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Scott's Notes > Neurology > Flashcards

Neurology Flashcards

1
Q

What does DANISH stand for?

A 
DANISH
Dysdiadokochinesia/Dysmetria
Ataxic gait
Nystagmus
Intention tremor
Slurred staccato speech
Hypotonia
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2
Q

What are some causes of cerebellar syndrome?

A 
DAISIES
Demyelination
Alcohol
Infarction
SOL
Inherited (wilsons, friedrichs)
Epilepsy medications (phenytoin)
Systemic: MSA
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3
Q

Cerebellar signs are ipsi or contralateral?

A

Ipsilateral

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4
Q

Lesion of the cerebellar vermis causes what picture?

A

Ataxic trunk and gait with normal arms

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5
Q

Cerebellar nystagmus versus vestibular nystagmus?

A

Cerebellar nystagmus: fast phase towards the lesion

Vestibular nystagmus: Fast phase away from the lesion

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6
Q

Hx questions for cerebellar syndrome?

A 
MS - parasthesia, visuals, weakness
Alcohol
Infarction (onset, RFs)
Schwannoma - hearing loss, tinnitus, vertigo
FH
DH
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7
Q

Ix for cerebellar syndrome?

A 
ECG - arrhythmia
Bloods - Etoh (FBC, U&E, LFT), thrombophilia (clotting), Wilsons (low caeruloplasmin)
CSF - oligoclonal bands
MRI 
Pure tone audiometry
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8
Q

Mx for cerebellar syndrome?

A

General: MDT, CV risk management, reduce ETOH
Specifics:
MS - methylpred
EtOH - Pabrinex, tapering chlordiazepoxide
Infarct - thrombolysis
Schwannoma - surgery
Wilson’s - penicillamine

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9
Q

What causes Lateral Medullary Syndrome (LMS)?

A

Vestibular artery or PICA occlusion

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10
Q

What are the signs of LMS?

A 
DANVAH
Dysphagia
Ataxia
Nystagmus
Vertigo
Anaesthesia
Horner's (miosis, ptosis, anhidrosis)
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11
Q

With which neurocutaneous syndrome are vestibular schwannomas associated

A

Neurofibromatosis type 2

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12
Q

How might a vestibular schwannoma present?

A

Unilateral SN hearing loss, tinnitus, vertigo
Headache (raised ICP)
Ipsilateral CN 5,6,7,8 palsies and cerebellar sign

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13
Q

What is the investigation of choice for vestibular schwannomas?

A

MRI of the cerebellopontine angle

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14
Q

Von Hippel-Lindau key points?

A 
Renal cysts
Bilateral RCC
Haemangioblastomas (cerebellar)
Phaeochromocytomas
Islet cell tumours
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15
Q

What are the main features of Friedrich’s ataxia?

A

Pes cavus
Bilateral cerebellar ataxia
Leg wasting with areflexia
Loss of vibration and proprioception

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16
Q

What are the features of Wilson’s disease?

A 
CLANK
Cornea - Kaiser Fleischer rings
Liver - CLD
Arthritis
Neuro - PD, ataxia, psych
Kidney - Fanconi's synd
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17
Q

What gaits would you see in patients with a) Unilateral UMN signs and b) Bilateral UMN signs?

A

a) Circumducting (ex>flex)

b) Scissoring

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18
Q

Causes of bilateral UMN signs (spastic paresis)

A

MS
Cord compression/trauma
Cerebral palsy

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19
Q

Causes of unilateral UMN signs?

A 
Stroke
MS
SOL
Cerebral palsy
Cord compression
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20
Q

Diagnosis if mixed UMN and LMN signs?

A

MND

Rarely: Friedrichs, Subacute combined degeneration of the cord (B12 deficiency)

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21
Q

Hx questions in UMN signs?

A

MS - tingling, eye probs, ataxia, other weakness
Cord compression - back pain, fever, weight loss
Trauma
FH

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22
Q

Ix in UMN signs

A

MRI - cord and brain
MS - LP
Compression - FBC (infection), CXR
SCDC - B12, pernicious anaemia antibodies

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23
Q

Mx for UMN signs?

A

Supportive - MDT, orthoses, mobility aids, baclofen for contractures

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24
Q

Differentials for bilateral, symmetrical, distal neuropathy?

A

Charcot Marie tooth
Paraneoplastic
GB syndrome

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25
Q

Proximal myopathy differentials?

A 
Inherited: Muscular dystrophy
Inflammation: Dermato/polymyositis
Endocrine: Cushings, acromegaly, thyrotoxicosis, osteomalacia
Drugs: EToH, statins, steroids
Malignancy: Paraneoplastic
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26
Q

Differentials for hand wasting?

A 
Syringomyelia
MND
Klumpke's
Charcot Marie Tooth
Diabetes
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27
Q

Stroke secondary prevention protocol?

A

Start atorvastatin after 48 hours
Asp 300 for 2 weeks
Clopi 75 or Asp 75 or ticagrelor 200 used for maintenance
Warfarin/DOAC if AF

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28
Q

What might you find on examination of a patient with diabetic neuropathy?

A

Inspection: Finger pricks, PVD, Charcot joints
Motor: Bilateral loss of ankle jerks, foot drop (mononeuritis multiplex)
Sensory - Stocking distribution

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29
Q

Ix for diabetic neuropathy?

A

Full exam - fundi, CN, upper limb
Urine - glucose, ACR
Blood - HbA1c, glucose, U&Es

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30
Q

Mx for diabetic neuropathy?

A

MDT, good glycaemic control, neuropathic pain management (amytryptilline, gabapentin, capcasin cream etc)

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31
Q

What might you find on examination of a patient with Charcot Marie Tooth (CMT) disease?

A

Insp - pes cavus, distal muscle wasting, thickened nerves
Motor - high stepping gait, weak dorsiflexion, absent ankle jerks
Sensory - stocking

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32
Q

Ix for CMT?

A

Nerve conduction studies

Genetic testing

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33
Q

Facial palsy syndromes accompanied by other CN involvement?

A

Pons -> Millard Gubler Syndrome (CN 6, 7, corticospinal tracts)
CPA (CN 5,6,7,8 + cerebellar signs)

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34
Q

Facial palsy differentials?

A 
75% idiopathic Bell's
Vascular
MS
SOL
CPA mass
Parotid tumour
Ramsay Hunt (zoster) /Cholesteatoma
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35
Q

Hx questions to ask in facial nerve palsy/

A

Sx: Eye dryness, drooling, hyperacusis, ageusia
Cause: Onset (rapid in bells), rash or ear pain, DM, SOL signs, vertigo, tinnitus, diplopia, weakness, fever

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36
Q

Ix for facial nerve palsy?

A 
Urine dip - glucose
Bloods - DM, VZV, Lyme, anti-ACh receptor antibodies
MRI of Posterior cranial fossa
LP
Audiometry
Nerve conduction studies
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37
Q

Mx of facial nerve palsies?

A

Prednisolone within 72 hours for 10 days + artificial tears and tape eyes closed at night
Valaciclovir if Ramsay Hunt suspected

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38
Q

What is a distinguishing feature of cholesteatoma?

A

Foul smelling white ear discharge

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39
Q

What else might you find on examination of a patient with facial anaesthesia?

A

Weak masseter and temporalis
Jaw jerk may be brisk (UMN) or absent (LMN)
Loss of corneal reflex (CN5)

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40
Q

What are some causes of facial anaesthesia?

A

Supranuclear, nuclear, peripheral

Supranuclear: Demyelination, Stroke, SOL
Nuclear: CPA lesion, LMS
Peripheral mononeuropathy: DM, sarcoid, vasculitis, cavernous sinus

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41
Q

What are the signs of Horner’s syndrome?

A 
PEAS
Ptosis
Enophthalmos
Anhydrosis
Small pupil
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42
Q

What are the differentials for Horner’s syndrome?

A

Central, pre-ganglionic, post-ganglionic

Central - MS, LMS
Pre-ganglionic - Pancoast’s tumour (T1), trauma (CVA insertion/endarterectomy)
Post-ganglionic - Cavernous sinus thrombosis

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43
Q

Causes of CN3 palsy?

A

Medical vs. Surgical

Medical: DM, MS, Weber’s syndrome (CN3 + Contralateral hemiplegia)
Surgical: Raised ICP (uncal herniation), cavernous sinus thrombosis, PICA (+pain)

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44
Q

What are the salient points and important causes regarding the Argyll Robertson pupil?

A

Small irregular pupils which accomodate but dont react to light
Causes: Quaternary syphillis, DM

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45
Q

Salient features and important causes of RAPD/Marcus Gunn pupil?

A

Minor constriction to direct light with dilatation on moving light from normal to abnormal eye.
Causes: MS, glaucoma

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46
Q

Difference in field defect between pituitary adenoma and craniopharyngioma?

A

Pit adenoma: superior quadrantopia

Craniopharyngioma: inferior quadrantopia

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47
Q

What might you find on examination of a patient with internuclear opthalmoplegia?

A

Failure of ipsilateral adduction
Nystagmus in contralateral abductin eye
Convergence preserved

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48
Q

What are some causes of internuclear opthalmoplegia?

A

MS (most common)
Infarction
Syringomyelia
Phenytoin toxicity

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49
Q

How would you interpret the results of Rinne’s test?

A

Positive (normal) = AC>BC

Negative = BC>AC, where true is conductive deafness and false is complete SNHL

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50
Q

How would you interpret the results of Weber’s test/

A

Central= normal

SNHL lateralises to normal ear

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51
Q

Interpret:
Weber - lateralises to the right
Rinne - positive bilaterally

A

Left sided sensorineural hearing loss

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52
Q

Interpret:
Weber - lateralises to the right
Rinne - negative on the right

A

Right sided conductive hearing loss

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53
Q

Interpret:
Weber - no lateralisation
Rinne - positive bilaterally

A

Normal OR bilateral sensorineural hearing loss

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54
Q

Interpret:
Weber - no lateralisation
Rinne - negative bilaterally

A

Symmetrical conductive hearing loss

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55
Q

What are some causes of a conductive hearing loss?

A

WIDENING

Wax/foreign body
Infection
Drum perforation
Extra (otosclerosis/trauma)
Neoplasia
INjury
Granuloma (sarcoid)
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56
Q

What are some causes of sensorineural hearing loss?

A

DDIVINITY

Developmnetal (Alports, TORCCH)
Degenerative - presbyacusis
Infection - VZV, measles, meningitis
Vascular - Stroke
Inflammation - Vascitis/Sarcoid
Neoplasia - CPA tumours
Injury
Toxins - Gent, Vanc, Furosemide, Aspirin
lYmph - Meniere's
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57
Q

Define the following terms:
Dysphonia
Dysarthria
Dysphasia

A

Dysphonia: Impaired sound production
Dysarthria: Impaired articulation of sounds into words
Dysphasia: Impairment of language

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58
Q

How do you test each of:
Dysphonia
Dysarthria
Dysphasia

A 
Dysphonia: Bovine cough, soft voice
Dysarthria: Yellow lorry, baby hippopotamus, the Leith police dismisses us
Dysphasia:
Name three objects - nominal
Three stage command - receptive 
Repeat back - conductive
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59
Q

What are the following tracts responsible and where do their fibres decussate?

a) Dorsal columns
b) Lateral spinothalamic
c) Lateral corticospinal

A

a) Fine touch, vibration, proprioception - Decussation in medulla
b) Pain and temperature - Decussation at entry level
c) Motor - Pyramidal decussation at ventral medulla

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60
Q

What is Beck’s syndrome?

A

Anterior spinal artery infarction affecting the ventral 2/3 of the cord, resulting in para/quadraparesis (depending on spinal level), impaired pain and temperature but touch and proprioception are preserved

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61
Q

Differentials for muscle weakness?

A

Work anatomically from brain to muscle

Brain - Vascular, MS, SOL, infection
Cord - Vascular, MS, trauma
Anterior horn - MND, polio
Roots - Spondylosis, cauda equina, carcinoma
Motor nerves - compression, GBS, CMT
NMJ - GBs, Myasthenia, botulism
Muscle - Steroids, poly/dermatomyositis, inherited musculodystrophies

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62
Q

Differentials for hand wasting?

A

Work anatomically from cord to muscle

Cord - MND, polio, syringomyelia
Roots (C8, T1) - compression
Brachial plexus - compression (cervical rib, Pancoast), klumpke’s palsy
Neuropathy- General (CMT), mononeuritis (DM), compressive
Muscle - RA (through disuse), myotonic dystrophy, cachexia

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63
Q

Differentials for gait disturbance?

A

Motor vs sensory

Motor
Basal ganglia - shuffling (Parkinsonism)
Bilat UMN - scissoring (cord comp/trauma or CP/MS cerebrally)
Unilat UMN - circumducting (CVA, MS, SOL)
Bilat LMN - (footdrop) (CMT, GBS, corda equina)
Unilat LMN - high stepping (common peroneal lesion, L5 root lesion, DM)
UMN + LMN =MAST (MND, ataxia (Friedrichs), SCDC, tabes dorsalis)

Sensory
Vestibular - Romberg +ve (Meniere’s, labyrinthitis, brainstem lesion)
Cerebellar - ataxic (EtOH, infarction)
Proprioceptive loss (B12 deficiency, peripheral neuropathy)
Visual loss

Other
Myopathy, MG/LEMS, postural hypotension, arthritis

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64
Q

What are the differentials for black out?

A

CRASH

Cardiac: Stokes Adams attack
Reflexes: Vagal - vasovagal, cough, micturation, effort etc. or Sympathetic underactivity (hypovolaemia, drugs, autonomic neuropathy, pooling)
Arterial: Vertebrobasilar insufficiency (CVA, TIA), shock, hypertension (phaeo)
Systemic: Metabolic (hypoglycaemia), resp (hypoxia/hypercapnia), blood (anaemia)
Head: Epilepsy, drop attacks

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65
Q

What is the definition of a postural drop?

A

Anything greater than 20/10 after 3 minutes

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66
Q

What investigations might you do after a collapse?

A

ECG (+24hr ECG/BP), bloods (UNE, FBC, glucose), tilt table, EEG, echo, CT

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67
Q

CRASH

C

Trigger, before, during, after, Ix

A 
Trigger - Exertion, drug
Before - palps, chest pain, dyspnoea
During - pale, slow/absent pulse, some clonic jerks
After - rapid recovery
Ix - ECG + 24hr ECG, Echo
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68
Q

CRASH

R

Trigger, before, during, after, Ix

A

Trigger - prolonged standing, heat, stress, fatigue
Before - gradual onset, nausea, pallor, sweating, CANNOT occur when lying down
During - pale, grey, clammy, clonic jerks and incontinence may occur but no tongue biting
After - rapid recovery
Ix - tilt table

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69
Q

CRASH

A

Trigger, before, during, after, Ix

A

Trigger - arm elevation, migraine, nothing
Before - gradual onset, nausea, pallor, sweating
During - pale, grey, clammy, clonic jerks and incontinence may occur but no tongue biting
After - rapid recovery
Ix - imaging

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70
Q

CRASH

S

Trigger, before, during, after, Ix

A 
Trigger - hypoglycaemia
Before - tremor, hunger, sweating, light headedness
During - as for vasovagal
After - as for vasovagal
Ix - BM
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71
Q

CRASH

H - epilepsy

Trigger, before, during, after, Ix

A

Trigger - flashing lights, fatigue, fasting
Before - aura, strange feeling deja vu, smells, lights, automatisms
During - tongue biting, incontinence, stiffness, jerking, eyes open, cyanosis, hypoxia
After - headache, confusion, drowsy
Ix - EEG, raised prolactin at 10-20 minutes

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72
Q

CRASH

H - drop attacks

Trigger, before, during, after, Ix

A

Trigger - nil
Before - no warning
During - sudden weakness of legs causes older woman to fall to ground
After - no post ictal phase

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73
Q

Differentials of vertigo?

A

IMBALANCE

Infection/injury - Ramsay hunt, labyrinthitis, trauma
Meniere’s - recurrent vertigo with fluctuating SNHL + tinnitus
BPV
Aminoglycosides/furosemide
Lymph
Arterial - migraine, CVA
Neoplasm - vestibular schwannoma
Central lesion - demyelination, tumour, infarct
Epilepsy - complex partial

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74
Q

What are the different types and causes of tremor?

A

RAPID

Resting: Abolished on movement, PD, Da agonists
Action/Postural: Worse on movement, causes inc BET, endocrine, ETOH withdrawal, beta-agonists, anxiety
Intention: Irregular, past pointing, cerebellar damage
Dystonic: mostly idiopathic

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75
Q

What would you give to treat acute dystonia?

A

Procyclidine (antimuscarinic)

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76
Q

What are some reversible causes of dementia?

A 
Infective (HSV, cysticercosis)
Vascular (chronic subdural)
Inflamm (SLE, sarcoid)
Neoplasia
Nutritional (thiamine, B12/fol, B3)
Hypothyroid
Hypoadrenal
Hypercalcaemia
Normal pressure hydrocephalus
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77
Q

What are the differentials for delirium?

A

DELiRIUMS

Drugs: opioids, sedatives, ldopa
Eyes, ears, etc
Low O2 states (MI, CVA, PE)
Infection
Retention
Ictal
Under hydration/nutrition
Metabolic (DM, post op, sodium, uraemia)
Subdural haemorrhage
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78
Q

What investigations would you do for delerium?

A

Bloods: FBC, LFT, U&E, CRP, glucose, ABG
ECG
Urine dip
Septic screen

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79
Q

Acute headache differentials?

A

VICIOUS

Vascular - haemorrhage, infarction, venous (sinous thrombosis)
Infection - Men/enceph/abscess
Compression - Tumour, pituitary
ICP - Spontaneous intracranial hypotension (worse on standing)
Ophthalmic - Acute glaucoma
Unknown
Systemic - HTN, infection (sinusitis), toxins

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80
Q

Chronic headache differentials?

A

MCD TINGS

Migraine
Cluster headaches
Drugs - analgesia, caffeine

Tension Headaches
ICP
Neuralgia (trigeminal)
Giant cell arteritis
Systemic (HTN, uraemia)
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81
Q

What are the features of venous sinus thrombosis?

A

Headache, vomiting, seizures, vision impairment, papilloedema

82
Q

What is the acute and prophylactic management of cluster headaches?

A

Acute: 100% O2 + sumatriptan
Prophylaxis: Verapamil, topiramate

83
Q

What are the signs and management of temporal arteritis?

A

Unilateral scalp pain/tenderness with thickened, pulseless temporal artery. May also have jaw claudication, amaurosis fugax. Raised ESR.

Management is with 60mg PO pred for 5-7 days guided by symptoms and ESR. Also give PPI with bisphosphonate

84
Q

What is the acute and prophylactic management of migraines?

A 
Acute: 
1st - Paracetamol + metoclopramide
2nd - NSAID + metoclopramide
3rd - Rizatriptan (CI in IHD and with SSRIs)
4th - Ergotamine (5-HT1b block)

Prophylaxis:
1st - Avoid triggers
2nd - Propranolol, topiramate
3rd - valproate, gabapentin

85
Q

What are Berry aneurysms associated with, and what type of haemorrhage do they cause when they rupture?

A

PKD, CoA, Ehlers Danlos

Subarachnoid

86
Q

What investigations would you do to diagnose a SAH?

A

CT - detects 90% in first 48hrs

LP - Xanthochromia

87
Q

What is the management of a SAH?

A

Frequent neuro obs
Maintain SBP > 160
Nimodipine for 3 weeks to reduce cerebral vasospasm
Endovascular coiling

88
Q

What are the complications of a SAH?

A

Rebleeding - 20%
Cerebral ischaemia
Hydrocephalus (arachnoid granulation blockage)
Hyponatraemia - common

89
Q

What is the Miller Fischer variant of GB syndrome?

A

Opthalmoplegia + ataxia + areflexia

90
Q

What are some common infective causes of GB syndrome?

A

Campylobacter, mycoplasma, CMB, EBV, vaccines

91
Q

What are the salient features of GB syndrome?

A 
SYMMETRICAL, ascending flaccid weakness with lower motor neuron signs.
Proximal > distal
Breathing and bulbar problems
Back pain is common
Parasthesia in extremities
Autonomic neuropathy
92
Q

What is the management of GB syndrome?

A

Supportive: Airway, analgesia, autonomic (inotropes/catheter), antithrombotic
Immunosuppression: Plasmapheresis and IVIG
Physiotherapy to prevent contractures

93
Q

What is the prognosis of GB syndrome?

A

85% make a complete recovery

94
Q

What are the clinical features of Charcot Marie Tooth disease?

A

Nerves: Thickened, enlarged
Motor: Foot drop, weak dorsiflexion, absent ankle jerks, symmetrical distal muscle atrophy, pes cavus
Sensory: Stocking loss, some experience neuropathic pain

95
Q

What are the salient points regarding polio?

A

RNA virus affecting anterior horn cells causing fever sore throat and myalgia.
0.1% develop paralytic polio characterised by:
Asymmetric LMN paralysis with NO sensory involvement

96
Q

What are the clinical features of myasthenia gravis?

A

Increasing muscle fatigue (ptosis, diplopia, voice softening, myasthenic smile, head droop, foot drop)
Normal tendon reflexes

97
Q

What investigations would you do if myasthenia is suspected?

A

(Tensilon test - edrophonium IC should improve power) Still done?
Anti-AChR Abs in 90%
EMG - reduced response to a train of impulses
Reduced FVC
TFTs

98
Q

What is the management of myasthenia?

A

Symptom control - Pyrostigmine
Immunosuppression - pred if relapse
Thymectomy - in young people

99
Q

What should be done in the event of a myasthenic crisis?

A

Plasmapheresis and IVIg

Monitor FVC and provide support if <20

100
Q

What antibodies are characteristic of myasthenia and Lambert Eaton syndrome?

A

Myasthenia - anti nAChR

LEMS - anti VGCaC

101
Q

What are the salient features of botulism?

A

Toxin which prevents ACh vesicle release
Sescending flaccid paralysis with no sensory change
Rx - BenPen and antiserum

102
Q

Describe Brown-Sequard syndrome

A

Hemisection of the spinal cord resulting in ipsilateral UMN signs, fine touch and proprioceptive loss with contralateral loss of pain and temperature sensation

103
Q

What is the strongest risk factor for an acute ischaemic stroke?

A

Hypertension

104
Q

What are the features of a total anterior circulation stroke?

A

ALL 3 of the following:

  1. Contralateral hemiplegia/paralysis
  2. Contralateral homonymous hemianopia
  3. Executive dysfunction (dominant= dysphasia, non-dominant= hemispatial neglect)
105
Q

What are the features of a partial anterior circulation stroke?

A

Two of the 3 TACS criteria

106
Q

What are the features of a posterior circulation stroke?

A

Any of the following:

  1. Ipsilateral cerebellar signs
  2. Contralateral homonymous hemianopia
  3. Brainstem syndrome
107
Q

What are the features of a lacunar infarct?

A

Crucially, there is absence of cortical dysfunction, visual dysfunction, drowsiness or brainstem signs.

There may be one of 5 syndromes:

  1. Pure motor (commonest)
  2. Pure sensory
  3. Mixed sensorimotor
  4. Dysarthria
  5. Ataxic hemiparesis
108
Q

What are the features of a brainstem infarction, and what structures do they correlate to?

A 
Hemi-quadriparesis - corticospinal tracts
Conjugate gaze palsy - CN3
Horner's syndrome - sympathetic trunk
Facial weakness - CN7
Nystagmus, vertigo - CN8
Dysphagia/dysarthria - CN9+10
Dysarthria/ataxia - Cerebellum
Reduced GCS - RAS
109
Q

What are some alternative differentials for strokes?

A 
Head injury +- haemorrhage
Abnormal glucose control
SOL
Hemiplegic migraine
Encephalitis
Opiate overdose
110
Q

What is the acute NON-medical management of stroke?

A 
ABCDE approach
Plce NBM
Maintain glucose between 4-11
Keep BP below 185/110 (caution)
Frequent neuro obs
Urgent CT/MRI (DW if poss)
111
Q

What is the acute medical management of acute ischaemic stroke?

A

If CT confirms ischaemic stroke and within 4.5 hrs of symptom onset, perform thrombolysis with alteplase
Also give 300mg aspirin + PPI

112
Q

What is the secondary prevention protocol following an acute ischaemic stroke?

A

Start statin after 48 hours
Ssp/clopi 300mg for 2 weeks followed by
1st line; Clopi 75
2nd line; Asp 75 + ticagrelor 200mg BD
Use Warfarin instead if cardioembolic stroke, or patient has chronic AF
Consider carotid endarterectomy if good recovery and ipsilateral stenosis >70%

113
Q

What is involved in stroke rehabilitation?

A

MENDS

MDT - physio, SALT, dietician, OT, spec nurses, neurologist, family
Eating - regular screening swallows, screen for malnutrition
Neurorehab - physio and speech therapy
DVT prophylaxis
Sores - avoid avoid avoid

114
Q

What investigations would you do following a suspected TIA?

A 
Bloods - FBC, U&amp;E, LFT, BM, ESR, lipids
CXR
ECG
Echo
?Brain imaging
Carotid doppler +_ angiography
115
Q

What is the management plan following a TIA?

A
  1. Anticoagulate - same protocol as for stoke
  2. Cardiac RF control - BP, lipids, DM, smoking, exercise, reduce salt intake
  3. ABCD2 to assess risk of subsequent stroke
116
Q

What is the ABCD2 score and when is it used?

A

Used to predict risk of subsequent stroke following a TIA
Age>60
BP>140/90
Clinical Fx (unilateral weakness or speech disturbance)
Duration (>1hr scores 2 points, 10mins-59 mins scores 1)
Diabetes

117
Q

Which vessels are affected in a subdural haemorrhage?

A

Bridging veins between the cortex and venous sinuses

118
Q

What is the management approach to an extradural haematoma?

A
  1. Provide neuroprotective ventilation (100% O2 aiming for CO2 3.5-4)
  2. Consider mannitol 1g/kg IV
  3. Craniectomy
119
Q

How might a venous sinus thrombosis present?

A

Insidiously over days-weeks, with signs of raised ICP, and proptosis/eyelid oedema/opthalmoplegia in the case of cavernous sinus thrombosis

120
Q

How might a cortical vein thrombosis present?

A

Over days, typically with stroke like focal symptoms. May also have thunderclap headache and focal seizures

121
Q

What are some causes of intracranial venous thrombosis?

A 
Pregnancy
COCP
Trauma
Dehydration
Malignancy
Thrombophilia
122
Q

What are Kernig’s and Brudzinski’s signs in the context of meningitis?

A

Kernigs - pain on hip flexion

Brudzinskis - neck flexion instigates lifting of legs

123
Q

What is the antibiotic management of bacterial meningitis?

A

Community - 1.2g BenPen IM
If <50 - Ceftriaxone 2g IM/IV BD
If >50, add ampicillin
If ?viral -> aciclovir

124
Q

How might an encephalitis present?

A

Infectious prodrome followed by bizarre behaviour, confusion, reduced GCS, headache, focal signs, seizures etc

125
Q

What investigations would you do for a suspected encephalitis?

A

Bloods - FBC, cultures, viral PCR, malaria film
Contrast CT - bilateral temporal lobe involvement suggests HSV
LP - Raised protein, lymphocytes
EEG

126
Q

What is the management of encephalitis?

A

Aciclovir infusion stat
Supportive measures in HDU
Phenytoin for seizures

127
Q

What are some predisposing factors for a cerebral abscess?

A 
Prev infection
Skull fracture
Congenital heart disease
Endocarditis
Bronchiectasis
Immunosuppression
128
Q

What are some causes of epilepsy?

A

2/3 are idiopathic
Congenital - NF, TS, CP
Acquired - Infection, vascular, trauma, SOL, MS, sarcoid
Non-epileptic - withdrawal, metabolic, raised ICP, infection, eclampsia, pseudoseizures

129
Q

What do the terms simple and complex refer to regarding seizures?

A 
Simple = awareness unimpaired
Complex = awareness impaired
130
Q

What are the 5As of complex partial seizures?

A 
Aura
Autonomic 
Awareness lost
Automatisms
Amnesia
131
Q

What are the features of a petit mal seizure?

A

ABSENCES

ABrupt onset
Short - <10s
Eyes - glazed
Normal - investigations
Clonus/automatisms
EEG - 3Hx spike and wave
Stimulated by hyperventilation
132
Q

What are some localising features to seizures arising from each of the cortical lobes?

A

Temporal - automatisms, deja vu, delusions, hallucinations
Frontal - motor Fx (Jacksonian march, arrest, Todd’s palsy)
Occipital - Visual phenomena
Parietal - numbness, parasthesia

133
Q

What investigations might you do following an unprovoked seizure?

A 
Bloods - FBC, UnE, glucose, prolactin (raised @10-20 mins if true seizure), AED levels
Urine - toxicology
ECG
EEG - supportive not definitive
MRI - not routine
134
Q

What are first and second line drug managements for the following types of epilepsy?

  1. Tonic clonic
  2. Absence
  3. Tonic/atonic/myoclonic
  4. Focal +-2 gen
A
  1. Valproate ->Lamotrigine
  2. Valproate/Ethosuximide -> Lamotrigine
  3. Valproate -> Levetiracetam
  4. Lamotrigine -> Carbamazepine
135
Q

What AEDs may be used in pregnancy?

A

Lamotrigine or carbamazepine

5mg Folic acid

136
Q

What are 3 side effects of lamotrigine?

A

Skin rash ->SJS
Hypersensitivity reaction
Diplopia

137
Q

What are the side effects of valproate?

A

ALPROATTTE

Appetite increase
Liver failure
Pancreatitis
Reversible hair loss
Oedema
Ataxia
Tremor, Teratogenicity, Thrombocytopaenia
Encephalopathy
138
Q

Wha are 3 side effects of carbamazepine?

A

Aplastic anaemia
Skin reactions
SIADH ->hyponatraemia

139
Q

What are 4 side effects of phenytoin?

A

Gingival hypertrophy
Hirsutism
Cerebellar syndrome
Peripheral sensory neuropathy

140
Q

What is the first thing to do in status epilepticus?

A

Check BMs

141
Q

What is the immediate management following head injury?

A 
A-E approach
Look for lacerations, fractures, CSF leak, signs of skull base fracture, blood behind TM
C-spine tenderness
Head to to examination
Log roll
142
Q

What are the indications for CT head in the context of head trauma?

A

BANGS LOC

Break in bone
Amnesia >30 mins
Neuro deficit/seizure
GCS <13 @any time or <15 2 hours after event
Sickness - more than one vomit
LOC
143
Q

What are the two ways in which IIH may present?

A

As a SOL

Visual - blurring, CN6 palsy, enlarged blind spot

144
Q

What is the management of IIH?

A 
Weight loss number 1
Acetazolamide
Loop diuretics
Prednisolone
LP shunt if necessary
145
Q

What is the acute management of raised ICP?

A 
A-E approach
Treat seizures and correct hypotension
Elevate bed to 40 deg
Neuropreotective ventilation
Mannitol or hypertonic saline
146
Q

How might each of the types of brain herniation present?

A

Tonsillar - CN6 palsy, UMN signs, apnoea
Transtentorial/uncal - CN3 palsy, contralateral hemiparesis
Subfalcine - May compress ACA causing a stroke

147
Q

What are the characteristic features of each of the Parkinsons- plus syndromes?

A

PSP - Postural instability, Speech disturbance, Palsy of vertical gaze

CBD - Aphasia, akinetic rigidity, dysarthria, apraxia

MSA - Autonomic dysfunction, cerebellar signs

LBD - Fluctuating cognition, visual hallucinations

148
Q

What are some other causes of parkinsonism?

A 
Dementia pugilistica
Infection: Syphillis, HIV, CJD
Vascular infracrtions
Antipsychotics, metoclopramide
Wilson's disease
149
Q

What are the features of Parkinson’s disease

A

TRAPPS PD

Tremor
Rigidity
Akinesia
Postural instability
Postural hypotension
Sleep disorders
Psychosis
Depression/Dementia
150
Q

What are the side effects of L-DOPA?

A

DOPAMINE

Dyskinesia
On-off effect
Psychosis
Arterial BP decrease
Mouth dryness
Insomnia
Nausea
Excessive daytime somnolescence
151
Q

What is the management of Parkinson’s disease?

A

If biologically fit:

  1. Da agonists e.g. ropinirole
  2. MOA-B inhibitors e.g. rasagiline, selegiline
  3. L-DOPA - co-careldopa

If biologically frail:

  1. L-DOPA
  2. MOA-B inhibitors

Other therapies
COMT inhibitors reduce end dose effect - e.g. Entacapone
Apomorphine is a potent Da agonist
Amantidine is useful for iatrogenic dyskinesias
Atypical antipsychotics where relevant
SSRIs

152
Q

What is Lhermitte’s sign and when is it seen?

A

Neck flexion causing shooting pains in trunk/limbs in MS patients

153
Q

What is the acute management of an MS attack?

A

Methylpred 1g for 3 days

154
Q

What is the role of steroids in the management of MS?

A

Used in acute scenarios to speed recovery but not alter the extent of recovery

155
Q

What is the longterm prophylactic management of MS?

A

IFN-beta - reduce relapse freq
Glatiramer - as above
Natilzumab - as above
Alemtuzumab

156
Q

What are some good prognostic signs in MS?

A 
Female
Under 25 yo
Sensory signs at onset
Long interval between relapses
Fewer MRI lesions
157
Q

What are the clinical features of cord compression?

A

Deep local spinal pain in dermatomal distribution
Sensory, reflex and motor level with progressing weakness and sensory loss
Painless urinary retention
Faecal incontinence

158
Q

What are the causes of cord compression?

A

Trauma
Infection
Malignancy (mostly mets)
Disc herniation

159
Q

What is the management of acute cord compression?

A

Neurosurgical emergency
For malignancy give dexamethasone IV and consider laminectomy
For abscess give Abx and surgical decompression

160
Q

What are the signs of conus medullaris lesions?

A

Early constipation and retention
Mixed UMN/LMN weakness
Back pain

161
Q

What are the signs of cauda equina syndrome?

A 
Saddle anaesthesia
Back pain
Poor anal tone
Radicular pain down legs
Bilateral Flaccid, Areflexic lower limb weakness
Incontinence
162
Q

What are some causes of spondylosis?

A

Trauma
Ageing
Disc/Vertebral collapse
Osteophytes

163
Q

How might a cervical spondylosis present?

A

Mostly asymptomatic
Neck stiffness
Arm pain with motor and sensory disturbances
Lhermitte’s sign
Hoffman’s sign (flicking middle finger pulp causes pincer grip response)

164
Q

What deficits are seen in a C5 root lesion?

A

Motor: Deltoid and supraspinatus weakness
Sensory: Numb elbow

165
Q

What deficits are seen in a C6 root lesion?

A

Motor: Biceps and brachioradialis weakness, with reduced biceps reflex
Sensory: Numb thumb and index finger

166
Q

What deficits are seen in a C7 root lesion?

A

Motor: Triceps and finger extension weakness with reduced triceps reflex
Sensory: Numb middle finger

167
Q

What deficits are seen in a C8 root lesion?

A

Motor: weak finger flexors and intrinsic hand muscles
Sensory: Numb little and ring fingers

168
Q

What is the management of cervical spondylosis?

A

Conservative: Collar, analgesia
Medica: Steroids
Surgical: Decompressive laminectomy

169
Q

How might lumbosacral spondylosis present? and which nerve roots are affected most commonly?

A

L5 and S1 most commonly affected

Presents with severe lower back pain +- sciatic pain, limited spinal flexion

170
Q

What deficits are seen in L5 root lesion?

A

Weak hallux plantarflexion +- foot drop, reduced sensation over dorsum of foot

171
Q

What deficits are seen in S1 root lesion?

A

Weak foot plantarflexion and eversion, loss of ankle jerk, calf pain, loss of sensation over sole of foot and back of calf

172
Q

How might spinal stenosis present?

A

Spinal claudication: Aching on walking, rapid onset, +-parasthesia
Pain alleviated on leaning forward

173
Q

What are some causes of mononeuritis multiplex (2 ore more peripheral nerves affected)

A

Diabetes
Amyloid
Rheumatoid
Sarcoid

174
Q

What are the features of NF 1?

A

CAFE NOIR

Cafe au lait spots (>6 in adults)
Axillary freckling
Fibromata (subcut - may compress local structures)
Eye - Lisch nodules are brown hamartomas of the iris
Neoplasia - various inc. CNS and phaeos
Ortho - kyphoscoliosis
IQ reduction
Renal - RAS dysfunction ->HTN
175
Q

What are the features of NF 2?

A

Cafe au lait spots
Bilateral ventricular schwannomas
Bilateral cataracts

176
Q

What is the mean survival of NF2?

A

15 years from diagnosis

177
Q

What are the causes of intrinsic cord disease?

A

DIVINITY

Degenerative - MND
Developmental - Friedrich's
Infection - HIV, Syphillis
Vascular infarction
Inflammation - MS, transverse myelitis
Neoplasia
Injury
Toxin - B12 def
sYringomyelia!!!
178
Q

What is the clinical history (symptom progression) of syringomyelia?

A

May be stable for years then worsen suddenly e.g. on coughing as pressure increase leads to lesion extension

179
Q

What are the major causes of syringomyelia?

A

Arnold- Chiari malformation
Masses (these two block CSF flow)
Spina bifida
secondary causes

180
Q

What are the cardinal signs of syringomyelia?

A
  1. Sensory loss: absent pain and temperature but preserved touch, proprioception and vibration as ventral tracts are affected. CAPE distribution
  2. Wasting of hands (claw)
  3. Loss of upper limb reflexes
  4. Charcot joints in shoulder and elbow
181
Q

What are the features of a median nerve (C6-T1) palsy?

A

Motor: LOAF muscle weakness and thenar wasting
Sensory: Radial 3.5 fingers and palm sensory loss, pain, imp proprioception, Tinels and Phalens positive

182
Q

What are the features of an ulnar nerve (C7-T1) palsy?

A

Motor: Partial claw, hypothenar wasting
Sensory: Ulnar 1.5 fingers sensory loss

183
Q

What are the features of a radial nerve (C5-T1) palsy?

A

Motor: Finger/wrist drop
Sensory: Snuff box sensory loss

184
Q

What are the features of a phrenic nerve (C3-C5) palsy?

A

Orthopnoea and raised hemidiaphriagm

185
Q

What are some causes of polyneuropathy?

A

Metabolic: DM, renal, B12, hypothyroid
Inflammation: GB synd, sarcoid
Vasculitis: RA, Wegener’s
Drugs: Isoniazid, EtOH, Phenytoin

186
Q

How would you investigate a polyneuropathy?

A

Bloods - FBC, LFT, UnE, B12, BM, Ca, ANA/ANCA, TFT, ESR
Nerve conduction studies
EMG

187
Q

What are the main causes of sensory neuropathy?

A

ABCDE

Alcohol
B12
CKD
DM
Every vasculitis
188
Q

What are the main causes of motor neuropathy?

A

GB syndrome
CMT
Paraneoplastic
Lead

189
Q

What are the main causes of autonomic neuropathy?

A 
DM
HIV
SLE
GBS
LEMS
190
Q

What are some features of autonomic neuropathy?

A 
Postural hypotension
ED
Reduced sweating
Constipation and urinary retention
Horners
191
Q

What are three cardinal negative features of MND

A

Never any sensory loss
Never any sphincter involvement
Never affects eye movement

192
Q

How would you investigate potential MND?

A

Brain/cord MRI and LP - both for exclusion

EMG shows denervation

193
Q

What is the picture of MND?

A

Mixed UMN and LMN signs
Speech or swallowing impairment
FTD

194
Q

What are the management options for MND?

A

Riluzole - prolongs life by 3

Supportive measures: Drooling, dysphagia, resp failure, pain, spasticity Rx

195
Q

What are the 4 types of MND and a distinguishing feature of each one

A

ALS - commonest
Bulbar palsy - most severe
PMA - LMN signs only
PLS - Mainly UMN signs

196
Q

What is the difference between bulbar and pseudobulbar palsy in terms of its presentation?

A

Bulbar = LMN so flaccid fasciculating tongue, quiet speech, reduced jaw jerk

Pseudobulbar = UMN so spastic tongue, hot potato speech, brisk jaw reflex

197
Q

How would you distinguish between a myopathy and a motor neuropathy?

A

Myopathy is slower onset and causes proximal rather than distal weakness. Dystrophies also tend to affect specific muscle groups and have preserved tendon reflexes

198
Q

How would you investigate a ?myopathy?

A 
ESR
CK
AST
LDH
EMG
199
Q

What are the features (and findings) of Duchenne’s?

A

Presents early (~4), Gower’s sign, calf pseudohypertrophy, respiratory failure

Ix: V raised CK

200
Q

How does Becker’s compare with Duchenne’s?

A

Presents later and is less severe

Scott's Notes (21 decks)

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