Neuro Flashcards
1
Q
Features of migraine
A
Typically lasts 4-72 hours
Unilateral headache: poudning or throbbing
Nausea + vomiting
Photopboia
Phonophobia
With/without aura
2
Q
Common triggers of migraine
A
CHOCOLATE
Chocolate (Cheese)
Hangover
Oral contraceptive
Caffeine
Orgasm
Anxiety/Alcohol
Travel
Exercise
Others: periods, injury, being hungry, smoking etc
3
Q
Medical management of acute migraine
A
Paracetamol
Triptans - sumatriptan 50mg as soon as migraine starts
NSAIDs
Antiemetics for vomiting
4
Q
Medications for migraine prophylaxis
A
Propanolol (preferred in women of child-bearing age)
Topiramate (teratogenic and can reduce effect of hormonal contraceptives)
Amitryptyline
5
Q
ABCD2 score
A
Used to predict risk of stroke after a TIA
Age >60 years = 1
Blood pressure >140/90 = 1
Clinical features:
- Unilateral weakness = 2
- Speech disturbance without weakness = 1
Duration of symptoms
- >60 minutes = 2
- 10-60 minutes = 1
- <10 minutes = 0
Diabestes = 1
6
Q
Risk of stroke following TIA using ABCD2
A
0-3 = 1%
4-5 = 4%
6-7 = 8%
7
Q
Prevention of stroke in patients with TIA
A
If scoring >/= 4 –> 300mg Aspirin immediately, specialist assessment within 24 hours of onset
</= 3 = low risk –> 300mg aspirin, refer to be seen by specialist and investigated within 1 week of onset
8
Q
TIA
A
Transient neurological dysfunction secondary to ischaemia without infarction
(Traditional definition = symptoms resolve completely within 24 hours of onset)
9
Q
Amaurosis fugax
A
Sudden loss of vision in one eye
Caused by infarct in retinal artery/ies or in ophthalmic artery
Described as black curtain coming across the vision
Important differential = migraine
10
Q
Presentation of TIA
A
Sudden, focal neurological deficit e.g.
Unilateral weakness or sensory loss
Dysphagia
Ataxia, vertigo or incoordination
Amaurosis fugax
Homonymous hemianopia
Cranial nerve defects
11
Q
Blood tests in TIA
A
FBC
HBA1c
ESR
U+Es
Bone profile
LFTs
Lipid profile
Routine coag/clotting screen
INR (if on warfarin)
12
Q
Main investigation in TIA
A
MRI head with diffusion-weighted imaging
CT used if MRI unavailable
13
Q
Other investigations in TIA
A
ECG - arrhythmias
Echo - only used if suspicion of heart disease or confirmed stroke
Carotid dopplers
14
Q
Level of carotid stenosis required for endarterectomy
A
> 70%
Only offered if patient is not severely disabled
15
Q
Crescendo TIA
A
> 1 TIA in the last week - severe risk for future stroke
16
Q
Acute management of TIA
A
300mg aspirin (continued for two weeks)
Clopidogrel 300mg if aspirin contraindicated/not tolerated
Immediate admission for imaging if on an anticoagulant, or has a bleeding disorder
17
Q
Long-term therapy for TIA
A
Clopidogrel 75mg od (aspirin if cannot have clopidogrel)
Statin (atorvastatin 20-80mg od) in all patients
Consider anti-coagulation for AF
Modification of other risk factor e.g. anti-hypertensives
18
Q
Triad of Parkinson’s disease
A
Resting tremor
Rigidity
Bradykinesia
19
Q
Pathophysiology of PD
A
Progressive decrease in dopamine produced by substantia nigra in the basal ganglia - responsible for coordinating habital movement, voluntary movement, and learning specific movement patterns
20
Q
Presentation of PD
A
Stooped posture
Facial masking
Forward tilit
Reduced arm swing
Pill-rolling tremor (at rest, worse if distracted)
Cogwheel rigidity
Bradykinesa
- Micrographia
- Shuffling gait
- Difficulty initiating movements
- Difficulting turning
- Hypomimia
21
Q
Other features of PD
A
Depression
Sleep disturbance + insomnia
Anosmia
Postural instability
Cognitive impairment + memory problems
22
Q
Differences between parkinson’s tremor + benign essential tremor
A
PD = asymmetrical, lower frequency, worse at rest, improves with intentional movement, no change with alcohol
BET = symmetrical, higher frequency, improves at rest, worse with intentional movement, improves with alcohol
23
Q
Management of benign essential tremor
A
Primidone
Propanolol
Deep brain stimulation if refractory to drug treatment and causes severe functional impairment
24
Q
Scan that can be used to identify Parkinson’s disease/atypical parkinsonian disorders
A
DAT scan
Shows evidence of nigrostriatal degeneration
25
Parkinson's-plus syndromes
Multiple system atrophy --> autonomic + cerebellar dysfunction
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration
26
Management of PD
Levodopa (dopamine cannot cross BBB)
Given with something to improve half-life (peripheral decarboxylase inhibitors) e.g. carbidopa, benserazide -->
Co-benyldopa, or co-careldopa
27
Side-effects of levodopa treatment
Efficacy decreases over time
On-off effect at end of dose
Nausea/GI upset
Dyskinesias: dystonia, chorea, athetosis
Psychosis
Compulsive behaviours
28
Other options for management of PD
Catechol-o-methyltransferanse (COMT) inhibitors e.g. entacapone - extends effective duration of levodopa
Non-ergot derived dopamine agonists e.g. ropinirole
Ergot-derived dopamine agonists e.g. bromocriptine, pergolide, carbergoline: prolonged use --> pulmonary fibrosis
Monoamine oxidase-B inhibitors e.g. selegiline, rasagiline
29
What drugs may induce Parkinsonism
Anti-psychotics
Antiemetics e.g. metoclopramide
Lithium
Methyldopa
Antiepileptic drugs
Calcum channel blockers
30
Four most common forms of MND
Amyotrophic lateral sclerosis
Progressive bulbar palsy - affects more swallowing + talking
Progressive muscular atrophy
Primary lateral sclerosis
31
Presentation of MND (ALS)
Signs of LMN disease
Signs of UMN disease
NO SENSORY PROBLEMS
Progressive weakness and wasting of limbs (symmetrical) - starts at hands and spreads. May begin unilateral, but will become bilateral
No pain usually
Important: Loss of muscle tone + spasticity rarely seen together
32
Signs of UMN disease
- Increased tone or spasticity
- Brisk reflexes
- Upgoing plantar responses
33
Signs of LMN disease
- Muscle wasting
- Reduced tone
- Fasciculations
- Reduced reflexes
34
Presentation of progressive bulbar palsy
Problems with speech and swallowing
Dysphagia
Dysarthria
Nasal regurgitation
Choking
Tongue may be immobile, or wasted + fasciculating
Progressive
35
Progressive muscular atrophy
Typically only affects LMNs of upper limbs
36
Spinal muscular atrophy
Characterised by wasting and weakness of mucles
37
Management of ALS
Riluzole - used to improve prognosis, but only by a few months. Sodium channel blocker. Most effective in patients with bulbar signs
Baclofen - GABA agonist, helps reduce spasticity
Amitriptyline/propantheline for drooling
Ventilation support
38
Important features that differentiate MND from other similar diseases
Bladder never affected
No sensory signs
Ocular muscles never affected
39
Commonest causative agents of bacterial meningitis (general population)
Neisseria meningitidis (gram negative diplococci)
Streptococcus pneumoniae
(also haemophilus influenzae in 3months - 6 years)
40
Commonest causative agent of bacterial meningitis in neonates
Group B streptococcus
41
Common causative agents of bacterial meningitis in children 0-3 months
E coli
Listeria monocytogenes
42
Presentation of meningitis
Fever
Neck stiffness
Vomiting/poor feeding
Hedache
Photophobia
Altered conciousness
Seuizures (infective causes)
43
Signs of meningitis
Tachycardia
Kernig's sign - flex hip with knee flexed, extend knee. Spasm in hamstrings = +ve
Brudzinski's sign = passively flex neck. Flexion of hip and/or knee = +ve
Fever (if infective)
44
Late signs of meningitis (in children)
Bulging fontanelle
Neck stiffness
Opisthotonos (arched back)
Rash (bacterial causes only) --> petechial + non-blancing (suggests septicaemia)
Fall in BP
45
Which children should receive an LP to rule out meningitis
Under 1 months presenting with fever
1-3 months with fever + unwell
Under 1 years with unexplained fever and other features of serious illness
46
Management of bacterial meningitis in community
- IM or IV benzylpenicillin
- Transfer to hospital
47
Management of bacterial meningitis in hospital
- Blood culture, LP for CSF prior to antibiotics where possible
- Meningococcal PCR testing
- <3 months old --> cefotaxime + amoxicillin (cover listeria)
- >3 months --> ceftriaxone
- + vancomycin if possible of penicillin resistant pneumococcal infection
- Steroids e.g. dexamethasone to prevent long-term deficitns
48
Post-exposure prophylaxis for bacterial meningitis
Single dose of ciprofloxacin (given orally)
Ideally given within 24 hours of initial diagnosis
Anyone with prolonged contact within 7 days prior to onset of illness
49
Commonest causes of viral meningitis
Herpes simplex virus
Enterovirus
Varicella zoster virus
50
Management of viral meningitis
Often just supportive management
Aciclovir if HSV
51
CSF findings in bacterial meningitis
Cloudy
High protein
Low glucose
High WCC (neutrophils)
Culture +ve for bacteria
52
CSF findings in viral meningitis
Clear
Protein mildly raised or normal
Normal glucose
High WCC (lymphocytes)
Negative culture
53
Complications of meningitis
Hearing loss
Seizures + epilepsy
Cognitive impairment + learning disability
Memory loss
Focal neurological deficits e.g. limb weakness or spasticity
54
C5 myotome
Shoulder abduction + external rotation
Elbow flexion
55
Nerve for wrist extension
C6
56
Nerve for elbow extension + wrist flexion
C7
57
Nerve for finger flexion + thumb extension
C8
58
Nerve for finger abduction
T1
59
Nerve for hip flexion
L2
60
Nerve for knee extension
L3
61
Nerve for ankle dorsiflexion
L4
62
Nerve for great toe extension
L5
63
Nerve for ankle plantarflexion
S1
64
C4 dermatome
Over acromioclavicular joint
65
C5 dermatome
Laterl aspect of lower edge of deltoid
66
C6 dermatome
Palmar side of thumb e.g. thenar eminence
67
C7 dermatome
Palmar side middle finger
68
C8 dermatome
Palmar side little finger
69
T1 dermatome
Medial aspect antecubital fossa, proximal to medial epicondyle of humerus e.g. soft upper underarm, closest to body
70
Common features of non-epileptic attack
Arms flexing + extending
Pelvic thrusting
Sudden drop at start
Eyes closed
Prolonged seizures (>30 minutes)
Symptoms wax and wane
71
Features of simple partial seizure
Patient remains conscious
Isolated limb jerking
Isolated head turning (away from side of seizure)
Isolated parasthesia
Weaness of limbs may follow
72
What is Todd's paralysis
Weakness of limbs following a seizure (usually a simple partial motor seizure e.g, Jacksonian)
73
Features of generalised tonic-clonic seizures
Loss of consciousness
Muscle tensing + muscle jerking episodes (usually this order)
Tongue biting
Incontinence
Groaning
Irregular breathing
Confused post-ictally: drowsy, irritable, depressed
74
Management of tonic-clonic seizures
1st line = sodium valproate
2nd line = lamotrigine/carbamazepine
75
Features of focal seizures/complex partial seizures e.g. temporal lobe seizures
Affects hearing, speech, memory and emotions
e.g.
Hallucinations
Memory flashbacks
Deja-vu/jamais-vu
Vertigo
Lip-smacking/other disturbances
76
Management of focal seizures
1st = carbamazepine or lamotrigine
2nd = sodium valproate or levetiracetam
77
Management of absence seizures
Sodium valproate or ethosuximide
78
Features of atonic seizures
Drop attacks
Brief lapses in muscle tone
Typically <3 minutes
Begin in childhood
May be associated with Lennox-Gastaut syndrome
79
Management of atonic seizures
1st = sodium valproate
2nd = lamotrigine
80
Definition of status epilepticus
Seizure >5 minutes
OR >3 seizures in 1 hour
81
Management of status epilepticus in hospital
Secure airway
O2 (high concentration)
Assess cardiac + resp function
Check blood glucose - rule out hypoglycaemia
Gain IV access
IV lorazepam 4mg, repeated after 10 minutes if seizures continue
--> IV phenobarbital or phenytoin
82
Options for management of status epilepticus in community
Buccal midazolam
Rectal diazepam
83
Medications that should be avoided in Parkinson's disease
Prochlorperazine
Metoclompramide
Haloperidol
Chlorpromazine
Promazine
84
Presentation of brain abscess
Headache - often dull, persistent
Fever - may be absent, not swinging pyrexia
Focal neurology e.g. oculomotor/abducens palsy secondary to raised intracranial pressure
Other features of raised ICP:
- Nausea
- Papilloedema
- Seizures
85
Investigations for brain abscess
CT head - rim-enhancing lesion with a central cavity, surrounding oedema
86
Most common pattern for multiple sclerosis
Relapsing-remitting
87
Risk factors for IIH
Obesity
Female sex
Pregnancy
Drugs: COCP, steroids, TCAs, Vitamin A, lithium
88
Features of IIH
Headache
Blurred vision
Papilloedema
Enlarged blind spot
Sixth nerve palsy may be present
89
Management of IIH
Weight loss
Diuretcis e.g. acetazolamide
Topiramata may be used --> can also help with weight loss
Repeat LP
Surgery
90
Definition of status epilepticus
Single seizure lasting >5 minutes, or
>/= 2 seizures within a 5-minute period without the person returning to normal between them
91
Features of third nerve palsy
Eye 'down and out'
Ptosis
Pupil may be dilated
Direct light reflex absent, consensual light reflex may be present
92
Causes of third nerve palsy
Diabetes mellitus
Vasculitis
Posterior communicating artery aneurysm
Cavernous sinus thrombosis
Weber's syndrome
Multiple sclerosis
93
Features of post-concussion syndrome
Headache
Fatigue
Anxiety/depression
Dizziness
94
International Headache Society for migraine without aura
A - at least 5 attacks, fulfilling criteria B-D
B - headaches lasting 4-72 hours
C - headache has at least two of:
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routine physical activity
D - during headahce, at least one of:
- Nausea and/or vomiting
- Photophobia + phonophobia
E - not attributred to another disorder
95
Difference in presentation of migraine in children
Attacks may be shorter lasting
Headache more commonly bilateral
Gastrointestinal disturbance is more prominent
96
Presentation of cluster headaches
Typically unilateral symptoms:
Red, swollen and watering eye
Miosis (pupil constriction)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating
Intense, sharp, stabbing pain around one eye
97
Timing of cluster headaches
Pain usually once or twice a day
Each episode lasts 15 minutes - 2 hours
Clusters typically last 4-12 weeks
98
Acute management of cluster headaches
Triptans e.g. sumatriptan 6mg injected subcutaneously
High flow 100% oxygen for 15-20 minutes
99
Prophylaxis of cluster headaches
Verapamil
Lithium
Prednisolone
100
Management of neuropathic pain
1st line: amitriptyline, duloxetine, gabapentin, or pregabalin
- If does not work, try one of the other three
- Typically used as monotherapy
- NB: carbamazepine used in trigeminal neuralgia
Tramadol - used as rescue therapy for exacerbations
Topical capsaicin - used or localised neuropathic pain
101
Features of encephalitis
Fever
Headache
Altered mental status
And/or neurological deficits
May also have seizures, behavioural changes (e.g. psychotic or affective features), brainstem dysfunction, memory problems
102
Pathophysiology of encephalitis
HSV-1 responsible for 95% cases in adults
Typically affects temporal + inferior frontal lobes
103
MRI findings on encephalitis
Prominent swelling
Increased signal of the brain in affected areas
104
Investigations in encephalitis
CSF: lymphocytosis, elevated protein
PCR for HSV
Neuroimaging: MRI is better, medial temporal + inferior frontal changes (or normal)
EEG: lateralised periodic discharges at 2Hz
105
Management of encephalitis
IV aciclovir
106
Withdrawing analgesia in medication overuse headache
Simple analgesia (e.g. paracetamol, NSAIDs) + triptans: stop abruptly
Opiods: withdraw gradually
107
Features of medication overuse headaches
Present for 15 days/more per month
Developed or worsened whilst taking regular symptomatic medication
Higher risk in patients using opioids and triptans
May be psychiatric co-morbidity
108
What to do when a PD patient cannot take oral medication
Levodopa can only be given orally --> use a dopamine agonist patch
109
Key difference between LMN and UMN facial nerve palsy
UMN palsy --> forehead sparing, due to bilateral innervation of the forehead
LMN palsy --> forehead not spared
110
Examples of UMN lesions causing facial nerve palsy
Unilateral:
Cerebrovascular accidents e.g. strokes
Tumours
Bilateral (rare):
Psuedobulbar palsies
Motor neurone disease
111
Bell's palsy
Unilateral LMN facial nerve palsy
112
Recovery from Bell's palsy
Majority of patients fully recover over several weeks
Recovery may take up to 12 months
1/3 are left with some residual weakness
113
Management of Bell's palsy
If patient presents within 72 hours of developing symptoms:
- 50mg prednisolone for 10 days, or
- 60mg pred for 5 days, followed by a 5-day reducing regime of 10mg/day
Antivirals may offer some benefit
Lubricating eye drops to prevent eye damage
Tape to keep eye closed at night
114
Features of Bell's palsy
Forehead does not rise
Drooping of eyelid - exposing eye
Loss of nasolabial fold
Patients may also notice post-auricular pain (prior to paralysis), altered taste, dry eyes, hyperacusis
115
Complication of Bell's palsy
Exposure keratopathy --> requires ophthalmology review
116
Follow-up in Bell's palsy
If paralysis shows no sign of improvement after 3 weeks --> urgent ENT referral
Plastic surgery referral may be required for patients with more long-standing weakness
117
What is Guillain-Barre syndrome
Acute paralytic polyneuropathy
Causes acute, symmetrical, ascending weakness, as well as sensory symptoms
Usually triggered by an infection
118
Infections associated with Guillain-Barre syndrome
Campylobacter jejuni
Cytomegalovirus
Epstein-Barr virus
119
Main features of GBS
Symmetrical ascending weakness - starting at feet, moving up body
Reduced reflexes
May have peripheral loss of sensation, or neuropathic pain (mild sensory symptoms)
May have history of gastroenteritis
120
Other features of GBS
Respiratory muscle weakness
May progress to cranial nerves --> facial nerve palsy, diplopia, oropharyngeal weakness
Autonomic involvements --> urinary retention, diarrhoea
Papilloedema may be present
121
Investigations in GBS
Lumbar puncture
- Rise in protein
- Normal WBC count (albuminocytologic dissociation)
- Normal glucose
Nerve conduction studies may be performed
- Decreased motor nerve conduction velocity (demyelination)
- Prolonged distal motor latency
- Increased F wave latency
122
Management of GBS
IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis
May require respiratory support
123
What is multiple sclerosis
Chronic and progressive condition
Involves demyelination of the myelinated neurones in the CNS
Caused by an inflammatory process involving activation of immune cells against the myelin
124
Diagnosis of MS
Lesions disseminated in time + space
However, if one episode of acute lesion e.g. optic neuritis, and an MRI showing a previous lesion, or positive oligoclonal bands on CSF --> can diagnose MS as these Ix show dissemination
For time dissemination: lasts longer than 24 hours + more than 1 month apart (typically)
125
Typical patient affected by MS
2-3x more common in women
Present around 20-40 years old
126
Classifications of MS
Relapsing-remitting
Primary progressive MS
Secondary progessive MS (50% of patients with relapsing-remitting will develop this within 15 years of onset)
127
Visual manifestations of MS
Optic neuritis
INO: disorder of conjugate lateral gaze (failure to adduct eg. look right, right eye abducts, left eye remains central)
Abducens nerve palsy eg. look right, right eye fails to abduct
128
Features of optic neuritis
- Visual loss
- Blurred vision
- Pain behind eye, and on movement
- Central scotoma (enlarged blind spot)
- Poor colour differentiation (dyschromatopsia --> typically cannot see red)
- Poor visual acuity
- Relevant afferent pupillary defect
- Optic nerve swelling seen on fundoscopy
129
Motor + coordination manifestations of MS
Progressve paraparesis
UMN signs: spasticity, reduced power, hyper-reflexia
Transverse myelitis: sensory + motor symptoms below level of lesion in spine, with potential bladder/bowel involvement
Cerebellar syndrome: ataxia, slurred speech, intention tremor, nystagmus, vertigo + clumsiness
130
Sensory + autonomic manifestations of MS
Paraesthesia
Pain
Heat sensitivity (Uhthoff phenomenon)
Sexual dysfunction
Bladder + bowel dysfunction
131
Uhthoff's phenomenon
Neuro symptoms are exacerbated by increases in body temperature
132
Lhermitte's sign
A sign on physical examination seen in MS
Shooting pain some patients expereicne when in neck flexion
133
Cognitive + psychological manifestations of MS
Cognitive impairment
Depression --> can also affect memory, attention + concentration
Fatigue
134
What is an MS attack
An episode of neurological symptoms that relate to an inflammatory demyelinating lesion
Lasts >24 hours, with or without recovery
Must be more than 30 days between attacks to count as separate episodes
135
Clinically isolated syndrome
First episode of demyelination + neurological signs + symptoms
Cannot diagnose MS from this as lesions must be 'disseminated in time + space'
136
Investigations in MS
MRI scans - demonstrate lesions
Lumbar puncture - detect oligoclonal bands in CSF (more than seen in serum, not specific to MS)
137
Non-MS causes of optic neuritis
Sarcoidosis
Systemic lupus erythematous
Diabetes
Syphilis/HIV
Measles
Mumps
Lyme disease
B12 deficiency
138
Management of acute relapse MS
High dose steroids e.g. oral or IV methylprednisolone for 5 days
Used to shorten duration of relapse, not alter degree of recovery
139
Management of MS
DMARDs + biologic therapy
Natalizumab
Fingolimod
Beta-interferon
Glatiramer acetate
140
Myasthenia Gravis
Autoimmune condition causing muscle weakness that gets progressively worse with activity and improves with rest
Disorder of neuromuscular junctions - prevention of binding of ACh to receptors
Typically affects women <40 years old, and men >60
141
Tumoir associated with myasthenia gravis
Thymoma (tumour of thymus gland)
142
Muscle weakness in myasthenia gravis
Weakness that gets worse with muscle use, and improves with rest - symptoms typically worse at end of day
Symptoms mostly affect proximal muscles + small muscles of head + neck
143
Presentation of myasthenia gravis
Diplopia (extraocular muscles)
Ptosis (eyelid weakness)
Weakness in facial movements
Difficulty swallowing
Fatigue in jaw with chewing
Slurred speech
Progressive weakness with repetitive movements
144
How to elicit signs of myasthenia gravis on examination
Repeated blinking --> exacerbate ptosis
Prolonged upward gazing --> exacerbate diplopia on further eye movement testing
Repeated abduction of one arm 20 times --> unilateral weakness when comparing sides
Test forced vital capacity
145
Diagnosis of myasthenia gravis
ACh-receptor antibodies (85% patients)
Muscle-specific kinase antibodies (MuS)
LRP4 antibodies (low-density lipoprotein receptor-related protein 4)
CT/MRI thymus - look for thymoma
Edrophonium test
146
Edrophonium test
Patients given IV dose of edrophonium chloride (or neostigmine)
Prevents breakdown of acetylcholine in NMJ
Briefly + temporarily relieves weakness
147
Management of myasthenia gravis
Reversible acetylcholinesterase inhibitors (pyridostigmine or neostigmine)
Immunosuppression e.g. prednisolone or azathioprine
Thymectomy (even if no thymoma)
Rituximab - reduces production of antibodies
148
Myasthenic crisis
Severe complication of myasthenia gravis
Causes an acute worsening of symptoms, often triggered by another illness e.g. resp tract infection
Can lead to respiratory failure --> may required ventilation
Perform bedside FVC + arterial blood fas analysis
Immunomodulatory therapies: IVIG and plasma exchange
149
Drugs that may exacerbate myasthenia
Penicillamine
Quinidine, procainamide
Beta-blockers
Lithium
Phenytoin
Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
150
Ptosis + dilated pupil vs. constricted pupil
Dilated = third nerve palsy
Constricted = Horner's
151
Presentation of Horner's syndrome
Ptosis
Miosis
Anhidrosis
May also have enopthalmos
Light + accomodation reflexes not affected
152
What is Horner's syndrome
Caused by damage to sympathetic nervous system supply to the face
153
Central causes of Horner's syndrome
Central lesions cause anhidrosis of trunk + arm as well as face (4Ss)
- Stroke
- Multiple Sclerosis
- Swelling (tumours)
- Syringomyelia (cyst in spinal cord)
154
Pre-ganglionic causes of Horner's syndrome
Anhidrosis of face only
4Ts
- Tumour (Pancoast's tumour)
- Trauma
- Thyroidectomy
- Top rib (cervical rib growing above first rib above clavicle)
155
Post-ganglionic causes of Horner's syndrome
No anhidrosis
4Cs
- Carotid aneurysm
- Carotid artery dissection
- Cavernous sinus thrombosis
- Cluster headache
156
Diagnosis of Horner syndrome
Cocaine eye drops - causes normal eye to dilate, but no reaction of Horner syndrome pupil
Low concentration adrenaline eye drops - won't dilate normal pupil, does dilate Horner syndrome pupil
157
Key features of progressive supranuclear palsy
PSP = problem seeing planes = vertical gaze palsy
Parkinsonism symptoms
Dysarthria
158
Key features of multi-system atrophy
Parkinsonism
Features of affect on other systems
e.g. postural hypotension
Ataxia
Urinary system --> incontinence/other bladder problems
Erectile dysfunction
159
Causes of homonymous hemianopia
Incongruous defects: Lesion of optic tract
Congruous defects: lesion of optic radiation, or occipital cortex
Macula sparing: lesion of occipital cortex
160
Causes of homonymous quadrantopias
Superior: lesion of inferior optic radiations in temporal lobe (Meyer's loop)
Inferior: lesion of superior optic radiations in parietal lobe
PITS (parietal - inferior, temporal-superior)
161
Cause of bitemporal hemianopia
Lesion of optic chiasm
Upper quadrant defect > lower quadrant = inferior chiasmal compression, commonly pituitary tumour
Lower > upper = superior chiasmal compression, commonly a craniopharyngioma
162
Timeframe for stroke thrombolysis
Only consider if <4.5 hours since symptoms
Must exclude haemorrhage first
163
Timeframe for stroke thrombectomy
Soon as possible - within 6 hours of symptom onset
Within 4.5 hours if given with thrombolysis
Can be given if known to be well between 6-24 hours previously depending on imaging
164
Secondary prevention for stroke after ischaemic stroke
In people who have had an ischaemic stroke: clopidogrel
2nd line = aspirin + dipyridamole
165
Features of anterior inferior cerebellar artery occlusion
Lateral pontine syndrome -->
Sudden onset vertigo + vomiting
Ipsilateral: facial paralysis, deafness, facial pain + temp loss
Contralateral: limb/torso pain + temperature loss
Ataxia
Nystagmus
166
Features of anterior cerebral artery lesion
Contralateral hemiparesis + sensory loss
Lower extremity > upper
May have personality changes
167
Features of middle cerebral artery lesion
Contralateral hemiparesis + sensory loss
Upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
168
Features of posterior cerebral artery lesion
Contralateral homonymous hemianopia with macular sparing
Visual agnosia - inability to recognise visually presnted objects
No facial blindness
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Features of lesion affecting branches of posterior cerebral artery supplying midbrain
Weber's syndrome
Ipsilateral CN III palsy
Contralateral weakness of upper + lower extremity
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Features of lesion affecting posterior inferior cerebellar artery
Wallenberg syndrome/lateral medullary syndrome
Ipsilateral: facial pain + temperature loss
Contralateral: limb/torso pain, and temperature loss
Nystagmus
Ataxia
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What is a lacunar stroke
Stroke involving the perforating arteries around the internal capsule, thalamus and basal ganglia
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Presentation of lacunar strokes
Isolated: hemiparesis, hemisensory loss or hemiparesis with limb ataxia
May have have dysarthria/clumsy hand syndrome
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What is autonomic dysreflexia
Clinical syndrome
Occurs in patients with spinal cord at, or above, T6 level
Afferent signals, commonly triggered by faecal impaction or urinary retention, cause a sympatheitc spinal reflex
Parasympathetic response prevented by cord lesion --> unbalanced physiologiccal response
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Features of autonomic dysreflexia
Commonly history of constipation or urinary retention
Hx of spinal cord lesion at, or above, T6 spinal level
Extreme hypertension
Sweating + flushing above level of cord lesion
Agitation
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Red flag features for headache
Sudden onset headache, reaching maximum intensity within 5 minutes
Vomiting without other obvious cause
Headache worse with fever
New-onset neurological deficit/cognitive dysfunction
Change in personality
Impaired level of consciousness
Headahce triggered by cough, valsalva, sneeze or exercise
Headache changing with posture
Substantial change in characteristics of headache
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Red flag features in personal history for headache
Recent (last 3 months) head trauma
Compromised immunity
<20 years old with history of malignancy
Hx malignancy known to have brain metastases
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Cushing reflex
Response to raised ICP
--> hypertension + bradycardia
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How to calculate cerebral perfusion pressure
Mean arterial pressure - intracranial pressure
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Features of subdural haemorrhage
Caused by rupture in bridging veins between dura + arachnoid mater
CT: crescent shape, not limited by cranial sutures
(bright if acute, hypodense if chronic)
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Features of extradural haemorrhage
Typically rupture of middle meningeal artery
Can be associated with fracture of temporal bone
CT: bi-convex shape, limited by cranial sutures
Typical: young patient, traumatic head injury, ongoing headache. Period of improved neuro symptoms + consciousness followed by rapid decline
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First line radiological investigation for suspected stroke
Non-contrast CT head - needed to rule out intracranial haemorrhage
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Causes of raised ICP
Idiopathic intracranial hypertension
Traumatic head injuries
Infection e.g. meningitis
Tumours
Hydrocephalus
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Features of raised ICP
Headache
Vomiting
Reduced levels of consciousness
Papilloedema
Cushing's triad: widening pulse pressure, bradycardia, irregular breathing
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Investigations for raised ICP
Neuroimaging to determine cause
Invasive ICP monitoring
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Management of raised ICP
Treat underlying cause
Head elevation to 30 degrees
IV mannitol may be used as an osmotic diuretic
Controlled hyperventilation --> aim to reduce pCO2
Removal of CSF e.g. repeated LP
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Features of intracranial venous thrombosis
Headache (may be sudden onset)
N+V
Reduced conciousness
Generally features of raised ICP
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Investigation for intracranial venous thrombosis
MRI venography = gold standard
- CT venography = alternative
D-dimer may be elevated
Non-contrast CT head often normal
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Management of intracranial venous thrombosis
Anticoagulation:
- LMWH acutely
- Warfarin for longer term
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Management of optic neuritis
Resolves in around 6 weeks
Oral steroids may speed up recovery/lessen pain
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Features of temporal lobe seizures
HEAD
Hallucinations
Epigastric rising/Emotional
Automatisms e.g. lip smacking/grabbing/plucking
Deja vu/Dysphasia post-ictal
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Features of frontal lobe seizures
Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march (clonic movements travelling proximally)
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Presentation of brain abscess
Headache: often dull, persistent
Fever: may be absent
Focal neurology e.g. oculomotor or abducens nerve palsy, secondary to raised ICP
Other features of raised ICP: nausea, papilloedema, seizures
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Investigations of brain abscess
Imaging with CT scanning - ring-enhancing lesion
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Management of brain abscess
Surgery: craniotomy + abscess cavity debrided
IV antibiotics: 3rd gen cephalosporin e.g. ceftriaxone, and metronidazole
Intracranial pressure management e.g. dexamethasone
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Inheritance of Charcot-Marie-Tooth disease
Most mutations are inherited in an autosomal dominant pattern
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Features of Charcot-Marie-Tooth
High foot arches (pes cavus)
Distal muscle wasting --> inverted champagne bottle legs
Weakness in lower legs (loss of ankle dorsiflexion)
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss
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Causes of peripheral neuropathy
A - Alcohol
B - B12 deficiency
C - Cancer + CKD
D - Diabetes + Drugs (e.g. isoniazid, amiodarone and cisplatin)
E - Every vasculitis
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Definition of overuse of medication (for headaches)
Applies to opioids + triptans
Using the medication on 10 days or more per month, for 3 months or more
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Features of medication overuse headaches
Often tension-type headache, but can have migraine-like characteristics
Present for 15 days or more per month
Worse after exercise
Worst in the morning
Resolve within 2 months of stopping the causative medication
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Causes of bilateral facial nerve palsy
Sarcoidosis
Guillain-Barre syndrome
Lyme disease
Bilateral acoustic neuromas
Bell's palsy
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What is an acoustic neuroma
Vestibular Scwannoma
Benign tumour of the Schwann cells surroudning the vestibulochoclear nerve
Occur at the cerebellopontine angle
Usually unilateral
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Disease associated with bilateral acoustic neruomas
Neurofibromatosis type II
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Presentation of acoustic neuromas
Typically patient aged 40-60
Gradual onset of symptoms
Unilateral sensorineural hearing loss (often first symptom)
Unilateral tinnitus
Dizziness or imbalance (vertigo)
Sensation of fullness in one ear
May also have a facial nerve palsy (CN VII)
Cranial nerve V may also be affected --> absent corneal reflex
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Management of acoustic neuroma
Conservative management may be appropriate
Surgery to remove the tumour
Radiotherapy to reduce growth
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Key features of normal pressure hydrocephalus
Urinary incontinence
Gait abnormality
Dementia
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Imaging in normal pressure hydrocephalus
Ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
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Management of normal pressure hydrocephalus
Ventriculoperitoneal shunting
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Most common causes of cervical myelopathy
Degenerative cervical spondylosis
Congenital stenosis
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Presentation of cervical myelopathy
Neck pain + stiffness
Extremeity paraesthesias - bilateral, non-dermatomal numbness + tingling
Bilateral weakness + clumsiness
Gait instability
Urinary retention (rare, and only appear late)
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Gold standard investigation for suspected cervical myelopathy
MRI cervical spine
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Management of cervical myelopathy
Typically surgical decompression + stabilisation
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Juvenile myoclonic epilepsy presentation
Myoclonus (jerking) in limbs
Normally bilateral myoclonus
Typically occur early in the morning or near bedtime
May have daytime absences
More common in girls + teenagers
Can progress to generalised seizures
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Benign roalndic epilepsy presentation
Typically children aged 4-12 years old
Partial seizures, occurring at night
Typically parasthesias (of the face)
No LOC or significant mental status change
More common in males
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What diet may be recommended in or help with epilepsy that is hard to control/is unresponsive
Ketogenic diet
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Genetics of Huntington's disease
Autosomal dominant
Trinucleotide repeat expanded disorder (CAG)
Involves genetic mutation in the HTT gene on chromosome 4
Shows anticipation: successive generations have more repeats --> earlier age of onset, increased severity
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Presentation of Huntington's disease
Insidious, progressive worsening of symptoms
Tend to present aged 30-50
Usually begins with cognitive, psychiatric or mood problems
Movement disorder then develops:
- Chorea (involuntary, abnormal movements)
- Eye movement disorders
- Dysarthria
- Dysphagia
Life expectancy around 15-20 years after symptom onset
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Medications to suppress disordered movement
Antipsychotics e.g. olanzapine
Benzodiazepines e.g. diazepam
Dopamine-depleting agents e.g. tetrabenazine
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Giant cell arteritis
Systemic vasculitis that affects medium + large arteries
Often known as temporal arteritis
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What condition is strongly associated with giant cell arteritis
Polymyalgia rheumatica
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Symptoms of giant cell arteritis
Severe unilateral headache, typically around temple + froehead
Scalp tenderness may be noticed e.g. when brushing hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly
Systemic symptoms also possible
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Investigations of giant cell arteritis
Raised ESR (usually >50mm/hour)
Temporal artery biopsy - showing multinucleated giant cells
Other possible findings:
FBC: normocytic anaemia + thrombocytosis
LFTs: raised ALP
CRP rasied
Duplex USS of temporal artery --> hypoechoic halo sign.
CTA due to risk of aortic aneurysm
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Management of giant cell arteritis
Steroids: given before confirmation of diagnosis to reduce risk of permanent sight loss
- 40-60mg prednisolone per day (60 if jaw claudication or visual symptoms)
- Review response within 48 hours: usually rapid and significiant
Aspiring 75mg daily: decrease visual loss + strokes
PPI for gastric prevention while on steroids
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Commonest recessive type of ataxia in UK
Friedrich's ataxia
Causes atrophy + thinning of dorsal root ganglia
GAA repeat disorder
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Papillitis
Inflammation of optic nerve head
Presents with pain on eye movement + blurred vision
Assciated with inflammatory + demyelinating disorders
Significant visual loss
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Types of manifest strabismus
One eye forwards with...
Esotropia: one eye inwards
Exotropia: one eye outwards
Hypertropia: one eye upwards
Hypotropia: one eye downwards
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Latent strabismus
Eyes are straight when both eyes are open, but deviation can be elicited when each eye is covered
Under occluder eye turning...
Esophoria - inwards
Exophoria - outwards
Hyperphoria - upwards
Hypophoria - downwards
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Causes of childhood strabismus
Hereditary
Refractive errors (requires glasses)
- Most common = uncorrected hypermetropia (long-sighted) and accomodative esotropia
- Anisometropia (difference in refractive error of each eye) and development of amblyopia (lazy eye)
Hydrocephalus
Cerebral palsy
Space occupying lesions
Trauma
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Amblyopia
Eye affected becomes passive and has reduced function compared to dominant eye (lazy eye)
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Examination of squint
Eye movements
Fundoscopy - rule out retinoblastoma, cataracts, or other retinal pathology
Visual acuity
Hirschberg's test: observe reflection of light source on cornea
Cover test: watch movement of previously covered eye
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Management of strabismus etc
Treatment needed before age of 8 (as visual fields still developing)
Occlusive patch: cover good eye + force weaker eye to develop
Atropine drops: alternative to patch, causes blurry vision in good eye
Ophthalmology input
Correct refractive errors
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Common location of lesion in painful third nerve palsy
Posterior communicating artery aneurysm
Associated headache also present
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Genetics of neurofibromatosis
NF1: gene found on chromosome 17, codes for neurofibromin (tumour suppressor protein); autosomal dominant
NF2: chromosome 22, codes for merlin (tumour suppresor protein, esp in Schwann cells); autosomal dominant
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Criteria for neurofibromatosis type 1
2/7 required for diagnosis
CRABBING
C- cafe-au-lait spots (6+) measuring >/= 5mm in children, or >/= 15mm in adults
R - relative with NF1
A - axillary or inguinal freckles
BB - Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I - iris harmatomas (Lisch nodules) (2+), yellow-brown spots on iris
N - neurofibromas (2+) or 1 plexiform neurofibroma
G - glioma of optic nerve
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Key features of neurofibromatosis type 2
Mutations in this gene --> schwannomas
Associated with aucostic neuromas -->
- Hearing loss
- Tinnitus
- Balance problems
Bilateral acoustic neuromas suggests NF2
Can also develop schwannomas in brain + spinal cord
Surgical resection may be useful
