the 1st line treatments for myoclonic seizures in males and females?

A

1st line - Sodium valporate (males)

1st line - Levetriacetam (females)

298
Q

What anti-epileptic should be avoided in myoclonic seizures? and why?

A

Carbamazepine

Can worse seizures

299
Q

What is the 1st line treatment for tonic/atonic seizures?

A

1st line - Sodium valporate or lamotrigine

300
Q

What scale is used to measure disability or dependence in activities of daily living in stroke patients?

A

Barthel index

301
Q

What scale categorises patients into levels of frailty according to function?

A

Rockwood frailty score

302
Q

Define myasthenia gravis

A

Describes an autoimmune disorder resulting in insufficient functioning of acetyl choline receptors.

Occurs due to generation of Acetyl Choline Receptor antibodies.

303
Q

How may myasthenia gravis present? (5)

A

Key feature - Muscle fatigability - Muscles become progressively weaker during periods of activity and slowly improve with rest.

Other features;

Extra ocular muscle weakness; diplopia

Proximal muscle weakness; face, neck, limb girdle

Ptosis

Dysphagia

304
Q

Myasthenia gravis is commonly associated with what? (3)

A

Thymomas (15%) - May present on anterior mediastinum

Thymic hyperplasia (50-70%)

Autoimmune disorders - pernicious anaemia, SLE, RA ect

305
Q

What is the 1st line for myasthenia gravis?

A

Pyridostigmine (acetylcholinesterase inhibitor)

Later add - Prednisolone

306
Q

Define myasthenic crisis

A

Describes an acute, life threatening exacerbation of myasthenic symptoms, leading to respiratory failure

307
Q

How is myasthenic crisis managed? (3)

A

Plasmapheresis

IV Immunoglobulin G

Early endotracheal intubation

308
Q

What cranial nerves are commonly affected in vestibular schwannomas?

A

V, VII, VIII (cerebellopontine junction)

309
Q

What is the classical presentation of vestibular schwannoma? (4)

A

Vertigo

Sensorineural hearing loss

Tinnitus

Absent corneal reflex (ophthalmic branch of trigeminal nerve)

310
Q

Describe the mechanism of adjusting ventilation in the management of patients with raised ICP

A

Controlled hyperventilation

Hyperventilation > reduces Co2 > Vasoconstriction of cerebral arteries > Reduced ICP

311
Q

How may a patient with a craniopharyngioma present? (2)

A

Lower bitemporal hemianopia

Diabetes insipidus (Polydipsia/Polyuria)

312
Q

How can Weber’s test be interpreted? (3)

A

Normal - Sound heard equally in both ears

Sensorineural hearing loss - Sound is louder on the side of the intact ear

Conductive hearing loss - Sound is louder on the side of the affected ear

313
Q

How can Rinne’s test be interpreted? (3)

A

Normal - Air conduction > bone conduction (positive)

Conductive hearing loss - Bone conduction > air conduction (negative)

Sensorineural hearing loss - Air conduction > bone conduction (positive)

314
Q

What are the 3 modalities of GCS?

A

Motor response

Verbal Response

Eye opening

315
Q

Describe the motor response modality of GCS (6)

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain (decorticate posture)
  5. Extending to pain
  6. None
316
Q

Describe the verbal response modality of GCS (5)

A
  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None
317
Q

Describe the eye opening modality of GCS (4)

A
  1. Spontaneous
  2. To speech
  3. To pain
  4. None
318
Q

What respiratory management should take place in a patient with a GCS <8?

A

Insert Cuffed Endotracheal Tube

319
Q

What triad of symptoms is typically seen in Normal Pressure Hydrocephalus?

A

Urinary incontinence

Dementia and bradyphrenia (slow thinking)

Gait abnormalities (ataxia)

320
Q

What is thought to be the cause of normal pressure hydrocephalus

A

Occurs secondary to reduced CSF absorption at the arachnoid villi.

May be secondary to head injury, subarachnoid haemorrhage or meningitis.

321
Q

What may be seen on MRI in a patient with Normal Pressure Hydrocephalus?

A

Ventriculomegaly (enlarged cerebral ventricles)

322
Q

How is normal pressure hydrocephalus managed?

A

Ventriculoperitoneal shunting

323
Q

How are medication overuse headaches managed?

A

Abruptly stop - Simple analgesics and Triptans

Gradually stop - Opioids (codeine)

324
Q

Define neurofibromatosis

A

Describes an autosomal dominant condition characterised by the formation of tumours on nerve tissue

325
Q

What are the 3 main types of neurofibromatosis?

A

NF-1

NF-2

Schwannomatosis

326
Q

Give 4 clinical features of neurofibromatosis 1

A

Multiple fibromas - Soft, painless nodules under the skin

Cafe au lait spots

Lisch nodules (pigmented iris haematomas)

Seizures

327
Q

Give 2 clinical features of neurofibromatosis 2

A

Bilateral vestibular schwannomas

Early onset cataracts (usually bilateral)

328
Q

Describe tuberous sclerosis

A

Describes an autosomal dominant condition characterised by the generation of non-cancerous tumours in different parts of the body.

329
Q

Give 4 pathogmonic cutaneous features of tuberous sclerosis

A

‘Ash lead spots’

Rough patches over lumbar spine (Shagreen patches)

Adenoma sebaceum (angiofibromas - butterfly distribution over nose)

Subungual fibromatoma (fibromata beneath nails)

330
Q

Give 3 extra-cutaneous features of tuberous sclerosis

A

Epilepsy

Retinal haemorrhage

Developmental delay

331
Q

Define glaucoma

A

Describes an optic neuropathy due to raised intraocular pressure

332
Q

Give 3 factors predisposing people to acute angle closure glaucoma (AACG)

A

Hypermetropia (long-sightedness)

Pupillary dilatation

Lens growth associated with age

333
Q

Give 5 clinical features of Acute Angle Closure Glaucoma

A

Severe pain - Ocular or Headache

Decreased Visual Acuity

Red eye

Haloes around lights

Semi-dilated non-reacting pupil

334
Q

How is acute angle closure glaucoma managed (acute)? (3)

A

Urgent referral to opthalmologist

Combination of eye drops;

Pilocarpine (parasympathomimetic)
Timolol (beta blocker)
Apraclonidine (alpha 2 agonist)

IV acetazolamide (reduces aqueous secretions)

335
Q

What is the definitive treatment for acute angle closure glaucoma?

A

Laser peripheral iridotomy

336
Q

How does pilocarpine alleviate symptoms of acute angle closure glaucoma?

A

Causes contraction of ciliary muscle > opening the trabecular meshwork > increased outflow of aqueous humour

337
Q

What is the protocol regarding driving for a patient whom experienced a TIA?

A

Can start driving if symptom free for 1 month - No need to inform DVLA

338
Q

What type of visual field defect is seen in pituitary adenoma?

A

Bitemporal Superior Quadrantanopia (as pituitary adenoma presses on optic chiasm from below)

339
Q

What type of visual field defect is seen in craniopharyngioma?

A

Bilateral inferior quadrantanopia (as craniopharyngioma presses on optic chiasm from above)

340
Q

Craniopharyngioma is derived from a remnant of what?

A

Rathke’s pouch

341
Q

What condition is associated with bilateral vestibular schwannomas?

A

Neurofibromatosis 2

342
Q

What is the most common primary brain tumour in adults?

A

Glioblastoma

343
Q

How may a glioblastoma appear on imaging?

A

Solid tumour with central necrosis

Has a rim that enhances on contrast

344
Q

What is the 2nd most common brain tumour in adults?

A

Meningioma

345
Q

Where do meningiomas arise? Where are they typically located?

A

From the arachnoid cap cells of the meninges, typically located next to the dura

Typically located at the flax cerebri

346
Q

How may a pontine haemorrhage (stroke) present? (3)

A

Reduced GCS

Paralysis (quadriplegia)

Bilateral pin point pupils

347
Q

How should a patient taking warfarin/doac presenting with TIA be managed? Why?

A

Immediate referral to emergency department for imaging

(to exclude haemorrhage - increased risk in bleeding disorders/on blood thinners)

348
Q

What is the gold standard investigation for Intracranial Venous thrombosis?

A

MRI venography

349
Q

Where do intracranial venous thromboses commonly occur?

A

Sagittal sinus

350
Q

How is intracranial thrombosis managed?

A

Acute - LMWH

Chronic - Warfarin

351
Q

How may sagittal sinus thrombosis present? (2)

A

Seizures and hemiplegia

Empty delta sign on venography

352
Q

Give 4 common features of non-epileptic attacks

A

Arms flexing and extending (may have pelvic thrusting)

Eyes are usually closed (eyes are open in epilepsy)

Prolonged seizure (>30 minutes)

Symptoms wax and wane

353
Q

How is postural hypotension defined? How is the test done?

A

Systolic drop of >20mm when going from sitting to standing.

Patient should lie or sit still for 5 minutes before taking their baseline measurement.

Then get them to stand and measure their BP at 1 min and 3 min.

354
Q

What is the 1st line treatment of peridcarditis?

A

NSAIDs

2nd line - Colchicine (for recurrent or continued symptoms beyone 14 days)

355
Q

Give 3 common features of PE on CXR

A

Fleischner sign (dilated central pulmonary vessel)

Westermark sign (collapse of vasculature distal to PE)

Hampton’s hump (Wedge shaped infarct)

356
Q

Give 2 ECG features of PE

A

Sinus tachycardia

ST depression

357
Q

What is the MOA of caffeine?

A

Blocks adenosine receptors

358
Q

What is the MOA of methotrexate?

A

Competitively inhibits dihydrofolate reductase

359
Q

Define Transient Ischaemic Attack (TIA)

A

Aka Mini Strokes

Defined as a brief, transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal infarction, without acute ischaemia.

360
Q

Give 4 causes of TIAs

A

Atherothromboembolism from the internal carotid artery (main cause)

Cardioembolism (post MI, or AF, or prosthetic valves)

Hyperviscosity (polycythemia, sickle cell, myeloma)

Vasculitis (rare)

361
Q

Give 4 symptoms/signs of TIA. Do symptoms resolve?

A

TIA patients tend to have complete resolution of symptoms within an hour.

Amaurosis fungax (unilateral progressive vision loss - like a curtain descending)

Unilateral weakness or sensory loss

Ataxia, vertigo or loss of balance

Aphasia or dysarthria

362
Q

Give 6 investigations useful in excluding other diagnoses in TIA patients

A

Serum glucose (exclude hypoglycaemia)

FBC (exclude anaemia/infection)

Prothrombin time, INR, PTT (exclude coagulopathy)

Fasting lipid profile (exclude hyperlipidaemia/atherosclerotic risk)

ECG (investigate AF or other arrhythmias)

Doppler +/- Angiography

363
Q

What risk assessment is used to estimate risk of stroke after TIA?

364
Q

Describe the immediate management of TIA

A

Immediate antithrombotic therapy:

Give Aspirin 300mg immediately.

365
Q

In TIA management, when should aspirin not be given? (3)

A

If;

The patient has a bleeding disorder or is taking an anticoagulant (needs admission for imaging to exclude haemorrhage)

The patient is already taking low dose aspirin regularly (continue the current dose of aspirin until reviewed by a specialist)

Aspirin is contraindicated (discuss management with a specialist team)

366
Q

What is the preferred diagnostic imaging test for TIA? What carotid imaging test should also be performed?

A

MRI is preferred imaging to determine the territory of ischaemia.

Carotid doppler should be conducted in all patients (unless not a candidate for carotid endartectomy)

367
Q

Describe the secondary prevention for TIA

A

Antiplatelet and lipid modification therapy to follow on from initial aspirin therapy;

1st line - Clopidogrel + atorvastatin (20-80mg)
2nd line - Aspirin + dipyridamole + atorvastatin (if clopidogrel not tolerated)

368
Q

In TIA patients, when is carotid artery endarterectomy recommended?

A

Recommended if patient has suffered stroke or TIA in the carotid territory and is not severely disabled.

Should only be considered if;
Carotid stenosis >70% according to European or >50% according to North American

369
Q

From what layer of brain tissue does a lumbar puncture extract CSF?

A

Sub arachnoid

370
Q

Where does the dura mater receive it’s blood and nerve supply?

A

Blood supply = middle meningeal artery/internal jugular veins

Nerve supply = Trigeminal Nerve

371
Q

Why should phenytoin and carbamazepine be avoided in patients taking the oral contraceptive pill?

A

They are enzyme induces so reduce the effectiveness of the oral contraceptive pill.

372
Q

Define meningitis

A

Describes an inflammation of the meninges, usually due to infection. (meninges are the lining of the brain and spinal cord)

373
Q

Name 5 common causes of bacterial meningitis

A

Neisseria meningitidis (most common)
Streptococcus pneumoniae (most common in adults)
Haemophilus influenzae
Group B streptococcus (GBS)
Listeral monocytogenes

374
Q

What 2 pathogens commonly cause meningitis in neonates?

A

Group B streptococcus (GBS) (as HBS can colonise the vagina)

Listeria monocytogenes

375
Q

Define meningococcal meningitis and meningococcal septicaemia.

A

Meningococcal meningitis - When the bacteria infects the meninges and the CSF

Meningococcal septicaemia - When the bacteria infects the bloodstream.

376
Q

What rash is commonly seen in meningococcal septicaemia?

A

Non-blanching rash

377
Q

What are the 3 most common causes of viral meningitis?

A

Enteroviruses (coxsackievirus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)

378
Q

What diagnostic test is performed to diagnose viral meningitis?

A

Viral PCR testing on CSF sample

379
Q

What is used to treat HSV and VZV (viral meningitis)?

380
Q

Give 6 typical symptoms of meningitis

A

Fever

Neck stiffness

Vomiting

Headache

Photophobia

Altered consciousness/Seizures

381
Q

How may meningitis present in babies/neonates?

A

Non-specific symptoms;

Hypotonia
Poor feeding
Lethargy
Hypothermia

Bulging fontanelle

382
Q

When do NICE recommend performing a lumbar puncture on a child with suspected sepsis? (2)

A

Children who are;

Under 1 month, presenting with fever

1-3 months and are unwell or have a low or high white blood cell count

383
Q

When performing a lumbar puncture, which vertebrae is the needle inserted?

A

L3/L4 or L4/L5 vertebral space

384
Q

What tests are performed on a sample of CSF when investigating meningitis?

A

Bacterial Culture

Viral PCR

Cell Count

Protein levels

Glucose levels

385
Q

What may CSF test results show in a patient with bacterial meningitis? (5)

A

Appearance - Cloudy

Protein - High (bacteria release proteins)

Glucose - Low (bacteria eat glucose)

White Cell Count - High (neutrophils)

Culture - Shows Bacteria

386
Q

What may CSF test results show in a patient with viral meningitis? (5)

A

Appearance - Clear

Protein - Mildly raised/normal

Glucose - Normal (viruses don’t eat glucose)

White cell count - High (lymphocytes)

Culture - Shows viruses

387
Q

Is bacterial meningitis a medical emergency?

A

Yes. Should be treated immediately.

388
Q

A child presenting with suspected meningitis and a non-blanching rash should be given what immediately?

A

Benzylpenicillin (IM or IV)

Under 1 = 300mg
1-9 years = 600mg
Over 10 = 1200mg

389
Q

What antibiotics are given to babies with suspected meningitis?

A

Under 3 months - Cefotaxime + Amoxicillin (to cover listeria)

Above 3 months - Ceftriaxone

390
Q

If there is a risk of penicillin-resistant pneumococcal infection (e.g recent foreign travel/prolonged antibiotic exposure), what should be added? (treatment of bacterial meningitis)

A

Vancomycin

391
Q

What medication is used to reduce the frequency and severity of hearing loss and neurological complications in patients with bacterial meningitis?

A

Steroids (Dexamethasone)

392
Q

Is bacterial meningitis and menigococcal infection an notifiable disease?

A

Yes. Both should be notified to the UK Health Security Agency

393
Q

When is the exposure risk highest for people in close contact with an individual with a meningococcal infection?

A

Risk is highest within 7 days before onset of illness.

Risk decreases 7 days after the diagnosis.

394
Q

What is given as post-exposure prophylaxis for meningococcal infection?

A

Single dose of Ciprofloxacin (preferred) or rifampicin

395
Q

Give 5 complications of meningitis

A

Hearing loss (key complication)

Seizures and epilepsy

Cognitive impairment and learning disability

Memory loss

Focal neuological deficits (limb weakness or spasticity)

396
Q

In what circumstances should a lumbar puncture be delayed? (4)

A

Signs of severe sepsis or a rapidly evolving rash

Severe respiratory/cardiac compromise

Significant bleeding

Signs of raised ICP (focal neuro deficits, papilloedema, continuous/uncontrolled seizures, GCS <12)

397
Q

How should patients with signs of raised ICP be managed? (6)

A

Get critical care input

Secure airway + high flow oxygen

IV access > take bloods and blood cultures

IV dexamethasone

IV antibiotics (ceftriaxone/cefotaxime)

Arrange neuroimaging

398
Q

If a lumbar puncture is performed for suspected meningitis, what should it be tested for? (5)

A

glucose, protein, microscopy and culture

lactate

meningococcal and pneumococcal PCR

enteroviral, herpes simplex and varicella-zoster PCR

consider TB investigations

399
Q

Bacterial meningitis - What is the initial empirical therapy for child aged <3 months?

A

IV cefotaxime + amoxicillin (or ampicillin)

400
Q

Bacterial meningitis - What is the initial empirical therapy for aged 3 months - 50 years?

A

IV cefotaxime (or ceftriaxone)

401
Q

Bacterial meningitis - What is the initial empirical therapy for patients aged >50?

A

IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin)

402
Q

Bacterial meningitis - What is the treatment for meningococcal meningitis?

A

IV benzylpenicillin or cefotaxime (or ceftriaxone)

403
Q

Bacterial meningitis - What is the treatment for pneumococcal meningitis?

A

IV cefotaxime (or ceftriaxone)

404
Q

Bacterial meningitis - What is the treatment for meningitis caused by haemophilus influenzae?

A

Intravenous cefotaxime (or ceftriaxone)

405
Q

Bacterial Meningitis - What is the treatment for meningitis caused by Listera?

A

IV amoxicillin (or ampicillin) + Gentamicin

Phase 3a (6 decks)

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