Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MY REVISION - ALL TO DO > TO DO NEURO > Flashcards

TO DO NEURO Flashcards

1
Q

STROKE
Give an example of how chronic HTN can cause a stroke.

A
  • Charcot-Bouchard aneurysms most often in the basal ganglia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

STROKE
What are some important differentials of stroke?

A
  • Metabolic (hypo or hyperglycaemia, electrolytes)
  • Intracranial tumours, hemiplegic migraine
  • Infection (meningitis)
  • Head injury, seizure (focal > Todd’s paralysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

STROKE
What classification system can be used for strokes?

A
  • Oxford stroke (Bamford) classification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

STROKE
How would a Total Anterior Circulation Infarct (TACI) present?

A

(involves middle and anterior cerebral arteries)
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

STROKE
how would a Partial Anterior Circulation Infarct present?

A

2 of the criteria are present:
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

STROKE
how does a lacunar infarct (LACI) present?

A

presents with one of the following:
- unilateral weakness (+/- sensory deficit) of face, arm and leg or all 3
- pure sensory stroke
- ataxic hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

STROKE
what vessels are affected in a lacunar infarct?

A

perforating arteries around the internal capsule, thalamus and basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

STROKE
how would a posterior circulation infarct (POCI) present?

A

presents with one of the following:
- cerebellar or brainstem syndromes
- loss of consciousness
- isolated homonymous hemianopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

STROKE
what is the presentation of lateral medullary syndrome?

A

IPSILATERAL
- ataxia
- nystagmus
- dysphagia
- facial numbness
- cranial nerve palsy

CONTRALATERAL
- limb sensory loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

STROKE
what vessels are affected in lateral medullary syndrome?

A

posterior inferior cerebellar artery
(also known as Wallenberg’s syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

STROKE
what is the presentation of Weber’s syndrome?

A
  • ipsilateral CN III palsy
  • contralateral weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

STROKE
How would a PCA stroke present?

A

visual issues

  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

STROKE
How would a brainstem/basilar artery infarct present?

A
  • Locked in syndrome – complete paralysis BUT eye movement + awareness preserved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

STROKE
How would a haemorrhagic stroke appear on CT head?

A
  • Acute = hyperdense
  • Subacte = isodense
  • Chronic = hypodense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

STROKE
What other investigations may you do in stroke?

A
  • ECG 72h tape to look for paroxysmal AF, MI.
  • ECHO to check for endocarditis or CHD
  • CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

STROKE
What is the treatment for an ischaemic stroke?

A

Immediate management:

  • CT/MRI to exclude haemorrhagic stroke
  • aspirin 300mg

Antiplatelet therapy

  • aspirin 300mg for 2 weeks
  • clopidogrel daily long term

Anticoagulation (e.g. warfarin) for AF

thrombolysis

  • within 4.5 hrs of onset
  • IV alteplase
  • lots of contraindications (can cause massive bleeds)

mechanical thromboectomy
- endovascular removal of thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

STROKE
What other treatment can be given in ischaemic stroke either alongside alteplase or after the time frame?

A
  • Thrombectomy (mechanical retrieval of clot)
  • Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
  • Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

STROKE
What other management is given for ischaemic strokes?

A
  • Control BP
  • 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

STROKE
What medication and general management may be given in stroke prevention?

A
  • Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
  • Anticoagulation if have AF but wait 2w post-stroke
  • Manage co-morbidities (HTN, DM)
  • Cholesterol >3.5mmol/L diet + 80mg atorvastatin
  • VTE assessment + monitor for infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

STROKE
What is the CHA2DS2-VaSc score

A
  • Congestive heart failure
  • HTN
  • Age 65-74 (1), ≥75 (2)
  • Diabetes
  • Prev stroke/TIA (2)
  • Vascular disease
  • Sex female
  • 1 = consider anticoagulation, ≥2 = anticoagulate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SAH
What are the investigations for SAH?

A
  • urgent non-contrast CT head = starburst sign
  • ECG

to consider
- lumbar puncture = xanthochromia (if CT negative, perform >12hrs after symptom onset)
- CT angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

SAH
What is the management of SAH?

A

1st line
- nimodipine 60mg 4hrly
- endovascular coiling (2nd line = surgical clipping)

  • if raised ICP = IV mannitol, hyperventilation + head elevation
  • conservative = bed rest, stool softeners
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

EDH
What is the pathophysiology of extra-dural haematoma (EDH)?

A
  • Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater over minutes to hours

After a lucid interval there is:
- rapid rise in ICP
pressure on the brain
- midline shift
- tentorial herniation
- coning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

EDH
What are some differentials for EDH?

A
  • Epilepsy,
  • CO poisoning,
  • carotid dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

EDH
What are the investigations for EDH?

A

Non-contrast CT head - hyperdense biconvex (lemon shape)

Skull x-ray - may show fracture lines

LP is contraindicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

EDH
What is the management for EDH?

A
  • bed position = tilted to 30 degrees
  • intubation if low GCS
  • maintain cerebral perfusion (hyperventilation, inotropes + vasopressors, fluids, hypertonic saline or IV MANNITOL)
  • hypothermia
  • burr hole

DEFINITIVE
- Craniotomy + haematoma evacuation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

SDH
What is the most common cause of subdural haematoma (SDH)?

A
  • Rupture of a vein running from hemisphere to the sagittal sinus of the dural venous sinuses (bridging veins) that’s beneath the dura leading to haematoma between arachnoid + dura mater
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

SDH
What are the investigations for SDH?

A

Non-contrast CT head
- crescentic collection
- not limited by suture lines

acute = hyperdense (light)
subacute = isodense
chronic = hypodense (dark)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

SDH
What is the management of SDH?

A

SURGERY
1* = irrigation via burr-hole craniostomy
2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

STATUS EPILEPTICUS
What is the step-wise management of status epilepticus?

A

PRE-HOSPITAL/EARLY STATUS (<10 MINS)
- in community 1st line = buccal midazolam (2nd line = rectal diazepam)
- in hospital 1st line = 4mg IV lorazepam (2nd line = IV diazepam)
two doses of benzodiazepine given 10 mins apart

ESTABLISHED STATUS (>10 MINS)
- alert on-call anaesthetist
- one of following: phenytoin, levetiracetam, sodium valproate
if one fails, try another agent on list

REFRACTORY STATUS (>30 MINS)
- phenobarbitone
- general anaesthesia with propofol, midazolam or thiopental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

LOC
What are the potential causes of LOC?

A

CRASH
- Cardiogenic (more alarming)
- Reflex (neurally mediated)
- Arterial
- Systemic
- Head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

NEAD
what is the management of NEAD?

A

correct Dx vital,
speak to pt,
reassure them,
wait for seizure to pass,
CBT,
avoid AEDs as can be fatal if mistreated excessively (respiratory depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

PARKINSON’S DISEASE
what are the clinical features of Parkinson’s disease

A

MOTOR SYMPTOMS
- bradykinesia (slow movements, festinant gait due to reduced arm swing + turning en bloc)
- tremor (resting, pill-rolling, 4-6Hz)
- cogwheel rigidity (tremor superimposed on a rigid movement)
- lead-pipe rigidity (stiffness throughout entire movement)

NON-MOTOR SYMPTOMS
- anosmia (early symptom)
- sleep disturbance
- depression
- anxiety
- dementia (usually develops after motor symptoms)
- constipation
- postural instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

PARKINSON’S DISEASE
How can you differentiate Parkinson’s resting tremor from benign essential tremor ?

A
  • Asymmetrical vs symmetrical
  • 4–6Hz vs 5–8Hz
  • Worse at rest vs improves at rest
  • Improves with intentional movement vs worse with intentional movement
  • No change with alcohol vs improves with alcohol (also Rx = propranolol)
  • Parkinson’s vs. autosomal dominant condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

PARKINSON’S DISEASE
What are 4 differential diagnoses to consider in Parkinson’s disease?

A

Parkinson’s plus syndromes –
- Progressive supranuclear palsy
- Multiple system atrophy
- Lewy Body dementia
- Corticobasal degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

PARKINSON’S DISEASE
What is progressive supranuclear palsy?

A
  • Early falls, cognitive decline or both sides being equally affected
  • Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
  • Impaired vertical gaze (down worse = issues reading or descending stairs)
  • Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

PARKINSON’S DISEASE
What is multiple system atrophy?

A
  • Neurones in multiple systems in the brain degenerate
  • Degeneration in basal ganglia > Parkinsonism
  • Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

PARKINSON’S DISEASE
What is Lewy Body dementia associated with?

A
  • Associated with Sx of visual hallucinations, delusions, REM sleep disorders, fluctuating consciousness, progressive cognitive decline + Parkinsonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

PARKINSON’S DISEASE
What is corticobasal degeneration?

A
  • Early myoclonic jerks, gait apraxia, agnosia + alien limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

PARKINSON’S DISEASE
What is the management of Parkinson’s disease?

A
  • Lifestyle: education, exercise, physio, MDT

1st line:
- if motor symptoms are affecting QoL = L-DOPA (CO-CARELDOPA)
- if motor symptoms not affecting QoL = dopamine agonist (ROPINIROLE) or MAO-B inhibitor (SELEGILINE or RASAGALINE)

2nd line
- COMT inhibitor (ENTACAPONE)
- amantadine
- SC apomorphine (in advanced disease with severe motor symptoms)
- deep brain stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

HUNTINGTON’S DISEASE
What is the pathophysiology of Huntington’s disease?

A
  • Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HUNTINGTON’S DISEASE
How does Huntington’s disease present?

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination

● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety
- rigidity
- dysarthria (speech problems)
- dysphagia (swallowing problems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HEADACHES
What is the management of cluster headaches?

A

ACUTE
- SC or intranasal sumatriptan
- 100% oxygen at 15L/min via non-rebreather mask
- avoid triggers
- avoid paracetamol, NSAIDs, opioids, ergots + oral triptans

PROPHYLAXIS
- verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected?

A
  • Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
  • Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

TRIGEMINAL NEURALGIA
How would you manage trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MIGRAINE
What is the pathophysiology of migraines?

A
  • Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
  • Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MIGRAINE
What are the triggers of migraines?

A

CHOCOLATE –
- Chocolate
- Hangovers
- Orgasms
- Cheese/caffeine
- Oral contraceptives
- Lie-ins
- Alcohol
- Travel
- Exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

MIGRAINE
What is the acute management of migraines?

A
  • PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID
  • Antiemetic like metoclopramide or prochlorperazine if vomiting occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

MIGRAINE
What is the prophylaxis for migarines?

A
  • Propranolol or topiramate are first line
  • Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
  • Also, amitriptyline, botulinum toxin or acupuncture.
  • 400mg OD of riboflavin (B2) may help
  • NOT gabapentin
  • Avoid indentified triggers (?headache diary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

MND
What is ALS?
What is a long-term consequence?

A
  • Loss of motor neurones in motor cortex + anterior horn of cord so mixed signs
  • Long term consequence is progressive spastic tetraparesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?

A
  • Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
  • Primarily affects muscles of talking, chewing, tongue palsy + swallowing
  • Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

MND
What is…

i) progressive muscular atrophy?
ii) primary lateral sclerosis?

A

i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

MND
What is the general clinical presentation of MND?

A

SYMPTOMS
- progressive weakness
- falls
- speech + swallow issues

SIGNS
- UMN + LMN issues
- spastic paraparesis
- fasciculations
- dysarthria
- dysphagia
- muscle wasting

NO SENSORY abnormalities
NO EXTRAOCULAR involvement
NO CEREBELLAR involvement
sphincter dysfunction is rare and only late feature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

MND
What are UMN signs?

A

Hypertonia or spasticity,
brisk reflexes
upgoing plantars,
muscle wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

MND
What are some investigations for MND?

A

EMG = fibrillation potentials
nerve conduction studies = reduction in amplitude
MRI spine (exclude spinal pathology)
pulmonary function tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

MND
What medication may be given in MND?

A
  • RILUZOLE – Na+ blocker inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

MULTIPLE SCLEROSIS
What are some classic sites for MS?

A
  • Periventricular white matter lesions
  • Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

MULTIPLE SCLEROSIS
What is the diagnostic criteria for MS?

A

McDonald criteria –
- >2 relapses
- Multiple CNS lesions (≥2)
- Sx that last >24h
- Disseminated in space (Clinically or on MRI) and time (>1m apart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MULTIPLE SCLEROSIS
What are the symptoms of MS?

A

SYMPTOMS
- blurred vision + red desaturation (optic neuritis)
- numbness + tingling
- weakness
- bowel + bladder dysfunction
- Uhtoff’s phenomenon (worsening symptoms following temperature rise e.g. hot bath/shower)

SIGNS
- visual (pale optic disc + inability to see red, relative afferent pupillary defect)
- internuclear ophthalmoplegia
- sensory loss
- UMN signs (spastic paraparesis)
- cerebellar signs (ataxia + tremor)
- Lhermitte’s phenomenon (electric shock sensation on neck flexion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?

A

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

MULTIPLE SCLEROSIS
What are some signs of MS?

A
  • UMN = spastic paraparesis, brisk reflexes, hypertonia
  • Sensory = loss of sensation, cerebellar signs
  • Relative afferent pupillary defect
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

MULTIPLE SCLEROSIS
What are the investigations for MS?

A
  • MRI head + spinal cord to show demyelination plaques = diagnostic
  • Lumbar puncture may show oligoclonal bands of IgG on CSF electrophoresis
  • Evoked potentials = delayed visual, auditory + somatosensory potentials
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

MULTIPLE SCLEROSIS
What is the management of MS relapses?
How does this affect disease prognosis?

A
  • oral/IV methylprednisolone for 5 days
  • plasma exchange (for sudden, severe relapses not responding to steroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

MULTIPLE SCLEROSIS
What is the management of MS remissions?

A

DMARDs
- natalizumab
- ocrelizumab
- fingolimod
- beta-interferon
- glatiramer acetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

MENINGITIS
What are the clinical signs of meningitis?

A
  • Meningism
  • +ve Kernig’s = pain or unable to extend leg at knee when it’s bent
  • +ve Brudzinski = involuntary flexion of hips + knees when neck flexed
  • Non-blanching purpuric rash = later sign in meningococcal septicaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

MENINGITIS
What are some complications following meningitis?

A
  • Hearing loss is key complication
  • Seizures + epilepsy
  • Sepsis or abscess
  • Hydrocephalus
  • Cognitive impairment + learning disability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

MENINGITIS
What is the management of bacterial meningitis

A

1st line = ceftriaxone/cefotaxime (+ amoxicillin if <3m or >55)
IV dexamethasone (avoid in meningococcal sepsis)

if penicillin allergic = IV chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

BRAIN ABSCESS
What are the most common causative organisms?

A
  • Staph. aureus + strep. pnuemoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

BRAIN ABSCESS
What is the management of brain abscess?

A

1ST LINE
- empirical antibiotics (IV ceftriaxone + metronidazole)
- treat underlying cause

2ND LINE
- abscess drainage/excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

BRAIN DEATH + COMA
What are the components of ‘eyes’ in GCS?

A

E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

BRAIN DEATH + COMA
What are the components of ‘verbal’ in GCS?

A

V5 = orientated in TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

BRAIN DEATH + COMA
What are the components of ‘motor’ in GCS?

A

M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

BRAIN DEATH + COMA
What is abnormal flexion to pain?
What does it indicate?

A
  • Decorticate posturing – arm adducted + flexed, wrist flexed, internal rotation, plantar flexed + stiff appearance
  • Indicates significant damage to cerebral hemispheres, internal capsule + thalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

BRAIN DEATH + COMA
What is abnormal extension to pain?
What does it indicate?

A
  • Decerebrate posturing – arms + legs extended, head extension, plantar flexion, internal rotation, pt rigid with teeth clenched
  • Indicates brainstem damage + so lesions in cerebellum or midbrain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

MYASTHENIA GRAVIS
What are the risk factors of myasthenia gravis?

A
  • female gender
  • family history
  • autoimmune (RA and SLE)
  • thymoma or thymic hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

MYASTHENIA GRAVIS
What are the clinical features of myasthenia gravis?

A

SYMPTOMS
- lethargy
- muscle weakness (worse at end of day)
- double vision
- slurred speech
- dysphagia
- shortness of breath

SIGNS
- proximal muscle weakness with fatiguability
- ptosis exacerbated on upward gaze (uni/bilateral)
- complex ophthalmoplegia
- head drop
- myasthenic snarl (snarling expression when attempting to smile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

MYASTHENIC CRISIS
What is the management of myasthenic crisis?

A
  • Urgent review by neurologists + anaesthetists
  • IV immunoglobulins or parapheresis
  • intubation
  • corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

MYASTHENIA GRAVIS
What is the management of myasthenia gravis?

A

1st line = acetylcholinesterase inhibitors (pyridostigmine)

2nd line = prednisolone

3rd line = azathioprine

other = methotrexate or rituximab

Thymectomy if thymoma present

80
Q

GUILLAIN-BARRE
What is the pathophysiology of GBS?

A
  • B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
81
Q

GUILLAIN-BARRE
What is Miller-Fisher syndrome?

A
  • GBS variant which affects CNS + eye muscles
  • Characterised by ophthalmoplegia + ataxia
82
Q

GUILLAIN-BARRE
What is the clinical presentation of GBS?

A

SYMPTOMS
- tingling + numbness in hands and feet (often precedes muscle weakness)
- symmetrical ascending progresive weakness
- unsteady when walking
- back and leg pain
- SOB
- facial weakness and speech problems

SIGNS
- reduced sensation in affected limbs
- symmetrical weakness
- ataxia with hyporeflexia
- autonomic dysfunction (tachycardia, HTN, postural hypotension, urinary retention)
- respiratory distress
- cranial nerve involvement and bulbar dysfunction (diplopia, facial droop)

83
Q

GUILLAIN-BARRE
What are the investigations for GBS?

A

BLOODS
- U&Es
- B12 + folate
- TFTs (exclude hypothyroidism)
- anti-ganglionside antibodies

CULTURES
- stool or sputum

LUMBAR PUNCTURE
- raised protein with normal WCC

To consider
- nerve conduction studies (not required for diagnosis)
- MRI brain + spinal cord

84
Q

GUILLAIN-BARRE
What is the main treatment for GBS?

A

1st line
- IV immunoglobulin (IVIG) = 5 day course commenced within first 2 weeks of symptom onset

or
- plasma exchange = 5 treatments of 2-3L over 2 weeks commenced within first 4 weeks of symptom onset

ADDITIONAL OPTIONS
- thromboprophylaxis
- physiotherapy
- ICU support (if ventilatory failure)

85
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the frontal lobe?

A

Personality + intellect change, hemiparesis, expressive dysphasia

86
Q

NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?

A
  • Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
87
Q

NEUROPATHY
What are the causes of peripheral neuropathy?

A

ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis

88
Q

NEUROPATHY
In terms of peripheral neuropathy, what conditions show a…

i) mostly motor loss?
ii) mostly sensory loss?

A

i) GBS, chronic inflammatory demyelination polyneuropathy (chronic GBS), Charcot-Marie-Tooth disease
ii) DM, CKD, deficiencies

89
Q

NEUROPATHY
What is Charcot-Marie-Tooth disease?

A
  • Autosomal dominant condition.
  • Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
90
Q

NEUROPATHY
Where is Baum’s loop located?
Where is Meyer’s loop located?
How can you remember which is superior/inferior?

A
  • Parietal lobe
  • Temporal lobe
  • PITS – Parietal Inferior Temporal Superior
91
Q

NEUROPATHY
What does a CN5 lesion cause?

A
  • Loss of sensation to face
  • Weak muscles of mastication
  • Loss of corneal reflex (afferent)
  • Jaw deviation to weak side
92
Q

NEUROPATHY
What does a CN7 lesion cause?

A

Face, ear, taste, tear –
- Muscles of expression
- Stapedius
- Anterior 2/3rd tongue
- Parasympathetic fibres to lacrimal + salivary glands

93
Q

CORD COMPRESSION
What is myelopathy?

A

Injury to the spinal cord due to severe compression resulting in UMN signs + specific symptoms based on compression

94
Q

CORD COMPRESSION
What are the causes of spinal cord compression?

A
  • Malignancy (mostly secondary, 5Bs = breast, bronchus, byroid, bidney, brostate)
  • Infection (epidural abscess), spinal osteophytes
  • Disc prolapse (slower onset), haematoma (warfarin)
  • Lumbar degeneration due to trauma or age (conservative Mx or steroid injections)
  • Myeloma
95
Q

CORD COMPRESSION
What are the signs of spinal cord compression?

A
  • Motor, reflex + sensory level = normal ABOVE lesion
  • LMN signs = AT level
  • UMN signs = BELOW level
  • Tone + reflexes usually reduced in acute cord compression
  • ?Sign of infection like tender spine, pyrexia
96
Q

CORD COMPRESSION
How does degenerative cervical myelopathy present?

A
  • Pain, loss of motor or sensory function affecting neck, upper or lower limbs
  • Loss of autonomic function
  • Hoffman’s sign +ve
97
Q

CORD COMPRESSION
What are the investigations of spinal cord compression?

A
  • PR to assess loss of sphincter control
  • Screening bloods (FBC, CRP/ESR, B12, LFT, U+Es)
  • MRI spine gold standard
  • If mass, ?biopsy/surgical exploration
98
Q

SPINAL CORD INJURY
What is Brown-Sequard syndrome?

A
  • Lateral hemisection of spinal cord
  • Ipsilateral weakness below the lesion (lateral corticospinal)
  • Ipsilateral loss of fine touch, proprioception + vibration (DCML)
  • Contralateral loss of pain + temp (lateral spinothalamic)
99
Q

ANTERIOR CORD SYNDROME
What is anterior cord syndrome?

A
  • Anterior spinal artery occlusion or compression
  • Bilateral spastic paresis (lateral corticospinal)
  • Bilateral loss of pain + temp (lateral spinothalamic)
100
Q

SPINAL CORD INJURY
What is posterior cord syndrome?

A
  • Trauma or posterior spinal artery occlusion
  • Loss of fine touch, proprioception + vibration (DCML)
101
Q

SPINAL CORD INJURY
What is central cord syndrome?

A
  • Hyperextension injury, often elderly with underlying cervical disease
  • Sensory + motor deficit (upper extremities > lower)
102
Q

MYOPATHY
How do myopathies present?

A
  • Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
  • Weakness > wasting
  • Reflexes + sensation normal, no fasciculations
103
Q

MYOPATHY
How does myotonic dystrophy present?

A
  • type 1 = distal weakness more prominent
  • type 2 = proximal weakness more prominent.
  • May have cataracts, testicular atrophy, cardiac lesions (heart block, cardiomyopathy), DM
104
Q

HYDROCEPHALUS
How does normal pressure hydrocephalus present?

A

‘Wet, wacky, wobbly’ –

SYMPTOMS
- poor concentration
- poor memory (particularly short term)
- poor insight into deficits
- increasing confusion

SIGNS
- bladder incontinence
- faecal incontinence
- shuffling gait
- magnetic gait (feet appear to be stuck to the floor)

  • Sx come on gradually + similar to Alzheimer’s so difficult to diagnose
105
Q

IDIOPATHIC INTRACRANIAL HYPERTENSION
What is the management of IIH?

A
  • # 1 weight loss (topiramate can be used + has benefit of weight loss)
  • Acetazolamide
  • Surgery = optic nerve sheath decompression + fenestration to prevent damage
  • Lumboperitoneal or ventriculoperitoneal shunt
106
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) carbamazepine?
ii) valproate?
iii) lamotrigine

A

i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia

107
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?

A

i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes

108
Q

NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?

A
  • Levodopa is dopamine precursor which can cross BBB to be converted to dopamine by dopa-decarboxylase
  • Must be combined with peripheral dopa-decarboxylase inhibitor like carbidopa so levodopa can reach brain
109
Q

NEURO PHARMACOLOGY
What are the side effects of Levodopa?

A
  • Postural hypotension
  • Confusion
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time (even with dose increase)
  • On-off effect
  • Psychosis
110
Q

NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?

A
  • Bromocriptine, cabergoline, ropinirole
  • Increases amount of dopamine in CNS
  • Hallucinations (more than levodopa), postural hypotension
  • ECHO, ESR, creatinine + CXR prior to Rx
111
Q

NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?

A
  • Pulmonary retroperitoneal + cardiac fibrosis
  • Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
112
Q

NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?

A
  • Catechol-o-methyltransferase (COMT) inhibitor = entacapone
  • Monoamine oxidase-B (MAO-B) inhibitor = selegiline
  • Inhibit enzymatic breakdown of dopamine
113
Q

NEURO PHARMACOLOGY
Examples of triptans.
Mechanism of action?
Used for?

A
  • Sumatriptan, naratriptan
  • 5-HT (serotonin) receptor agonists + act on smooth muscle in arteries > vasoconstriction, peripheral pain receptors > inhibit activation of pain receptors (vasoactive peptides) + reduce neuronal activity in CNS
  • Abort migraines when start to develop
114
Q

STROKE
What is the timeframe for thrombolysis for ischaemic strokes?

A
  • Within 4.5 hours of the onset of symptoms
115
Q

STROKE
what is the mechanism of action for alteplase / streptokinase (thrombolysis drugs for ischaemic stroke)?

A
  • Converts plasminogen > plasmin so promotes breakdown of fibrin clot
  • Alteplase (tPA) or can use streptokinase
116
Q

SDH
what are the risk factors of SDH?

A
  • Elderly - brain atrophy, dementia
  • Frequent falls - epileptics, alcoholics
  • Anticoagulants
  • babies - traumatic injury (“shaking baby syndrome”)bridging veins stretched so more likely to rupture,
117
Q

EPILEPSY
How would a partial seizure present in the parietal lobe?

A

paraesthesia
visual hallucinations
visual illusions

118
Q

NEAD
How can NEAD and a true epileptic seizure be differentiated?

A
  • Vital signs including lying-standing BP
  • FBC, U+Es, glucose, LFTs, TFTs (normal CK + prolactin in NEAD)
  • 24h 12-lead ECG + ECHO
  • EEG + CT/MRI if necessary
119
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte’s sign?

A

Neck flexion causes electric shock sensation down spine

120
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff’s phenomenon?

A

symptoms worsening in heat e.g. in the shower/exercise

121
Q

MENINGITIS
What are the aseptic causes of meningitis?

A

MS.
HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis

122
Q

ENCEPHALITIS
What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria
Lyme’s disease

123
Q

MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?

A

Abx, CCBs, beta-blockers, lithium + statins

124
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the temporal lobe?

A

Receptive dysphasia, amnesia

125
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the parietal lobe?

A

Hemisensory loss, dysphasia

126
Q

NEUROPATHY
What can cause mononeuritis multiplex?

A

Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis

127
Q

BELL’S PALSY
what are the symptoms?

A

unilateral LMN facial weakness (forehead is affected)
altered taste
post auricular pain - pain behind ears
- hyperacusis (noise sensitivity)
- dry mouth

128
Q

BELL’S PALSY
what is the management?

A
  • prednisolone
  • aciclovir
  • eye protection (eye lubricants or artificial tears should be considered
129
Q

NEUROFIBROMATOSIS
what are the clinical signs of NF1?

A
  • cafe-au-lait spots on the skin
  • pea-sized lumps under skin
  • skeletal abnormalities
  • tumour on optic nerve
130
Q

NEUROFIBROMATOSIS
what are the clincial signs of NF2?

A
  • acoustic neuromas (bilateral)
  • family history
  • meningioma, schwannoma, juvenile cortical cataracts or glioma
131
Q

NEUROFIBROMATOSIS
what are the causes of neurofibromatosis 1 and 2?

A

NF1 = chromosome 17 (autosomal dominant)
NF2 = chromosome 22 (autosomal dominant)

132
Q

NARCOLEPSY
what is the management?

A

1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate

133
Q

RADICULOPATHY
what are the causes?

A
  • intervertebral disc prolapse
  • degenerative diseases of the spine
  • fracture (trauma or pathological)
  • malignancy (metastatic)
  • infection (extradural abscesses, osteomyelitis)
134
Q

RADICULOPATHY
what is the management?

A

1st line
- NSAIDS (ibuprofen)
- physical therapy

2nd line
- epidural steroid injections
- surgery (laminectomy + discectomy)

135
Q

CATAPLEXY
what is the management?

A

sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs

136
Q

EPILEPSY
What is the emergency treatment for epilepsy?

A

ABCDE
check glucose
RECTAL/IV DIAZEPAM or LORAZEPAM
IV PHENYTOIN loading
mechanical ventilation

137
Q

EPILEPSY
what is the treatment for generalised myoclonic epilepsy?

A

male = sodium valproate
female = levetiracetam

138
Q

PARKINSON’S DISEASE
Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra
  2. Lewy bodies
139
Q

PARKINSON’S DISEASE
What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

140
Q

HUNTINGTON’S DISEASE
What is the triplet code that is repeated in Huntington’s disease?

A

Trinucleotide expansion repeat of CAG in HTT gene on chromosome 4
- >35 = HD

141
Q

MIGRAINE
What is the diagnostic criteria for a migraine?

A

classified as with or without aura
at least 2 of:
unilateral pain (usually 4-72hrs)
throbbing-type pain
moderate > severe intensity
motion sensitivity
plus at least 1 of:

  • nausea/vomiting
    -photophobia/phonophobia

there must also be a normal examination and no attributable cause

142
Q

MIGRAINE
How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

143
Q

MND
What are LMN signs?

A

Hypotonia + muscle wasting,
reduced reflexes,
fasciculations (particularly tongue)

144
Q

MND
What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes

145
Q

MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?

A

Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs

146
Q

GUILLAIN-BARRE
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?

A

If a patient has IgA deficiency - can cause severe allergic reaction

147
Q

ANTERIOR CORD SYNDROME
what are the causes?

A
  • iatrogenic - thoracic and thoracoabdominal AA repair
  • aortic dissection
  • atherothrombotic disease
  • emboli
  • vasculitis
148
Q

ANTERIOR CORD SYNDROME
what are the symptoms?

A
  • acute motor dysfunction
  • loss of pain and temperature sensation below level of infarction
  • autonomic dysfunction - neurogenic bowel/bladder
  • acute onset back pain
149
Q

ANTERIOR CORD SYNDROME
what are the investigations?

A

MRI - ‘owls eyes’ hyperintensities in anterior horns

lumbar puncture, CSF testing, blood and urine to rule out other causes

150
Q

HORNER’S SYNDROME
what are the causes of 1st order horner’s syndrome?

A

Stroke
Syringomyelia
MS
tumour
encephalitis

anhidrosis to face, arm and trunk

151
Q

HORNER’S SYNDROME
what are the causes of 2nd order horner’s syndrome?

A

Pancoast’s tumour
thyroidectomy
trauma
cervical rib

anhidrosis of face

152
Q

HORNER’S SYNDROME
what are the causes of 3rd order horner’s syndrome?

A

carotid artery dissection
carotid aneurysm
cavernous sinus thrombosis
cluster headache

no anhidrosis

153
Q

HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?

A

MAPLE

Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)

154
Q

BULBAR PALSY
what are the symptoms?

A
  • dysphagia
  • reduced/absent gag reflex
  • slurred speech
  • aspiration of secretions
  • dysphonia
  • dysarthria
  • drooling
  • difficulty chewing
  • nasal regurgitation
  • atrophic tongue
    weak jaw/facial muscles
155
Q

STRABISMUS
what are the risk factors?

A

FHx of strabismus
prematurity
low birth weight
maternal smoking during pregnancy

156
Q

SCIATICA
what are the risk factors?

A
  • previous injury
  • overweight
  • lack of core strength
  • physically demanding job
  • diabetes
  • osteoarthritis
  • inactivity
  • smoking
157
Q

SCIATICA
what are the causes?

A
  • herniated/slipped disc - puts pressure on nerve root
  • degenerative disc disease
  • spinal stenosis
  • spondylolisthesis
  • osteoarthritis
  • trauma
  • cauda equina syndrome
158
Q

MYOPATHY
what are the causes of myotonic dystrophy type 1 and 2?

A

type 1 - DMPK gene mutation on chromosome 19

type 2 = ZNF9 gene on chromosome 3

159
Q

TIA
what are the signs of a carotid TIA?

A

Amaurosis fugax = retinal artery occlusion –> vision loss
Aphasia
Hemiparesis
Hemisensory loss
hemianopia

160
Q

TIA
what are the signs of a vertebrobasilar TIA?

A

Diplopia, vertigo, vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
Hemianopic/bilateral visual loss
tetraparesis
loss of consciousness

161
Q

HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?

A

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue

  • injury
  • bleeding
  • infection
  • brain tumour
  • brain surgery
162
Q

ESSENTIAL TREMOR
what is the presentation?

A

HAND TREMOR
- upper limb
- worse on movement
- bilateral
- improves with sedation (alcohol, benzodiazepines, barbiturates + gabapentin)
- head or voice tremor
- difficulty performing fine motor tasks (writing, eating, dressing)

163
Q

ESSENTIAL TREMOR
what is the management?

A

mild disease
- observation

moderate disease
- 1st line: propranolol or primidone
- 2nd line: gabapentin or benzodiazepines
- 3rd line: deep brain stimulation, MRI guided thalamotomy

164
Q

EPILEPSY
how do lamotrigine and carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

165
Q

EPILEPSY
how does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

166
Q

PARKINSONS DISEASE
what is the pathway for dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

167
Q

HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?

A
  • Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
  • increased CSF production (choroid plexus tumour) but very rare
168
Q

DIABETIC NEUROPATHY
what is the management for gastroparesis?

A

metoclopramide, domperidone or erythromycin

169
Q

EPILEPSY
what are the risk factors?

A
  • premature birth
  • genetic (tuberous sclerosis, NF)
  • febrile convulsions as a child
  • traumatic brain injury
  • neurodegenerative disease
  • brain tumour
  • intracerebral infection
  • illicit drug use
  • dementia
170
Q

CHRONIC FATIGUE SYNDROME
what is the diagnostic criteria?

A

FATIGUE with all following features:
- persistent (>4 months)
- new or specific onset (not lifelong)
- unexplained by other conditions
- substancial reduction in activity level
- characterised by post-exertional malaise and/or fatigue

HAVE ONE OR MORE OF FOLLOWING FEATURES:
- muscle or joint pain
- headaches
- painful lymph nodes
- sore throat
- cognitive dysfunction
- worsening symptoms on physical or mental exertion
- general malaise or flu-like symptoms
- dizziness and/or nausea
- difficulty sleeping
- palpitations

171
Q

HUNTINGTON’S DISEASE
where is the genetic mutation located and what type of mutation is it?

A
  • mutation in HTT gene on chromosome 4
  • trinucleotide repeat disorder (CAG)
172
Q

BRAIN METASTASES
what are the most common cancers to metastasise to the brain?

A
  • lung cancer
  • breast cancer
  • melanoma
  • colorectal cancer
  • renal cell carcinoma
173
Q

BRAIN METASTASES
what is the management?

A
  • corticosteroids (DEXAMETHASONE)
  • radiotherapy
  • stereotactic radiosurgery
  • surgery
  • chemotherapy
  • targeted therapies
174
Q

CEREBELLAR DISEASE
what are the causes?

A
  • Friedreich’s ataxia
  • neoplastic (cerebellar haemangioma)
  • stroke
  • alcohol
  • MS
  • hypothyroidism
  • drugs (phenytoin, lead poisoning)
  • paraneoplastic (secondary to lung cancer)
175
Q

IDIOPATHIC INTRACRANIAL HYPERTENSION
what are the risk factors?

A
  • obesity
  • female sex
  • pregnancy
  • drugs (COCP, steroids, tetracyclines, retinoids, lithium)
176
Q

RADICULOPATHY
how can you distinguish an L5 radiculopathy from a common peroneal nerve injury?

A

both conditions cause foot drop

L5 RADICULOPATHY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- lower limb tendon reflex changes
- L5 dermatomal distribution of sensory loss

COMMON PERONEAL NERVE INJURY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- no changes to lower limb reflexes
- sensory loss over anterior aspects of foot and leg

177
Q

WERNICKE-KORSAKOFF SYNDROME
what is the clinical triad?

A
  • confusion
  • ataxia
  • ophthalmoplegia + nystagmus
178
Q

EPILEPSY
what is the management for different types of seizures?

A

GENERALISED TONIC-CLONIC
- male = sodium valproate
- female = lamotrigine or levetiracetam

FOCAL SEIZURES
- 1st line = lamotrigine or levetiracetam
- 2nd line = carbamazepine, oxcarbazepine or zonisamide

ABSENCE SEIZURES
- 1st line = ethosuximide
- 2nd line (male) = sodium valproate
- 2nd line (female) = lamotrigine or levetiracetam

MYOCLONIC SEIZURES
- male = sodium valproate
- female = levetiracetam

TONIC OR ATONIC SEIZURES
- male = sodium valproate
- female = lamotrigine

179
Q

MONONEUROPATHY
what are the nerve roots for median nerve?

180
Q

MONONEUROPATHY
what are the clinical features of median nerve palsy (carpal tunnel syndrome)?

A
  • sensory loss and/or paraesthesia over palmar + distal aspect of thumb, index, middle and half of ring ringer
  • weakness of hand
  • weak thumb abduction
  • thenar eminence wasting
  • hand pain (worse at night)
181
Q

MONONEUROPATHY
what are the investigations for carpal tunnel syndrome?

A

tinels test
phalens test

182
Q

MONONEUROPATHY
what are the nerve roots for the ulnar nerve?

183
Q

MONONEUROPATHY
what are the clinical features of ulnar neuropathy?

A
  • sensory loss and/or paraesthesia over little finger + medial side of ring finger
  • hand weakness (loss of dexterity, grip weakness)
  • muscle wasting (hypothenar eminence +/- interossei muscles)
  • claw hand deformity
184
Q

MONONEUROPATHY
what are the investigations for ulnar neuropathy

A

froments test - pinch paper between thumb + index finger

185
Q

MONONEUROPATHY
what are the nerve roots for the radial nerve?

186
Q

MONONEUROPATHY
what are the clinical features of radial neuropathy?

A
  • sensory loss and/or paraesthesia over dorsum or hand (may extend up forearm)
  • wrist drop
  • weakness in finger extension
  • weakness in brachioradialis
187
Q

MONONEUROPATHY
what are the nerve roots of the axillary nerve?

188
Q

MONONEUROPATHY
what are the clinical features of axillary neuropathy?

A

sensory loss over lateral shoulder

189
Q

MONONEUROPATHY
what are the nerve roots for the common peroneal nerve?

190
Q

MONONEUROPATHY
what are the clinical features of common peroneal neuropathy?

A
  • foot drop (weakness of dorsiflexion)
  • sensory loss over dorsum of foot + lateral shin
191
Q

MONONEUROPATHY
what are the nerve roots of the tibial nerve?

192
Q

MONONEUROPATHY
what are the clinical features of tibial neuropathy?

A
  • paraesthesia, pain or numbness over the sole of the foot (worse at night + with prolonged standing)
  • foot deformities (pes planus, pronated foot, abnormal gait)
193
Q

MONONEUROPATHY
what is meralgia parasthetica?

A

pain +/- sensory loss over anterolateral thigh due to neuropathy of lateral femoral cutaneous nerve

194
Q

MONONEUROPATHY
what is the management of carpal tunnel syndrome?

A
  • wrist splints
  • corticosteroid injections
  • surgical decompression (flexor retinaculum decompression)
195
Q

TIA
What is the secondary prevention following a stroke/TIA?

A
  • 1st line = clopidogrel 75mg
  • 2nd line = aspirin 75mg + MR dipyridamole
  • 3rd line = MR dipyridamole
  • 4th line = aspirin 75mg

all patients = high dose statin (atorvastatin 20-80mg)

manage HTN, DM, smoking and CVD risk factors

196
Q

ENCEPHALITIS
what is the management?

A

IV ceftriaxone
IV acyclovir

MY REVISION - ALL TO DO (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions