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Final Year > Neurology > Flashcards

Neurology Flashcards

1
Q

What are cluster headaches?

A

Unbearable unilateral headaches, centred around eye
Come in clusters and disappear for extended periods

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2
Q

What are the symptoms of cluster headaches?

A

3-4 episodes/d for wks/mths, then pain-free period lasting several yrs
Attacks last between 15mins and 3hrs
Unilateral

Red, swollen and watering eye
Pupil constriction
Eyelid drooping
Nasal discharge
Facial sweating

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3
Q

Outline acute management of cluster headaches

A

Triptans (eg: Sumitriptan)
High-flow 100% O2

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4
Q

Outline prophylactic management of cluster headaches

A

1st line: Verapamil
Occipital nerve block
Prednisolone- Given short course to break the cycle
Lithium

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5
Q

What are the 4 types of migraine?

A

Migraine w/o aura
Migraine with aura
Silent migraine (aura but no headache)
Hemiplegic migraine

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6
Q

What are the 5 stages of migraine?

A
  • Premonitory/prodromal- Several days before headache
  • Aura (lasts up to 60mins)
  • Headache- Lasts 4 to 72h
  • Resolution- Headache fades/relieved abruptly by vomiting or sleeping
  • Postdromal/recovery phase
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7
Q

What are the typical features of a migraine headache?

A

Lasts between 4 and 72h
Usually unilateral
Moderate-severe intensity
Pounding or throbbing
Photophobia
Phonophobia
Osmophobia (discomfort with smells)
Aura (visual changes)
N&V

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8
Q

What are the common features of an aura?

A

Affects vision/sensation/language
Sparks in vision
Blurred vision
Lines across vision
Loss of visual fields (eg: Scotoma)
Tingling/numbness
Dysphagia

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9
Q

What is a hemiplegic migraine?

A

Unilateral limb weakness
Ataxia (loss of coordination)
Impaired consciousness
Familial hemiplegic migraine- Autosomal dominant
Can mimic stroke or TIA

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10
Q

List some of the triggers of migraines

A

Stress
Bright lights
Strong smells
Certain foods (eg: Chocolate, cheese, caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

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11
Q

Outline acute management of migraines

A

NSAIDs
Paracetamol
Triptans (eg: Sumitriptan)
Antiemetics (eg: Metoclopramide or prochlorperazine)

Opiates can make migraine worse

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12
Q

Outline triptans

A

5-HT receptor agonists (bind to serotonin receptors

MoA:
Cranial vasoconstriction
Inhibit transmission of pain signals
Inhibit release of inflammatory neuropeptides

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13
Q

What are the CIs of triptans?

A

Associated with vasoconstriction:
HTN
Coronary artery disease
Previous stroke
TIA
MI

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14
Q

Outline prophylaxis of migraines

A

Headache diary and avoid triggers
Propanolol
Amitriptyline
Topiramate (teratogenic)

Specialist:
Pizotifen
Candesartan
Sodium valproate
MA- Erenumab or fremanezumab

CBT
Mindfulness and meditation
Acupuncture
Vit B2 (riboflavin)

Menstrual migraines- Prophylactic triptans (eg: Frovatriptan or zolmitriptan)

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15
Q

Which type of headache is the COCP CI in and why?

A

Migraine with aura
Associated with increased risk of stroke

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16
Q

What are the red flags of headaches?

A

Fever, photophobia, neck stiffness- Meningitis, encephalitis, brain abscess
New neuro symptoms- Haemorrhage, tumours
Visual disturbance- Giant cell arteritis, glaucoma, tumours
Sub-onset occipital headache- SAH
Worse on coughing or straining- Raised ICP
Postural, worse on standing/lying/bending over- Raised ICP
Vomiting- Raised ICP or CO poisoning
History trauma- ICH
History of cancer- Brain metastasis
Pregnancy- Pre-eclampsia

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17
Q

What is an important investigation in papilloedema?

A

Fundoscopy
Suggests raised ICP- Brain tumour, benign intracranial HTN, intracranial bleed

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18
Q

Outline tension headaches

A

Common
Mild ache or pressure in band-like pattern around head
Develop and resolve gradually
No visual changes

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19
Q

What are some of the associations of tension headaches?

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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20
Q

Outline management of tension headaches

A

Reassurance
Ibuprofen or paracetamol
Amitriptyline for chronic/frequent tension headaches

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21
Q

What are secondary headaches?

A

Similar presentation to tension headache, but with a clear cause

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22
Q

List some of the causes of secondary headaches

A

Infections- Viral URTI
OSA
Pre-eclampsia
Head injury
CO poisoning

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23
Q

Outline sinusitis

A

Inflammation of paranasal sinuses
Typically causes pain and pressure following recent viral URTI
Tenderness and swelling on palpation of affected areas
Resolve within 2-3wks

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24
Q

What is the management of sinusitis?

A

Usually spontaneously resolves within 10d
Steroid nasal spray
Antibiotics- Pen V

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25
Q

What is a medication overuse headache?

A

Analgesic headache caused by frequent analgesia use
Similar non-specific features as tension headache

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26
Q

Outline hormonal headaches

A

Related to low oestrogen
Similar to migraine features

Occur:
2d before and 1st 3d menstruation
Perimenopause
Early pregnancy

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27
Q

Outline management of hormonal headaches

A

Triptans
NSAIDs- Mefenamic acid

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28
Q

Outline cervical spondylosis

A

Caused by degenerative changes in cervical spine
Causes neck pain, worse with movement
Often presents with headaches

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29
Q

Outline trigeminal neuralgia

A

Intense facial pain in distribution of trigeminal nerve
90% unilateral
More common in MS

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30
Q

Outline presentation of trigeminal neuralgia

A

Pain comes on suddenly and lasts secs to hrs
Electricity-like, shooting, stabbing or burning pain
May be triggered by touch, talking, eating, shaving or cold
Attacks may worsen over time

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30
Q

Outline management of trigeminal neuralgia

A

Carbamazepine

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31
Q

What is tuberous sclerosus?

A

Autosomal dominant genetic condition that affects multiple systems
Characteristic feature- Hamartomas (benign tissue growths)

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32
Q

What are the common locations of hamartomas in tuberous sclerosus?

A

Skin
Brain
Lungs
Heart
Kidneys
Eyes

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32
Q

What are the common mutations causing tuberous sclerosus?

A

TSC1 gene on Chr 9- Hamartin
TSC2 gene on Chr16- Tuberin

Hamartin and tuberin interact to control size and growth of cells- Abnormality leads to abnormal cell size and growth

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33
Q

Outline skin features of tuberous sclerosus

A

Ash leaf spots- Depigmented areas of skin shaped like ash leaf
Shagreen patches- Thickened, dimpled, pigmented patches of skin
Angiofibromas- Small skin-coloured/pigmented papules that occur over nose and cheeks
Ungual fibromas- Circular painless lumps that grow from nail bed and displace nail
Cafe-au-lait spots
Poliosis- Isolated patch of white hair on head/eyebrows/eyelashes/beard

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34
Q

List neurological features of tuberous sclerosis

A

Epilepsy
LD
Brain tumours

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35
Q

Outline other features of tuberous sclerosus

A

Rhabdomyolysis in heart
Angiomyolipoma in kidneys
Lymphangioleiomyomatosis in lungs
Subependymal giant cell astrocytoma in brain
Retinal hamartomas in eyes

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36
Q

Outline management of tuberous sclerosus

A

No treatment for underlying gene defect
Supportive- Monitor and treat complications
mTOR inhibitors may be used to suppress growth of brain/lung/kidney tumours

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37
Q

What is neurofibromatosis?

A

Genetic condition causing nerve tumours (neuromas) to develop throughout nervous system
Benign but can cause neuro and structural problems

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38
Q

Outline NFT1

A

More common than type 2
Chr 17- Codes for neurofibromin- Tumour suppressor protein
Autosomal dominant

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39
Q

Outline features of NFT1

A

C- Cafe au lait spots
R- Relative with NF1
A- Axillary or inguinal freckling
BB- Bony dysplasia, such as Bowing of long bone or sphenoid wing dysplasia
I- Iris hamartomas- Yellow-brown spots on iris
N- Neurofibromas
G- Glioma of optic pathway

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40
Q

What do neurofibromas look like on the skin?

A

Skin-coloured, raised nodules or papules with smooth, regular surface

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41
Q

Outline management of NF1

A

Diagnosis based on presentation
No treatment
Manage complications

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42
Q

List complications of NF1

A

Migraines
Epilepsy
Renal artery stenosis, causing HTN
LD
ADHD
Scoliosis of spine
Vision loss (2ndary to optic nerve glioma)
*Malignant peripheral nerve sheath tumours
*GI stromal tumour
Brain tumour
Spinal cord tumour
Increased risk cancer

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43
Q

Outline neurofibromatosis type 2

A

Chr 22- Codes for Merlin (tumour suppressor protein in Schwann cells (PNS))
Mutations lead to Schwannomas
Autosomal dominant
Acoustic neuromas (tumours of auditory nerve)

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44
Q

What is the key characteristic of NF2?

A

Bilateral acoustic neuromas

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45
Q

What is Guillain-Barre syndrome?

A

Acute paralytic polyneuropathy affecting PNS
Acute symmetrical ascending weakness and sensory symptoms
Triggered by infection- Campylobacter jejuni, CMV, EBV

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46
Q

Outline presentation of Guillain-Barre syndrome

A

Symptoms start within 4wks of triggering infection
Symmetrical ascending weakness
Reduced reflexes
Recovery period- Mths to yrs
May have peripheral loss sensation or neuropathic pain
May progress to CNs and cause facial weakness
Autonomic dysfunction- Urinary retention, ileus or heart arrhythmias

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47
Q

Outline diagnosis of Guillain-Barre syndrome

A

Clinically
Nerve conduction studies- Reduced signal through nerves
Lumbar puncture- Raised protein, normal cell count and glucose

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48
Q

Outline management of Guillain-Barre syndrome

A

Supportive care
VTE prophylaxis- PE leading cause of death
IVIG 1st line
Plasmapheresis- Alternative to IVIG

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49
Q

Outline prognosis of Guillain-Barre syndrome

A

Recovery mths-yrs
5% mortality due to respiratory or CV complications

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50
Q

What is Charcot-Marie-Tooth disease?

A

Inherited disease that affects peripheral motor and sensory neurones
Myelin or axon dysfunction
Autosomal dominant
Symptoms usually present <10y

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51
Q

Outline features of Charcot-Marie-Tooth disease

A

High foot arches (pes cavus)
Distal muscle wasting- Inverted champagne bottle legs
Lower leg weakness- Loss of ankle dorsiflexion (high stepping gait due to foot drop)
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

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52
Q

List causes of peripheral neuropathy

A

Alcohol
B12 deficiency
Cancer and CKD
Diabetes and Drugs (isoniazid, amiodarone, leflunomide, cisplatin)
Every vasculitis

Charcot-Marie-Tooth disease

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53
Q

Outline management of Charcot-Marie-Tooth disease

A

Physio
Podiatrists
Analgesia (amitriptyline)

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54
Q

What is Myasthenia gravis?

A

AI condition affecting NMJ
Muscle weakness that progressively worsens with activity and improves with rest

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55
Q

Which condition has a strong link to myasthenia gravis?

A

Thymomas (thymus gland tumours)

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56
Q

Outline presentation of myasthenia gravis

A

Affects women <40y and men >60y
Associated with thymoma
Affects proximal muscles of limbs and small muscles of head and neck
Weakness worsens with muscle use and improves with rest

Difficulty climbing stairs, standing from a seat, raising hands above head
Extraocular muscle weakness- Diplopia
Eyelid weakness- Ptosis
Weak facial muscles
Difficulty swallowing
Fatigue in jaw when chewing
Slurred speech

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57
Q

How can you test muscles for fatiguability indicating myasthenia gravis?

A

Repeated blinking- Ptosis
Prolonged upward gazing- Diplopia
Repeated abduction of 1 arm 20 times- Unilateral weakness

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58
Q

Outline pathophysiology of myasthenia gravis

A

ACh receptor antibodies produced- Bind to postsynaptic ACh receptors- Blocked
More receptors used in activity= More blocked
Clear at rest

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59
Q

How do NMJ work?

A

Way for motor neurones to communicate with muscles
Axons release ACh from presynaptic membrane- Travels across synapse and attaches to receptors on postsynaptic membrane stimulating muscle contraction

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60
Q

Which antibodies can cause myasthenia gravis?

A

AChR antibodies
MuSK antibodies
LRP4 antibodies

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61
Q

Outline investigations in myasthenia gravis

A

Antibody tests
CT/MRI of thymus gland- Thymoma
Edrophonium test if doubt

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62
Q

Outline management of myasthenia gravis

A

Pyridostigmine- Cholinesterase inhibitor
Immunosuppression (eg: Prednisolone or azathioprine)
Thymectomy- Can improve symptoms even w/o thymoma
Rituximab

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63
Q

What is Myasthenic crisis?

A

Potentially life-threatening complication of myasthenia gravis
Acute worsening of symptoms- Often triggered by RTI
Respiratory muscles weaken- Can lead to respiratory failure

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64
Q

How is a myasthenic crisis managed?

A

NIV or mechanical ventilation
IVIGs
Plasmapheresis

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65
Q

What is Lambert-Eaton Myasthenic syndrome?

A

AI condition affecting NMJ
Symptoms less insidious/pronounced
Mostly paraneoplastic and occurs alongside SCLC

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66
Q

Outline pathophysiology of Lambert-Eaton Myasthenic syndrome

A

Antibodies against voltage-gated calcium channels in presynaptic membrane
Less ACh released- Weaker signal- Reduced muscle contraction

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67
Q

What is the role of voltage-gated calcium channels in muscle contraction?

A

Responsible for assisting release of ACh into synapse of NMJ

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68
Q

Outline presentation of Lambert-Eaton myasthenic syndrome

A

Proximal muscle weakness
Autonomic dysfunction- Dry mouth, blurred vision, impotence, dizziness
Reduced/absent tendon reflexes

*Signs and symptoms improve after periods of muscle contraction

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69
Q

Outline management of Lambert-Eaton Myasthenic syndrome

A

Exclude malignancy- SCLC
Amifampridine
Pyridostigmine
Immunosuppressants (eg: Prednisolone or azathioprine)
IVIGs
Plasmapheresis

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70
Q

What is Huntington’s Chorea?

A

Autosomal dominant- Trinucleotide repeat disorder
Progressive neurological dysfunction
Has anticipation

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71
Q

Outline presentation of Huntington’s Chorea

A

Symptoms begin 30-50y
Begins with cognitive/pschiatric/mood problems

Chorea
Dystonia
Rigidity
Eye movement disorders
Dysarthria
Dysphagia

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72
Q

What is chorea?

A

Involuntary, random, irregular and abnormal body movements

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73
Q

What is dystonia?

A

Abnormal muscle tone, leading to abnormal postures

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74
Q

What is rigidity?

A

Increased resistance to passive movement of joint

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75
Q

What is dysarthria?

A

Speech difficulties

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76
Q

What is dysphagia?

A

Swallowing difficulties

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77
Q

What is anticipation?

A

Huntington’s chorea
Feature of trinucleotide repeat disorders- Successive generations have more repeats

Earlier age of onset
Increased severity of disease

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78
Q

Give examples of trinucleotide repeat disorders

A

Huntington’s Chorea
Fragile X syndrome

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79
Q

Outline management of Huntington’s chorea

A

Diagnosis- Genetic testing
Genetic counselling
Physiotherapy
Speech and language therapy
Tetrabenazine- Chorea symptoms
SSRIs
Advanced directives and end-of-life care

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80
Q

Outline prognosis of Huntington’s disease

A

Progressive
Life expectancy- 10-20y after onset of symptoms
Death often due to aspiration pneumonia
Suicide also common

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81
Q

Outline presentation of brain tumours

A

As grow- Progressive focal neurological symptoms

Raised ICP symptoms:
Constant headache
Nocturnal
Worse on waking
Worse on coughing/straining
Vomiting
Papilloedema (fundoscopy)
Altered mental state
Visual field defects
Seizures (partial)
Unilateral ptosis
3rd and 6th nerve palsies

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82
Q

What are the causes of increased ICP?

A

Brain tumours
ICH
Idiopathic intracranial HTN
Abscess or infection

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83
Q

Outline papilloedema

A

Sign of raised ICP
Swelling of optic disc 2ndary to raised ICP
Paton’s lines on fundoscopy

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84
Q

Outline gliomas

A

Tumours of glial cells in brain/SC
Glial cells surround and support neurones- Astrocytes, oligodendrocytes, ependymal cells
Most common and aggressive form- Glioblastoma

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85
Q

Outline meningiomas

A

Tumour growing from meninges
Usually benign
Take up space- Mass effect

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86
Q

What are the most common cancers to spread to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

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87
Q

Outline management of brain tumours

A

MRI 1st line
Biopsy during surgery
Options- Surgery/chemotherapy/radiotherapy/palliative care

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88
Q

Outline pituitary tumours

A

Tend to be benign
Press on optic chiasm- Bitemporal hemianopia

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89
Q

Outline presentation of pituitary tumour

A

Bitemporal hemianopia
Acromegaly (excessive GH)
Hyperprolactinaemia (excessive prolactin)
Cushing’s disease (excessive ACTH and cortisol)
Thyrotoxicosis (excessive TSH and TH)

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90
Q

How can pituitary tumours be managed?

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine- Blocks excess prolactin
Somatostatin analogues (eg: Octreotide)- Block excess GH

91
Q

Outline acoustic neuromas

A

Benign tumours of Schwann cells that surround vestibulocochlear nerve
Occur at cerebellopontine angle
Bilateral= NF2

92
Q

Outline presentation of acoustic neuroma

A

40-60y
Gradual onset:
Unilateral sensorineural hearing loss
Unilateral tinnitus
Dizziness or imbalance
Sensation of fullness in ear
Facial nerve palsy

93
Q

Outline management of acoustic neuroma

A

Conservative- Monitor if no symptoms
Surgery
Radiotherapy

94
Q

What are the infectious causes of LMN FN palsy?

A

Otitis media
Otitis externa
HIV
Lyme disease

95
Q

What are the systemic disease causes of LMN FN palsy?

A

Diabetes
Sarcoidosis
Leukaemia
MS
Guillain-Barre

96
Q

What are the tumour causes of LMN FN palsy?

A

Acoustic neuroma
Parotid tumour
Cholesteatoma

97
Q

What are the trauma causes of LMN FN palsy?

A

Direct nerve trauma
Surgery
BoS fractures

98
Q

What is the pathway of the facial nerve?

A

Exits brainstem at cerebellopontine angle
Passes through temporal bone and parotid gland

99
Q

What are the 5 branches of the facial nerve?

A

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

100
Q

What is the motor function of the facial nerve?

A

Facial expression
Stapedius inner ear
Posterior digastric, stylohyoid and platysma muscles

101
Q

What is the sensory function of the facial nerve?

A

Taste from ant. 2/3 of tongue

102
Q

What is the parasympathetic supply of the facial nerve?

A

Submandibular and sublingual salivary glands
Lacrimal gland (tear production)

103
Q

What are the features of UMN FN palsy?

A

Urgent
Forehead sparing on affected side- Can move forehead
Can be unilateral or bilateral

104
Q

What are the features of LMN FN lesion?

A

Less urgent
Forehead not spared- Paralysis

105
Q

Give examples of unilateral UMN lesions

A

Stroke
Tumours

106
Q

Give examples of bilateral UMN lesions

A

Rare
Pseudobulbar palsies
MND

107
Q

What is Bell’s palsy?

A

Idiopathic
Unilateral LMN FN palsy
Recover over 12mths

108
Q

Outline management of Bell’s palsy

A

Prednisolone:
50mg for 10d
60mg for 5d, then 5d reducing regime

Lubricating eyedrops- Help prevent exposure keratopathy

109
Q

Outline Ramsay-Hunt Syndrome

A

VZV
Unilateral LMN FN palsy
Painful and tender rash in ear canal, pinna and around ear on affected side- Can extend to anterior tongue and hard palate

110
Q

Outline management of Ramsay-Hunt syndrome

A

Aciclovir and prednisolone
Lubricating eye drops

111
Q

What are the SEs of NSAIDs?

A

Gastritis with dyspepsia
Stomach ulcers
Exacerbation of asthma
HTN
Renal impairment
Coronary artery disease, HF, stroke- Rare

112
Q

What are the CIs of NSAIDs?

A

Asthma
Renal impairment
Heart disease
Uncontrolled HTN
Stomach ulcers

113
Q

What is often prescribed alongside NSAIDs and why?

A

PPI- Omeprazole or lansoprazole
Reduce risk of GI SEs

114
Q

What are the key SEs of opioids?

A

Constipation
Skin itching
Nausea
Altered mental state (sedation, cognitive impairment, confusion)
Respiratory depression

115
Q

What is the antidote to opioids?

A

Naloxone

116
Q

What are the options for opioid regimes in palliative care?

A

Background opiates- eg: 12hrly MR oral morphine or opioid patches
Rescue doses- For breakthrough pain, eg: Immediate-release oral morphine solution

Rescue dose is usually 1/6 of background 24h dose

117
Q

Give examples of opioid patches

A

Buprenorphine patches- 5mcg/h patches
Fentanyl patches- 12mcg/h patches

118
Q

What is complex regional pain syndrome?

A

Areas of abnormal nerve functioning, causing neuropathic pain, abnormal sensations and skin changes
Often triggered by an injury and isolated to one limb

119
Q

What are the features of complex regional pain syndrome?

A

Hypersensitive
Allodynia- Pain associated with normal sensations
Intermittent swelling/colour changes/skin flushing/abnormal sweating
Abnormal hair growth

120
Q

What are the 4 1st line treatments of neuropathic pain?

A

Amitriptyline- TCA
Duloxetine- SNRI
Gabapentin- Anticonvulsant
Pregabalin- Anticonvulsant

Tramadol- Only used as short-term rescue for flares

121
Q

What is the 1st line medication for trigeminal neuralgia?

A

Carbamazepine

122
Q

List common causes of neuropathic pain

A

Post-herpetic neuralgia from shingles in dermatome distribution on trunk
Nerve damage from surgery
MS
Diabetic neuralgia
Trigeminal neuralgia
Complex regional pain syndrome

123
Q

What is the difference between chronic primary and chronic secondary pain?

A

Primary- No underlying condition
Secondary- As a result of an underlying condition

124
Q

What are the options for managing chronic primary pain?

A

Supervised group exercises
Acceptance and commitment therapy
ABT
Acupuncture
Antidepressants (eg: Amitriptyline, duloxetine, SSRI)

125
Q

What should patients with chronic primary pain not be started on?

A

Paracetamol
NSAIDs
Opiates
Anti-epileptics (eg: Pregabalin or gabapentin)

126
Q

Outline a generalised tonic-clonic seizure

A

Tonic- Muscle tensing
Clonic- Muscle jerking
Associated with complete LOC
(also called Grand mal)
May have aura
Prolonged post-ictal phase

127
Q

Outline partial seizures

A

(focal seizures)
Often in temporal lobe
Affect hearing, speech, memory and emotions
Patient awake
Simple partial seizures- Aware
Complex partial seizures- Lose awareness

128
Q

What are some of the symptoms of partial seizures?

A

Deja vu
Strange smells, tastes, sight or sound
Unusual emotions
Abnormal behaviours

129
Q

Outline myoclonic seizures

A

Sudden, brief muscle contractions- Abrupt jump/jolt
Remain awake

130
Q

Outline tonic seizures

A

Sudden onset of increased muscle tone- Entire body stiffens
Usually results in fall if standing
Last seconds

131
Q

Outline atonic seizures

A

Drop attacks
Sudden loss of muscle tone resulting in fall
Usually aware
May be indicative of Lennox-Gastaut syndrome

132
Q

Outline absence seizures

A

Blank, stares into space, abruptly returns to normal
During episode- Unaware of surroundings, no response
Tend to stop as gets older

133
Q

Outline infantile spasms

A

West syndrome
Rare
Starts at 6mths age
Clusters of full body spasms
Developmental regression and poor prognosis

134
Q

What is a characteristic finding on EEG in West syndrome?

A

Hypsarrhythmia

135
Q

Outline management of West syndrome

A

ACTH
Vigabatrin

136
Q

Outline febrile convulsions

A

Tonic-clonic seizures occur during high fever
Not caused by epilepsy
Between 6mths and 5yrs
Don’t usually cause lasting damage
1/3 have more than one
Slight increased risk of developing epilepsy

137
Q

Outline investigations of seizures

A

EEG
MRI brain
ECG
Serum electrolytes
Blood glucose- Hypoglycaemia and diabetes
Blood cultures, urine cultures, lumbar puncture- If sepsis/encephalitis/meningitis suspected

138
Q

What is the criteria for driving with seizures?

A

No driving if had seizures within past yr

139
Q

What is the management of generalised tonic-clonic seizures?

A

1st line- Sodium valproate
2nd line- Lamotrigine or levetiracetam

140
Q

What is the management of partial/focal seizures?

A

Lamotrigine or levetiracetam

141
Q

Outline management of myoclonic seizures

A

1st line- Sodium valproate
2nd line- Levetiracetam

142
Q

Outline management of tonic and atonic seizures

A

1st line- Sodium valproate
2nd line- Lamotrigine

143
Q

Outline management of absence seizures

A

Ethosuximide

144
Q

What are the SEs of sodium valproate?

A

Teratogenic
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

145
Q

What is the effect of using sodium valproate in pregnancy?

A

Neural tube defects
Developmental delay

146
Q

What is status epilepticus?

A

Sezure lasting >5mins
Multiple seizures w/o regaining consciousness

147
Q

Outline management of status epilepticus

A

Secure airway
High-conc. O2
Check blood glucose levels
IV access

148
Q

Outline the medical management of status epilepticus

A

1st line- Benzo, repeat after 5-10mins if seizure continues
2nd line- IV levetiracetam, phenytoin or sodium valproate
3rd line- Phenobarbital or general anaesthesia

149
Q

List options for use of benzos in status epilepticus

A

Buccal midazolam
Rectal diazepam
IV lorazepam

150
Q

What are the acute complications of status epilepticus?

A

Hyperthermia
Pulmonary oedema
Cardiac arrhythmia
CV collapse

151
Q

What are the long term complications of status epilepticus?

A

Epilepsy
Encephalopathy
Focal neurological defects

152
Q

What is a benign essential tremor?

A

Fine tremor affecting all voluntary muscles

153
Q

Outline features of benign essential tremor

A

Fine tremor (6-12Hz)
Symmetrical
More prominent with voluntary movement
Worse when tired/stressed/caffeine
Improved by alcohol
Absent during sleep

154
Q

What are the differential diagnoses of tremor?

A

Parkinson’s
MS
Huntington’s chorea
Hyperthyroidism
Fever
Dopamine antagonists (eg: Antipsychotics)

155
Q

Outline management of benign essential tremor

A

Propranolol
Primidone (barbiturate anti-epileptic)

156
Q

Outline Parkinson’s disease

A

Progressive reduction in dopamine in basal ganglia leading to disordered movement

157
Q

What is the classic triad of features in Parkinson’s disease?

A

Resting tremor
Rigidity
Bradykinesia

158
Q

Outline features of Parkinson’s disease

A

Symptoms asymmetrical (one side of body affected more)
Gradual onset
Tremor 4-6Hz (pill-rolling)
Resting tremor (improves with movement)- Gets worse when patient distracted
Rigidity- Resistance to passive movement of joint- Cogwheel rigidity

Bradykinesia:
Handwriting smaller
Shuffling gait
Difficulty initiating movement
Difficulty turning (take lots of little steps)
Hypomimia (reduced facial movement/expression)

Depression
Sleep disturbance and insomnia
Anosmia
Postural instability
Cognitive impairment and memory problems

159
Q

What are Parkinson’s-Plus syndromes?

A

Multiple system atrophy
Dementia with Lewy bodies

160
Q

What is multiple system atrophy?

A

Parkinson’s-Plus syndrome
Rare
Neurones of various systems in brain degenerate
Basal ganglia- Leads to Parkinson’s presentation
Other areas- Autonomic dysfunction and cerebellar dysfunction

161
Q

What are signs of autonomic dysfunction?

A

Postural hypotension
Constipation
Abnormal sweating
Sexual dysfunction

162
Q

What are the signs of cerebellar dysfunction?

A

Ataxia

163
Q

Outline dementia with Lewy bodies

A

Dementia with features of Parkinsonism
Progressive cognitive decline
Associated symptoms- Hallucinations, delusion, REM sleep disorders, fluctuating consciousness

164
Q

Outline diagnosis of Parkinson’s disease

A

Diagnosed clinically

165
Q

Outline management of Parkinson’s disease

A

Levodopa
COMT inhibitors
Dopamine agonists
MAOB inhibitors

166
Q

Outline levodopa

A

Synthetic dopamine
Normally combined (eg: Co-careldopa or Co-beneldopa)- Stops it being metabolised in body before reaches brain
Most effective for treatment of Parkinson’s but declines over time

167
Q

What is the main SE of levodopa?

A

Dyskinesia- Abnormal movements associated with excessive motor activity:
Dystonia
Chorea
Athetosis

168
Q

What is dystonia?

A

Excessive muscle contraction leads to abnormal postures or exaggerated movement

169
Q

What is athetosis?

A

Involuntary twisting or writhing movements, usually in fingers/hands/feet

170
Q

What is an option for managing dyskinesia caused by levodopa?

A

Amantadine (glutamate antagonist)

171
Q

Outline COMT inhibitors

A

Eg: Entacapone
Slows breakdown of levodopa in body and brain
Extends effective duration of levodopa

172
Q

Outline Dopamine agonists

A

Mimic action of dopamine in basal ganglia, stimulate dopamine receptors
Less effective than levodopa in reducing symptoms
Eg: Bromocriptine, pergolide, cabergoline

173
Q

What is the most notable SE of dopamine agonists?

A

Pulmonary fibrosis

174
Q

Outline MAO-B inhibitors

A

Increase circulating dopamine
Eg: Selegiline, rasagiline

175
Q

What is motor neurone disease?

A

Variety of diseases affecting motor nerves
Progressive, eventually fatal condition where motor neurones stop functioning

176
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis (ALS)- Most common
Progressive bulbar palsy- Affects muscles of talking and swallowing

177
Q

Outline pathophysiology of MND

A

Progressive degeneration of upper and lower motor neurones
Increased risk with smoking, FHx, exposure to heavy metals, and certain pesticides

178
Q

Outline presentation of MND

A

Late middle-aged man
Insidious, progressive weakness of muscles throughout body
Weakness first noticed in upper limbs
May be increased fatigue when exercising
May complain of clumsiness/dropping things more often
Can develop dysarthria (Slurred speech)

179
Q

What are the signs of lower MND?

A

Muscle wasting
Reduced tone
Fasciculations
Reduced reflexes

180
Q

What are the signs of upper MND?

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

181
Q

Outline diagnosis of MND

A

Clinical presentation
Diagnosis of exclusion

182
Q

Outline management of MND

A

Riluzole can slow progression and extend survival by several months in ALS
NIV- Support breathing when respiratory muscles weaken
Baclofen- For muscle spasticity
Benzos- Help breathlessness caused by anxiety

183
Q

Outline pathophysiology of Parkinson’s disease

A

Basal ganglia- Coordinates habitual movement (walking/voluntary movement)
Dopamine- Essential for basal ganglia function
Slow progressive drop in dopamine production

184
Q

What is MS?

A

Chronic and progressive AI condition
Demyelination in CNS
Immune system attacks myelin sheath of myelinated neurones

185
Q

Outline pathophysiology of MS

A

Myelin covers axons of neurones to help electrical impulses travel faster
Ms affects CNS (oligodendrocytes)

186
Q

What are the different cells in myelin?

A

Oligodendrocytes- CNS
Schwann cells- PNS

187
Q

What is the characteristic feature of MS?

A

Disseminated in time and space:
Vary in location and symptoms change over time

188
Q

List causes of MS

A

Multiple genes
EBV
Low vit D
Smoking
Obesity

189
Q

Outline onset of MS

A

Symptoms progress over >24h and last days to weeks at 1st presentation then improve

190
Q

Outline optic neuritis and MS

A

Most common presentation of MS
Demyelination of optic nerve
Unilateral reduced vision

191
Q

What are the key features of optic neuritis?

A

Central scotoma (enlarged central blind spot)
Pain with eye movement
Impaired colour vision
RAPD

192
Q

What is RAPD?

A

Relative afferent pupillary defect
Pupil in affected eye constricts more when shining light in contralateral eye than when shining it in affected eye

193
Q

List causes of optic neuritis

A

MS
Sarcoidosis
SLE
Syphilis
Measles or mumps
Neuromyelitis optica
Lyme disease

194
Q

Outline symptomatic treatments of MS

A

Exercise
Fatigue- Amantadine, modafinil or SSRIs
Neuro pain- Amitriptyline or gabapentin
Depression- SSRIs
Urge incontinence- Solifenacin
Spasticity- Baclofen or gabapentin
Oscillopsia- Gabapentin or memantine

195
Q

How are MS relapses treated?

A

Steroids:
500mg orally daily for 5d
1g IV daily 3-5d if severe

196
Q

Outline diagnosis of MS

A

Clinical picture and symptoms
MRI scans
Lumbar puncture- Oligoclonal bands

197
Q

What is found on MS LP?

A

Oligoclonal bands

198
Q

Outline disease patterns of MS

A

Clinically isolated syndrome- 1st episode of demyelination and neuro signs/symptoms- Lesions on MRI suggest more likely to occur again
Relapsing-remitting- Most common
Secondary progressive- Was relapsing-remitting, now progressive worsening with incomplete remission
Primary progressive- Worsening disease from point of diagnosis, w/o relapses or remissions

199
Q

Outline ataxia and MS

A

Problem with coordinated movement
Sensory- Loss of proprioception- Positive Romberg’s and pseudoathetocis (involuntary writhing movement)- Lesion in dorsal column
Cerebellar ataxia- Problems with cerebellum coordinating movement- Cerebellar lesion

200
Q

Outline focal weakness in MS

A

Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis
Transverse myelitis

201
Q

Outline focal sensory symptoms in MS

A

Trigeminal neuralgia
Numbness
Paraesthesia
Lhermitte’s sign
Transverse myelitis

202
Q

What is Lhermitte’s sign?

A

Electric shock sensation travelling down spine and into limbs when flexing neck
Indicates disease in cervical spinal cord in dorsal column

203
Q

Outline management of complications in SAH

A

Hydrocephalus:
LP
External ventricular drain
VP shunt

Seizures:
Anti-epileptics

204
Q

Which eye movement abnormalities can occur in MS?

A

Oscillopsia- Visual sensation of environment moving, can’t create stable image
CN III/IV/VI- Diplopia and nystagmus
Internuclear ophthaloplegia- Lesion in medial longitudinal fasciculus- Impaired adduction in same eye as lesion, nystagmus in contralateral abducting eye
CN VI- Conjugate lateral gaze disorder- If lesion in L eye, look left, R eye adducts, L eye stays central

205
Q

What is a subarachnoid haemorrhage?

A

Bleeding in subarachnoid space
Between pia mater and arachnoid membrane
Cerebral aneurysms
High mortality- Approx. 30%

206
Q

List RFs for subarachnoid haemorrhage

A

45-70y
Women
Black ethnic origin
HTN
Smoking
Excessive alcohol intake
FHx
Cocaine use
SCA
Marfans or Ehlers-Danlos
Neurofibromatosis
ADPKD

207
Q

Outline presentation of subarachnoid haemorrhage

A

Sudden-onset occipital headache
During strenuous activity- Heavy lifting/sex
Thunderclap headache

208
Q

Outline investigations of subarachnoid haemorrhage

A

1st line- CT head- Hyper-attenuation in subarachnoid space
Lumbar puncture in normal CT head- Wait at least 12h after symptoms start (takes time for bilirubin to accumulate in CSF)
CT angiography- After confirmed diagnosis- Locates source of bleeding

209
Q

What will an LP of subarachnoid haemorrhage show?

A

Raised cell count
Xanthochromia- Yellow CSF due to bilirubin

210
Q

Outline management of SAH

A

Surgical intervention for aneurysms- Coils or clipping
Nimodipine- CCB- Prevents vasospasm (common complication following SAH- Causes brain ischaemia)

211
Q

What is an extradural haemorrhage?

A

Bleeding between skull and dura mater
Rupture of MMA in temporoparietal region
Bi-convex on CT, don’t cross suture lines
Lucid period

212
Q

Outline subdural haemorrhage

A

Between dura mater and arachnoid mater
Rupture of bridging veins
Crescent shape on CT, cross suture lines
Occur in elderly and alcoholics

213
Q

Outline intracerebral haemorrhage

A

Bleeding in brain tissue
Presents similar to ischaemic stroke with sudden-onset focal neuro symptoms
Occur spontaneously or secondary to ischaemic stroke/tumour/aneurysm rupture

213
Q

Outline management of intracranial haemorrhage

A

Immediate CT head
FBC (platelets) and coagulation screen
Avoid hypotension

Small bleed:
Conservative management
Close monitoring, repeat imaging

Surgical (extradural or subdural):
Craniotomy
Burr holes

214
Q

What are the two types of cerebrovascular accident?

A

Ischaemia or infarction (ischaemic stroke)
Intracranial haemorrhage (haemorrhagic stroke)

215
Q

What is the difference between ischaemia and infarction?

A

Ischaemia- Inadequate blood supply
Infarction- Tissue death

216
Q

What is a TIA?

A

Temporary neuro dysfunction (lasts <24h) caused by ischaemia w/o infarction
Rapid onset and resolve quickly

217
Q

What are crescendo TIAs?

A

2+ TIAs within 1wk
Indicate high risk of stroke

218
Q

Outline presentation of stroke

A

Limb weakness
Facial weakness
Dysphasia (speech disturbance)
Visual field defects
Sensory loss
Ataxia and vertigo (post. circulation infarction)

219
Q

List RFs for stroke

A

Previous stroke/TIA
AF
Carotid artery stenosis
HTN
Diabetes
Raised cholesterol
FHx
Smoking
Obesity
Vasculitis
Thrombophilia
COCP

220
Q

Outline management of TIA

A

Aspirin 300mg daily
Refer within 24h for specialist assessment
Diffusion-weighted MRI scan

221
Q

Outline management of stroke

A

Exclude hypoglycaemia
Immediate CT brain
Aspirin 300mg daily for 2wks after scan
Thrombolysis with alteplase- Consider once haemorrhage excluded- Give within 4.5h symptoms onset

222
Q

What is the difference between management of BP in haemorrhagic stroke and ischaemic stroke?

A

Ischaemic- Low BP can worsen ischaemia
Haemorrhagic- Aggressively treated to lower and reduce ICP

223
Q

How are the underlying causes of stroke assessed?

A

Carotid imaging- Carotid artery stenosis
ECG- AF

Start anticoagulation following stroke due to AF after finishing course of aspirin

224
Q

What are the top risk factors for stroke?

A

AF
Carotid artery stenosis

225
Q

Outline secondary prevention of stroke

A

Clopidogrel- 75mg OD
Atorvastatin- 20-80mg- Delay at least 48h
BP and diabetes control
Stop smoking, lose weight, exercise as required

226
Q
A

Final Year (14 decks)

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