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3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the signs of a migraine without aura?

A 
Unilateral throbbing headache
Worse upon activity 
Nausea and vomiting 
Photophobia
Phonophobia
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2
Q

How long does a migraine episode last?

A

4-72 hours

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3
Q

What are the signs of a migraine with aura?

A

Visual: blurred vision, loss of visual fields, lines
Motor: dysarthria
Somatosensory: Paraesthesia
Speech: dysphasia

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4
Q

What are the triggers of migraine?

A 
CHOCOLATE 
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie ins 
Alcohol
Tumult
Exercise
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5
Q

How would you medically treat a migraine?

A

Paracetamol
Triptan
NSAIDs
Antiemetics

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6
Q

What type of drugs are triptans?

A

5HT (serotonin receptor) receptor agonist

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7
Q

Which can be used for migraine prophylaxis?

A

Propranolol
Topiramate
Amitriptyline
Acupuncture

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8
Q

What sign on fundoscopy is a sign of raised ICP?

A

Papilloedema

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9
Q

What are the causes of raised ICP?

A

Brain tumour
Benign intracranial hypertension
Intracranial bleed

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10
Q

What are the symptoms of a tension headache?

A

Tight band around forehead

Scalp muscle tenderness

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11
Q

What is associated with tension headaches?

A

Stress
Depression
Alcohol
Dehydration

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12
Q

How would you treat tension headaches?

A

Analgesia

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13
Q

Name the 3 branches of the trigeminal nerve.

A

Ophthalmic
Maxillary
Mandibular

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14
Q

Which condition is associated with trigeminal neuralgia?

A

MS

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15
Q

What are the signs of trigeminal neuralgia?

A

Spontaneous facial pain, can last seconds-hours

Shooting pain

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16
Q

What are the triggers of trigeminal neuralgia?

A 
Cold weather
Spicy food
Caffeine 
Touching affected area
Eating
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17
Q

What is the first line treatment for trigeminal neuralgia?

A

Carbamazepine

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18
Q

What is the surgical treatment for trigeminal neuralgia?

A

Surgery at trigeminal ganglion

Microvascular decompression

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19
Q

Cluster headaches come in clusters of attacks and then disappear for a while. For example, a patient may suffer 3 – 4 attacks a day for weeks or months followed by a pain-free period lasting 1-2 years. How long does an attack episode last?

A

15 minutes - 3 hours

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20
Q

What are the symptoms of cluster headaches?

A 
Red, swollen watering eye
Miosis 
Ptosis
Unilateral severe unbearable pain, usually around eye
Facial sweating
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21
Q

What is a risk factor for cluster headaches?

A

Smoking

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22
Q

How would you manage a cluster headache?

A

High flow 100% oxygen

Sumatriptan

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23
Q

What can be done for the prophylaxis of cluster headaches?

A

Verapamil
Lithium
Prednisolone

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24
Q

A TIA is sudden onset of focal CNS phenomena due to temporary occlusion of cerebral circulation. What are the risk factors for TIA?

A 
Hypertension
Smoking 
Obesity
Diabetes
High alcohol intake
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25
Q

What are the features of a TIA?

A 
Symptoms <24 hours
Amaurosis fugax 
Aphasia
Hemiparesis
Vomiting 
Vertigo
Ataxia
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26
Q

What is amaurosis fugax?

A

Occlusion of retinal artery, leading to unilateral progressive vision loss (like curtain descending)

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27
Q

What are the differentials of a TIA?

A

Hypoglycaemia
Migraine aura
Focal epilepsy
Stroke

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28
Q

Which score is used to predict risk of stroke after a TIA?

A

ABCD2 score

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29
Q

Outline the components of the ABCD2 score.

A 
Age >60  - 1 pt
BP >140/90 - 1pt
Unilateral weakness - 2pts
Speech disturbance without weakness - 1pt 
Symptoms >1 hour - 2 pts
Symptoms <1 hour - 1pt
Diabetes - 1pt
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30
Q

How would you manage a TIA?

A

Start 300mg aspirin daily

Prevent CVS disease e.g. smoking cessation, control diabetes, statin

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31
Q

What are the two types of stroke?

A

Ischaemic

Haemorrhagic

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32
Q

What are the cause of ischaemic stroke?

A 
MI
AF
Prosthetic valves
Endocarditis 
Atherothromboembolism
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33
Q

What are the cause of haemorrhagic stroke?

A

Trauma
Anaeurysm rupture
Anticoagulation + thrombolysis
Subarachnoid haemorrhage

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34
Q

What are the risk factors of stroke?

A 
CVS disease
Previous TIA/stroke
AF
Hypertension
Diabetes
Smoking 
Vasculitis 
Thrombophilia
Combined OCP
Carotid artery dissection
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35
Q

What are the signs of stroke?

A

Sudden onset: Facial weakness, limb weakness, dysphasia, vision loss, locked in syndrome

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36
Q

What are the differentials of a stroke?

A 
Migraine with aura
Epilepsy
Intracranial tumour
Hypoglycaemia
Subdural haemorrhage
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37
Q

What is the immediate management for someone with stroke?

A

Admit patient to stroke centre
Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg stat after CT

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38
Q

How would you manage an ischaemic stroke?

A

IV alteplase
Thrombectomy
300mg aspirin for 2 weeks

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39
Q

What kind of drug is alteplase?

A

Tissue plasminogen activator

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40
Q

What is the time frame to give alteplase?

A

Within 4.5 hours of stroke

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41
Q

What is the time frame for a thrombectomy?

A

Within 24 hours of stroke

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42
Q

Outline secondary prevention of stroke after a TIA

A

Clopidogrel 75mg OD
Atorvastatin 80mg
Carotid endarterectomy/stenting
Treat modifiable risk factors

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43
Q

What are the causes of subarachnoid haemorrhage?

A

Berry aneurysm rupture

Aterio-venous malformations

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44
Q

What are the risk factors for subarachnoid haemorrhage?

A 
Hypertension
Smoking 
Excess alcohol
Cocaine 
FH
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45
Q

Where does subarachnoid haemorrhage occur?

A

Subarachnoid space, between pia mater nd arachnoid membrane

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46
Q

What are the signs of a subarachnoid haemorrhage?

A 
Sudden onset thunderclap headache - can occur during strenuous activity
Neck stiffness
Photophobia
Vision changes
Weakness
Speech changes 
Seizures
Kernig's sign: inability to straighten knee when hip is flexed at 90 degrees
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47
Q

What are the differentials of subarachnoid haemorrhage?

A

Meningitis
Migraine
Intracerebral bleeds

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48
Q

What investigations would you do if you suspect subarachnoid haemorrhage?

A

CT head, Lumbar puncture, angiography

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49
Q

How would a subarachnoid haemorrhage appear on CT?

A

Hyperattenuation in subarachnoid space, star shaped bleed

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50
Q

What are the signs of subarachnoid haemorrhage on lumbar puncture?

A

CSF will show: raised RBC and xanthochromia caused by bilirubin

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51
Q

How would you manage subarachnoid haemorrhage?

A

Coiling/clipping to treat aneurysm
Antiepileptic
Nimodipine to prevent vasospasm
Lumbar puncture to treat hydrocephalus

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52
Q

Where does subdural haemorrhage occur?

A

Bleeding from bridging veins between cortex and venous sinuses. Leads to hameatoma between dura and arachnoid

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53
Q

What occurs if a subdural haemorrhage is not treated?

A

ICP rises, midline structures are shifted away from clot. Tentorial hernia and coning occurs.

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54
Q

What are the causes of subdural haemorrhage?

A

Trauma, however sometimes this can be up to 9 months ago

Dural mets

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55
Q

What are the risk factors for subdural haemorrhage?

A

Elderly
Epileptics (increased fall risk + atrophy)
Alcoholics (increased fall risk)

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56
Q

What are the signs of subdural haemorrhage?

A 
Fluctuating levels of consciousness
Sleepiness
Personality change
Seizure
Local neurological symptoms
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57
Q

How would a subdural haemorrhage appear on CT?

A

Crescent shaped collection of blood

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58
Q

How would you manage subdural haemorrhage?

A

Craniotomy

Burr hole washout

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59
Q

Laceration of which vessel causes extradural haemorrhage?

A

Middle meningeal artery in temporo-parietal region

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60
Q

Where does extradural haemorrhage occur?

A

Between skull and dura mater. Associated with fracture of temporal bone

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61
Q

What are the signs of extradural haemorrhage?

A 
Traumatic head injury leads to headache 
Period of improving consciousness followed by rapid decline 
Vomiting 
Seizures
Coma
62
Q

How would an extradural haemorrhage appear on CT?

A

Bi-convex shape of bleed, that cannot cross cranial sutures

63
Q

How would you manage extradural haemorrhage?

A

Clot evacuation

Ligation of bleeding vessel

64
Q

Multiple sclerosis (MS) is a chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system. This is caused by an inflammatory process involving the activation of immune cells against the myelin. Which cells have myeli n the PNS and CNS?

A

PNS: Schwann cells
CNS: Oligodendrocytes

65
Q

A characteristic feature of MS is that lesions vary in their location over time, meaning that different nerves are affected and symptoms change over time. What term is used to describe this phenomena?

A

Disseminated in time and space

66
Q

What are the risk factors for MS?

A

EBV, low vitamin D, smoking, obesity

67
Q

Name focal weakness symptoms of MS

A

Horner’s syndrome, Bells palsy, limb paralysis, incontinence

68
Q

Name focal sensory symptoms of MS

A

Trigeminal neuralgia, numbness, paraesthesia, Lhermitte’s sign: electric shock travelling down spine when flexing neck

69
Q

Name the types of ataxia that occur in MS

A
  1. Sensory ataxia: loss of proprioception

2. Cerebellar ataxia

70
Q

What results in demyelination of the optic nerve?

A

Optic neuritis

71
Q

Name the two abnormalities that occur with a sixth nerve (abducens) palsy

A

Internuclear opthalmoplegia + conjugate lateral gaze disorder (eye will not be able to adduct)

72
Q

State the 3 types of disease progression in MS.

A
  1. relapsing-remitting
  2. primary progressive (no relapses)
  3. secondary progressive (relapsing at first but now progressive worsening)
73
Q

How would MS appear on lumbar puncture?

A

Oligoclonal bands in CSF

74
Q

What are the key features of optic neuritis?

A

Central scotoma = enlarged blind spot
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

75
Q

Which drugs can be used to treat relapses of MS?

A

IV methylprednisolone

Monoclonal antibodies

76
Q

Outline symptomatic management for MS

A

Exercise
Gabapentin for spasticity
Oxybutynin for incontinence
Botox for tremor

77
Q

What type of genetic inheritance is Huntington’s disease?

A

Autosomal dominant

78
Q

Huntington’s chorea is a trinucleotide repeat disorder that involves a genetic mutation in the HTT gene on chromosome 4. Which trinucleotide is affected?

A

CAG

79
Q

What is the term given to the phenomena where successive generations have more repeats in the gene, resulting in:

Earlier age of onset
Increased severity of disease?

A

Anticipation

80
Q

What are the signs of Huntington’s?

A 
Mood problems
Chorea = involuntary abnormal movements
Eye movement disorders
Dysarthria
Dysphagia
81
Q

How would you manage Huntington’s?

A

No treatment to stop disease. Counsel, offer speech and language therapy

82
Q

Which chemical becomes progressively lower in Parkinson’s?

A

Dopamine

83
Q

Which part of the brain is there reduced dopamine in Parkinson’s?

A

Substantia nigra in basal ganglia

84
Q

What are the clinical features of Parkinson’s?

A 
Unilateral tremor 
Cogwheel rigidity 
Bradykinesia: shuffling gait, handwriting gets smaller and smaller
Depression
Insomnia
Anosmia - loss of smell
Postural instability 
Cognitive impairment
Asymmetrical reduction in arm swing 
Dribbling
85
Q

Outline the features of a Parkinson’s tremor

A

Unilateral, worse at rest, improves with movement, no change with alcohol

86
Q

Outline the features of a benign essential tremor

A

Bilateral, improves at rest, worse with movement, improves with alcohol

87
Q

What are the complications of Parkinson’s?

A

Multiple system atrophy
Cerebellar dysfunction
Dementia with Lewy bodies

88
Q

How would you manage Parkinson’s?

A

Dopamine agonist e.g. ropinirole
Monoamine oxidase-B inhibitors
COMT inhibitors
L-dopa - give last

89
Q

What are the side effects of L-dopa?

A

Chorea, dystonia, athetosis

90
Q

What is a significant side effect of dopamine agonists?

A

Pulmonary fibrosis

91
Q

Guillain-Barré syndrome is an “acute paralytic polyneuropathy” that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms. It is usually triggered by which infections?

A

EBV, campylobacter jejuni and cytomegalovirus

92
Q

Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.

What are the symptoms of this?

A

Symmetrical ascending weakness from feet up
Reduced reflexes
Neuropathic pain
Peripheral loss of sensation

93
Q

How is Guillain-Barré syndrome diagnosed?

A

Nerve conduction studies (reduced signal)

Lumbar puncture: raised protein and normal WCC

94
Q

How would you manage Guillain-Barré syndrome?

A

IV immunoglobulins or plasma exchange
Ventilation
VTE prophylaxis - PE is a leading cause of death

95
Q

Myasthenia graves is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.

Which condition is a risk factor for myasthenia gravis?

A

Thymoma

96
Q

In around 85% of patients with myasthenia gravis, acetylcholine receptor antibodies are produced by the immune system. These bind to the postsynaptic neuromuscular junction receptors, preventing muscle contraction. These antibodies also activate the complement system within the neuromuscular junction, leading to damage to cells at the postsynaptic membrane. This further worsens the symptoms.

Which other antibodies cause myasthenia gravis?

A

Muscle specific kinase (MusK) and low-density lipoprotein receptor-related protein 4 (LRP4) - both are needed to create acetylcholine receptors

97
Q

What are the clinical features of myasthenia gravis?

A 
Weakness that gets worse with use and improves with rest
Diplopia
Ptosis
Slurred speech
Weak swallow
98
Q

What investigations would you do for myasthenia gravis?

A

ACH-R, MuSK and LRP4 antibodies
CT of thymus
Edrophonium test - briefly relieves weakness

99
Q

How would you manage myasthenia gravis?

A

Reversible acetylcholinesterase inhibitor
Prednisolone
Thymectomy
Rituximab

100
Q

Myasthenic crisis is a severe complication of myasthenia gravis. It can be life threatening. It causes an acute worsening of symptoms, often triggered by another illness such as a respiratory tract infection. This can lead to respiratory failure as a result of weakness in the muscle of respiration. How would you manage this?

A

Intubation and ventilation
IV immunoglobulins
Plasma exchange
Monitor FVC

101
Q

Which nerve is compressed in carpal tunnel syndrome?

A

Medial nerve

102
Q

What are the risk factors for carpal tunnel syndrome?

A 
Repetitive strain
Obesity
RA
Diabetes
Acromegaly
Hypothyroidism
103
Q

arpal tunnel syndrome causes sensory symptoms in the distribution of which branch of the median nerve?

A

Palmar digital cutaneous branch

104
Q

What are the sensory symptoms of carpal tunnel syndrome?

A 
Thumb, index, middle and lateral ring finger:
Numbness
Paraesthesia
Burning sensation
Pain
Relieved by shaking hand 
Worse at night
105
Q

What are the motor symptoms of carpal tunnel syndrome?

A

Weakness of thumb movements
Wasting of thenar muscles
Weakness of grip

106
Q

Which two special tests can be done to diagnose carpal tunnel syndrome?

A

Phalen’s: maximal wrist flexion for 1 min induces parathesia
Tinel’s: tapping over nerve induces paraesthesia

107
Q

How would you manage carpal tunnel syndrome?

A

Wrist splint, steroid injections, decompression surgery

108
Q

Motor neurone disease is an umbrella term that encompasses a variety of specific diagnoses. Motor neurone disease is a progressive, ultimately fatal condition where the motor neurones stop functioning. There is no effect on the sensory neurones and patients should not experience any sensory symptoms.

State 4 types of MND.

A
  1. ALS: amyotrophic lateral sclerosis
  2. Progressive bulbar palsy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis
109
Q

In MND, there is a progressive degeneration of both upper and lower motor neurones. The sensory neurones are spared.

What are the risk factors for developing MND?

A

Positive FH, smoking, exposure to heavy metals, pesticides

110
Q

What are the symptoms of MND?

A
  • insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech.
  • increased fatigue when exercising
  • clumsiness, dropping things more often or tripping over
  • slurred speech (dysarthria)
111
Q

What are the UMN signs of MND?

A

Increased tone or spasticity
Brisk reflexes
Up-going plantar responses

112
Q

What are the LMN signs of MND?

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

113
Q

How would you manage MND?

A
  • riluzole for ALS
  • non invasive ventilation
  • NG feeding tube
  • diazepam for spasticity
  • propantheline for excess saliva
114
Q

How can you distinguish between MND and myasthenia gravis?

A

MND never affects eye movements

115
Q

In ALS, there is moss of motor neurones in anterior horn and motor cortex. What are the features of ALS?

A

Weakness, LMN wasting

116
Q

In progressive bulbar palsy, cranial nerves 9-12 are affected. What are the features of this?

A

LMN lesion of tongue: flaccid, fasiculating tongue

Hoarse speech

117
Q

Progressive muscular dystrophy is due to lesions in the anterior horn cells. Would this present as UMN or LMN signs?

A

LMN

118
Q

In primary lateral sclerosis, there is loss of Bletz cells in the motor cortex. Would this present as UMN or LMN signs?

A

UMN

119
Q

Epilepsy is an umbrella term for a condition where there is a tendency to have seizures. Seizures are transient episodes of abnormal electrical activity in the brain. There are many different types of seizures.

State the types of seizures

A 
Generalised tonic clonic 
Absence 
Atonic
Myoclonic
Focal
Infantile spasms
120
Q

What are the features of a general tonic clonic seizure?

A
  • There is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) episodes.
  • associated tongue biting, incontinence, groaning and irregular breathing.

After the seizure there is a prolonged post-ictal period where the person is confused, drowsy and feels irritable or depressed.

121
Q

How would you manage a tonic clonic seizure?

A

First line: sodium valproate

Second line: lamotrigine or carbamazepine

122
Q

What are the features of focal seizures?

A 
Focal seizures start in temporal lobes:
Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot
123
Q

How would you manage focal seizures?

A

First line: carbamazepine or lamotrigine

Second line: sodium valproate or levetiracetam

124
Q

What are the features of atonic seizure?

A

Atonic seizures are also known as “drop attacks”. They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minutes.

125
Q

How would you manage atonic seizures?

A

First line: sodium valproate

Second line: lamotrigine

126
Q

What are the features of absence seizures?

A

The patient becomes blank, stares into space and then abruptly returns to normal. During the episode they are unaware of their surroundings and won’t respond. These typically only lasts 10-20 seconds.

127
Q

How would you manage absence seizures?

A

First line: sodium valproate or ethosuximide

128
Q

What are the features of myoclonic seizures?

A

Myoclonic seizures present as sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode. They typically happen in children as part of juvenile myoclonic epilepsy.

129
Q

How would you manage myoclonic seizures?

A

First line: sodium valproate

Other options: lamotrigine, levetiracetam or topiramate

130
Q

What are the features of infantile spasms?

A

Also known as West syndrome. Starts at 6 months of age. It is characterised by clusters of full body spasms. There is a poor prognosis: 1/3 die by age 25, however 1/3 are seizure free

131
Q

How would you manage infantile spasms?

A

Prednisolone

Vigabatrin

132
Q

How would you diagnose epilepsy?

A
  • EEG
  • MRI of brain
  • ECG
133
Q

State the non-epileptical causes of seizure

A
  • Trauma
  • Stroke
  • Raised ICP
  • Alcohol withdrawal
  • Infection e.g. HIV, syphillis
  • Cocaine use
134
Q

What is a severe side effect of sodium valproate?

A

Teratogenic

135
Q

Define status epilepticus

A

seizures lasting more than 5 minutes or more than 3 seizures in one hour.

136
Q

How would you manage status epilepticus?

A

Secure the airway
Give high-concentration oxygen
Check blood glucose levels
IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
If seizures persist: IV phenobarbital or phenytoin

137
Q

What is a sign of raised ICP on fundoscopy?

A

Papilloedema

138
Q

What are the causes of raised ICP?

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection

139
Q

What are the most common cancers to metastasise in the brain?

A

Breast
Lung
Prostate
Renal cell carcinoma

140
Q

State 2 types of benign brain tumour

A

Neurofibroma

Meningioma

141
Q

State types of malignant brain tumour

A

Glioma
Lymphoma
Medulloblastoma

142
Q

What are the symptoms of raised ICP?

A 
Nausea 
Headache that is nocturnal and worse on lying down and in morning
Worse when coughing 
Altered mental state
Visual field defects
Seizures (particularly focal)
Unilateral ptosis
Third and sixth nerve palsies
Papilloedema (on fundoscopy)
143
Q

If someone presented with personality change due to a brain tumour, where would the lesion be located?

A

Frontal lobe

144
Q

Papilloedema is the swelling of what structure?

A

Optic disc

145
Q

Gliomas are tumours of the glial cells in the brain or spinal cord. What are the 3 key types of glioma?

A

Astrocytoma
Oligodendroglioma
Ependymoma

146
Q

What occurs when pituitary tumours press on the optic chiasm?

A

Bitemporal hemianopia

147
Q

Acoustic neuromas are tumours of which cells?

A

Schwann cells surrounding auditory nerve

148
Q

What are the symptoms of acoustic neuroma?

A

Hearing loss
Tinnitus
Balance problems

149
Q

How would you investigate a suspected brain tumour?

A
  • CT/MRI of brain
  • Brain biopsy
  • Do not do lumbar puncture if you suspect raised ICP as this can cause coning
150
Q

How would you manage a high grade tumour?

A
  • IV dexamethasone to reduce cerebral oedema
  • Resection of tumour
  • Radiotherapy
  • Chemo

No cure

151
Q

How would you manage a pituitary tumour?

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine to block prolactin-secreting tumours
Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours

3a (13 decks)

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