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Year 3 - Neuro > General > Flashcards

General Flashcards

1
Q

What are 5 red flags in headache presentation?

A 
New onset >55
Previous malignancy
Immunosuppression
Early morning headache
Exacerbation by Valsalva
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2
Q

In headache more common in men or women?

A

Women

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3
Q

What is the criteria for a diagnosis of migraine without aura?

A

5+ attacks lasting 4-72 hours
2 of: unilateral throbbing pain, worse on movement
1 of: photophobia, phonophobia, autonomic features

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4
Q

What is an “aura”?

A

Full reversible, visual, sensory , motor or language symptoms lasting 20-60 minutes

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5
Q

What can trigger a migraine?

A

Sleep, foods, stress, hormones, exercise

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6
Q

How is migraine managed?

A

Avoid triggers
Relaxation and stress management
Pharmacological

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7
Q

How can migraine triggers be identified?

A

Use of headache diary

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8
Q

How can headaches be treated pharmacologically?

A

NSAID, 5HT agonists

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9
Q

What NSAIDs can be used for headache?

A

Aspirin 900mg
Naproxen 250mg
Ibuprofen 400mg

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10
Q

How are 5HT agonists taken for migraine?

A

Orally, sublingual or s/c

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11
Q

What 5HT agonist (triptans) can be used for migraine?

A

Frovatriptan

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12
Q

When would migraine prophylaxis be considered?

A

3 attacks/month or very severe

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13
Q

What prophylaxis can be used for migraine?

A

Propanolol 80-240mg
Topiramate (carbonic anhydrase inhibitor) 25-100mg
Amitriptyline 10-75mg

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14
Q

What lifestyle factors affect migraine?

A

Hydration
Caffeine
Stress
Exercise

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15
Q

What are the 6 types of migraine

A 
Acephalgic
Basilar
Retinal
Ophthalmic
Hemiplegic
Abdominal
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16
Q

What is an acephalgic migraine?

A

No headache but aura present

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17
Q

What is a basilar migraine?

A

Migraine with vertigo/dizziness

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18
Q

Which type of migraine is common in kids?

A

Abdominal

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19
Q

How are tension type headaches treated?

A

Relaxation physiotherapy and anti-depressants

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20
Q

What does a tension type headache feel like?

A

Pressing, tingling, bilateral headache

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21
Q

What is a trigeminal autonomic cephalgia?

A

Primary headache disorder

Causing unilateral trigeminal distribution pain with cranial autonomic features

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22
Q

What cranial nerve features are present in trigeminal autonomic cephalgia?

A

Ptosis, miosis, n&v, nasal stiffness, tearing, eye lid oedema

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23
Q

What are the 4 types of trigeminal autonomic cephalgias?

A

Cluster
Paroxysmal
Hemicrania continua
SUNCT

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24
Q

Who gets a cluster type trigeminal autonomic cephalgia?

A

Men 30-40s

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25
Q

What is a cluster type trigeminal autonomic cephalgia?

A

Unilateral, EXTREME, headache lasting 30mins to 2 hours

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26
Q

What is the pattern of cluster type trigeminal autonomic cephalgia?

A

1-8 per day for months

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27
Q

What is the treatment for a cluster type trigeminal autonomic cephalgia?

A

High flow oxygen for 20 mins
S/c sumatriptan 6mg
Steroids over 2 weeks
Verapamil for prophylaxis

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28
Q

Who gets paroxysmal hemicrania type trigeminal autonomic cephalgia?

A

Women 50-60s

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29
Q

How does paroxysmal hemicrania type trigeminal autonomic cephalgia present?

A

Unilateral with autonomic features

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30
Q

What is the pattern of paroxysmal hemicrania type trigeminal autonomic cephalgia?

A

Comes and goes
Lasts 10-30 mins
Get 1-40 per day

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31
Q

How is paroxysmal hemicrania type trigeminal autonomic cephalgia treated?

A

Indomethicin 50mg TDS always works

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32
Q

How does SUNCT type trigeminal autonomic cephalgia present?

A

Short, unilateral headache with tearing

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33
Q

How are SUNCT type trigeminal autonomic cephalgias treated?

A

Lamotrigine, gabapentin

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34
Q

What investigations should be done for headaches?

A

MRI, MR angiogram, CT

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35
Q

Who gets idiopathic cranial hypertension?

A

Obese females

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36
Q

How does headache from idiopathic cranial hypertension present?

A

Headache with diurnal variation, worse on lying down

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37
Q

How is headache from idiopathic cranial hypertension investigated?

A

MRI with sequence

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38
Q

Describe pressure in CSF with idiopathic cranial hypertension?

A

Elevated >30

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39
Q

How does idiopathic cranial hypertension affect vision?

A

Visual acuity probably stays normal but there is loss of visual fields
Eventually can go blind

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40
Q

Who gets trigeminal neuralgia?

A

Old women

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41
Q

How does trigeminal neuralgia present?

A

Severe stabbing unilateral pain lasting 1-90s

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42
Q

What is the pain in trigeminal neuralgia?

A

Lasts 1-90s, 10-100x daily

Weeks to months before remission

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43
Q

How is trigeminal neuralgia treated?

A

Carbamazepine, gabapentin, phenytoin, baclofen, surgical ablation and decompression

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44
Q

What investigation should be done in trigeminal neuralgia?

A

MRI

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45
Q

Which symptoms would a brain tumour present with?

A

Headache that wakes you up at night
Progressive neuro symptoms
Motor weakness
Seizures (25%)

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46
Q

What is the most common extra-axial brain tumour?

A

Meningioma

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47
Q

How likely is it for a meningioma to become malignant?

A

Not

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48
Q

What is the second most common malignancy in children?

A

Meningioma

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49
Q

How does increased intercranial pressure present?

A

Headache, vomiting, mental changes, seizures

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50
Q

What are signs that increased intercranial pressure needs treated immediately?

A

Blown pupil

Rapidly reducing gcs

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51
Q

What can you give in increased intercranial pressure to reduce pressure in cavity?

A

Mannitol

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52
Q

Which cell type is mostly likely to be involved in brain tumour?

A

Oligodendrocytes

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53
Q

Who gets glial tumours?

A

25-45 year olds

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54
Q

Which tumour is solid, grayish with a “toothpaste” morphology?

A

Oligodendrocyte tumour

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55
Q

What are the 4 types of astrocytic tumours?

A

Type I - Pilocytic, pleomorphic xanthoastrocytoma
Type II - Low grade, but becomes malignant
Type III - Anaplastic
Type IV - Glioblastoma multiforme

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56
Q

Who gets type I astrocytic tumours?

A

Children and young adults

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57
Q

Which type I astrocytic tumour is curable?

A

Cerebellar

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58
Q

How is a type I astrocytic tumour treated?

A

Surgery

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59
Q

How does a type II astrocytic tumour present?

A

Seizure

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60
Q

What are poor prognostic factors for type II astrocytic tumours?

A 
>50
Focal deficit
Short duration 
Raised ICP
Altered consciousness
Enhancement on contrast
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61
Q

How is a type II astrocytic tumour treated?

A

Surgery +/- radio or chemo

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62
Q

What is brachytherapy?

A

Placement of radioactive isotopes directly onto the tumour

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63
Q

What is the mean survival of a type III anaplastic astrocytic tumour?

A

2 years

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64
Q

What is the life expectancy with type IV astrocytic tumour?

A

15 months

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65
Q

How likely is a meningioma type III to become malignant?

A

90% are benign

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66
Q

How does a meningioma appear on a CT?

A

Homogenous
Oedema
Hyperostosis/skull blistering

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67
Q

How does a meningioma appear on an MRI?

A

Dural tail

Patent dural sinuses

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68
Q

What is the peak incidence of a germ cell tumour?

A

10-12 yrs

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69
Q

How does a germ cell tumour appear on CT?

A

Iso- or hyper-dense
Enhancing
Mixed histology

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70
Q

What is the most common CNS germ cell tumour?

A

Geminomas

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71
Q

What bloods should be done with any midline brain tumour in a child?

A

ALP
HCG
LDH

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72
Q

What are the features of POCS stroke?

A 
Cranial nerve deficit
Bilateral motor/sensory deficit
Eye movement disorders
Cortical blindness
Cerebellar deficits
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73
Q

What are the features of TACS stroke?

A

Hemiplegia

Cortical signs incl dysphagia, diploplia, nystagmus and neglect

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74
Q

What are the features of PACS?

A

2/3 TACS features

Isolated cortical dysfunction

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75
Q

What are the features of LACS?

A

Occlusion of single deep penetrating artery affecting 2 of: face, leg, arm

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76
Q

Which stroke classification has the best prognosis?

A

LACS

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77
Q

What is small vessel disease classified into?

A

Types 1-6

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78
Q

What type of small vessel disease is most common?

A

Type 1

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79
Q

What is type 1 small vessel disease?

A

Arteriosclerotic

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80
Q

What is type 2 small vessel disease?

A

Sporadic and hereditary cerebral amyloid angiopathy

blood vessel in brain problem

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81
Q

What is type 3 small vessel disease?

A

Genetic

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82
Q

What is type 4 small vessel disease?

A

Inflammatory and immunologically mediated

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83
Q

What is type 5 small vessel disease?

A

Venous collagenosis

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84
Q

What is type 6 small vessel disease

A

Post radiation

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85
Q

What are the two main causes of primary intracerebral haemorrhage?

A

Hypertension

Amyloid angiopathy

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86
Q

What are causes of secondary intracerebral haemorrhage?

A

Arteriovenous malformation, aneurysm, tumour

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87
Q

What investigations are done in stroke?

A 
Full lipid profile 
BP
Carotid scan
ECG
Echo
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88
Q

What is the acute management of stroke?

A 
Thrombolysis 
Imaging
Swallow assessment
Anti-platelets
Stroke care unit
DVT prophylaxis
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89
Q

What is the window of opportunity for TPA treatment in stroke?

A

4.5 hours

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90
Q

How much CSF is in the body?

A

150ml

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91
Q

What is the mean pressure of CSF?

A

14cmH20

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92
Q

Which drug reduces CSF production by 50%

A

Acetozolamide

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93
Q

When is the max volume of CSF?

A

Approx 2am

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94
Q

How heavy is the brain?

A

1.5kg

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95
Q

How does hydrocephalus present at birth?

A

Large head
Thin/shiny scalp
Bulging/tense fontalles

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96
Q

How can hydrocephalus be picked up prenatally?

A

USS

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97
Q

How does hydrocephalus present at infancy?

A 
Moving up head centiles
Poor feeding
Vomiting
Sleepiness
Muscle stiffness
Lack of up gaze
Pupils unreactive to light
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98
Q

How is hydrocephalus treated?

A

Shunt placed posterior to the parietal eminence

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99
Q

What are complications of getting a shunt placed?

A 
Over drainage
Underdrainage
Infection
Haemhorrage
Seizures
Dissemination of tumour
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100
Q

How does a blocked CSF shunt present?

A

Headache
Vomiting
Sunsetting in eyes
Blurred vision

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101
Q

How is a blocked shunt treated?

A

Tap shunt, CT, surgical intervention

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102
Q

What is ETV for hydrocephalus?

A

Opening created in the floor for the third ventricle to allow CSF to bypass the blockage prevent it from circulating

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103
Q

What major structure is at risk during ETV?

A

Basilar artery

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104
Q

Who gets normal pressure hydrocephalus?

A

Elderly

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105
Q

What is normal pressure hydrocephalus?

A

When the ventricles are enlarged but the pressure is normal

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106
Q

How does normal pressure hydrocephalus present?

A

Ataxia, memory decline, incontinence

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107
Q

How is normal pressure hydrocephalus investigated?

A

CT, MRI, LP tap test

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108
Q

What is an LP tap test for normal pressure hydrocephalus?

A

Measure pressure, drain 30mls CSF

If walking improves or general function is better after, this indicates hydrocephalus

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109
Q

How is normal pressure hydrocephalus managed?

A

70% success with shunt but only functional for 1 year

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110
Q

What is benign intracranial hypertension?

A

Normal ventricles but high intracranial pressure

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111
Q

Who gets benign intracranial hypertension?

A

Young, obese females with hypothyroidism
Abs use
Steroid withdrawal
Sleep apnoea

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112
Q

How does benign intracranial hypertension present?

A

Headaches
Visual loss
Papilloedema
Loss of VA

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113
Q

How is benign intracranial hypertension managed?

A

Acetazolamide
Heparin for thrombosis
Diuretics, shunt, decompression
Weight loss

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114
Q

What is the common side effect of acetazolamide?

A

Tingling in hands and feet

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115
Q

What type of history must be taken in epilepsy?

A

Collateral

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116
Q

What is epilepsy?

A

The tendency to have spontaneous/unprovoked seizures

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117
Q

What are the two types of epileptic seizure?

A

Focal

General

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118
Q

Who is most likely to have epilepsy?

A

Infancy and >55

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119
Q

What are risk factors for epilepsy?

A 
Pregnancy or delivery problems
Developmental delay 
Seizures in past
Head injury 
Substance misuse 
FHx
Medications
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120
Q

Which medication are risk factors for epilepsy? (8)

A 
Abs
Tramadol
Anti-emetics
Diamorphine
Theophylline
Lithium 
Ketamine
NSAIDs
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121
Q

What are the features of an epileptic fit?

A 
Rigid muscle
Head turned
Tongue biting 
Potentially wet yourself 
Sweaty
Drowsy 
No memory
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122
Q

Describe focal seizures

A

Specific jerking movement, somatosensory and memory symptoms
Focal part of the brain had abnormal structure and electrical activity

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123
Q

What makes a focal/partil epileptic seizure complex?

A

Impaired consciousness level

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124
Q

What are the types of general epileptic seizure?

A 
Absence
Myoclonic
Atonic
Tonic
Tonic clonic
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125
Q

Who mostly gets general absent epileptic seizures?

A

Young kids

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126
Q

What is an atonic general epileptic seizure?

A

No muscle tone at all

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127
Q

What is a tonic general epileptic seizure?

A

Stiff rigid muscles

Arms my bend as flexors typically stronger than extensors but this it not clonic

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128
Q

Describe a general tonic clonic seizure

A

Phase 1 - rigid muscles, tense and tight

Phase 2 - jerky movements, clonic

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129
Q

What examinations should be done with epileptic seizures?

A

Full neuro and cardio

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130
Q

What investigations should be done with epileptic seizures?

A

ECG
Imaging
EEG

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131
Q

What is a cardio exam and ECG done with seizures?

A

To check for arrhythmias

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132
Q

When would imaging be done urgently in seizure?

A

Suspected skull fracture, lesion, lowering gcs, focal neuropathy, haemorrhage, gcs <15 4 hours later

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133
Q

What is the only situation in which someone who is not a neurologist should do an EEG?

A

To confirm non-convulsive status

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134
Q

Is an EEG specific to epilepsy?

A

No - just helps to confirm clinically suspected epilepsy

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135
Q

When can you drive following a seizure?

A

Car - after 6 months

HGV - after 5 years

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136
Q

When can you drive after a nocturnal seizure?

A

Car - 6 months

After 1 year of having ONLY nocturnal seizures

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137
Q

When can you drive an HGV after confirmed epilepsy diagnosis?

A

10 years seizure free

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138
Q

What is SUDEP?

A

Sudden unexplained death in epilepsy

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139
Q

What are risks of SUDEP?

A

Drugs
Alcohol
Non-compliance
Sleeping alone

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140
Q

How is partial-seizure epilepsy treated?

A

Carbamazepine or lamotrigine

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141
Q

What should the patient be made aware of if taking carbamazepine?

A

Makes other drugs less effective including chemotherapy and OCP

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142
Q

Why is sodium valproate avoided?

A

Weight gain, hair loss, fatigue and teratogenic

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143
Q

What should NEVER be given to treat generalised epilepsy?

A

Carbamazepine

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144
Q

How is general epilepsy treated?

A

Sodium valprotate

Lamotrigine

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145
Q

Why is lamotrigine dose started low?

A

If too high can cause Steven-Johnsons syndrome

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146
Q

What can lamotrigine make worse?

A

Myoclonus

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147
Q

How are myoclonic seizures treated?

A

Sodium valproate
Levetiracetam
Clonazepam

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148
Q

How are absent seizures treated?

A

Sodium valproate
Ethosuximide
Topiramate

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149
Q

How effective is treatment for epilepsy?

A

65% seizure free with treatment

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150
Q

Which anti-convulsants should be used with caution when used together?

A

Sodium valproate and lamotrigine

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151
Q

Why shouldn’t you use sodium valproate and lamotrigine together?

A

Sodium valproate inhibits the metabolism of lamotrigine

Risk of Steven Johnson syndrome

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152
Q

What is phenytoin used for in epilepsy?

A

Acute management 6 months - 1 year

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153
Q

Which drug for epilepsy can be used which is well tolerated and causes some mood swings?

A

Levetiracetam

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154
Q

Which epileptic drug causes sedation, weight loss and isn’t well tolerated?

A

Topiramate

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155
Q

Which form of contraception should females on anti-convulsants not use?

A

Progesterone only

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156
Q

What should females on anti-convulsants also be prescribed?

A

Vit K

Folic acid

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157
Q

What epileptic situation are classed as emergencies?

A

Continuous seizures >30 mins
Recurrent fits without full recovery of consciousness
Conscious in altered state
Epilepsia partialis continua

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158
Q

What is a tic?

A

Involuntary stereotyped movement or vocalisation

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159
Q

What is chorea?

A

Brief irregular purposeless movement which flows from one body part to another

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160
Q

Why is epileptic status dangerous?

A

Excessive energy use leads to muscle damage, hyperthermia, rhabomyolsis, loss of BBB

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161
Q

What should be given in epileptic emergency?

A

Patient’s normal medication
Benzo - buccal midazolam, 10mg PR diazepam
Phenytoin
Valproate

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162
Q

When should someone in epileptic status be sent to intensive care?

A

If there is no improvement with medication after 30 mins

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163
Q

What is sleep?

A

Normal, recurring, reversible state in which you are not conscious or unconscious

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164
Q

In which type of sleep do you experience non-narrative images?

A

Non-REM

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165
Q

What are non-narrative images?

A

Dream without a story which has evoked an emotional response

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166
Q

Which type of sleep occurs at the start of the night?

A

Non-REM

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167
Q

Which type of sleep is associated with reduced cerebral flow, heart rate and BP?

A

Non-REM

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168
Q

During which type of sleep does protein synthesis occur?

A

Non-REM

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169
Q

During which type of sleep is there synchronised, rhythmic EEG activity?

A

Non-REM

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170
Q

Which type of sleep occurs at the end of the night?

A

REM

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171
Q

In which type of sleep is there fast EEG activity and increased brain activity?

A

REM

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172
Q

In which type of sleep is cerebral blow flow increased?

A

REM

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173
Q

In which type of sleep is there impaired thermal regulation?

A

REM

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174
Q

Which germ layer is microglia derived from?

A

Mesoderm

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175
Q

In which injury reaction is there shrinking and angulation of the neuron?

A

Acute

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176
Q

In which injury mechanism is there a “red neuron” ?

A

Acute

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177
Q

In which injury mechanism is the visibility of the nucleolus lost?

A

Acute

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178
Q

Describe axonal damage

A

Distal degeneration in the axon in response to injury

Increased protein synthesis

Chromatolysis causing loss of Nissl granules

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179
Q

Which response to injury involves reactive gliosis replacing neural tissue?

A

Simple neuron atrophy

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180
Q

What occurs during simple neuron atrophy?

A

Neurons shrink, angulate and are lost

Accumulation of lipofuscin pigment

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181
Q

Which type of damage are oligodendrocytes sensitive to?

A

Oxidative

De-myelination

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182
Q

Which cells line the ventricular system ?

183
Q

How do ependymal granulations occur?

A

Disruption and local proliferation of sub-ependymal astrocytes produce small irregularities on ventricular surfaces

184
Q

How do microglia respond in injury?

A

Proliferate and form aggregates

185
Q

What do M1 microglia do?

A

Encourages inflammation in chronic disease

186
Q

What do M2 microglia do?

A

Anti-inflammation, acute, phagocytic

187
Q

Define cerebrovascular disease

A

Abnormality of the brain caused by pathological process of blood vessels

188
Q

Give an example of a cause of focal hypoxia

A

Vascular obstruction

189
Q

Give an example of a cause of global hypoxia

A

Cardiac arrest, hypotension

190
Q

When does cytotoxic oedema occur?

A

Intoxication, Reye’s and severe hypothermia

191
Q

Why does cytotoxic oedema occur?

A

Dying cells accumulate water because osmotically active ions move into the cell

192
Q

Why does ionic oedema occur?

A

BBB dysfunction

Sodium ions cross BBB and drive chloride ion transport creating an osmotic gradient for water accumulation

193
Q

Why does vasogenic oedema occur?

A

Due to disruption of endothelial tight junctions and plasma proteins

194
Q

When does haemorrhagic conversion occur?

A

When endothelial integrity is lost and blood enters extracellular space

195
Q

What is a stroke?

A

A sudden disturbance of cerebral function of vascular origin which lasts >24 hours or causes death

196
Q

What is macroscopically and microscopically visible 0-12 hours after a stroke?

A

Very little

197
Q

What is macroscopically visible 12-24 hours after stroke?

A

Pale, soft, swollen ill defined margins between injured and non-injured brain

198
Q

What is microscopically visible 12-24 hours after stroke?

A

Red neuron, oedema

199
Q

What is microscopically visible 24-48 hours after stroke?

A

Neutrophils, extravasation of RBCs, haemorrhagic conversion and activation of astrocytes and microglia

200
Q

What is macroscopically visible 2-14 days after stroke?

A

Reduction in oedema

Gelatinous tissue

201
Q

What is microscopically visible 2-14 days after stroke?

A

Microglia become predominant cell type, myelin breakdown, reactive gliosis

202
Q

What is macroscopically visible several months after stroke?

A

Formation of cavity lined by dark grey tissue

203
Q

What is microscopically visible several months after stroke?

A

Phagocytosis brings increasing cavitation and surrounding gliotic scar formation

204
Q

Who presents with MS?

A

Females in 30s who live far from the equator

205
Q

How can vitamin D affect MS?

A

Lowers development risk but doesn’t help prevent disease

206
Q

What is the most common form of MS?

A

Relapsing and remitting

207
Q

What is secondary progressive MS?

A

Cases which get worse after several years of relapsing and remitting

208
Q

What is primary progressive MS?

A

Never relapse

209
Q

How does pyramidal dysfunction in MS present?

A

Spasticity, hyperreflexia, weakness in upper limbs

210
Q

What are common symptoms of MS?

A

Sensory impairment
Urinary tract disturbance
Cerebellar and brainstem features

211
Q

How is MS investigated?

A 
MRI
FBC
Renal, liver, bone profile
Auto anti-body screen 
HIV and syphilis screen
212
Q

How is pyramidal dysfunction in MS treated?

A 
Anti-spasmodic agents
Physio
OT
Botox
Baclofen, tizanidine, phenol
213
Q

How are sensory symptoms in MS treated?

A 
Gabapentin
Amitriptyline
TENS
Acupuncture
Lignocaine infusion
214
Q

How are urinary symptoms in MS treated?

A

Bladder drill
Anti-cholinergic
Desmopressin
Catheterisation

215
Q

What medication is given in moderate MS?

A

500mg weekly meta-prednisolone

216
Q

What medication is given in severe MS?

A

IV steroids 1000mg over 3 days

217
Q

What DMARDs can be given first line in severe MS?

A

Interferon beta
Glatiramer acetate
Tecidera

218
Q

What DMARDs can be given second line in MS?

A

Monoclonal antibodies

Fingolimod

219
Q

What can be done third line in severe MS?

A

Mitoxantrone

Stem cell transplant

220
Q

Given an example of primary demyelination disorders

A

MS
Acute disseminated encephalomyelitis
Acute haemorrhagic leukoencephalitis

221
Q

Give an example of secondary demyelination disorders

A

Progressive multifocal leukoencephalopathy

Central pontine myelinolysis

Toxins - CO, organic solvent, cyanide

222
Q

Which gene is associated with MS?

223
Q

What is the criteria for diagnosis of MS?

A

Two distinct neurological defects occurring at two different sites
Multiple distinct lesions on MRI

224
Q

What does MRI show in MS?

A

Irregular but well demarcated, glassy plaques

225
Q

Are perivascular inflammatory cells a marker of an active or inactive plaque in MS?

226
Q

Are oligodendrocytes involved in active or inactive MS plaques?

227
Q

Are microglia involved in active or inactive MS plaques?

228
Q

Does gliosis occur with active or inactive MS plaques?

229
Q

What is dementia?

A

Acquired, persistent and generalised disturbance of mental function in an otherwise fully alert person

230
Q

Which sex is more likely to get dementia?

231
Q

Which genes are implicated in Alzheimer’s?

A

Amyloid precursor protein

Presenilin 1 & 2

232
Q

What are the 3 main symptoms of Alzheimer’s?

A

Progressive disorientation, memory loss and aphasia

233
Q

What brain changes occur in Alzheimer’s ?

A 
Decreased size of brain
Widening of sulci
Narrowing of gyri
Compensatory dilatation of ventricles
Plaques
Neuronal atrophy
Neurofibrillary tangles
Amyloid angiopathy
234
Q

What part of the brain is spared in Alzheimer’s?

A

Cerebellum

235
Q

Where are neurofibrillary tangles found in the brain in Alzheimer’s?

A

Hippocampus and temporal lobe

236
Q

Which type of plaques are found in Alzheimer’s and where?

A

A-beta amyloid plaques

Around astrocytes

237
Q

How does Lewy body dementia present?

A

Progressive with hallucinations and fluctuating levels of attention and cognition

238
Q

Which part of the brain degenerates in Lewy body dementia?

A

Substantia nigra

239
Q

What is a classical Lewy body?

A

Intracytoplasmic eosinophilic body with a dense core and a pale halo
Made of alpha-synuclein

240
Q

Which set of symptoms are commonly found in Lewy body dementia?

A

Parkinsonian symptoms

241
Q

What is Pick’s disease otherwise known as?

A

Fronto-temporal dementia

242
Q

What is the common age of onset of Pick’s disease?

A

50-60 years

243
Q

How does Pick’s disease present?

A

Personality and behaviour changes
Communication problems
Change in eating habits
Reduced attention span

244
Q

How long does Pick’s disease last?

A

2-10 years

245
Q

What are the brain changes in Pick’s disease?

A

Extreme atrophy of cerebral cortex in frontal them temporal lobe
Brain weight <1kg
Neuronal loss
Pick’s cells and bodes found

246
Q

What is a Pick’s body?

A

Intracytoplasmic filamentous inclusion

247
Q

Which protein and Pick’s bodies enriched in in Pick’s disease?

248
Q

What is the typical age of onset of Huntington’s?

249
Q

How does Huntington’s present?

A

Chorea, myoclonus, clumsiness, slurred speech, depression, irritability, apathy

250
Q

What chromosome is implicated in Huntington’s?

A

4p

Additional CAG repeats

251
Q

What brain changes are seen in Huntington’s?

A

Atrophy of basal ganglia, caudate nucleus and putamen

252
Q

What are the four main primary causes of dementia?

A

Lewy body
Huntington’s
Alzheimer’s
Pick’s disease

253
Q

What are the main secondary causes of dementia?

A

Vascular, infection, trauma, substances

254
Q

What is vascular dementia?

A

Deterioration in mental function due to cumulative damage to the brain through hypoxia or anoxia

255
Q

Who is most likely to get vascular dementia?

A

Males, >60

Or middle aged hypertensives

256
Q

Why are those with vascular dementia more prone to depression and anxiety?

A

They are aware of the defects

257
Q

How does vascular dementia progress?

258
Q

What is parkinsonism?

A

Group of symptoms

Loss of facial expression, stooping, shuffling gait, slow initiation of movement, stiffness and rolling tremor

259
Q

In what conditions is Parkinsonism seen?

A 
Idiopathic Parkinson's disease
Lewy body dementia
Substance use
Medications - phenothiazines
Trauma
Multisystem atrophy
Progressive supranuclear palsy
Cortico-basal dengeneration
260
Q

What three things can cause hydrocephalus?

A

Obstruction to CSF flow
Decreased resorption of CSF
Overproduction of CSF

261
Q

What can lead to obstruction of CSF flow?

A

Inflammation, pus, tumours

262
Q

What can lead to decreased resorption of CSF?

A

SAH

Meningitis

263
Q

What can lead to overproduction of CSF?

A

Tumour of choroid plexus (rare)

264
Q

What are the two types of hydrocephalus?

A

Communicating and non-communicating

265
Q

What is non=communicating hydrocephalus?

A

Obstruction to flow of CSF occurring within the ventricular system

266
Q

What is communicating hydrocephalus?

A

Obstruction to CSF out with the ventricles

267
Q

What is the outcome if hydrocephalus occurs before the closure of the cranial sutures?

A

Cranial enlargement

268
Q

What is the outcome if hydrocephalus occurs after the closure of the sutures?

A

Raised ICP and expansion of ventricles

269
Q

What are the 4 types of herniation?

A

Subfalcine
Tentorial
Cerebellar
Transcalvarial

270
Q

What are the signs and symptoms of raised ICP?

A

Papilloedema
Headache
N&V
Neck stiffness

271
Q

What can cause a single brain abscess?

A

Local extension of mass

Direct implantation of pathogen

272
Q

What can cause multiple brain abscesses?

A

Haematogenous spread from pneumonia, endocarditis,etc

273
Q

How is a brain abscess investigated?

274
Q

What is a linear skull fracture?

A

Straight sharp fracture line that may cross sutures

275
Q

What does coup describe?

A

Injury with a response that occurs at the site of the injury

276
Q

What does contrecoup describe?

A

Injury with a response which occurs on the opposite side

277
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual tissue damage or described in terms of such damage

278
Q

Describe acute pain

A

Associated with (usually) obvious tissue damage
Protective function
Increased nervous system activity
Pain resolves on healing

279
Q

Describe chronic pain

A

Pain beyond an expected period of healing

Doesn’t serve a useful purpose

280
Q

Which fibres perceive painful stimuli?

A

A-delta and C fibres

281
Q

Which substance is released on activation of A-delta and C fibres?

A

Substance P

282
Q

Where is substance P released onto when a painful stimulus is perceived?

A

Laminae I and V

283
Q

Where does Laminae I signal painful stimuli information to?

A

Amygdala and hypothalamus

284
Q

Where does Laminae V signal to in the case of painful stimuli?

A

Thalamus then somatosensory cortex

285
Q

What is nociceptive pain?

A

Appropriate physiological response to painful stimuli

286
Q

What is neuropathic pain?

A

Inappropriate response caused by a dysfunction in the nervous system

287
Q

What is allodynia?

A

Experiencing pain from a stimulus which is not expected to be pain

288
Q

What is hyperalgesia?

A

More pain than expected from a painful stimulus

289
Q

What are common causes of chronic pain?

A 
Shingles
Surgery
Trauma
Diabetic neuropathy 
Amputation
290
Q

What can be given as adjuvants to pain medication in chronic pain?

A

Antidepressants

Anti-convulsants

291
Q

How do NSAIDs act?

A

inhibit COX1 and prostaglandin synthesis

292
Q

What are the side effects of NSAIDs?

A

GI irritation
GI bleed
CV side effects

293
Q

How does paracetamol work?

A

Inhibits central prostaglandin synthesis

294
Q

Give an example of a weak opioid

A

Tramadol

Codeine

295
Q

Give an example of a strong opioid

A

Morphine

Oxycodone

296
Q

What type of pain are opioids and NSAIDs used in?

A

Nociceptive

297
Q

How do opioids work?

A

Stimulates receptors in the limbic system to eliminate feeling pain

298
Q

What are common side effects of opioids?

A 
N&amp;V
Constipation
Dizziness
Somnolence
Pruritus
299
Q

What type of pain are anti-depressants and anti-convulsants used for?

A

Neuropathic pain

300
Q

What are side effects of tricyclic antidepressants?

A 
Constipation
Dry mouth 
Insomnia
Increased appetite 
Abnormalities in heart rate and rhythm
301
Q

What are the side effects of SSRIs and SNRIs?

A 
N&amp;V
Constipation
Somnolence 
Dry mouth 
Increased sweating
Loss of appetite
302
Q

Which anticonvulsants are used in neuropathic pain?

A

Gabapentin
Carbamazepine
Pregabalin

303
Q

What are the side effects of anticonvulsants?

A

Sedation, dizziness, ataxia, peripheral oedema, nausea and weight gain

304
Q

What channels does Gabapentin act on?

A

Voltage dependent calcium channels

305
Q

Which channels does pregabalin act on?

A

N-type calcium channels

306
Q

What does carbamazepine do?

A

Blocks Na+ and Ca2+ channels

307
Q

What are side effects of topical analgesics?

A

Rash, pruritic, erythema

308
Q

What physical treatments can be complementary to medication in chronic pain?

A

Massage
Aromatherapy
Reflexology
Acupuncture

309
Q

What psychological therapies can be used in chronic pain?

A

CBT

Solution focused brief therapy

310
Q

How can you localise a lesion in the cervical region of spinal cord?

A

Lateral may only affect arms

Central can affect anywhere in spinal cord down from that point

311
Q

How can you tell if there is a lesion in the spinal cord?

A

Some leg problems with little to no arm involvement

312
Q

How can you localise a legion to the lumbar region of spinal cord?

A

Only legs involved, no UMN features

313
Q

How is tone in UMN lesions?

314
Q

How is tone in LMN lesions?

315
Q

Is there more atrophy in UMN or LMN lesions?

A

LMN

UMN may have some but it comes later

316
Q

Are fasciculations found in UMN or LMN lesions?

317
Q

Describe the reflex change with an UMN lesions

318
Q

Describe the reflex changes with LMN lesions

A

Decreased or absent

319
Q

Is clonus present in UMN ro LMN lesions?

320
Q

How does a cervical disc prolapse present?

A

Arm pain
Pain in relevant dermatomes
LMN problems

321
Q

How does a thoracic disc prolapse present?

A

Thoracic back pain

322
Q

How does a lumbar disc prolapse present?

A

Leg pain

LMN symptoms

323
Q

How does spinal claudication present?

A

Intermittent burning, achey pain, worse on movement
Better on bending forward and walking up hill
Altered sensation
Weakness
Urinary dysfunction

324
Q

How is spinal claudication investigated?

A

MRI urgently

325
Q

How is spinal claudication treated?

A

Surgery - not curative, only to stop it getting worse

326
Q

What is a cervical myelopathy?

A

Compression in the cervical spine

327
Q

How does cervical myelopathy present

A

“Numb clumsy hands”
Paraesthesia in fingertips
Reduced mobility
UMN signs

328
Q

What is Hoffman sign positive in?

A

Cervical myelopathy

329
Q

What is failed back syndrome?

A

Chronic pain in the back

330
Q

What can cause failed back syndrome?

A 
Recurrence of previous problem 
Srugery causing instability 
Infection 
Depression and anxiety
Diabetes
Smoking 
Higher BMI
331
Q

What should be the treatment for pure neck/back pain only?

A

Physio

Risk of surgery not worth it

332
Q

What is a subarachnoid haemorrhage?

A

Blood in the SA space

333
Q

What abnormality is normally underlying in subarachnoid haemorrhage?

A

Berry aneurysm

334
Q

What is the most common finding when identifying underlying cause in subarachnoid haemorrhage?

A

No cause identified

335
Q

How does a subarachnoid haemorrhage present?

A 
Sudden onset thunderclap headache
Collapse
Vomiting
Neck pain
Photophobia
Decreased consciousness
336
Q

What is benign coital cephalgia?

A

Sudden onset headache before orgasm

337
Q

How is subarachnoid haemorrhage investigated?

A

CT immediately
LP
Cerebral angiography

338
Q

When is LP done in subarachnoid haemorrhage?

A

No papilloedema and after normal CT

339
Q

What does CSF look like in subarachnoid haemorrhage?

A

Bloodstained or xanthochromatic

340
Q

How would a traumatic tap be indicated in LP results?

A

Decreased levels of RBCs in ;labelled samples

341
Q

Why may an aneurysm be missed on cerebral angiography?

A

Vasospasm not allowing vessels to fill with contrast

342
Q

What are the five main complications of subarachnoid haemorrhage?

A 
Re-bleeding 
Delayed ischaemic deficit 
Hydrocephalus 
Hyponatraemia
Seizures
343
Q

How is re-bleeding of a subarachnoid haemorrhage treated?

A

Endovascular techniques

344
Q

When does a delayed ischaemic deficit occur after a subarachnoid haemorrhage?

345
Q

How is a delayed ischaemic deficit after subarachnoid haemorrhage treated?

A

Nimodipine

346
Q

Should you fluid restrict in hyponatraemia following subarachnoid haemorrhage?

347
Q

What is the risk of seizures following subarachnoid haemorrhage?

A

10% over 5 years

348
Q

What in an intracerebral haemorrhage?

A

Bleed into the brain parenchyma

349
Q

What abnormalities/conditions may precede intracerebral haemorrhage?

A

Hypertension (50%)

Aneurysms and AV malformations (30%)

350
Q

How does an intracerebral haemorrhage present?

A

Headache that is less intense and sudden than SAH
Focal neurological illness
Decreased conscious levels

351
Q

How is intracerebral haemorrhage investigated?

A

CT

Angiography if suspicion of underlying vascular abnormality

352
Q

How is an intracerebral haemorrhage treated?

A

Surgical evacuation of haematoma with treatment of underlying abnormality
Non-surgical more common

353
Q

What is an intraventricular haemorrhage?

A

Blood in the ventricles

Occurs with rupture of SA or intracerebral bleed

354
Q

What can AV malformations cause?

A

Seizure, haemorrhage, headache, steal syndrome

355
Q

How is an AV malformation treated?

A

Surgery to remove
Endovascular embolisation to block
Stereotactic radiotherapy - takes about 2 years to work

356
Q

Where does the corticospinal tract dessucate?

357
Q

What is the spinothalamic tract for?

A

Pain, temp, crude touch

358
Q

Where does the spinothalamic tract dessucate?

A

Spinal level

359
Q

What is the dorsal column for?

A

Fine touch, proprioception, vibration

360
Q

Where does the dorsal column pathway dessucate?

361
Q

What are acute causes of spinal cord compression?

A

Trauma, tumour, bony mets, infection, haemorrhage

362
Q

What are chronic causes of spinal cord compression?

A

Degenerative disease eg spondylosis, tumours, rh arthritis

363
Q

What is the flaccid areflexic paralysis after cord transection termed?

A

Spinal shock

364
Q

What does central cord syndrome follow?

A

Hyperflexion or hyperextension of a stenotic neck

365
Q

How does central cord syndrome present?

A

Distal upper limb weakness
Cape-like spinothalamic sensory loss is across a few dermatomes
Lower limb power preserved

366
Q

Where do extradural metastases normally come from?

A

Lung, breast, kidney, prostate

367
Q

Give an example of an intradural extramedullary tumour

A

Meningioma

Schwannoma

368
Q

Give an example of an intradural intramedullary tumour

A

Astroctyoma

Ependymoma

369
Q

What is spinal stenosis?

A

When the spinal canal gets narrowed by “weak and tear” changes

370
Q

What structural problems can cause spinal stenosis?

A

Osteophyte stenosis
Intervertebral disc bulging
Facet joint hypertrophy
Sublaxation

371
Q

Why is dexamethasone given in spinal mets?

A

To improve weakness

Not curative

372
Q

Which nuclear treatment is used on plasmacytoma?

373
Q

Who is most likely to get motor neurone disease?

A

50-75 year old white male

374
Q

What is the genetic link between ALS and frontotemporal dementia?

A

C9ORF repeat expansions

375
Q

What genes are implicated in motor neuron disease?

A

TDP43

C9ORF

376
Q

What are the 4 main subtypes of motor neuron disease?

A

Amyotrophic lateral sclerosis (ALS)
Progressive muscular atrophy (PML)
Primary lateral sclerosis (PLS)
Progressive bulbar palsy (PBP)

**Note these are most common –> least common

377
Q

Which subtype of motor neuron disease does not show LMN features?

A

Primary lateral sclerosis (PLS)

378
Q

Which subtype of motor neurone disease have the best survival?

A

Primary lateral sclerosis (PLS)

5 years

379
Q

How does motor neuron disease present?

A

Muscle weakness and wasting
Speech and swallow problems
Breathing problems
Cognitive impairment

380
Q

How does motor neuron disease begin and progress?

A

Begins are focal symptoms and spread until general paresis

381
Q

Give examples of UMN signs

A 
Increased tone
Hyper-reflexia
Extensor planter responses
Spastic gait
Exaggerated jaw-jerk
Slowed movements
Babinski sign
382
Q

Give examples of LMN signs

A 
Muscle wasting
Weakness
Fasciculations
Areflexia 
Muscle cramp
383
Q

What are the criteria for definite ALS?

A

UMN and LMN signs in bulbar and at least two of: lumbosacral, thoracic and cervical regions

384
Q

What are the bulbar UMN signs?

A

Exaggerated snout reflex, clonic jaw jerk, emotional lability, forced yawning

385
Q

How is motor neuron disease managed?

A

SALT, communication aids
Nutritional needs assessed via dietician based on swallow ability
Rilozole

386
Q

How do NSAIDs work, generally?

A

Act at site of injury to decrease nociceptor sensitisation in inflammation

387
Q

How do local anaesthetics work?

A

Block nerve conduction

388
Q

How do opioids and anti-depressants work as pain killers?

A

Supress transmission of nociceptive signals in the dorsal horn

389
Q

Give an example of an NSAID

A

Diclofenac, ibruprofen, indomethacin, naproxen

390
Q

Is codeine a weak or strong opioid?

391
Q

Is tramadol a weak or strong opioid?

392
Q

Is morphine a weak or strong opioid?

393
Q

Is oxycodone a weak or strong opioid?

394
Q

Is dextropropoxyphene a weak or strong opioid?

395
Q

Is hydromorphone a weak or strong opioid?

396
Q

Is fentanyl a strong or weak opioid?

397
Q

What is supraspinal anti-nociception?

A

When regions of the brain involved in pain perception project to the brainstem and spinal cord to modify input

398
Q

Which regions in the brain are involved in supraspinal anti-nociception?

A

Periaqueductal grey (PAG)
Nucleus raphe magnus (NRM)
Locus coeruleus

399
Q

Which receptors mediate opioid action?

A

beta-gamma units on GPCRs which signal to Gi/Go

400
Q

What does opioid action on GPCRs produce?

A

Inhibition of voltage activated Ca2+ channels

Opening of K channels

401
Q

What does the inhibition of Ca channels in opioid use do?

A

Suppresses neurotransmitter release therefore reducing signals in the dorsal horn

402
Q

What does the opening of K channels in opioid use do?

A

Hyperpolarises post-synaptic cell so that it can’t produce an AP, therefore reducing signalling

403
Q

What are the three classifications of opioid receptors?

A

Mu - mop
Delta - DOP
Kappa - KOP

404
Q

What type of opioid receptor can be pro-convulsant?

A

Delta (DOP)

405
Q

Which opioid receptor is associated with sedation, dysphoria and hallucination?

A

Kappa (KOP)

406
Q

How does opioid use produce apnoea?

A

Blunting of medullary respiratory centre to CO2

407
Q

How does opioid use produce orthostatic hypotension?

A

Reduce sympathetic tone and bradycardia (via medulla)

Histamine-evoked vasodilation due to mast cell degranluation

408
Q

How does opioid use produce GI effects?

A

Action on CTZ, increased smooth muscle tone, decrease motility

409
Q

What CNS effects can opioid use produce?

A

Confusion, euphoria, dyshphoria, hallucinations, dizziness, myoclonus, hyperalgesia

410
Q

How is morphine metabolised?

A

By the liver by glucuronidation at 3 and 6 positions

411
Q

What is morphine metabolised into?

A

M3G and M6G

412
Q

How are morphine metabolites excreted?

A

By the kidney

413
Q

By which route is diamorphine given?

414
Q

How is codeine metabolised?

A

By the liver by demethylation to morphine by CYP2D6 and CYP3A4

415
Q

How is codeine given?

416
Q

By which route is fentanyl given?

A

IV in maintenance

Transdermal and buccal in chronic pain

417
Q

How is pethidine given?

A

IV, IM, SC

418
Q

When is pethidine used?

A

Acute severe pain (like labour)

419
Q

Which class of drugs should pethidine not be given in conjunction with?

A

monoamine oxidase inhibitors

420
Q

Which metabolite of pethidine can cause seizures?

A

Norpethidine

421
Q

When is buprenorphine given?

A

Chronic pain

422
Q

How is buprenorphine given?

A

IV or sublingual

423
Q

Which opioid receptor does tramadol act on?

424
Q

How does tramadol work?

A

Excites descending serotonergic (NRM) and adrenergic (LC) pathways

425
Q

What condition should tramadol not be given in?

426
Q

Which opioid receptor does methadone work on?

427
Q

Other than opioid receptors, where does methadone act?

A

K channels, NMDA glutamate and 5HT receptors

428
Q

When in methadone used?

A

Chronic pain

Withdrawal from strong opioids

429
Q

When is naloxone used?

A

Reverse opioid toxicity

430
Q

How does naloxone work?

A

Competitive antagonist of mu (MOP) receptors

431
Q

What might cause the need for naloxone to be given to a newborn?

A

Respiratory depression caused by pethidine given to mother in labour

432
Q

What are alvimopan and methylnatrexone used for?

A

Reducing GI effects of chronic opioid use

433
Q

How do NSAIDs reduce inflammation?

A

Inhibit synthesis and accumulation of prostaglandins by COX

434
Q

What is prostaglandin’s affect on nociceptors?

A

Decreases the activation threshold

435
Q

How do gabapentin and pregabalin work as pain killers?

A

Reduce cell surface expression of alpha-2-delta subunits which are upregulated in damaged sensory neurons

436
Q

Give an example of when gabapentin is prescribed

A

In migraine prophylaxis

437
Q

Given an example of when pregabalin is prescribed

A

Painful diabetic neuropathy

438
Q

How does carbamazepine work as a pain killer?

A

Blocks subtypes of voltage activated Na channels that are upregulated in damaged cells

439
Q

What is given first line in trigeminal neuralgia?

A

Carbamazepine

440
Q

How to tricyclic anti-depressants work as painkillers?

A

Decrease uptake of noradrenaline

441
Q

What are the three most common causes of bacterial community acquired meningitis in <60?

A

Pneumococcus
Meningococcus
H. Influenzae

442
Q

What is the most common cause of bacterial community acquired meningitis in >60 or immunocompromisation?

443
Q

What is the treatment for bacterial community acquired meningitis?

A

Ceftriazone IV 2g bd
+
Dexamethasone IV 10mg qds

listeria cover is amoxicillin 2g 4 hourly

444
Q

Describe the CSF findings in viral meningitis

A 
Lymphocytes
Gram stain negative 
Bacterial antigen negative
Protein normal/slightly high
Glucose normal
445
Q

Describe the CSF findings in bacterial meningitis

A 
Polymorphs
Gram stain positive 
Bacterial antigen detection positive
Protein high
Glucose <70% blood glucose
446
Q

Describe the CSF findings in TB

A

Lymphocytes
Bacterial antigen detection negative
Protein very high
Blood glucose less than 60% blood glucose

447
Q

Where is S. pneumococcus found?

A

Nasopharynx

448
Q

What procedure puts kids at risk for S. pneumococcus infection?

A

Cochlear implant insertion

449
Q

Who gets Neisseria m. infections?

A

Young children and 10-21

450
Q

Who gets listeria infections?

A

> 60s, alcoholics, immunosuppressed people

451
Q

What antibiotics are used to treat TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

452
Q

Who gets H. influenza

453
Q

How does meningitis present?

A

Stiff neck, rash, irritability, seizures, fever, drowsy, headache, photophobia

Year 3 - Neuro (19 decks)

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