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*Phase 3a Julia > Neurology > Flashcards

Neurology Flashcards

1
Q

In MS, what is the name given to symptoms that worsen with heat / exercise?

A

Uhthoff’s phenomenon

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2
Q

List some brainstem / cerebellar symptoms of MS

A

ataxia
dysphagia
diplopia
vertigo

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3
Q

Tx MS relapse

A

Oral methylprednisolone 500mg OD for 5 days (or IV if severe)

Avoid steroid treatment more than 3x per year

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4
Q

What would 2 features be of LP and CSF studies in MS?

A

oligoclonal bands of increased immunoglobulin concentration

increased protein levels

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5
Q

Diagnostic criteria MS

A

2 or more CNS lesions disseminated in time and place

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6
Q

Subtypes MS

A

relapsing-remitting MS
secondary progressive MS
primary progressive MS

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7
Q

Prognosis MS

A

5-10 years below average

Pts often die from aspiration pneumonia

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8
Q

Pathophysiology Myasthenia Gravis

A

An AI disease mediated by antibodies against nicotinic anti-cholinergic receptors

AChR IgG

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9
Q

Mx of a myasthenic CRISIS

A

IV immunoglobulin

Plasma electrophoresis

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10
Q

Tx for MG (not crisis)

A

Pyridostigmine

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11
Q

What is the only drug licensed for Tx of MND?

A

Riluzole

RILUZOLE

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12
Q

What Tx for spasticity in MS and spasms in MND?

A

BACLOFEN

Baclofen

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13
Q

What type of dementia is ALS associated with?

A

frontotemporal dementia

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14
Q

What type of MND has the worst prognosis?

A

Progressive bulbar palsy

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15
Q

If ALS is familial, what chromosome does the gene responsible lie on?

A

Chromosome 21

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16
Q

Differentials for tension headaches

A

migraine, cluster, GCA, polymyalgia rheumatica, drug-induced, exertional

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17
Q

Chronic tension headache

A

> 15 days per month for at least 3 months

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18
Q

CFs tension headache

A

Bilateral, non-pulsative, chronic daily headache. ‘Tight-band like sensation’. Pressure behind eyes. Mild-moderate pain +/- scalp tenderness

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19
Q

Important -ves in tension headache

A

no vomiting, no aura, no sensitivity to head movement

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20
Q

What is the only prophylactic Tx recommended by NICE for tension headaches?

A

Acupuncture

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21
Q

Acute treatment of migraine

A

Combo of an oral triptan (e.g. sumatriptan) and NSAID / Paracetamol +/- an antiemetic if needed

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22
Q

Prophylactic treatment of migraine

A

If 2+ attacks a month, or acute Tx needed more than twice a week

  • Propanol or topiramate is 1st line
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23
Q

What class of drug is topiramate and what must you be cautious of?

A 
An anti-convulsant
Its teratogenicity (cleft palate)
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24
Q

Features of cluster headache

A

Rapid onset of excruciating pain around one eye
Rises to crescendo over minutes and lasts 15-160 mins once/twice a day

  • nocturnal / early mornings, often wakes from sleep
  • watery blood shot eye with swelling

+/- vomiting

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25
Q

Abortive Tx cluster headache

A

Subcut Sumatriptan + 100% O2

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26
Q

Preventative Tx cluster headache

A

Verapamil (a CCB)

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27
Q

Triggers cluster headache

A

alcohol

~ nocturnal sleep

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28
Q

1st Line Tx for trigeminal neuralgia?

A

Carbamazepine

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29
Q

Pathophysiology TN?

A

compression of the trigeminal nerve, causing demyelination and excitation of the trigeminal nerve –> erratic pain singaling

e.g. aneurysm, meningeal inflammation, tmours

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30
Q

RFs for TN and peak age

A

**Hypertension
F
Peak age = 50yrs

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31
Q

CF TN

A

Sudden unilateral paroxysms of knife-life, electric-shock like pain

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32
Q

Triggers TN

A

shaving, eating, talking

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33
Q

Red flag CFs in TN that suggest an underlying cause + prompt referral to neurologist

A 
Sensory changes
Deafness or other hearing problem
ONSET <40yrs
Pain only in ophthalmic division, or bilaterally
Optic neuritis
FHx of MS
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34
Q

who must have GCA excluded?

A

All >50year olds with a new headache that has lasted a few weeks

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35
Q

Pathophysiology GCA, aka Temporal Artery

A

inflammatory granulomatous vasculitis of large cerebral arteries

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36
Q

CFs GCA

A

scalp tenderness
jaw claudication
sudden blindness

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37
Q

Ix GCA

A

ESR and CRP raised
Temporal artery biopsy

Normochromic normocytic anaemia

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38
Q

Mx GCA

A

prednisolone

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39
Q

Why do you need to start treatment asap for GCA?

A

due to risk of permanent visual loss from anterior ischaemic optic neuropathy from vasculitis of ciliary arteries

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40
Q

What is GCA associated with?

A

Polymyalgia Rheumatica

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41
Q

RFs SAH?

A

Hypertension, known aneurysm, polycystic kidney disease

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42
Q

CFs SAH

A

Sudden onset severe occipital headache - ‘thunderclap’

Vomiting

Neck stiffness

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43
Q

How is SAH graded?

A

According to the GCS at presentation

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44
Q

What Investigations for SAH?

A

CT scan

LP (if CT head -ve but high clinical suspicion)

45
Q

What would CT scan SAH show?

A

Star shaped lesion - due to blood filling the gyral patterns around the brain adn the ventricles

46
Q

What would LP show and when should it be performed?

A

Xanthochromia (yellow) due to bilirubin from Hb breakdown

12hr after the onset of symptoms

47
Q

Cause of SAH?

A

Spontaneous not trauma

Most often due to rupture of a berry aneurysm

48
Q

Mx SAH

A
  1. Maintain good cerebral perfusion: hydration + give dexamethasone to reduce cerebral oedema
  2. Refer to neurosurgery: clipping or coiling of aneurysm
  3. NIMODIPINE (a CCB) to reduce risk of VASOSPASM
49
Q

Complications SAH?

A

Hyponatraemia (SIADH)
rebleeding
hydrocephalus
cerebral ischaemia due to vasospasm

50
Q

Peak age of onset PD

A

55-65 years

51
Q

Pathophysiology PD

A

Progressive degeneration of dopaminergic neurones in the substantia nigra of the basal ganglia

52
Q

Triad of Parkinsonism CFs

A

Rigidity
Bradykinesia
Resting tremour

53
Q

DDx Parkinsonism

A

LBD
Drug induced (typical antipsychotics e.g. haloperidol)
Wilson’s disease
Trauma

54
Q

Gold standard treatment for PD

A

Levodopa + decarboxylase inhibitor (e.g. carbidopa)

55
Q

limitations of levodopa, and what does it mean for starting the drug?

A

reduced efficacy over time, even with increased dose

L-dopa should not be started until absolutely necessary, only when motor symptoms are affecting their quality of life and other treatments are ineffective

56
Q

What can be used 1st line to delay starting L-dopa? and their side effects?

A
  1. Dopamine agonists e.g. ropinirole

SEs: drowsiness, nausea, hallucinations, compulsive behaviour*

57
Q

What can be used if parkinsons pt is NBM so can’t take levodopa?

A

Dopamine agonsit patch - to prevent actue dystonia

58
Q

What can be used 2nd line to delay starting L-dopa, and to reduce the wearing off of L-dopa? and their SEs?

A

Monoamine Oxidase B inhibitors e.g. selegiline

SEs: postural hypotension, AF

59
Q

Differentiating between LBD and PD?

A

If dementia occurs prior to or at the same time as the motor symptoms –> LBD

If dementia occurs >1yr after motor symptoms, it is a feature of the PD

60
Q

What is Guillain-Barre Syndrome?

A

An acute inflammatory, ascending polyneuropathy of the peripheral nervous system following an URTI or a GI infection

61
Q

Cause of Guillain-Barre Syndrome?

A

Campylobacter Jejuni
CMV

Infection –> production of antibodies that attack myelin –> demyelination and an acute polyneuropathy

62
Q

What might require ITU admission in Guillain-Barre Syndrome?

A

Respiratory involvement

Do FVC!!

63
Q

Dx Guillain-Barre Syndrome?

A

Nerve conduction studies: slow nerve conduction and prolonged distal motor latency

LP: increased proteins, WCC normal

64
Q

Mx Guillain Barre Syndrome?

A

IV Immunoglobulin for 5 days : decreases severity and duration of paralysis

65
Q

What is a meningioma

A

A typically benign tumor that develops from the dura mater of the meninges

(benign still have serious consequences due to the closed vault of cranium and risk of compression)

66
Q

What is coning and what does it result in?

A

herniation of the cerebella tonsils through foramen magnum –> resp depression, bradycardia and death

67
Q

CFs brain tumours

A

Increased intracranial pressure headache (worse in mornings / lying down / coughing / sneezing)
Vomiting
Personality change
Neurological focal symptoms

68
Q

How are brain tumours graded?

A

Histology of cell type

Grade I and II beningn, III and IV are malignant

69
Q

Mx brain tumours

A

Refer to neurosurgery,

Surgical resection, RT and supportive Tx, - very dependent on tumour type

70
Q

Define TIA

A

A transient and reversible episode of sudden onset neurological dysfunction caused by ischaemia, with acute infarction

Symptoms have generally fully resolved within 24hrs

71
Q

Driving and TIA

A

Can’t drive for at least 4 weeks after a TIA

72
Q

What score for risk of stroke for someone with AF? - and why they at increased risk?

A

CHA2DS2VASC score

Stagnation of blood in the poorly contracting atria –> thrombus formation

73
Q

What must be done for suspected stroke pt before thrombolysis is give?

A

CT head to exlude haemorrhagic stroke (30%)

74
Q

Immediate Tx ischaemic stroke

A
  1. Thrombolysis: ALTEPLASE (IV tissue plasminogen activator) within 4.5hrs of onset
  2. Antiplatalet therapy (75mg clopidogrel) started 24hrs after thrombolysis
75
Q

Tx If miss the immediate Tx window for ischaemic stroke?

A

300mg aspirin for 2 weeksn, THEN lifelong clopidogrel 75mg (+statin)

76
Q

What sign to differentiate between organic and non-organic lower leg weakness?

A

Hoover’s sign

77
Q

What is site of lesion in stroke if: contralateral hemiparesis and sensory loss, lower extremity > upper?

A

Anterior cerebral artery

78
Q

What is the site of lesion in stroke if: contralateral hemiparesis and sensory loss, upper extremity > lower?

A

Middle cerebral artery

79
Q

What CFs would lateral medullary syndrome manifest in?

A

Ipsilateral: facial pain and temp loss

Contra: limb / torso pain and temp loss

Ataxia, nystagmus

80
Q

What infarct cause aphasia?

A

Dominant hemisphere middle cerebral infart

81
Q

RFs Subdural haematoma

A

Traumatic head injury
Anticoagulation medication
PMHx of coagulopathy
Alcoholism

82
Q

What is key about the CFs for Subdural haematoma?

A

The interval between injury and symptoms can be days –> months

83
Q

CFs acute subdural haematoma

A

Signs of raised ICP: headache, vom, nausea, raised BP

Alternating level of consciousness

84
Q

CFs chronic subdural haematoma

A

Personality change, cognitive decline, headache - may have no memory of initial trauma

85
Q

Ix subdural haematoma

A

Crescent shaped- mass

86
Q

What might the Dx be in an elderly patient with progressive peronality change and declining GCS?

A

Chronic Subdural haematoma

due to decreased brain weight, and increased subdural space, may evolve slowly

87
Q

What is the lucid interval in an extradural haematoma?

A

The time between Traumatic Brain Injury and decrease in consciousness

88
Q

Cause of extradural haematoma?

A

Trauma to the temporal / parietal bone –> laceration of middle meningeal artery

89
Q

What would CT show in extradural haematoma?

A

Hyperdense biconvex / ‘ lemon’ shape next to the skull

90
Q

Most common cause of encepahlitis in UK?

A

Herpes simplex virus 1 + 2

91
Q

What is the predominant symptom in encepahlitis?

A

decreased LoC and confusion

92
Q

Cause of meningitis

A

Neisseria Meningitidis transmitted

93
Q

What is meningococcal septicaemia caused by?

A

When Neisseria Meningitidis invades into flood, presence of endotoxin leads to inflammatory cascade

94
Q

CFs meningitis

A

fever, headache, meningism, seizures,

NON-BLANCHING petechial rash

95
Q

CSF findings for bacterial meningitis?

A

Raised protein, low glucose
Polymorphs (neutrophils)

Turbid color

96
Q

Difference on CSF findings between TB and bacterial meningitis?

A

TB- cells are lymphocytes

Bacteria - cells are polymorphs (neutrophils)

97
Q

Viral meningitis CSF findings

A

cells are lymphocytes

protein and glucose normal

98
Q

Define epilepsy

A

A recurrent tendency to spontaneous, intermitted abnormal electrical activity in part of the brain, manifesting as seizures

99
Q

What are generalised seizures characterised by?

A

Loss of consiousness from the start

100
Q

which type of seizure might have awareness impaired and automatisms such as lip smacking and chewing?

A

Complex partial seizure

101
Q

What does the clinical diagnosis of epilepsy require?

A

2 or more unprovoked seizures occuring >24hrs apart

102
Q

Mx Primary generalised epilepsy?

A

Sodium valporate or lamotrigine

103
Q

Mx absence seizure?

A

Sodium valporate or ethosuxamide

104
Q

Mx Partial / focal seizure?

A

Carbemazepine or lamotrigine

105
Q

DVLA and epilepsy

A

cant drive until free of daytime seizures for at least 1yr

106
Q

When and how can you stop anti-epileptic drugs?

A

If seizure free for >2yrs, with AEDs being stopped over 2-3 months

107
Q

Cause of huntingtons?

A

AD inheritance
Mutation on Chromosome 4, repeated expression of CAG sequence

Decreased ACh synthesis and GABA in struatum

108
Q

CFs huntingtons?

A

Often a prodromal phase of mild psychotic and behavioural symptoms before the development of chorea

progresses to rigidity, writhing and abnormal posture

behavioural change

dementia

109
Q

What is brown-sequard syndrome?

A

Loss of pain temp and light touch on opposite side to lesion

Loss of motor function and vibration, position, and deep touch sensation on same side as the cord damange

*Phase 3a Julia (8 decks)

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