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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

Examples of primary headaches ?

A

Migraine
Tension headache
Clusher headache

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2
Q

What are secondary headaches ?

A

Headaches caused by a medication or medical illness

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3
Q

What are red flag symptoms for secondary headaches ?

A

HIV or immunosuppressed patients
Fever
Thunderclap headache
Seizure with new headache
Suspected meningitis, encephalitis
Acute glaucoma
Papilloedema

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4
Q

What is the most common cause of headache?

A

Medication overuse

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5
Q

What is a tension headache?

A

Generalised facial pain involving frontal and occipital region described as a tight band across the head

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6
Q

How can tension headaches be classified?

A

Episodic; less than 15 days per month
Chronic; More than 15 days per months for 3 months

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7
Q

What is the epidemiology for tension headaches?

A

Most common primary headache
2:3 male to female ratio
Onset between 20 and 30 years

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8
Q

What is the pathophysiology of tension headache ?

A

Release of inflammatory agents leads to sensitisation of peripheral trigeminal afferents leading to central hypersensitivity
Noicicentor is pericranial musculture
Chronic headaches lead to generalised hyperalgesia

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9
Q

Risk factors for tension headaches ?

A

Stress
Mental tension
Hunger
Sleep deprivation
Fatigue
Bad posture
Eye strain
Anxiety
Depression
Missed meals
Noise

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10
Q

What is the clinical presentation of tension headache?

A

Bilateral, pressure-like, non-throbbing and constricting pain
Dull non-pulsatile symptoms of varying intensity
Worsen as day progresses
Symptoms not aggravated by physical activity
Pressure behind eyes

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11
Q

How long does a tension headache last?

A

30 minutes to 7 days

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12
Q

Differentials to consider in tension headache?

A

Chronic migraine
Medication overuse headache
Sphenoid sinusitis
Giant cell arteritis
Temporomandibular joint disorders
Pituitary/brain tumour
Chronic subdural haematoma

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13
Q

Investigations for tension headaches?

A

Clinical diagnosis based on history and examination findings, headache diary

Investigations to rule out other causes

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14
Q

What investigations can be done to rule out differentials of tension headaches?

A

CT sinus; exclude spheroid simisitis
MRI brain; exclude brain tumour
Lumbar puncture; infection, sinus venous thrombosis

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15
Q

What is the management for episodic tension headache?

A

Over the counter simple analgesia ( Paracetamol, aspirin, NSAID)
Assess and manage triggers

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16
Q

What is the management of chronic tension headache?

A

6-10 sessions of acupuncture
Physiotherapy and regular exercise
CBT and relaxation techniques
10mg Amitriptyline prophylaxis

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17
Q

Which medication should not be used in treatment of tension headache?

A

Opioids

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18
Q

Complications of tension headache?

A

Impact on quality of life
Depression and low mood
Medication overuse causing more headache

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19
Q

What is a migraine?

A

Recurrent, throbbing headache preceded by aura and associated with nausea, vomiting and visual changes

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20
Q

What is the epidemiology of migraines ?

A

More common in females
90% of cases have onset before 40
Severity decreases with increasing age
Affects 1 in 6 patients
Most common cause of episodic headache

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21
Q

What is the most common cause of episodic headache?

A

Migraine

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22
Q

What are the trigger for migraine?

A

Chocolate
Hangover
Orgasm
Cheese
Oral contraceptives
Lie -ins
Alcohol
Tumult
Exercise

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23
Q

What is the aetiology of migraines ?

A

Any of the triggers
Brain chemical imbalance
Changes in brainstem and interactions with trigeminal nerve

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24
Q

What is the pathophysiology of migraines?

A

Neuronal and glial depolarisation spreads across cerebral cortex causing migraine aura and release of inflammatory mediators
Neurogenic inflammation of first division of trigeminal sensory neurones which innervate large vessels and meninges . releases substances causing dilation of blood vessels, leakage of plasma proteins into surround tissue and pain
These changes lead to unstable trigeminal nerve nucleus

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25
Q

What is the clinical presentation of migraine?

A

Headache lasting 4-72 hours
Unilateral throbbing pain
Nausea and vomiting
Decreased ability to function
Headache worsens with activity
Photophobia, phonophobia

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26
Q

What are the components of aura?

A

Positive phenomena; Visual sparkles, flashing lights
Negative cnomena; Visual loss, scotoma
Sensory aura; Numbness and tingling

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27
Q

What investigations can be used to diagnose migraines?

A

Clinical diagnosis; headache diary can be helpful to identify pattern

ESR; rule out temporal arteritis
Lumbar puncture; infection
MRI brain; space occupying/ischaemic lesion
CT head; intracranial haemorrhage
Fundoscopy; papilloedema

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28
Q

What are the differentials for migraines?

A

Other primary headache
Subarachnoid haemorrhage
Cerebral neoplasm
Temporal arteritis
Arterial dissection
Ischaemic stroke

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29
Q

What is the acute management for migraine?

A

Simple analgesia; Ibuprofen, Aspirin, Paracetamol
Triptan medication; Sumatriptan
Antiemetic; Prochlorperazine, Metoclopramide

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30
Q

What is prophylactic therapy for migraine?

A

Propanolol
Topiramate
Amitriptyline
Acupuncture and behavioural intervention

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31
Q

Which medication should not ble ased in migraines?

A

Opioids

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32
Q

What monitoring is required for migraine?

A

2-8 weeks from starting treatment

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33
Q

What are the complications of migraine?

A

Migrainous infarction
Depression
Cardiovascular disease
Chronic migraine
Complications of pregnancy

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34
Q

What is the prognosis of migraines?

A

Patients cope well with diagnosis
Impact on quality of life and ADL

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35
Q

What is a cluster headache?

A

Rare and severe headache associated with unilateral excruciating pain

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36
Q

What is the most disabling primary headache?

A

Cluster headache

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37
Q

What is the epidemiology of cluster headache ?

A

More common in males
Age of onset between 20 and 40 years
90% episodic and 10% chronic

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38
Q

What is the aetiology of cluster headaches?

A

Autosomal dominant gene association
Environmental influence

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39
Q

What are the risk factors for cluster headaches?

A

Head trauma
Heavy alcohol intake and smoking
Family history
Male sex
Sleep apnoea

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40
Q

What is the pathophysiology of cluster headache?

A

Trigeminal autonomic reflex causes pain and autonomic features of attack

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41
Q

What are the cardinal features of cluster headache?

A

Trigeminal distribution of pain
Ipsilateral cranial autonomic symptoms
Circadian pattern of attack

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42
Q

Clinical presentation of cluster headaches?

A

Repeated attack of unilateral, periorbital excruciating pain
Lacrimation, conjunctival injection
Rhinorrhoea
Agitation and restlessness
Partial horner’s syndrome
Nausea, vomiting
Photophobia, phonophobia, Migrainous aura

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43
Q

Investigations used to diagnose cluster headaches?

A

Clinical diagnosis based on history
Brain MRS; rule out tumour, cavernous sinus pathology
ESR; Giant call arteritis
Pituitary function test; pituitary adenoma

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44
Q

What are differential diagnosis for cluster headache?

A

Migraine
Paroxysmal berniciavia
Trigeminal neuralgia
Cluster-tic syndrome
Subarachnoid haemorrhage

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45
Q

What is the acute management for cluster headache?

A

Sumatriptan - SC/nasal
High flow 100% oxygen at flow rate of 12-15 L/ min via non rebreathable Mask for 15-20 minutes

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46
Q

What is the prophylactic therapy for cluster headache?

A

Verapamil
Corticosteroid
Avoid smoking /drinking

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47
Q

What is the monitoring requirement for cluster headache?

A

See neurologist
ECG, TFT, U+E for those on lithium

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48
Q

What are the complications of cluster headaches?

A

Depression
Poor quality of life

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49
Q

What is trigeminal neuralgia?

A

Facial pain syndrome in distribution of one or more divisions of the trigeminal nerve with no neurological deficit

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50
Q

What is the epidemiology of trigeminal neuralgia?

A

More common in females
Peak age between 50 and 60 years
Prevalence increases with age
20 times more prevalent in patients with MS

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51
Q

What medical condition is associated with trigeminal neuralgia?

A

Multiple sclerosis

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52
Q

What is the primary cause of trigeminal neuralgia?

A

Intracranial vascular compression

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53
Q

What are secondary causes for trigeminal neuralgia?

A

Pathology in brainstem; tumour MS, infarction
Pathology at cerebellopontine angle; acoustic neuroma, tumour
Pathology within petrous bone; middle ear infection
Pathology within cavernous sinus; Aneurysm of internal caratic, tumour, thrombosis of cavernous sinus

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54
Q

What is the pathophysiology of trigeminal neuralgia?

A

Compression of trigeminal nerve root at the root entry zone by aberrant vascular loop
Typically superior cerebellar artery
Results in focal demyelination and resultant conduction aberrations result in neuropathic pain

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55
Q

Risk factors you trigeminal neuralgia?

A

Hypertension
Multiple sclerosis
Increasing age
Female

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56
Q

What is the clinical presentation of trigeminal neuralgia?

A

Pain in trigeminal distribution, recurring and paroxysmal pair, intense, sheurp, superficial stabbing unilateral pain
Pain lasts seconds the minutes

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57
Q

What is needed for a diagnosis of trigeminal neuralgia?

A

Atleast 3 attacks of unilateral facial pain

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58
Q

What are triggers for trigeminal neuralgia?

A

Facial /oral mechanical stimulation
e.g tooth brushing, eating, cold, washing area, eating, talking, shaving, dental prostheses

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59
Q

Investigations for trigeminal neuralgia?

A

Clinical diagnosis based on history
Trigeminal reflex test ; Early blink reflex or early masseter reflex
Intra-oral reflex the rule out dental cause
MRI scan

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60
Q

Differential diagnosis in trigeminal neuralgia?

A

Dental caries
Dental fractures
Mandibular osteomyelitis
TMJ syndrome
Migraine
Temporal arteritis
Glossopharyngeal neuralgia

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61
Q

What medications are used in trigeminal neuralgia?

A

Carbamazepine

Phenytoin, gabapenting lamotrigine; less effective and should be started by specialist

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62
Q

Which mediations are not effective in trigeminal neuralgia?

A

Typical analgesic, opioids

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63
Q

What is the management if medications fail in trigeminal neuralgia?

A

Microvascular decompression; anomalous vessel separated from trigeminal nerve root
Gamma knife surgery
Stereotactic radiosurgery

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64
Q

What is giant cell arteritis?

A

Immune mediated granulomatous vasculitis of large/ medium sized arteries

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65
Q

What is the epidemiology of giant cell arteritis ?

A

Most common form of systemic vasculitis
More common in females over age of 50 years
More common in white, North European ancestry

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66
Q

What is the aetiology of giant cell arteritis?

A

Genetics; Polymorphism of HLA class II region
Infection; Mycoplasma Pneumoniae, parovirus B 19, parainfluenza virus, chlamydia pneumonia, varicella zoster

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67
Q

What is the pathophysiology of giant cell arteritis?

A

Immune insult to adventitia of arterial wall results in inflammation of artery
Fragmentation of internal elastic lamina
Inflammatory changes lead to vessel narrowing and occlusion which leads to ischaemia

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68
Q

Risk factors for giant cell arteritis?

A

Age over 50 years
Increasing age
Female sex
Genetics
Smoking
Atherosclerosis
Environmental factors

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69
Q

Clinical presentation of giant cell arteritis?

A

Severe pulsating temporal headache
Scalp pain or tenderness
Aching and stiffness
Loss of vision/ abnormal fundoscopy
Jaw pain and tongue claudication

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70
Q

Investigations for giant cell arteritis?

A

Elevated CRP and ESR
Normocytic, normochromic anaemia
Vascular ultrasound
Temporal artery biopsy

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71
Q

What is seen on vascular ultrasound in giant cell arteritis?

A

Wall thickening
Stenosis/ occlusion

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72
Q

What is seen on temporal artery biopsy in giant cell arteritis?

A

Granulomatous inflammation
Multinucleated giant cells

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73
Q

Differentials for giant cell arteritis?

A

Polymyalgia rheumatica
Solid organ cancer
Haematological malignancy
Takayasu’s arteritis
Amyloidosis
SLE
Connective tissue disease

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74
Q

What is the treatment for giant cell arteritis?

A

High dose corticosteroids which are weaned over 12-24 months
If visual symptoms persist give IV methylprednisolone for 3 days
Long term bone and GI protection

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75
Q

What are the monitoring requirements for giant cell arteritis?

A

Every 2-8 weeks for first 6 months
Every 12 weeks during second 6 months
Every 12-24 weeks during second year
Any point during relapse
When glucocorticoid therapy is modified

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76
Q

What are the complications of giant cell arteritis?

A

Large vessel stenosis
Aortic aneurysm
Glucocorticoid related adverse effects
Vision loss

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77
Q

What is the prognosis of giant cell arteritis?

A

Increased risk of aortic aneurysm and cardiovascular disease

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78
Q

What is a transient ischaemic attack?

A

Brief episode of neurological dysfunction caused by focal brain, spinal or retinal ischaemia without infarction with symptom lasting less than 24 hours

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79
Q

What is the epidemiology of TIA?

A

15% of first strokes are preceded by TIA
More common in males
Black ethnicity has a higher risk

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80
Q

Pathophysiology of TIA?

A

Cerebral ischaemia results in lack of oxygen and nutrients resulting in cerebral dysfunction with infarction of cerebral tissue

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81
Q

Aetiology of TIA?

A

In- situ thrombosis of intracranial artery
Cardioembolic events; AF, impaired ejection fraction
Small vessel occlusion; Microatheroma, hypercoaguability, dissection, vasculitis, vasospasm, sickle cell anaemia
Hypoperfusion; cardiac arrhythmia, postural hypotension, decreased flow through narrowed artery

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82
Q

Risk factors for TIA/ stroke?

A

Male
Family history
Increasing age
Atrial fibrillation
Valvular disease
Carotid stenosis
Congestive heart failure
Hypertension
Diabetes mellitus
Cigarette smoking
Alcohol
Hyperlipidaemia
Patent foramen ovale
Obesity
Hypercoaguability
Lack of exercise

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83
Q

What systems are used to classify TIA?

A

Bamford classification; Based on presenting symptoms and clinical signs

TOAST criteria; Based on aetiology

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84
Q

What is the Bamford classification?

A

TIA classification based on presenting symptoms

Total anterior circulation
Partial anterior circulation
Posterior circulation ( vertebrobasilar territory )
Lacunar

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85
Q

What is the TOAST criteria?

A

Classification system used for TIA based on aetiology

Large artery atherosclerosis
Cardio-embolism
Small vessel occlusion
Other determined aetiology ( Non atherosclerotic vasculopathy, haematological disorder )
Undetermined aetiology

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86
Q

What are the features of anterior circulation TIA?

A

Affects frontal and medial parts of cerebrum
Weakness, paraesthesia in contralateral limb
Hemiparesis
Hemi sensory disturbance
Dysphagia
Amaurosis fugax

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87
Q

What percentage of TIA affect anterior and posterior circulation?

A

Anterior; 90%
Posterior; 10%

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88
Q

What is the presentation of a posterior circulation TIA?

A

Diplopia
Vertigo
Vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
Loss of consciousness
Hemianopia vision loss
Transient global amnesia
Tetraparesis

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89
Q

What is the classical features of TIA?

A

Transient sudden sensory/ motor dysfunction
No evidence of infarction on imaging

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90
Q

Investigations performed in TIA?

A

Blood glucose
Bloods; FBC, coagulation screen
ECG
CT scan; look for evidence of infarction

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91
Q

Differentials for TIA?

A

Stroke
Hypoglycaemia
Todd’s paralysis
Complex migraine
Space occupying lesion
Multiple sclerosis
Peripheral neuropathy

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92
Q

Management for TIA?

A

Calculate ABCD2 score
Loading dose aspirin
Seen by specialist within 7 days
Secondary prevention of stroke

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93
Q

What is secondary prevention of stroke following TIA?

A

Lifestyle counselling and risk factor optimisation
Antiplatelet therapy; 75 mg clopidogrel
Atorvastatin 20-80mg daily
Anti hypertensives

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94
Q

What is ABCD2 score?

A

Age; over 60 years
Blood pressure; > 140/90
Clinical presentation; Speech impairment (2 points), Unilateral weakness (1 point)
Diabetes mellitus
Duration; 10-59 minutes (1 point), >60 minutes (2 points)

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95
Q

Complications of TIA?

A

Stroke
Myocardial infarction

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96
Q

Prognosis of TIA?

A

8% of patients will have a stroke following TIA hospitalisation
Over 10% will have stroke within 3 months of TIA

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97
Q

What is a Stroke?

A

Rapid onset syndrome of neurological deficit caused by focal cerebral, spinal or retinal infarction
Symptoms last over 24 hours

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98
Q

Epidemiology of stroke?

A

Incidence increases with age
Higher in asian ethnicity
Incidence is falling due to rigorous management of risk factors
Trauma included stroke is common in younger patients

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99
Q

Aetiology of stroke?

A

Ischaemic stroke (80%)
Haemorrhagic stroke (15%)
Trauma
Vasculitis

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100
Q

What is the pathophysiology of ischaemic stroke?

A

Blood supply in cerebral vascular territory is reduced, leading to irreversible cell death and infarction of cerebral tissue

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101
Q

What is the pathophysiology of haemorrhagic stroke?

A

Rupture of intracerebral vessel causes bleeding into brain parenchyma
Expanding haematoma can sheer or occlude neighbouring arteries
Results in raised ICP, cerebral hypoperfusion, and ischaemic injury

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102
Q

What is a Charcot-Bouchard aneurysm?

A

Microaneurysm caused by hypertension

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103
Q

Primary causes of intracerebral haemorrhage?

A

Idiopathic
Anticoagulation

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104
Q

What are secondary causes of intracerebral haemorrhage?

A

Vasculitis
Connective tissue disease
Amyloid angiopathy
Aneurysm

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105
Q

What is the presentation of an anterior cerebral artery stroke?

A

Leg weakness
Sensory disturbance in leg
Gait apraxia
Truncal ataxia
Incontinence
Drowsiness
Akinetic mutism

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106
Q

What is the presentation of a middle cerebral artery stroke?

A

Contralateral arm and leg weakness
Contralateral sensory loss
Hemianopia
Aphasia
Dysphagia
Facial drop

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107
Q

What is the presentation of posterior cerebral artery stroke?

A

Contralateral homonymous hemianopia
Cortical blindness
Visual agnosia
Prosopagnosia
Unilateral headache

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108
Q

What is the presentation of a posterior circulation stroke?

A

Motor deficit; hemiparesis, tetraparesis, facial paralysis
Dysarthria
Vertigo, nausea, vomiting
Visual.disturbance
Altered conciousness

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109
Q

What is the presentation of a lacunar stroke?

A

Unilateral weakness
Sensory deficit of face, arm, leg or all three
Pure sensory loss
Ataxic hemiparesis

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110
Q

In which stroke is patient more likely to get locked in?

A

Posterior circulation (Vertebrabasilar artery)

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111
Q

Investigations performed in stroke?

A

Bloods; FBC, U+E, glucose, LFT, clotting screen
Non contrast CT head

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112
Q

What is seen on a non contrast head CT in ischaemic stroke?

A

Hypoattenuation of brain parenchyma
Loss of grey matter

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113
Q

What is seen on a non contrast CT in a haemorrhagic stroke?

A

Hyperattenuation suggesting acute blood
Surrounding hypoattenuation due to oedema

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114
Q

Differentials for stroke?

A

Transient ischaemic attack
Hypertensive encephalopathy
Hypoglycaemia
Complicated migraine
Subdural haematoma
Wernicke encephalopathy
Brain tumour
Sepsis

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115
Q

What is the treatment of ischaemic stroke?

A

Maximise ischaemic tissue; fluids and maintain sats over 95%

tPA thrombolysis within 4.5 hours of symptom presenting, followed by aspirin and clopidogrel for 2 weeks, then clopidogrel lifelong

Mechanical thrombectomy

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116
Q

What is the management of haemorrhagic stroke?

A

Frequently monitor GCS
Reverse pre- existing anticoagulation (vitamin K, beriplex)
Control hypertension
Manual decompression (mannitol)
Decompressive surgery

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117
Q

What prophylactic measures are taken to prevent stroke?

A

Antiplatelet therapy ( aspirin + clopidogrel )
Cholestrol management
Atrial fibrillation treatment and anticoagulation
Blood pressure management

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118
Q

Contraindications for thrombolysis?

A

Recent surgery in last 3 months
Recent arterial puncture
History of active malignancy
Evidence of aneurysm in brain
Patient is on anticoagulation
Severe liver disease
Acute pancreatitis
Clotting disorder
Above 80 years

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119
Q

What is the alternative if clopidogrel is not tolerated?

A

dipyramidole

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120
Q

What parameters are monitored in stroke patients in hospital?

A

GCS
Blood pressure
Blood glucose
Oxygen saturations
Hydration
Temperature
Cardiac rhythm, rate
Development of seizures

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121
Q

Complications of stroke?

A

Infection
Seizures
Deep vein thrombosis
Delerium
Aspiration pneumonia
Alteplase related orolingual oedema
Haemorrhagic transformation of ischaemic stroke

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122
Q

Prognosis of stroke?

A

Leading cause of serious long term disability
Patients treated with alteplase have better functional outcome

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123
Q

What is a subarachnoid haemorrhage?

A

Spontaneous bleeding into subarachnoid space

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124
Q

Epidemiology of subarachnoid haemorrhage?

A

Accounts for 5% of strokes
Decreasing incidence due to better management of risk factors
Incidence increases with age

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125
Q

Aetiology of subarachnoid haemorrhage?

A

Spontaneous rupture of intra-cranial saccular berry aneurysm
Arteriovenous malformations
Bleeding disorders
Anticoagulation use
Acute bacterial meningitis
Tumours

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126
Q

What is the pathophysiology of subarachnoid haemorrhage?

A

Cerebral aneurysm arises at the bifurcation of arteries in the circle of willis
Weaking in the arterial walls increases risk of rupture
Rupture leads to bleeding into subarachnoid space

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127
Q

Risk factors for subarachnoid haemorrhage?

A

Hypertension
Smoking
Family history
ADPKD
Alcohol/ Cocaine use
Marfans/ Ehlers-Danlos syndrome
Neurofibromatosis type I

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128
Q

Clinical presentation of subarachnoid haemorrhage?

A

Sudden onset headache (thunderclap)
Reduced/ loss of consciousness
Neck stiffness
Eyelid drooping, diplopia, mydriasis, orbital pain
Papilloedema
Kernig sign
Brudzinski sign

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129
Q

What is Kernig sign?

A

Unable to extend leg at knee when thigh is flexed

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130
Q

What is Bridzinski sign?

A

When neck is flexed by doctor, patient will flex knees and thighs

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131
Q

Investigations performed in subarachnoid haemorrhage?

A

Urgent non contrast CT of head
Lumbar puncture
CT cerebral angiogram
Bloods, ECG

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132
Q

What is seen on non contrast CT in subarachnoid haemorrhage?

A

Hyperdense star shaped lesion in subarachnoid space

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133
Q

What is seen on lumbar puncture in subarachnoid haemorrhage?

A

Xanthochromia, 12 hours after symptom onset

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134
Q

What are the differentials for subarachnoid haemorrhage?

A

Non-aneurysmal perimesencephalic SAH
Arterial dissection
AV malformation
Vasculitis
Anticoagulation use
Migraine
Cortical vein thrombosis

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135
Q

What is the management for subarachnoid haemorrhage?

A

Maintain cerebral perfusion; IV fluids and keep blood pressure below 160mmHg
Nimodipine to reduce vasospasm
Mannitol to prevent raised ICP
Endovascular coiling/ clipping
Surgery

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136
Q

What are the monitoring requirements for subarachnoid haemorrhage?

A

If aneurysmal disease then frequency and imaging modality is determined on a case basis

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137
Q

Complications of subarachnoid haemorrhage?

A

Neuropsychiatric problems
Chronic hydrocephalus

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138
Q

Prognosis of subarachnoid haemorrhage?

A

Responsible for 1/3 of premature deaths
Highest mortality in black and female patients
Poor quality of life and reduced functional capabilities

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139
Q

What is a subdural haemorrhage?

A

Bleeding between dura mater and arachnoid mater of the meninges following rupture of bridging veins between cortex and venous sinus

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140
Q

Epidemiology of subdural haemorrhae?

A

More common in people with small brains (elderly, alcoholics and babies)
Incidence increases with age

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141
Q

What is the aetiology of subdural haemorrhage?

A

Trauma, usually deceleration injury
Dural metastasis
Venous malformation

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142
Q

What is the pathophysiology of a subdural haemorrhage?

A

Torsion, sheering forces causes causes disruption of bridging cortical veins that empty into dural venous sinus and formation of haematoma .

As haematoma gorwns the rise in pressure is able to stop bleeding.

After a few days haematoma starts to autolyse and an increase in oncotic pressure raises ICP over couple of weeks

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143
Q

What is the consequence of raised ICP?

A

Leads to midline shift of structures
Tectorial herniation and coning

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144
Q

Risk factors for subdural haemorrhage?

A

Traumatic head injury
Cerebral atrophy
Increasing age
Alcoholism
Male
Physical abuse, shaken baby syndrome

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145
Q

What is the classification of subdural haematoma?

A

Acute subdural haematoma; less than 3 days old, diffusely hyperdense

Subacute subdural haematoma; 3-21 days old, heterogeneously hyperdense/ isodense

Chronic subdural haematoma; more than 21 days, diffusely hypodense

Acute on chronic subdural haematoma; areas of hyperdensity with hypodense haematoma

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146
Q

What is the clinical presentation of subdural haematoma?

A

Recent trauma
Headache
Nausea/ vomiting
Diminished eye/ motor response
Confusion
Focal neurology
Stupor/ coma

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147
Q

Investigations in subdural haemorrhage?

A

Non contrast CT
MRI

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148
Q

What is seen on non contrast CT in subdural haemorrhage?

A

Crescent shaped collection
Hyperdense -> isodense -> hypodense
May be a midline shift if raised ICP

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149
Q

What is the treatment for subdural haemorrhage?

A

Assess ABCDE and monitor GCS
Mannitol to reduce ICP
Neurosurgical management irrigation/ evacuation via burr hole craniotomy

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150
Q

Monitoring requirement for subdural haemorrhage?

A

Follow up CT 1-2 months post discharge

Consult cardiology for when to restart anticoagulation

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151
Q

Complications of subdural haemorrhage?

A

Neurological deficit
Coma
Stroke
Surgical site infection
Epilepsy
Recurrence of subdural haematoma

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152
Q

What factors are associated with a poorer prognosis in subdural haemorrhage?

A

Older age
Greater severity of injury
Low GCS
Midline shift on imaging
Early need for surgery
Raised ICP

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153
Q

What is an extradural haemorrhage?

A

Acute haemorrhage between dura mater and the bone usually caused by head injury

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154
Q

What is the epidemiology of extradural haemorrhage?

A

Usually occurs in young adults, common in males aged 20-30 years
75% of cases are a result of skull fractures

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155
Q

What is the aetiology of extradural haemorrhage?

A

Skull trauma in temporoparietal region
Ruptured middle meningeal artery, vein
AV malformations
Bleeding disorder

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156
Q

Pathophysiology of extradural haemorrhage?

A

Vessel damage leads to bleeding between dura mater and cranium
As volume of blood in extradural space increases it begins to pull dura away from skull
Can lead to raised ICP

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157
Q

Risk factors of extradural haemorrhage?

A

Trauma
Male
Young age

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158
Q

Clinical presentation of extradural haemorrhage?

A

Headache
Nausea and vomiting
Confusion
Loss of consciousness
Lucid interval
Confusion, reduced GCS
Neurological, sensory and motor deficits
Cushing’s triad
Babinski sign

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159
Q

Investigations to diagnose extradural haemorrhage?

A

Bedside glucose and ECG
Blood work; FBC, U+E, CRP, Coagulation, Group and save
Imaging; CT, MRI, cerebral angiography

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160
Q

What is seen on CT in extradural haemorrhage?

A

Bi-convex lemon shaped mass
Secondary features; midline shift, brainstem herniation

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161
Q

Differentials for extradural haemorrhage?

A

Epilepsy
Carotid dissection
CO poisoning
Subdural haematoma
Subarachnoid haemorrhage
Meningitis

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162
Q

Management in extradural haemorrhage?

A

ABCDE, correction of anticoagulation, mannitol

Surgical management

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163
Q

Monitoring requirement in extradural haemorrhage?

A

Serial scans to monitor ICP
Close observation post operatively

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164
Q

Complications of extradural haemorrhage?

A

Infection
Cerebral ischaemia
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus due to ventricular obstruction
Brainstem injury

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165
Q

Factors that worsen prognosis following extradural haemorrhage?

A

Low GCS at presentation
No history of lucid interval
Pupil abnormalities
Pre-existing brain injury

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166
Q

What is multiple sclerosis?

A

Chronic auto-immune T-cell mediated inflammatory demyelinating disease resulting in episodic neurological dysfunction in at least 2 areas of the CNS separated in time and space

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167
Q

What cells are attacked in MS?

A

Oligodendrocytes

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168
Q

What is the epidemiology of MS?

A

More common in females
Most common age at diagnosis is 20-40 years
More prevalent in European countries

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169
Q

Aetiology of MS?

A

EBV exposure
Low sunlight exposure and Vit D deficiency

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170
Q

Pathophysiology of MS?

A

Infection/ metabolic stress triggers inflammatory response
Activated T-cells seek entry into CNS via attachment to receptor on endothelial cells and td enter trough BBB
Once in BBB inflammatory cascade causes destruction of oligodendrocytes

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171
Q

Where are demyelinating placques in MS likely to be found?

A

Optic nerve
Ventricles of the brain
Corpus callosum
Brainstem and cerebellar connections
Cervical cord

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172
Q

What are the types of MS phenotypes?

A

Relapsing
Relapsing remitting
Primary progressive
Secondary progressive

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173
Q

What s the most common MS phenotype?

A

Relapsing remitting

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174
Q

Risk factors for MS?

A

Female
Lack of sunlight/ vitamin D
Exposure to EBV
Northern latitude
Smoking
Personal/ family history of auto-immune disease
Obesity

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175
Q

Clinical presentation of MS?

A

Unilateral optic neuritis
Numbness or tingling of limbs
Leg weakness
Brainstem demyelination
Cerebellar symptoms
Trigeminal neuralgia
Constipation
Spasticity and weakness
Bladder and sexual dysfunction
Lhermitte’s sign
Cognitive decline

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176
Q

What is the presentation of optic neuritis?

A

Pain in one eye on movement
Greying/ blurring of vision
Reduced central vision

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177
Q

What are symptoms of brainstem demyelination?

A

Diplopia, vertigo, facial weakness, dysarthria, dysphagia
Clumsy
Loss of proprioception

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178
Q

What is Lhermitte’s sign?

A

Electric shock like sensation extending down

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179
Q

What evidence is needed in history to diagnose MS?

A

Two or more attacks
Affecting different parts of the CNS disseminated in time and space

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180
Q

Investogations performed in MS?

A

Bloods to rule out differentials; FBC, CRP, U+E, glucose, HIV serology, auto-antibodies, Ca2+, B12
MRI
Lumbar puncture
Electrophysiology

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181
Q

What is seen on MRI in MS?

A

Demyelinating lesions in spinal cord
Hyperintensities in periventricular white matter in brain

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182
Q

What is seen in lumbar puncture in MS?

A

Oligoclonal IgG bands in 90% of cases
CSF cell count

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183
Q

Differentials for MS?

A

Myelopathy
Fibromyalgia
Sleep disorder
Sjorgens syndrome
B12 deficiency
Ischaemic stroke
Lymphoma
GBS
ALS
SLE

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184
Q

What is the management for MS?

A

Lifestyle management
Regular exercise
Smoking cessation
Optimise co-morbidities
Yearly flu vaccine
Fertility and pregnancy counselling

Managing relapse
Methylprednisolone for 5 days
SC interferon 1B or 1A
Disease modifying agents; alemtuzumab, natalizumab, dimethyl fumarate
Symptom management; physiotherapy, baclofen, tizanidine, botox

Stem cell therpay can be considered

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185
Q

Monitoring requirements for MS?

A

Frequency of monitoring depends on patient situation, commonly every 6-12 months

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186
Q

Complications of MS?

A

UTI
Osteopenia, osteoporosis
Depression
Visual impairment
Cognitive impairment
Impaired mobility

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187
Q

What is the prognosis of MS?

A

Life expectancy is reduced by 5-10 years
Often die from aspiration pneumonia

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188
Q

What is myasthenia gravis?

A

Chronic autoimmune disorder against nicotinic acetylcholine receptors in the postsynaptic membrane of neuromuscular junction

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189
Q

Epidemiology of Myasthenia gravis?

A

More common in females
Women present under 40 years and men over 60 years
Increasing prevalence, especially in developed countires

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190
Q

Aetiology of Myasthenia gravis?

A

Antibody mediated autoimmune destruction

Transient symptoms can be caused by D-penicillamine treatment for Wilsons disease

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191
Q

Risk factors for Myasthenia gravis?

A

Autoimmune conditions; Pernicious anaemia, SLE, rheumatoid arthritis
Thymic hyperplasia
Family history of Myasthenia gravis/ autoimmune conditions
Cancer therapy

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192
Q

Pathophysiology of Myasthenia gravis?

A

Anti-AChR autoantibodies result in complement mediated destruction of postsynaptic membrane of neuromuscular junction
Reduced number of binding sites available for ACh resulting in inconsistent generation of muscle fibre action potentials and manifesting as skeletal muscle weakness

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193
Q

What is the classification of Myasthenia gravis?

A

Class I; eye muscle weakness, ptosis, all other muscle strength is normal
Class II; mild weakness of other muscles and eye muscle weakness of any severity
Class III; moderate weakness of other muscles and eye muscle weakness of any severity
Class IV; severe weakness of other muscles and eye muscle weakness of any severity
Class V; need intubation to maintain airway

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194
Q

Clinical presentation of Myasthenia gravis?

A

Increasing muscle fatigue
Ptosis, diplopia
Myasthenic snarl on smiling
Respiratory difficulties in generalised myasthenia gravis
Fatigable tendon reflexes
Proximal limb weakness

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195
Q

Weakness is myasthenia gravis worsens in which situations?

A

Pregnancy
Hypokalaemia
Infection
Exercise
Drugs; opiates, beta-blockers, gentamycin, tetracycline

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196
Q

What is seen on examination in myasthenia gravis?

A

When asked to count to 50, voice will become less audible

When asked to focus on finger after a while patient will be unable to hold their vision

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197
Q

Investigations performed in Myasthenia gravis?

A

Serum anti-AChR (if negative look for anti-MuSK)
EMG and nerve conduction studies
CT scan of thymus to look for hyperplasia

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198
Q

Differentials for Myasthenia gravis?

A

Lambert-Eaton myasthenic syndrome
Botulism
Penicillamine induced myasthenia gravis
Primary myopathies

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199
Q

Management in Myasthenia gravis?

A

Thymectomy if onset is over 50 years and poorly controlled symptoms
Pyridostigmine for symptoms control
Immunosuppression with steroids and azathioprine/ methotrexate

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200
Q

What is the management in myasthenic crisis?

A

Intubation
Plasmapheresis and IVIG
Steroids

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201
Q

Monitoring requirements for Myasthenia gravis?

A

Every 3-12 months depending on situation
Blood work if immunosuppressed
Lung function tests
Assess for symptoms affecting ADL, difficulties with swallowing/ breathing, and effect of medications

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202
Q

Complications of Myasthenia gravis?

A

Pyridostigmine induced reactions
Respiratory failure
Impaired swallowing
Acute aspiration
Secondary pneumonia
Cardiac complications
Pregnancy complications

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203
Q

Prognosis of Myasthenia gravis?

A

Older patients, with poorer response to therapy and multiple co-morbidities have poorer prognosis

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204
Q

What is meningitis?

A

Inflammation of the meninges caused by bacterial, viral or fungal infection

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205
Q

What is the epidemiology of meningitis?

A

Occurs in all age groups
More common in infants, young children and elderly
Immunisation routine has changed epidemiology and incidence rates
Viral meningitis is more common in men

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206
Q

Aetiology of meningitis?

A

Bacterial; Streptococcus pneumoniae is most common cause worldwide, Neisseria meningitidis is predominant in Europe

Viral; Human enterovirus is most common cuase, HSV-2, varicella zoster

Fungal

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207
Q

What is a common causative agent for meningitis in pregnant women?

A

Listeria monocytogenes

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208
Q

What is a common causative agent for meningitis in neonates?

A

Group B haemolytic streptococcus

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209
Q

Pathophysiology of bacterial meningitis?

A

Bacteria reach CNS and multiply in subarachnoid space
Bacterial components in CSF induce an inflammatory response
This leads to cerebral oedema, raised ICP contributing to neurological damage

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210
Q

What is the pathophysiology of viral meningitis?

A

Virus enters through faeco-oral route and virus replicates in non CNS tissue
The virus is carried to CNS by haematological spread and enters subarachnoid space leading to inflammatory response and meningitis

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211
Q

Risk factors for meningitis?

A

Genetic predisposition
Advancing age
Crowding; military base, university students
Intrathecal access
Immunocompromised patients; HIV, malignancy, asplenia, congenital
Exposure to pathogens
Bacterial endocarditis
IVDU
Sickle cell disease
Diabetes

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212
Q

Clinical presentation of meningitis?

A

Headache
Neck stiffness
Fever
Altered mental status
Nausea, vomiting
Photophobia
Seizures
Petechial non blanching rash
Papilloedema
Kernig’s sign
Brudzinski’s sign

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213
Q

Investigations in meningitis?

A

Blood culture
Serum PCR
Bloods; FBC, U+E, CRP, VBG, LFT, coagulation screen
Lumbar puncture; CSF protein/ cells/ glucose, microscopy and gram staining, lactate, viral serology

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214
Q

What is the CSF findings in bacterial meningitis?

A

Polymorph neutrophils
Raised protein
Low glucose

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215
Q

What is the appearance of CSF in bacterial infection?

A

Turbid

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216
Q

What are the CSF findings in viral meningitis?

A

Lymphocytes
Normal protein count
Normal glucose

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217
Q

What are the indications for LP?

A

Age over 60
Immunocompromised
History of CNS disease
New onset seizures
Decreasing GCS
Focal neurological signs
Papilloedema

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218
Q

Differentials for meningitis?

A

Encephalitis
Toxic/ metabolic encephalitis
Drug induced meningitis
Tuberculous meningitis
Intracranial haemorrhage

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219
Q

Management of bacterial meningitis?

A

Transfer patient to hospital
Administer stat dose of IM benzylpenicillin
Once causative agent has been identified give appropriate antibiotic course
Consider steroids to reduce cerebral oedema
Give Ciprofloxacin to close contacts

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220
Q

What is the antibiotic course for Strep.pneumoniae, Haemophilus influenzae meningitis?

A

Ceftriaxone/ cefotaxime for 10 days

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221
Q

What is the antibiotic course for listeria monocytogenes?

A

Amoxicillin for 21 days

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222
Q

What is the antibiotic course for staphylococcus aureus meningitis?

A

Flucloxacillin for 14 days

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223
Q

What is the management for viral meningitis?

A

Supportive management
Consider acyclovir

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224
Q

Complications of bacterial meningitis?

A

Shock
Raised
ICP
Hydrocephalus
Cognitive, behavioral and academic problems
Seizures
Subdural effusion
Hearing loss

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225
Q

Complications of viral meningitis?

A

Persistent headache and malaise
Neurodevelopmental deficits in infants

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226
Q

Prognosis in meningitis?

A

Excellent with therapy
Poorer prognosis is associated with increasing age, co-morbidities, causative pathogen, severity of presentation, low GCS

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227
Q

What is encephalitis?

A

Infection and inflammation of the brain parenchyma

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228
Q

Epidemiology of encephalitis?

A

Bimodal age distribution (below 1 year and over 65 years)
More common in immunocompromised

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229
Q

Aetiology of encephalitis?

A

Viral is most common
Bacterial
Fungal
Auto-immune

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230
Q

Pathophysiology of encephalitis?

A

Causative agents induces inflammation in brain tissue resulting in neurological dysfunction

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231
Q

Risk factors for encephalitis?

A

Young and elderly
Immunocompromised
Geographic location
Smoking
Autoimmune disease
Seasonal changes

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232
Q

Clinical presentation of encephalitis?

A

Features of viral illness; Fever, myalgia, headache, nausea

Progresses to;
Personality and behavioral change
Decreased consciousness
Focal neurological deficit
Seizures
Raised ICP

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233
Q

Investigations for encephalitis?

A

Blood tests; FBC, U+E, LFT
Blood film to detect malaria
Throat swab and sputum culture
MRI
Lumbar punture

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234
Q

What is seen on MRI in encephalitis?

A

Inflammation and swelling of brain parenchyma
Midline shift in context of raised ICP

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235
Q

Differentials for encephalitis?

A

Meningitis
Stroke
Brain tumour
Toxic/ metabolic encephalopathy
Intracranial bleed

236
Q

Management of encephalitis?

A

Supportive care and monitor vitals
IV acyclovir for viral aetiology

237
Q

Monitoring requirements in encephalitis?

A

Neuropsychological testing in childhood survivors due to increased risk of ADHD and cognitive problems

238
Q

Complications of encephalitis?

A

Death
Hypothalamic and autonomic dysfunction
Ischaemic stroke
Seizures
Cerebral haemorrhage
Cerebral vasculitis
Neurodevelopmental problems

239
Q

Prognosis of encephalitis?

A

Based on aetiology
Older age, decreased consciousness, delayed treatment associated with poorer prognosis

240
Q

What is a brain abscess?

A

Suppurative collection of microbes within gliotic capsule occurring within brain parenchyma

241
Q

What is the epidemiology of brain abscess?

A

Highest prevalence in adult men under 30 years
In children common between 4-7 years
More common in men
Most common cause of space occupying lesion worldwide

242
Q

What is the aetiology of brain abscess?

A

Infection with bacterial, fungal, parasitic organisms

243
Q

Pathophysiology of brain abscess?

A

Originate in ischaemic white matter adjacent to cortex
Entry of infective organism through haematogenous spread
Early cerebritis (3 days); local inflammation, tissue necrosis, neutrophilic infiltration, activation of microglia and astrocytes
Late cerebritis (day 4-9); increased organisation where lymphocytic and microglial infiltration
Frank abscess; encapsulation, suppurative collection

244
Q

Risk factors for brain abscess?

A

Immunocompromised
Cancer/ chronic illness
Congenital heart disease
Major head trauma, surgery or injury
Meningitis
Chronic sinus or middle ear infection
IVDU
Diabetes mellitus
Infective endocarditis

245
Q

Clinical presentation of brain abscess?

A

Altered mental status; increased confusion, decreased responsiveness, irritability, change in personality
Decreased speech, sensation and movement
Changes in vision
Vomiting
Fever, chills
Neck stiffness
Photophobia

246
Q

Investigations to diagnose brain abscess?

A

MRI/ CT scan
Ultrasound scan in infants
Bloods; FBC, U+E, CRP, LFT, glucose

247
Q

When can ultrasound be used to image brain?

A

When fontanelles are open

248
Q

What is seen on imagining in brain abscess?

A

One or more ring enhancing lesion

249
Q

Differentials for brain abscess?

A

Primary CNS neoplasm
Metastatic lesion
Recurrent tumour/ irradiation necrosis
Multiple sclerosis
Acute disseminated encephalomyelitis
Ischaemic stroke

250
Q

Management of brain abscess?

A

Antibiotics; vancomycin, metronidazole/ clindamycin, ceftriaxone
Supportive care; corticosteroids, anticonvulsants, monitor vitals, surgical evacuation

251
Q

Monitoring requirements for brain abscess?

A

Periodic CT with contrast until lesion have resolved, minimum for 1 year

252
Q

Complications of brain abscess?

A

Ventriculitis
Hyponatraemia
Cognitive dysfunction
Seizures
Death
Hydrocephalus

253
Q

Prognosis of brain abscess?

A

Mortality of 10%
Major factor is patients neurological status upon presentation
Early diagnosis and treatment improves outcome

254
Q

What is Guillain-Barre syndrome?

A

Acute inflammatory demyelinating ascending polyneuropathy against Schwann cells of peripheral sensory and motor nerves

255
Q

What are the defining features of GBS?

A

Motor difficulty
Absence of deep tendon reflexes
Paraesthesia without objective sensory loss
Increased CSF albumin with normal cell count

256
Q

Epidemiology of GBS?

A

Most common acute polyneuropathy
More common in men
Associated with infection

257
Q

Aetiology of GBS?

A

Campylobacter jejuni
Cytomegalovirus
Mycoplasma
Zoster
HIV
EBV

258
Q

Pathophysiology of GBS?

A

Auto-immune reaction
Molecular mimicry where antibodies or T cells stimulated in response to pathogenic antigen epitopes cross react with neural epitopes
Results in immune mediated damage to neural schwann cells resulting in reduced peripheral nerve conduction

259
Q

Risk factors for GBS?

A

Preceding viral or bacterial infection
Mosquito bites
Hepatitis E
Immunisation
Cancer
Male

260
Q

Clinical presentation of GBS?

A

1-3 weeks post infection
Symmetrical ascending muscle weakness ( proximal muscles affected more; trunk, respiratory, cranial nerve)
Back and leg pain
Respiratory weakness/ distress
Speech problems, diplopia
Areflexia, hyporeflexia, absent deep tendon reflexes
Facial/ extra-ocular muscle weakness
Pupillary dysfunction

261
Q

Investigations to diagnose GBS?

A

Nerve conduction studies
Lumbar puncture
Spirometry/ LFT

262
Q

What is seen on nerve conduction studies in GBS?

A

Prolonged distal and F-wave latency
Reduced conduction velocity
H reflex prolonged/ absent

263
Q

Differentials for GBS?

A

Transverse myelitis

Myasthenia gravis

Lambert- eaton myastenic syndrome

Botulism

Polymyositis

Vasculitic neuropathy

264
Q

Management of GBS?

A

Without IgA deficiency or renal failure; IVIG, supportive therapy, plasma exchange
With lgA deficiency or renal failure, plasma exchange, supportive treatment

265
Q

Monitoring requirements in GBS?

A

Follow-up within 2 weeks of acute syndrome

Every 4-6 weeks for 6 months

Followed by annual follow ups

Access to physiotherapy, occupational therapy and psychological support

266
Q

Complications of GBS?

A

Respiratory failure
Bladder areflexia
Adynamic ileus
Paralysis
Fatigue
DVT
Immobilisation hypercalcaemia

267
Q

Factors predicting poorer prognosis in GBS?

A

Severe weakness
Rapid onset
Older age
Muscle wasting
Electrically inexcitable nerves
Preceding diarrhoeal illness

268
Q

What in epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting in seizures

Disease of brain with atleast two unprovoked seizures occuring more than 24 hours apart

269
Q

What is an epileptic seizure?

A

Paroxysmal/ unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharge

270
Q

What is the epidemiology of epilepsy?

A

Incidence is age dependent; highest before 20 years and after 60 years
Focal seizures are most common

271
Q

What is the cause of generalised epilepsies?

A

Unprovoked
Provoked; toxins, illicit substance, medications, metabolic derangement and mutations in genes coding for ion channels

272
Q

What is the cause of focal epilepsy?

A

Traumatic brain injury
CNS infection
Brain tumour and space occupying lesions
Stroke
Alzehimer’s
Perinatal injury
Alcohol withdrawal
Malformation in cortical development

273
Q

Pathophysiology of epilepsy?

A

Inappropriate hyperexcitability and hypersynchrony
Neurones have abnormal capability to generate intrinsic discharge bursts with decreased GABA inhibition and activation of local excitatory currents
Genetic and structural abnormality contribute to neurones behaving in this manner

274
Q

What are the elements of a seizure?

A

Prodrome
Aura
Ictal
Post- ictal

275
Q

What happens during seizure prodrome?

A

Lasts hours/ days
Not part of the seizure
Results in change in mood and behaviour

276
Q

What happens during seizure aura?

A

Strange feeling in gut, deja vu, strange smells, and visual changes

Patient is aware of symptoms and can feel seizure coming

277
Q

What happens during ictal stage?

A

The seizure; presentation depends on type of seizure

278
Q

Risk factors for generalised epilepsy?

A

Family history
Previous CNS infection
Head trauma
Substance abuse
Premature birth
Multiple or complicated febrile seizures

279
Q

Risk factors for focal epilepsy?

A

Febrile seizure
Traumatic brain injury
CNS infection
Stroke
Brain tumour
Intellectual disability
Cerebral palsy
Dementia
Family history of seizures
Intracranial vascular malformations
Male sex

280
Q

Presentation of generalised tonic clonic seizure?

A

Often no aura
Loss of consciousness
Tonic phase; rigid, stiff limbs, person will fall to the floor
Clonic phase; generalised bilateral rhythmic muscle jerking lasting seconds to minutes
Eyes remain open
Tongue biting
Urine and faecal incontinence
Post ictal phase of drowsiness, confusion and muscle ache

281
Q

Presentation of absence seizure?

A

Disorder of childhood
Ceases activity, stares and pales for a few seconds
Suddenly stops talking mid sentence
Often does not realise this has happened
EEG shows 3-Hz spike and wave activity
Children tend to develop generalised tonic-clonic seizures in adult life

282
Q

Presentation of myoclonic seizure?

A

Sudden isolated jerk of limb, face or trunk
Patient may be thrown suddenly to the ground or violently disobedient limb

283
Q

Presentation of tonic seizure?

A

Sudden sustained increased tone
Characteristic cry/ grunt
Stiffening not followed by jerking

284
Q

Presentation of atonic seizure?

A

Sudden loss of muscle tone and cessation of movement
Results in falling

285
Q

What seizures are classed as generalised seizures?

A

Generalised tonic clonic
Absence
Myoclonic
Tonic
Atonic

286
Q

Presentation of simple partial seizure?

A

Not affecting consciousness or memory
Awareness if unimpaired with focal motor, sensory, autonomic or psychic symptoms
No post-ictal symptoms

287
Q

Presentation of complex partial seizure?

A

Affects awareness or memory before, during or after seizure
Commonly arise from temporal lobe
Post ictal confusion is common in those originating from temporal lobe
Rapid recovery in those originating from frontal lobe

288
Q

Investigations to diagnose epilepsy?

A

Bloods; FBC, U+E, LFT, TFT, glucose
Lumbar puncture and CSF analysis; rule out infection
CT/ MRI; identify anatomical abnormalities and space occupying lesion
EEG

289
Q

Differentials for epilepsy?

A

Syncope
Transient ischaemic attack
Parkinsons
Meniere’s disease
Panic attack
Psychiatric illness

290
Q

Management of generalised seizure?

A

Sodium valproate/ lamotrigine
Carbamazepine

If medications are not helpful consider surgery or vagal nerve stimulation

291
Q

What other medication can be offered to treat absence seizures?

A

Ethosuximide

292
Q

Monitoring requirements in epilepsy?

A

Patients on anticonvulsants should be monitored every 6-12 months
Every 1-2 months if medication dose is altered
Ask patients to keep seizure diaries
Routine blood tests to monitor blood biochemistry

293
Q

Complications of epilepsy?

A

Head trauma
Bone fracture
Memory loss
Mood disorder
Sudden unexpected death in epilepsy
Status epilepticus

294
Q

Prognosis of epilepsy?

A

Majority of patients achieve adequate seizure control
If a single identifiable cause can be found, surgical treatment can offer 70% chance of seizure free

295
Q

What is status epilepticus?

A

Neurological emergency
Convulsive seizures that continue for a prolonged period of time with no recovery in between

296
Q

Aetiology of status epilepticus?

A

Epilepsy
Drug withdrawal
Neurological insult or systemic abnormality
Hypoxia, stroke
Metabolic abnormality
Alcohol intoxication or withdrawal

297
Q

Pathophysiology of status epilepticus?

A

When seizure aborting mechanisms fail, excessive and normally persistent excitation or ineffective inhibition result in rapid and random neural firing.

Accumulation of excitatory neurotransmitters leads to cerebral damage

298
Q

Risk factors for status epilepticus?

A

Poor anticonvulsant therapy adherence
Alcohol abuse
Stroke
Recreational drug use

299
Q

Clinical presentation in status epilepticus?

A

Prolonged/ repeated tonic- clonic seizures with altered level of consciousness
Confusion
Change in personality

300
Q

Differentials for status epilepticus?

A

Psychogenic non-epileptic status
Delirium
Coma

301
Q

Management of status epilepticus?

A

ABCDE
Supportive care; ECG, GCS, glucose
Benzodiazepine rectal if no IV access
Consider; levetiracetam, sodium valproate, phenytoin

302
Q

Monitoring requirements for status epilepticus?

A

Neurological observations
Standards observations
NICE recommends regular anticonvulsant drug levels

303
Q

Complications of status epilepticus?

A

Focal neurological deficit
Cognitive dysfunction; notably memory deficits
Behavioral problems

304
Q

What is diabetic neuropathy?

A

Peripheral nerve dysfunctions with/ without autonomic nerve dysfunction as a complication of diabetes mellitus

305
Q

Epidemiology of diabetic neuropathy?

A

Most common complication of diabetes mellitus

306
Q

What is the most common type of diabetic neuropathy?

A

Chronic sensorimotor polyneuropathy
Autonomic dysfunction

307
Q

Causes of neuropathy?

A

Toxins; alcohol
B12 deficiency
Medication induced; metformin, proton pump therapy
Chemotherapy
Hypothyroidism
Renal disease
Malignancy
Monoclonal gammopathy
Infections
Chronic inflammatory demyelinating neuropathy
Vasculitis

308
Q

Pathophysiology of diabetic neuropathy?

A

Metabolic and vascular factors result in low grade inflammation
Impaired mitochondrial function mediates Schwann cell injury
Progressive damage and loss of peripheral nerve fibres
Results in impaired sensory function and sometimes autonomic dysfunction

309
Q

Risk factors for diabetic neuropathy?

A

Duration of diabetes
Poorly controlled hyperglycaemia
Dyslipidaemia with elevated triglycerides
Immune dysregulation
Height
Body mass index
Age over 70 years

310
Q

Clinical presentation of diabetic neuropathy?

A

Peripheral pain; prickling, burning, aching, worse at night
Loss of peripheral sensation; proceeds proximally causing symmetrical distal sensory loss, glove and stocking pattern
Painless foot injuries/ ulceration
Dysaesthesia; abnormal sensation of burning, tingling and numbness
Absent ankle reflexes
Autonomic features

311
Q

What autonomic features present with diabetic neuropathy?

A

Resting tachycardia
Impaired heart rate variability
Urinary frequency, urgency, nocturia incontinence, hesitancy, weak stream, retention
Erectile dysfunction
Decreased sexual desire
Increased pain during intercourse
Orthostatic hypotension

312
Q

Investigations performed to diagnose diabetic neuropathy?

A

Clinical diagnosis
HbA1c/ fasting glucose
Routine baseline bloods
Corneal confocal microscopy

313
Q

Differentials for diabetic neuropathy?

A

Uraemia
B12 deficiency
Hypothyroidism
Chronic raised alcohol intake
Heavy metal poisoning
Drug induced neuropathy
Chronic inflammatory demyelinating neuropathy
Cauda equina
Myasthenia gravis

314
Q

Management of diabetic neuropathy?

A

Improve glycaemic control
Neuropathic pain management; pregabalin/ gabapentin, topical capsacin, TENS/ PENS

315
Q

Monitoring requirements for diabetic neuropathy?

A

Foot screen and podiatry
Fundoscopy
HbA1c

316
Q

Complications of diabetic neuropathy?

A

Foot wounds/ ulcers
Wound infection/ gangrene
Amputation
Silent MI
Death
Depression
Charcot foot

317
Q

Prognosis of diabetic neuropathy?

A

Depends of glycaemic control
Neuropathy is associated with increased mortality

318
Q

What is an essential tremor?

A

Progressive tremor of the upper extremities in posture and action, without other neurological signs or symptoms

319
Q

What does an essential tremor look like?

A

Symmetrical, rhythmic, involuntary, oscillation movement disorder of hands and forearm

Usually absent at rest and present during posture and intentional movements

320
Q

Epidemiology of essential tremor?

A

Most common movement disorders
Incidence increases with age
More common in white ancestry

321
Q

Aetiology of essential tremor?

A

Ageing, genetics
Environmental toxin exposure

322
Q

Pathophysiology of essential tremor?

A

Involves cerebellum, brainstem and thalamus
GABAnergic dysfunction of cerebellar dentate nucleus in brainstem due to neurodegeneration leads to tremulous activity within cerebellothalamocortical circuit resulting in involuntary movement of upper limb

323
Q

Risk factors for essential tremor?

A

Advanced age
Family history
White ancestry
Exposure to environmental toxins

324
Q

Clinical presentation of essential tremor?

A

Postural/ kinetic tremor; bilateral upper limb action tremor with absence of other neurological signs
Problems with fine motor tasks
Medications suppress tremor

325
Q

What medications suppress action tremor?

A

Alcohol, benzodiazepines, gabapentin, barbiturates

326
Q

Investigations to diagnose essential tremor?

A

Clinical diagnosis from history
EMG silence in all muscles groups except tremulous muscles
CT/ MRI head to rule out other causes

326
Q

Differentials for essential tremor

A

Parkinson’s disease
Dystonia
Wilson’s disease
Enhanced physiological tremor
Drug- induced tremor
Psychogenic tremor
Orthostatic tremor

327
Q

Management of essentials tremor?

A

Watch and wait
Medications; propanolol, primidone, gabapentin, alprazolam, topiramate
Deep brain stimulation
Gamma knife thalamotomy

328
Q

Monitoring requirements for essential tremor?

A

Annual visits to monitor progression

329
Q

Complications of essential tremor?

A

Deep brain stimulation related paraesthesia, dysarthria, gait disorder

330
Q

Prognosis of essential tremor?

A

Persistent and progressive disorder
Many patients are mildly affected
Some can have social handicap and embarrassment
No cure, but treatment to improve quality of life

331
Q

Classification of tremor?

A

Essential tremor
Rest tremor
Action tremor
Mixed action/ rest tremor

332
Q

Causes of rest tremor?

A

Parkinson’s disease
Dementia with lewy bodies
Multisystem atrophy
Progressive supranuclear palsy
Toxin induced parkinsonism; carbon disulphide, carbon monoxide, cyanide, manganese, herbicides, organic solvents

333
Q

Causes of action tremor?

A

Enhanced physiological tremor
Essential tremor
Cerebral tremor; MS, trauma, stroke
Fragile X tremor ataxia syndrome
Orthostatic tremor
Primary writing tremor
Neuropathic tremor

334
Q

Causes of mixed action/ resting tremor?

A

Drug induced tremor
Dystonic tremor
Tremor secondary to wilsons disease
Psychogenic tremor
Holmes tremor; Rubral, midbrain tremor

335
Q

What is Parkinson’s disease?

A

Chronic progressive neurodegenerative disorder characterised by presence of bradykinesia with resting tremor and/ or rigidity
Reduced dopaminergic neurones in the substantia nigra

336
Q

Epidemiology of Parkinson’s disease?

A

Mean age of onset is 65 years
Increasing prevalence with increasing age
Rare condition
Greater incidence in men
More common in white people

337
Q

Aetiology of Parkinson’s disease?

A

Autosomal dominant and recessive forms of disease have been identified
Mitochondrial dysfunction
Environmental factors; chronic heavy metal exposure, oxidative damage by free radicals, pesticides, MTP

338
Q

Pathophysiology of Parkinsons disease?

A

Degeneration of dopaminergic neurones in pars compacta of substantia nigra as a result of mitochondrial dysfunction and oxidative stress
Reduced striatal dopamine resulting in inhibition of thalamus hence bradykinesia

339
Q

How is Parkinson’s classified?

A

According to age of onset; juvenile (under 21 years), Young onset (between 21 and 40 years)

340
Q

Risk factors for Parkinson’s?

A

Increasing age
Family history
Mutations in glucocerebrosidase gene
MPTP exposure
Male sex
Head injury
Occupational

341
Q

Classic triad for Parkinsons?

A

Bradykinesia, Resting tremor, Cogwheel rigidity

342
Q

Clinical presentation of Parkinsons?

A

Asymmetrical presentation
Bradykinesia
Resting tremor
Rigidity
Parkinsonian gait
Postural instability
Marked facies
Hypophonia, drooling, swallowing difficulty
Fatigue, dementia, sleep disorder
Dementia
Urinary problems

343
Q

Investigations to diagnose Parkinsons?

A

Clinical based on history and examination
Dopaminergic agent trial; Symptoms Improve
MRI head; Brain atrophy, Lewy bodies in late disease

344
Q

Differentials of parkinsons?

A

Essential tremor
Dementia
Drug induced parkinsonism
Metabolic abnormalities
Corticobasal degeneration

345
Q

Management of Parkinsons?

A

Non medical management; physiotherapy, occupational therapy, speech therapy, psychiatric management

Medical management; Levodopa+decarboxylase inhibitor, dopamine antagonist, MAO-B/ COMT inhibitors

346
Q

Monitoring requirements for Parkinson’s disease?

A

Serial monitoring of movement disorder
History and neurological examination to monitor progression

347
Q

Complications of Parkinson’s?

A

Levodopa induced dyskinesia
Motor fluctuations
Dementia
Constipation, bladder dysfunction
Depression, psychosis, anxiety

348
Q

Prognosis of Parkinsons?

A

No curative or disease modifying agents
Factors favoring poorer prognosis; older age of symptoms, rigidity hypokinesia, reduced response to dopaminergic medications

349
Q

What is Huntington’s disease?

A

Autosomal dominant neurodegenerative disorder characterised by chorea, incoordination, cognitive decline, personality change and psychiatric symptoms

350
Q

Epidemiology of Huntington’s disease?

A

20 years from diagnosis to death
Affects men and women equally
Onset between 35 and 45 years
More common in North American and European ancestry

351
Q

Aetiology of Huntington’s disease?

A

Expanded CAG repeats at N-terminus of gene coding for huntingtin protein

352
Q

How many CAG repeats are needed to develop Huntington’s?

A

40 or more

353
Q

Which parent is more likely to pass on Huntington’s?

A

Father as pathogenic trinucleotide repeat is less stable in spermatogenesis

354
Q

Pathophysiology of Huntington’s?

A

CAG repeat produces elongated polyglutamine tail on huntingtin protein leading to cleavage and generation of toxic fragments of abnormal protein , predisposing cross linking and aggregation resistant to deformation

Aggregates interfere with normal cellular function, mitochondrial metabolism, apoptosis, proteosome function

355
Q

Which region of brain is most affected by Huntington’s?

A

Striatum

356
Q

Risk factors for Huntington’s?

A

Family history
European, North American ancestry

357
Q

Clinical presentation of Huntington’s?

A

Chorea
Personality change
Impaired performance at work/ school
Impulsivity
Twitching/ restlessness
Milk maids grip
Saccadic eye movements
Loss of coordination

358
Q

Describe Huntington’s chorea?

A

Continuous flow of jerky, semi purposeful movements
Occasional peculiar postures of hands, trunk or limbs and odd facial expressions

359
Q

Investigations to diagnose Huntington’s?

A

Clinical diagnosis
CAG repeat genetic testing
MRI or CT scan

360
Q

Differentials for Huntington’s?

A

Tardive dyskinesia
Benign hereditary chorea
Hyperthyroid chorea
Wilson’s disease
Lupus cerebritis
Antiphospholipid antibody syndrome

361
Q

Management of Huntington’s?

A

No disease modifying treatment
Chorea; benzodiazepines, sulphide, tetrabenazine
Antidepressants, antipsychotics
Aggression; risperidone

362
Q

Monitoring requirements for Huntington’s?

A

Every 6-12 months
Aim to review symptom, identify cover fatigue

363
Q

Complications of Huntington’s?

A

Weight Ioss
Dysphagia
Falls
Suicide risk
Incontinence

364
Q

Prognosis of Huntington’s?

A

Duration of disease is 20 years from diagnosis to death

365
Q

What is normal pressure hydrocephalus?

A

Clinical features of hydrocephalus without significantly raised CSF pressure

366
Q

Aetiology of normal pressure hydrocephalus?

A

Abnormal absorption of CSF
Build up of toxic metabolites in CSF
Abnormal arterial pulsatility compressing venous vasculature

367
Q

Pathophysiology of normal pressure hydrocephalus?

A

Imbalance between CSF production and drainage through arachnoid granulations, either through scarring or obstruction

368
Q

Risk factors for normal pressure hydrocephalus?

A

Age over 65 years
Vascular disease
Diabetes mellitus

369
Q

Clinical presentation of normal pressure hydrocephalus?

A

Gait apraxia
Cognitive impairment; mental slowing, memory impairment
Urinary frequency/ incontinence/ urgency

370
Q

Describe features of gait disturbance in normal pressure hydrocephalus?

A

Unresponsive to levodopa
Slow, cautious, unsteady gait
Reduced stride length
Insidious onset
Symmetrical
Predominantly affects lower body

371
Q

Investigations performed in normal pressure hydrocephalus?

A

CT/ MRI; enlarged ventricles, periventricular leukomalacia, cerebral infarction
Levodopa challenge; No response
Lumbar puncture; assess CSF properties, look for improvement in symptoms
Continuous intracranial pressure monitoring

372
Q

Differentials for normal pressure hydrocephalus?

A

Parkinson’s disease
Alzheimer’s
Other dementia
Urinary outflow obstruction

373
Q

Management of normal pressure hydrocephalus?

A

Surgical options; ventriculoperitoneal shunt, endoscopic third ventriculostomy

Serial CSF tap

374
Q

Monitoring requirements of normal pressure hydrocephalus?

A

Post operative monitoring for shunt function and infection

375
Q

Complications of normal pressure hydrocephalus?

A

Stroke
Subdural haematoma
Bleeding
Shunt infection
Vascular disease
Cognitive impairment

376
Q

Prognosis of normal pressure hydrocephalus?

A

Extensive radiological change on neuroimaging
Gait is most improved symptom and urinary symptoms show least improvement

377
Q

What is Wernicke’s encephalopathy?

A

Neurological emergency with varied neurocognitive manifestations including change in mental status, gait and oculomotor disturbance

378
Q

Epidemiology of Wernicke’s encephalopathy?

A

Prevalence between 0.8 and 2.8%
More common in alcoholics and people with AIDS
More prevalent in men

379
Q

Aetiology of Wernicke’s encephalopathy?

A

Acute or subacute thiamine deficiency as a result of decreased intake, relative deficiency compared to increased demand, malabsorption from GI tract

380
Q

Pathophysiology of Wernicke’s encephalopathy?

A

Thiamine deficiency leads to reduced activity of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase

Energy compromise leads to neuronal death

Can affect memory circuits leading to Korsakoff’s psychosis

381
Q

Risk factors for Wernicke’s encephalopathy?

A

Exclusive breast feeding
Alcoholism
AIDS
Malnutrition of any cause; malignancy, gastric bypass surgery, haemodialysis, hyperemesis gravidarum
Bone marrow transplantation
Gastrointestinal surgery
Genetic susceptibility
Male sex

382
Q

Clinical presentation of Wernicke’s encephalopathy?

A

Mental slowing, impaired concentration and apathy
Frank confusion
Oculomotor disturbance; gaze palsies, sixth nerve palsy, impaired vestibular ocular reflex
Change in mental status
Opthalmoplegia
Gait disturbance

383
Q

Investigations to diagnose Wernicke’s encephalopathy?

A

Finger prick glucose and screening full set of bloods
Thiamine level

384
Q

Differentials of Wernicke’s encephalopathy?

A

Alcohol intoxication/ withdrawal
Viral encephalitis
Miller- Fisher syndrome
Bickerstaff brainstem encephalitis
Primary CNS lymphoma
Toxic/ metabolic encephalopathies

385
Q

Management of Wernicke’s encephalopathy?

A

ABCDE management
Thiamine, magnesium, folic acid and multivitamin supplementation

386
Q

Monitoring requirements for Wernicke’s encephalopathy?

A

Neurocognitive evaluation for residual deficits
Work appropriate neuropsychological evaluation
Patients should be followed periodically to ensure they do not relapse and are adherent to supplementation

387
Q

Complications of Wernicke’s encephalopathy?

A

Ataxia
Varying degree of ophthalmoparesis
Korsakoff’s psychosis
Hearing loss
Seizures
Spastic paraparesis

388
Q

Prognosis of Wernicke’s encephalopathy?

A

If not recognised and treated can cause permanent brain injury with impairment in recent and remote memory, apathy and confusion

389
Q

What is Bell’s palsy?

A

Acute unilateral peripheral facial nerve palsy with deficits affecting all facial zones

390
Q

What is Ramsy- Hunt syndrome?

A

Specific form of facial nerve palsy caused by varicella zoster infection

391
Q

Epidemiology of Bell’s palsy?

A

Most common cause of facial nerve palsy
No dominant gender or side of face affected
Common between 15 and 45 years of age

392
Q

Aetiology of Bell’s palsy?

A

Reactivation of HSV-1
Inflammation and immune response

393
Q

Pathophysiology of Bell’s palsy?

A

Reactivation of HSV-1 destroys ganglion cells and infection of Schwann cells leads to demyelination and neural inflammation causing oedema in exit canal of CN8 compression the nerve and causing transient ischaemia and nerve dysfunction

394
Q

Risk factors for Bell’s palsy?

A

Intranasal influenza vaccination
Pregnancy
Upper respiratory tract infection
Arid/ cold climate
Hypertension
Family history of Bell’s palsy
Diabetes
Dental procedures

395
Q

Clinical presentation of Bell’s palsy?

A

Unilateral facial muscle weakness
Keratoconjunctivitis sicca
Post auricular pain with mild to moderate otalgia
Facial synkinesis

396
Q

Investigations to diagnose Bell’s palsy?

A

Clinical diagnosis from hsitory
EMG

397
Q

Differentials for Bell’s palsy?

A

Ramsay hunt syndrome
Lyme disease
Benign/ malignant facial nerve tumour
Chronic otitis media

398
Q

Treatment for Bell’s palsy?

A

Prednisolone within 72 hours of symptom onset
Eye drops
If severe disease then decompression surgery and antiviral therapy may be needed

399
Q

Monitoring requirements for Bell’s palsy?

A

1-2 weeks following initial visit
Then monthly or 3-monthly follow-up to monitor recovery

400
Q

Complications associated with Bell’s palsy?

A

Keratoconjunctivitis sicca
Ectropion (eyelid sagging)
Contracture and synkinesis
Gustatory hyperlacrimation

401
Q

Prognosis of Bell’s palsy?

A

Majority make full recovery
Poorer prognostic factors; advancing age, diabetes mellitus, taste disturbance on presentation

402
Q

What is Meniere’s disease?

A

Episodic auditory/ vestibular disease characterised by sudden onset vertigo, low frequency hearing loss, low frequency tinnitus and sudden sensation of fullness in ear

403
Q

Epidemiology of Meniere’s disease?

A

Affects adults, typically in 4th decade
Slight female predominance

404
Q

Aetiology of Meniere’s disease?

A

Idiopathic
Allergies
Congenital or acquired syphilis, lyme disease
Hypothyroidism
Stenosis of internal auditory canal

405
Q

Pathophysiology of Meniere’s disease?

A

Impaired endolymph absorption forms endolymphatic hydrops increasing endolymphatic fluid pressure leading to reupture of Reissner’s membrane
This releases K+ rich endolymph into peri-lymphatic space injuring sensory and neural elements
In between attacks membrane may reattach and symptoms remit

406
Q

Risk factors for Meniere’s disease?

A

Viral infection
Genetic pre-disposition; autosomal dominant, X-linked
Autoimmune disease

407
Q

Clinical presentation of Meniere’s disease?

A

Vertigo
Hearing loss
Tinnitus
Aural fullness

408
Q

Investigations to diagnose Meniere’s disease?

A

Positive romberg’s test
Pure- tone air and bone conduction with masking; Unilateral sensorineural hearing loss
Speech audiometry
Tympanometry/ immittance/ stapedial reflex levels
Oto-acoustic emissions

409
Q

Differentials for Meniere’s disease?

A

Acoustic neuroma
Vestibular migraine
Vestibular neuronitis
Viral labyrinthitis
Benign paroxysmal positional vertigo
Vertebrobasilar insufficiency

410
Q

Acute management for Meniere’s disease?

A

Thiazide diuretic +/- K+ sparring diuretic
Vertigo; anti-emetic, corticosteroid, vestibular suppressant
Tinnitus; benzodiazepine

411
Q

Long term management for Meniere’s disease?

A

Dietary and lifestyle change
Hearing aid
Endolymphatic sac surgery, vestibular nerve resection, labyrinthectomy

412
Q

Monitoring requirements for Meniere’s disease?

A

Follow- up with audiologist and otologist
Regular hearing tests and monitor symptoms

413
Q

Complications of Meniere’s disease?

A

Falls
Profound hearing loss

414
Q

Prognosis of Horner’s syndrome?

A

Symptoms worsen regardless of interventions
Unpredictable course, may have periods of remission

415
Q

What is Horner’s syndrome?

A

Compression of sympathetic trunk presenting with ptosis, miosis, anhidrosis

416
Q

Epidemiology of Horner’s syndrome?

A

Uncommon, occuring 1 in 6000
No gender, age or ethnicity predominance

417
Q

Aetiology of Horner’s syndrome?

A

First order neurons; stroke, tumour, demyelinating disease, neck trauma, cyst in spinal cord

Second order neuron; lung cancer, schwannoma, damage to aorta, surgery in chest cavity, traumatic injury

Third order neurons; damage to carotid/ jugular, tumour or infection near base of skull, migraines

418
Q

Pathophysiology of Horner’s syndrome?

A

Compression of sympathetic chain

419
Q

Clinical presentation of Horner’s syndrome?

A

Classic triad; anhidrosis, miosis, ptosis
Notable difference in size of pupil
Delayed dilation of pupil in dim light
Slight elevation of lower lid
Sunken appearance in affected eye

420
Q

Investigations to diagnose Horner’s syndrome?

A

Look for cause of compression; CXR, CT, MRI, angiography

421
Q

Differentials for Horner’s syndrome?

A

Carotid artery dissection
Neuroblastoma
Neurosyphilis

422
Q

Management of Horner’s syndrome?

A

Treat the cause of compression
No particular treatment for Horner’s syndrome

423
Q

Complications/ prognosis of Horner’s syndrome?

A

Depends on aetiology

424
Q

What is neurofibromatosis?

A

Autosomal dominant genetic disorder with characteristic features; cafe au lait spots, multiple neurofibroma, irish lisch nodules

425
Q

What are the classic features of NF?

A

Café au lait spots
Multiple neurofibroma
Irish Lisch nodules

426
Q

Epidemiology of NF?

A

Autosomal dominant mutation

427
Q

Where is the genetic mutation in NF1?

A

NF 1 gene on chromosome 17

428
Q

Pathophysiology of Neurofibromatosis 1?

A

Reduction in NF1 gene product neurofibromin which is a tumour suppressor protein, disrupts Ras-oncogene mediated signaling in Schwann cells, glia, melanocytes and other cells derived from ectoderm
Tissue specific dysplasia/ neoplasia

429
Q

Risk factors for neurofibromatosis?

A

Parent with NF
Severe crush trauma

430
Q

Clinical presentation of NF?

A

Pain in any location; usually due to peripheral neurofibroma
Neurological deficit; gross motor delay, incoordination, performance problems
Skin changes; cafe au lait spits, axillary freckling, cutaneous neurofibroma
Visual change; optic disk pallor, irish lisch nodules, visual compramise
CNS signs; hydrocephalus, cerebellar abnormalities
PNS signs; palpable mass in neck, brachial plexus, groin, popliteal fossa
Skeletal signs; tibial dysplasia, pseudoarthrosis, sphenoid wing dysplasia
Gastrointestinal; constipation, abdominal pain, gastrointestinal bleeding

431
Q

Investigations to diagnose NF?

A

MRI/ CT/ PET scan; look for tumours, hydrocephalus
Biopsy
Genetic test to confirm NF1 mutation

432
Q

Differentials for NF?

A

Neurofibromatosis type 2
McCune-Albright syndrome
Familial cafe au lait spots
Age related cutaneous neurofibromas
Schwannomatosis

433
Q

Management of NF?

A

Surgical removal of tumours
Physiotherapy, psychological therapy
Frequent follow-up

434
Q

Monitoring requirements for NF?

A

Annual review including history, physical exam of eyes, nervous system, skeleton, skin and CVS
Women offered mammogram from 30 years

435
Q

Complications of NF?

A

Migraine
Epilepsy
Renal artery stenosis causing hypertension
Learning and behavioural problems
Scoliosis of spine
Vision loss
Malignant peripheral sheath tumours
Gastrointestinal stromal tumour
Spinal cord tumour
Breast cancer
Leukaemia

436
Q

Prognosis of NF?

A

Reduced life-expectancy due to cardiovascular complications and malignancy

437
Q

What is the cause of NF 2?

A

Mutation on chromosome 22 coding for protein merlin (tumour suppressor protein)

438
Q

Which cells does NF2 affect more?

A

Schwann cells

439
Q

What is the inheritance pattern of NF2?

A

Autosomal dominant

440
Q

What type of NF is associated with acoustic neuroma?

A

NF 2

441
Q

What sign is indicative of NF2?

A

Bilateral acoustic neuroma

442
Q

What is acoustic neuroma?

A

Benign cerebellopontine angle tumour

443
Q

Epidemiology of acoustic neuroma?

A

Female predominance

444
Q

Aetiology of acoustic neuroma?

A

Sporadic
Neurofibromatosis type 2

445
Q

Pathophysiology of acoustic neuroma?

A

Benign growth at cerebello- pontine angle causing compression of vestibulocochlear nerve producing problems with hearing and balance

446
Q

Risk factors for acoustic neuroma?

A

NF type 2

447
Q

Clinical presentation of acoustic neuroma?

A

Unilateral sensorineuronal hearing loss, tinnitus
Dizziness, imbalance
Fullness in inner ear
If bilateral think of NF type 2

448
Q

Investigations to diagnose acoustic neuroma?

A

Audiometry; sensorineural pattern hearing loss
Auditory brainstem reflexes
MRI/ CT; look for tumour

449
Q

Differentials for acoustic neuroma?

A

Meningioma
Facial/ trigeminal nerve schwannoma

450
Q

Management of acoustic neuroma?

A

Conservative monitoring if not surgical candidate
Surgery to remove tumour
Radiotherapy

451
Q

Monitoring requirements of acoustic neuroma?

A

MRI every 6 months to monitor growth, then yearly when stable

After surgery a baseline MRI and one after a few months, then annually for 5 years

452
Q

Complications of acoustic neuroma?

A

Surgical complications; injury to vestibulocochlear nerve, facial weakness/ paraesthesia, CSF fluid leak

Radiation complications; Hydrocephalus, secondary malignancy, hearing loss, facial nerve palsy

453
Q

Prognosis of acoustic neuroma?

A

Good prognosis with minimal complications

40-60% of tumours do not require treatment

454
Q

What is cauda equina syndrome?

A

Compression of lumbosacral nerve roots that extend below spinal cord

455
Q

Epidemiology of cauda equina syndrome?

A

1-2 cases per 100,000
Equal incidence between race, gender
Under 50 more likely to have acute presentation, over 50 more progressive

456
Q

Aetiology of cauda equina syndrome?

A

Disk herniation at L4/L5
Spinal stenosis
Traumatic injury
Spinal tumour
Epidural haematoma, abscess

457
Q

Most common cause of cauda equina syndrome?

A

Disk herniation

458
Q

Pathophysiology of cauda equina syndrome?

A

Bundle of spinal nerves L1- S5 which innervate bladder, bowel, lower limb muscle and sexual function

Compression of these nerve roots produces symptoms

459
Q

Classification of cauda equina syndrome?

A

Incomplete; thecal sac compression with no urinary retention

Complete; thecal sac compression with established neurogenic urinary retention

460
Q

Risk factors for cauda equina syndrome?

A

Lumbar disk herniation
Spinal trauma
Spinal surgery
Spinal epidural abscess
Anticoagulation therapy; increases risk of haematoma
Spinal stenosis
Spinal tumour

461
Q

Clinical presentation of cauda equina syndrome?

A

Lower limb weakness
Saddle paraesthesia/ anaesthesia
Bowel dysfunction
Bladder dysfunction and retention
Lower back pain
Sciatica
Sexual dysfunction

462
Q

Investigations to diagnose cauda equina syndrome?

A

CT/ MRI; visualise compression
Urodynamic testing

463
Q

Differentials for cauda equina syndrome?

A

Spinal epidural abscess
Osteoporotic spinal compression fracture
Transverse myelitis
GBS
Traumatic conus medullaris

464
Q

Management of cauda equina syndrome?

A

Decompression surgery
Bladder and bowel management `

465
Q

Monitoring requirements in cauda equina syndrome?

A

Long term bladder, bowel, sexual and physical dysfunction monitoring
Physiotherapy

466
Q

Complications of cauda equina syndrome?

A

Bladder dysfunction
Bowel dysfunction
Sexual dysfunction
Sensory impairment
Leg weakness

467
Q

Prognosis of cauda equina syndrome?

A

Degree of neurological dysfunction at surgery indicates prognosis

Poorer prognostic factors; urinary retention, delay of surgery

468
Q

What is chronic spinal cord injury?

A

Symptoms of spinal cord injury that have been present for at least 12 months resulting in permanent/ progressive interruption in conduction of impulses across neurons and tracts of spinal cord

469
Q

Epidemiology of chronic spinal cord injury?

A

75% of patients are male
Children and elderly are most at risk
Falls are most common cause?

470
Q

Why are children and elderly at highest risk of chronic spinal cord injury?

A

Less developed neck musculature
Horizontal orientation of facets
Relative ligamentous laxity

471
Q

Aetiology of chronic spinal cord injury?

A

Traumatic; compression from haematoma, dissection/ shearing/ laceration trauma
Non traumatic injury; degeneration, compression from tumours, infection
Congenital narrowing of spinal column
Vascular injury

472
Q

Pathophysiology of chronic spinal cord injury?

A

Inflammatory response secondary to initiating factor resulting in disability and depends on which region of the spinal cord is affected

473
Q

Risk factors for chronic spinal cord injury?

A

Spinal cord trauma or ischaemia
Extremes of age
Narrow spinal canal
Male sex

474
Q

Clinical presentation of chronic spinal cord injury?

A

Motor weakness
Loss of fine motor coordination
Spasticity
Paraesthesia, numbness, dysaesthesia
Hyperreflexia and ankle clonus
Autonomic dysreflexia

475
Q

Signs of autonomic dysreflexia?

A

Sudden uncontrolled rise in blood pressure
Pounding headache
Sweating
Shivering
Anxiety
Chest tightness
Blurred vision

476
Q

Investigations to diagnose chronic spinal cord injury?

A

MRI; look for lesions, spinal column abnormalities
EMG; localise neuromuscular pathology
Urodynamic studies

477
Q

Differentials for chronic spinal cord injury?

A

Compressive myelopathy
Non compressive myelopathy

478
Q

Management of chronic spinal cord injury?

A

If compressive; surgical decompression in timely manner and vasodilatory therapy if autonomic dysreflexia

Rehabilitation, pain control, physiotherapy, spasticity management

479
Q

Monitoring requirements in chronic spinal cord injury?

A

VTE prophylaxis
If on opiates monitor respiratory drive

480
Q

Complications of chronic spinal cord injury?

A

Disturbance in bowel and bladder control
Respiratory dysfunction
Sexual dysfunction
Joint contractures
Neuropathic pain
Autonomic dysreflexia

481
Q

Prognosis of chronic spinal cord injury?

A

Depends on severity of neurological deficit
Decreased life expectancy

482
Q

What is Narcolepsy?

A

Chronic sleep disorder affecting control of sleep and wakefulness with REM sleep intrusion into wake state

483
Q

Characteristic of narcolepsy?

A

Excessive daytime sleepiness
Cataplexy; generalised muscle weakness leading to partial or complete collapse
Hypnagogic/ hypnopompic hallucinations; visual or auditory perceptions on falling asleep or awakening
Sleep paralysis

484
Q

Epidemiology of narcolepsy?

A

2 per 1000 cases
Second most common cause of disabling daytime sleepiness after obstructive sleep apnoea

485
Q

Aetiology of narcolepsy?

A

Head trauma
Stroke
Brain or hypothalamic tumours
CNS infection/ inflammation
Arteriovenous malformations
Multiple sclerosis
Paraneoplastic anti-Ma antibodies
Niemann-Pick disease type C, Norrie’s disease, Prader-Willi syndrome

486
Q

Risk factors for narcolepsy?

A

HLA-2 DQA1, DQB2
Prader-Willi syndrome
Low CSF hypocretin
Hypothalamic tumours, infarct, haemorrhage

487
Q

Investigations to diagnose narcolepsy?

A

Actigraphy and sleep diary
Overnight polysomnography
Multiple sleep latency tests

488
Q

Differentials for narcolepsy?

A

Obstructive sleep apnoea
Periodic limb movement of limbs
Restless leg syndrome
Behaviourally induced insufficient sleep syndrome
Hypersomnia due to medications/ psychiatric conditions
Idiopathic hypersomnia
Menstrual related hypersomnia

489
Q

Management of narcolepsy?

A

Regular and adequate amounts of sleep during night
Schedule naps to optimise daily function
Avoid heavy meals and afternoon caffeine/ alcohol

Medications; Modafinil, pitolisant, sodium oxalate

490
Q

Monitoring requirements in narcolepsy?

A

Follow up every 6-12 months to re-evaluate social support, symptoms and medications

491
Q

Complications of narcolepsy?

A

Traffic accidents
Depression

492
Q

Prognosis of narcolepsy?

A

Lifelong condition
Almost half patients have daily impairment from symptoms

493
Q

What is myalgic encephalomyelitis?

A

Chronic fatigue syndrome for more than 6 months, with combination of cognitive dysfunction, total body pain, unrefreshing sleep, post exertional malaise

494
Q

Epidemiology of myalgic encephalomyelitis?

A

Peak onset between 30 and 50 years
2-3 times more common in women
More common in ethnic minority groups

495
Q

Aetiology of myalgic encephalomyelitis?

A

Post COVID syndrome
Viral and bacterial infections; EBV, mycoplasma pneumonia
Neuroendocrine
Genetic
Gastrointestinal
Psychological
IgG subclass deficiencies

496
Q

Risk factors of myalgic encephalomyelitis?

A

Female sex
EBV infection in adolescents
COVID
Family history
Genetic factors
Autoimmune disease
Gut microbiome

497
Q

Clinical presentation of myalgic encephalomyelitis?

A

Persistent disabling fatigue for over 6 months
Post exertional malaise
Short term memory/ concentration impairment
Sore throat
Generalised arthralgia without inflammation
Unrefreshing sleep
Orthostatic intolerance

498
Q

Investigations to diagnose myalgic encephalomyelitis?

A

DePaul symptom questionnaire/ clinical diagnosis
FBC with WCC differential, CRP, ESR, comprehensive metabolic panel, TSH, anti- ANA, anti- RF
HIV antibody test

499
Q

Differentials for myalgic encephalomyelitis?

A

COVID
Migraine
Anxiety
Major depressive episode
Sleep apnoea
Fibromyalgia
Reaction to life crisis
Dehydration
Psychiatric illness

500
Q

Management of myalgic encephalomyelitis?

A

No curative treatment, treat the symptoms and improve functional capacity
Occupational therapy, physical therapy
CBT and psychiatry referral

501
Q

Monitoring requirements for myalgic encephalomyelitis?

A

Management with single primary care physician

See patient every 3 months to counsel and reassess situation and symptoms

502
Q

Complications of myalgic encephalomyelitis?

A

Major depressive episode

503
Q

Prognosis of myalgic encephalomyelitis?

A

Lifelong condition with symptom management as there is no treatment

504
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis
Primary lateral sclerosis
Progressive muscular dystrophy
Progressive bulbar palsy

505
Q

What is ALS?

A

Neurogenerative disorder characterised by progressive muscle weakness that can start in any limb, axial, bulbar or respiratory muscles and then become generalised causing progressive disability

506
Q

Epidemiology of ALS?

A

Mean age of onset is 62 years
Peak incidence between 60 and 75 years
More common in men
Higher incidence in white ethnicity

507
Q

Aetiology of ALS?

A

Sporadic

508
Q

Pathophysiology of ALS?

A

Progressive loss of cortical, bulbar and ventral cord motor neurons
After motor cell death retrograde axonal degeneration followed by denervation and reinnervation in corresponding muscles

Glutamate toxicity, protein misfolding, oxidative stress, inflammation, mitochondrial dysfunction are involved in pathophysiological changes

509
Q

Risk factors for ALS?

A

Genetic/ family history
Age over 40 years
Military service
Professional athletic activity
Smoking
Agricultural chemical exposure
Lead exposure

510
Q

Clinical presentation of ALS?

A

UMN symptoms
Upper extremity weakness; Difficulty in performing ADL
Stiffness with poor coordination and balance
Stiffness and decreased balance with impact on gait; UMN truncal weakness
Hyperreflexia
Dyspnoea
Strained slow speech
Hypophonic speech

LMN symptoms
Spasticity and unsteady gait
Painful muscle spasm
Difficulty arising from chair or going up stairs
Foot drop
Head drop; LMN axial weakness
Difficulty maintaining erect posture
Muscle atrophy

511
Q

Investigations to diagnose ALS?

A

Clinical presentation and history
Neuroimaging and bloods to rule out other causes

512
Q

Differentials for ALS?

A

Cervical spondylosis with myelopathy and radiculopathy
Inclusion body myositis
Monomelic amyotrophy
Myasthenia gravis
Post- polio syndrome
Other types of motor neurone disease

513
Q

Management for ALS?

A

Riluzole at diagnosis

Respiratory symptoms; Non invasive ventilation
Dysphagia and weight loss; diet modification, feeding tube
Dysarthria; alternative communication methods
Muscle weakness; physiotherapy
Spasticity; physiotherapy, baclofen, tizanidine, botox
Psychiatric management

514
Q

Which medication is prognostic in ALS?

A

Riluzole

515
Q

Monitoring requirements for patients taking riluzole?

A

LFT and FBC every 3 months due to risk of neutropenia and hepatotoxicity

516
Q

Monitoring requirements in ALS?

A

Respiratory function and nutritional status every 3 months

Bloods every 3 months if on riluzole

517
Q

Complications of ALS?

A

Respiratory failure
Nutritional deficit
Aspiration pneumonia
Riluzole related hepatotoxicity/ neutropenia

518
Q

Poorer Prognostic factors for ALS?

A

Older age at diagnosis
Bulbar onset
Comorbid frontotemporal dementia
Baseline FVC below 75%
Substantial weight loss

519
Q

Good prognostic factors for ALS?

A

Treatment with non-invasive ventilation
Enteral nutrition
Younger age at diagnosis
Limb onset
Line first vital capacity over 75%
Longer time from symptom onset to diagnosis

520
Q

Prognosis of ALS?

A

Mean survival is 3-5 years from diagnosis
Progressive illness

521
Q

What is brown sequard syndrome?

A

Lesion of spinal cord resulting in weakness/ paralysis, sensory distrubance on the same side as lesion and contralateral pain and temperature sensory disturbance due to hemisection of the spinal cord

522
Q

Epidemiology of brown sequard syndrome?

A

Accounts for 4% of spinal cord injuries
Most common cause is trauma

523
Q

Aetiology of brown sequard syndrome?

A

Trauma; puncture, wound, penetrating trauma, gunshot wound, motor accident
Ischaemia/ infarction/ haemorrhage
Infectious disease
Inflammatory disease
Spinal cord tumour

524
Q

Pathophysiology of brown sequard syndrome?

A

Clean cut hemi-section of spinal cord

525
Q

Risk factors for brown sequard syndrome?

A

Penetrating trauma
Infection

526
Q

Clinical presentation of brown sequard syndrome?

A

Loss of voluntary function on same side of body below lesion
Loss of pain and temperature sensation on contralateral body side below level of injury
Incontinence

527
Q

Investigations to diagnose brown sequard?

A

Clinical diagnosis
Neuroimaging

528
Q

Differentials for Brown sequard?

A

Stroke/ tumour/ cyst causing spinal cord compression
Cauda equina syndrome

529
Q

Management of brown sequard syndrome?

A

Decompressive surgery
VTE prophylaxis
Breathing support
Rehabilitation; maintain strength and range of motion, improve mobility

530
Q

Monitoring requirements in brown sequard syndrome?

A

Rehabilitation and physiotherapy involvement

Monitor healing of injury

531
Q

Complications of brown sequard syndrome?

A

Abdominal distention
Depression
Hypotension
Pulmonary embolism
Infection
Permanent paralysis

532
Q

Prognosis of brown sequard?

A

Depends of cause and degree of spinal cord injury

533
Q

What is mononeuropathy?

A

Damage to single nerve lying close to skin or bone resulting in pain, loss of movement and sensation

534
Q

Which nerves are commonly affected by mononeuropathy?

A

Median nerve; carpal tunnel syndrome
Ulnar nerve; elbow
Radial nerve; upper arm
Peroneal nerve; below knee
Lateral femoral cutaneous nerve; in the leg

535
Q

What is the difference between mononeuropathy and radiculopathy?

A

Radiculopathy affects nerves as they leave the spinal canal and typically affects nerve roots

Mononeuropathy affects peripheral nerves that lye close to skin and bone

536
Q

Epidemiology of mononeuropathy?

A

Carpal tunnel syndrome is the most common form of entrapment neuropathy

537
Q

Aetiology of mononeuropathy?

A

Poorly fitted casts/ crutches
Pressure from staying fixed in a position for a long time/ paralysis
Injury from radiation therapy

538
Q

Pathophysiology of mononeuropathy?

A

Stiffness of soft tissue or pressure from underlying bone damages peripheral nerve causing impingement and nerve dysfunction

539
Q

Risk factors for mononeuropathy?

A

Obesity
Diabetes
Pregnancy

540
Q

Clinical presentation of mononeuropathy?

A

Loss of sensation in affected area
Weakness in affected area
Pain or burning
Feelings of pins and needles

541
Q

Investigations to diagnose mononeuropathy?

A

Clinical diagnosis from history
Electromyography and nerve conduction studies
Neuromuscular ultrasound and MRI imaging

542
Q

Differentials for mononeuropathy?

A

Radiculopathy
Chronic pain syndrome
Alcoholic neuropathy
Brachial neuritis
GBS
Acute compartment syndrome

543
Q

Management of mononeuropathy?

A

Decompression surgery
Corticosteroid injections
Splints to immobilise the area

544
Q

Complications of mononeuropathy?

A

Permanent weakness
Impaired dexterity
Permanent disability
Loss of sensation
Pain

545
Q

Prognosis of mononeuropathy?

A

If caught and treated early then improved prognosis

546
Q

What is radiculopathy?

A

Injury/ damage to nerve roots at the region the leave the spine

547
Q

Aetiology of radiculopathy?

A

Degeneration wear and tear
Arthritis
Herniated discs
Spondylosis
Degenerative spondyloarthropathies
Bone spurs

548
Q

Pathophysiology of radiculopathy?

A

The point at which spinal nerve roots leave the vertebral column can become narrowed and pinch on the nerve
Causing muscle weakness, pain and sensory disturbance

549
Q

Types of radiculopathy?

A

Cervical radiculopathy
Lumbar radiculopathy (sciatica)
Thoracic radiculopathy

550
Q

Risk factors for radiculopathy?

A

Heavy manual labour
Poor posture
Smoking
Operating vibrating equipment
Spinal trauma
Previous spinal nerve injury

551
Q

Clinical presentation of radiculopathy?

A

Cervical radiculopathy
Numbness and tingling in the fingers, hands
Weakness in muscles of the arm, shoulder or hand
Loss of sensation in the arms and shoulders

Thoracic radiculopathy
Sharp, burning, shooting pain present at back, scapula, chest or abdominal wall

Lumbar radiculopathy
Burning sharp pain radiating down leg

551
Q

Investigations to diagnose radiculopathy?

A

History and examination; abnormalities in sensation, reflexes, muscle power
X-ray; bone alignment
MRI/ CT; nerve root compression

552
Q

Differentials for radiculopathy?

A

Brachial plexus injury
Cervical disk injuries
Cervical facet syndrome
Rotator cuff injury

553
Q

Management for radiculopathy?

A

Non surgical; rest, physical therapy, NSAIDs, steroid injections

Surgical; spinal decompression. discectomy, laminectomy, spinal fusion, foraminotomy, disc replacement surgery

554
Q

Monitoring requirements in radiculopathy?

A

Annual review with surgeons
Monitor for pain, loss of function

555
Q

Complications of radiculopathy?

A

Prolonged nerve damage
Decreased quality of life
Cauda equina syndrome
Chronic pain syndrome
Muscle atrophy, deconditioning and wasting

556
Q

What is cerebellar disease?

A

Dysfunction of cerebellum resulting in ataxia, coordination, balance and gait disturbance

557
Q

Aetiology of cerebellar disease?

A

Multiple sclerosis
Posterior circulation stroke
Bilateral cerebellopontine angle lesions
Paraneoplastic syndromes
Drugs and toxins
Metabolic; thyroid, B12 deficient, coeliac, wilson’s disease
Infectious; HIV, neurosyphilis, toxoplasmosis
GBS
Hereditary; friedreich ataxia, Von hippel- lindau syndrome

558
Q

Pathophysiology of cerebellar disease?

A

Dysregulation of cerebellar activity affects patients gait, balance and coordination

559
Q

Risk factors for cerebellar disease?

A

Toxin ingestion
Poor nutrition
Traumatic injury
Pre-existing neurological condition

560
Q

Clinical presentation of cerebellar disease?

A

Nystagmus
Hypometric/ hypermetric saccadic eye movements
Cerebellar staccato speech
Upper limb signs; Intention tremor, Past- pointing, Dysmetria, Dysdiadochokinesis , Hypotonia
Truncal ataxia
Ataxic gait
Heel to shin ataxia

561
Q

Investigations to diagnose cerebellar disease?

A

Neuroimaging
Blood tests; FBC, ESR, CRP, B12, TFT, copper, paraneoplastic screen, auto anti-bodies, tox screen
Lumbar puncture

562
Q

Differentials for cerebellar disease?

A

Parkinson’s
Dementia
Stroke
Motor neuron disease
Diabetes mellitus
Encephalopathy
B12 deficiency

563
Q

Management for cerebellar disease?

A

If cause is identified, treat the cause
Physiotherapy and coordination training

564
Q

Monitoring requirements for cerebellar disease?

A

Regular follow- up with neurologist
Serial neuroimaging

565
Q

Complications of cerebellar disease?

A

Falls
Paralysis
Dizziness
Gait disorder
Worsening tremor
Psychosocial stigma
Raised ICP
Developmental delay in children

566
Q

Prognosis of cerebellar disease?

A

Depends on aetiology
Metabolic and nutritional have better prognosis

567
Q

What is the nature of benign brain tumours?

A

Low grade, less likely to return after treatment

568
Q

What is the nature of malignant tumours?

A

High grade, more likely to return after treatment

569
Q

Epidemiology of brain tumours?

A

More prevalent in men and in developed countries
Highest incidence in people aged 85 to 89 years

570
Q

Aetiology of brain tumours?

A

Primary brain tumours originate in the brain
Secondary brain tumours have a primary tumour elsewhere and metastasise to brain

571
Q

Pathophysiology of brain tumours?

A

Creates a space occupying lesion which compresses local structures causing neurological dysfunction
If malignant then also has systemic effects of lethargy, weakness, weight loss, fevers

572
Q

Risk factors for brain tumours?

A

Increasing age
Radiation exposure
Family history of certain genetic conditions; Tuberous sclerosis, NF1, NF2, turner’s syndrome

573
Q

Clinical presentation of brain tumours?

A

Headache
Seizures
Persistent nausea, vomiting, drowsiness
Mental, behavioural changes
Vision and speech problems

574
Q

Investigations to diagnose brain tumours?

A

Neuroimaging
Bloods

574
Q

Differentials for brain tumours?

A

Essential tremor
Stroke
Chronic subdural hematoma
Meningitis
Orbital optic neuritis
AV malformation
Intraocular optic neuritis
Brain abscess
Neurosyphilis

574
Q

Management of brain tumours?

A

Steroids
Pain relief, antiemetics for symptom control
Surgery, radiotherapy, chemotherapy

575
Q

Monitoring requirements for brain tumours?

A

Seek specialist advice
Different for different tumours

576
Q

Complications of brain tumours?

A

Treatment induced toxicity
Compression of brain structures
Altered mental status
Raised ICP

577
Q

Prognosis of brain tumours

A

Depends on stage and grade of tumour, location and radiological findings

578
Q

Mechanism of action of lamotrigine?

A

Sodium channel blocker

579
Q

Side effects of lamotrigine?

A

Stevens- Johnson syndrome

580
Q

Mechanism of action of pyridostigmine?

A

Acetylcholine esterase inhibitor

581
Q

Side effects of pyridostigmine?

A

Diarrhoea
Vomiting
Sweating
Muscle cramps/ muscle weakness
Increased salivation
Miosis
Bradycardia
Headache

Phase 3A (7 decks)

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