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Neurology Flashcards

1
Q

What can cause disruption of blood supply that leads to a stroke?

A

Thrombus formation or embolus, atherosclerosis, shock, vasculitis

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2
Q

What is the definition of TIA?

A

Transient neurological dysfunction secondary to ischaemia without infarction

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3
Q

What is the presentation of stroke/TIA?

A

Sudden onset of any neurological symptoms - weakness, dysphasia, visual/sensory loss, swallowing problems, balance problems, dizziness, confusion, ataxia, N+V

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4
Q

What are the 3 requirements for a total anterior circulation stroke?

A

All 3 of the following are present:
1. Unilateral weakness and/or hemisensory loss of face, arm and leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphasia

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5
Q

Which extremity (upper or lower) is affected more in anterior/middle cerebral artery strokes?

A

Anterior = upper
Middle = lower

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6
Q

What are the requirements for something to be described as a partial anterior circulation stroke?

A

Two of the following 3 are present:
1. Unilateral weakness and/or hemisensory loss of face, arm and leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphasia

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7
Q

What are the symptoms of lacunar infarcts?

A

Presents with one of the following:
1. Unilateral weakness (or sensory loss) of face and arm, arm and leg or all 3
2. Pure sensory stroke
3. Ataxic weakness

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8
Q

What are the symptoms of posterior circulation strokes?

A

One of the following:
1. Cerebellar or brainstem syndromes
2. Loss of consciousness
3. Isolated homonymous hemianopia

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9
Q

What is lateral medullary syndrome/Wallenberg’s syndrome?

A

Stroke of the posterior inferior cerebellar artery

Cerebellar signs
Ipsilateral - Horner’s, facial numbness
Contralateral - sensory loss

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10
Q

What is Weber’s syndrome?

A

Ipsilateral cranial nerve III palsy
Contralateral weakness

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11
Q

What tool is designed to recognise stroke in the emergency room?

A

ROSIER - stroke is likely if patient scores anything above 0

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12
Q

What needs to be ruled out in someone presenting with stroke symptoms?

A

Hypoglycaemia

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13
Q

What is the 1st line investigation for someone presenting with stroke symptoms?

A

Non-contrast CT head to exclude haemorrhage

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14
Q

Once haemorrhage has been excluded what is the management for stroke?

A

Aspirin 300mg STAT (continued for 2 weeks)

Thrombolysis e.g. alteplase within 4.5 hours of onset of symptoms (if not contraindicated)

+/- thrombectomy - done if there is confirmed occlusion of the proximal anterior circulation (needs to be done within 6 hours of symptom onset in addition to thrombolysis)

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15
Q

What is the management of TIA when someone presents within a week of the symptoms?

A

Start aspirin 300mg daily
Start secondary prevention for CVD
Need to be seen in rapid access TIA clinic within 24 hours

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16
Q

What imaging investigations are done for people during TIA clinic?

A

Diffusion-weight MRI - aim to establish the vascular territory affected
Carotid USS to assess for carotid stenosis

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17
Q

What is the secondary prevention of stroke?

A

Clopidogrel 75mg OD = 1st line
Aspirin 75mg with MR dipyridamole 200mg = 2nd line
Atorvastatin 80mg
Carotid endarterectomy or stenting

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18
Q

How long can people who have had stroke/TIA not drive for?

A

TIA/stroke = 1 month
Multiple TIAs = 3 months

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19
Q

What are the risk factors for intracranial bleeds?

A

Head injury, hypertension, aneurysms, brain tumours, anticoagulants

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20
Q

What are the symptoms of intracranial haemorrhage?

A

Sudden onset headache, seizures, weakness, vomiting, reduced consciousness, sudden onset neurological symptoms

In subdural there is fluctuating consciousness

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21
Q

Which vessel is ruptured in an extradural hameorrhage?

A

Middle meningeal artery - can be associated with fracture of the temporal bone

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22
Q

What are the CT findings of someone with extra dural?

A

Bi-convex (lemon) hyperdense collection that is limited by the cranial sutures

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23
Q

What is the definitive management of extradural?

A

Craniotomy and evacuation of the haematoma

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24
Q

Which vessel is ruptured in a subdural bleed?

A

Bridging veins between the cortex and the venous sinus

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25
Q

What are the CT findings in subdural?

A

Hyperdense crescent shaped collection not limited by suture lines

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26
Q

What is the management of acute subdurals?

A

Decompressive craniectomy

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27
Q

What people are at risk of chronic subdurals?

A

Elderly and alcoholic patients due to brain atrophy and fragile vessels

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28
Q

What is the management for chronic subdurals?

A

If small can be managed conservatively

Otherwise surgical decompression with burr holes is required

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29
Q

What are the causes of SAH?

A

Rupture of cerebral aneurysm, trauma, AV malformation, pituitary apoplexy

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30
Q

What are the symptoms of SAH?

A

Sudden onset thunderclap headache that occurs during strenuous activity such as weightlifting/sex

Neck stiffness, photophobia, N+V, vision changes, loss of consciousness

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31
Q

What are the risk factors for SAH?

A

Hypertension, smoking, excessive alcohol, cocaine use, family history, sickle cell anaemia, connective tissue disorders, neurofibromatosis, PKD

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32
Q

What is seen on LP in those with SAH?

A

Red cell count raised
Xanthochromia - yellow discolouration of CSF caused by bilirubin

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33
Q

What is the management of SAH?

A

Endovascular coiling or clipping
Nimodipine is used to prevent vasopasm

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33
Q

What investigations are done in epilepsy?

A

EEG, MRI head, ECG to exclude heart problems, baseline bloods

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34
Q

When are antiepileptics started?

A

After 2 seizures have occured

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35
Q

How long must a person be fit-free for before they are able to drive?

A

Cannot drive for 6 months following seizures, for those with established epilepsy must be fit free for 12 months

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36
Q

What symptoms are associated with tonic-clonic seizures?

A

Tongue biting, incontinence, groaning, irregular breathing, prolonged post-ictal period, unprovoked event

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37
Q

What is the 1st line and 2nd line treatment for tonic-clonic epilepsy?

A

1st = sodium valproate
2nd = lamotrigine or levetiracetam (1st line in women)

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38
Q

What is the presentation of focal seizures?

A

Level of awareness can vary dramatically, hallucinations, memory flashbacks, deja vu

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39
Q

What is the 1st and 2nd line management for focal seizures?

A

1st line = levetiracetam or lamotrigine
2nd line = carbamazepine, oxcarbazepine

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40
Q

What is the presentation of absence seizures?

A

Typically occur in children, becomes blank and stare into space before abruptly returning to normal

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41
Q

What is the management of absence seziures?

A

1st line = ethosuximide
2nd line = sodium valproate or lamotrigine/levetiracetam (females)

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42
Q

What are the symptoms of atonic seizures?

A

Brief lapses in muscle tone (drop attacks), begin typically in childhood

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43
Q

What is the 1st and 2nd line management for atonic seizures?

A

1st line = sodium valproate
2nd line = lamotrigine (1st in females)

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44
Q

What is the presentation of myoclonic seizures?

A

Sudden brief muscle contractions like a sudden jump, patient usually remains awake during the episode (can occur as part of juvenile myoclonic epilepsy)

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45
Q

What is the 1st and 2nd line management for myoclonic seziures?

A

1st line = sodium valproate
2nd line = lamotrigine/levetiracetam (1st in females)

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46
Q

What is the presentation for infantile spasms?

A

Starts around 6 months of age, characterised by clusters of full body spasms

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47
Q

What is the management of infantile spasms?

A

Prednisolone and vigabatrin

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48
Q

What are the side effects of sodium valproate?

A

Teratogenic, liver damage and hepatitis

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49
Q

What are the side effects of carbamazepine?

A

Agranulocytosis, SIADH, induces the P450 system

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50
Q

What are the side effects of phenytoin?

A

Folate and vitamin D deficiency, megaloblastic anaemia, P450 inducer

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51
Q

What are the side effects of ethosuximide?

A

Night terrors and rashes

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52
Q

What are the side effects of lamotrigine?

A

Stevens Johnsons, leukopenia

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53
Q

What is the definition of status epilepticus?

A

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

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54
Q

What is the management of status epilepticus?

A

Secure airway, check blood glucose
IV lorazepam 4mg repeated after 10 minutes if the seizure continues
If they persist give IV Phenobarbital or phenytoin

55
Q

Which area of the brain is affected in Parkinson’s?

A

Substantia nigra (part of the basal ganglia) which is responsible for producing dopamine

56
Q

Are Parkinson’s symptoms bilateral or unilateral?

A

Unilateral to start with but as disease progresses may become more bilateral

57
Q

What symptoms are common in Parkinson’s?

A

Pill rolling resting tremor, cogwheel rigidity, small handwriting, shuffling gait, difficulty initiating movement, hypomimia, reduced arm swing, fine motor issues

58
Q

What is multi system atrophy?

A

Parkinson plus syndrome which leads to autonomic dysfunction –> postural hypotension, constipation, abnormal swearing, sexual dysfunction, ataxia

59
Q

What is dementia with lewy bodies?

A

Parkinson plus syndrome which causes progressive cognitive decline, hallucinations, delusions, disorders of REM and fluctuating consciousness

60
Q

How can you differentiate true Parkinson’s from drug induced Parkinson’s?

A

Drug induced Parkinsonism typically presents with motor symptoms, rapid onset, no resting tremor or rigidity

61
Q

What are the side effects of Levodopa?

A

Dystonia - excessive muscle contraction
Chorea - abnormal involuntary movements
Athetosis - involuntary twisting or writhing movements

62
Q

What is an example of a COMT inhibitor and how does it work ?

A

Entacapone
Prevents the metabolism of levodopa in the body and brain

63
Q

What is an example of a dopamine agonsits, how does it work and what are the side effects?

A

Bromocriptine, pramipexole, ropinirole
Mimics dopamine in the basal ganglia and stimulates dopamine receptors
Side effects = impulse control disorders and excessive daytime sleepiness

64
Q

What is an example of a monoamine oxidase-B inhibitor and how does it work?

A

Selegiline, rasagiline
Block the action of enzymes that break down dopamine

65
Q

When is levodopa used as 1st line management in Parkinson’s?

A

If motor symptoms are affecting the patients quality of life at time of diagnosis/starting medication

66
Q

What are the symptoms of benign essential tremor?

A

Fine tremor, symmetrical, worse on voluntary movement, improved by alcohol and worse when tired/stressed

67
Q

What can be done to manage benign essential tremor?

A

Propranolol and primidone can help improve symptoms

68
Q

What are red flag headache symptoms?

A

Fever, neck stiffness, new onset neurological symptoms, dizziness, visual disturbance, sudden onset, worse on coughing/straining, severe enough to wake from sleep, vomiting, trauma

69
Q

What are the features of tension headache?

A

Mild ache across forehead like a tight band, 30 minutes to 7 days, bilateral , come on and resolve gradually, no visual symptoms, associated with stress, depression, alcohol etc.

70
Q

What is the management of tension headaches?

A

Reassurance, simple analgesia, relaxation techniques (ensure they do not use simple analgesia too frequently)

71
Q

How does sinusitis present?

A

Usually facial pain behind nose/forehead, tenderness over the affected sinus, lasts for 2-3 weeks

72
Q

How is sinusitis treated?

A

Nasal irrigation, steroid nasal spray

73
Q

What is the presentation of cervical spondylosis?

A

Neck pain made worse by movement, headache

74
Q

How does trigeminal neuralgia present?

A

90% of cases are unilateral, intense facial pain that comes on spontaneously and last anywhere between a few seconds to hours, electric shock type pain

75
Q

What is the management of trigeminal neuralgia?

A

Carbamazepine

76
Q

What is the presentation of idiopathic intracranial hypertension?

A

Seen in young, overweight females
Headache, blurred vision, papilloedema, six nerve palsy

77
Q

What is the management of idiopathic intracranial hypertension?

A

CT/MRI head may be done to rule out other causes but will be normal
Weight loss and acetazolamide

78
Q

What is the definition of medication overuse headache?

A

Headache occurring on at least 15 days per month for at least 3 months with pre-existing headache disorder

Regularly for more than 3 months used one or more drugs that can be taken for headache

79
Q

What are the headache symptoms associated with migraines?

A

Last between 4 and 72 hours, moderate to severe, pounding/throbbing, unilateral, photophobia, phonophobia, N+V

80
Q

What are the symptoms of a migraine aura?

A

Sparks in vision, blurring vision, lines across vision, loss of different visual fields, motor weakness, sensory symptoms

Lasts 5-60 minutes

81
Q

What are the symptoms of a hemiplegic migraine?

A

Typical migraine symptoms but also associated with unilateral weakness of limbs, ataxia and changes in consciousness - need to rule out stroke

82
Q

What are some typical triggers for migraines?

A

Stress, bright lights, strong smells, foods, dehydration, menstruation, abnormal sleep patterns, trauma

83
Q

What medications can be used in the acute management of migraines?

A

Paracetamol, NSAIDs, triptans + antiemetics if required

84
Q

What can be used as migraine prophylaxis?

A

Propranolol 80-160mg
Topiramate 50-100mg
Amitriptyline 25-75mg
Acupuncture
Vitamin B2 supplementation

85
Q

What are the symptoms of cluster headaches?

A

Red, swollen watering eye, severe headache around the eye area, pupil constriction, nasal discharge, facial sweating

Last between 15 minutes and 3 hours

Occur in clusters 3-4 attacks a day fro a week followed by pain free period

86
Q

What is the management of cluster headaches?

Immediate and prophylaxis

A

Refer to neurology during first bout

Triptans and high flow 100% oxygen can be used during acute attack

Prophylaxis - verapamil, lithium, prednisolone (short course)

87
Q

What are some presentations of MS?

A

Symptoms progress over more than 24 hours last for a week or so then improve

Optic neuritis - pain behind the eye and loss of colour discrimination, enlarged blind spot, RAPD (unilateral)

Focal sensory symptoms, focal weakness, ataxia

88
Q

What is Uhthoff’s phenomenon?

A

Transient worsening of any neurological symptoms related to MS when the body becomes overheated in hot weather, exercise, hot showers etc.

89
Q

What is Lhermitte’s sign?

A

Electrical shock sensation that travels down the spine and into the limbs when flexing the neck

90
Q

What investigations are done in MS?

A

Clinical diagnosis, MRI head, LP will show oligoclonal bands

91
Q

How are MS relapses treated?

A

Methylprednisolone - 500mg OD or 1g IV for 3-5 days

92
Q

What is the long term management of MS?

A

DMARDs and biologic therapy

93
Q

What are the types of motor neurone disease?

A

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

94
Q

What is the presentation of MND?

A

Both UMN and LMN signs but no sensory symptoms

Progressive weakness of muscles throughout the body, clumsy, tripping over, slurred speech

95
Q

What are LMN signs?

A

Muscle wasting, reduced tone, fasciculations, reduced relfexes

96
Q

What are UMN signs?

A

Increased tone/spasticity, brisk reflexes, upgoing plantar reflexes

97
Q

What investigations are done in MND and what do they show?

A

Clinical diagnosis but done to aid diagnosis

Nerve conduction studies - normal
Electromyography - reduced number of action potentials
MRI - normal

98
Q

What is the management of MND?

A

Riluzole can slow progression but otherwise control symptoms

99
Q

What antibodies are found in myasthenia gravis?

A

Acetylecholine receptor antibodies, anti-MuSK, anti-LRP4

100
Q

What are the symptoms of myasthenia gravis?

A

Weakness that gets worse with use and improves with rest

Double vision
Eyelid weakness
Facial weakness
Fatigue in jaw
Slurred speech

101
Q

What test can be done to confirm diagnosis of myasthenia gravis?

A

Edrophonium/Tensilon test

102
Q

What is the management of myasthenia gravis?

A

Acetylcholinesterase inhibitors e.g. pyridostigmine or neostigmine - increases the amount of ACh in the NMJ and improves symptoms

Avoid beta blockers as they can make MG worse

103
Q

What is a myasthenic crisis?

A

Severe acute worsening of symptoms triggered by another illness, can lead to respiratory failure (monitor with FVC)

104
Q

What is Lambert Eaton myasthenic syndrome?

A

Condition associated with SCLC

Progressive muscle weakness, repeated muscle contractions leads to increased muscle strength (in contrast to MG), proximal muscles are most notably affected, autonomic symptoms

105
Q

What is the management of Lambert-Eaton myasthenic syndrome?

A

Diagnose and manage the underlying malignancy

Amifampridine

106
Q

What are the symptoms of raised intracranial pressure?

A

Constant headache, waking up from sleep, worse on coughing/straining/bending forward, vomiting, papilloedema on fundoscopy, altered mental state, visual field defects, cranial nerve palsies

107
Q

What is Cushing’s triad?

A

Physiological response to raised ICP

Bradycardia, hypertension, wide pulse pressure

108
Q

What tumours commonly metastasise to the brain?

A

Lung, breast, RCC, melanoma

109
Q

What are the symptoms of normal pressure hydrocephalus?

A

Dementia, incontinence and disturbed gait

110
Q

What investigations are done in someone with hydrocephalus?

A

CT = 1st line
MRI will give more detail
LP = diagnostic and therapeutic

111
Q

What are the symptoms of a third nerve palsy?

A

Eye is down and out, ptosis, pupil may be dilated

112
Q

What are the symptoms of a fourth nerve palsy?

A

Vertical diplopia noticed when looking down, eye may appear to deviate upwards/rotated outwards

113
Q

What are the symptoms of a sixth nerve palsy?

A

Eye will be adducted, horizontal diplopia, inability to look laterally

114
Q

What are the symptoms of a fifth nerve palsy?

A

Altered sensation over face and tongue, weakness in muscles of mastication, jaw deviates to side of lesion, absent jaw and corneal reflex

115
Q

What are the causes of UMN and LMN facial palsies?

A

UMN = stroke or tumour
LMN = Bell’s palsy and Ramsay-hunt syndrome

116
Q

How can you differentiate between LMN and UMN facial nerve palsy?

A

UMN = there is forehead sparing
LMN = forehead is not spared

117
Q

What is the management of Bell’s palsy?

A

50mg prednisolone for 10 days and eye care advice

118
Q

What is Ramsay-Hunt syndrome and how is it managed?

A

Caused by varicella zoster virus, have painful and tender vesicular rash in ear canal + LMN facial nerve palsy

Management = aciclovir and prednisolone + eye care advice

119
Q

What are the causes of GBS?

A

Usually triggered by infection - campylobacter jejuni, CMV and EBV

120
Q

What are the symptoms of GBS?

A

Symptoms start 1-4 weeks after infection

Ascending (starts at feet and works up) weakness and reduced reflexes, may be some sensory loss

121
Q

What investigations are done in GBS and what will they show?

A

Clinical diagnosis

Nerve conduction studies - reduced signal through the nerves

LP - raised protein with normal cell count and glucose

122
Q

What is the management of GBS?

A

VTE prophylaxis, IV immunoglobulins = 1st line, plasmapheresis = 2nd line

123
Q

What is the pathophysiology of Huntington’s?

A

Autosomal dominant condition that causes progressive neurological dysfunction due to trinucleotide repeats of CAG

124
Q

What is genetic anticipation?

A

Successive generations have more repeats which leads to earlier onset and increased severity of disease

125
Q

What are the symptoms of Huntington’s?

A

Cognitive, psychiatric or mood problems
Chorea, dystonia, rigidity, eye movement disorders, speech difficulties, swallowing difficulties

126
Q

How is Huntington’s diagnosed?

A

Genetic testing - must be at least 18

127
Q

What are the features of neurofibromatosis type 1?

A

Cafe-au-lait spots, axillary or inguinal freckling, bony dysplasia, iris hamartomas, neurofibromas (nodules on the skin), glioma

128
Q

What cancers are associated with neurofibromatosis type 1?

A

Malignant peripheral nerve sheath tumours, GI stromal tumours, brain tumours, spinal cord tumours

Increased risk of breast cancer and leukaemia

129
Q

What are the features of neurofibromatosis type 2?

A

Bilateral acoustic neuromas

130
Q

What is the inheritance pattern of both neurofibromatosis?

A

Autosomal dominant

131
Q

What are the features of Charcot-Marie-Tooth disease?

A

High foot arches, distal muscle wasting, lower leg weakness particularly ankle dorsiflexion, peripheral sensory loss (glove and stocking)

132
Q

What are the differentials of peripheral neuropathy?

A

Alcohol, B12 deficiency, myeloma, CKD, diabetes, isoniazid, amiodarone, vasculitis

133
Q

What is tuberous sclerosis and what are the features?

A

Autosomal dominant condition that affects skin, brain, lungs, heart and kidneys

Learning difficulties, brain tumours, epilepsy, shagreen patches, ash lead spot, angiofibromas, ungual fibromas, cafe-au-lait spots

134
Q

What is nacrolepsy?

A

Condition that results in excessive sleepiness, sleep paralysis, hallucinations on waking up and sudden loss of muscle tone triggered by emotion (cataplexy)

Managed with modafinil and night time sodium oxybate

Finals (21 decks)

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