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Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

Presentation of a tension headache

A

Mild ache / pressure in a band like pattern around the head

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2
Q

Management of tension headache

A
  • Reassurance
  • Simple analgesia (e.g., ibuprofen or paracetamol)
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3
Q

4 associations with tension headahces

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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4
Q

Presentation of sinusitis and it’s management

A
  • Recent URTI
  • Tenderness and swelling on palpation
  • Prolonged cases (>10 days) = steroid nasal spray or Abx (phenoxymethylpenicillin)
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5
Q

Presentation of cervical spondylosis

A
  • Neck pain, worse with movements
  • Headahces
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6
Q

Presentation of trigeminal neuralgia and 1st line management ?

A
  • Electric shock like pain
  • Triggered by touch, talking, eating, shaving or cold
  • First line = carbamazepine
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7
Q

Presentation of a cluster headache

A
  • Unilateral severe pain
  • Red, swollen and watering eye
  • Miosis
  • Ptosis
  • Nasal discharge
  • Facial sweating
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8
Q

Management of acute cluster headache attacke

A

-> Triptans (e.g., subcutaneous or intranasal sumatriptan)
-> High-flow 100% oxygen (may be kept at home)

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9
Q

1st line prophylaxis of cluster headaches

A

Verapamil

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10
Q

Typical symptoms of a migraine

A

Last between 4 and 72 hrs

  • Usually unilateral
  • Moderate-severe intensity
  • Pounding or throbbing in nature
  • Photophobia (discomfort with lights)
  • Phonophobia (discomfort with loud noises)
  • Osmophobia (discomfort with strong smells)
  • Aura (visual changes)
  • N&V
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11
Q

common migraine triggers

A
  • Stress
  • Bright lights
  • Strong smells
  • Certain foods (e.g., chocolate, cheese and caffeine)
  • Dehydration
  • Menstruation
  • Disrupted sleep
  • Trauma
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12
Q

Presentation of hemiplegic migraine

A
  • Hemiplegia
  • Ataxia
  • Impaired consciousness
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13
Q

Acute management of migraine

A
  • NSAIDs (e.g., ibuprofen or naproxen)
  • Paracetamol
  • Triptans (e.g., sumatriptan)
  • Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)
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14
Q

How do triptans work >

A

-> 5-HT receptor agonist, binding to serotonin receptors.
- > Cranial vasoconstriction, inhibit transmission of pain signals and inhibit release of inflammatory neuropeptides

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15
Q

3 prophylactic options for migraines

A
  • Propranolol (a non-selective beta blocker)
  • Amitriptyline (a tricyclic antidepressant)
  • Topiramate (teratogenic and very effective contraception is needed)
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16
Q

Prophylaxis of menstrual migraines

A

Prophylactic triptans (e.g., frovatriptan or zolmitriptan)

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17
Q

definition of tuberous sclerosis and mutations involved

A
  • AD condition causing development of hamartomas
  • TSC1 gene on chromosome 9, which codes for hamartin
  • TSC2 gene on chromosome 16, which codes for tuberin
  • Leads to abnormal cell size and growth
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18
Q

skin features of tuberous sclerosis

A

-> Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
-> Shagreen patches (thickened, dimpled, pigmented patches of skin)
-> Angiofibromas (small skin-coloured or pigmented papules that occur over the nose and cheeks)
-> Ungual fibromas (circular painless lumps that slowly grow from the nail bed and displace the nail)
-> Cafe-au-lait spots (light brown “coffee and milk” coloured flat pigmented lesions on the skin)
-> Poliosis (an isolated patch of white hair on the head, eyebrows, eyelashes or beard)

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19
Q

Neurological features of tuberous sclerosis

A

Epilepsy
Learning disability
Brain tumours - glioma

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20
Q

Define MS

A
  • Autoimmune demyelination of the CNS
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21
Q

What cells produce myelin in the CNS and in the PNS ?

A

-CNS : oligodendrocytes
-PNS : schwann

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22
Q

How do the episodes of demyelination present in MS?

A

-Episodes disseminated in time and space

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23
Q

What is optic neuritis ?

A

-Unilateral painful reduced vision developing over hrs to days.

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24
Q

Give 4 key features of optic neuritis

A

-Central scotoma (blind spot)
-Pain on eye movement
-Impaired colour vision
-Relative afferent pupillary defect

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25
Q

Give 7 other causes of optic neuritis other than MS

A

-Sarcoidosis
-SLE
-DM
-Syphilis
-Measles
-Mumps
-Lyme disease

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26
Q

What investigations can support a diagnosis of MS

A
  • MRI with contrast -> demyelinating lesions
  • LP -> oligoclonal bans in CSF
  • McDonald criteria for diagnosing
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27
Q

Give the 4 disease patterns of MS

A

-Clinically isolated syndrome
-Relapsing-Remitting
-Secondary progressive
-Primary progressive

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28
Q

Explain the relapsing-remitting pattern of MS

A

-Episodes of disease followed by recovery. Classified on whether active and/or worsening

-Active : new symptoms developing
-Not active : no new symptoms developing
-Worsening : overall worsening of disability over time
-Not worsening : no worsening of disability over time

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29
Q

Explain secondary progressive pattern of MS

A

-Was relapsing/remitting but now a progressive worsening of symptoms
-Can also be classified as active and/or worsening

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30
Q

Explain primary progressive pattern of MS

A

-Worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions

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31
Q

Give two common characteristics of MS

A

-Lhermitte’s sign : tingling electric shock shooting up the spine when flexing the neck
-Uhthoff’s phenomenon : symptoms are worse when hpt (e.g. in bath, hot weather, exercise).

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32
Q

What can be used to treat relapses in MS?

A

-Methylprednisolone
-500mg orally for 5 days or 1g IV for 3-5 days if treatment fails

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33
Q

What is the pathophysiology behind MND?

A

-Progressive degeneration of both upper and lower motor neurones
-Sensory neurones are spared

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34
Q

What can increase the risk of MND?

A

-Smoking
-Exposure to heavy metals
-Certain persticides

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35
Q

What is a typical presentation of MND

A
  • Late middle aged man
  • Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech
  • Weakness often first noticed in upper limbs
  • Fatigue when exercising
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36
Q

Give 4 signs of lower MND

A

-Muscle wasting
-Reduced tone
-Fasciculations
-Reduced reflexes

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37
Q

GIve 3 signs of upper MND

A

-Increased tone or spasticity
-Brisk reflexes
-Upgoing plantar responses

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38
Q

What is the most common presentation of MND ?

A

-Amyotrophic lateral sclerosis (ALS)
- Typically LMN signs in the arms and UMN signs in the legs

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39
Q

What can be used to slow the progression of MND ?

A

-Riluzole : prevents stimulation of glutamate receptors

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40
Q

Signs seen in primary lateral sclerosis (MND)

A

UMN signs only

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41
Q

Signs seen in progressive muscular atrophy (MND)

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

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42
Q

Signs seen in progressive bulbar palsy

A
  • Palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
  • Carries worst prognosis
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43
Q

What is myasthenia Gravis ?

A

-Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
- Affects the NMJ

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44
Q

What is strongly associated with myasthenia Gravis?

A

-Thyoma : tumour of the thymus gland

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45
Q

Explain the pathophysiology behind myasthenia gravis

A

-In most cases, acetylcholine receptor antibodies are produced
-These bind to the postsynaptic receptors
-This prevents the stimulation of the receptor and so prevents muscle contraction
-The antibodies also activate the complement system, leading to damage to the cells of the postsynaptic membrane further worsening the symptoms

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46
Q

Why do the symptoms of myasthenia gravis get worse with exercise ?

A

-The receptors are used more during muscle activity and so more of them become blocked up.
-This leads to less effective stimulation of the muscle with increased activity
-There is more muscle weakness the more the muscles are used
-This improves with rest as more receptors are freed up again for use

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47
Q

What are 2 other antibodies involved in myasthenia gravis?

A

-Muscle-specific kinase (MuSK)
-Low density lipoprotein receptor-related protein (LRP4)
-These proteins are imprtant for the creation of acetylcholine receptor
-Destruction of these by the antibodies leads to inadequate acetylcholine receptors

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48
Q

What is a characteristic feature of myasthenia gravis

A

-Weakness that gets worse with muscle use and improves with rest

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49
Q

What muscles are most affected in myasthenia gravis ?

A

-Proximal muscles and small muscles of the head and neck

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50
Q

Give 8 common symptoms of myasthenia gravis

A
  • Diplopia : extraocular muscle weakness
  • Ptosis
  • Weak upwards gaze
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
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51
Q

Give 3 things to assess of examination for myasthenia gravis

A

-Thymectomy scar
-FVC
-Elicit fatiguability of muscles : repeated blinking will exacerbate ptosis ; prolonged upward gaze with exacerbate diplopia ; repeated abduction of one arm 20 times with result in unilateral weaknes when comparing both sides

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52
Q

Give 3 investigations for diagnosing myasthenia gravis

A
  • Test for antibodies
  • CT/MRI of the thymus to check for thymoma
  • Edrophonium test if in doubt (tensilon)
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53
Q

What is the edrophonium test

A

-Used to aid diagnosis of myasthenia gravis
-IV edrophonium chloride is given which will prevent the breakdown of acetylcholine
-Acetycholine levels will rise giving temporary relief from the weakness

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54
Q

Give 3 treatment options for myasthenia gravis

A

-Pyridostigmine -> reversible acetylcholinesterase inhibitors -> increase the amount of acetylcholine at the junction (or rivastigmine)
-Immunosuppression with prednislone or azathioprine : suppress antibody production
-Thymectomy

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55
Q

What 2 monoclonal antibodies can be used in myasthenia gravis ?

A

-Rituximab -> targets b cells reducing antibody production
-Eculizumab -> targets complement protein C5.

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56
Q

What is a myasthenic crisis?

A

-Acute worsening of symptoms often triggered by a viral infection
-Can lead to resp failure due to weakness in the muscle of respiration
- FVC needs monitoring

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57
Q

What is used in the management of a myasthenic crisis?

A
  • IV immunoglobulins
  • Plasmapheresis

If needed :
- BiPAP
- Intubation and ventilation

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58
Q

what drugs can exacerbate myasthenia ?

A
  • penicillamine
  • quinidine, procainamide
  • beta-blockers
  • lithium
  • phenytoin
  • antibiotics: gentamicin, macrolides, quinolones, tetracyclines
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59
Q

What is Lambert-Eaton myasthenic syndrome ?

A

autoimmune condition affecting the neuromuscular junction

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60
Q

Who is usually affected by Lambert-Eaton myasthenic syndrome ?

A

-Patients with small cell lung cancer

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61
Q

Explain the pathophysiology behind Lambert-Eaton myasthenic syndrome

A
  • Antibodies against voltage-gated calcium channels in the SCLC are produced.
  • These target and damage the same channels in the presynaptic terminals of the neuromuscular junction
  • This results in less acetylcholine being released into the synapse
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62
Q

How does lambert-eaton syndrome present ?

A

-Proximal muscles most affected -> leg muscle weakness (difficulty climbing stairs)
- Reduced or absent tendon reflexes
-Autonomic dysfunction : dry mouth, blurred vision, impotence and dizziness

-Double vision
-Ptosis
-Dysphagia

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63
Q

What is post-tetanic potentiation ?

A

-In lambert-eaton syndrome, tendon reflexes are normally reduced
-They can become temporarily normal for a short period following a period of strong muscle contraction

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64
Q

How is lambert-eaton syndrome managed?

A

-Treat underlying malignancy if present
-Amifampridine
-Immunosuppressants
-IV immunoglobulins
-Plasmaphersis

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65
Q

How does amifampridine work in the treatment of Lambert-Eaton?

A

-It blocks voltage-gated potassium channels in the presynaptic cells
-This prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action

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66
Q

Define Gullian-Barre syndrome (GBS)

A

-Acute paralytic polyneuropathy affecting the peripheral nervous system

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67
Q

What usually triggers GBS ?

A

-Infection
-Campylobacter jejuni (food poisoning), cytomegalovirus, EBV

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68
Q

How does GBS present ?

A
  • Back/leg pain in initial stages
  • Symmetrical ascending weakness
  • Reduced reflexes
    -+/- peripheral loss of sensation or neuropathic pain
  • May progress to cranial nerves and cause diplopia, bilateral facial nerve palsy and oropharyngeal weakness
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69
Q

What is the clinical course of GBS?

A

-Preceding infection
-Symptoms begin 4 wks later
-Symptoms peak after 2-4 wks
-Recovery period lasting mnths to years

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70
Q

What investigations support the diagnosis of GBS?

A

-Once clinically diagnosed using Brighton criteria :

-Nerve conduction studies showing reduced signal through the nerves
-LP : raised protein with normal cell count and glucose

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71
Q

How is GBS managed ?

A
  • IV immunoglobulins
  • Plasmapheresis can be an alternative to IVIG
  • VTE prophylaxis with LMWH
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72
Q

What are the features of a benign essential tremor ? (6)

A

-Fine tremor
-Symmetrical
- 6-12 Hz
-MORE prominent on VOLUNTARY movement
-Worse when tired, stressed or after caffeine
-Improved by alcohol
-Absent during sleep

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73
Q

Give 6 differentials of a tremor

A

-Parkinson’s
-MS
-Huntington’s chorea
-Hyperthyroidism
-Fever
-Medications (e.g. antipsychotics)

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74
Q

What 2 medications can improve the symptoms of a benign essential tremor ?

A
  • First line = Propranolol
  • Primidone
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75
Q

What is the cause of parkinson’s ?

A
  • Progressive reduction of dopamine in the basal ganglia
  • Leads to disorders of movement
  • Symptoms are ASYMMETRICAL
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76
Q

What is the classic triad of parkinson’s

A
  • Cogwheel rigidity
  • Pill-rolling resting tremor (4-6Hz)
  • Bradykinesia : smaller handwriting, shuffling gate, difficulty initiating movements, reduced facial expressions (hypomimia)

postural instability is an extra

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77
Q

Where is dopamine produced ?

A

-Substantia nigra of the basal ganglia

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78
Q

Give 5 other features of parkinson’s

A

-Depression
-Sleep disturbance and insomnia
-Anosmia
-Postural instability (caused by autonomic failure)
-Cognitive impairment and memory problems

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79
Q

Describe a parkinson’s tremor

A

-Asymmetrical / unilateral
-WORSE at REST
-IMPROVES with INTENTIONAL movement
-No change with alcohol

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80
Q

Give 4 treatment options for parkinson’s

A
  • Co-benyldopa or co-careldopa
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine Oxidase-B Inhibitors
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81
Q

Explain how levodopa works

A

-Synthetic dopamine
-Most effective but becomes less effective over time

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82
Q

What is usually given with levodopa and why?

A

-Peripheral decarboxylase inhibitor
-Stops is being broken down before it reaches the brain
-Examples : carbidopa, benserazide

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83
Q

What is the main side effect of levodopa?

A
  • Too high dopamine = dyskinesias = abnormal movements associated with excessive motor activity.
  • E.g. dystonia, chorea, athetosis
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84
Q

How do COMT inhibitors work?

A

-Example : entacapone
-Inhibits catechol-o-methyltransferase which is responsible for metabolising levodopa
-Extends to duration of levodopa

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85
Q

How do dopamine agonists work ?

A
  • Mimic dopamine in the basal ganglia and stimulate dopamine receptors
  • Less effective than levodopa
  • Examples : bromocryptine, pergolide, cabergoline
86
Q

What is the most notable side effect of dopamine agonists with prolonged use ?

A
  • Pulmonary fibrosis
87
Q

How do monoamine Oxidase-B Inhibitors work?

A

-They block Monoamine Oxidase-B enzyme which is responsible for breaking down dopamine
-Examples are selegiline and rasagiline

88
Q

what can be given with levodopa to help with the dyskinesia ?

A

-> Amantadine (glutamate antagonist)

89
Q

what causes multiple system atrophy and how does it present

A

-> Neurones in various areas of brain degenerate
-> Parkinsonism
-> Autonomic disturbance : erectile dysfunction: often an early feature, postural hypotension, atonic bladder
-> Cerebellar signs : ataxia

90
Q

Presentation of lewy body dementia

A

-> Progressive cognitive impairment FOLLOWED BY parkinsonism
-> Visual hallucinations
-> Delusions
- > REM sleep disorders
-> Fluctuating consciousness

91
Q

Features of progressive supranuclear palsy

A

-> postural instability and falls
-> Impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
-> Parkinsonism : bradykinesia is prominent
-> Cognitive impairment : primarily frontal lobe dysfunction

92
Q

what usually causes an extradural haemorrhage

A
  • Rupture of the middle meningeal artery in the temporoparietal region
  • Often associated with fracture of temporal bone
93
Q

What does an extradural haemorrhage look on a CT ?

A
  • Bi-convex shape
  • Limited by cranial sutures
  • Hyperdense
94
Q

Typical history of an extradural haematoma

A
  • Pt with traumatic head injury
  • Period of improved neurological Sx and consciousness
  • Followed by rapid decline over hrs
95
Q

Cause of a subdural haematoma

A

Rupture of bridging veins in outermost layer

96
Q

Appearance of subdural haemorrhage on CT

A

Crescent shaped
Can cross suture lines

97
Q

Who often presents with subdural haemorrhages

A
  • Elderly or alcoholic patients
  • Atrophy in their brains make the vessels more prone to rupture
98
Q

Presentation of subarachnoid haemorrhage

A
  • Sudden onset occipital headache during strenuous activity
  • N&V
  • Meningism (photophobia, neck stiffness)
  • Coma
  • Seizures
99
Q

first line investigation for subarachnoid haemorrhage

A

Non contrast CT

100
Q

Investigation required if CT is done >6 hrs after onset of SAH symptoms and is normal

A
  • LP
  • Needs to be done 12 hrs after start of symptoms
101
Q

LP results in SAH

A

-> Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
-> Xanthochromia (a yellow colour to the CSF caused by bilirubin)

102
Q

usual cause of SAH

A

Cerebral aneurysm

103
Q

Management options of SAH

A
  • Endovascular coiling OR
  • Neurosurgical clipping
104
Q

3 common complications of SAH and necessary treatment options

A
  1. Vasospasm -> Nimodipine (CCB)
  2. Seizures -> anti-epileptic meds
  3. Hydrocephalus -> LP, external ventricular drain, ventriculoperitoneal (VP)V shunt.
105
Q

Presentation of intracerebral haemorrhage

A
  • Sudden onset focal neurological symptoms (e.g. limb or facial weakness, dysphasia or vision loss)
106
Q

What is Charcot-Marie-Tooth disease and what is the usual inheritance pattern?

A
  • Hereditary motor and sensory neuropathy
  • Autosomal dominant
107
Q

Give 7 features of Charcot-Marie-Tooth ?

A

-High foot arches (pes cavus)
-Distal muscle wasting causing ‘inverted champagne bottle legs’
-Weakness in lower legs, particularly loss of ankle dorsifelxion (with high stepping gait due to foot drop)
-Weakness in the hands
-Reduced muscle tone
-Reduced tendon reflexes
-Peripheral sensory loss

108
Q

Give 5 causes of peripheral neuropathy

A

-A : alcohol
-B : B12 deficiency
-C : cancer and chronic kidney disease
-D : diabetes and drugs (e.g isoniazid, amiodarone & cisplatin)
-E : every vasculitis

109
Q

Explain the facial nerve pathway

A

-> Exits brainstem at cerebellopontine angle
-> Passes through the temporal bone and parotid gland
-> Divides into 5 branches :
~ Temporal
~ Zygomatic
~ Buccal
~ Marginal mandibular
~ Cervical

110
Q

Motor function of the facial nerve

A
  • Facial expression
  • Stapedius in the inner ear
  • Posterior digastric, stylohyoid and platysma muscles
111
Q

Sensory function of facial nerve

A

Taste from anterior 2/3 of the tongue

112
Q

Parasympathetic function of the facial nerve

A

-> Submandibular and sublingual salivary glands
-> Lacrimal gland (stimulating tear production)

113
Q

Explain the differing presentations of UMN and LMN lesions after the facial nerve

A

-> UMN = forehead sparing
-> LMN = NO forehead sparing

  • Each side of the forehead has UMN innervation from BOTH sides of the brain but LMN innervation from ONE side
114
Q

what is Bell’s palsy

A

-> Acute idiopathic unilateral LMN facial palsy
-> Forehead affected, drooping of eyelide, loss of nasolabial fold

115
Q

Management of Bell’s palsy

A

If pt presents with 72 hrs : PREDNISOLONE either :

-> 50mg for 10 days
-> 60mg for 5 days followed by a 5-day reducing regime, dropping the dose by 10mg per day

+

-> Artificial tears

116
Q

Cause of Ramsay-Hunt syndrome

A

Varicella Zoster Virus (VZV)

117
Q

Presentation of Ramsay-Hunt Syndrome

A
  • Unilateral LMN faical nerve palsy
  • Painful and tender vesicular rash in the ear canal, pinna and around the ear on affected side
118
Q

Management of ramsay-Hunt syndrome

A

-> Oral aciclovir and prednisolone.
-> Patients also require lubricating eye drops.

119
Q

Role and inheritance of neurofibromatosis type 1 gene

A
  • Found on chromosome 17
  • Codes for neurofibromin -> tumour suppressor protein
  • Inherited in AD pattern
120
Q

Diagnostic criteria for neurofibromatosis type 1

A

CRABBING :

  • C – Café-au-lait spots (more than 15mm diameter is significant in adults)
  • R – Relative with NF1
  • A – Axillary or inguinal freckling
  • BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
  • I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
  • N – Neurofibromas
  • G – Glioma of the optic pathway
121
Q

2 unique complications of NF1

A
  1. Malignant peripheral nerve sheath (MPNST)
  2. Gastrointestinal stromal tumours (GIST)
122
Q

Role and inheritance of neurofibromatosis type 2

A
  • Chromosome 22
  • Codes for merlin -> tumour suppressor protein important in Schwann cells
123
Q

Common finding in neurofibromatosis type 2

A
  • Bilateral vestibular schwannomas (tumours of the auditory nerve)
  • Unilateral sensorineural hearing loss (often the first symptom)
  • Unilateral tinnitus
  • Dizziness or imbalance
  • Sensation of fullness in the ear
  • Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)
124
Q

Cause of Huntington’s disease

A
  • AD genetic condition
  • Caused by trinucleotide repeat disorder affecting the HTT gene on chromosome 4
125
Q

Define anticipation and what disease is it seen in ?

A
  • Successive generations have more repeats resulting in “
  1. Earlier age of onset
  2. Increased severity of disease
126
Q

Presentation of Huntington’s

A

Usually cognitive / psychiatric / mood problems FOLLOWED by movement disorders :

  • Chorea (involuntary, random, irregular and abnormal body movements)
  • Dystonia (abnormal muscle tone, leading to abnormal postures)
  • Rigidity (increased resistance to the passive movement of a joint)
  • Eye movement disorders
  • Dysarthria (speech difficulties)
  • Dysphagia (swallowing difficulties)
127
Q

Explain generalised seizures and the different specific types

A
  • Involve both sides of the brain
    • > Tonic-clonic (grand mal)
    • > Tonic
    • > Clonic
    • > Typical absence (petit mal)
    • > Atonic
128
Q

Explain focal seizures

A
  • Involve specific area, on one side of the brain
  • Simple/focal aware
  • Complex/ focal impaired awareness
129
Q

Seizure type seen in those affecting temporal lobe

A

-> Typically a rising epigastric sensation
- > Deja vu
- > Hallucinations
-> Automatisms (lip smacking/grabbing/plucking)
-> Post-ictal dyspahsia

130
Q

Seizure type seen in frontal lobe seizures

A
  • Head/leg movements
  • Post-ictal weakness
  • Jacksonian march
131
Q

Features of parietal lobe seizure

A

Paraesthesia

132
Q

Features of occipital lobe seizure

A

Floaters / flashes

133
Q

Management of generalised tonic clonic seizures

A
  • Male : SV
  • Female : Lamotrigine / Levetiracetam
134
Q

Management of focal seizures

A

1st : Lamotrigine / levetiracetam
2nd : Carbamazepine

135
Q

Management of absence seizures

A

1st : ethosuximide

136
Q

Management of myoclonic seizures

A
  • Male : SV
  • Female : levetiracetam
137
Q

Management of tonic or atonic seizures

A
  • Male : SV
  • Female : Lamotrigine
138
Q

How does sodium valporate work ?

A
  • Increasing activity of gamma-aminobutyric acid (GABA) -> which has a calming effect on the brain
139
Q

5 notable SE of sodium valporate

A
  • Teratogenic
  • Liver damage and hepatitis
  • Hair loss
  • Tremor
  • Reduce fertility
140
Q

what advice should be given to women planning on becoming pregnancy with epilepsy

A

Take 5mg folic acid

141
Q

Definition of status epilepticus

A
  • A seizure lasting more than 5 minutes
  • Multiple seizures without regaining consciousness in the interim
142
Q

Medical management of status epilepticus

A

-> A benzodiazepine (IV lorazepam) first-line, repeated after 5-10 minutes if the seizure continues
-> Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
-> Third-line options are phenobarbital or general anaesthesia

143
Q

Dosage of rectal diazepam for status epilepticus based on age

A
  • Neonate : 1.25 - 2.5 mg
  • Child 1 month - 1 year : 5 mg
  • Child 2 years - 11 years : 5 - 10 mg
  • Child 12 years - 17 years : 10 mg
  • Adult : 10 - 20 mg (max. 30 mg)
  • Elderly : 10 mg (max. 15 mg)
144
Q

Explain the analgesic ladder

A
  • > Step 1: Non-opioid medications such as paracetamol and NSAIDs
    -> Step 2: Weak opioids such as codeine and tramadol
    -> Step 3: Strong opioids such as morphine, oxycodone, fentanyl and buprenorphine
145
Q

Key SE of NSAIDs

A
  • Gastritis with dyspepsia (indigestion)
  • Stomach ulcers
  • Exacerbation of asthma
  • Hypertension
  • Renal impairment
  • Coronary artery disease, heart failure and strokes (rarely)

PPI co-prescribed to reduce GI effects

146
Q

CI to NSAIDs

A

Asthma
Renal impairment
Heart disease
Uncontrolled hypertension
Stomach ulcers

147
Q

5 SE of opioids

A
  • Constipation
  • Pruritus
  • Nausea
  • Altered mental state (sedation, cognitive impairment or confusion)
  • Respiratory depression (usually only with larger doses in opioid-naive patients)
148
Q

What is used for opioid overdose

A

Naloxone

149
Q

Explain the combination of opioids used to control pain in palliative patients

A

-> Background opioids
-> Rescue doses for breakthrough pain

  • The dose of the rescue opioid should be 1/6th of the background dose
150
Q

what do the NICE guidelines clearly state in regards to chronic primary pain

A
  • Avoid essentially all forms of analgesia in chronic primary pain, except antidepressants.
151
Q

Typical features of neuropathic pain

A

Burning
Tingling
Pins and needles
Electric shock like sensation

152
Q

Causes of neuropathic pain

A
  • Post-herpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk
  • Nerve damage from surgery
  • Multiple sclerosis
  • Diabetic neuralgia (typically affecting the feet)
    -Trigeminal neuralgia
  • Complex regional pain syndrome
153
Q

four first line treatments for neuropathic pain

A
  • Amitriptyline – a tricyclic antidepressant
  • Duloxetine – an SNRI antidepressant
  • Gabapentin – an anticonvulsant
  • Pregabalin – an anticonvulsant

Should be used as monotherapy, if one doesn’t work SWITCH don’t add

154
Q

which tumours most commonly spread to the brain

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney (renal cell carcinoma)

155
Q

What is the most common primary brain tumour in adults and how do they appear on imaging

A
  • Glioblastoma
  • Solid tumours with central necrosis and a rim that enhances with contrast
156
Q

How do brain tumours present ?

A
  • Progressive focal neurological symptoms
  • Signs and symptoms of raised ICP
157
Q

What concerning features of a headache might suggest raised ICP

A

Constant headache
Nocturnal (occurring at night)
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
Papilloedema on fundoscopy

158
Q

Other than a headache, what are the other features of raised ICP

A

Altered mental state
Visual field defects
Seizures (particularly partial seizures)
Unilateral ptosis (drooping upper eyelid)
Third and sixth nerve palsies

159
Q

First line investigation for a brain tumur

A

MRI

160
Q

what criteria is used to assess the type of stroke ?

A

Bamford classification, assesses :

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
161
Q

Total anterior circulation infarct

A
  • Involves middle and anterior cerebral arteries
  • All 3 of bamford criteria
162
Q

Partial anterior circulation infarct

A
  • Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
  • 2 of the bamford classification
163
Q

Lacunar infarcts

A
  • Involves perforating arteries around the internal capsule, thalamus and basal ganglia
    presents with 1 of the following:
  1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
  2. pure sensory stroke.
  3. Ataxic hemiparesis
164
Q

Posterior circulation stroke

A
  • Involves vertebrobasilar arteries presents with 1 of the following:
  1. cerebellar or brainstem syndromes
  2. loss of consciousness
  3. isolated homonymous hemianopia
165
Q

Lateral medullary syndrome stroke

A

-> Involves posterior inferior cerebellar artery (Wallenberg’s syndrome)

  • Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  • Contralateral: limb sensory loss
166
Q

Weber’s syndrome (stroke)

A
  • Ipsilateral CN III palsy
  • Contralateral weakness of upper and lower extremity

Stroke in the branches of the posterior cerebral artery that supply the midbrain

167
Q

Management of TIA

A
  • > Aspirin 300mg daily (started immediately)
    -> Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
    -> Diffusion-weighted MRI scan is the imaging investigation of choice.
168
Q

What score is used to assess probablity of a stroke ?

A

ROSIER (one or more = stroke is possible)

169
Q

Initial management of suspected stroke

A
  • Exclude hypoglycaemia
  • Immediate non contrast CT head to exclude haemorrhage
  • Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
  • Admission to a specialist stroke centre
170
Q

when should thrombolysis with alteplase and thrombectomy be considered for acute stroke management

A

-> If it can be administered within 4.5 hours of onset of stroke symptoms
-> Haemorrhage has been definitively excluded (i.e. Imaging has been performed)

171
Q

when can thrombectomy be offered for the management of acute stroke

A
  • In patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation.
    -> It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.
172
Q

What underlying conditions are all patients with a TIA or stroke investigated for ?

A

-> Carotid artery stenosis : Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
-> AF : ECG or ambulatory ECG monitoring

173
Q

Secondary prevention following a stroke

A

-> Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
-> Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
-> Blood pressure and diabetes control
-> Addressing modifiable risk factors (e.g., smoking, obesity and exercise)

174
Q

Anterior cerebral artery stroke

A
  • Contralateral hemiparesis and sensory loss, - - Lower extremity > upper
175
Q

Middle cerebral artery stroke

A
  • Contralateral hemiparesis and sensory loss, - - Upper extremity > lower
  • Contralateral homonymous hemianopia
  • Aphasia
176
Q

Posterior cerebral artery stroke

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia
177
Q

Most important causes of status epilepticus to rule our first

A

Hypoxia
Hypoglycaemia

178
Q

Management of status epilepticus in a pre hospital setting

A

PR diazepam or buccal midazolam

179
Q

Underlying condition that can cause prolonged reliance on a ventilator following anaesthesia

A

Myasthenia gravis

180
Q

What other symptom could be elicited on cranial nerve examination in Bell’s palsy

A
  • Loss of taste on anterior two-thirds of the tongue (one same side as facial weakness).
181
Q

simple initial management of raised ICP

A

Elevate the bed to 30 degrees

182
Q

long term prophylaxis of stroke / TIA ?

A

Antiplatelet therapy -> clopidogrel

183
Q

Common trigger for cluster headaches

A

Alochol

184
Q

Headache associated with valsalva manoeuvres suggests what underlying cause and what would be the investigation of choice

A
  • Raised ICP
  • Ix = CT head (LP is CI until raised ICP excluded).
185
Q

Explain the therapeutic guidelines for what anti-emetic is used depending on the underlying cause

A
  • Ondansetron for chemotherapy-induced nausea
  • Haloperidol for intracranial causes (raised ICP, direct effect of tumour)
  • Prochlorperazine for vestibular causes
  • Metoclopramide for gastrointestinal causes
186
Q

How does onsansetron work

A

5-HT-3 receptor antagonist (serotonin receptor)

187
Q

Points in glasgow coma scale

A

M : motor response /6
V : verbal response /5
E : eye opening /4

188
Q

Motor response in GCS

A

6 : Obeys commands
5 : Localises to pain
4 : Withdraws from pain
3 : flexes to pain
2 : extends to pain
1 : none

189
Q

Verbal response in GCS

A

5 : Orientated
4 : Confused
3 : words
2 : sounds
1 : none

190
Q

Eye opening in GCS

A

4 : spontaneous
3 : to voice
2 : to pain
1 : none

191
Q

what is often spared in MND

A

Eye movements

192
Q

what medication should be avoided in myasthenia gravis and why

A

Bisoprolol
Can worsen MG and cause drop in FVC

193
Q

Signs of a fourth nerve palsy (Trochlear)

A
  • Vertical diplopia (WORSE ON GOING DOWNSTAIRS).
  • When looking straight, the affected eye may deviate upwards and rotate outwards
  • May develop head tilt
194
Q

Action of fourth nerve on eyeb

A

Trochlear = superior oblique
Depresses eye and move inwards

195
Q

example of a medication that should be stopped following dementia diagnosis

A

Amitriptyline - can worsen cognitive impairment

196
Q

Illicit drug, blood condition and kidney condition associated with SAH

A
  • Drug = cocaine
  • Blood condition = sickle cell
  • Kidney condition = ADPKD
197
Q

Presentation of complex regional pain syndrome

A
  • Previous injury (e.g. fracture)
  • Pain, skin flushing, swelling and abnormal hair growth in the area
198
Q

Name for experiencing pain from stimuli that are not normally painful

A

Allodynia

199
Q

Most malignant brain tumour

A

Glioblastoma

200
Q

4 secondary mets of a brain tumour

A

Renal cell carcinoma
Breast
Lung
Melanoma

201
Q

3 presenting symptoms of acoustic neuroma

A

Tinnitus
Unilateral hearing loss
Balance problems

202
Q

pathology in the heart, brains, kidneys, retina and lungs in tuberous slerosis

A
  • Heart : rhabdomyomas
  • Brain : gliomas
  • Kidneys : polycystic kidneys
  • Retina : hamartomas
  • Lungs : Lymphangioleimyomatosis
203
Q

Management of idiopathic intracranial hypertension

A
  • Weight loss
  • Topiramate
  • Acetazolamide
  • LP and drainage
  • CN II decompression
204
Q

Mechanism of action of acetazolamide

A

Carbonic anhydrase inhibitor

205
Q

Presentation of a third nerve palsy

A
  • ‘Down and out’ eye
  • Ptosis
  • Dilated pupil
  • Absent light reflex but intact consensual constriction (third nerve carries efferent fibres hence absent light reflex but afferent still in tact = consensual)
206
Q

most common long term complication of bacterial meningitis

A

Sensorinerual hearing loss

207
Q

Typical presentation of a brain abscess

A
  • Triad : fever, headache and focal neurological deficit
  • Can also present with seizure
208
Q

likely nerve injury followung mid-shaft humeral fracture and how to test it

A
  • Radial
  • Extend the wrist
209
Q

Signs and symptoms of a pontine haemorrhage

A
  • Reduced GCS
  • Paralysis
  • Bilateral small / pin point pupils
  • Hx of long standing HTN
210
Q

3 investigations you would do in someone with suspected TIA

A

ECG : AF
Head CT / MRI
Carotid artery doppler USS

211
Q

3 TIA RF

A

Smoking
DM
HTHN

Finals (92 decks)

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