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Phase 2a > Neurology 3 > Flashcards

Neurology 3 Flashcards

1
Q

How do you investigate a migraine?

A

Mainly clinical
Exclude differentials - bloods, consider for CT/MRI

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2
Q

If you take the OCP and have a migraine with aura, what are you at risk of?

A

Ischaemic stroke

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3
Q

What triggers a migraine?

A

CHOCOLATE

CHeese
OCP
Caffeine
AlcohOL
Anxiety/stress
Travel
Exercise

Also too much/little sleep, sensory stimuli, dehydration

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4
Q

What are migraines?

A

Recurrent acute attacks of unilateral frontal pulsating headache

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5
Q

What worsens migraines?

A

Head movement or physical activity

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6
Q

What are migraines associated with?

A

N+V + photo/phonophobia

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7
Q

What are the features of migraines?

A

POUND

Pulsating
Onset 4-72hrs
Unilateral
Nausea
Disabling

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8
Q

How do migraines start?

A

25% with an aura

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9
Q

What is an aura of a migraine like?

A

Usually visual - flashes/lines/zigzags = fortification spectra, scotoma (black hole in visual field)

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10
Q

What are the less common features of migraines?

A

Paraesthesia, dysphasia etc

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11
Q

What is the acute management of a migraine?

A

Triptans (sumatriptan) + NSAIDs +/- anti-emetic if nauseous

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12
Q

What is the non-medicated prophylaxis for migraines?

A

Reduce triggers
Stop OCP

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13
Q

What is the 1st line medicated prophylaxis for migraines?

A

Beta blocker (propranolol)

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14
Q

What are the other options for medicated prophylaxis of migraines?

A

Anticonvulsant (topiramate), amitriptyline, botulinum toxin type A

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15
Q

What is there a risk of when treating a migraine?

A

Medication overuse headache - avoid offering opioids or ergots

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16
Q

What is the most common headache?

A

Tension headache

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17
Q

What triggers a tension headache?

A

Stress/anxiety, sleep deprivation, eye strain, noise etc.

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18
Q

How does a tension headache present?

A

Bilateral tight pressing band-like sensation +/- scalp tenderness

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19
Q

How long do tension headaches last?

A

30 mins to 7 days, can be chronic or episodic

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20
Q

What are the key differentials of a tension headache from a migraine?

A

Non-pulsatile

Not worsened on head movement/physical activity

No N+V

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21
Q

How do you diagnose a tension headache?

A

Clinical diagnosis from history

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22
Q

How do you manage a tension headache?

A

Lifestyle advice e.g. regular exercise, avoid triggers

Stress relief

NSAIDs for symptoms

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23
Q

How do you reduce the risk of a medication overuse headache?

A

Limit use of analgesia to no more than 6 days/month

Avoid opioids

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24
Q

Where is a tension headache felt?

A
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25
Q

Where is a migraine felt?

A
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26
Q

What is the most disabling primary headache?

A

Cluster headache

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27
Q

What triggers a cluster headache?

A

Alcohol

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28
Q

How do you diagnose a cluster headache?

A

Clinical

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29
Q

How does a cluster headache present?

A

Rapid abrupt onset excruciating pain around one eye, temple or forehead - always unilateral, usually affects same side + ipsilateral autonomic features

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30
Q

What are the autonomic features of cluster headaches?

A

Bloodshot eye, miosis, ptosis, lacrimation, rhinorrhea

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31
Q

How long do cluster headaches last?

A

15-60 mins

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32
Q

When do cluster headaches occur?

A

A couple of times a day, usually at the same time - often nocturnal/wakes patient from sleep

Last several weeks, followed by pain-free periods before next cluster

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33
Q

What is the acute management of a cluster headache?

A

100% oxygen for 15 mins via non-rebreathable mask + SC sumatriptan

Analgesics unhelpful

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34
Q

How do you prevent a cluster headache?

A

Verapamil (CCB) = 1st line

Avoid alcohol during

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35
Q

How does trigeminal neuralgia present?

A

Paroxysmal severe sharp stabbing pain

Unilateral in distribution of trigeminal nerve branches - patient’s face screws up with pain

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36
Q

How long does trigeminal neuralgia last?

A

seconds - 2 mins

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37
Q

What causes trigeminal neuralgia?

A

Due to compression of trigeminal nerve usually due to loop of vein/artery

Can be secondary e.g. aneurysm, tumour

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38
Q

What triggers trigeminal neuralgia?

A

Cutaneous stimuli e.g. touch, shaving, washing face, eating etc.

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39
Q

How do you treat trigeminal neuralgia?

A

Anticonvulsants - carbamazepine

Analgesics do not work

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40
Q

What is giant cell arteritis?

A

Granulomatous arteritis of large arteries

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41
Q

Which artery is commonly affected in giant cell arteritis?

A

Temporal artery

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42
Q

What is the epidemiology of giant cell arteritis?

A

F>M

>50

Caucasian

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43
Q

What condition is GCA strongly associated with?

A

Polymyalgia rheumatica

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44
Q

How do you treat GCA?

A

Corticosteroids - prednisolone immediately

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45
Q

What do you prescribe alongside steroids for GCA?

A

PPI for gastric protection

Bisphosphonates/vitamin D for osteoporosis prophylaxis

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46
Q

How do you investigate GCA?

A

Bloods - ESR/CRP raised

Gold standard - temporal artery biopsy

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47
Q

How does GCA present?

A

Headache

Scalp tenderness - often noticed when brushing hair

Jaw claudication

Malaise

Visual disturbance

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48
Q

What is a serious complication that can occur with GCA?

A

Vision loss - irreversible + painless, monocular

Can happen rapidly + suddenly

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49
Q

What visual disturbances can happen with GCA?

A

Blurred/double vision, diplopia, amaurosis fugax

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50
Q

How does the affected vessel in GCA present?

A

Palpable, tender and non-pulsatile

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51
Q

What is Parkinson’s disease?

A

Degenerative movement disorder caused by the loss of dopaminergic neurons in the substantia nigra

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52
Q

What are the 2 main pathological hallmarks of Parkinson’s disease?

A

Presence of lewy bodies

Dopaminergic neuron loss

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53
Q

How do you investigate parkinson’s disease?

A

Diagnosis is clinical

MRI head/DaTscan may help differentiate

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54
Q

How does Parkinson’s disease present?

A

Rigidity (lead-pipe)

Bradykinesia

Resting tremor

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55
Q

What is bradykinesia?

A

Slow to initiate movement (especially repetitive ones), fine movements e.g. micrographia, expressionless face

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56
Q

Where is resting tremor in PD patients most obvious?

A

In hands (pill-rolling tremor), improves on movement

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57
Q

Describe the onset of PD.

A

Asymmetrical, one side is always worse

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58
Q

Describe the gait of a PD patient.

A

Short shuffling gait with stooped posture, narrow base and reduced arm swing

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59
Q

What symptoms present first in a PD patient?

A

Anosmia, depression/dementia, pain, REM sleep disorders, urinary symptoms, constipation

60
Q

How is PD managed?

A

Co-careldopa (levodopa + carbidopa - decarboxylase inhibitor) - symptom relief, doesn’t alter disease progression

MAO-B inhibitors and COMT inhibitors - inhibit dopamine breakdown

61
Q

What are the side effects of co-careldopa?

A

Causes serious long-term mbility complications - start as late as possible

62
Q

What is the 1st line treatment for PD patients <60?

A

Dopamine agonist

63
Q

How does carbidopa work?

A

Prevents peripheral breakdown of levodopa before it gets to the brain. Allows for lower dose of L-dopa to cause less side effects.

64
Q

What is HD?

A

Hereditary hyperkinetic neurodegenerative disorder affecting the striatum and other areas

65
Q

What is the inheritance pattern of HD?

A

Autosomal dominant

66
Q

What causes HD?

A

CAG repeat in Huntington gene

67
Q

Describe the onset of HD.

A

100% penetrance

Number of repeats increases as disease passed on so symptoms beccome more severe and appear earlier with each generation (anticipation)

68
Q

How does HD present?

A

Hyperkinesia - chorea, dystonia, incoordination

Psychiatric issues e.g. psychosis, depression, dementia

Behavioural difficulties, cognitive impairment

69
Q

What is chorea?

A

Involuntary, irregular, unpredictable jerky muscle movements

70
Q

How is HD treated medically?

A

No cure, symptom control

Chorea - benzodiazepines

Neuroleptic drugs - haloperidol for psychosis

71
Q

What is MS?

A

Chronic inflammatory disorder involving a T-cell mediated immune response (autoimmune) causing demyelination in the CNS

72
Q

What is the typical onset of MS?

A

20-40 yrs

73
Q

What are the different types of MS?

A

RRMS (80%)

Primary progressive

Secondary progressive

74
Q

Describe the presentation of RRMS.

A

Partial/complete recovery between attacks, gets worse with each epidsode, attack must last >48 hours

75
Q

What is primary progressive MS?

A

Gradually worsens from onset without relapse/remissions

76
Q

What is secondary progressive MS?

A

Follows on from RRMS, late stage with gradually worsening symptoms and fewer remissions

77
Q

What is clinically isolated syndrome?

A

First episode of MS, must last >24 hours, about half progress on to MS

78
Q

What are the visual S+S of MS?

A

Optic neuritis (often first sign), internuclear ophthalmoplegia, Uhtoff’s phenomenon

79
Q

What is Uhtoff’s phenomenon?

A

Worsening of visual symptoms when body temperature is increased e.g. hot bath, fever

80
Q

What are the sensory S+S of MS?

A

Numbness, tingling, Lhermitte’s sign

81
Q

What is Lhermitte’s sign?

A

Electric shock like sensation spreads from neck to limbs on neck flexion

82
Q

What are the motor S+S of MS?

A

UMN signs - brisk reflexes, hypertonia, spastic weakness

83
Q

What are the cerebellar S+S of MS?

A

Ataxia, diplopia, nystagmus, intention tremor, vertigo

84
Q

What are the spinal cord S+S of MS?

A

Urinary incontinence, sexual dysfunction

85
Q

What are the miscellaneous S+S of MS?

A

Fatigue, intellectual impairment

86
Q

How do you manage an acute relapse of MS?

A

Methylprednisolone for 5 days (shortens relapse)

87
Q

What is the long term management of MS?

A

DMARDs e.g. beta interferon, glatiramer acetate, natalizumab

88
Q

What do you treat MS spasticity with?

A

Baclofen

89
Q

What do you treat MS urinary issues with?

A

Self-catheterisation, laxatives, anti-cholinergic alpha blockers e.g. doxazosin for urinary incontinence

90
Q

What do you treat MS fatigue with?

A

Amantidine. physio, exercise

91
Q

What do you treat MS neuropathic pain with?

A

Gabapentin, amitriptyline

92
Q

What do you treat MS depression with?

A

SSRI, psychotherapy

93
Q

How do you investigate MS?

A

McDonald’s criteria

MRI - diagnostic > demyelination

LP - oligoclonal IgG bands > inflammation

94
Q

What is McDonald’s criteria?

A

Evidence of damage to CNS that is disseminated in time and space

Time - shown by relapses or new lesions on MRI compared to previous one

Space - shown by lesions in different places on MRI or symptoms indicating damage to a new part of CNS

95
Q

What is optic neuritis?

A

Unilateral eye pain on movement, loss of central vision

96
Q

What is internuclear ophthalmoplegia?

A

Decreased adduction of IL eye + nystagmus on abduction of CL eye

97
Q

What is MND?

A

Progressive degeneration of motor neurons in the brain and spinal cord

98
Q

What causes MND?

A

Unknown, could be familial

99
Q

What is the most common MND?

A

Amyotrophic lateral sclerosis (ALS)

100
Q

What is ALS?

A

Asymmetrical patchy distribution of both UMN and LMN features with evidence of spread to other regions

101
Q

What muscles does MND involve?

A

Weakness and atrophy eventually involves muscles of all 4 extremities, trunk and bulbar muscles

102
Q

How is MND diagnosed?

A

Diagnosis based on clinical findings - no diagnostic test

Nerve conduction studies + EMG to support diagnosis

MRI/LP/bloods to exclude differentials

103
Q

How is MND managed without medication?

A

MDT care, feeding and respiratory support when required

104
Q

What is the prognosis of MND?

A

Involvement of respiratoy muscles associated with poor prognosis - death usually respiratory failure due to bulbar palsy

105
Q

MND significantly overlaps with what condition?

A

Frontotemporal dementia

106
Q

How do you differentiate MND from MS/polyneuropathies?

A

No sensory loss or sphincter disturbance in MND

107
Q

How do you differentiate MND from myasthenia gravis?

A

No effect on eye movement in MND

108
Q

How is electromyography (EMG) used for MND?

A

Shows denervation of muscles due to degeneration of LMNs

109
Q

What is bulbar palsy?

A

LMN lesion of CN 9-12 (affects muscles of mouth and throat responsible for speech and swallowing)

110
Q

What is meningitis?

A

Inflammation of the meninges due to infection

111
Q

Who is meningitis most common in?

A

Infants then teenagers/young adults

112
Q

What are the common bacteria which cause meningitis?

A

Neisseria meningitidis (meningicoccus), strep. pneumoniae, haemophilus influenzae type B, listeria monocytogenes

113
Q

What are the common viruses that can cause meningitis?

A

HSV, enterovirus, varicella zoster, EBV

114
Q

Which meningitis is more serious?

A

Bacterial

115
Q

How does meningitis present early on?

A

Fevers, rigors, headache

116
Q

What are the signs of meningism (meningitis)?

A

Neck stiffness

Photophobia

Non-blanching purpura rash (meningococcal only)

Kernig’s sign

117
Q

What are the other signs of meningitis?

A

Raised ICP - vomiting, altered consciousness, seizures

Risk of septic shock (suggestive of meningococcal septicaemia) - tachycardia, hypotensive, slow cap refill etc.

118
Q

How do you investigate meningitis?

A

Bloods - blood cultures ASAP (first line)

LP - gold standard. Done ASAP but shouldn’t delay treatment

119
Q

When is an LP contradicated?

A

Raised ICP - may cause coning

120
Q

How does viral meningitis present?

A

Much more mild than bacterial

121
Q

How is bacterial meningitis treated?

A

All cases treated as bacterial until proven otherwise

In community - urgent injection of benzylpenicillin + transfer to hospital

Hospital - treat empirically immediately - IV ceftriaxone

Once organism is confirmed, treat according to this

122
Q

What happens after a confirmed case of bacterial meningitis?

A

Notify public health

Prophylactic antibiotics for close contacts - ciprofloxacin

123
Q

What are the features of CSF in bacterial meningitis?

A

Cloudy

High protein

Low glucose

High neutrophils

Bacteria

124
Q

What are the features of CSF in viral meningitis?

A

Clear

Mildly raised or normal protein

Normal glucose

High lymphocytes

Negative for bacteria

125
Q

How is viral meningitis managed?

A

Often only requires supportive treatment, no specific treatment

Aciclovir for suspected HSV meningitis/concerned about encephalitis

126
Q

What organism is neisseria meningitidis?

A

Gram -ve diplococci

127
Q

What organism is strep pneumoniae?

A

Gram +ve diplococci

128
Q

What is Kernig’s sign?

A

Lie patient on back, flex one hip and knee to 90 degrees, slowly straighten knee whilst keeping hip flexed (stretches meninges) > +ve = spinal pain/resistance to movement

129
Q

What causes meningococcal septicaemia?

A

Neisseria meningitidis

130
Q

What is meningococcal septicaemia?

A

Infection is in bloodstream = cause of non-blanching rash (bad news!)

131
Q

What is the prognosis of meningitis?

A

Treat ASAP, high mortality rate especially in children

132
Q

What are the long term complications of meningitis?

A

Hearing loss, seizures, learning disabilities/cognitive impairment, focal neuro deficits

133
Q

What is encephalitis?

A

Inflammation of cerebral cortex due to infection

134
Q

What viruses can cause encephalitis?

A

HSV, enterovirus, EBV

135
Q

What is the most common cause of encephalitis?

A

Virus

136
Q

What other organisms can cause encephalitis?

A

Bacteria e.g. listeria monocytogenes or parasitic/fungal/non-infectious

137
Q

How does encephalitis present?

A

1st symptoms = fever, flu-like symptoms, headache

Focal neurological deficits

Seizures

Behavioural change, confusion, coma

138
Q

How do you investigate encephalitis?

A

Bloods and blood cultures

LP - CSF shows lymphocytosis

Viral PCR to identify virus

CT/MRI - asymmetrical but often bilateral inflammation

139
Q

How is encephalitis treated?

A

Aciclovir if viral cause

140
Q

What causes spinal cord compression?

A

Central disc protrusion (mostly lumbar) - disc herniation, bulging

Degenerative discs > osteophyte formation in osteoarthritis/spondylosis

Tumour/haematoma/abscess

Trauma

141
Q

What cancers are most likely to metastasise to the spine?

A

Breast, prostate, lung

142
Q

How do you treat spinal cord compression?

A

Surgery ASAP - doesn’t improve condition, stops progression e.g. laminectomy, decompression

Pain relief

Treat underlying cause e.g. tumour

143
Q

How do you investigate spinal cord compression?

A

MRI spine

144
Q

How does spinal cord compression present?

A

Motor deficit below level of compression

UMN signs e.g. cervical myelopathy > clumsy hands, difficulty walking

Sensory loss up to level of compression

Aching back pain radiating distally

145
Q

What is the presentation of spinal cord compression dependent on?

A

Location and injury type

146
Q

How is MND managed with medication?

A

Antiglutametergic drugs e.g. riluzole

Symptomatic relief

147
Q

Describe the headache of GCA.

A

New onset severe unilateral headache around temple/forehead

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