Neurology Flashcards
(291 cards)
1
Q
Features of migraine
A
Severe, unilateral, throbbing headache
Typically lasts 4-72 hours
Associated with nausea, photonics and phonophobia
1/3 of patients experience aura (visual (transient hemianoptic disturbance or a spreading scintillating scotoma), progressive, last 5-60 min)
2
Q
Migraine: epidemiology (gender)
A
3 times more common in women
3
Q
Common triggers for a migraine attack
A
Chocolate / Cheese / Citrus fruits
Combined Oral Contraceptive Pill / Hormonal (menstruation)
Alcohol (especially red wine)
Lights
Lack of food / dehydration / Tiredness / Stress
4
Q
Migraine diagnostic criteria (5)
A
- At least FIVE attacks fulfilling the criteria
- Two classic features: unilateral, pulsating, moderate-severe pain, aggravation by routine physical activity
- At least ONE: nausea/vomiting and/or photophobia/phonophobia
- Lasts 4-72 hours
- Not attributed to another disorder
5
Q
General rule of migraine acute vs prophylactic management
A
5-HT receptor agonists (e.g. triptans) are used in acute treatment, 5-HT receptor antagonists are used in prophylaxis (e.g. propranolol, amitriptyline)
6
Q
1st line treatment of acute migraine
A
Oral triptan + NSAID
Or
Oral triptan + paracetamol
Antiemetics e.g. metoclopramide for vomiting - can lead to EPSEs
Aged 12-17: consider nasal triptans
7
Q
Options for medical prophylaxis of migraines
A
Propranolol
Amitriptyline
Topiramate (AVOID in women of childbearing age)
8
Q
Menstrual migraine treatment
A
Frovatriptan or zolmitriptan 2.5mg BD around menstruation
9
Q
‘Complementary medicine’ option for migraine prophylaxis
A
Acupuncture
10
Q
Vitamin supplement useful in migraine prophylaxis
A
Vitamin B2 (riboflavin)
11
Q
Hemiplegic migraine features
A
can mimic stroke - act fast
Typical migraine symptoms
Sudden or gradual onset
Hemiplegia (unilateral weakness of limbs)
Ataxia
Changes in consciousness
12
Q
Contraception contraindicated in patients with migraine with aura
A
COC (due to increased risk of stroke)
13
Q
1st line pain relief migraine in pregnancy
A
1st line: Paracetamol 1g
2nd line: NSAIDs can be used in first and second trimester, avoid aspirin and opioids e.g. codeine
14
Q
Red flag aura symptoms
A
Motor weakness
Double vision
Visual symptoms affecting only one eye
Poor balance
Decreased level of consciousness
15
Q
Most common cause of primary headache in children
A
Migraine without aura
16
Q
ABCD2 score
A
Risk of stroke after a suspected TIA
Age > 60
BP > 140/90
Clinical features
Duration
Diabetes diagnosis
17
Q
TIA definiton
A
A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction
(No longer time based definition)
18
Q
Clinical features of TIA
A
Stroke symptoms that typically resolve within 1 hour
- Unilateral weakness or sensory loss
- Aphasia or dysarthria
- Ataxia, vertigo
- Visual problems
19
Q
Immediate management of TIA
A
Aspirin 300mg daily (unless contraindicated or already on aspirin)
Referral for specialist assessment within 24 hours if TIA occurred in last 7 days
If > 7 days ago, refer for assessment within 7 days
20
Q
Initial management of patient with suspected TIA who is on warfarin/a DOAC or has a bleeding disorder
A
Admit immediately for imaging to exclude haemorrhage
Aspirin 300mg is contraindicated
21
Q
Investigations to assess the underlying cause of TIA or stroke (2)
A
All patients should have an urgent carotid doppler to assess for carotid artery stenosis
ECG to assess for atrial fibrillation
22
Q
Surgical intervention where there is significant carotid artery stenosis (> 70%)
A
Carotid endarterectomy
Note: only available if the patient is not severely disabled
23
Q
Preferred modality in patients with suspected TIA who require brain imaging
A
MRI brain with diffusion-weighted imaging
24
Q
1st and 2nd line secondary prevention for TIA or stroke
A
1st: Clopidogrel 75mg once daily + Atorvastatin 20-80mg daily
2nd: Aspirin + dipyridamole (anti-platelet) + Atorvastatin 20-80mg daily
25
Crescendo TIA
Two or more TIAs within a week - indicate a high risk of stroke
26
4 pathological causes of disruption of blood supply to the brain
Thrombus or embolus
Atherosclerosis
Shock
Vasculitis
27
1st line radiological investigation for suspected stroke
+ signs for ischaemic vs haemorrhagic
**Non-contrast CT head scan**
Ischaemic signs: hyperdense artery corresponding with the responsible arterial clot
Haemorrhagic signs: hyperdense material (blood) surrounded by low density (oedema)
28
ROSIER score
Recognition of stroke in the ER
29
Management of stroke (4)
Exclude hypoglycaemia
Immediate CT scan
Aspirin 300mg daily for 2 weeks (once haemorrhage is excluded)
Admission to specialist stroke centre
30
Indications for IV thrombolysis with alteplase in stroke management
Within 4.5 hours of onset of stroke symptoms
Haemorrhage has been definitely excluded
31
Indication for thrombectomy in the management of ischaemic stroke
Within 6-24 hours
Offer to patients where there is confirmed occlusion of the proximal anterior circulation and if there is potential to salvage brain tissue (scans show limited infarct core volume)
32
Indication for thrombectomy with IV thrombolysis
Within 4.5 hours
Confirmed occlusion of proximal posterior circulation (basilar or PCA) and potential to salvage brain tissue (i.e. scans show limited infarct core volume)
33
Parkinson’s triad
ASYMMETRICAL:
Bradykinesia
Tremor
Rigidity
34
Bradykinesia presentation in Parkinson’s
Movement gets slower and smaller:
- Short, shuffling steps with reduced arm swinging
- Difficulty in initiating movement e.g. standing to walking
35
Tremor presentation in Parkinson’s
Most marked at REST
3-5 Hz
Worse when stressed or tired
Improves with voluntary movement
Typically ‘pill-rolling’, i.e. thumb and index finger
36
Rigidity presentation in Parkinson’s
‘Cogwheel’ due to superimposed tremor / resistance to passive movement of joint
37
Psychiatric features in Parkinson’s (4)
Depression (most common - 40%)
Dementia
Psychosis
Sleep disturbances
38
What can autonomic dysfunction in Parkinson’s cause
Postural hypotension
39
Parkinsonism vs Parkinson’s
Parkinsonism:
Motor symptoms are generally RAPID onset and BILATERAL
Rigidity and rest tremor are UNCOMMON
40
Who can diagnose Parkinson’s disease
A specialist with expertise in movement disorders
41
1st line treatment for Parkinson’s where the motor symptoms are affecting the patients QOL
Levodopa
*(Co-carelodopa/Co-beneldopa)*
42
Treatment for Parkinson’s where motor symptoms are not affecting patients QOL
Dopamine agonist (non-ergot derived)
Levodopa
Monoamine Oxidase B inhibitor
43
Which antiparkinson drug is associated with the greatest improvement in symptoms and ADLs but has more motor complications
Levodopa
44
Which antiparkinsonian medication has the highest chance of inhibition disorders
Dopamine agonist therapy
45
What is levodopa usually combined with to prevent peripheral metabolism
Peripheral decarboxylase inhibitors e.g. carbidopa or benserazide
46
Types of dyskinesias (side effect of levodopa at peak dose)
Dystonia
Chorea
Athetosis
47
Adverse effects of levodopa (5)
Dry mouth
Orthostatic hypotension
Palpitations, Psychosis
Anorexia
48
2 phenomenons regarding levodopa use
End-of-dose wearing off: symptoms worsen towards end of dosage interval resulting in decline of motor activity
On-off phenomenon: normal function during ‘on’ period, weakness and restricted mobility during ‘off’ period
49
Levodopa is an example of a critical medicine, what does this mean?
Must not be acutely stopped
50
What can be given as a rescue medicine if levodopa cannot be given orally
Dopamine agonist patch
- to prevent acute dystonia
51
Mechanism of action of COMT inhibitors
COMT enzyme metabolises levodopa in both the body and brain
COMT inhibitors extend the effective duration of levodopa by slowing down the breakdown in the brain
52
What kind of drug is entacapone
COMT inhibitor
53
Indication for the use of dopamine receptor agonists and Monoamine oxidase-B inhibitors in Parkinson’s
Less effective than levodopa in reducing symptoms, therefore used to *delay the use of levodopa* and then used in *combination with levodopa* to *reduce the dose of levodopa required*
54
Examples of ergot-derived dopamine receptor agonists (2nd line to non ergot-derived)
Bromocriptine
Carbergoline
55
Complications of the use of ergot-derived dopamine receptor agonists e.g. bromocriptine
Pulmonary, retroperitoneal and cardiac fibrosis
56
Example of MAO-B inhibitor
Selegiline
Rasagiline
57
Action of Monoamine oxidase enzymes
Break down neurotransmitters such as dopamine, serotonin and adrenaline
MAO-B is specific to dopamine
58
Prognosis of MND
Poor - 50% of patients die within 3 years
59
Riluzole mechanism in MND
**prevents** stimulation of glutamate receptors = slows progression/prognosis of disease
***only** licensed medication to treat MND*
60
ALS presentation
Age around 60 / Male
Asymmetric progressive weakness (limbs, trunk, face, speech)
Mixture of lower motor neuron and upper motor neuron signs
Absence of sensory signs
61
What motor features are preserved in MND
External ocular muscles
Cerebellar signs
Abdominal reflexes
62
Diagnosis of MND
Clinical diagnosis based on presentation and exclusion of other neuropathies (nerve conduction studies are normal)
63
Lower motor neurone signs
Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes
64
Upper motor neurone signs
Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex
65
Which muscles are primarily affected in progressive bulbar palsy
Muscles of **talking** and **swallowing** (the bulbar muscles)
66
Most common cause of meningitis in neonates (0-3 months)
Group B Streptococcus (usually contracted during birth from GBS bacteria that live harmlessly in the mothers vagina)
67
Most common cause of bacterial meningitis in children and adults
Streptococcus pneumoniae (pneumococcus)
Neisseria meningitidis (gram negative meningococcus)
68
Causal organisms of meningitis in: > 60 years
Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes
69
Causal organisms of meningitis in: immunosuppressed
Listeria monocytogenes
70
Explain the lumbar puncture results of a bacterial sample
Appearance: cloudy (proteins)
Protein: high (bacteria release proteins)
Glucose: low (bacteria eat up the glucose) - typically < 1/2 plasma glucose
WCC: high (immune system releases **neutrophils** in response to bacteria)
71
What level is a lumbar puncture needle inserted
L3-L4
72
Explain the lumbar puncture results of a viral sample
Appearance: clear
Protein: mildly raised/normal (viruses may release a small amount of protein)
Glucose: normal (viruses don’t use glucose: 60-80% of plasma glucose present)
WCC: high (immune system releases lymphocytes in response to viruses)
73
Complications of meningitis
Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity
74
Most common causes of viral meningitis
Herpes simplex virus (HSV)
Enterovirus
Varicella zoster virus (VZV)
75
Management of viral meningitis
Tends to be **milder than bacterial** and often only requires supportive treatment
Acyclovir can be used to treat HSV or VZV
76
Post exposure prophylaxis for close prolonged contact of bacterial meningitis 7 days before onset
Single dose of **ORAL ciprOflOxacin**
(Rifampicin can be used but ciprofloxacin is preferred)
77
Management of suspected meningococcal disease in a primary care setting
Urgent stat injection (IM or IV) of **benzylpenicillin**
+ dexamethasone to reduce complications
78
Red flag of a non-blanching rash in children accompanied by headache, fever, neck stiffness
Meningococcal septicaemia - indicates that the infection has caused DIC and subcutaneous haemorrhages
79
Typical symptoms of meningitis
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered conciousness
Seizures
80
2 special tests to look for meningeal irritation
Kernigs test
Brudzinskis test
81
Antibiotic management of bacterial meningitis
Over 3 months: IV cefotaxime or ceftriaxone
Under 3 months: IV cefotaxime + amoxicillin (to cover listeria)
82
Which medication is given in meningitis management to reduce the frequency and severity of hearing loss and neurological damage
Dexamethasone - 4 times daily for 4 days to children over 3 months
83
Circumstances where lumbar puncture should be delayed in the investigation of meningitis
Signs of severe sepsis or a rapidly evolving rash
Severe respiratory/cardiac compromise
Significant bleeding risk
Signs of raised intracranial pressure
84
4 signs of raised intracranial pressure
Focal neurological signs
Papilloedema
Continuous or uncontrolled seizures
GCS <12
85
Who should not receive IV dexamethasone in the management of meningitis
Septic shock
Meningococcal septicaemia
Immunocompromised
86
When would neuroimaging be indicated in suspected bacterial meningitis
**Raised ICP** - otherwise not normally indicated
87
Most common cause of foot drop
Common peroneal nerve lesion causing weakness of the foot dorsiflexor muscles
88
Risk of having a stroke with AF score
CHADSVAS
Congestive heart failure
Hypertension
Aged 75 years or older
Diabetes mellitus
Stroke (previous)
Vascular disease
Age 65-74
Sexual category (female)
89
Total anterior circulation stroke (TACS) criteria
*Bamford classification of ischaemic stroke*
Stroke affecting both the MCA and ACA
Diagnosis requires all 3 of the following:
Unilateral weakness of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction e.g. dysphasia
90
Posterior circulation stroke key symptoms
**Dizziness**
Diplopia
Dysarthria
Dysphagia
Dystaxia
91
what are Lewy Bodies
alpha synuclein cytoplasmic inclusions
*seen in LBD, Parkinson's + Alzheimer's*
92
Lilluptian bodies
Lewy body dementia associated **visual hallucinations**, classically of small creatures/children/figures
93
Lewy body dementia vs parkinson's disease dementia
Lewy Body Dementia: starts at the top and eventually descends to the substantia nigra / dementia and movement disorder *develop within a year of each other*
Parkinson's Disease Dementia: inclusions affect the substantia nigra (to cause the movement disorder) before ascending to involve the paralimbic and neocortical areas to result in **dementia** / movement disorder and dementia *develop a year apart*
94
Fronto-temporal dementia features
Onset before 65
Insidious onset
cognitive impairment
personality change
repetitive checking behaviour
disinhibition
Memory loss is a late feature
Constructional apraxia i.e. failure to draw interlocking pentagons may be a key feature in the early stages
95
3 variants of frontotemporal dementia
**Behavioural variant** (60%), characterised by loss of social skills, personal conduct awareness, disinhibition, and repetitive behaviour
**Semantic dementia** (20%), characterised by an inability to remember words for things, calling them 'thingy'
**Progressive non fluent aphasia** (20%), where the patient can't verbalise; their speech is laboured and difficult
96
Risk factor for frontotemporal dementia
repetitive head injury
97
Pick's disease
one cause of FTD / diagnosed on post-mortem where "Pick's bodies" (accumulations of TAU protein that stain with silver) are found in the neurons
97
Second most common cause of dementia
Vascular dementia
98
Dementia assessment tools recommended by NICE for the non-specialist setting
10-point cognitive screener (10-CS)
6-Item cognitive impairment test (6CIT)
*AMTS and MMSE are also widely used but not recommended by NICE*
99
Primary care blood screening for dementia
FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels
100
Secondary care primary investigation for dementia
Neuroimaging (exclude other reversible conditions e.g. subdural haematoma) and provide aetiological information
101
Dementia most likely to present with **fluctuating cognition**
Lewy Body Dementia
102
Which medication should be avoided in LBD
Neuroleptics *may cause irreversible parkinsonism*
103
When should antipsychotics be used in Alzheimer's patients
patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
**antipsychotics in AD are associated with a sig. risk of increased mortality**
104
Middle cerebral artery presentation (4)
Contralateral hemiparesis and sensory loss
**Upper extremity > lower**
**Contralateral homonymous hemianopia**
Aphasia
105
Anterior cerebral artery key presentation
Contralateral hemiparesis and sensory loss
**Lower extremity > Upper**
106
Horner's syndrome features
Unilateral
Anhidrosis (absence of sweating of the face)
Miosis (constricted pupil)
Ptosis (drooping eyelid)
Enophthalmos (inset eye)
107
Which lung cancer tumour can lead to Horner's syndrome
Pancoast (apical) tumour compressing the sympathetic chain
108
Pharmacological medication in Alzheimer's
1st line:
**Acetylcholinesterase inhibitors** (donepezil, galantamine and rivastigmine)
Severe (as an add on) or if Acetylcholinesterase i are contraindicated: **Memantine** (NMDA receptor antagonist)
*NICE does not recommend antidepressants for mild to moderate depression in dementia patients*
109
Trigeminal neuralgia features
unilateral
brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
the pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors)
110
Red flag signs in trigeminal neuralgia
Onset before 40
Family history of MS
Optic neuritis
Sensory changes
Deafness
Bilateral pain
*refer to neurology*
111
1st line treatment trigeminal neuralgia
Carbamazepine
*if contraindicated or not tolerated, refer to neurology*
112
Mixed dementia (2 most common types)
AD and VD
113
Non-ergot derived dopamine agonists examples
Ropinirole
Rotigotine
114
Major non-modifiable risk factor for TIA
Age - risk doubles every decade after 55
115
Huntington's disease genetic features (4)
1. Autosomal dominant
2. Trinucleotide repeat disorder (repeat CAG expansion)
3. Defect in huntingtin gene on chromosome 4
4. Anticipation
116
Huntington's disease pathophysiology
Results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
117
Clinical features of Hungtington's disease
Features typically develop after 35 years of age
Chorea
Personality changes (e.g. irritability, apathy, depression) and intellectual impairment
Dystonia
Saccadic eye movements
118
Progressive supranuclear palsy
Parkinson plus condition
Typically reduced movement and **vertical gaze palsy**
119
Wernicke's encephalopathy triad
Confusion
Opthalmoplegia (may present as CN6 palsies/nystagmus)
Ataxia (broad-based gait)
120
Korsakoff syndrome symptoms
Retrograde amnesia
Anterograde amnesia
Confabulation
Loss of insight
**occurs when Wernicke's is left untreated**
121
Which motor neuron lesion 'spares' the upper face
**upper** motor neuron lesion
122
Bell's palsy
**lower** motor neuron facial nerve (VII) palsy (forehead affected on ipsilateral side)
*Dumbell's are heavy = low*
123
Temporal arteritis
Also known as giant cell arteritis
idiopathic vasculitis affecting medium and large sized vessel arteries
124
What disorder does temporal arteritis overlap with in 50% of cases
Polymyalgia rheumatica: *aching, morning stiffness in proximal limb muscles (not weakness)*
125
Features of temporal arteritis
Typical patient is > 60 years old
Usually rapid onset (e.g. < 1 month)
Headache
Jaw claudication
Vision (amaurosis fugax can occur)
Tender, palpable temporal artery
126
2 investigations in temporal arteritis
Raised inflammatory markers (ESR and CRP)
Temporal artery biopsy (skip lesions)
127
1st line Treatment temporal arteritis
**urgent high dose steroids** should be given as soon as the diagnosis is suspected and **before** the temporal artery biopsy
- **no visual loss** = high-dose prednisolone
- **evolving visual loss** = IV methylprednisolone given first then prednisolone
*give bone protection with bisphosphonates as treatment requires long course of steroids*
128
Causative organism of the gastroenteritis that precedes guillain-barre syndrome
Campylobacter jejuni
129
Characteristic features of Guillain-barre syndrome
Progressive, symmetrical weakness of all the limbs
Classically ascending i.e. the legs are affected first
Very few + mild sensory signs
130
Guillain-Barre 1st line treatment
IV immunoglobulins
2nd line: plasma exchange
131
Investigation guillain-barre
Nerve conduction studies
Lumbar puncture (raised protein, normal WCC, normal glucose)
132
Convergent squint
commonest form of childhood squint
hypermetropia (long sightedness) causes the image to focus behind the retina when the eye is at rest
excessive accommodation brings the image into focus but causes squint
133
Cluster headache features
Intense sharp, stabbing pain around one eye:
- once or twice a day / 15 mins - 2 hours
- typically lasts 4 - 12 weeks
- redness, lacrimation, lid swelling
- ptosis, miosis
134
Common trigger for cluster headaches
Alcohol
135
Investigation of choice cluster headache
MRI with contrast
*underlying brain lesions are sometimes found*
136
Acute management of cluster headache
100% oxygen + subcutaneous triptan
*triptans are C/I in CAD*
137
Prophylaxis management of cluster headache
Verapamil
138
Antibodies found in myasthenia gravis
Anti-acetylcholine receptor (positive in 85-90%)
139
2 associations myasthenia gravis
Thymomas
Autoimmune disorders
140
Key symptoms of myasthenia gravis
Fatiguability
Ptosis
Diplopia
Facial weakness
141
Investigations myasthenia gravis
Single fibre electromyography
CT thorax (thymoma)
Antibodies to Ach-receptors
CK = normal
142
1st line drug myasthenia gravis
Pyridostigmine (long acting acetylcholinesterase inhibitor)
143
3 components of GCS
Motor response e.g. 2 = extending to pain, 6 = obeys commands
Verbal response e.g. 3 = words, 5 = orientated
Eye opening e.g. 2 = to pain, 4 = spontaneous
144
Uhthoff's phenomenon
Small increases in body temperature can temporarily worsen current or pre-existing symptoms of MS e.g. reduced visual acuity after **exercise**
145
Most common presentation of MS
Optic neuritis
*demyelination of the optic nerve = unilateral reduced vision*
146
4 features of optic neuritis
1. **Central scotoma** (enlarged central blind spot)
2. **pain** with **eye movement**
3. Impaired **colour vision**
4. Relative afferent pupillary defect (affected eye pupil constricts **more** when shining a light in the **contralateral** eye than when shining light in the affected eye)
5. Typically resolves in days or weeks
6. Phosphenes (images of light or colour whilst eye closed)
7. Optic disc swelling
8. Unilateral presentation
147
Treatment optic neuritis
High dose steroids
148
4 examples of focal weakness in MS
Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis
149
4 examples of focal sensory symptoms in MS
Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte's sign
150
MS: Clinically isolated syndrome
First episode of demyelination and neurological signs/symptoms
*Patients with CIS may never have another episode or may go on to develop MS - lesions on MRI scan have poorer prognosis for MS diagnosis*
151
Most common pattern of MS when first diagnosed
Relapsing-remitting
152
Secondary progressive MS
Relapsing-remitting disease that turns into a progressively worsening disease (symptoms with incomplete remissions)
153
Primary progressive MS
Worsening disease and neurological symptoms from point of diagnosis without relapses and remissions
154
Investigations that support a clinical diagnosis of MS
**MRI brain + spinal with contrast** - *high signal T2 lesions, periventricular plaques*
Lumbar puncture - oligoclonal bands in CSF
155
Management of acute relapse in MS
High dose steroids (e.g. oral or IV methylprednisolone)
156
1st line DMARD for MS
Natalizumab
157
Management of specific problems in MS:
1. Fatigue
2. Spasticity
3. Bladder dysfunction
4. Oscillopsia *(visual fields appear to oscillate)*
1. Exclude anaemia, thyroid, depression then offer trial of amantadine
2. Baclofen and Gabapentin
3. **KUB ultrasound** to assess bladder emptying, significant residual volume = intermittent self catheterisation, if no significant residual volume = anticholinergics
4. Gabapentin
158
Common non-specific early feature of MS
Lethargy (75%)
159
Risk factors subarachnoid haemorrhage
Smoking
Cocaine use
Excess alcohol intake
Ehlers Danos syndrome
Polycystic kidney disease
Coarctation of the aorta
160
What can be given in cauda equina syndrome before surgery to reduce malignant compression
High dose dexamethasone (reduces oedema around the tumour site)
161
Most common cause of cauda equina syndrome
Central disc prolapse (typically L4/L5 or L5/S1)
162
Features of cauda equina syndrome
Low pack pain
Bilateral sciatica
Reduced sensation in perianal area
Decreased anal tone
Urinary dysfunction (incontinence is a late sign)
163
Investigation cauda equina syndrome
Urgent MRI
164
Management cauda equina syndrome
Surgical decompression
165
1st line investigation in suspicion of pituitary tumour
CT head - quick and easily available, to then triage patient
166
Most common cause of vertigo
Benign paroxysmal positional vertigo
167
Average age of onset BPPV
55 years
168
BPPV features
Vertigo triggered by change in head position
May be associated w nausea
Lasts 10-20 seconds
Positive Dix-Hallpike manoeuvre (pathgnomonic) i.e. rotatory nystagmus
169
Vestibular neuronitis
Inflammation of the vestibular portion of CN8
Causes vertigo
Often develops following a viral infection
170
Features of vestibular neuronitis
Recurrent vertigo attacks lasting hours or days
Nausea and vomiting
Horizontal nystagmus
No hearing loss or tinnitus
171
key differential diagnosis in vertigo
Posterior circulation stroke
172
Labyrinthitis vs vestibular neuritis
Labyrinthitis = hearing impairment
173
4 A's of alzheimer's presentation
Amnesia
Aphasia
Agnosia (naming an object)
Apraxia
174
What causes brown-sequard syndrome
Lateral hemisection of the spinal cord
175
3 features of brown-sequard syndrome
1. **Ipsilateral weakness** below lesion
2. **Ipsilateral** loss of **proprioception and vibration sensation**
3. **Contralateral** loss of **pain and temperature** sensation
176
what movement worsens a benign essential tremor
Arms outstretched (postural tremor)
177
Management of benign essential tremor
1st line: propranolol
If C/I: reassure + explain treatment isn't possible
178
3 other features outside of the core features of PD
- Handwriting gets smaller and smaller (micrographia)
- Reduced facial movements and expressions (hypomimia)
- Soft speech (hypophonia)
179
4 causes of brain abscess
Sepsis form middle ear
Trauma or surgery to the scalp
Penetrating head injuries
Embolic events from endocarditis
180
features of raised intracranial pressure
Headache (dull, persistent)
Vomiting
Focal neurology (**CN III/CN VI**)
Nausea, papilloedema on fundoscopy, seizures
Cushing’s triad (wide pulse pressure, bradycardia, irregular breathing)
181
Brain abscess investigations
CT head
182
Brain abscess management
Craniotomy
IV antibiotics (IV 3rd gen cephalosporin + metronidazole)
ICP management e.g. dexamethasone
183
Causative organism of 95% of cases of encephalitis in adults
HSV-1
184
Features of encephalitis
**first features: fever + lethargy**
headache
psychiatric symptoms (typically **temporal** and **inferior frontal** lobes affected e.g. irritability or focal seizures)
vomiting
Focal features e.g. aphasia
*peripheral lesions have no relation to the presence of HSV encephalitis*
185
Investigations encephalitis
Lumbar puncture/CSF: **lymphocytosis, elevated protein**, PCR for HSV, VZV and enteroviruses
Neuroimaging (MRI)
EEG
186
Management encephalitis
**IV aciclovir** in all cases of suspected encephalitis
187
Shingles pathophysiology
Following primary infection with varicella-zoster virus (VZV/chickenpox), the virus lies dormant in the dorsal root or cranial nerve ganglia
Herpes zoster infection/shingles is caused by reactivation of the varicella-zoster virus (VZV)
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Shingles risk factors
Increasing age
HIV (x 15)
Other immunosuppressive conditions (steroids, chemo)
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Features of shingles
Prodromal period: burning pain over affected dermatome for 2-3 days
Rash: painful erythematous, macular rash over affected dermatome, quickly becomes vesicular, UNILATERAL
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When is shingles no longer infectious
When the vesicles have crusted over (usually 5-7 days following onset)
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Management of shingles
Antivirals **within 72 hours** (unless <50 with mild symptoms) e.g. **aciclovir**
*reduces incidence of post-herpetic neuralgia*
Analgesia:
1st line: **paracetamol and NSAIDs**
2nd line: neuropathic agents e.g. amitriptyline
3rd line: oral corticosteroids (in first 2 weeks only in immunocompetent adults)
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Complications of shingles
**Post-herpetic neuralgia** (most common)
Herpes zoster opthlamicus (trigeminal nerve)
Herpes zoster oticus (Ramsay Hunt syndrome): ear lesions + facial paralysis
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Most common form of brain tumour
Metastatic brain cancer *often multiple and not treatable with surgical intervention*
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Tumours that most commonly spread to the brain
**Lung (most common)**
Breast
Bowel
Skin (melanoma)
Kidney
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What kind of spread to metastases spread to the brain
Haematogenous spread
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Most common primary tumour in adults
Glioblastoma
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Presentation of vestibular schwannoma (acoustic neuroma)
**Vertigo** (CN VIII)
**Unilateral sensorineural hearing loss** (CN VIII)
**Unilateral tinnitus** (CN VIII)
**Absent corneal reflex** (CN V)
**Facial nerve palsy** (CN VII)
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Condition most commonly associated with **bilateral** vestibular schwannomas
Neurofibromatosis type 2
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Vestibular schwannoma investigation of choice
MRI of the **cerebellopontine angle**
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4 endocrinology pathologies caused by pituitary tumours
Acromegaly (GH)
Hyperprolactinaemia (prolactin)
Cushing’s (ACTH and cortisol)
Thyrotoxicosis (TSH and thyroid hormone)
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Symptoms of cerebellar disease
**DANISH**
**D**ysdiadochokinesia
**A**taxia
**N**ystagmus
**I**ntention tremor
**S**lurred speech
**H**ypotonia
*Unilateral lesions cause **ipsilateral** signs*
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Causes of cerebellar disease
PASTRIES
**P**araneoplastic (e.g. secondary to lung cancer)
**A**lcohol
**S**troke,
**T**rauma
**R**arer causes
**I**nherited
**E**pilepsy treatment (phenytoin)
Multiple **S**clerosis
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4 risk factors for hypoxic-ischaemic encephalopathy (Intra partum asphyxia)
Prolapsed cord
Placental abruption
Trauma
Cephalopelvic disproportion
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Who is Bell’s palsy most common in
Pregnant women
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2 treatments for Bell’s palsy
1. Oral prednisolone within 72 hours of onset
2. Eye care (drops, lubricants) to prevent exposure keratopathy
*Antivirals may be of small benefit*
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When should someone with Bell’s palsy be referred to ENT
No sign of paralysis improvement after 3 weeks
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Causes of most Extradural haematoma
Low impact trauma (blow to head/fall) to the temporal region
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Vessel affected in Extradural haematoma
Middle meningeal artery
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Classical presentation Extradural haematoma
Patient who initially loses, briefly regains and then loses again consciousness after a low impact head injury
**Fixed and dilated pupil** (**temporal lobe herniates** and the parasympathetic fibres of **CNIII** are **compressed**)
*regain in consciousness = lucid interval*
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Imaging signs Extradural haematoma
Biconvex (lentiform) hyperdense collection around the surface of the brain
Limited by the suture lines of the skill
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Definitive treatment Extradural haematoma
Craniotomy and evacuation of the haematoma
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Most common cause of **spontaneous** SAH
Intracranial aneurysm (saccular ‘berry’ aneurysm) - 85%
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Presentation subarachnoid haemorrhage
Headache: Occipital, worst ever, sudden-onset, thunderclap
Meningism (photophobia, neck stiffness)
Nausea and vomiting
ECG changes inc ST elevation
Star shaped lesion on CT
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Management if subarachnoid haemorrhage is suspected but a CT head is done within **6 hours of symptom onset** and is **normal**
Do **not** do a lumbar puncture, consider alternative diagnosis
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Management if subarachnoid haemorrhage is suspected but a CT head is done **more than 6 hours of symptom onset** and is **normal**
Lumbar puncture (at least 12 hours following onset to allow xanthochromia)
- Other findings include normal or raised opening pressure
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How is vasospasm prevented in subarachnoid haemorrhage
Nimodipine
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Definitive treatment subarachnoid haemorrhage
Most patients will have a coil (interventional neuroradiology) but some may require craniotomy and clipping (neurosurgery)
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4 complications of aneurysmal SAH
Re-bleeding (Ix: repeat CT)
Hydrocephalus (Mx: external ventricular drain)
Vasospasm
Hyponatraemia (caused by SIADH)
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Predictive factors in SAH
Conscious level on admission
Age
Amount of blood visible on CT head
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Definition of acute, subacute and chronic subdural haematoma
Acute = within **48 hours of injury** (rapid neurological deterioration)
Subacute = days to weeks post-injury
Chronic = weeks to months (patients may not recall a specific head injury, common in elderly)
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4 neurological symptoms subdural haematoma
Altered mental status
Focal neurological deficits e.g. nystagmus
Headache
Seizures
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4 physical examination findings subdural haematoma
Papilloedema
Pupil changes (unilateral dilated pupil - compression of CNIII)
Gait abnormalities (ataxia or weakness)
Hemiparesis or hemiplegia
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Behavioural and cognitive changes in subdural haematoma
Memory loss
Personality changes
Cognitive impairment
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Who is most at risk of subdural haematomas
**Elderly and alcoholic patients** - brain atrophy with fragile or taut bridging veins
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CT imaging acute vs chronic subdural haematoma
Both will be crescent in in shape, not restricted by suture lines and compress the brain ‘mass effect’
Acute = hyperdense/bright (fresh blood)
Chronic = hypodense/dark (old blood)
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Most likely operation for symptomatic chronic subdural bleeds
Burr hole evacuation
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Neurofibromatosis inheritance pattern
Autosomal dominant
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Ménière’s disease
Disorder of the inner ear *of unknown cause*
Characterised by excessive pressure and progressive dilation of the endolymphatic system
*Common in middle-aged adults*
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Features of Ménière’s disease
Recurrent episodes of **vertigo**, tinnitus and sensorineural hearing loss
Aural fullness/pressure
Nystagmus
Positive Romberg test
Lasts minutes to hours
Typically **unilateral**
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Management Ménière’s disease (4)
ENT assessment
Inform DVLA
**Buccal or IM prochlorperazine for acute attacks** (same as vestibular neuritis)
Betahistine and vestibular rehabilitation for prophylaxis
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Chronic fatigue syndrome diagnostic definition
At least 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms
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Screening tests for chronic fatigue (name 4)
FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening, urinalysis
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Advice regarding physical activity and exercise in a patient with chronic fatigue syndrome
do not advise people with ME/CFS to undertake exercise that is not part of a programme overseen by an ME/CFS specialist team
should only be recommended if patients 'feel ready to progress their physical activity beyond their current activities of daily living'
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Features of narcolepsy
Typical onset = teenage years
Hypersomnolence (excessive sleep)
Cataplexy (sudden loss of muscle tone triggered by emotion)
Sleep paralysis
Vivid hallucinations going to sleep or waking up
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Investigations narcolepsy
Multiple sleep latency EEG
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Management narcolepsy
Daytime stimulants e.g. modafinil
Nighttime sodium oxybate
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Peripheral neuropathies which cause predominantly sensory loss
Diabetes
Leprosy
Alcoholism
Vitamin B12 deficiency
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Radiculopathy definition
Conduction block in the axons of a spinal nerve or its roots with motor and sensory affects, most commonly due nerve compression
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5 causes of Radiculopathy
Intervertebral disc prolapse
Degenerative diseases of the spine
Fracture
Malignancy (commonly metastatic)
Infection
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Damage to ulnar nerve presentation
‘Claw hand’
Wasting and paralysis of intrinsic hand muscles and hypothenar muscles
Sensory loss to the medial 1 1/2 fingers
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2 presentations of radial nerve damage
Wrist drop
Sensory loss to small area between dorsal aspect of the 1st and 2nd metacarpals
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Which nerve is affected in carpal tunnel syndrome
Median nerve
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Presentation carpal tunnel syndrome
1. Pain/pins and needles in thumb, index, middle finger
2. Patient classically has to shake hand at night to obtain relief
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Examination findings in carpal tunnel syndrome (4)
1. Weakness of thumb abduction
2. Wasting of **thenar** eminence
3. Tinel’s sign (tapping causes paraesthesia)
4. Phalen’s sign (flexion of wrist causes symptoms)
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4 causes of carpal tunnel syndrome
Idiopathic
Pregnancy
Oedema e.g. HF
Rheumatoid arthritis
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Electrophysiology findings carpal tunnel syndrome
Motor and sensory axon action potential prolongation
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Treatment mild-moderate carpal tunnel syndrome
6 week trial:
**Wrist splints** at night (particularly helpful in transient conditions such as pregnancy)
**Corticosteroid injection**
*Severe/no improvement*: surgical decompression
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4 features of anterior cord syndrome
Bilateral weakness
Bilateral loss of pain and temperature
Autonomic dysfunction (abnormal BP)
Bladder dysfunction
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2 causes of anterior cord syndrome
Vascular/ischaemia (thromboembolism, aortic disease, hypotension)
Pathology to spinal cord (tumour, trauma, disc hernia)
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3 visual symptoms in posterior cerebral artery stroke
Diplopia
Contralateral homonymous hemianopia **with macular sparing**
Visual agnosia
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Posterior **inferior cerebellar artery** stroke
Loss of temperature and pain sensation to the ipsilateral face and Contralateral trunk and limbs
Slurring of speech and ataxic gait
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Hoover’s sign
When examining a patient lying down, you place your hand under one leg and ask them to raise the contralateral leg and test whether you feel pressure against your hand
Tests for functional weakness
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Idiopathic intracranial hypertension classic patient
Young, overweight female
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Management of **idiopathic intracranial hypertension**
Carbonic anhydride inhibitors e.g. **acetazolamide** and **topiramate** (also helpful for weight loss)
Repeated lumbar puncture (temporary measure)
Optic nerve sheath decompression and fenestration may be needed to prevent optic nerve damage
Lumboperitoneal or ventriculoperitoneal shunt
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Tension headache features
Bilateral
‘Tight band’ around the head
May be related to stress
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Chronic tension headache definition
15 or more days per month
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Management of tension headache
Acute: aspirin, paracetamol or NSAID
Prophylaxis: up to 10 sessions of acupuncture over 5-8 weeks
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cerebellar hemisphere vs cerebellar vermis lesions
Hemisphere = peripheral (finger-nose ataxia)
Vermis = gait ataxia
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Diet used for children with epilepsy unresponsive to treatment
Ketogenic diet
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Medication overuse headache
present for 15 days or more per month
developed or worsened whilst taking regular symptomatic medication
patients using opioids and triptans are at most risk
may be psychiatric co-morbidity
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Mydriasis vs miosis
Dilated pupil vs constricted pupil
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Visual field defect pathway
Superior = temporal
Inferior = parietal
Bitemporal hemianopia = pituitary
Macular sparing = posterior
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Anti-epileptics in pregnancy
Lamotrigine: safe
Sodium valproate: neural tube defects
Carbamazepine: relatively safe
Phenytoin: associated with cleft palate
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Benign Rolandic epilepsy
4-12 years
Occur at night
Focal seizures (e.g. paraesthesia affecting the face)
Child is otherwise well
EEG: centrotemporal spikes
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Ataxic gait
Wide-based gait with loss of heel to toe walking
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Post-lumbar puncture headache
Usually develops within 24-48 hours following LP
Worsens with upright position
Treatment: blood patch, epidural saline fluids and IV caffeine
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Associated drugs with idiopathic intracranial hypertension
COC
Steroids
Tetracyclines
Retinoids
Lithium
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Headache red flags
History of malignancy + < 20
Thunderclap
New onset cognitive dysfunction
Impaired consciousness
Triggered by cough, valsalva, sneeze, exercise
Orthostatic
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Dorsal columns
Proprioception
Vibration sense
Tactile discrimination
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Corticospinal tracts
Muscle weakness
Hyperreflexia
Spasticity and persistent weakness if not treated
Babinski sign
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Spinothalamic tracts
Loss of pain and temperature sensation
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Oxford stroke classification 3 criteria
1. Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphasia
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Total vs partial anterior circulation infarcts
Total:
Middle and anterior cerebral arteries
All 3 of the Oxford criteria
Partial:
Smaller arteries of anterior circ e.g. upper or lower division of MCA
2 of the Oxford criteria
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Lacunar infarcts presentation
Presents with 1 of the following:
1. Unilateral weakness of face, arm, leg or all three
2. Pure sensory stroke
3. Ataxic hemiparesis
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Chemoreceptor trigger zone
Medulla oblongata
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2 contraindications lumbar puncture
Any signs of raised ICP
Meningococcal septicaemia
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Management of medication overuse headache
Simple analgesics and triptans can be withdrawn abruptly
Opioid analgesics should be gradually withdrawn
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Key symptom of posterior communicating artery aneurysm
Painful third nerve palsy
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Epilepsy and the DVLA
All patients must not drive and must inform the DVLA
1st seizure: 6 months
Established epilepsy: can drive if seizure-free for 12 months
Withdrawal of epilepsy medication: 6 months after last dose
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Treatment for cerebral oedema in patients with brain tumours
Dexamethasone
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Key feature of basilar artery stroke
Locked-in syndrome
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Features of Weber’s syndrome (posterior cerebral artery that supply the midbrain)
Ipsilateral CNIII palsy
Contralateral weakness of upper and lower extremity
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Most common complication of meningitis
Sensorineural hearing loss
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Creutzfeldt-Jakob disease
Degenerative brain disorder caused by infectious prion proteins
Key features: rapidly progressive dementia and **myoclonus**
MRI: hyperintense signals in the basal ganglia and thalamus
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Atonic seizure
Sudden loss of muscle tone
Last 15 seconds or less
After effects of confusion
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Focal impaired awareness seizures
Emotional disturbance
Automatism e.g. lip smacking
Disturbance of consciousness/awareness
Post-ictal state/tiredness
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3rd nerve palsy vs Horner’s
3rd nerve: ptosis + **dilated pupil/mydriasis**
Horner’s: ptosis + **constricted pupil/miosis**
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Mechanism of action of ondansetron
Anti-emetic: 5-HT3 receptor antagonist in chemoreceptor trigger zone in medulla oblongata
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syncope vs epilepsy
Short ictal period
Stressful event participating the syncope e.g. phobia or upcoming interview
Can be associated with mild twitching or jerking
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Management options for raised intracranial pressure
Head elevation to 30 degrees
IV mannitol (osmotic diuretic)
Controlled hyperventilation
Removal of CSF (drain, repeated LP e.g. IIH)
