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Phase 3a > Neurology Notes > Flashcards

Neurology Notes Flashcards

1
Q

How long do TIAs last

A

Less than 24 hours

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2
Q

What is the ABCD2 score used for?

A

Assessing a patient who has had a TIAs subsequent risk of having a stroke (Age, Blood Pressure, Clinical Features (unilateral weakness, dysphasia without weakness, Duration, Diabetes)

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3
Q

Treatment for stroke where intracranial haemorrhage has been excluded

A

Thrombolysis with IV Alteplase, as long as within 4.5 hours

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4
Q

What is the gold standard imaging technique for stroke

A

Diffusion weighted MRI

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5
Q

What are 4 examples of secondary prevention of Stroke?

A
  • clopidogrel 75mg daily
  • atorvastatin
  • carotid endarectomy or stenting
  • treat modifiable RF
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6
Q

At what point on the GCS should airways be secured

A

8/15

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7
Q

What is the pathophysiology of subdural haemorrhage

A

Rupture of bridging veins

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8
Q

How does a subdural haemorrhage appear on a CT scan

A

Crescent shape and are not limited by the cranial sutures

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9
Q

What is the pathophysiology of an extra Dural haemorrhage

A

Rupture if the middle meninges artery in the temporal-parietal region (can be associated with fracture of the temporal bone)

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10
Q

What is the shape of an extra dural haemorrhage on a CT scan

A

Bi Convex shape and limited by the cranial sutures

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11
Q

What are risk factors (other than aneurysm) for SAH

A

Cocaine, sickle cell anaemia

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12
Q

What are the features of essential tremour?

A
  • postural: worse if arms outstretched
  • improved by alcohol and rest
  • strong family history
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13
Q

What should be investigated in essential tremour?

A

Check U + Es, calcium, LFT, TFT (checks for other causes)

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14
Q

What is the inheritance of essential tremour?

A

Autosomal dominant

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15
Q

What is the management of essential tremor?

A

Propranolol (first line), primidone

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16
Q

What are the triad of symptoms of Parkinsons?

A

Rest tremor, rigidity, bradykinesia

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17
Q

What conditions can present similarly to PArkinsons?

A

Supranuclear palsy, normal pressure hydrocephalus, multiple system atrophy, Wilson’s disease, post-encephalitis

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18
Q

How can you differentiate supranuclear palsy to parkinsons?

A

Will present additionally with gaze issues, swallowing issues, early falls

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19
Q

What drugs can cause Parkinsonisms?

A

Anti-psychotics, metoclopramide

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20
Q

Why does domperidone not cause extra-pyramidal side effects?

A

Doesn’t cross the blood brain barrier

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21
Q

Why do Parkinsons patient get chorea?

A

Due to medication (over stimulation of basal ganglia). Typically levodopa

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22
Q

Why does Wilson’s disease cause Parkinsonism?

A

Copper is mostly deposited in the basal ganglia (particularly putamen and globus pallidus)

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23
Q

Outside of the typical triad, what presentation can Parkinsons have?

A
  • depression (common)
  • sleep disturbance
  • anmosia
  • mask like facies
  • micrographia
  • drooling of saliva
  • sleep disturbance
  • fatigue
  • autonomic dysfunction, such as postural hypotension
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24
Q

What type of sleep disturbance occurs in Parkinsons?

A

REM sleep behaviour disorder. Can occur many years before diagnosis

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25
Q

What sort of tremor is seen in Parkinsons?

A

Pill rolling

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26
Q

When does the tremor in Parkinsons improve and worse?

A

It is more noticeable when resting and improves on voluntary movement. It gets worse when the patient is distracted. Performing a task with the other hand (e.g., miming the act of painting a fence) exaggerates the tremor

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27
Q

What frequency is the tremor in Parkinsons?

A

4-6 hertz

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28
Q

What sort of rigidity is seen in Parkinsons?

A

Cogwheel

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29
Q

What is hypomimia? What condition is it seen in?

A

Reduced facial movements and facial expressions. Seen in Parkinsons

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30
Q

What are the main side effects of levodopa?

A

Dyskinesia (abnormal movements associated with excessive motor activity)

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31
Q

What advantage does dopamine agonists have over levodopa?

A

Less dyskinesia

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32
Q

What Parkinsons medication offers the most improvement in motor symptoms?

A

Levodopa

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33
Q

What is the distribution of Parkinsons symptoms?

A

Asymmetrical

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34
Q

What is the pathophysiology of Parkinsons?

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra. Reduction in dopamine output results in the classical triad of symptoms.

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35
Q

What autonomic disturbances are seen in Parkinsons?

A

Postural hypotension, urinary frequency, hypersalivation

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36
Q

What surgical treatment can be given for Parkinsons?

A

Deep brain stimulation: electrodes stimulate basal ganglia

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37
Q

Are symptoms sudden or gradual onset in Parkinsons?

A

Gradual

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38
Q

What ways can bradykinesia present in Parkinsons?

A
  • handwriting getting smaller (micrographia)
  • small steps when walking (shuffling gait)
  • rapid frequency of steps to compensate for small steps and avoid falling (festinating gait)
  • difficulty initiating movement
  • reduced facial movements + expressions (hypomimia)
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39
Q

What worsens/improves essential tremors?

A

Alcohol improves, rest improves. Worsens with intentional movement, worsens when arms outstretched

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40
Q

What is multiple system atrophy?

A

condition where neurones of various systems in the brain degenerate, including basal ganglia

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41
Q

What is the presentation of multiple system atrophy?

A

Parkinson’s presentation, autonomic dysfunction, cerebellar dysfunction (-> ataxia)

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42
Q

What are Parkinson’s plus syndrome?

A

Multiple system atrophy, dementia with Lewy bodies, progressive supranuclear palsy, corticobasal degeneration

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43
Q

What is a dementia associated with Parkinsons?

A

Lewy body dementia

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44
Q

How can lewy body dementia and Parkinsons be differentiated?

A

Cognitive symptoms start before motor symptoms in Lewy body dementia. Other way round in Parkinsons

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45
Q

How can Lewy body dementia be differentiated to other forms of dementia?

A
  • fluctuating cognition
  • early impairments in attention and executive function rather than just memory loss
  • visual hallucinations
  • Parkinsonism
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46
Q

What are the two types of multiple system atrophy?

A

Predominant Parkinsonian features and predominant cerebellar features

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47
Q

What condition does Parkinsonism with associated autonomic symptoms indicate?

A

Multiple system atrophy

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48
Q

What autonomic disturbance is often seen as an early feature of multiple system atrophy?

A

Erectile dysfunction

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49
Q

How is Parkinsons typically diagnosed?

A

Clinically: history and examination findings. By a specialist in movement disorders

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50
Q

What is the first line treatment in Parkinsons patients, where motor symptoms are affecting quality of life?

A

Levodopa

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51
Q

What is the first line treatment in Parkinsons patients, where motor symptoms are NOT affecting quality of life

A

Dopamine agonist, MAO-B inhibitor

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52
Q

Of the antiparkinsonism drugs, which offers the most improvements in motor symptoms and ADLs?

A

Levodopa

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53
Q

Which Parkinsons drug has the most motor complications?

A

Levodopa

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54
Q

Which Parkinsons drug has the most associated adverse events?

A

Dopamine agonists (excessive sleepiness, hallucinations, impulse control disorders)

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55
Q

What are common s/e of levodopa?

A

Dry mouth, anorexia, palpitations, postural hypotension, psychosis

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56
Q

What drug is levodopa nearly always given with?

A

Decarboxylase inhibitor (carbidopa)

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57
Q

Why is levodopa usually given with a carboxylase inhibitor?

A

This prevents the peripheral metabolism of levodopa to dopamine outside the brain, which can reduce side effects

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58
Q

What are examples of dopamine receptor agonists?

A

Bromocriptine, ropinirole, cabergoline, apomorphine

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59
Q

What are ergot derived dopamine receptor agonists?

A

Bromocriptine, cabergoline

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60
Q

What s/e are ergot derived dopamine agonists associated with, and what monitoring should occur?

A

Associated with pulmonary, retroperitoneal, cardiac fibrosis. Thus, prior to starting do a ECHO, ESR, creatinine and CXR. Requires careful monitoring

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61
Q

What are possible s/e of dopamine agonists?

A

Impulse control disorders, hallucinations, excessive daytime sleeping

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62
Q

How does MAO-B inhibitors work for Parkinsons treatment?

A

Inhibits the breakdown of dopamine secreted

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63
Q

How can dosage of Levodopa change over time?

A

May have to increase, as it becomes less effective over time

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64
Q

What are examples of dyskinesia due to Levodopa?

A
  • dystonia (excessive muscle contraction leads to abnormal postures/exaggerated movements)
  • chorea
  • athetosis (involuntary twisting/writhing movements)
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65
Q

When is amantadine used in Parkinsons?

A

Used to reduce the dyskinesia associated with levodopa

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66
Q

What drug class is amantadine?

A

Glutamate antagonist

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67
Q

What is the action of COMT enzyme in Parkinsons/Levodopa tx?

A

Metabolises levodopa in the body and brain

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68
Q

Why are COMT inhibitors given?

A

To extend the effective duration of levodopa; inhibits the breakdown of the drug

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69
Q

What drug is entacapone?

A

COMT inhibitor

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70
Q

What are examples of MAO-B inhibitors?

A

Selegiline, rasagiline

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71
Q

What Parkinsons drug has the highest risk of impulse control disorder?

A

Dopamine agonist therapy

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72
Q

What medication can be used to treat excessive salivation in Parkinsons?

A

Glycopyrronium bromide

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73
Q

What is the role of anti muscarinics in Parkinsonisms?

A

Treat drug induced parkinsonism, can help tremor and rigidity. Procyclidine also in acute dystonia in anti psychosis medication

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74
Q

What muscles are affected by benign essential tremor?

A

Voluntary muscles: head, jaw, vocal tremor

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75
Q

What are possible causes of tremors?

A

Parkinsonism, essential tremor, anxiety, thyrotoxicosis, hepatic encephlopathy, CO2 retention (CO2), cerebellar disease, drug withdrawal

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76
Q

What age does MND rarely present before?

A

40 years

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77
Q

What are the types of MND?

A

ALS, primary lateral sclerosis, progressive muscular atrophy, progressive bulbar palsy

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78
Q

What is the most common type of MND?

A

ALS

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79
Q

How does progressive bulbar palsy typically present?

A

Palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei

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80
Q

What type of MND has the poorest prognosis?

A

Progressive bulbar palsy

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81
Q

What type of MND has the best prognosis?

A

Progressive muscular atrophy

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82
Q

What is the typical distribution of signs in ALS?

A

LMN signs in arms, UMN signs in legs

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83
Q

What is the most common presentation of ALS?

A

Asymmetric limb weakness

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84
Q

What disease should fasciculations make you consider?

A

MND

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85
Q

What is the presentation of MND?

A
  • asymmetric limb weakness
  • mixture of LMN and UMN
  • wasting of small hand muscles/tibialis anterior
  • fasciculations
  • absence of sensory signs/symptoms
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86
Q

What muscles are characteristically spared in MND?

A

External ocular

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87
Q

What investigations can support a dx of MND?

A

Nerve conduction studies, MRI, electromyography

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88
Q

Why is nerve conduction studies done in MND? What is the typical result?

A

Exclude a neuropathy. Show normal motor conduction

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89
Q

What is the typical results for electromyography in MND?

A

Reduced number of action potentials with increased amplitude

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90
Q

Why is MRI done in MND?

A

To exclude the differential diagnosis of cervical cord compression and myelopathy

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91
Q

What are the potential differential dx in MND?

A

Neuropathy, cervical cord compression, myelopathy

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92
Q

What are the cognitive domains?

A

Memory, visuospatial, language, executive function, social cognition/behavioural, attention

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93
Q

What are symptoms of episodic memory loss?

A

reptititive in conversation, limited knowledge of current affairs, may forget appointments

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94
Q

What are signs of episodic memory loss?

A

Cannot recall breakfast, cannot recall pictures from naming test, Ribot’s phenomenoma

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95
Q

What is Ribot’s phenomenoma

A

More recent memories lost more than remote ones

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96
Q

What are symptoms of visuospatial memory loss?

A

Difficulty reading unusual fonts, optician visits, misperceptions, hallucinations, loss of confidence driving

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97
Q

What are signs of visuospatial memory loss?

A

Unable to draw clock faces or intersecting pentagons, prosopagnosia (can’t recognise faces)

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98
Q

What is symptoms of language memory loss?

A

Forgetting words, stumbling over words, neologisms, vague descriptions, asking what things are/mean

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99
Q

What are signs of language memory loss?

A

Unable to repeat difficult words, phrases or follow complex commands. Unable to read unusual words, unable to demonstrate use of object

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100
Q

What is the symptoms of executive function loss?

A

Disorganised, unable to multitask, frequently distracted, lacking initiative, odd decisions made

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101
Q

What are signs of executive function loss?

A

Poor estimates, impaired letter fluency, stroop test

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102
Q

What are symptoms of social cognition loss?

A

Loss of empathy, inappropriate behaviour, callous, self obsessed, humourless, preference for sweet foods (lol)

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103
Q

What is praxis?

A

Conception, planning, executive of a specific action (eg, gait apraxia)

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104
Q

What are causes of rapid onset dementia?

A

CDJ, vasculitis, limbic encephalitis, space occupying lesion, seizures, infections (HIV, HSV), metabolic

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105
Q

What are LMN signs?

A

Muscle wasting, reduced tone, fasciculations, reduced reflexes

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106
Q

What are UMN signs?

A

Increased tone or spasticity, brisk reflexes, upgoing plantar reflexes

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107
Q

What is used in the treatment of MND?

A

Riluzole, non invasive ventilation (BiPAP)

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108
Q

What is the MoA of riluzole?

A

Prevents stimulation of glutamate receptors

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109
Q

What conditions has association with epilepsy?

A

Cerebral palsy, tuberous sclerosis, mitochondrial diseases

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110
Q

What age does febrile convulsions typically occur between?

A

6 months and 5 years

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111
Q

What are the features of a typical febrile convulsion?

A

Early in viral infection as temperature rises rapidly, brief, tonic-clonic

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112
Q

What are the features of a simple febrile convlusion?

A

<15 minutes, generalised seizure, no recurrence in 24 hours, complete recovery within an hour

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113
Q

What are the features of a complex febrile seizure?

A

15-30 minutes, focal, repeated seizures

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114
Q

What is the management following a paediatric febrile seizure?

A

Children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics

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115
Q

When should a parent ring an ambulance in a febrile seizure?

A

If it has lasted longer than 5 minutes

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116
Q

Do antipyretics reduce the chances of a febrile seizure?

A

No

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117
Q

What is the treatment for recurrent febrile seizures?

A

BDZ rescue medication (Rectal diazepam or buccal midazolam)

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118
Q

What are focal siezures?

A

Start in a specific area, typically on one side of the brain

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119
Q

Do patients remain conscious in generalised seizures?

A

No, all patients become immediately unconscious

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120
Q

What are the types of generalised seizure?

A

Tonic-clonic, tonic, clonic, typical absence, myoclonic, atonic

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121
Q

What is West’s syndrome?

A

Infantile spasms in the first few months of life

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122
Q

How do infantile spasms present?

A

Flexion of the head, trunk, and limbs. This is followed by extension of the arms

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123
Q

What typically causes West’s syndrome?

A

Neurological abnormality

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124
Q

What is the typical features of juvenile myoclonic epilepsy?

A

Infrequent generalised seizures, often in the morning. Daytime absences, and sudden shock like myoclonic seizures. Worse after drinking alcohol

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125
Q

What is the treatment of juvenile myoclonic epilepsy?

A

Sodium valproate

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126
Q

How can post ictal phases differentiate seizures and syncope?

A

Following a seizure: patients have a post ictal phase where they feel drowsy and tired for around 15 minutes. Syncopal episodes have quicker recovery

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127
Q

What symptoms may be associated with epilepsy?

A

Tongue biting, incontinence of urine

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128
Q

What type of seizures of seen in febrile convulsion?

A

Tonic/tonic-clonic

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129
Q

What features may be seen in temporal seizures?

A

Epigastric aura and automatism, deja vu, jamais vu, less commonly hallucinations

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130
Q

What features may be seen in frontal lobe partial seizures?

A

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

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131
Q

What is the difference between tonic, clonic, myoclonic and atonic?

A

Tonic: muscle tensing
Clonic: muscle jerking
Myoclonic: brief rapid muscle jerks
Atonic: less of muscle tone

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132
Q

Do eyes shut or stay open in an epileptic seizure?

A

Typically remain open

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133
Q

What are the differential diagnoses for epileptic seizures?

A

Vasovagal syncope, pseudoseizures, cardiac syncope, hypoglycaemia, TIA

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134
Q

When are AEDs started?

A

After second epileptic seizure

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135
Q

How can AEDs affect the P450 system?

A

Many epileptics can induce/inhibit the P450 system resulting in varied metabolism of other medications, for example warfarin

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136
Q

What are the possible s/e of sodium valproate?

A

P450 enzyme inhibitor, increased appetite and weight gain, alopecia, tremor, hepatitis, pancreatitis, thrombocytopaenia

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137
Q

What is the MoA of sodium valproate?

A

Increases GABA activity

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138
Q

When is sodium valproate used?

A

Generalised seizures in men (teratogenic)

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139
Q

What is the MoA of carbamazepine?

A

Binds to sodium channels, increasing refractory period

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140
Q

What are the possible s/e of carbamazepine?

A

P450 enzyme inhibitor, dizziness and ataxia, drowsiness, agranulocytosis, visual disturbance

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141
Q

What is the possible s/e of lamotrigine?

A

Stevens Johnson syndrome

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142
Q

What is the first line treatment of seizure? What time is it administered?

A

5-10 minutes, give benzodiazepine

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143
Q

When is status epilepticus?

A

> 5 mins

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144
Q

What is the first line treatment for generalised seizures (men vs women)?

A

Men: sodium valproate
Women: lamotrigine or levetiracetam

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145
Q

What is the treatment for partial seizures (men vs women)?

A

Both lamotrigine or levetiracetam

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146
Q

What is the treatment of absence seizures?

A

Ethosuximide

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147
Q

Are eyes open or closed in a seizure?

A

Open. Closed in syncope

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148
Q

What benzodiazepine is given in status epilepticus?

A

Pre-hospital: PR diazepine or buccal midazolam
Hospital: IV lorazepam

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149
Q

How many doses of IV lorazepam can be given in status epilepticus?

A

Maximum two doses

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150
Q

What is second line for status epilepticus?

A

Levetiracetam, phenytoin, sodium valproate

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151
Q

Is consciousness affected in focal seizures?

A

No, not impaired

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152
Q

Can mothers on AEDs breastfeed?

A

Yes

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153
Q

What birth defects can sodium valproate be associated with?

A

Neural tube defects

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154
Q

What is the prognosis of benign rolandic epilepsy?

A

Excellent; most will outgrow by adolescence?

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155
Q

What is the cause of Lateral medullary syndrome?

A

Occlusion of the posterior inferior cerebellar artery

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156
Q

What are the symptoms of lateral medullary syndrome?

A

Ipsilateral facial pain and temperature loss, contralteral limb/torso pain, ataxia (cerebellar signs), nystagmus

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157
Q

What are the typical symptoms of neuromalignant syndrome?

A

Pyrexia, muscle rigidity, autonomic lability (HTN, tachycardia, tachypnoea), agitated delirium with confusion, raised creatine kinase, AKI, leukocytosis

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158
Q

What is the pattern of damage for the radial nerve?

A

Wrist drop, sensory loss to area between dorsal aspect of the 1st and 2nd metacarpals

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158
Q

What type of fracture puts the radial nerve at risk?

A

Shaft fracture of the humerus

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159
Q

What is the treatment of Bell’s palsy?

A

Prednisolone

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160
Q

What is MS?

A

A chronic cell mediated autoimmune disorder characterised by demyelination in the CNS

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161
Q

What gender is MS more common in?

A

Women

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162
Q

What is the most common form of MS?

A

Relapsing remitting disease

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163
Q

What is a very common (non specific) presentation of MS?

A

Lethargy

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164
Q

What are common visual presentations of MS?

A

Optic neuritis, optic atrophy, Uhthoff’s phenomenon

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165
Q

How does optic neuritis present?

A

Pain, unilateral vision loss, visual field loss, loss of colour vision, flashing lights, central scotoma (enlarged central blind spot)

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166
Q

What is Uhthoff’s phemomenom?

A

Worsening of vision and other symptoms following rise in body temperature

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167
Q

What are the sensory features of MS?

A

Pins/needles, numbness, trigeminal neuralgia, Lhermitte’s syndrome

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168
Q

What is Lhermitte’s syndrome?

A

Parasethesiae in limbs on neck flexion

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169
Q

What motor symptom is seen in MS?

A

Spastic weakness (most commonly in legs), limb paralysis

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170
Q

What general symptoms are seen in MS? (not motor, sensory or visual)

A

Urinary incontinence, sexual dysfunction, intellectual deterioration

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171
Q

What is required for a diagnosis of MS?

A

Demonstration of lesions disseminated in time and space

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172
Q

What is the pathophysiology of MS?

A

Myeline covers axons of neurones, helps the travel of electrical impulses. In MS, inflammation damages myelin. In early stages, re-myelination can occur and symptoms can resolve. Further on in disease, this happens less.

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173
Q

Does MS affect central or peripheral nervous system?

A

Central (the oligodendrocytes)

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174
Q

What are the differential diagnosis of optic neuritis?

A

Sarcoidosis, SLE, syphilis, measles, mumps, Lyme disease, MS

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175
Q

What is the treatment of optic neuritis?

A

High dose steroids

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176
Q

Lesions in what cranial nerves cause double vision and nystagmus?

A

Oculomotor (III), trochlear (IV), abducens (VI)

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177
Q

What is internuclear ophthalmoplegia?

A

Nerve fibres of the medial longitudinal fasciculus connect the cranial nerve nuclei that control eye movements and ensure the eyes move together.

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178
Q

Where is the lesion that causes internuclear ophthalmoplegia?

A

Medial longitudinal fasciculus

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179
Q

What is the presentation of internuclear ophthalmoplegia?

A

Causes impaired adduction on the same side as the lesion and nystagmus in the contralteral eye

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180
Q

What causes conjugate lateral gaze disorder?

A

Lesion in the abducens nerve

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181
Q

How does conjugate lateral gaze disorder present?

A

When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion involving the left eye, when looking to the left, the right eye will adduct (move towards the nose), and the left eye will remain in the middle.

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182
Q

What is the difference in sensory and cerebellar ataxia?

A

Sensory: due to loss of proprioception
Cerebellar: due to problems from the cerebellum coordinating movement

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183
Q

What test comes back positive in sensory ataxia?

A

Rombergs (lose balance with eye’s closed)

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184
Q

Where is the lesion in ataxia?

A

Dorsal columns of the spine

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185
Q

How is MS diagnosed?

A

MRI (can demonstrate lesions) or lumbar puncture (detect oligoclonal bands in the CSF)

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186
Q

How is acute relapse treated in MS?

A

High dose steroids (oral or IV methylprednisolone)

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187
Q

What are drug options for reducing risk of relapse in MS?

A

Natalizumab, ocrelizumab, fingolimod, beta interferon

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188
Q

What is first line drug treatment for reducing the risk of relapse in MS?

A

Natalizumab (recombinant monoclonal antibody)

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189
Q

What is the first line treatment of spasticity in MS?

A

Baclofen and gabapentin

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190
Q

What additional investigation should patients with bladder dysfunction in MS undergo and why?

A

Ultrasound to assess bladder emptying: if there is significant residual volume, anticholinergics may worse

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191
Q

What is the treatment for bladder dysfunction in MS?

A

Anti cholinergics

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192
Q

What is the treatment of fatigue in MS?

A

Amantadine (1st line: unknown mechanism), modafinil or SSRI

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193
Q

What are the features of an ataxic gait?

A

Wide based, falls, cannot walk heel to toe

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194
Q

What are the cerebellar causes of an ataxic gait?

A

MS, posterior fossa tumour, alcohol, phenytoin toxicity

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195
Q

If there is right ataxia and the cause is cerebellar, where will the cerebellar lesion be?

A

Same side

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196
Q

What are the proprioceptive causes of an ataxic gait?

A

Sensory neuropathies (low B12), inner ear problem (affecting vestibular system)

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197
Q

What are the mechanisms that blood supply to the brain can be disrupted?

A

Thrombus/embolus, atherosclerosis, shock, vasculitis

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198
Q

What is the onset time of a stroke?

A

Rapid

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199
Q

What is the main risk factor for an embolic stroke?

A

AF

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200
Q

What are the risk factors for haemorrhagic stroke?

A

Age, HTN, AVM, anticoagulation therapy

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201
Q

What are the typical features of a stroke?

A

Asymmetrical. Limb weakness, facial weakness, dysphasia, visual field defects (homonymous hemianopia), sensory loss, ataxia and vertigo

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202
Q

What specific symptoms are seen in brainstem infarcts?

A

Severe stroke symptoms including quadroplegia and lock-in-syndrome

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203
Q

What are the specific symptoms of cerebral hemisphere infarcts?

A

Contralateral hemiplegia (initially flaccid then spastic), contralateral sensory loss, homonymous hemianopia, dysphasia

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204
Q

What are the symptoms of lacunar infarcts?

A

Pure sensory stroke OR ataxic hemiparesis OR unilateral weakness (and/or sensory deficit)

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205
Q

What are lacunar infarcts?

A

Small infarcts around the basal ganglia, internal capsule, thalamus, pons

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206
Q

What is the Bamford classification?

A

Classifies strokes based on the initial symptoms

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207
Q

What are the criteria for the Bamford classification?

A
  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction (eg, dysphasia)
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208
Q

What arteries are involves in total anterior circulation infarcts?

A

Middle and anterior cerebral arteries

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209
Q

What criteria of the Bamford classification is present in a total anterior circulation infarct?

A

All 3

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210
Q

What arteries are affected in partial anterior circulation infarcts?

A

Smaller arteries of anterior circulation

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211
Q

What arteries are affected in lacunar infarcts?

A

Arteries around the internal capsule, thalamus and basal ganglia

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212
Q

What type of stroke is likely in a patient who presents with isolated unilateral hemiplegia without speech or vision problems?

A

Lacunar infarct

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213
Q

What arteries are affected in posterior circulation infarcts?

A

Vertebrobasilar arteries

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214
Q

What symptoms are more likely in a haemorrhagic stroke?

A

Decrease in level of conciousness, headache, nausea and vomiting, seizures

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215
Q

When can patients be offered thrombolysis?

A

Confirmed ischaemic stroke, and within 4.5 hours of stroke symptoms. IV alteplase given

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216
Q

What is the management of TIA?

A

Immediate 300mg aspirin unless C/I

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217
Q

What is the associated affects with anterior cerebral artery stroke?

A

Contralateral hemiparesis (weakness) and sensory loss, more often lower extremity

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218
Q

What is the most and least common location of stroke infarcy?

A

MCA= most common
ACA = least likely

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219
Q

What is the symptoms of MCA infarct?

A

Contralateral hemiparesis and sensory loss, more often upper body. Hemiplegia. Aphasia (Broca’s)

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220
Q

What blood supply has infarcted if there is Broca’s aphasia?

A

MCA

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221
Q

Where is Broca’s located?

A

Frontal lobe

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222
Q

How is LMN and UMN distinguished in a patient with facial palsy?

A

Forehead sparing will have UMN origin (due to bilateral innervation)

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223
Q

What commonly causes LMN facial paralysis?

A

Bell’s palsy

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224
Q

What is the presentation of a stroke in PCA region?

A

Visual issues: often contralateral homonymous hemianopia with macular sparing

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225
Q

What is Weber’s syndrome?

A

Midbrain stroke syndrome

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226
Q

What is the presentation of Weber’s infarct?

A

Ipsilateral CN III palsy (down and out), contralateral weakness of upper and lower extremity

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227
Q

What is the presentation of anterior inferior cerebellar artery occlusion?

A

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

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228
Q

What is seen in ophthalmic artery infarct?

A

Amaurosis fugax

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229
Q

What is seen in basilar artery infarct?

A

Locked in syndrome

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230
Q

Which area of the brain affected by a stroke which causes expressive dysphasia?

A

Broca’s area (dominant hemisphere, usually left)

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231
Q

Which area of the brain would a stroke cause receptive dysphasia?

A

Wernicke’s

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232
Q

What should be prescibed alongside steroids?

A

PPI (steroids can cause gastric irritation)

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233
Q

How would you assess someone’s risk of a stroke if they have AF?

A

CHADSVASC

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234
Q

What are the general clinical features of a posterior circulation infarct?

A

Vertigo, imbalance, unilateral limb weakness, slurred speech, double vision, headache, N+V, cerebellar signs

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235
Q

What are the features of a total anterior circulation infarct?

A

Cognitive impairment, speech troubles, unilateral weakness/incoordination, unilateral numbness or loss of sensation, dysarthria, unilateral visual loss, loss in 1 visual field

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236
Q

What arteries are involves in posterior circulation infarcts?

A

vertebrobasilar arteries

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237
Q

What should be given as soon as a haemorrhagic stroke has been excluded?

A

300mg aspirin

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238
Q

What is the target time that thrombectomy should be offered within?

A

6 hours

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239
Q

What imagine should be done prior to thrombectomy and why?

A

Computed tomographic angiography (CTA) or magnetic resonance angiography (MRA). This is to confirm which vessel is infarcted

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240
Q

What vessel area is always offered thrombectomy if within timeframe?

A

proximal anterior circulation

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241
Q

When would thrombectomy be done if more than 6 hours have passed?

A

If there is potential to salvage brain tissue as shown by CT perfusion or diffusion weighted MRI

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242
Q

What is first line secondary prevention of a stroke?

A

Clopidogrel

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243
Q

What is second line secondary prevention of a stroke?

A

Aspirin plus MR dipyridamole

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244
Q

When is carotid artery endartectomy recommended?

A

If they have had a stroke/TIA in the carotid territory, not severley disabled, and have >70% carotid stenosis

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245
Q

What investigations are done after a stroke to identify if a specific risk factor caused the event?

A
  • carotid imaging: identify carotid artery stenosis
  • ECG: identify AF
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246
Q

What is a validated tool that assesses stroke in hospital?

A

ROSIER score

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247
Q

What should be immediately excluded if a patient is presenting with a possible stroke?

A

Hypoglycaemia

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248
Q

What is assessed as part of the ROSIER tool?

A

Loss of consciousness or syncope, seizure activity (these make stroke LESS likely). Points if new, acute: asymmetric facial weakness, asymmetric arm weakness, asymmetric leg weakness, speech disturbance, visual field defect

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249
Q

What is the first line investigation for suspected stroke?

A

non contrast CT head scan

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250
Q

What will be seen on a non contrast CT head scan if there is an acute ischaemic stroke?

A

Hyperdense artery

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251
Q

What will be seen on a non contrast CT head scan if there is a haemorrhagic stroke?

A

Area of hyperdensity surrounded by low density (oedema)

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252
Q

What is the first line agents used to control BP in a patient post stroke? Why?

A

intravenous labetalol, nicardipine and clevidipine as first-line agents, due to the possibility for rapid and safe titration to control blood pressure

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253
Q

What should be done to blood pressure prior to thrombolytic therapy in stroke patients?

A

Reduced to 185/110, as elevated BP can affect thrombolytic eligibility

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254
Q

What is the treatment of TIA?

A

Immediately give 300mg aspirin

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255
Q

What is the management of a patient with a suspected TIA who has a bleeding disorder or taking an anticoagulant?

A

Admit immediately to exclude haemorrhage

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256
Q

When do TIA symptoms typically resolve?

A

Within an hour

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257
Q

When should a patient who has had a suspected TIA in the last 7 days be reviewed by a specialist?

A

Within 24 hours

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258
Q

When should a patient who has had a suspected TIA which has occurred more than a week ago by reviewed by a specialist?

A

Within 7 days

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259
Q

When should a patient who has had more than 1 TIA or has a suspected cardioembolic source or severe carotid stenosis by reviewed?

A

Discuss need for admission/observation urgently.

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260
Q

What neuroimaging is recommended in TIA patients?

A

MRI (including diffusion weight and blood sensitive sequences)

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261
Q

Is CT done for a TIA?

A

Generally no, unless there is clinical suspicion of an alternative diagnosis

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262
Q

What imaging should all TIA patients have done urgently, and why?

A

Carotid doppler, due to risk of carotid artery atherosclerosis

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263
Q

What is the first line treatment for TIA patients?

A

Clopidogrel, after initial aspirin therapy

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264
Q

What secondary therapy should be given to TIA patients, aside for antiplatelet?

A

High intensity statin

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265
Q

What layers of the brain do subarachnoid haemorrhages occur between?

A

The pia mater and arachnoid membrane

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266
Q

What is associated with SAH risk?

A

Cocaine use, FHx, sickle cell anaemia, connective tissue disorders, neurofibromatosis, autosomal dominant polycystic kidney disease

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267
Q

What is the first line investigation for a SAH?

A

Non contrast CT head

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268
Q

Is traumatic or spontaneous SAH more common?

A

Traumatic

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269
Q

What are the causes of spontaneous SAH?

A

Intracranial aneurysm (berry), AVM, pituitary apoplexy

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270
Q

What are conditions associated with berry aneurysms

A

HTN, adult polycystic kidney disease, ehlers danlos, coartication of the aorta

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271
Q

What are the features of SAH?

A

Thunderclap headache (severe, occipital), potential sentinel headache, nausea and vomiting, meningism, coma, seizures, ECG changes

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272
Q

What ECG changes might be seen during SAH?

A

ST elevation

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273
Q

Should a LP be done if CT head is negative within 6 hours of suspected SAH?

A

No: consider alternative dx

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274
Q

What course of action should be taken if CT head is done >6 hours after SAH and is normal?

A

Do a lumbar puncture

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275
Q

What are LP results consistent with a SAH?

A

Xanthichromia (RBC break down), normal or raised opening pressure

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276
Q

What time should LP be done within suspected SAH?

A

<12 hours

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277
Q

If a SAH is confirmed via CT, what should be the next steps of investigation?

A

Identify causative pathology via CT intracranial angiogram (to identify vascular lesion)

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278
Q

What medication is used to prevent vasospasm after a SAH?

A

Nimodipine

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279
Q

What is the risk of confirmed aneurysmal SAH?

A

Risk of rebleeding: most treated by interventional coil clipping, and some craniotomy and neurosurgical clipping

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280
Q

What is the investigation of potential aneurysmal SAH rebleeding?

A

Repeat CT

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281
Q

What are the potential complications of SAH?

A

Rebleeding, hydrocephalus, vasospasm, hyponatraemia, seizures

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282
Q

How is hydrocephalus after SAH treated?

A

External ventricular drain or long term VP shunt

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283
Q

What electrolyte imbalance is commonly seen after SAH and why?

A

Hyponatraemia due to SIADH

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284
Q

What most commonly causes a extradural haematoma?

A

Low impact trauma

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285
Q

What is the typical presentation of a patient with an extradural haematoma?

A

Patient who initially loses, briefly regains, and then loses consciousness after a low impact head injury

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286
Q

What pupillary sign is seen in patients with ED haematoma and why?

A

Fixed and dilated pupil due to the compression of the parasympathetic fibres of the third cranial nerve as the brain swells

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287
Q

What is the definitive treatment of ED haematoma?

A

Craniotomy and evacuation of the haematoma

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288
Q

What are the three types of subdural haemorrhage?

A

Acute, subacute, chronic

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289
Q

What is an acute subdural haematoma?

A

Collection of fresh blood within the subdural space

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290
Q

What are subacute subdural haematomas associated with?

A

High impact injuries, therefore often associated with other underlying brain injuries

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291
Q

What are the surgical options for an acute subdural haematoma?

A

Monitoring of intracranial pressure and decompressive craniectomy

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292
Q

What causes chronic subdural haematoma?

A

Rupture of the small bridging veins, causes slow bleeding

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293
Q

What is the time frame for symptoms developing in chronic subdural haematoma?

A

Typically several weeks or a month after

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294
Q

How do acute vs chronic subdurals appear on CT?

A

Acute: hyperdense (bright)
Chronic: hypodense (dark)

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295
Q

What are the indications for operating on a chronic subdural?

A

If the patient is confused, has an associated neurological deficit or severe imaging findings

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296
Q

What is the surgery of choice in chronic subdural haematoma?

A

Surgical decompression with burr holes

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297
Q

What are the features of intracranial venous thrombosis?

A

Slow onset headache, nausea and vomiting, reduced consciousness, diplopia, facial pain, signs of raised intracranial pressure

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298
Q

What is the investigation of choice for intracranial venous thrombosis?

A

MRI venography. Additionally d-dimer may be raised

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299
Q

What is the management of intracranial venous thrombosis?

A

Anticoagulation with LMWH acutely, warfarin in longer term

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300
Q

What sign is seen on venography with sagittal sinus thrombosis?

A

Empty delta sign

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301
Q

What are the risk factors for intracranial venous thrombosis?

A

Smoking, COC pill, hx of clots

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302
Q

What are factors that favour pseudoseizures?

A

Pelvic thrusting, family member with epilepsy, female, crying after seizure, don’t occur when alone, gradual onset

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303
Q

What blood test may be elevated after a true seizure, which can help differentiate from pseudoseizures?

A

Serum prolactin

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304
Q

What is the inheritance of Duchennes?

A

X-linked recessive

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305
Q

How does Duchennes typically present?

A

With a child who has vague symptoms of muscle weakness, and uses their hands on their legs to help them stand up (Gower’s sign)

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306
Q

What blood test may come back raised in Duchenne’s?

A

Creatinine kinase

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307
Q

What protein is the mutation in with Duchennes + Beckers?

A

Dystrophin

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308
Q

What is myopathy?

A

A disease that affects muscles that control voluntary movement in the body; patients experience muscle weakness

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309
Q

What are the typical features of myopathies?

A

Symmetrical muscle weakness (proximal > distal), common problems are rising from a chair/getting up stairs/rushing hair.

Sensation + reflexes normal

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310
Q

What are the potential causes of myopathy?

A

Polymyositis, Duchenne/Becker dystrophy, myotonic dystrophy, Cushing’s, thyrotoxicosis, alcohol

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311
Q

What is Bell’s palsy?

A

Facial nerve paralysis

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312
Q

Is Bell’s palsy uni or bilateral?

A

Unilateral

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313
Q

Is Bell’s palsy UMN or LMN?

A

LMN

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314
Q

What is the features of Bell’s palsy?

A

Entire facial paralysis (including the forehead). Can also have altered taste, dry eyes, hyperacusis (reduced tolerance to sound)

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315
Q

What is the treatment of Bell’s palsy?

A

Oral prednisolone within 72 hours, and eye care (artificial tears and eye lubricants)

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316
Q

When should patient’s with Bell’s palsy be referred?

A

No improvement after 3 weeks, refer to ENT

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317
Q

What are the 5 branches of the facial nerve?

A

Temporal, zygomatic, buccal, marginal mandibular, cervical

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318
Q

What is the facial nerve pathway?

A

Exits the brainstem at the cerebellopontine angle. On its journey to the face it passes through the temporal bone and parotid

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319
Q

What is the motor function of the facial nerve?

A

Facial expression, stapedius in the inner ear

320
Q

What is the sensory function of the facial nerve?

A

Taste to anterior 2/3 of the tongue

321
Q

What is the parasympathetic function of the facial nerve?

A

Supplies the submandibular, sublingual, and lacrimal glands

322
Q

What can cause bilateral UMN lesions?

A

Pseudobulbar palsies, MND

323
Q

What causes Bell’s palsy?

A

It is generally idiopathic, though there may be links with some viral causes

324
Q

What is Ramsay-Hunt syndrome?

A

Reactivation of the varicella zoster virus in the geniculate ganglion of the 7th cranial nerve

325
Q

What is the presentation of Ramsay Hunt syndrome?

A

Unilateral LMN facial nerve palsy, with the addition of a painful + tender vesicular rash in and around the ear. Can also have vertigo and tinnitus

326
Q

What is normally the first feature of Ramsay Hunt syndrome?

A

Auricular pain

327
Q

What is the management of Ramsay Hunt syndrome?

A

Oral aciclovir and corticosteroids, lubricating eye drops

328
Q

What structures does the facial nerve supply?

A

Structures of the second embyronic branchial arch

329
Q

What are causes of bilateral facial nerve palsy?

A

Sarcoidosis, guillain barre syndrome, lyme disease, bilateral acoustic neuromas (as in neurofibromatosis typ 2), Bell’s palsy (though normally unilateral)

330
Q

What are the possible causes of unilateral facial nerve palsy?

A

Sarcoidosis, GBS, Lyme disease, acoustic neuroma, Bell’s palsy, Ramsay-Hunt syndrome, parotid tumours, MS, HIV, diabetes mellitus, trauma (direct nerve trauma, base of skull fractures)

331
Q

What are the features of carbon monoxide poisoning?

A

Headache, N+V, vertigo, confusion, weakness

332
Q

What is the key investigation in patients with potential carbon monoxide poisoning?

A

Carboxyhaemoglobin levels

333
Q

When might carboxyhaemoglobin be falsely raised?

A

In smokers (<10%, vs <3% in non smokers)

334
Q

What are the three branches of the trigeminal neuralgia?

A

Ophthalmic, maxillary, mandibular

335
Q

What types seizures will carbamazepine worsen?

A

Absence or myoclonic seizures

336
Q

What are the possible causes of trigeminal neuralgia?

A

Idiopathic mostly, but also potentially due to compression of the trigeminal roots by tumours or vascular problems

337
Q

What are the triggers for pain in trigeminal neuralgia?

A

Light touch: such as washing, shaving, smoking, talking, brushing teeth

338
Q

What is the pain experienced in trigeminal neuralgia?

A

Unilateral. Brief, electric shock like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve

339
Q

What are trigger areas in trigeminal neuralgia?

A

Small areas of the nasolabial fold or chin

340
Q

What are red flag symptoms in trigeminal neuralgia that may suggest a serious underlying problem?

A

Sensory changes, deafness, pain only in the opthalmic division of the nerve (eye socket, forehead, nose), bilateral pain, optic neuritic, FHx of MS, onset before 40 years

341
Q

What is the first line treatment for trigeminal neuralgia?

A

Carbamazepine

342
Q

What condition frequently is co-concurrent with trigeminal neuralgia?

A

MS

343
Q

What is myasthenia gravis?

A

An autoimmune condition affecting the neuromuscular junction

344
Q

What age are patients typically with myasthenia gravis?

A

Men: over 60
Women: under 40

345
Q

What condition does myasthenia gravis have a strong link with?

A

Thymomas

346
Q

What is the pathophysiology of myasthenia gravis?

A

Acetylcholine receptor (AChR) antibodies bind to the postsynaptic acetylcholine receptors, blocking them and preventing stimulation. Therefore, the more receptors are used during muscle activity, the more they become blocked. The antibodies also activate the complement system at the neuromuscular junction, which leads to cell damage

347
Q

Which gender is more commonly affected by myasthenia gravis?

A

Women

348
Q

What antibodies are seen in myasthenia gravis?

A

ACh-AB, MuSK (muscle specific kinase antibodies), low density lipoprotein receptor related protein 4 antibodies (LRP4)

349
Q

What is the function of MuSK and LRP4 normally, and why does this lead to M.G?

A

MuSK and LRP4 are important proteins for the creation and organisation of the acetylcholine receptor. Destruction of these proteins leads to inadequate acetylcholine receptors

350
Q

What is the typical presentation of myasthenia gravis?

A

Muscle fatigability (worsen on activity, improve on rest), extraocular muscle weakness (diplopia), proximal muscle weakness, ptosis, dysphagia, jaw fatigue, slurred speech

351
Q

What set of disorders is M.G associated with?

A

Autoimmune conditions (pernicious anaemia, autoimmune thyroid disorders, SLE, rheumatois)

352
Q

What are methods for eliciting fatigability in muscles in M.G examination?

A

Repeated blinking exacerbates ptosis, prolonged upward gazing exacerbates diplopia

353
Q

What are the investigations for myasthenia gravis?

A

Single fibre electromyography (nerve conduction studies: action potentials decrease after repeated stimulation), CT thorax to exclude thymoma, antibodies to ACh-AB

354
Q

What is the tensilon/edrophonium test, and why is it no longer used?

A

Patients given IV edrophonium chloride, which will reduce muscle weakness temporarily. Rarely done as risk of cardiac arrythmia

355
Q

What is the first line treatment of M.G?

A

Long acting acetylcholinesterase inhibitors; pyridostigmine is first line

356
Q

What medication is usually given alongside acetylcholinesterase inhibitors in AG?

A

Immunosuppression; usually prednisolone

357
Q

What is myasthenic crisis?

A

The potentially life threatening complication of myasthenia gravis which is usually triggered by another illness

358
Q

What is the treatment of myasthenic crisis?

A

Non-invasive ventilation or mechanical ventilation. Also give IV immunoglobulins and plasmapheresis

359
Q

What is the Barthel index?

A

A scale that measures disability or dependence in activities of daily living in stroke patients

360
Q

What anti emetic should be prescribed in Parkinsons?

A

Domperidone: it doesn’t cross the blood brain barrier and therefore doesn’t exacerbate symptoms of Parkinsons

361
Q

What is the inheritance of Huntingtons?

A

Autosomal dominant

362
Q

What occurs on a genetic level to cause huntingtons?

A

Trinucleotide repeat disorder involving a mutation which does for huntington

363
Q

Why is the way that Huntingtons is inherited particularly important?

A

Displays genetic anticipation, which is a feature of trinucleotide repeat disorders. Leads to earlier age of onset through generations and increased severity of disease

364
Q

What are the first features usually noticed in Huntingtons?

A

Begins with cognitive, psychiatric or mood problems. General personality changes

365
Q

What is seen in the mood disorder component of huntingtons?

A

Chorea, dystonia, rigidity, eye movement disorders, dysarthria, dysphagia

366
Q

How is huntingtons diagnosed?

A

Via genetic testing

367
Q

What is the treatment for huntingtons?

A

There is no medication that stops/slows the disease

368
Q

What is used to manage chorea in Huntingtons?

A

Tetrabenazine

369
Q

What is often the cause of death for someone with Huntingtons?

A

Aspiration pneumonia

370
Q

What is the prognosis for Huntingtons?

A

Around 20 years

371
Q

What is bulbar palsy?

A

Signs and symptoms linked to the impaired function of the lower cranial nerves

372
Q

Which nerves are typically affected in bulbar palsy?

A

9, 10, 11, 12 (the cranial nerves that arise directly from the brainstem)

373
Q

What symptoms are seen in bulbar palsy?

A

Depends on cranial nerve, but dysphagia, reduced gag reflex, slurred speech, dysphonia and difficulty articulating words (dysarthria), weakness of jaw and facial muscles

374
Q

What is the difference in presentation between bulbar palsy and pseudobulbar palsy?

A

In pseudobulbar palsy there is changes to emotions, whereas there are no changes in bulbar palsy. There will also be an exaggerated jaw jerk in pseudobulbar palsy

375
Q

What is damaged in pseudobulbar palsy?

A

Damage to UMN

376
Q

What are the causes of bulbar palsy?

A

Brainstem strokes and tumours, degenerative diseases (ALS, MND), autoimmune diseases (GBS), genetic conditions

377
Q

What is the inheritance of neurofibromatosis type 1?

A

Dominant

378
Q

What are 7 features of neurofibromatosis type 1?

A
  1. Cafe au lait spots
  2. Relative with RF1
  3. Axillary or inguinal freckling
  4. Bony dysplasia (presents as bowing of long bone)
  5. Iris haemartomas
  6. Neurofibromas
  7. Glioma of the optic pathway
379
Q

What is seen on eye examination in a patient with neurofibromatosis type 1?

A

Iris hamartomas (Lisch nodules): yellow brown spots on the iris

380
Q

What are neurofibromas?

A

Skin coloured, raised nodules with a smooth regular surface

381
Q

How many neurofibromas are required to be significant?

A

2 or more

382
Q

What is a plexiform neurofibromas?

A

Large, irregular, complex neurofibroma containing multiple cell types

383
Q

How many plexiform neurofibromas are significant?

A

More than 1

384
Q

What are the possible complications of neurofibromatosis?

A

Migraines, epilepsy, renal artery stenosis, learning disability, scoliosis of the spine, vision loss (due to optic nerve gliomas), malignant peripheral nerve sheath tumours, gastrointestinal stromal tumour, brain tumours, spinal cord tumours, increased general risk of cancer

385
Q

What are the possible oncological complications of neurofibromatosis type 1?

A

Gastrointestinal stromal tumour, malignant peripheral nerve sheath tumours, brain tumour, spinal cord tumours, and just general increased risk of cancer, phaeochromocytoma

386
Q

What might vision loss occur in neurofibromatosis type 1?

A

Due to optic nerve gliomas

387
Q

What is the pathophysiology of neurofibromatosis type 2?

A

Schwannomas form (benign tumours of schwann cells) due to mutation in the merlin protein, which is a tumour suppressor protein in Schwann cells

388
Q

What is a common association with neurofibromatosis type 2?

A

Bilateral acoustic neuromas (tumours of the auditory nerve)

389
Q

What size/frequency of cafe au lait spots are required to be significant?

A

More than 6, more than 15mm

390
Q

Why are regular blood pressure checks required in neurofibromatosis type 1?

A

Due to risk of pheochromocytomas

391
Q

What does phaeochromocytomas secrete an excessive amount of?

A

Catecholamines (adrenaline)

392
Q

Where is adrenaline produced?

A

In the chromaffin cells in the medulla of the adrenal cells

393
Q

What is the 10% rule in phaeochromocytomas?

A

10% bilateral, 10% cancerous, 10% outside the adrenal gland

394
Q

What are the presentations of phaeochromocytomas?

A

Related to excessive adrenaline: anxiety, sweating, headache, tremor, palpitations, HTN, tachycardia

395
Q

Why aren’t phaeochromocytomas dx via serum adrenaline?

A

Due to very short half life, this is not reliable

396
Q

What is the tests performed for phaeochromocytoma?

A

Plasma free metanephrines, 24-hour urine catecholamines

397
Q

What is the management of phaeochromocytomas?

A

Alpha blockers, beta blockers, surgical removal of the tumour

398
Q

What causes Wernicke’s encephalopathy?

A

Thiamine deficiency. Commonly in alcoholics, persistent vomiting

399
Q

What is the classic triad of Wernickes?

A

Ophthalmoplegia/nystagmus, ataxia, encephalopathy

400
Q

What are the features of encephalopathy in Wernicke’s?

A

Confusion, disorientation, indifference, inattentiveness –> personality change

401
Q

What is the pathophysiology of Wernicke’s encephalopathy?

A

Petechial haemorrhages in the brain

402
Q

What is the features of Korsakoff’s syndrome?

A

Wernickes triad + retrograde/anteretrograde amnesia, and confabulation

403
Q

What should the loss of corneal reflex make you consider?

A

Acoustic neuroma

404
Q

What is the cushing reflex?

A

A physiological nervous system response to increased intracranial pressure that results in HTN and bradycardia

405
Q

What is the largest risk factor for dementia?

A

Increasing age

406
Q

How can dementia only be definitively diagnosed?

A

Post mortem

407
Q

What manner inheritance is shown in Alzheimer’s disease (for those who have a genetic component)?

A

Autosomal dominant

408
Q

What are risk factors for Alzheimer’s disease?

A

Increasing age, FHx, genetics, caucasian, Down’s syndrome

409
Q

What is the macroscopic changes seen in Alzheimer’s?

A

Widespread cerebral atrophy, particularly involving the cortex and hippocampus

410
Q

What is the microscopic pathological changes seen in Alzheimers? How does this lead to disease?

A

Plaques due to deposition of beta-amylois protein, and intraneuronal neurofibrillary tangles due to abnormal aggregation of tau protein. This leads to reduction in transmissions in the brain, and death of cells

411
Q

What is the first line pharmocological treatment of Alzheimers?

A

Acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine)

412
Q

What is the second line treatment for Alzheimer’s?

A

Memantine

413
Q

When is donepezil used, and what is it’s contraindication?

A

First line tx of Alzheimers. C/I in patients with bradycardia

414
Q

What is the adverse effects of donepezil?

A

Insomnia

415
Q

Should antidepressants be used in patients with mild/moderate depression with dementia?

A

No

416
Q

What are levels of ACh usually reported as in patients with Alzheimers?

A

Reduced

417
Q

What is the most common presentation of Alzheimers?

A

Memory loss, particularly recent. Associated changes in planning, reasoning, speech and orientation

418
Q

What is memory loss is depression like in comparison to dementia?

A

Global memory loss in depression, recent memory loss in dementia

419
Q

What are the risk factors of vascular dementia?

A

Hx of stroke/TIA, AF, HTN, DM, hyperlipidaemia, smoking, obesity, CHD

420
Q

How do patients with vascular dementia typically present?

A

Stepwise deterioration of cognitive impairment

421
Q

What are typical features of vascular dementia?

A

Focal neurological abnormalities (visual disturbance, sensory, motor symptoms), difficulty with attention/concentration, seizures, memory + speech + gait disturbance, mood disturbance and disorders

422
Q

How is vascular dementia diagnosed?

A

MRI can show infarcts and extensive white matter changes. Can also do CT

423
Q

What areas of the brain are most affected by vascular dementia?

A

White matter of hemispheres, grey nuclei, thalamus, striatum

424
Q

What is the management of vascular dementia?

A

Generally symptomatic, and reducing cardiovascular risk factors to reduce progression. No use of AChE inhibitors or memantine is indicated

425
Q

What type of dementia is associated with MND?

A

Frontotemporal dementia (Pick’s disease)

426
Q

What is the pathophysiology of Lewy Body dementia?

A

Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas

427
Q

What disease is strongly associated with Lewy body dementia?

A

Parkinsons

428
Q

What are the features of LewyBody dementia?

A

Progressive cognitive impairment comes first, then parkinsonism (triad), visual hallucinations

429
Q

What is unique about cognition impairment in Lewy Body dementia in comparison to other dementias?

A

Cognition may be fluctuating, which is unique

430
Q

What is the diagnosis of a patient with visual hallucinations and dementia?

A

LewyBody dementia

431
Q

How does Lewy Body dementia typically present?

A

Problems multitasking and performing complex cognitive actions (rather than memory)

432
Q

What dementia classical affects younger people?

A

Frontotemporal dementia (including Pick’s disease)

433
Q

What are the three recognised types of frontotemporal lobar degeneration?

A
  • frontotemporal dementia (Pick’s disease)
  • semantic dementia
  • progressive non fluent aphasia
434
Q

What are the common features of frontotemporal lobar dementias?

A

Onset before 65 years, insidious onset, relatively preserved memory and visuospatial skills, personality change and social conduct problems

435
Q

How does Pick’s disease typically present?

A

Personality change, impaired social conduct, disinhibition, increased appetite

436
Q

What is seen on imaging in Pick’s disease?

A

Focal gyral atrophy with a knife blade appearance

437
Q

What is the microscopic changes in Pick’s disease?

A
  • Pick bodies (spherical aggregations of tau protein)
  • neurofibrillary tangles
  • plaques
438
Q

What are the features of progressive non fluent aphasia (type of frontotemporal lobar degeneration)

A

Non fluent speech, issues with grammar and literacy skills

439
Q

What category of dementias does semantic dementia fall under?

A

Frontotemporal lobar degeneration

440
Q

What is the presentation of semantic dementia?

A

Decline in understanding of word meaning, issues with word retrieving. Empty speech with no meaning. Memory better for recent events than remote ones

441
Q

What are differential dx for dementia?

A

Prion protein diseases (CJD), HIV dementia, normal pressure hydrocephalus, severe depression, mild cognitive impairment, late syphilis

442
Q

What is Creutzfeldt-Jakob disease?

A

Rapidly progressive neurological condition caused by prion proteins. Causes the brain to fold abnormally. Sporadic or variant

443
Q

What is the aetiology of variant CJD?

A

Caused by meat infected by bovine spongiform encephalopathy

444
Q

What is the disease course of CJD?

A

Disease can be indolent for many years. Then presents as minor memory lapses, mood disturbance, loss of interest. Quickly becomes more prominent, with unsteadiness, stiffness, jerking movements, incontinence. Death occurs within 6 months.

445
Q

What is normal pressure hydrocephalus?

A

Secondary to reduced CSF absorption at the arachnoid villi

446
Q

What is the common causes of normal pressure hydrocephalus?

A

Head injury, SAH, meningitis

447
Q

What is the classic triad of normal pressure hydrocephalus?

A

Urinary incontinence, dementia, gait abnormality (wet, wacky, wobbly)

448
Q

What is seen on imaging of normal pressure hydrocephalus?

A

Ventriculomegaly in the absence of, or out of proportion, to sulcal enlargement

449
Q

What is the treatment of normal pressure hydrocephalus?

A

VP shunt: can reverse the condition

450
Q

Where is CSF produced, and where is it absorbed?

A

CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles. CSF is absorbed into the venous system by the arachnoid granulations.

451
Q

What is the most common cause of paediatric hydrocephalus?

A

Aqueductal stenosis, leading to insufficient drainage of CSF

452
Q

What are possible congenital causes of paediatric hydrocephalus?

A

Arachnoid cysts, arnold-Chiari malformation, chromosomal abnormalities

453
Q

What is arnold chiari malformation?

A

Where the cerebellum herniates downwards through the foramen magnum, blocking CSF outflow

454
Q

How to children with hydrocephalus typically present?

A

Rapidly enlarging head circumference, bulging anterior fontanelle, poor feeding and vomiting, poor tone, sleepiness

455
Q

What are possible VP shunt complications?

A

Infection, blockage, excessive drainage, intraventricular haemorrhage during shunt related surgery

456
Q

What factors suggest depression over dementia?

A

Short history, rapid onset, biology symptoms (weight loss, sleep disturbance), patient worried about poor memory, reluctant to take tests + dissappointed with results, variable MMSE results, global memory loss

457
Q

How are MMSE results interpreted?

A

Any score of 24 or more indicates a normal cognition. Below this can indicate Alzheimers

458
Q

What is mild cognitive impairment?

A

Term used for those with memory problems or higher cortical thinking, but not severe enough to interfere with everyday life

459
Q

Why might AF and anaemia worsen cognitive impairment?

A

Leads to mild brain hypoxia

460
Q

What is pellagra? What causes it

A

Deficiency disease of vitamin niacin (B3)

461
Q

What groups of people are more at risk of pellagra?

A

Those having isoniazid therapy (TB), and alcoholics

461
Q

What are the classical symptoms of Pellagra?

A

Dermatitis, diarrhoea, dementia, death if not treated

462
Q

What are possible reversible causes of dementia?

A

Subdural haematoma, normal pressure hydrocephalus, vitamin deficiency, hypothyroidism

463
Q

What factors indicate a diagnosis of delirium is more likely than dementia?

A

Acute onset, impairment of consciousness, fluctuation of symptoms (worse at night), abnormal perceptions (hallucinations), agitation, fear, delusions, inattention

464
Q

What factors increase risk of delirium?

A

> 65 years, hx of dementia, significant injury (eg, hip fracture), frailty or multimorbidity, polypharmacy

465
Q

What is delirium?

A

Acute confusional state that causes disturbed consciousness, attention, congition and perception

466
Q

What are possible causes of delirium?

A

Infection (particularly UTI), metabolic (hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration), change of environment, severe pain, alcohol withdrawal, constipation, hypothermia, organ dysfunction, new medications, nutrition changes

467
Q

What are the features of delirium?

A

Memory disturbances (loss of short term), agitation, withdrawn, disorientation, mood change, visual hallucinations, disturbed sleep, poor attention

468
Q

What are the three types of delirium?

A

Hypoactive, hyperactive, mixed

469
Q

What is the presentation of hyperactive delirium?

A

Agitation, delusions, hallucinations, wandering, aggression

470
Q

What are the symptoms of hypoactive delirium?

A

Lethargy, slowness w/ everyday tasks, excessive sleeping, inattention

471
Q

What is the management of delirium?

A

Treat the cause. First line medication is haliperidol

472
Q

What is the first line medication in delirium?

A

Haloperidol

473
Q

What cognitive tests can be used in delirium?

A

CAM (confusion assessment method), 4A’s test, AMT (abbreviated mental test)

474
Q

What is the investigations in delirium?

A

ECG, cultures, FBC, U+Es, LFTs, calcium, HbA1c, CRP, drug levels, syphilis serology, CXR, CT head

475
Q

What is Sundowner syndrome in dementia?

A

As evening approaches confusion increases and there is more falls

476
Q

What is the mechanism that causes the presentations of alcohol withdrawal?

A

Chronic alcohol consumption enhances GABA mediation and inhibits glutamates. Thus opposite in withdrawal (less GABA, more glutamate)

477
Q

When do features of alcohol withdrawal begin?

A

6-12 hours

478
Q

What features are seen at 6-12 hours after alcohol withdrawal?

A

Tremor, sweating, tachycardia, anxiety, nausea and vomiting

479
Q

What symptom is at peak incidence at 36 hours after alcohol withdrawal?

A

seizures

480
Q

What is the peak incidence of delirium tremens after alcohol withdrawal?

A

48-72 hours

481
Q

What symptoms are seen in delirium tremens?

A

Coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia, autonomic hyperactivity

482
Q

What is first line in management of alcohol withdrawal?

A

Long acting benzo: chlordiazepoxide or diazepam

483
Q

What is the treatment of Wernicke’s?

A

Pabrinex IV (vitamin B and C), and thiamine

484
Q

What vessel sizes are affected in temporal arteritis?

A

Medium and large sized vessels

485
Q

What condition has a strong link with giant cell arteritis?

A

Polymyalgia rheumatica

486
Q

What are the features of polymyalgia rheumatica?

A

Rapid onset acheing morning stiffness in proximal limb muscles (girdle) with no weakness. Also lethargy, depression, low grade fever, anorexia, night sweats

487
Q

What is the treatment of polymyalgia rheumatica?

A

Prednisolone: if no response, consider alternative diagnosis

488
Q

What is seen on investigation of polymyalgia rehumatica?

A

Raised inflammatory markers, normal creatine kinase

489
Q

What is the main complication of giant cell arteritis?

A

Irreversible vision loss

490
Q

What age is a typical patient with giant cell arteritis?

A

> 60 years old

491
Q

What are the features of giant cell artertis?

A

Unilateral headache (severe, around temple and jaw), scalp tenderness, jaw claudication, blurred or double vision, amaurosis fugax (though may become permanent)

492
Q

What might be noticed on examination of the face in giant cell arteritis?

A

Temple artery may be tender and thickened to palpate, with reduce/absent pulsation

493
Q

What is a key testing in all patients with giant cell arteritis?

A

Vision testing

494
Q

Why would diplopia occur in giant cell arteritis?

A

If there is involvement of the cranial nerves

495
Q

What is the main ocular complication in giant cell arteritis?

A

Anterior ischaemic optic neuropathy (leads to ischaemic of the optic nerve head)

496
Q

What is seen on fundoscopy of giant cell arteritis?

A

Anterior ischaemic optic neuropathy; swollen pale disc and blurred margins

497
Q

What investigations are done in giant cell arteritis?

A

Raised inflammatory markers, temporal artery biopsy, ultrasound of temporal artery

498
Q

What is seen on duplex ultrasound in giant cell arteritis?

A

Halo sign, and stenosis of the temporal artery

499
Q

What is the immediate treatment of GCA?

A

High dose steroids: no visual loss then high dose prednisolone, if evolving visual loss then methylprednisolone first then prednisolone

500
Q

When should steroids be given in GCA?

A

Immediately: before temporal artery biopsy

501
Q

What is long term management in GCA patients?

A
  • bone protection with bisphosphonates due to long course of steroids required
  • low dose aspirin
  • PPI for gastroprotection on steroids
502
Q

What is the diagnosis criteria for chronic fatigue syndrome?

A

Disabling fatigue for 3 months, for more than 50% of time, affecting mental and physical function in absence of other disease which could explain symptoms

503
Q

What are the features of chronic fatigue syndrome?

A

Fatigue made worse by activity and not relieved by rest, sleep problems (insomnia, hypersomnia, unrefreshing sleep), muslce/joint pains, headaches, painful lymph nodes, sore throat, cognitive dysfunction, flu like symptoms, dizziness, nausea, palpitations

504
Q

How long must symptoms be present for chronic fatigue syndrome to be diagnosed?

A

3 months

505
Q

What investigations should be carried out for chronic fatigue syndrome?

A

Large numbers of screening blood tests to exclude other pathology (eg, FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screen)

506
Q

What is the management for chronic fatigue syndrome?

A
  • refer to specialist service
  • energy management (spoons theory)
  • only physical exercise where possible for them
  • CBT
507
Q

What are the features of Horner’s syndrome?

A

Miosis (small pupil), ptosis, enopthalmos (sunken eye), anhidrosis (loss of sweating on one side)

508
Q

Where does head/arm/trunk anhidrosis suggest the lesion is and what has potentially caused it?

A

Central lesion. Caused by Stroke, spingomyelia, MS, brain tumours

509
Q

Where is the lesion if there is anhidrosis of only the face? What are possible causes?

A

Pre-ganglionic lesion. Pancosts tumour (apical lung cancer), trauma, thyroidectomy

510
Q

Where is the lesion if there is Horner’s syndrome without anhidrosis? What could cause this?

A

Post ganglionic. In carotid artery (dissection) or cavernous sinus thrombosis

511
Q

What causes Horner’s syndrome?

A

Lesion of the sympathetic chain supplying the eye

512
Q

What structures does the sympathetic nervous system supply in the eye?

A

Dilator pupillae (dilation of the pupil), sweat gland, muscle response for raising upper eyelid

513
Q

How is Horner’s syndrome classified?

A

Via the site of the lesion in the sympathetic chain. There are three consecutive neurons which transmit signals from the hypothalamus to the eye

514
Q

What type of Stroke does Central Horner’s typically present with?

A

Lateral medullary syndrome (posterior inferior cerebellar artery) –> ipsilateral ataxia, dysphagia, ipsilateral facial pain and temperatre loss, nystagmus

515
Q

Where does the first order neurone of the sympathetic chain run between?

A

Hypothalamus and T1 spinal cord

516
Q

Where does the second order neurone of the sympathetic chain run between?

A

T1 spinal cord to the superior cervical ganglion. Goes near to the upper lobe of the lung and subclavian artery

517
Q

Where does the third order neurone of the sympathetic chain run between?

A

From superior cervical ganglion to the cavernous sinus, where sympathetic fibres join the ophthalmic nerve

518
Q

What is a classic finding in congenital Horner’s syndrome?

A

Iris heterochromia

519
Q

How does Pancoast’s tumour present?

A

Horners syndrome with anhidrosis of the face, shoulder pain, upper limb neurological symptoms

520
Q

How is Horner’s diagnosed (if clinical signs unclear)

A

Eye drops: apraclonidine which will reverse pupillary constriction in Horners, but not in a normal pupil

521
Q

How is Horners syndrome treated?

A

By treating the cause!

522
Q

How is neuropathic pain treated?

A

Amitriptyline, duloxetine, gabapentin, pregabalin

523
Q

How does diabetic neuropathy typically present?

A

Sensory loss, not motor. This is typically in a glove and stocking distribution. Lower lengths affected first

524
Q

What can be used as rescue therapy in exacerbations of neuropathic pain?

A

Tramadol

525
Q

How is diabetic neuropathy managed?

A

The same way as other forms of neuropathic pain (amitriptyline, duloxetine, gabapentin, pregabalin)

526
Q

What should be used for localised neuropathic pain?

A

Topical capsaicin

527
Q

What two types of neuropathy can occur in diabetes?

A

Peripheral neuropathy and gastrointestinal autonomic neuropathy

528
Q

How does gastrointestinal autonomic neuropathy present?

A

Gastroparesis, chronic diarrhoea, GORD

529
Q

What are the symptoms of gastroparesis?

A

Erratic blood glucose control, bloating, vomiting

530
Q

How is gastroparesis managed?

A

Metoclopramide, domperidone, erythromycin

531
Q

What are causes of predominantly motor loss peripheral neuropathy?

A

GBS, lead poisoning, Charcot Marie Tooth, diphtheria

532
Q

What causes predominantly sensory loss peripheral neuropathy?

A

Diabetes, uraemia, leprosy, alcoholism, B12 deficiency, amyloidosis

533
Q

What occurs in vitamin B12 deficiency that leads to peripheral neuropathy?

A

Subacute combined degeneration of the spinal cord. Dorsal column affected first

534
Q

What does the dorsal column convey?

A

Fine touch vibration, two point discrimination, proprioception

535
Q

What does the spinothalamic tract convey?

A

Pain, thermal stimuli, pressure, crude touch

536
Q

What is Phalen’s test?

A

Assess Carpal tunnel. Hold wrist in maximum flexion, and if the test is positive there is numbness in the median nerve distribution

537
Q

What type of headache occurs in migraine?

A

Severe, unilateral, throbbing, aggravated by physical activity

538
Q

How do migraines present in children?

A

Can be bilateral, more commonly also have GI disturbance

539
Q

How long do migraine attacks last?

A

Up to 72 hours

540
Q

What sort of aura is seen in migraine?

A

Visual, progressive, last 5-60 minutes

541
Q

What gender are migraines more common in?

A

Women

542
Q

What are common triggers for migraines?

A

Tiredness, stress, alcohol, COC, lack of food or dehydration, cheese, chocolate, red wine, menstruation, bright lights

543
Q

How many migraine attacks must have occurred for a diagnosis to be made?

A

At least 5

544
Q

What is a hemiplegic migraine?

A

A variant of migraine in which motor weakness is a manifestation of aura

545
Q

What percentage of migraines present with an aura?

A

25%

546
Q

What are atypical aura symptoms that should be investigated?

A

Motor weakness, double vision, visual symptoms affecting only one eye, poor balance, decreased level of consciousness

547
Q

What is the general rule of migraine management in terms of drug classes?

A

5-HT agonists are used in acute treatment, 5-HT receptor antagonists are used in prophylaxis

548
Q

What is first line treatment in acute migraine attack?

A

Oral triptan + NSAID, or oral triptan and paracetamol

549
Q

What can be added onto acute first line migraine treatment?

A

Anti emetics: metoclopramide, domperisone, prochloperazine

550
Q

Why should metoclopramide not be prescribed to young people?

A

Increased risk of acute dystonic reaction

551
Q

When should migraine prophylaxis be given?

A

When there is significant impact on quality of life, and occur frequently

552
Q

What is the first line migraine prophylaxis?

A

Propanolol or topiramate (teratogenic!) or amitriptyline

553
Q

What vitamin medication may reduce migraines?

A

Riboflavin (Vit B2)

554
Q

What is the treatment for women with predictable menstrual migraine treatment?

A

Frovatriptan or zolmitriptan

555
Q

What is first line medication of migraine in pregnancy?

A

Paracetamol

556
Q

What is second line management of migraine in pregnancy?

A

NSAIDs (only 1st and 2nd trimester)

557
Q

Why can some migraine patients not have the COC?

A

If migraine with aura, due to increased risk of stroke

558
Q

Can patients with history of migraines be prescribed HRT?

A

Yes, but may make migraines worse

559
Q

What are the four types of migraine?

A

With aura, without aura, silent (with aura but no headache), hemiplegic

560
Q

What are the 5 stages of migraine?

A

Prodromal, aura, headache, resolution, post dromal

561
Q

What is the strongest risk factor for hemiplegic migraine?

A

Family history: autosomal dominant condition

562
Q

What is the drug class of triptans?

A

5-HT receptor agonists

563
Q

What is the MoA of triptans?

A

Cranial vasoconstriction, inhibition of transmission of pain signals, inhibiting the release of inflammatory neuropeptides

564
Q

How many doses of triptans can be taken in migraine?

A

2 (Additional one taken if the first doesn’t work)

565
Q

What are contraindications for triptans?

A

Being on SSRIs, HTN, coronary artery disease, previous stroke, TIA (aka risks related to vasoconstriction)

566
Q

What is a tension headache?

A

Recurrent, bilateral headache, non-disabling, often described as a ‘tight band’

567
Q

Who are cluster headaches more common in?

A

Men and smokers

568
Q

What is the frequency and duration of cluster headaches?

A

Once or twice a day, episodes lasting 15 mins -2 hours, clusters lasting 4-12 weeks

569
Q

What are the symptoms of cluster headaches?

A

Intense pain around eye (always same side), patient restless during attack, accompanied by redness, lacrimation, lid swelling

570
Q

What is the typical presentation of medication overuse headache?

A

Present for 15 days or more per month, despite using regular sumitriptan

571
Q

What are possible causes of acute single episode of headache?

A

Meningitis, encephalitis, SAH, head injury, sinusitis, glaucoma (acute closed angle), tropical illness (eg, malaria)

572
Q

What are possible causes of chronic headache?

A

Chronically raised ICP, Paget’s disease, psychological

573
Q

What is the most common cause of primary headache in children?

A

Migraine without aura

574
Q

What are the side effects of triptans?

A

Tingling, heat, heaviness/pressure sensations

575
Q

What is the first line in children for migraine?

A

Ibuprofen (more effective than paracetamol in kids)

576
Q

When can triptans be used in children, and what type is preferred?

A

If over 12, and oral spray is preferred

577
Q

What is the second most common cause of headache in children?

A

Tension type headache

578
Q

What are red flags for headaches?

A

Immunocompromised, under 20 + hx of malignancy, hx of malignancy to brain, vomiting without other obvious cause, w/ fever, thunderclap, new onset neurological deficit, new onset cognitive dysfunction, change in personality, impaired level of consciousness, recent head trauma, triggered by cough/sneeze/valsalva , changes with posture, change in character of headache

579
Q

What are sinister signs of headaches that require urgent head CT?

A

Cognitive dysfunction, impaired level of consiousness, thunderclap

580
Q

What are the features of post lumbar puncture headache?

A

Develops a day after LP, lasts several days, worsens when upright, improves lying down

581
Q

Who are post LP headaches more common in?

A

Women with low BMI

582
Q

What are factors that contribute to potential post LP headache?

A

Increased needle size, direction of bevel, increased number of LP attempts

583
Q

Does opening pressure + volume of CSF removed in an LP affect the change of a post LP headache?

A

Nope

584
Q

What is the treatment for post LP headache?

A

Initially supportive, eventually may need epidural saline and IV caffeine

585
Q

What can trigger an attack of cluster headaches?

A

Alcohol

586
Q

What is the investigation of choice in cluster headaches?

A

MRI with contrast (sometimes there are underlying brain lesions)

587
Q

What is the acute treatment of cluster headaches?

A

100% oxygen, subcut triptan

588
Q

What is the prophylaxis of cluster headaches?

A

Verapamil

589
Q

What can differentiate a tension headache from a migraine?

A

Bilateral, lower intensity, no aura or N+V or aggravation by physical activity

590
Q

What is the definition of a chronic tension type headache?

A

Present on 15 or more days per month

591
Q

What is the acute treatment of tension type headache?

A

aspirin, paracetamol or NSAID

592
Q

What is prophylaxis of tension headache?

A

NOT TRIPTANS! Course or acupuncture

593
Q

Which patients are most at risk of medication overuse headache?

A

Patients using opioids or triptans

594
Q

What is the management of medication overuse headache?

A

Withdraw simple analgesic and triptans abruptly. Opioid analgesic withdrawn gradually

595
Q

What investigations can be done in migraine to identify red flag causes? (not radiological)

A

Fundoscopy for papilloedema

596
Q

Why is it worrying if ipsilateral signs start in a patient who has had a cerebrovascular event?

A

Midline has occurred and the other side has started to be affected

597
Q

Why is it worrying if a pupil is blown in a patient who has had a cerebrovascular event?

A

Means that the brain is starting to cone (herniation), as it is compressing the 3rd nerve nucleus in the midbrain

598
Q

What side is most people’s language centres located?

A

Left

599
Q

When are hormonal headaches more likely to occur?

A

Two days before or 3 days after the menstrual period, in the perimenopausal period, early pregnancy

600
Q

What is cervical spondylosis and how does it typically present?

A

Common condition that results from OA. Presents as neck pain that may be referred and mimic headaches

601
Q

What are possible complications of cervical spondylosis?

A

Radiculopathy and myelopathy

602
Q

What is radiculopathy?

A

Pinched nerve: an injury or damage to nerve roots in the area where they leave the spine

603
Q

What is myelopathy?

A

An injury to the spinal cord caused by severe compression that may be due to spinal stenosis, disc degeneration, disc herniation, AI disorders, trauma

604
Q

What causes brain abscess?

A

Extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries, embolic events from endocarditis

605
Q

What is the presentation of brain abscess?

A

Depends on the site. Also: headache, fever, focal neurology. Symptoms of raised intracranial pressure (nausea, papilloedema, seizures)

606
Q

What is the primary infection of a suspected brain abscess? How does it present?

A

MRI: ring enhancing lesion with surrounding oedema

607
Q

What is the management of brain abscess?

A

Surgery (craniotomy + drainage), IV abx (IV ceft/cefotaxime + metronidazole), intracranial pressure management (eg, dexamethasone)

608
Q

What is normal ICP?

A

7-15

609
Q

What is cerebral perfusion pressure and how is it calculated?

A

Net pressure gradient causing cerebral blood flow to the brain. CPP=mean arterial pressure-ICP

610
Q

What causes raised ICP?

A

Idiopathic intracranial HTN, traumatic head injury, infection (meningitis, abscess), tumours, hydrocephalus

611
Q

What is Cushing’s triad?

A

Widening pulse pressure, bradycardia, irregular breathing

612
Q

How is raised ICP investigated/monitored?

A

Neuroimaging, invasive ICP monitoring

613
Q

What is the cutoff for determining if further treatment is needed to reduce ICP?

A

> 20 mmHg

614
Q

What is the management of raised ICP?

A

Head elevation to 30 degrees, IV mannitol, controlled hyperventilation, removal of CSF (shunt/drain/LPs in idiopathic intracranial HTN)

615
Q

When is controlled hyperventilation used?

A

In raised ICP

616
Q

How is controlled hyperventilation helpful in raised ICP?

A

Reduces pCO2 which leads to vasoconstriction of cerebral arteries, which reduces ICP

617
Q

What are risk factors for idiopathic intracranial HTN?

A

Obesity, female, pregnancy, certain drugs

618
Q

What drugs can cause Idiopathic intracranial HTN?

A

COCP, steroids, tetracyclines (doxycycline), lithium

619
Q

What cranial nerve is most likely to be affected by idiopathic intracranial HTN?

A

6th (abducens) (because of its long course)

620
Q

What are the features of idiopathic intracranial hypertension?

A

Headache, blurred vision, papilloedema, enlarged blind spot, 6th nerve palsy

621
Q

What is the lifestyle management of idiopathic intracranial HTN?

A

Weight loss

622
Q

What is the medical/surgical management of idiopathic intracranial hypertension?

A

Carbonic anhydrase inhibitors (acetazolamide), as they reduced CSF production at the choroid plexus. Topiramate also inhibits it. Can do repeated lumbar puncture

623
Q

What is GBS?

A

Acute paralytic polyneuropathy affecting the PNS

624
Q

What are common causative organisms of GBS?

A

Campylobacter jejuni, CMV, EBV

625
Q

What is the pathophysiology of GBS?

A

B cells create antibodies against the antigens on the triggering pathogens, which also match the proteins of the peripheral neurones. They target the myelin sheath or nerve axon itself

626
Q

What antibodies are typically found in GBS?

A

anti-GM1 antibodies (anti ganglioside)

627
Q

What is Miller Fisher syndrome?

A

Variant of Guillain Barre syndrome: descending paralysis. Eyes are typically affected first, also ataxia.

628
Q

What is the most common symptom seen in initial stages of illness in GBS?

A

Back/leg pain

629
Q

What are the characteristic features of Guillain Barre syndrome?

A

Progressive, symmetrical weakness of all limbs, ascending. Reduced/absent reflexes. Few sensory signs

630
Q

What is the differential diagnosis if there is symmetrical limb weakness following gastroenteritis?

A

GBS

631
Q

What are later stage symptoms of GBS?

A

respiratory muscle weakness, cranial nerve involvement

632
Q

What is the first line investigation in GBS? What also may be done?

A

Lumbar puncture: rise in protein with normal WBC. Also, nerve conduction studies which will show decreased motor nerve conduction velocity

633
Q

What is first line management of GBS?

A

Iv immunoglobulins

634
Q

What is the leading cause of death in GBS and thus what prophylaxis should be given?

A

Pulmonary embolism is leading cause. VTE prophylaxis should be given

635
Q

Does unilateral cerebellar lesions cause ipsilateral or contralateral lesions?

A

Ipsilateral

636
Q

What are the symptoms of cerebellar disease?

A

DANISH. Dysdiadochokinesia/dysmetria (past pointing), ataxia (limb, truncal), nystagmus (horizontal), intention tremour, slurred speech, hypotonia

637
Q

What are causes of cerebellar syndrome?

A

Friedreich’s ataxia, neoplasms (cerebellar haemangioma), stroke, alcohol, MS, hypothyroidism, brain mets (eg, secondary to lung cancer)

638
Q

What is Friedreich’s ataxia?

A

Early onset ataxia

639
Q

What is the inheritance of Friedreich’s ataxia?

A

Autosomal recessive

640
Q

How does Friedreich’s ataxia present?

A

Gait ataxia and kyphoscoliosis in young teenagers

641
Q

What are the neurological signs Friedreich’s ataxia?

A

Absent ankle jerks, cerebellar ataxia, optic atrophy, spinocerebellar tract degeneration

642
Q

What is the most common cause of death in Friedreich’s ataxia?

A

Hypertrophic obstructive cardiomyopathy

643
Q

What are the features of encephalitis?

A

Fever, headache, psychiatric symptoms, seizures, vomiting, focal features

644
Q

What causes encephalitis most commonly?

A

Herpes zoster virus 1

645
Q

What areas of the brain are most likely to be affected by encephalitis?

A

Temporal and inferior frontal lobes

646
Q

What are the investigations of encephalitis?

A

LP: high white cells, elevated proteins, and do PCR for HSV/VZV. Neuroimaging (MRI), and EEG

647
Q

What is the management of suspected encephalitis?

A

IV aciclovir: start immediately

648
Q

What is first line imaging in encephalitis?

A

MRI

649
Q

What characteristically causes temporal lobe encephalitis?

A

Herpes simplex

650
Q

How does primary infection of herpes simplex virus often present?

A

Severe gingivostomatitis (infection of the mouth and gums, with swelling)

651
Q

What causes malaria?

A

Plasmodium protozoa. There are four types, but plasmodium falciparum causes nearly all episodes, and plasmodium causes some

652
Q

What are protective factors against malaria?

A

G6PD deficiency, HLA-B53

653
Q

What are the features of severe malaria?

A

Schizonts on a blood film, parasitaemia >2%, hypoglycaemia, acidosis, pyrexia, severe anaemia, experiencing complications

654
Q

What are possible complications of malaria?

A

Cerebral malaria (seizures, coma), acute renal failure, acute respiratory distress syndrome, hypoglycaemia, DIC

655
Q

What are first line treatment of uncomplicated malaria?

A

Artemisinin-based combination therapies. Usually artemether with lumefantrine

656
Q

What vector spreads malaria?

A

Female anopheles mosquitos

657
Q

What is the presentation of malaria?

A

Unspecific: fever (very high and spikes at 48 hours), fatigue, myalgia, headache, nausea, vomiting

658
Q

What signs are seen on examination in malaria?

A

Pallor due to anaemia, hepatosplenomegaly, jaundice

659
Q

How is malaria diagnosed, and how is it proven to be negative?

A

Malaria blood film (shows parasite, concentration, and type). Three negative samples needed over 3 consecutive days due to parasites being released from red blood cells into the blood every 48-72 hours

660
Q

What is the treatment for severe or complicated malaria?

A

Artesunate

661
Q

What are acoustic neuromas?

A

Vestibular Schwannomas: a cerebellopontine angle tumour

662
Q

What is the classical history of vestibular schwannoma?

A

Combination of vertigo, hearing loss, tinnitus, absent corneal reflex

663
Q

What cranial nerves are involved in Vestibular schwannoma?

A

5, 7, 8,

664
Q

What is an important differential in unilateral hearing loss or tinnitus?

A

Vestibular schwannoma

665
Q

What is the first line investigation for vestibular schwannoma?

A

MRI of the cerebellopontine angle. Also audiometry

666
Q

What are the symptoms of spinal metastases?

A

Unrelenting lumbar back pain, any thoracic or cervical back pain, worse with coughing/sneezing, nocturnal, associated with tenderness. Later: neurological features

667
Q

What is the most common form of brain cancer?

A

Metastatic

668
Q

What are the 2 important features of brain mets?

A

There are often multiple, and often not treatable with surgical intervention

669
Q

What tumour most commonly spread to the brain?

A

Lung, breast, bowel, skin (melanoma), kidney

670
Q

What tumour most commonly spreads to the brain?

A

Lung

671
Q

What is gliobastoma multiforme? What is their unique feature?

A

Highly malignant and invasive brain tumour which crosses the corpus callosum (midline)

672
Q

What is the most common primary brain tumour in adults?

A

GMB (glioblastoma multiforme)

673
Q

How are GBMs treated?

A

Surgery with postoperative chemo and/or radiotherapy. Dexamethasone to treat oedema

674
Q

How do GBMs appear on imaging?

A

Solid tumours with central necrosis and rim that enhances with contrast

675
Q

What is olgiodendroma? How do they appear on histology?

A

Benign and slow growing tumour. On histology: fried egg appearance

676
Q

What are meningiomas?

A

Benign, superficial (extrinsic), arachnoid origin

677
Q

What are the symptoms of meningiomas?

A

Compression rather than invasion: can cause very late onset of symptoms!

678
Q

How do meningiomas present on histology?

A

Spindle cells + psammoma bodies?

679
Q

What is haemangioblastoma, and what syndrome is it associated with?

A

Vascular tumour of the cerebellum, can produce EPO. Associated with von Hippel-Lindau syndrome (syndrome that causes haemangioblastomas of multiple locations)

680
Q

What are the two types of pituitary adenoma?

A

Secretory or non secretory

681
Q

What are the common presentations of pituitary adenoma?

A

Bitemporal hemianopia due compression of optic chiasm (due to closeness) due to mass effect. Also consequences of hormone excess. Headache

682
Q

What surgery is done in pituitary adenoma?

A

Transphenoidal resection

683
Q

What is the most common brain tumour in children?

A

Pilocytic astrocytoma

684
Q

What brain tumour is a remnants of Rathke’s pouch?

A

Craniopharyngioma

685
Q

What is cerebral palsy?

A

The disorder of movement and posture due to a non progressive lesion of the motor pathways of the developing brain

686
Q

What are the antenatal causes of cerebral palsy?

A

Maternal infections, trauma around pregnancy

687
Q

What are the perinatal causes of cerebral palsy?

A

Birth asphyxia, pre-term birth

688
Q

What are postnatal causes of cerebral palsy?

A

Meningitis, severe neonatal jaundice, head injury

689
Q

What are the 4 types of cerebral palsy?

A

Spastic, dyskinetic, ataxic, mixed

690
Q

What causes spastic cerebral palsy, and what are the features?

A

Damage to UMN. Hypertonia and reduced function.

691
Q

What causes dyskinetic cerebral palsy, and what are the features?

A

Damage to the basal ganglia. Presents as issues controlling muscle tone, with hypertonia and hypotonia. Causes athetosis (slow, writhing movements of distal extremities), and oro-motor problems

692
Q

What causes ataxia cerebral palsy, and what are the features?

A

Cerebellum. Issues with coordinating movement

693
Q
A
694
Q

What are the four patterns of spastic cerebral palsy?

A

Monoplegia, hemiplegia, diplegia, quadraplegia

695
Q

What are signs and symptoms of cerebral palsy?

A

Failure to meet milestones, increased or decreased tone, hand preference before 18 months, problems with coordination/speech/walking, feeding or swallowing problems, learning difficulties

696
Q

What gait indicates an upper motor neurone lesion?

A

Hemiplegic/diplegic gait (gait where the leg is held stiffly and abducted with each step and swung around to the ground infront).

697
Q

What gait indicates a cerebellar lesion?

A

Broad based/ataxic gait

698
Q

What does a high stepping gait indicate?

A

Foot drop of LMN

699
Q

What does waddling gait suggest?

A

Pelvic muscle weakness due to myopathy

700
Q

What does gait in cerebral palsy present as?

A

Diplegic gait. Abnormally narrow base, dragging both legs and scrapping toes. Can have some circumduction. Arms will likely be flexed

701
Q

What are complications and associated conditions with cerebral palsy?

A

Learning disability, epilepsy, kyphoscoliosis, muscle contractures, hearing and visual impairment, GORD

702
Q

What is the treatment of spasticity in children with cerebral palsy?

A

Oral diazepam, baclofen, surgery (release tendons)

703
Q

What treatment might be offered to neonates with hypoxic ischaemic encepholopathy?

A

Therapeutic cooling: reduces neuronal damage

704
Q

What causes hypoxic ischaemic encepholopathy?

A

Hypoxic perinatal brain injury: caused by a decrease in the amount of oxygen supplied to infant’s brain during labour

705
Q

What is the pathophysiology of hypoxic brain birth injuries?

A

Biphasic model of neuronal death: death at time of insults and secondary death. Therapeutic cooling can reduce extent of secondary neuronal death

706
Q

When is hypoxic ischaemic encepholopathy in neonates?

A

Acidosis on umbilical artery blood gas, poor apgar scores, multi organ failure, seizures

707
Q

What are examples of causes of hypoxic-ischaemic encepholopathy?

A

Maternal shock, intrapartum haemorrhage, prolapsed cord, nuchal cord

708
Q

How is temperature monitored in therapeutic hypothermia?

A

A rectal probe

709
Q

What is the target temperature of neonatal cooling, and for how long?

A

33 to 35 degrees celsius. Done for 72 hours

710
Q

What time must therapeutic cooling be initiated in?

A

6 hours

711
Q

What is the most common area for spinal stenosis?

A

Lumbar spine

712
Q

What are the causes of spinal stenosis?

A

Congenitla, degenerative changes, herniated discs, thickening of ligaments in spine, fracture, tumours

713
Q

What is the typical presentation of spinal stenosis?

A

Gradual onset. Back pain, neuropathic pain, symptoms mimicking claudication (worse on movement, better on rest)

714
Q

What relieves spinal stenosis pain? What condition does this differentiate it from?

A

Sitting forward and walking uphill (expands the spinal canal). Differentiates this from claudication.

715
Q

What are the symptoms of intermittent neurogenic claudication that are seen in lumbar spinal stenosis?

A

Lower back pain, buttock and leg pain, leg weakness. Numbness. Better at rest, occur when moving.

716
Q

How does lateral spinal stenosis and foramina stenosis of the lumbar spine present?

A

Sciatica

717
Q

What is a key differential for central lumbar stenosis?

A

Peripheral arterial disease: however, there will be normal peripheral pulses and ABI, and presence of back pain

718
Q

What is the first line investigation for spinal stenosis?

A

MRI

719
Q

What is the surgical management of spinal stenosis?

A

Laminectomy

720
Q

What are red flags for lower back pain?

A

<20 years old or >50 years old, hx of previous malignancy, night pain, history of trauma, systemically unwell

721
Q

What is the typical presentation of ankylosing spondylitis?

A

Young man with lower back pain and stiffness, which is worse in the morning and improves with activity

722
Q

What are possible causes of foot drop?

A

Common peroneal nerve lesion, L5 radiculopathy, sciatic nerve lesion

723
Q

What is often the cause of common peroneal nerve lesion?

A

Compression at the neck of the fibula

724
Q

What are precipitating factors of common peroneal nerve lesion?

A

Prolonged confinement, recent weight loss, Baker’s cysts, plaster casts

725
Q

What symptoms suggest L5 radiculopathy?

A

Weakness of hip adbuction, foot drop

726
Q

What are the symptoms of Carpal Tunnel syndrome?

A

Pain/pins and needles in the thumb, index, middle finger. Symptoms ascend.

727
Q

What is seen on examination in carpal tunnel syndrome?

A

Weakness of thumb abduction, wasting of thenar eminence, tinel’s sign, phalen’s sign

728
Q

What are the causes of carpal tunnel syndrome?

A

Idiopathic, pregnancy, oedema, rheumatoid arthritis (often bilateral), acromgealy, diabetes, repetitive strain

729
Q

How does carpal tunnel syndrome affect action potentials?

A

Prolongs motor and sensory action potentials

730
Q

What is the treatment of carpal tunnel syndrome?

A

6 week of conservative treatments: corticosteroid injection, wrist splints at night. If severe: surgical decompression

731
Q

What reflexes would be reduced with L3/4 radiculopathy?

A

Knee reflex

732
Q

How can nerve root pain be identified?

A

Dermatomal distribution, associated neurological signs

733
Q

How can S1 radiculopathy be identified?

A

Reduced ankle reflex, positive sciatic nerve stretch test, sensory loss of posterior leg and lateral foot

734
Q

What is first line tx for lower back pain?

A

NSAIDS (with PPI)

735
Q

What is first line Ix for non specific back pain?

A

MRI (can see neurological and soft tissue structures)

736
Q

What spinal nerves form the sciatic nerve?

A

L4-S3

737
Q

What nerves does the sciatic nerve divide into?

A

Tibial nerve and common peroneal nerve

738
Q

What are the symptoms of sciatica?

A

Unilateral pain from the buttock down the back of thigh to below the knee or feet. Paraesthesia, numbness, motor weakness

739
Q

What cancers most commonly metastasise to bone?

A

Breast, Lung, Thyroid, Kidney, Prostate

740
Q

What is the sciatic stretch test?

A

Diagnoses sciatica: patient lies on their back with leg straight up, then dorsiflexes ankle. This should cause sciatic nerve root irritation

741
Q

What is cauda equina?

A

Compression of lumbosacral nerve roots beneath the spinal cord

742
Q

What is the most common cause of cauda equina?

A

Central disc prolapse at L4/L5 or L5/S1

743
Q

What are possible causes of cauda equina?

A

Central disc prolapse, tumours, infection, trauma, haematoma

744
Q

What is the presentation of cauda equina?

A

Lower back pain, bilateral sciatica, reduced sensation (saddle distribution), decreased anal tone, urinary dysfunction

745
Q

What is the investigation in cauda equina?

A

Urgent MRI

746
Q

What is the treatment of cauda equina and possible complications?

A

Emergency decompression, or there may be permanent neurological dysfunction

747
Q

What level does the spinal cord terminate?

A

L2/L3

748
Q

What is a key feature of metastatic spinal cord compression?

A

Back pain that is worse on coughing or straining

749
Q

What is the treatment of metastatic spinal cord compression?

A

High dose dexamethasone to reduce swelling, analgesia, surgery, chemo, radiotherapy

750
Q

Why is neuropathic pain difficult to treat?

A

Responds poorly to standard analgesia

751
Q

What are examples of neuropathic pain?

A

Diabetic neuropathy, post herpetic neuralgia, trigeminal neuralgia, prolapsed intervertebral disc

752
Q

What is unique about treatment for neuropathic pain?

A

Monotherapy: if not working, drugs should be switched, not added

753
Q

What are signs of neuropathic pain?

A

Burning, tingling, pins and needles, electric shocks, loss of sensation to touch of the affected area

754
Q

What are potential side effects of NSAIDs?

A

Gastritis with dyspepsia, stomach ulcers, asthma exacerbation, HTN, renal impairment, coronary artery disease

755
Q

What are potential side effects of opioids?

A

Constipation, skin itching, nausea, altered mental state, respiratory depression

756
Q

What is the treatment of patients with chronic primary pain?

A

No analgesia should be started, only depression

757
Q

What questionnaire assesses neuropathic pain?

A

DN4 questionnaire

758
Q

What occurs in a dorsal column lesion?

A

Loss of vibration and proprioception

759
Q

What occurs in a spinothalamic tract lesion?

A

Loss of pain, sensation and temperature

760
Q

What are the symptoms of a central cord lesion?

A

Flaccid paralysis of the upper limbs

761
Q

How does infarction of the spinal cord present?

A

Dorsal column signs (loss of proprioception and fine touch discrmination)

762
Q

What is Froment’s sign and what is it testing for?

A

Ulnar nerve palsy. Ask to ‘break the O’

763
Q

What nerves innervate the anal sphincter?

A

S2-4

764
Q

What is the area of lesion in Huntington’s Chorea?

A

Striatum

765
Q

What is presentation of anterior cord syndrome?

A

Motor paralysis below the level of the lesion, loss of pain and temperature at and below the lesion

766
Q

What causes anterior cord syndrome?

A

anterior spinal artery injury, usually due to flexion/compression injury

767
Q

What is the pattern of brown sequard syndrome?

A

Ipsilateral LMN paralysis at level of the segment, ipsilateral loss of fine touch, proprioception and vibration. Contralateral loss of pain and temperature below level of lesion

768
Q

Which spinal tract crosses over?

A

Spinothalamic: decussates at the level of the spinal cord

769
Q

What is narcolepsy?

A

A condition where the brain loses its ability to regulate the sleep-wake cycle

770
Q

What is the pathophysiology of narcolepsy?

A

Low levels of orexin, a protein which is responsible for controlling appetite and sleep patterns

771
Q

What are the features of narcolepsy?

A

Excessive day time sleepiness, cataplexy, distrupted nighttime sleep, hypnagogic/hypnopompic hallucinations, sleep paralysis

772
Q

What is cataplexy?

A

Conscious collapse caused by muscle atonia, often in response to sudden emotion. Seen in narcolepsy

773
Q

What is the investigations for narcolepsy?

A

Multiple sleep latency EEG, CSF levels of orexin

774
Q

What is the treatment of narcolepsy?

A

Daytime stimulants (modafinil) and sodium oxybate for improving nighttime sleep

775
Q

What is menieres disease?

A

Long term inner ear disorder

776
Q

What is the typical triad of Menieres disease?

A

Hearing loss, vertigo, tinnitus. Unilateral

777
Q

What type of hearing loss is seen in Menieres?

A

Sensorineural, associated with vertigo attacks and low frequency

778
Q

What is the pathophysiology of Menieres disease?

A

Excessive pressure and buildup of endolymph in the labryinth of the inner ear. Causes a higher pressure than normal, disrupts sensory signals. This is called endolymphatic hydrops

779
Q

What are symptoms other than the usual triad in Menieres?

A

Sensation of fullness in the ear, unexplained falls (‘drop attacks’), imbalance, nystagmus

780
Q

What triggers vertigo in Menieres?

A

Nothing: random

781
Q

How long do episodes last in menieres disease?

A

Minutes to hours

782
Q

How can driving be affected in patients with Menieres?

A

They should inform the DVLA and cease driving until symptoms are controlled

783
Q

What is the acute treatment of Menieres?

A

Prochlorperazine

784
Q

What is the prevention of Menieres disease attacks?

A

Betahistine

785
Q

What is the most common mononeuropathies?

A

Median nerve

786
Q

What is myelopathy?

A

Pathology involving the spinal cord

787
Q

What is syringomyelia?

A

Collection of CSF in the spinal cord

788
Q

What is syringobulbia?

A

Fluid filled cavity within the medulla of the brainstem. Often an extension of syringomyelia

789
Q

What are causes of syringomyelia?

A

Chiari malformation, trauma, tumours, idiopathic

790
Q

What are the symptoms of syringomyelia?

A

‘Cape like’ distribution: loss of sensation to temperature, preservation of light touch, proprioception, vibration. Patients might burn their hands without realising. Neuropathic pain, spastic weakness

791
Q

What is the investigations of syringomyelia?

A

MRI

792
Q

What is the treatment of syringomyelia?

A

The cause of syrinx, or a shunt

793
Q

What is Charcot-Marie-Tooth disease?

A

Most common hereditary peripheral neuropathy

794
Q

What is the inheritance of Charcot Marie Tooth?

A

Autosomal dominant

795
Q

What are the symptoms of Charcot-Marie-Tooth?

A

Mostly motor symptoms. High foot arches, distal muscle wasting (inverted champagne muscle legs), lower leg weakness (foot drop), weakness in hands, reduced reflexes, reduced muscle tone, peripheral sensory loss

796
Q

How do you differentiate a 3rd nerve palsy that requires medical vs surgical treatment?

A

If there is a dilated pupil alongside ‘down and out’, it requires surgical management. This is controlled by parasympathetic fibres, which are on the surface of the nerve, which suggests a compression of the nerve (tumour or bleed).

Phase 3a (19 decks)

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