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Neuro Flashcards

1
Q

Which lobe of the brain is responsible for voluntary motor function?

A

Frontal lobes

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2
Q

Which lobe of the brain is responsible for language and calculation?

A

Parietal lobes

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3
Q

Where is the primary sensory cortex?

A

Post-central gyrus, parietal lobe

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4
Q

Where is the primary motor cortex?

A

Pre-central gyrus, frontal lobes

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5
Q

Where is the primary visual cortex?

A

Occipital lobes

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6
Q

What are the basal ganglia responsible for?

A

Motor refinement

Modulation of cognitive and emotional responses

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7
Q

What three sections make up the brainstem?

A

Midbrain
Pons
Medulla

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8
Q

What is the bloody supply to the circle of willis?

A

2x vertebral arteries

2x internal carotid arteries

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9
Q

A clot in which artery would cause locked-in syndrome?

A

Basilar artery

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10
Q

At which level does the spinal cord terminate and become the caudal equina?

A

L1-2

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11
Q

What functions are carried within the dorsal columns?

A

Fine sensation, vibration and proprioception

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12
Q

What functions are carried within the spinothalamic tracts?

A

Pain, temperature and crude touch

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13
Q

Where do the dorsal column and spinothalamic tracts decussate?

A

Dorsal column tracts- decussate in medulla oblongata

Spinothalamic tracts decussate lower in the spinal cord

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14
Q

What is the neurological pattern of GBS?

A

Peripheral neuropathy- polyradiculopathy with no involvement of brain or spinal cord

Generally starts in the feet, spreading proximally to the legs, hands etc
Sensory symptoms often precede motor
Initially pain and paraesthesia -> progressive muscle weakness
Flaccid weakness and numbness

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15
Q

What are the clinical features of GBS?

A

Usually presenting following recent infection
- most commonly campylobacter gastroenteritis but can be a range of infections

Initially pain and paraesthesia affecting the feet -> spreading proximally
Followed by progressive weakness in similar pattern
Eventually central weakness -> dysarthria, extra ocular weakness, respiratory distress

LMN signs: areflexia, flaccid paralysis, ataxia

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16
Q

What are the triad of features which make up Miller Fisher Syndrome?

A

Ophthalmoplegia
Areflexia
Ataxia

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17
Q

How is GBS diagnosed?

A

Neuroimagine: NAD
Nerve conduction: slowed LMN conduction velocity
LP: elevated protein with normal cytology
Blood cultures and PCR for search for causative agent

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18
Q

How is GBS managed?

A

Regular spirometry & ABG to monitor respiratory function and need for intubation
VTE prophylaxis

IVIG for 5 days or plasma exchange if IVIG not available
NO BENEFIT of steroids

Physio, OT, neuro rehab

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19
Q

What are differential diagnoses for GBS?

A

Diabetic neuropathy- much more chronic course, prev DM, usually only sensation initially
MG- chronic, weakness varies throughout day, no pain, sensation and reflexes in-tact
Botulism- similar except DESCENDING paralysis rather than ascending, normal CSF, reflexes in-tact
Cauda equina- only affects lower body, sphincter involvement
Transverse myelitis- UMN syndrome

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20
Q

What is the cause of Myasthenia Gravis?

A

Auto-antibodies against acetylcholine receptors

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21
Q

What is the symptom pattern of MG?

A

Usually oculobulbar symptoms initially - worst in the evening

  • Progressive ptosis and diplopia (horizontal mostly)
  • Dysarthria, dysphagia aspiration

Progressive muscle weakness, mostly in proximal muscle groups e.g. raising arms, climbing stairs
Symptoms improve with rest

Reflexes and sensation remain in-tact

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22
Q

How is MG diagnosed?

A

Presence of AChR-autoantibodies
Nerve conduction studies: progressively decremental response on repetitive stimulation
PFTs to rule out MG crisis

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23
Q

How is MG managed?

A

1st line= pyridostigmine (AChE antagonist)

Corticosteroids
Thymectomy
Plasma exchange in crisis

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24
Q

What are differentials for MG?

A

LEMS: same but IMPROVES with repeated use rather than worsens
Botulism
Primary myopathy

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25
Q

What is a myasthenic crisis?

A

Worsened MG symptoms affecting respiratory muscles
Requiring respiratory support
Oropharyngeal involvement can also cause airway obstruction + aspiration

Most commonly triggered by supervening infection

Rx= IVIG or plasma exchange as soon as possible

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26
Q

What are the causes of botulism?

A

Clostridium botulinum toxin

  • > GI via food ingestion
  • > Respiratory via inhalation
  • > Iatrogenic
  • > Skin breaks
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27
Q

What are the symptoms of botulism?

A

Most common= GI so preceded by D&V

Descending flaccid paralysis with areflexia

  • > Starts in cranial nerves and descends
  • > Ptosis, diplopia, facial droop, ophthalmoplegia, mydriasis, poor reactivity/accomodation, hypoglossal weakness, dysarthria, dysphagia

Sensation remains in-tact, afebrile
Can cause respiratory failure

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28
Q

How is botulism diagnosed?

A

Mouse bioassay
Nerve conduction studies: small action potentials in response to supramaximal stimulation
Assessment of airway and respiratory function -> intubation

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29
Q

How is botulism managed?

A

Botulism anti-toxin administration ASAP
Respiratory support
Wound debridement and supportive care

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30
Q

Where do the corticospinal tracts decussate?

A

Lateral tract decussates in the medulla, anterior tract lower in the cord

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31
Q

What is acute cervical cord syndrome?

A

Hyperextension injury of the C-spine- mostly traumatic but can be caused by osteoporosis and collapse

Causes motor deficit in all 4 limbs but most pronounced in the arms
Sensory deficit in a cape-like distribution below level of injury- may have some arm sparing depending on level
Neck pain at site of impingement
Hyperreflexia and increased tone (UMN lesion)
May suffer urinary retention

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32
Q

How should anterior cervical cord syndrome be managed?

A

Cervical immobilisation and C-spine MRI
Steroids to reduce inflammation
Physio and OT

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33
Q

What are the causes of caudal equina syndrome?

A 
Disc herniation= most common
MSCC / bony tumour
Epidural abscess
Fracture
Spinal dural haematoma
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34
Q

What are the symptoms of caudal equina syndrome?

A

> 97% suffer back pain and bilateral sciatica

Saddle anaesthesia, loss of anal tone +/- incontinence
Urinary retention, erectile dysfunction
Areflexia and lack of tone in the legs
Bilateral leg weakness
Ataxia
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35
Q

How is cauda equina diagnosed?

A

Emergency MRI spine
CT myelogram if MRI not available
Bladder scan

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36
Q

How should cauda equina be managed?

A

A-E assessment
Catheter
Adequate analgesia
Neurosurgical input

Surgery should be performed <24 hours to reduce the risk of tetraplegia

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37
Q

What is Bell’s palsy?

A

Acute unilateral palsy of the facial nerve (CN7)
LMN lesion
Commonly thought to be viral cause e.g. HSV1

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38
Q

How does Bell’s palsy present?

A

Subacute onset (72 hours) of facial nerve palsy affecting all branches of the nerve
Forehead involvement
Unilateral
Loss of blink-> dry eye and ulcerative keratitis if not managed

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39
Q

How is Bell’s palsy investigated?

A

Usually clinical diagnosis

NCS will show >90% decrease in amplitude compared to other side

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40
Q

How is Bell’s palsy managed?

A

High dose corticosteroids - oral prod tapering course starting at 60mg
Eye protection: tape shut, artificial tears, glasses

Most people with Bell’s palsy make a full recovery within 3–4 months

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41
Q

What is Ramsay-Hunt syndrome?

A

Reactivation of VZV in the geniculate ganglion of the facial nerve

Causes facial nerve palsy affecting all 3 branches- no forehead sparing
LMN lesion

Associated with vesicular rash in/on the ear, otalgia and may get tinnitus/vertigo/SN deafness

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42
Q

How is Ramsay Hunt syndrome managed?

A

Oral aciclovir <72 hours
Oral steroids
Carbamazepine for any neuropathic pain
Eye protection- sunglasses, taping shut, artificial tears/lubricants

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43
Q

What are the symptoms of common peroneal nerve palsy?

A

Footdrop -> high-stepping gait
Inability to dorsiflex or evert the foot
Sensory disturbance on dorsum of foot and lateral leg
Unable to walk on heels

Ankle reflexes spared
Tinel’s sign positive

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44
Q

How is common peroneal nerve palsy managed?

A

Footdrop splint
Physiotherapy
Surgical repair in some

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45
Q

What are the clinical features of tarsal tunnel syndrome?

A

Pain BEHIND medial malleolus + planter aspect of medial heel
Pain with dorsiflexion and eversion

Initially worse with walking -> constant

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46
Q

What nerve is affected in tarsal tunnel syndrome?

A

Posterior tibial nerve

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47
Q

What are the symptoms of obturator nerve palsy?

A

Numbness/paraesthesia of the medial thigh
Weakened thigh ADduction
Wide-based, circumducting gait
Wasting of medial thigh muscles

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48
Q

What are symptoms of pudendal nerve palsy?

A

Pain/paraesthesia/numbness of the perineum, genitalia
Urinary urgency and frequency
Erectile dysfunction

S2-4 control the pelvic floor

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49
Q

What are the symptoms of suprascapular nerve palsy?

A

Wasting of the supra/infraspinatous muscles
Inability to abduct/externally rotate the arm
Impingement pain

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50
Q

Compression WHERE tends to cause radial nerve palsy?

A

Compression against the humerus, where there is the radial groove

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51
Q

What are the symptoms of radial nerve palsy?

A

Wrist-drop
Weakened triceps
Loss of extension of fingers and thumb
Sensory loss to dorsum of lateral 3.5 digits

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52
Q

What is the most common cause of ulnar nerve palsy?

A

Prolonged pressure on the elbow

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53
Q

What are the symptoms of ulnar nerve palsy?

A

Inability to extend medial 1.5 fingers (little and ring)
Inability to abduct/adduct fingers
Impaired thumb ADDuction
Decreased grip strength

Sensory loss to medial half of the hand
Muscle atrophy

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54
Q

What does Froment’s sign indicated?

A

Ulnar nerve palsy

Inability to hold piece of paper with thumb- impaired thumb adduction

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55
Q

What causes median nerve palsy?

A

Carpal tunnel syndrome

56
Q

What are the symptoms of carpal tunnel syndrome?

A

Numbness, tingling and pain in the palmar aspect of lateral aspect of lateral 3.5 fingers
Pain can radiate to wrist and forearm + generally worse in the morning
Pain can wake from sleep

Inability to grip properly, clumsiness
Wasting of the thenar eminence

57
Q

What is Phalen’s test?

A

Test for carpal tunnel syndrome

Hold wrist in flexion for 60s-> elicits numbness or pain in median nerve distribution

58
Q

What is the gold standard test for carpal tunnel syndrome?

A

EMG: slowed conduction velocity across carpal tunnel, decreased amplitude and prolonged latency

59
Q

How is carpal tunnel syndrome managed?

A

Dorsiflexed splint (20degree extension)
Steroid injection
Surgical decompression

60
Q

What should you consider when changing epilepsy medication?

A

Risk of breakthrough seizures
Consider interactions between new medication and current (both epilepsy and others)
Tolerability of new medication- new side effects etc
Implications for driving- recommended to stop driving for 6m during changeover, HAVE to after 6 months
Usual advice: no working at height/care near water etc

61
Q

What considerations should be taken in pregnancy for epileptic women?

A

5mg folic acid
Lamotrigine = 1st line, carbemazepine also safe
MDT input into pregnancy
Change medication over when THINKING about getting pregnant to reduce the risk of breakthrough seizures

62
Q

What are the driving rules with seizures?

A

Have to stop 6m after first seizure
Recommended to stop 6m when changing medication
Legally must stop for 6m after breakthrough seizure
In established epilepsy, must stop for 12m after an established seizure if not due to medication change

Can’t drive for work until seizure free for 10 years.

63
Q

What is first line for absence seizures?

A

Ethosuximide

64
Q

What is first line for myoclonic seizures?

A

Leviteracetam

65
Q

What needs to be in place before initiating sodium valproate?

A

Pregnancy prevention plan
Baseline FBC and LFTs

Need counselling on signs of hepatotoxicity and thrombocytopenia

66
Q

Which anti-epileptic is especially associated with SJS/TEN?

A

Lamotrigine

67
Q

Which anti-epileptic can interact with SSRIs to increase availability?

A

Lamotrigine

68
Q

Which anti-epileptics interact with the oral contraceptive pill?

A

Carbamazepine

Topiramate

69
Q

What are the causes of optic neuritis?

A 
MS
Neuromyelitis optica 
Infection: encephalitis, meningitis
SOL/compression of the optic nerve
Medication: ethambutol
Toxins: lead, methanol
70
Q

What are the clinical features of optic neuritis?

A 
Retrobulbar pain
Visual disturbance- often central scotoma
Photophobia 
Painful movement of the eye
RAPD
Papilloedema
71
Q

How is optic neuritis diagnosed?

A

MRI of the optic nerve

72
Q

How is optic neuritis treated?

A

Methylprednisolone: 1g IV 3 days, 500mg oral 5 days
+ gastroprotection

Most episodes resolve spontaneously in a matter of months

73
Q

What are the causes of transverse myelitis?

A 
MS
Neuromyelitis optica
Post-vaccine
Rheumatological diseases
Viral disease and encephalitis
74
Q

How does transverse myelitis commonly present?

A

Acute/subacte onset
May have back/sciatic pain
Paraesthesia and sensory loss below spinal level of lesion
Weakness in the limbs below the lesion which can progress to paralysis
May have bladder/bowel/sexual dysfunction
Spasticity and hyper-reflexia

75
Q

How is transverse myelitis diagnosed?

A

MRI brain and spinal cord to try and identify focus of inflammation
Bloods to rule out B12 deficiency, HIV, low copper, autoantibodies
LP + CSF analysis may show raised protein

76
Q

What is the management of transverse myelitis?

A

IV methylprednisolone: 1g 3-5 days
IVIG/plas ex if no improvement
Analgesia
Antivirals if indicated

77
Q

What is the clinical definition of MS?

A

2 discrete episodes of neurological dysfunction separated in space and time

Demyelinating disease with neuronal loss and axonal transection

78
Q

How does MS classically present?

A

Classically white women 20-40s

Often starts with episode of optic neuritis

79
Q

What is the most common pattern of MS?

A

Relapse-remitting: 85-90%

Often become secondary progressive (approx 50% of patients)

May also be primary progressive or progressive relapsing MS.

80
Q

What is L’Hermitte’s phenomenon?

A

Electric-shock like sensations running down the back of the neck, spine and sometimes into the limbs

  • Triggered by forward neck flexion
  • Often due to lesion in the upper posterior cervical cord
81
Q

How is MS diagnosed?

A

MRI brain and spinal cord- looking for areas of high signal which may indicate current or past inflammation

LP: oligoclonal banding in CSF, raised IgG

Evoked potentials in affected nerves

82
Q

How is MS managed?

A

For a relapse: High dose methylprednisolone IV 1g 3/7 or 500mg PO 5/7
+ PPI + bisphosphonates

Disease modifying medication:
B-interferon + glatiramer = most common agents

Symptomatic:
Baclofen for spasticity
Sertraline for associated depression
Pregabalin/gabapentin/TCAs for neuropathic pain
Oxybutynin for urinary urgency/frequency
83
Q

What are the differentials for MS?

A

Neuromyelitis optica
Standalone episode of optic neuritis or transverse myelitis
Stroke
GBS
Vitamin B12 deficiency- subacute combined degeneration of the cord
Autoimmune inflammatory conditions

84
Q

What is neuromyelitis optica?

A

Auto-inflammatory condition affecting the optic nerve and spinal cord
Characterised by optic neuritis and transverse myelitis
Caused by auto-antibodies: Anti-AQP4 and MOG antibodies

85
Q

How is NMO differentiated from MS?

A

MRI brain and spine- NMO only optic nerve and transverse myelitis, MS may show inflammation in other areas

Bloods: anti-AQP4 and MOG antibodies + rule out other causes

CSF analysis: no oligoclonal bands in NMO

86
Q

How is NMO managed?

A

High-dose IV corticosteroids- methylprednisolone
Plasma exchange if limited response to steroids
Long-term immunosuppressants can be used to reduce the risk of relapse

Symptomatic treatment

87
Q

What causes trigeminal neuralgia?

A

Compression of the nerve root at the skull base

  • Cyst/tumour, skull malformation
  • Meningeal inflammation
  • Facial injury
  • Demyelinating conditions, MS
88
Q

How is trigeminal neuralgia managed?

A

Carbamazepine = first line
Gabapentin/Pregabalin second line

If treatment resistant: surgical decompression

89
Q

How does venous sinus thrombosis cause death?

A

Mass effect from the thrombus + inflammation/oedema around it can cause trans-tentorial herniation and coning

90
Q

Where is the most common site of a venous sinus thrombus?

A

Sagittal sinus

Headache, vomiting, seizures, papilloedema, reduced vision

91
Q

How is venous sinus thrombosis diagnosed?

A

MRI/CT brain and venogram (venogram most diagnostic)

LP to rule out other causes- only FOLLOWING imagine

92
Q

How is venous sinus thrombosis managed?

A

LMWH and warfarin for 6 months

May need decompressive hemi-craniotomy

93
Q

What is the most common form of MND?

A

Amyotrophic Lateral Sclerosis

94
Q

What are the symptoms of MND?

A

Combination of upper and lower motor neurone symptoms
Muscle fasciculation- especially tongue
Limb weakness, usually proximal muscles first
Stiffness, spasticity, poor balance, ataxia, painful spasm, hyperreflexia
Dyspnoea, dysphagia, aspiration

95
Q

Which medication is thought to alter the disease course of MND?

A

Riluzole

96
Q

What medications can be used to relieve migraine?

A

Paracetamol/ibuprofen
Domperidone for vomiting
Triptans

97
Q

What medications can be used for migraine prophylaxis?

A

Propranolol first line
Topiramate but not in women of childbearing age
Amitriptyline

98
Q

What can be used to treat cluster headaches?

A

High-flow oxygen (12-15L non-rebreathe)

Nasal/SC triptans

99
Q

What can be used as cluster headache prophylaxis?

A

Verapamil

100
Q

What are the initial measures for raised ICP?

A

Hyperventilation
Bed at 30-40 degrees
IV mannitol
Fluid restriction

101
Q

What is the management for benign intracranial hypertension?

A

Acetazolamide +/- furosemide
Amitriptyline
CSF shunting

102
Q

What is the treatment of choice for focal seizures?

A

Carbamazepine

103
Q

What are the causes of spastic paraparesis?

A

Thoracic cord lesions- only legs affected
UMN

Trauma, tumour, TB, transverse myelitis, B12 deficiency, spinal artery thrombosis

104
Q

What are the causes of flaccid paraparesis?

A

Lesion below the level of the spinal cord i.e. Cauda equina, Initial phases of GBS, trauma to spine lower than conus medullaris

LMN signs in both legs

105
Q

What are the causes of spastic tetraparesis?

A

Cervical spine lesion, UMN

Neck trauma, catastrophic stroke

106
Q

What is cervical myeloradiculopathy?

A

Compression of the nerve roots of the C-spine
Causes LMN symptoms in the arms +/- UMN symptoms in the legs depending on the compression of the cord

Most commonly result of osteoporosis or c-spine herniation

107
Q

What is Brown-Sequard syndrome?

A

Hemi-cord syndrome: lesion affecting only one side of the cord e.g. stab wound
Loss of pain and temperature on contralateral side
Loss of fine touch and proprioception on affected side
UMN symptoms in the leg on the same side

108
Q

What are the causes of peripheral neuropathy?

A 
GBS
Diabetic neuropathy
Vitamin deficiency
Alcohol-induced
Thyroid disease
109
Q

What pattern of symptoms would you expect in a brainstem lesion?

A

Cranial nerve palsy on the side of the lesion

Contralateral limb/long-tract signs

110
Q

What is a RAPD?

A

Loss of afferent reflex on affected side but consensual constriction still in-tact
When swinging light test, paradoxical dilation of the affected eye when the torch is shone into it

Optic nerve palsy e.g. optic neuritis

111
Q

What is internuclear ophthalmoplegia?

A

Impaired adduction of the affected eye
Affected eye does not adduct past the midline and the other eye abducts with nystagmus as if trying to pull the affected eye along with it

Caused by a lesion in the MEDIAL LONGITUDINAL FASCICULUS

Most commonly caused by MS or stroke

112
Q

What is the management of status epilepticus?

A

5 min: 4mg IV lorazepam or 10mg buccal/rectal alternatives
Repeat if no improvement after further 5 mins
If still no improvement after further 5 mins: IV phenytoin 18mg/kg

After 30 mins, general anaesthesia, I&V

113
Q

What monitoring is required in the patients needing phenytoin to terminate seizures?

A

Continuous BP and ECG monitoring due to arrhythmogenic quality

114
Q

What is the most common cause of encephalitis?

A

Viral- particularly HSV 1 and other herpes viruses

115
Q

What are the symptoms of encephalitis?

A

Prodromal: fever, rash, lymphadenopathy, cold sores, meningeal irritation, conjunctivitis
Altered mental state / lower GCS
Focal neurological signs
Seizures, meningism

116
Q

How should you investigate suspected encephalitis?

A

Full neurological examination + A-E
Full set of obs
Bloods: cultures, viral PCR, FBC, U&E, LFT, glucose, ABG
Throat swabs / CXR
CT head with contrast- may show meningeal inflammation
LP: may show raised protein + lymphocytes, low glucose -> CSF send for viral PCR
EEG

117
Q

How should you manage encephalitis?

A

IV aciclovir ASAP- treat if suspicious, don’t wait for any viral PCR
May need I&V and ICU care
Symptomatic and supportive treatment

118
Q

What are differentials for encephalitis?

A 
Meningitis
Intracerebral abscess / SOL
Hypoglycaemia
Stroke
Metabolic encephalopathy: uraemia, hypercapnic, hepatic
Wernicke-Korsakoff
Alcohol withdrawal
119
Q

What are the features of epidural haematoma?

A

Biconcave lesion that will not cross suture lines
Caused by bleed of a meningeal artery- most commonly MMA after pterion fracture?
Patients often lose consciousness, come round and have a lucid period and then lose consciousness again due to raised ICP and brainstem compression

Signs: headache, vomiting, confusion, seizure
bradycardia with hypertension
ipsilateral pupil dilatation

120
Q

What are the features of subdural haematoma?

A

Crescent-shaped lesion beneath the dura which can cross sutural lines
Caused by rupture in the bridging veins -> increased risk in elderly fall and alcoholic/coagulopathy

Often presents with confusion, drowsiness, headache, unsteadiness
Also: vomiting, seizures, ICP signs

Can cause midline shift and tentorial herniation -> coning

Small ones often conservative watch/wait management

121
Q

What are the features of subarachnoid haemorrhage?

A

Bleeding from circle of willis
Usually due to berry aneurysms, AV malformation, trauma, severe HTN

Thunderclap occipital headache, reduced GCS, vomiting, meningism, seizures

May be visible on plain CT head
Xanthochromia on LP
CT angiogram can show source

122
Q

How are subarachnoid haemorrhages managed?

A

A-E
Keep SBP<160
Nimodipine prevents vasospasm
Endovascular clipping or coiling

123
Q

What are the complications of subarachnoid haemorrhage?

A

Rebleeding is the most common cause of death
Cerebral ischaemia due to vasospasm
Blocked venous sinuses -> hydrocephalus
Hyponatraemia due to SIADH

124
Q

What is the name of the aphasia where people make little sense?
What area of the brain is responsible for this?

A

Wernicke’s aphasia

Left superior temporal gyrus

125
Q

What is the name of the aphasia where people can’t form words properly?
What part of the brain is generally affected here?

A

Broca’s aphasia

Left inferior frontal gyrus.
It is typically supplied by the superior division of the left MCA.

126
Q

How would you manage a patient with suspected TIA?

A

300mg aspirin loading dose - continue 2-3 weeks
Referral to TIA clinic in 24 hours
Secondary prevention of stroke: clopidogrel, statin 80mg (after 2 weeks), HTN and DM management

127
Q

What is the most important thing to exclude before making a diagnosis of stroke?

A

Hypoglycaemia

128
Q

What is the management of confirmed Ischaemic stroke?

A
  1. Loading dose 300mg aspirin
  2. <4.5 hours: thrombolysis +/- thrombectomy if eligible

Continue 300mg aspirin + PPI for 2 weeks
75mg clopidogrel should be continued following this + 80mg atorvastatin
Manage HTN, DM and other risk factors

129
Q

How is stroke/TIA managed differently in people with AF?

A

After the 2 week interim period with aspirin, long-term anticoagulation should be initiated
EITHER
DOAC
Warfarin (INR target 2.5)

Anticoagulation should not routinely be prescribed in those in normal sinus rhythm

130
Q

How long after a TIA can you drive?

A

1 month

3 months if you have had multiple TIAs- aka must be 3 month TIA free

131
Q

What score can be used to identify stroke in ED?

A

ROSIER

Score >0 = increased risk of stroke

132
Q

What are the three features of total anterior circulation stroke?

A
  1. Hemiplegia
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction
133
Q

What are the features of partial anterior circulation stroke?

A

Any 2 of:

  1. Hemiplegia
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction
134
Q

What are the features of lacunar stroke?

A

Presents with 1 of:

  1. Unilateral weakness of face and arm, arm and leg or all 3
  2. Pure sensory stroke
  3. Ataxic hemiparesis
135
Q

What are the features of posterior circulation stroke?

A

Presents with 1 of:

  1. Cerebellar or brainstem syndromes
  2. Loss of consciousness
  3. Isolated homonymous hemianopia
136
Q

What are contraindications to thrombolysis?

A
  • Previous intracranial haemorrhage
  • Seizure at stroke onset
  • Intracranial neoplasm
  • Lumbar puncture in last 7 days
  • GI bleed in last 3 days
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120
  • Stroke or traumatic brain injury in the past 3 months

Finals Revision (23 decks)

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