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Neurology Flashcards

1
Q

Causes of blackouts - 7

A

Vasovagal (neurocardiogenic) syncope
Situational syncope ie cough or micturition
Carotid sinus syncope
Epilepsy
Stokes-Adams sacks - transient arrhythmia
Hypoglycaemia
Orthostatic hypotension

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2
Q

What is vasovagal syncope, onset and what happens during

A

Reflex bradycardia with or without peripheral vasodilation provoked by emotion, pain, fear, standing
Onset over seconds, preceded by nausea, pallor, sweating, closing in of visual fields
Unconscious for around 2 mins, may have brief clonic jerking of limbs (reflex anoxic)
May have urinary incontinence
Post ictal recovery rapid

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3
Q

Differentiate reflex anoxic jerks in vasovagal from epilepsy - 4

A

No stiffening
No tonic - clonic sequence
No tongue biting
Rapid post-ictal recovery

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4
Q

What is situation syncope

A

Sx same as vasovagal - preceding nausea, pallor, sweating, unconscious +- reflex anoxic myoclonic jerks, urinary incontinence
Caused by cough, effort (exercise, from cardiac origin ie aortic stenosis) or micturition (mostly men at night)

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5
Q

What is carotid sinus syncope

A

Hypersensitive baroreceptors cause excessive reflex bradycardia +- vasodilatation on minimal stimulation eg head turning

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6
Q

Features of LOC suggestive of epilepsy - 8

A 
When asleep or lying down
Aura
Identifiable trigger
Altered breathing, cyanosis 
Tonic-clonic movements
Tongue biting
Urinary incontinencce
Prolonged post-ictal drowsiness, confusion, amnesia and transient focal paralysis
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7
Q

What is syncope related to arrhythmia and features, and how often?

A

Stokes-Adams attacks - transient arrhythmia eg bradycardia from complete heart block, reduces CO and causes LOC
Often with no warning except palpitations
Pale, slow/absent pulse
Recovery within seconds, with flushing, pulse speeding up and consciousness returns
Can be several times a day and in any posture

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8
Q

What is a cause of sudden fall with no LOC in the elderly - 3

A

Drop attacks - sudden weakness in legs, generally older women
Benign and spontaneously resolves after a few attacks
Cataplexy - triggered by emotion
Hydrocephalus - may not be able to get up for hours

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9
Q

What makes orthostatic hypertension more likely? - 4

A 
Inadequate vasomotor reflexes:
Elderly
Autonomic neuropathy
Antihypertensives, overdiuresis
Multi system atrophy
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10
Q

Features of anxiety attack - 7

A 
Hyperventilation
Tremor
Sweating
Tachycardia
Paraesthesia
Light headed ness
No LOC
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11
Q

What exams to do for LOC - 3

A

Cardiovascular
Neurological
BP standing and lying

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12
Q

Investigation for LOC

A 
ECG +-24h for arrhythmia, long qt; echo
UE, FBC, glucose
Tilt table test
EEG, sleep eeg
CT/MRI brain
PaCO2 - low = hyperventilation
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13
Q

What is vertigo?

A

Illusion of movement, often rotator, of patient or surroundings
Always worsened by movement

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14
Q

Associated sx with vertigo - 4

A

Difficulty walking or standing
Relief on sitting still or lying
NV, pallor, sweating
Hearing loss or tinnitus = labyrinth or CN8 involvement

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15
Q

Anatomical locations of causes of vertigo - 4 most common

A

Labyrinth
Vestibular nerve
Vestibular nuclei
Central connections

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16
Q

7 common causes of vertigo

A
  1. Benign paroxysmal vertigo due to canalolithiasis
  2. Acute labyrinthitis/vestibular neuronitis
  3. Ménière’s disease
  4. Ototoxicity - aminoglycosides, loop diuretics, cisplatin - also dizziness
  5. Vestibular schwannoma (also known as acoustic neuroma incorrectly)
  6. Traumatic damage of patrons temporal bone or cerebello-pontine angle affecting auditory nerve
  7. Herpes zoster - eruption of external auditory meatus
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17
Q

Features of BPV and treatment

A

Canalolithiasis - debris in semicircular canal disturbed by head movement, resettles causing vertigo for a few seconds after movement
Nystagmus on performing Hallpike manoeuvre = diagnostic
Cleared by Epley manoeuvre

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18
Q

What is acute labyrinthitis and features

A

Abrupt onset of severe vertigo, NV +- prostration
No deafness or tinnitus
Caused by virus or vascular lesion
Severe vertigo subsides in days, complete recovery in 3-4w
Treat = reassure, sedate

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19
Q

What is Ménière’s disease, 3 features and treatment

A

Endolymphatic hydrops causing 1. recurrent attacks of vertigo lasting >20m +- nausea, 2. fluctuating sensorineural hearing loss (may be permanent), 3. Tinnitus with sense or aural fullness
Treat with bed rest and reassurance, and antihistamine if prolonged

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20
Q

What causes ototoxicity

A

Aminoglycosides
Loop diuretics
Cisplatin

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21
Q

Features of vestibular schwannoma

A 
Unilateral hearing loss
Vertigo occurs later
Progresses to affect ipsilateral CN5, 6, 9, 10 and ipsilateral cerebellar signs
Late = signs of RICP
A type of cerebello-pontine angle tumour
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22
Q

How does traumatic damage cause vertigo

A

To petrous temporal bone or cerebello-pontine angle, affects auditory nerve, causing vertigo, deafness, tinnitus

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23
Q

What infection can cause vertigo and what else does it cause?

A

Herpes zoster - herpetic eruption of external auditory meatus, causes facial palsy +- deafness, tinnitus, vertigo = Ramsay Hunt syndrome

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24
Q

What causes related to the brain stem, cerebellum and cerebello-pontine angle can cause vertigo and what other sx are there

A 
Also nystagmus and CN lesions
MS
Stroke/TIA
Haemorrhage
Migraine
Vestibular schwannoma
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25
Q

Management and progress of vestibular schwannoma

A

Serial MRIs for a few years to predict growth
30% don’t progress, 50% grow slowly and 20% grow quickly
Malignancy rare
Microsurgical removal can cause damage to CN7

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26
Q

Causes of conductive deafness and finding on tuning fork test

A

Wax, otosclerosis, otitis media or glue ear
Weber - localises to ear with conductive loss
Rinne = negative = bone conduction louder than air conduction

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27
Q

Causes of sensorineural deafness - 3 chronic 8 acute

A 
Chronic 
- accumulated environmental noise toxicity
- presbyacusis (loss of higher frequency sounds from age 30)
- inherited disorders 
Acute
- V vasculitis
- V stroke
- I mumps
- I TB
- T noise exposure
- A MS
- I toxin eg gentamicin
- N acoustic neuroma
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28
Q

Tests for sudden sensorineural deafness

A 
ESR, FBC, LFT
Viral titres and TB
Evoked response audiometry
CXR
MRI
Lymph node and nasopharyngeal biopsy for malignancy and TB culture
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29
Q

Result of tuning fork tests for sensorineural hearing loss

A

Tuning fork = 512hz
SNAC-RIP
Sensorineural loss and Normal ears, Air Conduction better - Rinne Is Positive
Weber localises sound to contralateral ear from affected ear in sensorineural loss

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30
Q

Causes of tinnitus

A

Focal hyper-excitability in auditory cortex
Viral
Presbyacusis, Meniere’s, hearing loss
Excess noise, wax
Head injury
Septic otitis media
Hypertension
Drugs - aspirin, loop diuretic, aminoglycosides
Psychological - diverse
Pulsatile = carotid artery stenosis or dissection, AV fistulae

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31
Q

Investigate tinnitus

A

Pulsatile may be audible with stethoscope
MRI
If unilateral, exclude vestibular schwannoma

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32
Q

Complications of tinnitus

A

Depression, insomnia

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33
Q

Manage tinnitus

A

Psychological support, reassure
Hypnotics at night
White noise through noise generator like a hearing aid
Cochlear nerve section if disabling - causes deafness
Repetitive transcranial magnetic stimulation of auditory cortex

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34
Q

Key questions for weak legs - 6

A
  1. Onset gradual or sudden
  2. Progressing at what rate
  3. Spastic or flaccid legs
  4. Sensory loss. Level = spinal cord disease
  5. Loss of sphincter control
  6. Signs of infection - spinal tenderness, raised WCC, eg extradural abscess
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35
Q

Sx in progressive weakness

A

Spinal or root pain first
Then leg weakness and sensory loss
- arm weakness is less severe as suggests cervical cord lesion
Bladder sphincter involvement is late = hesitancy, frequency then painless retention (neurogenic)
Signs:
- motor, reflex and sensory level - normal above, LMN signs at level, UMN signs below level
- tone and reflexes are usually reduced in acute cord compression

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36
Q

Causes of progressive weakness due to cord compression - 7

A

Most common = secondary malignancy - breast, lung, prostate, thyroid, kidney - in spine
Infection - epidural abscess
Cervical disc prolapse, atlanto-axial subluxation
Haematoma (warfarin)
Intrinsic cord tumour, myeloma

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37
Q

Differentials for progressive weakness (not due to cord compression)

A

Transverse myelitis
MS, Guillaun-Barre
Spinal artery thrombosis, dissecting aneurysm
Trauma

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38
Q

Investigations for cord compression

A

MRI sine
Biopsy or surgical exploration to investigate mass
CXR for primary lung malignancy, secondaries or TB
Screening bloods - FBC, ESR, B12, LFTs, syphilis, UE, PSA
Serum electrophoresis

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39
Q

treatment cord compression

A

Dexamethasone IV 4mg/6h if malignancy then consider C/RT, decompressive laminectomy
Surgical decompression and abx if epidural abscess

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40
Q

Main difference in sx of cauda equina/conus medullary lesions and higher up lesions

A

Leg weakness is flaccid and areflexic instead of spastic and hyperreflexic

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41
Q

Clinical features of conus medullary lesions

A

Mixed UMN/LMN leg weakness
Early urinary retention and constipation
Back pain and sacral sensory disturbance
Erectile dysfunction

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42
Q

Clinical features of cauda equina

A

Back pain and radicular pain down legs
Asymmetrical, atrophic, areflexic paralysis of legs
Sensory loss in root distribution
Reduced sphincter tone

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43
Q

Sensation of dorsal column damage

A

Hypersensitive or vibratory feelings

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44
Q

Causes of unilateral foot drop - 5

A 
Diabetes
Common peroneal nerve palsy
Stroke
Prolapsed disc
MS
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45
Q

Causes of weak legs with no sensory loss - 2

A

MND

Poliomyelitis

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46
Q

Causes of chronic flaccid paraparesis - 2

A

Peripheral neuropathy

Myopathy

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47
Q

Causes of spastic paraparesis - 5

A 
MS
Intrinsic cord tumours
Cord mets
MND
Syringomyelia
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48
Q

Causes of absent knee jerks and extensor planters - 5

A 
Cervical and lumbar disc disease
Conus medullaris lesions
MND
Friedreich’s ataxia
Subacute combined degeneration of cord - vit B12 deficiency
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49
Q

Spastic gait appearance

A

Stiff, circumduction of legs

Scuffing of foot

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50
Q

Extrapyramidal gait disorder

A

Flexed posture, shuffling feet, slow to start, postural instability
Parkinson’s

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51
Q

Apraxia gait disorder

A

Feet glued to floor or wide based unsteady gait with tendency to fall
Caused by normal pressure hydrocephalus or multi-infarcts

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52
Q

Ataxic gait

A

Wide based, falls, cannot walk heel to toe
Caused by
- cerebellar lesions (MS, alcohol)
- proprioceptive sensory loss (sensory neuropathy, B12 def)
Worse in dark or eyes closed

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53
Q

Myopathic gait abnormality

A

Waddle - hip girdle weakness

Cannot climb stairs or sit from standing

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54
Q

Psychogenic gait abnormalities

A

Bizarre, not conforming to pattern

Can’t stand despite no signs when examined

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55
Q

Tests for gait disorders

A 
Spinal X-ray, MRI
FBC, ESR, syphilis serology, B12, UE, LFT
PSA, serum electrophoresis
CXR
LP
EMG, muscle +- sural nerve biopsy
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56
Q

Examples of symptoms movement disorders

A 
Ataxia
Dystonia, dyskinesia
Gait problems
Parkinsonism
Chorea
Myoclonus
Spasticity
Tics and tremor
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57
Q

3 things to note on tremor

A

Frequency
Amplitude
Exacerbating factors eg stresss, fatigue

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58
Q

4 types of tremor

A

Rest - abolished on voluntary movements, caused by Parkinsonism
Intention tremor - irregular, large amplitude, worse at end of purposeful act eg finger-pointing, caused by cerebellar damage (MS, stroke)
Postural tremor - absent at rest, present on maintained posture eg arms outstretched , may persist but not worse on movement, caused by benign essential tremor, thyrotoxicosis, anxiety, B agonist
Re-emergent tremor - postural, developing after delay of 10s (Parkinson’s). Can be helped by surgery or deep brain stimulation

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59
Q

What is chorea and 7 causes

A

Non-rhythmic jerky purposeless movements eg facial grimacing, raising shoulders
Caused by basal ganglia lesion (Huntingdon’s, stroke), strep, SLE, wilson’s, neonatal kernicterus, drugs (L-dopa)

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60
Q

What is the chorea which causes significant large amplitude proximal muscle movements

A

Hemiballismus, contralateral to vascular lesion on subthalamic nucleus
Unilateral proximal joint
Recover spontaneously in a few months

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61
Q

What is common in cerebral palsy and often confused with chorea

A

Athetosis - slow, sinuous, confident, purposeless writhing movements - also known as dystonia.
Caused by lesion in putamen

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62
Q

What are tics?

A

Brief, repeated, stereotyped movements, most common in children and usually resolve
Tourette’s = motor and vocal
Manage = psych support, clonazepam, clonidine if severe

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63
Q

What are sudden involuntary focal/general jerks, and its 2 main types

A

Myoclonus, from cord, brain stem or cerebral cortex
In metabolic problems, neurodegenerative disease, CJD
Benign essential myoclonus - childhood onset, may respond to valproate or clonazepam
Asterixis/metabolic flap - jerking 1-2/s of outstretched hands with wrists extended, from loss of extensor tone - caused by liver/kidney failure, gabapentin

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64
Q

What is the complication of antipsychotics long term

A

Tardivesyndromes - chronic exposure to dopamine antagonists (antipsychotics and antiemetics)
Can be permanent
Can be dyskinesia (choreiform), dystonia (twisting spasms), akathisia (inner restlessness), myoclonus, tourettism or tremor

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65
Q

What antipsychotics are less likely to cause tardive dyskinesia?

A

Quetiapine, olanzapine, clozapine - atypical antipsychotics

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66
Q

Cause of acute dystonia, presentation and treatment

A

From starting drugs eg neuroleptic and antiemetics (metoclopramide, cyclizine)
Torticolis, trismus (oromandibular spasm), oculogyric crisis
Sx disappear with anticholinergic procyclidine IM

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67
Q

Risk factors for drug induced acute dystonia

A

Male
Young
Previous acute dystonia
Recent cocaine use

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68
Q

Which tracts transmit which sensations in the spinal cord?

A

Anterolateral/spinothalamic - pain and temperature

Dorsal columns - joint position and vibration sense

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69
Q

What results from hemicord lesions?

A

Brown-Sequard syndrome - dorsal column (proprioception and vibration) loss on side of lesion and contralateral spinothalamic (pain and temperature) loss

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70
Q

What is dissociated sensory loss?

A

Cervical cord lesion causes loss of pain ad temperature with sparing of proprioception and vibration
Caused by syringomyelia or cord tumour

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71
Q

Sensory loss in cortical lesions?

A

Confined to discriminating sensory functions eg 2 point discrimination

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72
Q

Where can an UMN lesion be?

A 
Motor nerve cells in precentral gyrus of frontal cortex
Internal capsule
Brain stem
Cord
Anterior horn cells in cord
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73
Q

Pattern of weakness/spasticity with UMN lesion

A

Stronger muscles become spastic - arm flexors and leg extensors, with weakness in opposing muscles
Loss of skilled fine finger movements

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74
Q

Findings on exam for UMN lesion

A

Spasticity is velocity dependent so can suddenly be overcome, eg clasp-knife
Hyperreflexia
Positive babinski (upgoing plantars)
Clonus

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75
Q

Where is damage that causes LMN lesions?

A

Anterior horn cells in cord
Nerve root
Plexus
Peripheral nerves

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76
Q

Features of LMN lesion

A

Wasting, fasciculation
Hypotonia, flaccidity
Reduced reflexes
Flexor plantars

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77
Q

Differentiate between LMN and primary muscle disease eg myasthenia gravis

A

Muscle disease - symmetrical, reflexes lost later, no sensory loss
Myasthenia gravis = fatiguability, little wasting, normal reflexes, no sensory loss

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78
Q

Muscle weakness grading

A 
MRC classification:
Grade 0 = no muscle contraction
1 = flicker
2 = some active movement
3 = active movement against gravity 
4 = active movement against resistance
5 = normal power
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79
Q

3 impairments causing difficulty speakign

A

Dysphasia - impairment of language
Dysarthria - difficulty articulating due to incoordination or weakness of musculature for speech, language is normal
Dysphonia - difficultly with speech volume due to weakness of resp muscles or vocal cords

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80
Q

Dysphasia associated with difficulty saying words, location of lesion

A

Broca’s/expressive - non-fluent, malformed words. Reading and writing impairment but comprehension relatively intact. understand question, attempts to convey meaningful answer
Lesion = inferolateral dominant frontal lobe

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81
Q

Dysphasia associated with meaningless speech and location of lesion

A

Wernicke’s/receptive - empty fluent speech with neologisms, oblivious of errors, inappropriate speech
Reading, writing, comprehension all impaired
Lesion = posterior superior dominant temporal lobe

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82
Q

2 types of aphasia which are not expressive or receptive

A

Conduction - interrupted communication between Broca’s and Wernicke’s. Impaired repetition, some comprehension and fluency
Nominal - all fine except naming objects, Posterior dominant temperoparietal lesions

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83
Q

What to assess in assessment for dysphasia - 4

A
  1. Comprehension - follow 1/2/3 step commands
  2. Repetition
  3. Naming
  4. Reading and writing
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84
Q

Assessing dysarthria and 4 causes and their features

A

Diffficuty with articulation due to incoordination/weakness of musculature of speech. Repeat phrase eg British constitution

  1. Cerebellar disease - slurring and irregular volume, scanning speech
  2. Extrapyramidal diseases - soft, indistinct, monotonous speech
  3. Pseudobulbar palsy - spastic dysarthria (UMN), slow, nasal and effortful, from MND or severe MS
  4. Bulbar palsy - LMN eg facial nerve palsy or guillain-barre - palatal paralysis gives nasal speech
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85
Q

Identifying dysphonia and what causes it?

A

Weakness of resp muscles/cords, precipitated in myasthenia by counting to 100
Dysarthria and dysphonia in Parkinson’s

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86
Q

What is dyspraxia and 4 types

A

Poor performance of complex movements despite ability to do each component, eg mime object’s use
Dressing - unsure of orientation of clothes on body. Nondominant hemisphere lesions
Constructional - difficulty drawing 5 point star - nondominant hemisphere lesions or hepatic encephalopathy
Gait - bilateral frontal lesions, posterior temporal region or hydrocephalus

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87
Q

Treat chorea

A

Dopamine antagonist tetrabenazine

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88
Q

Cerebellar signs

A

DANISH
Dysdiadochokinesia and fingerto nose tests
Ataxia - broad based gait, fall to side of lesion
Nystagmus
Intention tremor
Slurred/staccato speech
Hypotonia andreduced power

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89
Q

Test for ataxia

A

Romberg test - stand with eyes closed

  • pos (loses balance) = posterior column disease
  • neg = cerebellar disease
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90
Q

Findings on exam for complete optic nerve lesion

A

Ipsilateral blindness and no direct pupillary reflex

Indirect pupillary reflex intact

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91
Q

Findings on exam for optic chiasm lesion

A

Bitemporal hemianopia as fibres from nasal halves both retinas will be involved
Normal direct, consensual light reflex and accommodation reflex

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92
Q

Findings on exam for optic tract lesion

A

Homonymous hemianopia: right side optic tract lesion = right nasal. And left temporal hemianopias
Normal direct, consensual light and accommodation reflexes

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93
Q

Optic radiation lesion findings

A

Homonymous hemianopia, or inferior quadrantinopia if more posterior to cortex

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94
Q

Visual cortex lesion

A

Homonymous hemianopia
Pupils react normally to reflex stimuli
Macula often spared due to posterior/middle cerebral artery anastamosis

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95
Q

Scotoma found with glaucoma

A

Arcuate scotoma

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96
Q

Unilateral horizontal hemianopia cause - 3

A

Arterial occlusion, retinal vein thrombosis, inferior retinal detachment

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97
Q

Cause of central scotoma - 2

A

Macular degeneration or macular oedema

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98
Q

Test for macular disease - 2

A

Central scotoma

Amsler grid for distortion in central vision

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99
Q

Pituitary tumour findings and why

A

Disrupts chiasm so bitemporal field defects, can superimpose central optic nerve. Defect icon onesidemore

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100
Q

Process from optic nerve to brain

A 
Optic chiasm
Optic tract
Lateral geniculate body
Optic radiations
Visual cortex
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101
Q

Temporal lobe tumour visual defect

A

Contralateral upper homonymous quadrantinopia

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102
Q

Causes of visual cortex field defects

A 
Ischaemia - TIA, migraine, stroke
AVM
Glioma, meningioma
Abscess
Drugs - ciclosporin
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103
Q

What is dementia

A

Progressive global decline in cognitive function

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104
Q

2 types of dementia and causes of each

A

Degenerative - AD, PD, multi-infarct, Lewy body, Huntingdon’s, Wilson’s
Reversible - brain (SDH, NPH), drugs, infections (HIV, neurosyphilis), metabolic (low T4, low B12, high calcium) [DIM]

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105
Q

Inv for dementia?

A

Confusion screen:
Collateral history, MMSE
Bloods - FBC, UE, LFT, TFT, haematinic (ferritin, B12), bone screen (calcium), glucose
Other fluids - urine mcs
X-ray - cxr, CT head (small vessel disease = variant on multi infarct dementia)
[BOX]

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106
Q

Manage areas in dementia

A

Social - Activity, Adl help (mobility, nutrition, continence), Anticipatory planning
Psycho - Ask about depression
Bio - Address reversible, Ad drugs (acetylcholinesterase inhibitor, NMDA antagonist)
[6As]

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107
Q

Adv and disadvantages of MMSE

A

Adv - quick and easy, monitor changes

Dis - bias against blind or uneducated, poor sens for mild dementia

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108
Q

Marks for MMSE

A

20-24 = mild
12-20 = moderate
<12 - severe

109
Q

Drugs for dementia

A

ACh inhibit for - donezepil, galantamine, rivastigmine for mild/mod
+ or swap for memantine - glutamate receptor antag when severe

110
Q

NPH features

A

Triad:
Dementia
Gait disturbance ‘magnetic’
Urine incontineince

111
Q

NPH inv

A

Dilated ventricles, no RICP on CT

112
Q

Manage NPH

A

VP shunt helps if CSF removal post-LP improves sx

113
Q

Features of Lewy body

A

Fluctuating memory loss
Visual hallucinations - kids animals
Parkinsonism features - eventually

114
Q

Pathology of Lewy body

A

A synuclein inclusions bodies

>65yo

115
Q

Causes of delirium

A

Brain - bleed (EDH, SDH, SAH), infection (meningitis, encephalitis), stroke, tumour
[DIM] - others - drugs (opiates, benzo and withdrawals), infection, metabolic (hypovolaemia, hypoxia, electrolyte, anaemia)

116
Q

What is delirium

A

Acute confusional state characterised by fluctuating cognitive impairment

117
Q

Types of delirium and features of each

A

Most common - hypoactive - decreased arousal, apathy
Hyperactive - increased arousal, agitation
Both - altered sleep, wake; hallucinations

118
Q

Manage delirium

A

Confusion screen - treat cause
Optimise factors - light, glasses, hydration, nutrition, bowels, pain
Sedatives if last resort and disruptive - haloperidol

119
Q

Assessing delirium - 2

A 
AMT:
Time
Year
Current place
Address
DOB
Time
Age
2 people
Monarch
WW1 end date
Count back 20-1

Or Confusion Assessment Method

120
Q

Feature of SDH and cause

A

Fluctuating confusion for a while

Rupture off weak bridging vessels between cortex and venous sinuses leading to haemorrhage between dura and arachnoid

121
Q

CT blood on SDH

A

Black - chronic blood

122
Q

COPD with uncontrolled oxygen and confusion - what investigation

A

ABG = T2 respiratory failure

123
Q

What is a fall

A

Unintentional loss of blance resulting in coming to rest below knee level

124
Q

Causes of non-syncope fall

A 
Mobility
Balance
Visual
Cognitive
Hazards - wet floor
125
Q

Syncope causes of fall

A

Cardiogenic - arrhythmia, HOCP (ask about sudden cardiac death), AS, MI, PE
Neurogenic - seizure, CVA, hydrocephalus
Vasogenic - vasovagal, carotid sinus/micturition

126
Q

Causes of fall - syncope or nonsyncope

A 
Hypoglycaemia
Postural drop
Drugs
Infection 
Metabolic
127
Q

Post-falls assesment key questions

A

1) why did they fall, 2) did it cause an injury
History
Exam
Investigations

128
Q

Hx in post falls assessment

A

Hx -
before (trigger, warning sx),
during (timing, consciousness, incontinence, tongue biting),
after (recovery time, postictal)

129
Q

Exam post falls

A

Obs - lying/standing BP, BM
Drug chart - anticoagulants (brain bleed), psychotropic, htn
Full CVS, neuro incl CN, injury sites - head, c spine, hips, knees

130
Q

Inv in post fall assessmsent

A

ECG, 24h tape

Imaging - CT head, X-ray neck, X-ray pelvis

131
Q

Aims of falls risk assessment

A

Prevent future fall

Protective measures if do fall

132
Q

Who is at risk of falling

A

Age >65yo
>1 fall in last year
RF - mobility, visual, balance, cognitive and refer on

133
Q

Manage fall risk in clinic - 5

A 
RF
Home hazards
Timed up and o test, turn 180 degrees
Medication review - anticoagulation etc
Osteoporosis risk
134
Q

Bone assessment in elderly - 3

A

FRAX - 10y risk of fracture
DEXA
Bisphosphonates

135
Q

DEXA scan results

A

T score:
-1 - -2.5 = osteopoenia
< -2.5 = ostoporosis

136
Q

Manage low DEXA score

A

1st line - alendonate
2 - other PO Bisphosphonates
3 - newer agents, zoledronate IV

137
Q

CT head immediate criteria - 4

A

GCS <13 at assessment of <15 2h after
Suspected basal skull, open or dep[ressed fracture
Seizures or focal neuro
vomiting >1

138
Q

CT head urgent criteria - 4

A

Retrograde amnesia >30m
High impact trauma
Bleeding diathesis - warfarin, clotting disorder
Age >65yo

139
Q

Hx of weakness?

A

[STEERS]
Start point - morning? (Stroke)
Timings - come and go, getting better/worse
Explain it - where (asymmetrical) and effects on life
Exacerbating
Relieving factors
Sx screen:
- Sensory
- Functions - speech, swallow, sphincter
- Fits, faints, funny turns
- meningism - headache, vomiting, neck stiff, photophobia

140
Q

Focal weakness causes - 5 areas

A 
UMN only - 
Stroke
MS
Tumour
Bleed
Meningitis

UMN and LMN (mostly cord) -
MND
Cord disease

LMN only - neuropathy

NMJ - MG

Muscle - myopathy

141
Q

Generalised causes of weakness

A 
Frailty
Anaemia
Sarcopoenia
Hypoglycaemia
Electrolytes
Hypoxia
Infection
Drug related
142
Q

Ischaemic stroke - 3 types and exam findings

A

Emboli - cardiac, carotid
Thrombotic in situ - large vessel, small perforated
Rare - [3Vs] vasospasm for SAH, Vasculitis, Vvatershed stroke

AF, murmur, carotid bruit

143
Q

Haemorrhagic stroke - 6 causes and exam findings

A

[HHAATT]
Head injury and Htn
Anticoagulation and AVN
Thrombolysis and Tumour

Meningism, seizures, LOC

144
Q

Stroke mimics - 4

A

Hypoglycaemia, Hemiplegic migraine
Todd’s palsy (frontal lobe epilepsy), Tumour/haemrrange
[HHTT]

145
Q

Cardiac emboli strokes

A

TACS and PACS

146
Q

Small vessel thrombotic diseae

Large vessel thrombotic disease

A

LACS

POCS

147
Q

Why is macular spared in POCS

A

Bilateral supply

148
Q

MCA stroke features

A

[Ms]
Mouth and arms
Mechanical speech impairment - broca’s

149
Q

ACA stroke features

A

Legs and Wernicke’s

150
Q

Cerebellar stroke

A

DANISH

151
Q

Brainstem stroke features

A

Same side = CN problems

Other side = peripheral nerve problems

152
Q

Wallenberg - PICA

A

IL Horner, dysphagia, DANISH

CL sensory

153
Q

Weber - PCA midbrain

A

IL CN3

CL weakness

154
Q

Pontine stroke

A

IL CN6/7

CL weakness

155
Q

Types of brainstem stroke

A

PICA, MCA midbrain, pontine

156
Q

Manage stroke immediate

A 
[ACT]
Aspirin 300mg 2w then clopidogrel 75mg
Consider thrombolysis (<4.5h, contraindications, <80yo) and neuro referral if cerebellar (coning) or malignant MCA (oedema on infarct)
Transfer to stroke unit - monitor BP and BM (enough supply to penumbra by keeping BP in range)
157
Q

VTE after stroke?

A

Dont’ start LMWH as increased risk of haemorrhagic stroke

Aspirin 300mg

158
Q

LT stroke management

A

Cannot drive for 1m, tell DVLA if permissive neuro defecit
Statin >2d, warfarin >2w ifAF, stop clopidogrel
CEA <2w if symptomatic stenosis
PT/OT/dietician
NBM then SALT

159
Q

TIA assessment?

A 
ABCD2 criteria
Age
BP
Clinical features
Duration of sx
Diabetes

<4 - clinic <1
>=4 clinic in 24h

160
Q

Manage TIA

A

Aspirin 300mg, statin, ECG
TIA clinic within 24h
ABCD2 assessment

161
Q

MS ?

A

AI CNS demyelination - discrete plaques disseminated in time and space

162
Q

Types of MS

A

Relapsing remitting

Secondary or primary progressive

163
Q

MS ?

A

AI CNS demyelination - discrete plaques disseminated in time (different times) and space (different probems)
T cell demyelination repairs slowly

164
Q

Types of MS

A

Relapsing remitting

Secondary or primary progressive

165
Q

Features of MS

A

Visual - optic neuritis (most common presentation), bilateral INO, uhthoff phenomenon (worse in heat)
Sensory - limb tingling, Lhermitte’s sign
Motor - spastic paralysis (UMN), bowel/bladder dysfunction
Cerebellar - dAnish (A most common in relapsing)

166
Q

inv MS

A

MRI brain and spinal cord
T2 [2 letters in MS] with gadloneum contrast
LP - oligoclonal bands, ensure no inf before starting steroids

167
Q

Manage MS

A

Relapse - steroids IV 3d (ensure no inf first) then PO

Remission - DMARDs eg interferons (if >2 relapse in 2y), biologics, symptomatic (spasticity, pain, urinary retention)

168
Q

Open angle glaucoma fundoscopy

A

Optic disc cupping

169
Q

Complication when DMARD started for MS

A

Misdiagnosis - Neuromuscular optica = optic neuritis and transverse myelitis
Check anti-NMO antibodies when diagnosing MS
Gets worse with DMARDs

170
Q

Manage spasticity in MS

A

1 - Baclofen

2 - Botulinum

171
Q

Which ascending tract crosses

A

Lateral spinothalamic

172
Q

MND?

A

Degeneration of upper motor neurones,
CN and anterior horn nuclei - LMNs
Loss of corticospinal, corticobulbar tracts and anterior horn cells
Generally UMN signs in legs and LMN in arms

173
Q

Most common MND

A

Asymmetrical lateral sclerosis in anterior horn

174
Q

Features of asymmetrical lateral sclerosis

A

LMN arms - thenar wasting, split thumb, fasciculations

Umn legs

175
Q

4 types of MND

A

Asymmetric lateral sclerosis
Primary lateral sclerosis
Progressive muscular atrophy
Progressive bulbar palsy

176
Q

Diagnosis of MND

A

Exclusion

Motor only, mixed umn/lmn or fasciculatins - suspect

177
Q

Manage MND

A

MDT
Riluzole - anti glutaminergic
Symptomatic/supportive
Baclofen, diazepam

178
Q

Causes of cord ccompression - 5

A 
Trauma - post disc prolapse
Tumour - myeloma, mets
Bleeding - haematoma
Infection - abscess
Degeneration - spondylosis
179
Q

Red flags for cord compression

A

[4Bs]
Back pain
Bilateral neurology incl saddle anaesthesia
Bowel/bladder accident
B symptoms - fever, night sweats, weight loss

180
Q

Bottom of cord?

A

Conus medularis L1 - S5

181
Q

Intrinsic cord disease? - 5

A

Tracts:
Vascular - ASA infarction = anterior lateral tracts
Inflammation - MS
Infection - HTLV1
Metabolic - SACCD in b12 def
Congenital - syringomyelia, Friedrich ataxia

182
Q

Immediate management of malignant cord compression

A

Dexamethasone
MRI
Neurosurgery referral

183
Q

What are polyneuropathyies

A

symmetrical and distal - demyelination gets or axonal

184
Q

Motor polyneuropathy

A

LMN features

Guillan barre, paraneoplastic

185
Q

sensory neuropathy eg feature and causes

A

Glove and stocking

DM, alcohol, b12

186
Q

Mixed neuropathy features and causes

A

Postural drops
Retention/constipation
Point and Shoot

Diabetes, Guillan barre, HIV

187
Q

Myasthenia gravis?

A

AI - anti achr, anti musk

188
Q

Motor polyneuropathy features and causes

A

LMN features

Guillan barre, paraneoplastic

189
Q

Sensory polyneuropathy feature and causes

A

Glove and stocking

DM, alcohol, b12

190
Q

Manage MG

A

Anticholinesterase - pyridostigmine
Immunosuppression - rescue IVIG, plasma X; DMARDs
Thymectomy

191
Q

Myopathy?

A

Symmetrical proximal muscle wasting/weakness

Inherited or acquired

192
Q

Inv myopathy

A

Raised CK
EMG shows short action potential
Muscles biopsy diagnostic

193
Q

Inherited myopathies - 3

A

Musclular destroy
Myotonic dystrophy
Mitochndrial

194
Q

Acquired myopathies - 3

A

Myositis
Metabolic
Medicatios

195
Q

Assessing resp muscle weakness in neuromuscular disorder

A

FVC <1.5l
= ABG - T2RF
== ITU

196
Q

Cause of guillan barre and process

A

Campylobacter jejuni produces antibodies that cross reacts

2w before weakness starts

197
Q

Inherited of DMD

A

X linked recessive

198
Q

Causes of incontinence

A

Stress:
[Ps]
Pelvic floor weakness

Urge:
[Ds]
Detrusor overactivity

199
Q

Manage incontinence

A

Stress -
Pelvic floor exercises
PV tension free tape

Urge -
Diary and retraining therapy
Drugs - anti muscarinics

200
Q

Retention of urine causes

A

Inpatient - 4Cs - constipation, Catheter blocked, colonised (inf), chemicals
Outpatient - prostate, pelvic mass, paralysed bladder

201
Q

Presentation of urine retentiona n

A

No uterine
Distended palpable bladder
Delirium

202
Q

Inv urine retention

A

Bladder scan.- >500lm residual
US KUB for hydronephrosis
UE AKI

203
Q

Treat retention of urine

A

Identify cause and reverse
Catheterise - clot washout, tamsulosin, gentamycin
Chronic - catheterise with long term and refer

204
Q

Key drugs involved in cyp DDIs

A 
Statin
Warfarin
OCP
Theophylline
[SWOT]
205
Q

Red flag sx headache

A

Meningitic - neck stiff, photophobia, fever, vomiting rash
Pressure - worse on strain or morning, vision
GCA in elderly - jaw claudication, scap tenderness (brushing hair)

206
Q

Red flag diagnoses

A 
Inf - meningitis, encephalitis
Bleed (EDH, SDH, SAH)
Clot (pill?)
SOL
Acute closed angle glaucoma
GCA
207
Q

Chronic headaches - 3 causes

A

Tension headache
Migraine
Cluster headache

208
Q

Migraine diagnosis

A 
5 attacks
Lasting 4 hours to 3 days
2 of unilateral, pulsating, severe affecting life
1 of NV, phonophobia, photophobia
[54321]
209
Q

Aura type in migraine?

A

Visual

Motor

210
Q

Common triggers for migraine

A

Crap time - stress
Certain food - cheese, chocolate, caffeine
COCP

211
Q

Treat mild headache with hx of asthma?

A

Paracetamol

No naproxen as asthma

212
Q

Severe occipital headache with hx of aut dom polycystic kidney disease

A

SAH - CT head or LP after 12h if neg CT

213
Q

Why wait for 12h to do LP for SAH

A

Wait for blood to breakdown to bilirubin - xanthochromia, as can get blood on LP anyway from trauma

214
Q

Treat idiopathic intracranial htn - 4

A

Weight loss
Acetazolamide
Topiramate - prevent seizures
VP shunt/ON fenestration

215
Q

Sx of IIH - 4

A

Bilateral blurred vision with blurred discs on fundoscopy

Long term headache, worse with sex

216
Q

Unilateral headache
Pale optic disc
Amaurosis fugax

A

GCA - steroids and hospital

= Anterior ischaemic optic neuropathy

217
Q

GCA fundoscopy findings

A

Pale optic disc - anterior ischaemic optic neuropathy

218
Q

2 causes of pale optic disc

A

Anterior ischemic optic neuropathy - arteritic or nonarteritic (clot)
GCA

219
Q

Classify seizure

A

Epilepsy vs provoked
Partial.- simple, complex
Generalised - tonic clonic, absence

220
Q

Inv epiepsy

A

EEG, MRI brain

221
Q

seizure treatment

A

First fit clinic
Driving - no drivin 6m after 1st seizure, 1y seizure free to restart
AED - cbz for partial (not in absence), valproate for generalised, lamotrigine/levitiricitam

222
Q

Temporal epilepsy sx - 4

A

Hallucinations
Epigastric rising
Automatisms
Deja vu, dysphasia post ictal

223
Q

Frontal epilepsy sx - 3

A

Motor - posturing, head movements
Jacksonian march
Weakness post ictal - Todd’s

224
Q

Parietal epilepsy sx

A

Sensory

225
Q

Occipital epilepsy sx

A

Visual

226
Q

AED in pregnancy

A

Lamotrigine

227
Q

Manage status epilepticus

A 
A-E, recovery position
After 5m - IV lorazepam 2-4mg, 
After 15m - repeat bolus
After 20m - phenytoin, anaesthetist
After 30m - RSI, intubate, ITU
228
Q

Status epilepticus OSCE activities - 2

A

1) Start timing

2) Start drawing up lorazepam 2-4mg 2x boluses, and phenytoin

229
Q

Pseudoseizures - 3

A

Unexplained movements
Rapid resolution
Triggers eg stress

230
Q

Rapidly resolving unpredictable seizures?

A

Pseudoseizure

231
Q

Types of tremor

A

[RAPID]
Resting - sow, asymmetrical, pill rolling, relieved by movement and worse with distraction
- PArkinson’s
Action/postural - rapid, symm, both arms, worse with outstretched arms, relieved at rest
- BEATS
Intention - rapid, large amplitude, irregular, worse with finger pointing end, better with rest
- cerebellar causes
Dystonic - variable

232
Q

Causes of action or postural tremor

A 
Benign essential tremor
Endocrine - hyperthyroid 
Alcohol withdrawal 
Toxins - b agonist 
Stress//anxiety 
[BEATS}
233
Q

Parkinson’s diseae?

A

Reduced dopamnergic neutrons in pars compacta of substantianigra

234
Q

Sx parkinson’s

A 
Motor change - hypokinesia, rigidity, resting tremor - UL onset 
Autonic instability
Sleep disorder
Krazy - depression
[MASK]
235
Q

Manage Parkinson’s

A

Levidopa if unwell and carbidopa (prevents peripheral breakdown to improve brain action) - only last <5y
- SE = motor - on/off fluctuations (off when wearing off), dyskinesia

Dopamine agonist if well
- SEs - postural drop, nausea, visual hallucinations, fibrosis if ergo-derived

Prolong on time: MOA-B inhibitor selegiline, COMT inhibitor entacapone
Reduce dyskinesia: NMDA inhibitor

236
Q

When to rule out parkinson’s disease with tremor

A

Bilateral/symmetrical at start - Parkinsonism

237
Q

Manage benign essential tremor

A

Propanolol

238
Q

Features of benign essential tremor

A

Aut dom
Better with alcohol
Worse with specific movements

239
Q

What is Bell’s palsy 2 RF and inv and management

A 
CN7 palsy, diagnosis of exclusion 
Unilateral weakness including forehead
Decreased taste
Numbness or pain around ear
Abrupt onset
RF pregnancy, diabetes

ESR
MRI for SOL, MS or stroke
Can do nerve conduction study after 2w predicts prognosis - slow if axonal degeneration

Incomplete recovers in a few weeks, complete paralysis mostly will make full recovery

Prednisolone in first 72h, protect eye with tape

240
Q

Types of delirium and key features

A

Acute confusional state, hyperactive, hypoactive or mixed
Primary = personality abnormalities, found after crisis eg loss of spouse
Assess with AMTS, MoCA, MMSE

  1. Cognitive impairment
  2. Rapid onset - days to weeks
  3. Fluctuating severity - worse at night
241
Q

Predisposing factors for delirium

A 
Dementia
Old
Polypharmacy
Functional or sensory impairment
Malnutrition 
Comorbidities
242
Q

Precipitating factors for delirium

A 
Hospitalisation 
Catheterisation 
Acute illness
Electrolyte disturbances - sodium
Drugs - opiates, anticholinergics, sedation
Renal impairment
Alcohol
Peri-op
Constipation
243
Q

Differentiate delirium from dementia

A

Delirium - sudden onset, reversible, impaired consciousness, inattentive, psychomotor changes

Dementia - insidious, permanent, no impairment of consciousness, normal attention, no psychomotor changes

244
Q

What is dementia and diagnosis

A

Progressive impairment of higher cortical functions, including memory, language, emotional control and social behaviour
Must affect ADLs

Clinical cognitive assesments eg AMT, MMSE, MoCA - attention, memory, language, execute, apraxia, visuospatial
Focal neurology, FBC including calcium, BM, B12, folate, TFT
ECG, EEG, CXR, MSU
CT/MRI

245
Q

Alzheimer’s, what is it, 4 RF for dementia and management

A

Amyloid deposits - progressive degeneration of cortex - global impairment

Female
Family hx
Caucasian
Apolipoprotein E

Treat - supportive
Mild - AChEi galantamine or donepezil
Mod - NMDA antagonist memantine

246
Q

Vascular dementia

A

Macroscopic - single insult, or microscopic - number of microemboli
RF - male, CVD, smoker, obestiy,, DM, htn

Acute or subacute, focal or functional sx eg mood change
Treat contributing factors

247
Q

Lewy body dementia

A

A synuclein deposits in brainstem and neocortex
Multitasking lost first, then memory. Fluctuating cognitive impairment, hallucinations, sleep disorder

Treat - ?rivastigmine
Avoid PD drugs, antipsychotics and sedatives

248
Q

Differentials for dementia

A 
Alzheimer’s
Vascular
Lewy body
Frontotemporal - Pick’s
Normal pressure hydrocephalus
Depression

Mild cognitive impairment - objective cognitive impairment but doesn’t meet dementia criteria

249
Q

Features of extradural haemorrhage

A

Lucid interval then deterioration consciousness, headache, confusion, fits
Hemiparesis, brisk reflexes, upwards plantar
Eventually, ipsilateral pupil dilates

250
Q

What is Horner’s syndrome and causes

A
  1. miosis
  2. Partial ptosis
  3. Anhydrosis

From interruption to sympathetic supply - thoracic outlet (pancoast), brainstem (demyelination or vascular) or cord (syringomyelia)

251
Q

ABx for meningitis in adults

A

Cefotaxime and ampicillin if >55yo

Cefotaxime alone if <55yo

252
Q

Triptans and CI to triptans

A

5-HT3 agonist
Coronary artery spasm
Uncontrolled ypertension
SSRIs

253
Q

Prevention of migraine

A

If >=2 a month or not responding to treatment
1 - Propranolol, amitryptiline, calcium channel blockers
2 - Valproate, gabapentin,

254
Q

What is MND and sx

A

Selective loss of UMN in cortex, cranial nuclei and anterior horn cells
- UMN, LMN and bulbar signs
Sx - stumbling spastic gait, foot drop, prox myopathy
Doesn’t affect eyes or sphincters

Treat: sx eg baclofen for spasms, analgesia
Anti-NMDA drugs

255
Q

Grading of SAH and management and 4 complicatiotns

A 
1 - no sx
2 - neck stiffness and CN palsy
3 - drowsy
4 - drowsy with hemiplegia
5 - coma

Immediate surgery and endovascular coiling, measure GCS, pupils and BP and repeat CT if deteriorate
Nimodipine - calcium ch antagonist reduces vasospasm and morbidity from cerebral ischaemia

Rebleeding
Cerebral ischaemia from vasospasm
Hyponatraemia
Hydrocephalus from blocking arachnoid granulations

256
Q

What drugs to start for temporal arteritis

A

Prednisolone
PPI
Alendronate

257
Q

Wernicke’s encephalopathy features

A

Confusion
Ataxia
Opthalmoplegia

Memory loss, hypothermia, hypotension, reduced consciousness

From thiamine B1 deficiency

Treat with thiamine IV then PO

258
Q

Requirements for diagnosis of different strokes

A
  1. Unilateral weakness
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction
TACS = 3
PACS = 2

POCS: 1 of:

  1. Cerebellar dysfunction
  2. LOC
  3. homonymous hemianopia

LACS: 1 of:

  1. Unilateral weakness +- sensory of face, arm or leg
  2. Pure sensory
  3. Ataxic hemiparesis
259
Q

Manage TIA

A 
Aspirin 300mg and statin
ABCD2 score -age (60yo), bp (140), clinical features (1-2), duration (1 = <1h or 2), diabetic 
1-2 = clinic in 7d
3 = clinic in 24h
4+ = admit
260
Q

What is Huntingdon’s disease

A

Aut dom chronic progressive chorea and marked mental deterioration, present 30-50yo

Cerebral atrophy with loss of neutrons in putamen and caudate nucleus
Personality, mood and cognition change
Chorea, walking, speech - eventual akinesia and rigidity
Dementia
Early depression and increased suicide risk
Death in 10-20y of onset

Manage:
Antipsychotics
Tetrabenazine suppresses chorea
Antidepressants

261
Q

Cellulitis classification

A

Eron classification:
1 - no systemic sx
2 - systemically unwell or has comorb that may delay resolution
3 - significant systemic illness or comorbidity that may interfere with treatment or lead to vascular compromise and limb threatening infection
4 - sepsis or life threatening infection

Admit if: 3-4, severe or deteriorating, immunocompromised of facial
Stage 1 - oral flucloxacillin 7d

262
Q

Signs of degenerative cervical myelopathy and treatment

A

Neck pain
Bilateral median nerve dysfunction
Sensory, motor, autonomic

MRI - cervical canal stenosis

Manage: surgical decompression, physio and analgesia

263
Q

Chronic inflammatory demyelinating polyneuropathy

A

Widespread neuropathy, motor symptoms predominant
MRI to rule out MS
CSF = high protein
Treat - high dose steroids

264
Q

Subacute degeneration of cord

A

B12 deficiency
Posterior column first = proprioception, light touch, vibration
Lateral = spastic weakness, UMN signs

265
Q

Brown sequard

A

Contralateral pain, temperature and crude touch

Ipsilateral UMN, vibration, proprioception and fine touch

266
Q

Cause of CN3 palsy and sx

A

Posterior communicating artery aneurysm - severe headache and loss of visual acuity
down and out, ptosis, dilated

267
Q

Encephalitis causes and inv and treatmetn

A

Virus - HSV1/2, EBV, CMV, measles
Bacteria, Tb, malaria

Inv - bloods, cultures, PCR
Throat and urine swabs
CT
LP
EEG

Empirical acyclovir for HSV
Then treat identified cause and supportive

268
Q

Sx and inv and management of cerebral abscess

A

Sx - fever, seizures, localising sign, RICP, coma, sign of sepsis eg ear, tooth, lungs

Inv - WCC and ESR high, CT/MRI

Manage - neurosurgery, treat RICP

Finals (13 decks)

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