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
Management and progress of vestibular schwannoma
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
26
Causes of conductive deafness and finding on tuning fork test
Wax, otosclerosis, otitis media or glue ear Weber - localises to ear with conductive loss Rinne = negative = bone conduction louder than air conduction
27
Causes of sensorineural deafness - 3 chronic 8 acute
``` 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 ```
28
Tests for sudden sensorineural deafness
``` ESR, FBC, LFT Viral titres and TB Evoked response audiometry CXR MRI Lymph node and nasopharyngeal biopsy for malignancy and TB culture ```
29
Result of tuning fork tests for sensorineural hearing loss
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
30
Causes of tinnitus
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
31
Investigate tinnitus
Pulsatile may be audible with stethoscope MRI If unilateral, exclude vestibular schwannoma
32
Complications of tinnitus
Depression, insomnia
33
Manage tinnitus
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
34
Key questions for weak legs - 6
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
35
Sx in progressive weakness
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
36
Causes of progressive weakness due to cord compression - 7
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
37
Differentials for progressive weakness (not due to cord compression)
Transverse myelitis MS, Guillaun-Barre Spinal artery thrombosis, dissecting aneurysm Trauma
38
Investigations for cord compression
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
39
treatment cord compression
Dexamethasone IV 4mg/6h if malignancy then consider C/RT, decompressive laminectomy Surgical decompression and abx if epidural abscess
40
Main difference in sx of cauda equina/conus medullary lesions and higher up lesions
Leg weakness is flaccid and areflexic instead of spastic and hyperreflexic
41
Clinical features of conus medullary lesions
Mixed UMN/LMN leg weakness Early urinary retention and constipation Back pain and sacral sensory disturbance Erectile dysfunction
42
Clinical features of cauda equina
Back pain and radicular pain down legs Asymmetrical, atrophic, areflexic paralysis of legs Sensory loss in root distribution Reduced sphincter tone
43
Sensation of dorsal column damage
Hypersensitive or vibratory feelings
44
Causes of unilateral foot drop - 5
``` Diabetes Common peroneal nerve palsy Stroke Prolapsed disc MS ```
45
Causes of weak legs with no sensory loss - 2
MND | Poliomyelitis
46
Causes of chronic flaccid paraparesis - 2
Peripheral neuropathy | Myopathy
47
Causes of spastic paraparesis - 5
``` MS Intrinsic cord tumours Cord mets MND Syringomyelia ```
48
Causes of absent knee jerks and extensor planters - 5
``` Cervical and lumbar disc disease Conus medullaris lesions MND Friedreich’s ataxia Subacute combined degeneration of cord - vit B12 deficiency ```
49
Spastic gait appearance
Stiff, circumduction of legs | Scuffing of foot
50
Extrapyramidal gait disorder
Flexed posture, shuffling feet, slow to start, postural instability Parkinson’s
51
Apraxia gait disorder
Feet glued to floor or wide based unsteady gait with tendency to fall Caused by normal pressure hydrocephalus or multi-infarcts
52
Ataxic gait
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
53
Myopathic gait abnormality
Waddle - hip girdle weakness | Cannot climb stairs or sit from standing
54
Psychogenic gait abnormalities
Bizarre, not conforming to pattern | Can’t stand despite no signs when examined
55
Tests for gait disorders
``` Spinal X-ray, MRI FBC, ESR, syphilis serology, B12, UE, LFT PSA, serum electrophoresis CXR LP EMG, muscle +- sural nerve biopsy ```
56
Examples of symptoms movement disorders
``` Ataxia Dystonia, dyskinesia Gait problems Parkinsonism Chorea Myoclonus Spasticity Tics and tremor ```
57
3 things to note on tremor
Frequency Amplitude Exacerbating factors eg stresss, fatigue
58
4 types of tremor
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
59
What is chorea and 7 causes
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)
60
What is the chorea which causes significant large amplitude proximal muscle movements
Hemiballismus, contralateral to vascular lesion on subthalamic nucleus Unilateral proximal joint Recover spontaneously in a few months
61
What is common in cerebral palsy and often confused with chorea
Athetosis - slow, sinuous, confident, purposeless writhing movements - also known as dystonia. Caused by lesion in putamen
62
What are tics?
Brief, repeated, stereotyped movements, most common in children and usually resolve Tourette’s = motor and vocal Manage = psych support, clonazepam, clonidine if severe
63
What are sudden involuntary focal/general jerks, and its 2 main types
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
64
What is the complication of antipsychotics long term
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
65
What antipsychotics are less likely to cause tardive dyskinesia?
Quetiapine, olanzapine, clozapine - atypical antipsychotics
66
Cause of acute dystonia, presentation and treatment
From starting drugs eg neuroleptic and antiemetics (metoclopramide, cyclizine) Torticolis, trismus (oromandibular spasm), oculogyric crisis Sx disappear with anticholinergic procyclidine IM
67
Risk factors for drug induced acute dystonia
Male Young Previous acute dystonia Recent cocaine use
68
Which tracts transmit which sensations in the spinal cord?
Anterolateral/spinothalamic - pain and temperature | Dorsal columns - joint position and vibration sense
69
What results from hemicord lesions?
Brown-Sequard syndrome - dorsal column (proprioception and vibration) loss on side of lesion and contralateral spinothalamic (pain and temperature) loss
70
What is dissociated sensory loss?
Cervical cord lesion causes loss of pain ad temperature with sparing of proprioception and vibration Caused by syringomyelia or cord tumour
71
Sensory loss in cortical lesions?
Confined to discriminating sensory functions eg 2 point discrimination
72
Where can an UMN lesion be?
``` Motor nerve cells in precentral gyrus of frontal cortex Internal capsule Brain stem Cord Anterior horn cells in cord ```
73
Pattern of weakness/spasticity with UMN lesion
Stronger muscles become spastic - arm flexors and leg extensors, with weakness in opposing muscles Loss of skilled fine finger movements
74
Findings on exam for UMN lesion
Spasticity is velocity dependent so can suddenly be overcome, eg clasp-knife Hyperreflexia Positive babinski (upgoing plantars) Clonus
75
Where is damage that causes LMN lesions?
Anterior horn cells in cord Nerve root Plexus Peripheral nerves
76
Features of LMN lesion
Wasting, fasciculation Hypotonia, flaccidity Reduced reflexes Flexor plantars
77
Differentiate between LMN and primary muscle disease eg myasthenia gravis
Muscle disease - symmetrical, reflexes lost later, no sensory loss Myasthenia gravis = fatiguability, little wasting, normal reflexes, no sensory loss
78
Muscle weakness grading
``` 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 ```
79
3 impairments causing difficulty speakign
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
80
Dysphasia associated with difficulty saying words, location of lesion
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
81
Dysphasia associated with meaningless speech and location of lesion
Wernicke’s/receptive - empty fluent speech with neologisms, oblivious of errors, inappropriate speech Reading, writing, comprehension all impaired Lesion = posterior superior dominant temporal lobe
82
2 types of aphasia which are not expressive or receptive
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
83
What to assess in assessment for dysphasia - 4
1. Comprehension - follow 1/2/3 step commands 2. Repetition 3. Naming 4. Reading and writing
84
Assessing dysarthria and 4 causes and their features
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
85
Identifying dysphonia and what causes it?
Weakness of resp muscles/cords, precipitated in myasthenia by counting to 100 Dysarthria and dysphonia in Parkinson’s
86
What is dyspraxia and 4 types
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
87
Treat chorea
Dopamine antagonist tetrabenazine
88
Cerebellar signs
DANISH Dysdiadochokinesia and fingerto nose tests Ataxia - broad based gait, fall to side of lesion Nystagmus Intention tremor Slurred/staccato speech Hypotonia andreduced power
89
Test for ataxia
Romberg test - stand with eyes closed - pos (loses balance) = posterior column disease - neg = cerebellar disease
90
Findings on exam for complete optic nerve lesion
Ipsilateral blindness and no direct pupillary reflex | Indirect pupillary reflex intact
91
Findings on exam for optic chiasm lesion
Bitemporal hemianopia as fibres from nasal halves both retinas will be involved Normal direct, consensual light reflex and accommodation reflex
92
Findings on exam for optic tract lesion
Homonymous hemianopia: right side optic tract lesion = right nasal. And left temporal hemianopias Normal direct, consensual light and accommodation reflexes
93
Optic radiation lesion findings
Homonymous hemianopia, or inferior quadrantinopia if more posterior to cortex
94
Visual cortex lesion
Homonymous hemianopia Pupils react normally to reflex stimuli Macula often spared due to posterior/middle cerebral artery anastamosis
95
Scotoma found with glaucoma
Arcuate scotoma
96
Unilateral horizontal hemianopia cause - 3
Arterial occlusion, retinal vein thrombosis, inferior retinal detachment
97
Cause of central scotoma - 2
Macular degeneration or macular oedema
98
Test for macular disease - 2
Central scotoma | Amsler grid for distortion in central vision
99
Pituitary tumour findings and why
Disrupts chiasm so bitemporal field defects, can superimpose central optic nerve. Defect icon onesidemore
100
Process from optic nerve to brain
``` Optic chiasm Optic tract Lateral geniculate body Optic radiations Visual cortex ```
101
Temporal lobe tumour visual defect
Contralateral upper homonymous quadrantinopia
102
Causes of visual cortex field defects
``` Ischaemia - TIA, migraine, stroke AVM Glioma, meningioma Abscess Drugs - ciclosporin ```
103
What is dementia
Progressive global decline in cognitive function
104
2 types of dementia and causes of each
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]
105
Inv for dementia?
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]
106
Manage areas in dementia
Social - Activity, Adl help (mobility, nutrition, continence), Anticipatory planning Psycho - Ask about depression Bio - Address reversible, Ad drugs (acetylcholinesterase inhibitor, NMDA antagonist) [6As]
107
Adv and disadvantages of MMSE
Adv - quick and easy, monitor changes | Dis - bias against blind or uneducated, poor sens for mild dementia
108
Marks for MMSE
20-24 = mild 12-20 = moderate <12 - severe
109
Drugs for dementia
ACh inhibit for - donezepil, galantamine, rivastigmine for mild/mod + or swap for memantine - glutamate receptor antag when severe
110
NPH features
Triad: Dementia Gait disturbance ‘magnetic’ Urine incontineince
111
NPH inv
Dilated ventricles, no RICP on CT
112
Manage NPH
VP shunt helps if CSF removal post-LP improves sx
113
Features of Lewy body
Fluctuating memory loss Visual hallucinations - kids animals Parkinsonism features - eventually
114
Pathology of Lewy body
A synuclein inclusions bodies | >65yo
115
Causes of delirium
Brain - bleed (EDH, SDH, SAH), infection (meningitis, encephalitis), stroke, tumour [DIM] - others - drugs (opiates, benzo and withdrawals), infection, metabolic (hypovolaemia, hypoxia, electrolyte, anaemia)
116
What is delirium
Acute confusional state characterised by fluctuating cognitive impairment
117
Types of delirium and features of each
Most common - hypoactive - decreased arousal, apathy Hyperactive - increased arousal, agitation Both - altered sleep, wake; hallucinations
118
Manage delirium
Confusion screen - treat cause Optimise factors - light, glasses, hydration, nutrition, bowels, pain Sedatives if last resort and disruptive - haloperidol
119
Assessing delirium - 2
``` AMT: Time Year Current place Address DOB Time Age 2 people Monarch WW1 end date Count back 20-1 ``` Or Confusion Assessment Method
120
Feature of SDH and cause
Fluctuating confusion for a while | Rupture off weak bridging vessels between cortex and venous sinuses leading to haemorrhage between dura and arachnoid
121
CT blood on SDH
Black - chronic blood
122
COPD with uncontrolled oxygen and confusion - what investigation
ABG = T2 respiratory failure
123
What is a fall
Unintentional loss of blance resulting in coming to rest below knee level
124
Causes of non-syncope fall
``` Mobility Balance Visual Cognitive Hazards - wet floor ```
125
Syncope causes of fall
Cardiogenic - arrhythmia, HOCP (ask about sudden cardiac death), AS, MI, PE Neurogenic - seizure, CVA, hydrocephalus Vasogenic - vasovagal, carotid sinus/micturition
126
Causes of fall - syncope or nonsyncope
``` Hypoglycaemia Postural drop Drugs Infection Metabolic ```
127
Post-falls assesment key questions
1) why did they fall, 2) did it cause an injury History Exam Investigations
128
Hx in post falls assessment
Hx - before (trigger, warning sx), during (timing, consciousness, incontinence, tongue biting), after (recovery time, postictal)
129
Exam post falls
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
Inv in post fall assessmsent
ECG, 24h tape | Imaging - CT head, X-ray neck, X-ray pelvis
131
Aims of falls risk assessment
Prevent future fall | Protective measures if do fall
132
Who is at risk of falling
Age >65yo >1 fall in last year RF - mobility, visual, balance, cognitive and refer on
133
Manage fall risk in clinic - 5
``` RF Home hazards Timed up and o test, turn 180 degrees Medication review - anticoagulation etc Osteoporosis risk ```
134
Bone assessment in elderly - 3
FRAX - 10y risk of fracture DEXA Bisphosphonates
135
DEXA scan results
T score: -1 - -2.5 = osteopoenia < -2.5 = ostoporosis
136
Manage low DEXA score
1st line - alendonate 2 - other PO Bisphosphonates 3 - newer agents, zoledronate IV
137
CT head immediate criteria - 4
GCS <13 at assessment of <15 2h after Suspected basal skull, open or dep[ressed fracture Seizures or focal neuro vomiting >1
138
CT head urgent criteria - 4
Retrograde amnesia >30m High impact trauma Bleeding diathesis - warfarin, clotting disorder Age >65yo
139
Hx of weakness?
[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
Focal weakness causes - 5 areas
``` UMN only - Stroke MS Tumour Bleed Meningitis ``` UMN and LMN (mostly cord) - MND Cord disease LMN only - neuropathy NMJ - MG Muscle - myopathy
141
Generalised causes of weakness
``` Frailty Anaemia Sarcopoenia Hypoglycaemia Electrolytes Hypoxia Infection Drug related ```
142
Ischaemic stroke - 3 types and exam findings
Emboli - cardiac, carotid Thrombotic in situ - large vessel, small perforated Rare - [3Vs] vasospasm for SAH, Vasculitis, Vvatershed stroke AF, murmur, carotid bruit
143
Haemorrhagic stroke - 6 causes and exam findings
[HHAATT] Head injury and Htn Anticoagulation and AVN Thrombolysis and Tumour Meningism, seizures, LOC
144
Stroke mimics - 4
Hypoglycaemia, Hemiplegic migraine Todd’s palsy (frontal lobe epilepsy), Tumour/haemrrange [HHTT]
145
Cardiac emboli strokes
TACS and PACS
146
Small vessel thrombotic diseae | Large vessel thrombotic disease
LACS | POCS
147
Why is macular spared in POCS
Bilateral supply
148
MCA stroke features
[Ms] Mouth and arms Mechanical speech impairment - broca’s
149
ACA stroke features
Legs and Wernicke’s
150
Cerebellar stroke
DANISH
151
Brainstem stroke features
Same side = CN problems | Other side = peripheral nerve problems
152
Wallenberg - PICA
IL Horner, dysphagia, DANISH | CL sensory
153
Weber - PCA midbrain
IL CN3 | CL weakness
154
Pontine stroke
IL CN6/7 | CL weakness
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Types of brainstem stroke
PICA, MCA midbrain, pontine
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Manage stroke immediate
``` [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) ```
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VTE after stroke?
Dont’ start LMWH as increased risk of haemorrhagic stroke | Aspirin 300mg
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LT stroke management
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
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TIA assessment?
``` ABCD2 criteria Age BP Clinical features Duration of sx Diabetes ``` <4 - clinic <1 >=4 clinic in 24h
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Manage TIA
Aspirin 300mg, statin, ECG TIA clinic within 24h ABCD2 assessment
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MS ?
AI CNS demyelination - discrete plaques disseminated in time and space
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Types of MS
Relapsing remitting | Secondary or primary progressive
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MS ?
AI CNS demyelination - discrete plaques disseminated in time (different times) and space (different probems) T cell demyelination repairs slowly
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Types of MS
Relapsing remitting | Secondary or primary progressive
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Features of MS
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)
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inv MS
MRI brain and spinal cord T2 [2 letters in MS] with gadloneum contrast LP - oligoclonal bands, ensure no inf before starting steroids
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Manage MS
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)
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Open angle glaucoma fundoscopy
Optic disc cupping
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Complication when DMARD started for MS
Misdiagnosis - Neuromuscular optica = optic neuritis and transverse myelitis Check anti-NMO antibodies when diagnosing MS Gets worse with DMARDs
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Manage spasticity in MS
1 - Baclofen | 2 - Botulinum
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Which ascending tract crosses
Lateral spinothalamic
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MND?
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
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Most common MND
Asymmetrical lateral sclerosis in anterior horn
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Features of asymmetrical lateral sclerosis
LMN arms - thenar wasting, split thumb, fasciculations | Umn legs
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4 types of MND
Asymmetric lateral sclerosis Primary lateral sclerosis Progressive muscular atrophy Progressive bulbar palsy
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Diagnosis of MND
Exclusion | Motor only, mixed umn/lmn or fasciculatins - suspect
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Manage MND
MDT Riluzole - anti glutaminergic Symptomatic/supportive Baclofen, diazepam
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Causes of cord ccompression - 5
``` Trauma - post disc prolapse Tumour - myeloma, mets Bleeding - haematoma Infection - abscess Degeneration - spondylosis ```
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Red flags for cord compression
[4Bs] Back pain Bilateral neurology incl saddle anaesthesia Bowel/bladder accident B symptoms - fever, night sweats, weight loss
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Bottom of cord?
Conus medularis L1 - S5
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Intrinsic cord disease? - 5
Tracts: Vascular - ASA infarction = anterior lateral tracts Inflammation - MS Infection - HTLV1 Metabolic - SACCD in b12 def Congenital - syringomyelia, Friedrich ataxia
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Immediate management of malignant cord compression
Dexamethasone MRI Neurosurgery referral
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What are polyneuropathyies
symmetrical and distal - demyelination gets or axonal
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Motor polyneuropathy
LMN features Guillan barre, paraneoplastic
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sensory neuropathy eg feature and causes
Glove and stocking DM, alcohol, b12
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Mixed neuropathy features and causes
Postural drops Retention/constipation Point and Shoot Diabetes, Guillan barre, HIV
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Myasthenia gravis?
AI - anti achr, anti musk
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Motor polyneuropathy features and causes
LMN features Guillan barre, paraneoplastic
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Sensory polyneuropathy feature and causes
Glove and stocking DM, alcohol, b12
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Manage MG
Anticholinesterase - pyridostigmine Immunosuppression - rescue IVIG, plasma X; DMARDs Thymectomy
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Myopathy?
Symmetrical proximal muscle wasting/weakness | Inherited or acquired
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Inv myopathy
Raised CK EMG shows short action potential Muscles biopsy diagnostic
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Inherited myopathies - 3
Musclular destroy Myotonic dystrophy Mitochndrial
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Acquired myopathies - 3
Myositis Metabolic Medicatios
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Assessing resp muscle weakness in neuromuscular disorder
FVC <1.5l = ABG - T2RF == ITU
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Cause of guillan barre and process
Campylobacter jejuni produces antibodies that cross reacts | 2w before weakness starts
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Inherited of DMD
X linked recessive
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Causes of incontinence
Stress: [Ps] Pelvic floor weakness Urge: [Ds] Detrusor overactivity
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Manage incontinence
Stress - Pelvic floor exercises PV tension free tape Urge - Diary and retraining therapy Drugs - anti muscarinics
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Retention of urine causes
Inpatient - 4Cs - constipation, Catheter blocked, colonised (inf), chemicals Outpatient - prostate, pelvic mass, paralysed bladder
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Presentation of urine retentiona n
No uterine Distended palpable bladder Delirium
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Inv urine retention
Bladder scan.- >500lm residual US KUB for hydronephrosis UE AKI
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Treat retention of urine
Identify cause and reverse Catheterise - clot washout, tamsulosin, gentamycin Chronic - catheterise with long term and refer
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Key drugs involved in cyp DDIs
``` Statin Warfarin OCP Theophylline [SWOT] ```
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Red flag sx headache
Meningitic - neck stiff, photophobia, fever, vomiting rash Pressure - worse on strain or morning, vision GCA in elderly - jaw claudication, scap tenderness (brushing hair)
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Red flag diagnoses
``` Inf - meningitis, encephalitis Bleed (EDH, SDH, SAH) Clot (pill?) SOL Acute closed angle glaucoma GCA ```
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Chronic headaches - 3 causes
Tension headache Migraine Cluster headache
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Migraine diagnosis
``` 5 attacks Lasting 4 hours to 3 days 2 of unilateral, pulsating, severe affecting life 1 of NV, phonophobia, photophobia [54321] ```
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Aura type in migraine?
Visual | Motor
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Common triggers for migraine
Crap time - stress Certain food - cheese, chocolate, caffeine COCP
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Treat mild headache with hx of asthma?
Paracetamol | No naproxen as asthma
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Severe occipital headache with hx of aut dom polycystic kidney disease
SAH - CT head or LP after 12h if neg CT
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Why wait for 12h to do LP for SAH
Wait for blood to breakdown to bilirubin - xanthochromia, as can get blood on LP anyway from trauma
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Treat idiopathic intracranial htn - 4
Weight loss Acetazolamide Topiramate - prevent seizures VP shunt/ON fenestration
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Sx of IIH - 4
Bilateral blurred vision with blurred discs on fundoscopy | Long term headache, worse with sex
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Unilateral headache Pale optic disc Amaurosis fugax
GCA - steroids and hospital | = Anterior ischaemic optic neuropathy
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GCA fundoscopy findings
Pale optic disc - anterior ischaemic optic neuropathy
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2 causes of pale optic disc
Anterior ischemic optic neuropathy - arteritic or nonarteritic (clot) GCA
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Classify seizure
Epilepsy vs provoked Partial.- simple, complex Generalised - tonic clonic, absence
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Inv epiepsy
EEG, MRI brain
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seizure treatment
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
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Temporal epilepsy sx - 4
Hallucinations Epigastric rising Automatisms Deja vu, dysphasia post ictal
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Frontal epilepsy sx - 3
Motor - posturing, head movements Jacksonian march Weakness post ictal - Todd’s
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Parietal epilepsy sx
Sensory
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Occipital epilepsy sx
Visual
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AED in pregnancy
Lamotrigine
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Manage status epilepticus
``` A-E, recovery position After 5m - IV lorazepam 2-4mg, After 15m - repeat bolus After 20m - phenytoin, anaesthetist After 30m - RSI, intubate, ITU ```
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Status epilepticus OSCE activities - 2
1) Start timing | 2) Start drawing up lorazepam 2-4mg 2x boluses, and phenytoin
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Pseudoseizures - 3
Unexplained movements Rapid resolution Triggers eg stress
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Rapidly resolving unpredictable seizures?
Pseudoseizure
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Types of tremor
[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
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Causes of action or postural tremor
``` Benign essential tremor Endocrine - hyperthyroid Alcohol withdrawal Toxins - b agonist Stress//anxiety [BEATS} ```
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Parkinson’s diseae?
Reduced dopamnergic neutrons in pars compacta of substantianigra
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Sx parkinson’s
``` Motor change - hypokinesia, rigidity, resting tremor - UL onset Autonic instability Sleep disorder Krazy - depression [MASK] ```
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Manage Parkinson’s
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
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When to rule out parkinson’s disease with tremor
Bilateral/symmetrical at start - Parkinsonism
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Manage benign essential tremor
Propanolol
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Features of benign essential tremor
Aut dom Better with alcohol Worse with specific movements
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What is Bell’s palsy 2 RF and inv and management
``` 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
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Types of delirium and key features
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
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Predisposing factors for delirium
``` Dementia Old Polypharmacy Functional or sensory impairment Malnutrition Comorbidities ```
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Precipitating factors for delirium
``` Hospitalisation Catheterisation Acute illness Electrolyte disturbances - sodium Drugs - opiates, anticholinergics, sedation Renal impairment Alcohol Peri-op Constipation ```
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Differentiate delirium from dementia
Delirium - sudden onset, reversible, impaired consciousness, inattentive, psychomotor changes Dementia - insidious, permanent, no impairment of consciousness, normal attention, no psychomotor changes
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What is dementia and diagnosis
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
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Alzheimer’s, what is it, 4 RF for dementia and management
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
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Vascular dementia
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
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Lewy body dementia
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
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Differentials for dementia
``` Alzheimer’s Vascular Lewy body Frontotemporal - Pick’s Normal pressure hydrocephalus Depression ``` Mild cognitive impairment - objective cognitive impairment but doesn’t meet dementia criteria
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Features of extradural haemorrhage
Lucid interval then deterioration consciousness, headache, confusion, fits Hemiparesis, brisk reflexes, upwards plantar Eventually, ipsilateral pupil dilates
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What is Horner’s syndrome and causes
1. miosis 2. Partial ptosis 3. Anhydrosis From interruption to sympathetic supply - thoracic outlet (pancoast), brainstem (demyelination or vascular) or cord (syringomyelia)
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ABx for meningitis in adults
Cefotaxime and ampicillin if >55yo | Cefotaxime alone if <55yo
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Triptans and CI to triptans
5-HT3 agonist Coronary artery spasm Uncontrolled ypertension SSRIs
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Prevention of migraine
If >=2 a month or not responding to treatment 1 - Propranolol, amitryptiline, calcium channel blockers 2 - Valproate, gabapentin,
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What is MND and sx
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
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Grading of SAH and management and 4 complicatiotns
``` 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
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What drugs to start for temporal arteritis
Prednisolone PPI Alendronate
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Wernicke’s encephalopathy features
Confusion Ataxia Opthalmoplegia Memory loss, hypothermia, hypotension, reduced consciousness From thiamine B1 deficiency Treat with thiamine IV then PO
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Requirements for diagnosis of different strokes
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
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Manage TIA
``` 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 ```
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What is Huntingdon’s disease
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
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Cellulitis classification
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
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Signs of degenerative cervical myelopathy and treatment
Neck pain Bilateral median nerve dysfunction Sensory, motor, autonomic MRI - cervical canal stenosis Manage: surgical decompression, physio and analgesia
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Chronic inflammatory demyelinating polyneuropathy
Widespread neuropathy, motor symptoms predominant MRI to rule out MS CSF = high protein Treat - high dose steroids
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Subacute degeneration of cord
B12 deficiency Posterior column first = proprioception, light touch, vibration Lateral = spastic weakness, UMN signs
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Brown sequard
Contralateral pain, temperature and crude touch | Ipsilateral UMN, vibration, proprioception and fine touch
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Cause of CN3 palsy and sx
Posterior communicating artery aneurysm - severe headache and loss of visual acuity down and out, ptosis, dilated
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Encephalitis causes and inv and treatmetn
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
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Sx and inv and management of cerebral abscess
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