NEURO

Question 1

STROKE
What is a stroke?

Answer 1

Rapid onset of neurological deficit due to a vascular lesion lasting >24 hours and associated with infarction of central nervous tissue

poor blood flow to the brain causes cell death

Question 2

STROKE
What are the two main classifications of stroke?

Answer 2

• Ischaemic (85%) – cerebral ischaemia leads to infarction of neural tissue + so loss of functionality
• Haemorrhagic (15%) – ruptured blood vessel leads to reduced blood flow

Question 3

STROKE
What are the causes of ischaemic strokes?

Answer 3

small vessel occlusion by thrombus
atherothromboembolism (e.g. from carotid artery)
cardioembolism (post MI, valve disease, IE)
hyper viscosity
hypoperfusion
vasculitis
fat emboli from a long bone fracture
venous sinus thrombosis

Question 4

STROKE
What are the causes of haemorrhagic stroke?

Answer 4

Bleeding from the brain vasculature

1. Hypertension - stiff and brittle vessels, prone to rupture
2. Secondary to ischaemic stroke - bleeding after reperfusion
3. Head trauma
4. Arteriovenous malformations
5. Vasculitis
6. Vascular tumours
7. Carotid artery dissection

Question 5

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

Answer 5

• Charcot-Bouchard aneurysms most often in the basal ganglia

Question 6

STROKE
What are the risk factors for ischaemic strokes?

Answer 6

Age
Male
Hypertension
Smoking
Diabetes
Recent/past TIA
Heart disease - IHD, AF, valve disease
Combined oral contraceptive

Question 7

STROKE
What are some important differentials of stroke?

Answer 7

• Metabolic (hypo or hyperglycaemia, electrolytes)
• Intracranial tumours, hemiplegic migraine
• Infection (meningitis)
• Head injury, seizure (focal > Todd’s paralysis)

Question 8

STROKE
What classification system can be used for strokes?

Answer 8

• Oxford stroke (Bamford) classification

Question 9

STROKE
How would an ACA stroke present?

Answer 9

1. Leg weakness - contralateral
2. Sensory disturbance in legs
3. Gait apraxia
4. Incontinence
5. Drowsiness
6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
7. truncal ataxia - can’t sit or stand unsupported

Question 10

STROKE
How would a MCA stroke present?

Answer 10

1. Contralateral arm and leg weakness and sensory loss
2. Hemianopia
3. Aphasia
4. Dysphasia
5. Facial droop

Question 11

STROKE
How would a PCA stroke present?

Answer 11

visual issues

1. Contralateral homonymous hemianopia
2. Cortical blindness
3. Visual agonisa
4. Prosopagnoisa
5. Dyslexia
6. Unilateral headache

Question 12

STROKE
How would a brainstem/basilar artery infarct present?

Answer 12

• Locked in syndrome – complete paralysis BUT eye movement + awareness preserved

Question 13

TIA
What is a transient ischaemia attack (TIA)?

Answer 13

sudden onset, brief episode of neurological deficit due to temporary, focal cerebral ischaemia
symptoms are maximal at onset and lasts 5-15 mins (<24hrs)

Question 14

TIA
What is it essential to do in someone who has had a TIA?

Answer 14

Assess their risk of having stroke in the next 7 days = ABCD2 score

Question 15

TIA
What do the scores from ABCD2 mean?

Answer 15

• ≥4 or crescendo TIAs = specialist assessment within 24h (give aspirin 300mg OD)
• ≤3 = specialist assessment within 1 week, ?brain imaging

Question 16

STROKE
What tools can be used to identify stroke?

Answer 16

• FAST = Facial drooping, Arms floppy, Slurred speech, Time critical (999)
• ROSIER = Recognition Of Stroke In Emergency Room

Question 17

STROKE
What investigation is crucial for the management of stroke and why?

Answer 17

• Non-contrast CT head to exclude haemorrhagic before treatment given.

Question 18

STROKE
How would an ischaemic stroke appear on CT head?

Answer 18

• Hypodensity in region affected with hyperdense vessel
• Loss of grey-white matter differentiation + sulcal effacement (squishing) in cortical infarction
• Hypodense basal ganglia may be seen in deep vessel infarcts

Question 19

STROKE
How would a haemorrhagic stroke appear on CT head?

Answer 19

• Acute = hyperdense
• Subacte = isodense
• Chronic = hypodense

Question 20

STROKE
What are the pros of CT head imaging?

Answer 20

• Quick, readily available, can distinguish site affected + if ischaemic or haemorrhagic

Question 21

STROKE
What bloods may be taken in suspected stroke?

Answer 21

• FBC, ESR + clotting screen (polycythaemia, vasculitis, thrombocytopenia)
• U+Es, creatinine, LFTs, Ca2+ (electrolytes)
• Blood glucose (hypo)
• TFTs, lipid profile (hypercholesterolaemia)

Question 22

STROKE
What other investigations may you do in stroke?

Answer 22

• 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

Question 23

STROKE
What are some potential complications following a stroke?

Answer 23

• Raised ICP, aspiration pneumonia due to dysphagia, pressure sores
• Cognitive impairment, long-term disability, depression
• VTE due to immobility

Question 24

STROKE
What is the treatment for an ischaemic stroke?

Answer 24

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

Question 25

STROKE What must be done after alteplase treatment?

Answer 25

- Repeat CT head after 24h to check for haemorrhagic transformation

Question 26

STROKE What are some contraindications to treatment with alteplase?

Answer 26

- Haemorrhagic stroke - Recent surgery - GI bleeding - Pregnancy - Hx of intracranial haemorrhage - Active cancer

Question 27

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

Answer 27

- 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

Question 28

STROKE What other management is given for ischaemic strokes?

Answer 28

- Control BP - 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel

Question 29

STROKE What is the management of a haemorrhagic stroke?

Answer 29

- Stop anticoagulants if on any + warfarin reversal with vitamin K + beriplex - Aggressive BP control (140–160mmHg systolic) - Surgical decompression (either endovascular clipping or coiling)

Question 30

STROKE What lifestyle advice should be given post-stroke?

Answer 30

- Smoking + alcohol cessation - Improve diet + exercise - Cannot drive for 1m post-stroke or 1y if HGV driver

Question 31

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

Answer 31

- 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

Question 32

STROKE When assessing whether to anticoagulate a patient, what scores could you use?

Answer 32

- CHA2DS2-VaSc (risk of stroke due to AF) - HAS-BLED (risk of serious bleeding)

Question 33

STROKE What is the CHA2DS2-VaSc score

Answer 33

- Congestive heart failure - HTN - Age 65-74 (1), ≥75 (2) - Diabetes - Prev stroke/TIA (2) - Vascular disease - Sex female - 1 = consider anticoagulation, ≥2 = anticoagulate

Question 34

STROKE What is the HAS-BLED score?

Answer 34

- HTN >160mmHg - Abnormal liver/renal function - Stroke - Bleeding Hx or predisposition - Labile INR - Elderly >65y - Drug/alcohol use - ≥3 = high risk of bleeding

Question 35

TIA What treatment may be considered after a TIA?

Answer 35

- Carotid endarterectomy if >70% carotid artery stenosis within 2w of Sx (TIA/stroke)

Question 36

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

Answer 36

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

Question 37

SAH What are the causes of SAH?

Answer 37

- Traumatic injury - Berry aneurysm rupture (70-80%) - at common points round Circle of Willis - Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins - Idiopathic (15-20%)

Question 38

SAH What conditions are linked to SAH?

Answer 38

- Polycystic kidneys - coarctation of aorta - Ehlers-Danlos syndrome

Question 39

SAH What are the clinical features of SAH?

Answer 39

SYMPTOMS - headache (severe, sudden onset, occipital, 'thunderclap') - meningism (photophobia + neck stiffness) - nausea + vomiting - confusion, coma + seizures SIGNS - CN III palsy (fixed dilated pupil) - CN VI palsy - reduced GCS

Question 40

SAH What are some complications of SAH?

Answer 40

- 50% die suddenly or soon after haemorrhage - Rebleeding (20% within first few days) - Cerebral ischaemia due to vasospasm can cause permanent CNS deficit (most common cause of morbidity) - Obstructive hydrocephalus due to blockage of arachnoid granulations (requires ventricular or lumbar drain) - Hyponatraemia (IV 0.9% NaCl saline)

Question 41

SAH What is often associated with better outcomes in SAH?

Answer 41

- GCS >12 on arrival

Question 42

SAH What are the investigations for SAH?

Answer 42

- urgent non-contrast CT head = starburst sign - ECG to consider - lumbar puncture = xanthochromia (if CT negative, perform >12hrs after symptom onset) - CT angiogram

Question 43

SAH What is the management of SAH?

Answer 43

1st line - nimodipine 60mg 4hrly - endovascular coiling (2nd line = surgical clipping) - if raised ICP = IV mannitol, hyperventilation + head elevation - conservative = bed rest, stool softeners

Question 44

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

Answer 44

- 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

Question 45

EDH where does bleeding occur?

Answer 45

in the epidural space

Question 46

EDH What do the ventricles do to prolong survival in someone with an extradural haematoma?

Answer 46

- Ventricles get rid of their CSF to prevent the rise in ICP

Question 47

EDH What is the clinical presentation of EDH?

Answer 47

- initial injury followed by lucid period - period of rapid deterioration - rapid decline in GCS - increasing severe headache - vomiting - seizures - hemiparesis - coma - UMN signs - ipsilateral pupil dilation - bilateral limb weakness - deep and irregular breathing - due to coning late signs = bradycardia and raised BP (cushing's reflex) - death from respiratory arrest

Question 48

EDH what are the signs of ICP ± focal neurology in EDH?

Answer 48

- Increasingly severe headache, - vomiting, - confusion + seizures ± hemiparesis with brisk reflexes - upgoing plantars

Question 49

EDH What are some differentials for EDH?

Answer 49

- Epilepsy, - CO poisoning, - carotid dissection

Question 50

EDH What are the investigations for EDH?

Answer 50

Non-contrast CT head - hyperdense biconvex (lemon shape) Skull x-ray - may show fracture lines LP is contraindicated

Question 51

EDH What investigation is contraindicated in EDH and why?

Answer 51

- Lumbar puncture - Drop in CSF pressure in spinal column will speed up brain herniation through the foramen magnum as CSF + brain mass may shift towards low pressure outlet > brainstem compression + respiratory arrest

Question 52

EDH What is the management for EDH?

Answer 52

- 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

Question 53

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

Answer 53

- 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

Question 54

SDH What is the pathophysiology of a SDH?

Answer 54

1. bleeding from bridging veins into the subdural space forms a haematoma 2. then bleeding stops 3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges 4. gradual rise in ICP over weeks 5. midline structures shift away from side of clot - causes tentorial herniation and coning

Question 55

SDH what is an acute SDH?

Answer 55

< 3 days old traumatic rupture of bridging cortical veins

Question 56

SDH what is a chronic SDH?

Answer 56

- >21 days old - traumatic rupture of bridging cortical veins - associated with cortical atrophy (elderly, alcoholics)

Question 57

SDH what is a sub-acute SDH?

Answer 57

3-21 days old

Question 58

SDH What are the clinical features of SDH?

Answer 58

ACUTE SDH - symptom onset <3 days of event - may have lucid interval - reduced consciousness - headaches + vomiting - slurred speech - focal neurological deficit - cushings reflex - seizures CHRONIC SDH - insidious onset - progressive confusion + cognitive deficit - headaches + vomiting - focal neurological deficit (weakness or fixed dilated pupil)

Question 59

SDH What are the investigations for SDH?

Answer 59

Non-contrast CT head - crescentic collection - not limited by suture lines acute = hyperdense (light) subacute = isodense chronic = hypodense (dark)

Question 60

SDH What is the management of SDH?

Answer 60

SURGERY 1* = irrigation via burr-hole craniostomy 2* = craniotomy IV MANNITOL - to reduce ICP address cause of trauma

Question 61

EPILEPSY Define epilepsy

Answer 61

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

Question 62

EPILEPSY What are the causes of epilepsy?

Answer 62

1. Idiopathic (2/3) 2. cortical scarring 3. tumour 4. stroke 5. alzheimers dementia 6. alcohol withdrawal

Question 63

EPILEPSY What is a focal/partial seizure?

Answer 63

- Confined to one area of cortex with recognisable pattern, usually unilateral meaning 1 hemisphere affected, may affect one body part

Question 64

EPILEPSY What is a simple-partial seizure?

Answer 64

Consciousness + awareness is preserved (e.g. foot twitch)

Question 65

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

Answer 65

strange smells, motor movements, Jacksonian march

Question 66

EPILEPSY What is Jacksonian march?

Answer 66

Starts on one side of body then "marches" over a few seconds to affect larger parts of body like entire hand, foot or facial muscles + may generalise

Question 67

EPILEPSY What is a generalised seizure?

Answer 67

- Activity in both hemispheres, diffuse throughout the brain with bilateral movement abnormalities

Question 68

EPILEPSY Explain what an absence seizure is.

Answer 68

- Brief <30s pauses where activity stops (still, no talking, stares) - Begins in childhood, may progress to tonic-clonic later in life

Question 69

EPILEPSY Explain what a tonic clonic seizure is.

Answer 69

- Tonic = vague warning, rigid, pt falls + may make sound, LOC + may stop breathing - Clonic = convulsions, bilateral rhythmic muscle jerks, irregular breathing, may bite tongue (lateral) or urinary incontinence - Post-ictal = drowsy, confused, irritable or depressed

Question 70

EPILEPSY Explain what a myoclonic seizure is.

Answer 70

- Brief, sudden muscle contractions like jerk of a limb, face or trunk - Usually remains awake, can occur in juvenile myoclonic epilepsy

Question 71

EPILEPSY Explain what an atonic (akinetic) seizure/drop attack is.

Answer 71

- Brief, sudden loss of muscle tone causing a fall but no LOC - Typically begin in childhood, ?indicate Lennox-Gastaut syndrome

Question 72

EPILEPSY What are some differentials of epilepsy?

Answer 72

- Cardiac = postural or cardiogenic syncope - Non-epileptic attack disorder, hypoglycaemia, TIA

Question 73

EPILEPSY what is the management for different types of seizures?

Answer 73

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

Question 74

EPILEPSY what is the treatment for generalised tonic-clonic epilepsy?

Answer 74

1st line = Sodium Valproate for Males & women unable to childbear, 2nd line = Lamotrigine to females of childbearing potential for myoclonic

Question 75

EPILEPSY what is the treatment for absence (petit mal) epilepsy?

Answer 75

1st line = ethosuximide 2nd line - male = sodium valproate - female = lamotrigine or levetiracetam

Question 76

EPILEPSY What driving advice should be given to patients regarding seizures and established epilepsy?

Answer 76

- Cannot drive for 6m following seizure + must inform DVLA - Established epilepsy must be seizure free for 12m before driving

Question 77

STATUS EPILEPTICUS What is status epilepticus?

Answer 77

- Medical emergency where a seizure does not self-limit – seizures lasting >5m or ≥2 within a 5-minute period

Question 78

STATUS EPILEPTICUS What are some causes of status epilepticus?

Answer 78

- Poor adherence #1 - Infections (meningitis, encephalitis) - Worsening of primary cause of epilepsy (e.g. brain tumour growing) - alcoholism - electrolyte imbalance (hyponatraemia, hypocalcaemia)

Question 79

STATUS EPILEPTICUS What is the clinical presentation of status epilepticus?

Answer 79

continuous seizure lasting >5 mins or >2 seizures in 5 minute period without regaining consciousness SYMPTOMS - tonic-clonic seizure - tongue biting - urinary incontinence SIGNS - loss of consciousness - post-ictal confusion

Question 80

STATUS EPILEPTICUS What are the complications of status epilepticus?

Answer 80

- 10% mortality - Long-term morbidity after episode, esp. if hypoxic brain injury occurred (rhabdomyolysis, metabolic acidosis, renal failure)

Question 81

STATUS EPILEPTICUS What investigations might you do for aetiologies of status epilepticus?

Answer 81

- ECG - ABG/VBG - metabolic screen - FBC, U&Es and LFTs - inflammatory markers to consider - anti-epileptic drug levels - toxicology screen - CT head - lumbar puncture

Question 82

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

Answer 82

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

Question 83

STATUS EPILEPTICUS What considerations should be made in status epilepticus?

Answer 83

- Community – buccal midazolam or rectal diazepam as step 1 - If ?alcohol related treat with IV thiamine or Pabrinex - If medication not working or no response ?non-epileptic

Question 84

LOC What is LOC?

Answer 84

Partial or complete loss of perception of yourself + surroundings

Question 85

LOC What are the potential causes of LOC?

Answer 85

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

Question 86

LOC How might cardiogenic LOC present/causes?

Answer 86

- Transient arrhythmias (SVT, WPW, Brugada, long QT) - Bradyarrhythmias like complete heart block > asystole - Structural (aortic stenosis, hypertrophic cardiomyopathy) where may have palpitations, dyspnoea + CP *BLACKOUT ON EXERCISE IS CARDIOGENIC UNTIL PROVEN OTHERWISE*

Question 87

LOC How might reflex LOC present?

Answer 87

- Vasovagal syncope = intense fear like watching surgery, needles > faint - Situational syncope = coughing, post-micturition - Carotid sinus syncope = hypersensitive baroreceptors cause excessive reflexive bradycardia on minimal stimulation (turn head, shaving, reaching high) - Postural hypotension (iatrogenic autonomic failure)

Question 88

LOC What are some important questions to ask in LOC?

Answer 88

- Collateral Hx/witness account is crucial - Head banging - Triggers, before, during, after (how they felt, warning signs, incontinence, injury like tongue biting, sleepy or muscle aches) - Previous episodes

Question 89

SYNCOPE How might syncope present in terms of... i) patient? ii) triggers? iii) prodrome? iv) ictal? v) post-ictal?

Answer 89

i) Older, co-morbidities or young + FHx of young deaths ii) Posture, exertion, metabolic iii) Pale, clammy, palpitations, CPs, 'going dark' iv) Floppy, seconds, eye closed ± few jerks v) Rapid recovery, seconds

Question 90

EPILEPSY How might epilepsy present in terms of... i) patient? ii) triggers? iii) prodrome? iv) ictal? v) post-ictal?

Answer 90

i) Any age, ?CNS lesion, FHx of epilepsy ii) Alcohol, decreased sleep, illness, hyperventilation, none iii) No warning or ?aura, staring/vacant, vocalisation (cry out), posturing iv) Tonic>clonic, symmetrical, few minutes, eyes open, incontinence, lateral tongue biting v) Slow recovery, amnesia, confused, drowsy, agitated

Question 91

NEAD How might NEAD present in terms of... i) patient? ii) triggers? iii) prodrome? iv) ictal? v) post-ictal?

Answer 91

i) Younger, F>M, social/personal stressors, psych Hx, deprivation, abuse ii) Heightened emotion, stress or panic iii) No warning, upset/panic, aware of impending seizure iv) Thrashing/asymmetrical, long (up to 1h), pelvic thrusting, violent, back arching, eyes + mouth forcibly closed, crying, ?distractible, tongue biting (tip), waxing/waning v) unusually rapid, emotional ± amnesia

Question 92

NEAD what is the management of NEAD?

Answer 92

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)

Question 93

PARKINSON'S DISEASE What is the pathophysiology of Parkinson's disease?

Answer 93

destruction of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms Lewy body formation in basal ganglia

Question 94

PARKINSON'S DISEASE What are the causes of Parkinson's disease?

Answer 94

- Unknown, some genetic link, typically 70y/o M - Haloperidol (dopamine blockade) - Metoclopramide + domperidone (anti-emetics which blockade dopamine)

Question 95

PARKINSON'S DISEASE What are the cardinal features of Parkinson's disease?

Answer 95

- BRADYKINESIA (slow, difficult initiating movement, small movements) - RIGIDITY (pain, problems turning in bed) – cogwheel rigidity with tension in arm that gives way to movement in small increments (little jerks) - RESTING TREMOR – 'pill-rolling' - Shuffling gait, small steps + postural instability (stooped)

Question 96

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

Answer 96

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

Question 97

PARKINSON'S DISEASE In terms of tremor, what is an intention tremor?

Answer 97

Worse at end of movement (past-pointing) indicative of cerebellar issue

Question 98

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

Answer 98

- 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

Question 99

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

Answer 99

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

Question 100

PARKINSON'S DISEASE What is progressive supranuclear palsy?

Answer 100

- 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

Question 101

PARKINSON'S DISEASE What is multiple system atrophy?

Answer 101

- 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

Question 102

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

Answer 102

- Associated with Sx of visual hallucinations, delusions, REM sleep disorders, fluctuating consciousness, progressive cognitive decline + Parkinsonism

Question 103

PARKINSON'S DISEASE What is corticobasal degeneration?

Answer 103

- Early myoclonic jerks, gait apraxia, agnosia + alien limb

Question 104

PARKINSON'S DISEASE What investigations would you do in Parkinson's disease?

Answer 104

DaTscan Functional neuroimaging - PET Can confirm by reaction to levodopa MRI (to exclude other causes)

Question 105

PARKINSON'S DISEASE What are some complications of Parkinson's disease?

Answer 105

- Infections - Falls - Depression - Aspiration pneumonia

Question 106

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

Answer 106

- 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

Question 107

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

Answer 107

- Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)

Question 108

HUNTINGTON'S DISEASE What is the inheritance pattern of Huntington's disease?

Answer 108

- Autosomal dominant inheritance with 100% penetrance

Question 109

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

Answer 109

- mutation in HTT gene on chromosome 4 - trinucleotide repeat disorder (CAG)

Question 110

HUNTINGTON'S DISEASE Huntington's disease shows anticipation. What does this mean? When do symptoms typically occur?

Answer 110

- Successive generations have more repeats leading to earlier age of onset + increased severity of disease - Around middle age

Question 111

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

Answer 111

● 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)

Question 112

HUNTINGTON'S DISEASE What investigations would you do for Huntington's disease?

Answer 112

- GENETIC TESTING - with pre- + post-test counselling (cannot give to children have to be old enough to decide themselves), high risk of suicide with diagnosis - MRI HEAD - shows atrophy of striatum

Question 113

HUNTINGTON'S DISEASE What is the management of Huntington's disease?

Answer 113

poor prognosis - no treatment - physiotherapy - speech and language therapy - tetrabenazine (for chorea) - SSRIs for depression - advanced directives

Question 114

HEADACHES What are the two types of headaches and give some examples?

Answer 114

- Primary (no underlying cause) such as migraine, cluster + tension (most common) - Secondary due to an underlying cause.

Question 115

HEADACHES What do these red flags for headaches indicate... i) fever, photophobia, neck stiffness, rash? ii) sudden onset occipital? iii) vomiting, worse on coughing or straining? iv) Hx of trauma + may resist analgesia? v) dizziness or new neuro Sx? vi) visual disturbance? vii) pregnancy? viii) subacute or sudden with papilloedema? ix) travel Hx + flu-like illness?

Answer 115

i) Meningitis/encephalitis ii) SAH iii) Raised ICP (?SOL) iv) Head injury or haemorrhage v) Stroke vi) GCA or glaucoma vii) Pre-eclampsia viii) Venous sinus thrombosis ix) Malaria

Question 116

CLUSTER HEADACHES what are they?

Answer 116

intensely painful, unilateral, periorbital headaches associated with autonomic dysfunction (lacrimation, conjunctival injection, nasal congestion + rhinorrhoea)

Question 117

CLUSTER HEADACHES How does a cluster headache present and how long does it last?

Answer 117

- 15m–3h SYMPTOMS - unilateral, periorbital or temporal headache - ipsilateral autonomic symptoms (lacrimation, conjunctival injection, nasal congestion, rhinorrhoea, ptosis + miosis) - nausea + vomiting - photophobia (with agitation + restlessness) SIGNS - lacrimation - conjunctival injection - rhinorrhoea

Question 118

HEADACHES How does a tension headache present?

Answer 118

- 30m– 7 days - Bilateral, non-pulsatile headache ± scalp tenderness - Pressing/tight-band like sensation - Mild–moderate intensity (Med overuse headache is similar)

Question 119

HEADACHES How does a sinusitis headache present?

Answer 119

- Facial pain behind nose, forehead + eyes, pain on leaning forward - Tenderness over affected sinus - Post-nasal drip, common with coryza - Pain lasts 1–2w, viral

Question 120

HEADACHES How does acute glaucoma present?

Answer 120

- Constant aching pain rapidly develops around 1 eye, radiates to forehead, markedly reduced vision, visual halos, N+V - Signs = red, congested eye, cloudy cornea, dilated non-responsive eye (may be oval shaped) - Can be precipitated by dilating eye-drops, emotions or sitting in dark

Question 121

CLUSTER HEADACHES How can you diagnose cluster headaches?

Answer 121

clinical diagnosis - must rule out alternative - all patients should be referred to a neurologist to consider - CT or MRI brain (to rule out space occupying lesion) - ESR (to rule out giant cell arteritis)

Question 122

HEADACHES What is the management of cluster headaches?

Answer 122

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

Question 123

HEADACHES What is the management of tension headaches?

Answer 123

- Reassure, stress relief (Exercise, avoid triggers, massage) - Simple analgesia like paracetamol (<15d/m) or complex analgesia (<10d/m)

Question 124

HEADACHES What is the management of medication overuse headache?

Answer 124

- Withdrawal of analgesia (may be challenging if pt thinks necessary for headache)

Question 125

HEADACHES What is the management of sinusitis headache?

Answer 125

- Nasal irrigation w/ saline - Prolonged Sx with steroid nasal spray

Question 126

HEADACHES What is the management of acute glaucoma?

Answer 126

- Immediate expert help + IV acetazolamide (carbonic anhydrase inhibitor)

Question 127

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

Answer 127

- 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

Question 128

TRIGEMINAL NEURALGIA What are the causes of trigeminal neuralgia?

Answer 128

Compression of trigeminal nerve by a loop of vein or artery Aneurysms Meningeal inflammation Tumours

Question 129

TRIGEMINAL NEURALGIA What is the clinical presentation of trigeminal neuralgia?

Answer 129

PAIN - trigeminal distribution - severe - unilateral - electric-shock like - lasts seconds to minutes - provoked (washing, shaving, talking, brushing hair, brushing teeth) AUTONOMIC SYMPTOMS - lacrimation - facial swelling - rhinorrhoea - ptosis SIGNS - pain provoked by touch

Question 130

TRIGEMINAL NEURALGIA How would you diagnose trigeminal neuralgia?

Answer 130

- Clinically with ≥3 attacks with pain in ≥1 division + classical Sx - ?CT/MRI head to exclude secondary causes

Question 131

TRIGEMINAL NEURALGIA How would you manage trigeminal neuralgia?

Answer 131

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

Question 132

MIGRAINE What is the pathophysiology of migraines?

Answer 132

- 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

Question 133

MIGRAINE What are the triggers of migraines?

Answer 133

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

Question 134

MIGRAINE What are the stages of migraine?

Answer 134

- Prodromal (up to 3d before with fatigue + mood change) - Aura - Headache - Resolution (headache fades or resolved by vomiting/sleep) - Postdromal (Not typical, some experience a few stages)

Question 135

MIGRAINE What are the 4 main types of migraine?

Answer 135

- Migraine without aura (most common) - Migraine with aura - Silent migraine - Hemiplegic migraine

Question 136

MIGRAINE Describe the pain of a migraine

Answer 136

- Unilateral - Throbbing - Moderate/severe pain - Aggravated by physical activity

Question 137

MIGRAINE How does a migraine with aura present?

Answer 137

Same as without but – - Sparks/zig-zag lines in vision, blurred vision or loss of different visual fields - Aura usually unilateral + lasts up to 60m before headache

Question 138

MIGRAINE What investigations would you do in migraine?

Answer 138

- Mostly clinical Dx - Exclude other causes with bloods, CRP/ESR, CT/MRI head, LP if any red flag concerns

Question 139

MIGRAINE What is the acute management of migraines?

Answer 139

- PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID - Antiemetic like metoclopramide or prochlorperazine if vomiting occurs

Question 140

MIGRAINE What is the prophylaxis for migarines?

Answer 140

- 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)

Question 141

MND What is the pathophysiology of motor neurone disease (MND)?

Answer 141

- Relentless + unexplained destruction/degeneration of UMN + anterior horn cells in the brain + spinal cord - Motor cortex = UMN signs - Anterior horn cells = LMN signs - Cranial nerve nuclei = mixed signs

Question 142

MND What is the cause of MND?

Answer 142

- Most spontaneous + idiopathic with no FHx - Rare familial cases with SOD-1 implication (suggests free radicals like smoking, pesticides + heavy metals) can cause MN destruction - M>F, 60y/o, associated with frontotemporal dementia

Question 143

MND What are the 4 types of MND? Best and worse prognosis?

Answer 143

- Amyotrophic lateral sclerosis (ALS) - Progressive bulbar palsy (worst prognosis) - Progressive muscular atrophy (best prognosis) - Primary lateral sclerosis

Question 144

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

Answer 144

- Loss of motor neurones in motor cortex + anterior horn of cord so mixed signs - Long term consequence is progressive spastic tetraparesis

Question 145

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

Answer 145

- 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

Question 146

MND What is... i) progressive muscular atrophy? ii) primary lateral sclerosis?

Answer 146

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

Question 147

MND What is the general clinical presentation of MND?

Answer 147

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

Question 148

MND What are UMN signs?

Answer 148

Hypertonia or spasticity, brisk reflexes upgoing plantars, muscle wasting

Question 149

MND What are some important differentials of MND and how can they be differentiated?

Answer 149

- Cervical spine lesion as may present with UMN signs - Myasthenia gravis but MND NEVER affects eye movements - Multiple sclerosis but MND NEVER affects sphincters or sensation

Question 150

MND What are some investigations for MND?

Answer 150

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

Question 151

MND How rapidly does MND progress?

Answer 151

Half of patients die <3y from onset, monitor FVC closely for respiratory distress as most die from bulbar palsy respiratory failure

Question 152

MND What medication may be given in MND?

Answer 152

- 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

Question 153

MND What MDT management is given for MND?

Answer 153

- NG/PEG tube for feeding, blend food if dysphagia (SALT) - Exercise for spasticity (physio, orthotics) - Non-invasive ventilation at home to support breathing at night - Palliative care (advanced directives, EOL planning)

Question 154

MULTIPLE SCLEROSIS What is the pathophysiology of MS?

Answer 154

- Inflammation leads to infiltration of immune cells + damages the myelin causing focal loss - Demyelination heals poorly leaving thinner, inefficient myelin - Initially relative preservation of axons but as neurodegenerative, eventually axonal loss leading to fixed + progressive deficits

Question 155

MULTIPLE SCLEROSIS What are some classic sites for MS?

Answer 155

- Periventricular white matter lesions - Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles

Question 156

MULTIPLE SCLEROSIS What is the aetiology of MS?

Answer 156

- Unknown as autoimmune but influenced by genes, EBV, lifestyle factors such as low vitamin D, smoking + obesity

Question 157

MULTIPLE SCLEROSIS What is a clinically isolated syndrome?

Answer 157

- First episode of demyelination + neuro Sx – not diagnosis as does not meet criteria - More likely to develop MS if lesions on MRI

Question 158

MULTIPLE SCLEROSIS What are the 4 types of MS?

Answer 158

- Relapsing remitting (most common) - Secondary progressive - Primary progressive - Benign

Question 159

MULTIPLE SCLEROSIS What is relapsing remitting MS?

Answer 159

- Characterised by episodes of Sx in attacks (relapses) - Followed by periods of stability (remission) - May accumulate disability if don't fully recover

Question 160

MULTIPLE SCLEROSIS What is secondary progressive MS?

Answer 160

Initially RR but now progressive worsening of Sx + incomplete remissions

Question 161

MULTIPLE SCLEROSIS What is the diagnostic criteria for MS?

Answer 161

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

Question 162

MULTIPLE SCLEROSIS What are the symptoms of MS?

Answer 162

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)

Question 163

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

Answer 163

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

Question 164

MULTIPLE SCLEROSIS What are some signs of MS?

Answer 164

- 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

Question 165

MULTIPLE SCLEROSIS What is relative afferent pupillary defect?

Answer 165

- Seen on swinging light test (retina or optic nerve lesion – afferent issue) - The affected and normal eye appears to dilate when light is shone on the affected eye

Question 166

MULTIPLE SCLEROSIS What is internuclear ophthalmoplegia?

Answer 166

- CN VI/medial longitudinal fasciculus lesion - Disorder of conjugate lateral gaze with; – Decreased adduction of ipsilateral eye – Nystagmus on abduction of contralateral eye

Question 167

MULTIPLE SCLEROSIS What are the investigations for MS?

Answer 167

- 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

Question 168

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

Answer 168

- oral/IV methylprednisolone for 5 days - plasma exchange (for sudden, severe relapses not responding to steroids)

Question 169

MULTIPLE SCLEROSIS What is the management of MS remissions?

Answer 169

- First line = beta-interferons (1b) - 2nd line = DMARDs (monoclonal antibody) - natalizumab, dimethyl fumarate

Question 170

MULTIPLE SCLEROSIS What is the general symptomatic management for MS?

Answer 170

Spasticity - BACLOFEN (GABA analogue, reduces Ca2+ influx)/GABAPENTIN - TIZANIDINE (alpha-2 agonist) urinary incontinence = catheterisation incontinence - DOXAZOSIN or OXYBUTYNIN (anti-cholinergic alpha blocker drugs

Question 171

MENINGITIS What is meningitis?

Answer 171

- Inflammation of the meninges which line the brain + spinal cord

Question 172

MENINGITIS What are the bacterial causes of meningitis?

Answer 172

N. meningitidis S. pneumoniae H. influenzae

Question 173

MENINGITIS What are the viral causes of meningitis?

Answer 173

Enterovirus (most common viral) HSV CMV Varicella zoster virus

Question 174

MENINGITIS What are the symptoms of meningitis?

Answer 174

Neck stiffness Photophobia Papilloedema (due to increased ICP) Petechial non-blanching rash Headache Fever Decreased GCS

Question 175

MENINGITIS What are the clinical signs of meningitis?

Answer 175

- 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

Question 176

MENINGITIS What are some differentials of meningitis?

Answer 176

- Malaria - Encephalitis - SAH - Septicaemia - Tetanus - Dengue fever

Question 177

MENINGITIS What investigations would you do for meningitis?

Answer 177

Blood cultures (pre LP) Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate Lumbar puncture (contraindicated with raised ICP) CT head - exclude lesions Throat swabs - bacterial and viral

Question 178

MENINGITIS What would you expect the lumbar puncture result for meningitis to be in bacterial causes for... i) appearance? ii) protein? iii) glucose? iv) white cell count? v) other?

Answer 178

i) Cloudy/turbid ii) ++ iii) –– iv) ++ neutrophils v) Gram stain

Question 179

MENINGITIS What would you expect the lumbar puncture result for meningitis to be in viral causes for... i) appearance? ii) protein? iii) glucose? iv) white cell count? v) other?

Answer 179

i) Clear ii) Mild + or normal iii) Mild – or normal iv) ++ lymphocytes v) PCR

Question 180

MENINGITIS What would you expect the lumbar puncture result for meningitis to be in TB causes for... i) appearance? ii) protein? iii) glucose? iv) white cell count? v) other?

Answer 180

i) Fibrin web ii) ++ iii) –– iv) ++ lymphocytes v) Acid fast bacilli

Question 181

MENINGITIS When is a lumbar puncture contraindicated in meningitis?

Answer 181

- Drowsy, signs of raised ICP + in meningococcal septicaemia due to risk of coning of cerebellar tonsils

Question 182

MENINGITIS What are some complications following meningitis?

Answer 182

- Hearing loss is key complication - Seizures + epilepsy - Sepsis or abscess - Hydrocephalus - Cognitive impairment + learning disability

Question 183

MENINGITIS You see a patient in General Practice with a non-blanching petechial rash and suspect meningococcal septicaemia. What immediate treatment should be given whilst awaiting for hospital transfer?

Answer 183

- IM benzylpenicillin

Question 184

MENINGITIS What is the management of bacterial meningitis

Answer 184

- IV cefotaxime - + amoxicillin to cover listeria (potential contraction in birth) in <3m - Dexamethasone to reduce frequency + severity of neurological sequelae - Adjust treatment according to sensitivities

Question 185

MENINGITIS What is the management of viral meningitis?

Answer 185

- Supportive therapy mainly - IV aciclovir for HSV

Question 186

MENINGITIS Who must you notify about cases of meningitis?

Answer 186

- Public Health England immediately as notifiable disease

Question 187

ENCEPHALITIS What is encephalitis?

Answer 187

- Infection + inflammation of the brain parenchyma (cortex, white matter, brainstem, basal ganglia)

Question 188

ENCEPHALITIS What are the viral causes of encephalitis?

Answer 188

Herpes simplex (most common) CMV Epstein Barr varicella zoster HIV measles mumps

Question 189

ENCEPHALITIS What is the clinical presentation of encephalitis?

Answer 189

SYMPTOMS - fever - headache - behavioural changes (memory disturbance, psychotic behaviour, withdrawal or change in personality) - confusion - seizures SIGNS - reduced GCS - focal neuro deficit (aphasia, hemiparesis, cerebellar signs)

Question 190

ENCEPHALITIS What are the differentials of encephalitis

Answer 190

- Meningitis - Stroke - Brain tumour - Hypoglycaemia, SLE, hypoxic brain injury, DKA

Question 191

ENCEPHALITIS What investigations would you do for encephalitis?

Answer 191

BLOODS - FBC, CRP, U&Es BLOOD CULTURES HIV SEROLOGY MRI - shows areas of inflammation, may be midline shifting CSF - lymphocytosis EEG - periodic sharp and slow wave complexes lumbar puncture

Question 192

ENCEPHALITIS What would the CSF look like in encephalitis for... i) appearance? ii) protein? iii) glucose? iv) white cell count?

Answer 192

i) Clear ii) Raised iii) Normal/low iv) + lymphocytes

Question 193

ENCEPHALITIS What is the management of encephalitis?

Answer 193

IV Acyclovir immediately - even before investigation results Primidone = anti-seizure medication if needed IV benzylpenicillin if meningitis is suspected

Question 194

BRAIN ABSCESS What are the most common causative organisms?

Answer 194

- Staph. aureus + strep. pnuemoniae

Question 195

BRAIN ABSCESS What are the aetiologies of brain abscesses?

Answer 195

- Local infection spread (otitis media, sinusitis, mastoiditis) - Penetrating head injuries, trauma or surgery to the scalp - Haematogenous spread (more common in immunocompromised) from CHD (esp. R>L shunt), pneumonia, embolic events from infective endocarditis

Question 196

BRAIN ABSCESS What is the clinical presentation of a brain abscess?

Answer 196

SYMPTOMS - headache (severe, local to one area, refractory to analgesia) - altered mental state - slurred speech - seizure - nausea + vomiting SIGNS - fever - muscle weakness - hemiplegia - CN III + VI palsies - nuchal rigidity (sign of meningism)

Question 197

BRAIN ABSCESS What are the investigations for brain abscess?

Answer 197

- BLOODS - FBC/CRP - BLOOD CULTURES - CT HEAD - shows ring-enhancing lesion ± surrounding oedema - LP is contraindicated due to raised ICP

Question 198

BRAIN ABSCESS What is the management of brain abscess?

Answer 198

1ST LINE - empirical antibiotics (IV ceftriaxone + metronidazole) - treat underlying cause 2ND LINE - abscess drainage/excision

Question 199

BRAIN DEATH + COMA What is a coma?

Answer 199

Unarousable unresponsiveness

Question 200

BRAIN DEATH + COMA What are some neurological causes of brain death and coma?

Answer 200

- Trauma, tumours - Infection (meningitis, encephalitis) - Vascular (stroke, haemorrhages) - Epilepsy (status epilepticus, post-ictal)

Question 201

BRAIN DEATH + COMA What are some metabolic causes of brain death + coma?

Answer 201

- Drugs, poisoning (alcohol, TCAs, CO, opiates) - Hyperglycaemia (DKA, HHS) or hypoglycaemia - Septicaemia - Hypothermia - Hepatic/uraemia encephalopathy due to liver/renal failure - CO2 narcosis in COPD where too much oxygen leads to hypoxic drive slowing down so CO2 builds up

Question 202

BRAIN DEATH + COMA In terms of clinical presentation in brain death and coma, what are some... i) focal neurological deficits? ii) brainstem signs?

Answer 202

i) Asymmetry of motor function, tendon reflexes + plantar responses ii) Pupil size (pinpoint vs. dilated + pupillary reactions), eye movements, corneal reflexes, cough + gag reflexes, ice cold water in ears > nystagmus

Question 203

BRAIN DEATH + COMA What are lateralising signs? Give an example of one

Answer 203

- Signs that occur from one hemisphere of the brain but not the other, helps to localise pathology - Fixed dilated pupil (CN3 palsy)

Question 204

BRAIN DEATH + COMA Explain the pathophysiology of a third nerve palsy?

Answer 204

- CN3 comes out of brainstem + goes over apex of petrous part of temporal bone as it goes through cavernous sinus to supply eye so susceptible to damage if brain swollen, bleeding + trauma. - Outside CN3 are parasympathetic fibres which constrict pupil so if damaged > fixed + dilated

Question 205

BRAIN DEATH + COMA What is the main differential of a third nerve palsy? How can they be differentiated?

Answer 205

- Blind eye - Blind eye will not give contralateral responsiveness but other causes will + if you shine light in good eye then dilated pupil will restrict

Question 206

BRAIN DEATH + COMA What are some investigations for brain death and coma?

Answer 206

- Bloods – FBC, cultures, U+Es, Ca2+, phosphate, LFTs, glucose, clotting screen, toxicology (+ alcohol), ABG - CT/MRI head, EEG + LP for infection

Question 207

BRAIN DEATH + COMA What is the Glasgow Coma Scale (GCS)? What is it based on? What scores should prompt action?

Answer 207

- Universal consciousness assessment tool - BEST eye, verbal + motor response – 15 max, 3 min - 'GCS ≤8 = intubate' secure airway as may be unable to maintain on own - GCS >8 is greatest prognostic indicator in patients with traumatic brain injury

Question 208

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

Answer 208

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

Question 209

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

Answer 209

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

Question 210

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

Answer 210

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

Question 211

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

Answer 211

- Decorticate posturing – arm adducted + flexed, wrist flexed, internal rotation, plantar flexed + stiff appearance - Indicates significant damage to cerebral hemispheres, internal capsule + thalamus

Question 212

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

Answer 212

- 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

Question 213

BRAIN DEATH + COMA What does the progression from decorticate to decerebrate posturing suggest?

Answer 213

- Uncal (transtentorial) or tonsillar brain herniation 'coning'

Question 214

BRAIN DEATH + COMA What is the management of brain death + coma?

Answer 214

- ABCDE as emergency - Measure vitals, GCS, neuro signs (pupils) + re-check - IV access - Stabilise c-spine if trauma - Management in ICU

Question 215

MYASTHENIA GRAVIS What is myasthenia gravis?

Answer 215

- Autoimmune disorder against acetylcholine receptors in the pre-synaptic membrane of the neuromuscular junction

Question 216

MYASTHENIA GRAVIS What is the pathophysiology of myasthenia gravis?

Answer 216

- Anti-ACh receptor antibodies (IgG) interfere with NMJ via depletion of working post-synaptic receptor sites for ACh to bind to leading to fewer action potentials firing, blocking excitatory effect of ACh on receptors (all or nothing principle) - Both B + T cells implicated

Question 217

MYASTHENIA GRAVIS What are the risk factors of myasthenia gravis?

Answer 217

- female gender - family history - autoimmune (RA and SLE) - thymoma or thymic hyperplasia

Question 218

MYASTHENIA GRAVIS What is the main symptom of myasthenia gravis?

Answer 218

- Fatiguable weakness of muscles which improves with rest - Affects ocular, bulbar + proximal limb muscles - Dysphagia + dysarthria (bulbar)

Question 219

MYASTHENIA GRAVIS What will patients with myasthenia gravis struggle with?

Answer 219

- Hairs, chairs + stairs (proximal muscle weakness) - Speech, mastication, face + neck weakness - Resp muscles (breathing difficulty + dysphagia dangerous features which indicates advancing disease)

Question 220

MYASTHENIA GRAVIS What are the clinical features of myasthenia gravis?

Answer 220

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)

Question 221

MYASTHENIA GRAVIS What antibodies are implicated in myasthenia gravis?

Answer 221

- Anti-AChR antibodies (90%) - Muscle-specific tyrosine kinase (MuSK, esp. males) - Low density lipoprotein receptor-related protein 4 (rare)

Question 222

MYASTHENIA GRAVIS What investigations would you do for myasthenia gravis?

Answer 222

- antibodies - AchR antibodies - electrophysiological studies = repetitive nerve stimulations show decremental muscle response - CT thorax (to exclude thymoma) - thyroid function

Question 223

MYASTHENIC CRISIS What is the main complication of myasthenia gravis?

Answer 223

- Myasthenic crisis

Question 224

MYASTHENIC CRISIS What are the causes of myasthenic crisis?

Answer 224

- Infection (resp), natural disease cycle, under/overdosing meds

Question 225

MYASTHENIC CRISIS What is the management of myasthenic crisis?

Answer 225

- Urgent review by neurologists + anaesthetists - IV immunoglobulins or parapheresis - intubation - corticosteroids

Question 226

MYASTHENIA GRAVIS What is the management of myasthenia gravis?

Answer 226

1st line = acetylcholinesterase inhibitors (pyridostigmine) 2nd line = prednisolone 3rd line = azathioprine other = methotrexate or rituximab Thymectomy if thymoma present

Question 227

GUILLAIN-BARRE What is Guillain-Barré syndrome (GBS)?

Answer 227

- Acute inflammatory demyelinating polyneuropathy which targets Schwann cells in the peripheral nervous system - often triggered by infection

Question 228

GUILLAIN-BARRE What is the pathophysiology of GBS?

Answer 228

- 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

Question 229

GUILLAIN-BARRE What is Miller-Fisher syndrome?

Answer 229

- GBS variant which affects CNS + eye muscles - Characterised by ophthalmoplegia + ataxia

Question 230

GUILLAIN-BARRE What are the causes of GBS?

Answer 230

- Often triggered by preceding illness 4w before symptoms Bacteria - Camplylobacter jejuni - Mycoplasma Viruses - CMV - EBV - HIV - Herpes zoster

Question 231

GUILLAIN-BARRE What is the clinical presentation of GBS?

Answer 231

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)

Question 232

GUILLAIN-BARRE What are some differentials for GBS?

Answer 232

- Other causes of neuromuscular paralysis = hypokalaemia, polymyositis, botulism - Cord compression, transverse myelitis

Question 233

GUILLAIN-BARRE What are the investigations for GBS?

Answer 233

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

Question 234

GUILLAIN-BARRE What is the prognosis of GBS?

Answer 234

- 80% fully recover - 15% recover with neurological disability - 5% die, mostly from PE, resp failure or infection

Question 235

GUILLAIN-BARRE What is the main treatment for GBS?

Answer 235

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)

Question 236

BRAIN TUMOURS What is a brain tumour? What is the prognosis? Where do they come from?

Answer 236

- Abnormal growths in the brain - Poor (12m median survival time) - Most commonly secondary (lungs > breast > melanoma > GI tract > kidney)

Question 237

BRAIN TUMOURS Give 4 examples of different brain tumours

Answer 237

- Gliomas - Meningiomas - Pituitary tumours - Acoustic neuromas (vestibular Schwannomas)

Question 238

BRAIN TUMOURS What are gliomas? Give some examples

Answer 238

- Glial cell in origin in the brain or spinal cord - Graded 1–4 (1 = most benign ?cure, 4 = most malignant glioblastomas) - Astrocytomas like glioblastoma multiforme most common (90%), oligodendrogliomas + ependymoma

Question 239

BRAIN TUMOURS What are meningiomas?

Answer 239

- Benign tumours growing from cells of the meninges in the brain + spinal cord

Question 240

BRAIN TUMOURS What are pituitary tumours?

Answer 240

- Often benign, if large can press on optic chiasm causing bitemporal hemianopia - Can cause hypopituitarism or release excessive hormones > acromegaly, Cushing's, hyperthyroidism

Question 241

BRAIN TUMOURS What are the 3 cardinal signs of brain tumours?

Answer 241

- Progressive focal neurological deficit depending on location of tumours - Sx of raised ICP - Seizures/epilepsy (focal rather than generalised, recent new onset suggest sinister aetiology)

Question 242

BRAIN TUMOURS Why is the neurological deficit progressive in brain tumours?

Answer 242

- Mass effect of tumour + surrounding cerebral oedema as it grows

Question 243

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

Answer 243

Personality + intellect change, hemiparesis, expressive dysphasia

Question 244

BRAIN TUMOURS What are some symptoms of raised ICP?

Answer 244

- Headache – worse in morning, coughing, bending forwards or lying - Drowsiness, confusion, vomiting - Papilloedema (cardinal sign = swollen optic disc) on fundoscopy

Question 245

BRAIN TUMOURS What investigations would you perform for brain tumours?

Answer 245

- CT/MRI head (MRI gold standard) - LP C/I if Sx of raised ICP until after imaging - Audiogram + gadolinium enhanced MRI head for acoustic neuroma - MR angiography may be useful to define site or blood supply of mass

Question 246

BRAIN TUMOURS When would surgery be indicated as management in brain tumours?

Answer 246

- Single mets in younger pts with controlled primary with aim to improve QOL - Meningiomas may be removed entirely without unacceptable damage to surrounding structures

Question 247

BRAIN TUMOURS Other than surgery, what management is there for brain tumours?

Answer 247

- Radio/chemotherapy – stereotactic radiotherapy (gamma knife) - Medical – dexamethasone or mannitol to reduce cerebral oedema but can cause insomnia so give in mornings - AEDs for seizures - Palliative care involvement

Question 248

NEUROPATHY What is a neuropathy?

Answer 248

- Dysfunction/disease of the nerves typically causing weakness or numbness

Question 249

NEUROPATHY What are the peripheral nerve causes of muscle weakness?

Answer 249

- Peripheral neuropathy = lots of nerves affects all over body, often symmetrical + systemic causes - Mononeuropathy = 1 nerve affected, usually due to entrapment - Mononeuritis multiplex = various, individual nerve defects all over the place, randomly

Question 250

NEUROPATHY What is the pathophysiology of mononeuritis multiplex?

Answer 250

- Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit

Question 251

NEUROPATHY What are the causes of peripheral neuropathy?

Answer 251

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

Question 252

NEUROPATHY In terms of peripheral neuropathy, what conditions show a... i) mostly motor loss? ii) mostly sensory loss?

Answer 252

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

Question 253

NEUROPATHY What is Charcot-Marie-Tooth disease?

Answer 253

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

Question 254

NEUROPATHY What is the generic clinical presentation of mononeuropathy?

Answer 254

Individual nerve deficits in isolation, mostly upper limb nerves affected at compression points

Question 255

NEUROPATHY What is the generic clinical presentation of peripheral neuropathy?

Answer 255

- Chronic + slowly progressive - Starts in legs + longer nerves first (furthest from heart) - Sensory/motor/both - Glove + stocking distribution

Question 256

NEUROPATHY What does a CN1 lesion cause?

Answer 256

- Anosmia

Question 257

NEUROPATHY In terms of the optic nerve, what does a... i) L optic nerve lesion ii) Optic chiasma lesion iii) L optic tract lesion iv) L Baum's loop lesion v) L Meyer's loop lesion cause?

Answer 257

i) No vision through L eye ii) Bitemporal hemianopia iii) Contralateral (R) homonymous hemianopia iv) Inferior R homonymous quadrantanopia v) Superior R homonymous quadrantanopia

Question 258

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

Answer 258

- Parietal lobe - Temporal lobe - PITS – Parietal Inferior Temporal Superior

Question 259

NEUROPATHY What does a CN3 lesion cause?

Answer 259

- Tramps' palsy (eye down + out) - Ptosis - Fixed dilated pupil (loss of parasympathetic outflow, exclude a surgical 3rd nerve)

Question 260

NEUROPATHY What does a CN4 lesion cause?

Answer 260

- Vertical diplopia noticed when reading book or going downstairs - Defective downward gaze as innervates superior oblique

Question 261

NEUROPATHY What does a CN5 lesion cause?

Answer 261

- Loss of sensation to face - Weak muscles of mastication - Loss of corneal reflex (afferent) - Jaw deviation to weak side

Question 262

NEUROPATHY What does a CN6 lesion cause?

Answer 262

- Issues abducting eye beyond midline as innervates lateral rectus

Question 263

NEUROPATHY What does a CN7 lesion cause?

Answer 263

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

Question 264

NEUROPATHY What is Bell's palsy?

Answer 264

- CN7 lesion with complete facial paralysis, hyperacusis, - Differentiate from stroke as no forehead sparring as LMN - Often post-viral (HSV), treat with pred + eye care

Question 265

NEUROPATHY What does a CN8 lesion cause?

Answer 265

- Sensorineural deafness - Tinnitus, vertigo, nystagmus

Question 266

NEUROPATHY What does a CN9/10 lesion cause?

Answer 266

- Swallow, gag + cough issues - Uvula deviated away from side of lesion

Question 267

NEUROPATHY What does a CN11 lesion cause?

Answer 267

- Weakness turning head to contralateral side

Question 268

NEUROPATHY What does a CN12 lesion cause?

Answer 268

- Tongue deviation towards side of lesion

Question 269

NEUROPATHY What are the investigations used in neuropathy?

Answer 269

- Neuropathy screen (symmetrical) = FBC, CRP/ESR, U+E, glucose, TFT, B12 + folate - Vasculitis screen (asymmetrical) = first 3 + ANA, ANCA, anti-dsDNA, RhF, complement - EMG + nerve conduction studies

Question 270

NEUROPATHY What is the management of neuropathy?

Answer 270

- Sx relief with neuropathic analgesia (gabapentin, pregabalin, amitriptyline) - Treat underlying cause - Inflammatory = pred + steroid-sparing agents like azathioprine (+ IVIg or plasmapheresis in CIDP) - Vasculitis = rapid pred + immunosuppressant (cyclophosphamide) to avoid irreversible damage

Question 271

CORD COMPRESSION What is myelopathy?

Answer 271

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

Question 272

RADICULOPATHY How does radiculopathy present?

Answer 272

SYMPTOMS - radiating pain (may originate in neck or back) - paraesthesia or numbness - muscle weakness SIGNS - positive straight leg raise test - sensory deficits in dermatomal distribution - reduced muscle power

Question 273

CORD COMPRESSION What are the causes of spinal cord compression?

Answer 273

- 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

Question 274

CORD COMPRESSION What are the symptoms of spinal cord compression?

Answer 274

SYMPTOMS - onset (acute = trauma or disc herniation, insidious = malignancy, osteoporosis) - back pain - paraesthesia - weakness - bladder or bowel dysfunction SIGNS - UMN weakness below lesion (loss of muscle power, increased tone, hyperreflexia) - sensory deficit - spinal shock (hypo/areflexia below, motor paralysis below) - neurogenic shock (bradycardia, peripheral vasodilation, poikilothermia, decreased CO, priapism)

Question 275

CORD COMPRESSION What are the signs of spinal cord compression?

Answer 275

- 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

Question 276

CORD COMPRESSION How does degenerative cervical myelopathy present?

Answer 276

- Pain, loss of motor or sensory function affecting neck, upper or lower limbs - Loss of autonomic function - Hoffman's sign +ve

Question 277

CORD COMPRESSION What are the differentials for spinal cord compression?

Answer 277

- Transverse myelitis (inflammation of both sides of one section of spinal cord) - MS - Trauma - Dissecting aneurysm

Question 278

CORD COMPRESSION What are the investigations of spinal cord compression?

Answer 278

- 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

Question 279

CORD COMPRESSION What is the main complication of spinal cord compression?

Answer 279

- Cauda equina syndrome - Cord compression below the level of the termination of the spinal cord at L1/2 vertebral level = medical emergency

Question 280

CORD COMPRESSION What can cause cauda equina syndrome? How does it present?

Answer 280

- Mostly malignancy, disc prolapse (L4/5, L5/S1), trauma - Back pain, early urinary retention + constipation, saddle anaesthesia, decreased sphincter tone, mixed UMN/LMN leg weakness, erectile dysfunction, asymmetrical paralysis of legs

Question 281

CORD COMPRESSION What is spinal stenosis?

Answer 281

- Narrowing of lower spinal canal almost always due to degeneration

Question 282

CORD COMPRESSION What is the management of spinal cord compression?

Answer 282

- Malignancy = stat dexamethasone + consider chemo, radio, surgery - Epidural abscess = surgical decompression + Abx - Cauda equina = surgery for emergency pressure relief - Degenerative cervical myelopathy = urgent spinal surgery referral for surgical decompression

Question 283

SPINAL CORD INJURY What is Brown-Sequard syndrome?

Answer 283

- 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)

Question 284

ANTERIOR CORD SYNDROME What is anterior cord syndrome?

Answer 284

- Anterior spinal artery occlusion or compression - Bilateral spastic paresis (lateral corticospinal) - Bilateral loss of pain + temp (lateral spinothalamic)

Question 285

SPINAL CORD INJURY What is posterior cord syndrome?

Answer 285

- Trauma or posterior spinal artery occlusion - Loss of fine touch, proprioception + vibration (DCML)

Question 286

SPINAL CORD INJURY What is central cord syndrome?

Answer 286

- Hyperextension injury, often elderly with underlying cervical disease - Sensory + motor deficit (upper extremities > lower)

Question 287

MYOPATHY What are myopathies?

Answer 287

- Neuromuscular disorders where the primary Sx is muscle weakness due to dysfunction of muscle fibres

Question 288

MYOPATHY What are the aetiologies of myopathies?

Answer 288

- inflammatory - metabolic - inherited - polio - drugs - steroids, statins

Question 289

MYOPATHY How do myopathies present?

Answer 289

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

Question 290

MYOPATHY How does myotonic dystrophy present?

Answer 290

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

Question 291

MYOPATHY What are the investigations for myopathies?

Answer 291

- CRP/ESR, creatinine kinase elevated - Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy

Question 292

MYOPATHY What is the management of myopathies?

Answer 292

- Remove causative agent (statins, steroids) - Immunosuppression (steroids, azathioprine) if inflammatory cause.

Question 293

MYOPATHY What is the general supportive management of myopathies?

Answer 293

- OT = aids + adaptations to help live with condition - Physio = prevent contractures - Renal protection = myoglobin can cause kidney damage - Diet = ideally low BMI with good nutrition

Question 294

HYDROCEPHALUS What is hydrocephalus?

Answer 294

- Abnormal build-up of CSF around the brain causing compression to nearby brain tissue as the ventricles dilate

Question 295

HYDROCEPHALUS What is the purpose of CSF?

Answer 295

- Protects brain from damage - Removes waste products from the brain - Provides brain with nutrients to function properly

Question 296

HYDROCEPHALUS What is the usual flow of CSF in the brain?

Answer 296

- Lateral ventricles - Foramen of Munro - 3rd ventricle - Cerebral aqueduct - 4th ventricle - Subarachnoid space (Medially by foramen of Magendie, Laterally by Luschka) - Dural sinus via arachnoid granulations

Question 297

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 297

- Obstructive (non-communicating) = structural pathology blocking flow of CSF with dilatation superior to site of obstruction - Non-obstructive (communicating) = imbalance of CSF production/absorption - Normal pressure = unknown, can develop after head injury or stroke, >60s

Question 298

HYDROCEPHALUS What are some causes of obstructive hydrocephalus?

Answer 298

Tumour, acute haemorrhages, developmental abnormalities (aqueduct stenosis)

Question 299

HYDROCEPHALUS How does hydrocephalus present?

Answer 299

- Signs of raised ICP - Headache (worse in morning or lying down) - N+V, papilloedema, blurred vision

Question 300

HYDROCEPHALUS How does normal pressure hydrocephalus present?

Answer 300

'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

Question 301

HYDROCEPHALUS What are the investigations for hydrocephalus?

Answer 301

- CT head = enlarged ventricles - MRI head if suspected underlying lesion - levodopa challenge to consider: - LP is both diagnostic + therapeutic (caution in obstructive as difference in cranial/spinal pressures can cause brain herniation)

Question 302

HYDROCEPHALUS What is the management of hydrocephalus?

Answer 302

1st line - ventriculo-peritoneal shunting (VPS) 2nd line - Torkildsen procedure (ventriculocisternostomy)

Question 303

IDIOPATHIC INTRACRANIAL HYPERTENSION What is idiopathic intracranial hypertension (IIH)?

Answer 303

- Build up of CSF pressure around the brain causing signs of raised ICP - Associated with obese young women

Question 304

IDIOPATHIC INTRACRANIAL HYPERTENSION what are the risk factors?

Answer 304

- obesity - female sex - pregnancy - drugs (COCP, steroids, tetracyclines, retinoids, lithium)

Question 305

IDIOPATHIC INTRACRANIAL HYPERTENSION What are the causes of IIH?

Answer 305

- Primary = idiopathic - Secondary (often causing chronic intracranial HTN) = brain tumour, chronic SDH, meningitis/encephalitis, venous sinus thrombosis, drugs (nitrofurantoin, vitamin A)

Question 306

IDIOPATHIC INTRACRANIAL HYPERTENSION What is the clinical presentation of IIH?

Answer 306

- headache - blurred vision - papilloedema - enlarged blind spot - CN VI palsy may be present

Question 307

IDIOPATHIC INTRACRANIAL HYPERTENSION What are the investigations for IIH?

Answer 307

- Routine bloods + CT head to exclude organic causes - LP to exclude infection = increased opening pressure (can be therapeutic)

Question 308

IDIOPATHIC INTRACRANIAL HYPERTENSION What is the management of IIH?

Answer 308

- #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

Question 309

NEURO PHARMACOLOGY Give some examples of anti-epileptic drugs (AEDs). What is their mechanism of action?

Answer 309

- Carbamazepine, valproate, lamotrigine, levetiracetam, phenytoin, ethosuximide. - Inhibit voltage-gated Na+ channels which prevents excitability of neurones > reduced firing > stops seizure, some promote GABA release

Question 310

NEURO PHARMACOLOGY What are some side effects and important information for... i) carbamazepine? ii) valproate? iii) lamotrigine

Answer 310

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

Question 311

NEURO PHARMACOLOGY What are some side effects and important information for... i) phenytoin? ii) levetiracetam? iii) ethosuximide?

Answer 311

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

Question 312

NEURO PHARMACOLOGY What is the mechanism of action of Levodopa?

Answer 312

- 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

Question 313

NEURO PHARMACOLOGY What are the side effects of Levodopa?

Answer 313

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

Question 314

NEURO PHARMACOLOGY A side effect of high dopamine are dyskinesias. What is dystonia? What is chorea? What is athetosis?

Answer 314

- Excessive muscle contraction > abnormal postures/movements - Abnormal involuntary movements may be jerky - Involuntary twisting or writhing movements, usually in fingers/hands/feet

Question 315

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

Answer 315

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

Question 316

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

Answer 316

- Pulmonary retroperitoneal + cardiac fibrosis - Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)

Question 317

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

Answer 317

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

Question 318

NEURO PHARMACOLOGY Why are dopamine receptor agonists + COMT/MAO-B inhibitors used in Parkinson's disease?

Answer 318

- Delay use of levodopa + then used in combination to reduce levodopa dose as levodopa is most effective treatment

Question 319

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

Answer 319

- 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

Question 320

NEURO PHARMACOLOGY What are some SEs + C/Is of triptans?

Answer 320

- Dizziness, dry mouth, sleepy, nausea - C/I in CVD

Question 321

DIZZINESS/VERTIGO What is vertigo? What is it characterised by?

Answer 321

- Hallucination of movement, often rotary, of the pt/their surroundings - Spinning, tilting, veering sideways, feeling as if being pushed/pulled - Always worse with movement, relief on lying or sitting still - Difficulty walking or standing - N+V, pallor, sweating

Question 322

DIZZINESS/VERTIGO What is benign paroxysmal positional vertigo (BPPV)? What is it caused by? What is the treatment?

Answer 322

- Brief vertigo on head movements (rolling in bed) due to disruption of debris in semi-circular canal of ears (canalolithiasis) - Idiopathic, secondary to head trauma, labyrinthitis - Reassurance, Epley manoeuvre

Question 323

DIZZINESS/VERTIGO How does traumatic damage present?

Answer 323

- Trauma affecting petrous temporal bone or cerebellopontine angle then auditory nerve may be damaged > vertigo, deafness ± tinnitus.

Question 324

DIZZINESS/VERTIGO What are other causes of dizziness/vertigo?

Answer 324

- Alcohol - Motion sickness - Ototoxicity (aminoglycoside Abx like gentamicin, thiazide diuretics, lithium) - Vestibular neuronitis – recent viral, recurrent vertigo attacks, no hearing loss.

Question 325

DIZZINESS/VERTIGO What is the management of dizziness/vertigo?

Answer 325

- Tilt-table test + Dix-Hallpike manoeuvre - FBC, ESR/CRP, U+Es, LFTs, TFTs to exclude causes - MRI head if ?acoustic neuroma or other brain issue - Sx relief with anti-emetic (prochlorperazine), dizziness use antihistamine cinnarizine

Question 326

STROKE What are the various classifications of strokes?

Answer 326

- Total anterior circulation stroke (TACS) - Partial anterior circulation stroke (PACS) - Posterior circulation syndrome (POCS) - Lacunar syndrome (LACS)

Question 327

TIA What is a crescendo TIA?

Answer 327

- ≥2 TIAs within a week (high risk of stroke)

Question 328

STROKE What is the gold standard imaging for stroke if nothing can be seen on CT head?

Answer 328

- Diffusion-weighted MRI head as shows changes within minutes + higher sensitivity for infarcts

Question 329

STROKE What is the timeframe for thrombolysis for ischaemic strokes?

Answer 329

- Within 4.5 hours of the onset of symptoms

Question 330

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

Answer 330

- Converts plasminogen > plasmin so promotes breakdown of fibrin clot - Alteplase (tPA) or can use streptokinase

Question 331

STROKE What are the benefits of alteplase?

Answer 331

- Improves chance of independence on discharge, - benefit decreases with time (time=brain), - risk of death same

Question 332

STROKE What are the risks of alteplase?

Answer 332

- Haemorrhage (1 in 20), reaction to tPA

Question 333

TIA How would you assess suitability for a carotid endarterectomy after a TIA??

Answer 333

- Carotid doppler USS

Question 334

SAH What are some risk factors for SAH?

Answer 334

Hypertension Known aneurysm Previous aneurysmal SAH Smoking Alcohol Family history Bleeding disorders - associated with berry aneurysms: - Polycystic Kidney Disease - Coarctation of aorta - Ehlers-Danlos syndrome & Marfan syndrome

Question 335

EDH Which vessels most commonly are affected in extradural haematomas? which other vessels can be affected?

Answer 335

- Middle meningeal artery - 25% venous if fracture disrupts the venous sinuses

Question 336

EDH What causes an EDH?

Answer 336

Traumatic head injury (typically to temple, just lateral to eye e.g. punch) - often the temproal bone

Question 337

EDH what is Cushing's reflex?

Answer 337

Bradycardia and increased BP

Question 338

EDH What are some complications of EDH?

Answer 338

- Brainstem compression can cause deep + irregular breathing, - death may follow period of coma due to respiratory arrest

Question 339

SDH what are the risk factors of SDH?

Answer 339

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

Question 340

EPILEPSY Define seizure

Answer 340

a paroxysmal alteration of neurological function as a result of excessive, hypersynchronous discharge of neurons within the brain

Question 341

EPILEPSY what are the risk factors?

Answer 341

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

Question 342

EPILEPSY Define ictal phase

Answer 342

Early phase w/ +ve Sx (excessive/jerky actions)

Question 343

EPILEPSY Define post-ictal phase

Answer 343

Later phase w/ -ve Sx (weakness, drowsy)

Question 344

EPILEPSY What is a complex-partial seizure?

Answer 344

Without consciousness or awareness

Question 345

EPILEPSY What is a secondary generalised seizure?

Answer 345

Seizures starts in 1 hemisphere but spreads to both (focal > general)

Question 346

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

Answer 346

aura (déjà/jamais-vu), automatisms (chewing, lip smacking, picking), hallucinations, aura/sensations, amnesia

Question 347

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

Answer 347

paraesthesia visual hallucinations visual illusions

Question 348

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

Answer 348

visual hallucinations transient blindness rapid + forced blinking movement or head or eyes to opposite side

Question 349

EPILEPSY What is Todd's paresis?

Answer 349

Focal weakness in a part or all of the body after a seizure

Question 350

EPILEPSY What are the 4 main types of generalised seizure?

Answer 350

- Absence seizures, - tonic-clonic seizures, - myoclonic seizures - atonic (akinetic) seizures/drop attacks

Question 351

EPILEPSY What is the general management in the ictal phase?

Answer 351

- Ensure little harm as possible, maintain airway, do not restrain

Question 352

EPILEPSY what is the treatment for generalised tonic/atonic epilepsy?

Answer 352

male = sodium valproate female = lamotrigine

Question 353

EPILEPSY What is the management of epilepsy if anti-epileptic drugs fail to control it?

Answer 353

Vagal stimulation, surgery (hemispherectomy or non-dominant lobectomy)

Question 354

STATUS EPILEPTICUS When might status epilepticus be the first presentation of epilepsy?

Answer 354

First presentation in alcohol abuse (most commonly) or acute brain problem (stroke, trauma, infections, hypoglycaemia)

Question 355

SYNCOPE What is syncope?

Answer 355

Transient global cerebral hypoperfusion

Question 356

NEAD What is NEAD?

Answer 356

Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges, physical manifestation of psychological distress

Question 357

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

Answer 357

- 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

Question 358

PARKINSON'S DISEASE what can exacerbate parkinson's disease?

Answer 358

Anticholinergics can precipitate confusion

Question 359

PARKINSON'S DISEASE In terms of tremor, what is resting tremor?

Answer 359

Tremor seen in Parkinson's disease

Question 360

PARKINSON'S DISEASE In terms of tremor, what is postural tremor?

Answer 360

Anxiety, increased adrenaline, salbutamol, valproate, lithium, benign essential tremor

Question 361

HUNTINGTON'S DISEASE What is the life expectancy from Sx onset?

Answer 361

15–20y + death mostly respiratory disease

Question 362

HEADACHES How can you diagnose tension headaches?

Answer 362

Clinical Dx

Question 363

HEADACHES How can you diagnose medication overuse headaches?

Answer 363

- Present >15d/month, - regular use for >3m of >1 symptomatic treatment drugs - headache developed or worsened during drug use

Question 364

TRIGEMINAL NEURALGIA What are some triggers?

Answer 364

Washing affected area, shaving, eating, talking + dental prostheses

Question 365

TRIGEMINAL NEURALGIA What is the epidemiology?

Answer 365

peak age = 50-60yrs women > men

Question 366

MIGRAINE How long do they last for and who are they more common in?

Answer 366

4–72h, F>M

Question 367

MND What are some complications of MND?

Answer 367

- UTI, pneumonia + respiratory failure (common cause of death), constipation, pressure sores

Question 368

MULTIPLE SCLEROSIS What is the epidemiology of MS?

Answer 368

Commonly presents in young females living further away from equator

Question 369

MULTIPLE SCLEROSIS What is benign MS?

Answer 369

Relapses + Remissions but overall progress will never worsen

Question 370

MULTIPLE SCLEROSIS What is primary progressive MS?

Answer 370

Gradually worsening of disease from point of diagnosis without any RR

Question 371

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

Answer 371

Neck flexion causes electric shock sensation down spine

Question 372

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

Answer 372

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

Question 373

MULTIPLE SCLEROSIS What is the criteria for treatment of MS remissions?

Answer 373

- 2 relapses in past 2y

Question 374

MENINGITIS How does it occur?

Answer 374

Microorganisms can reach the meninges either by direct extension from ears, nasopharynx or via blood

Question 375

MENINGITIS What are the aseptic causes of meningitis?

Answer 375

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

Question 376

MENINGITIS How does viral meningitis present?

Answer 376

benign + self-limiting, no rash but blurred vision or headache

Question 377

ENCEPHALITIS What are the non-viral causes of encephalitis?

Answer 377

Bacterial meningitis TB Malaria Lyme’s disease

Question 378

BRAIN ABSCESS What is a brain abscess?

Answer 378

- Pus-filled swelling in the brain

Question 379

BRAIN DEATH + COMA What is brain death?

Answer 379

Irreversible cessation of all brain function, usually from widespread injury to brain indicated by lack of brainstem signs

Question 380

BRAIN DEATH + COMA What is a persistent vegetative state?

Answer 380

State of wakefulness with sleep-wake cycles but no detectable awareness

Question 381

MYASTHENIA GRAVIS What is the natural course of myasthenia gravis?

Answer 381

- Eventually leads to atrophy - Fluctuating relapsing + remitting pattern

Question 382

MYASTHENIA GRAVIS What medications can exacerbate myasthenia gravis?

Answer 382

Abx, CCBs, beta-blockers, lithium + statins

Question 383

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

Answer 383

Receptive dysphasia, amnesia

Question 384

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

Answer 384

Hemisensory loss, dysphasia

Question 385

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

Answer 385

Contralateral visual defects

Question 386

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

Answer 386

Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia (DANISH)

Question 387

NEUROPATHY What can cause mononeuritis multiplex?

Answer 387

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

Question 388

RADICULOPATHY What is radiculopathy?

Answer 388

the nerve root in the spinal column becomes inflamed or compressed, causing pain, numbness or weakness radiating along the nerve root's pathway

Question 389

RADICULOPATHY What is the most common radiculopathy?

Answer 389

Sciatica (L5) = lower back pain that travels to buttocks + down back of thigh to calf

Question 390

MYOPATHY What are dystrophies?

Answer 390

If they're inherited = dystrophies

Question 391

MYOPATHY How do myopathies compare to neuropathies?

Answer 391

Weakness is proximal in muscle disease (nerves = distal)

Question 392

SHINGLES what is the cause of shingles?

Answer 392

reactivation of herpes varicella zoster virus

Question 393

SHINGLES what is the pathophysiology of shingles?

Answer 393

- latent virus is reactivated in the dorsal root ganglia + travels down affected nerve via sensory root - affects one dermatome

Question 394

SHINGLES what is the clinical presentation?

Answer 394

- rash - restricted to same dermatome - neuritic pain - malaise, myalgia, headache and fever

Question 395

SHINGLES how is it diagnosed?

Answer 395

clinical diagnosis

Question 396

SHINGLES what is the management?

Answer 396

1st line - antivirals = acyclovir - simple analgesia = paracetamol/ibuprofen 2nd line - neuropathic agents = amitriptyline or gabapentin - corticosteroids

Question 397

SHINGLES what are the complications?

Answer 397

- post herpetic neuralgia - pain which lasts >4 months - damage to opthalmic branch of trigeminal nerve - results in sight loss

Question 398

CEREBELLAR DISEASE what are the signs of cerebellar dysfunction?

Answer 398

DANISH dysdiadochokinesia ataxia nystagmus intention tremor slurred speech hypotonia

Question 399

CEREBELLAR DISEASE what are the causes?

Answer 399

- Friedreich's ataxia - neoplastic (cerebellar haemangioma) - stroke - alcohol - MS - hypothyroidism - drugs (phenytoin, lead poisoning) - paraneoplastic (secondary to lung cancer)

Question 400

BELL'S PALSY what are the causes?

Answer 400

viral infection - reactivation of herpes simplex virus 1 (HSV1) this leads to swelling of CN VII

Question 401

BELL'S PALSY what is the pathophysiology?

Answer 401

reactivation of HSV-1 results in destruction of ganglion cells and infection of schwann cells leading to demyelination and neural inflammation

Question 402

BELL'S PALSY what are the symptoms?

Answer 402

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

Question 403

BELL'S PALSY what is the management?

Answer 403

- prednisolone - aciclovir - eye protection (eye lubricants or artificial tears should be considered

Question 404

BELL'S PALSY what are the investigations?

Answer 404

- can be clinical diagnosis other investigations to consider: - CT/MRI - infectious disease screen - ACE

Question 405

NEUROFIBROMATOSIS what are the clinical signs of NF1?

Answer 405

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

Question 406

NEUROFIBROMATOSIS what are the clincial signs of NF2?

Answer 406

- acoustic neuromas (bilateral) - family history - meningioma, schwannoma, juvenile cortical cataracts or glioma

Question 407

NEUROFIBROMATOSIS what are the causes of neurofibromatosis 1 and 2?

Answer 407

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

Question 408

NEUROFIBROMATOSIS what is the treatment for NF1 and NF2?

Answer 408

- no cure - pain management - growths can be surgically removed

Question 409

NARCOLEPSY what are the clinical features?

Answer 409

- excessive daytime sleepiness/sleep attacks - cataplexy - hypnagogic/hypnopompic hallucinations - sleep paralysis - excessive fatigue/impaired memory

Question 410

NARCOLEPSY what are the investigations?

Answer 410

- actigraphy and sleep diary - overnight polysomnography - multiple sleep latency test (MSLT)

Question 411

NARCOLEPSY what is the management?

Answer 411

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

Question 412

CORD COMPRESSION How is spinal stenosis managed?

Answer 412

MRI + canal decompression surgery

Question 413

CORD COMPRESSION How does spinal stenosis present?

Answer 413

- Spinal claudication > pain in buttocks/legs when walking - pain eased by bending forward as canal opens - negative straight leg raise

Question 414

RADICULOPATHY what are the causes?

Answer 414

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

Question 415

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

Answer 415

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

Question 416

RADICULOPATHY what are the investigations?

Answer 416

- MRI - nerve conduction studies - EMG

Question 417

RADICULOPATHY what is the management?

Answer 417

1st line - NSAIDS (ibuprofen) - physical therapy 2nd line - epidural steroid injections - surgery (laminectomy + discectomy)

Question 418

WERNICKE-KORSAKOFF SYNDROME what is it?

Answer 418

- includes wernicke's encephalopathy and korsakoff's syndrome - it is a spectrum (wernicke's = acute, korsakoff's = chronic)

Question 419

WERNICKE-KORSAKOFF SYNDROME what is the clinical triad?

Answer 419

- confusion - ataxia - ophthalmoplegia + nystagmus

Question 420

WERNICKE-KORSAKOFF SYNDROME what are the clinical features?

Answer 420

- confusion - ataxia (wide-based gait) - ophthalmoplegia (diplopia, horizontal/vertical nystagmus, conjugate gaze palsy - slow pupillary response - anisocoria - ptosis - autonomic dysfunction (hypotension, tachycardia)

Question 421

WERNICKE-KORSAKOFF SYNDROME what is the cause?

Answer 421

vitamin B1 (thiamine) deficiency - most commonly caused by alcoholism

Question 422

WERNICKE-KORSAKOFF SYNDROME what are the investigations?

Answer 422

can be clinical diagnosis - evidence of long term alcohol abuse (macrocytic anaemia, deranged LFTs + clotting) - therapeutic trial of IV thiamine - erythrocyte transkelotase activity - VBG = lactic acidosis - MRI brain

Question 423

WERNICKE-KORSAKOFF SYNDROME what is the management?

Answer 423

TREATMENT IV pabrinex for 5 days followed by long-term oral thiamine IV magnesium PROPHYLAXIS oral thiamine

Question 424

MYASTHENIC CRISIS What are the clinical features?

Answer 424

- Resp failure or death

Question 425

MYASTHENIC CRISIS what are the complications?

Answer 425

Resp failure or death

Question 426

CATAPLEXY what is it?

Answer 426

sudden muscle weakness triggered by strong emotions such as laughter, anger and surprise

Question 427

CATAPLEXY what happens during an attack?

Answer 427

- slurred speech - impaired eyesight (double vision, unable to focus) - hearing and awareness are undisturbed (remain conscious)

Question 428

CATAPLEXY what are the causes?

Answer 428

- 75% of people with narcolepsy have cataplexy - it is rare for cataplexy to be only symptom

Question 429

CATAPLEXY what is the management?

Answer 429

sodium oxybate tricyclic antidepressants (clomipramine) SSRIs

Question 430

SAH what is the appearance of SAH on CT head?

Answer 430

white star-shaped lesion as blood fills gyro patterns around brain + ventricles

Question 431

EDH what is the appearance of EDH on non-contrast head CT?

Answer 431

lens shaped haematoma = LEMON SHAPE doesn’t cross suture lines shows midline shift

Question 432

SDH What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?

Answer 432

Clot starts to break down and there is massive increase in oncotic pressure –> water is sucked up by osmosis into the haematoma

Question 433

SDH what is the appearance of SDH on non-contrast head CT?

Answer 433

crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time) unilateral shows midline shift

Question 434

EPILEPSY What is the emergency treatment for epilepsy?

Answer 434

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

Question 435

EPILEPSY what is the treatment for generalised myoclonic epilepsy?

Answer 435

male = sodium valproate female = levetiracetam

Question 436

BELL'S PALSY how do you tell the difference between bell's palsy and a stroke?

Answer 436

- stroke = forehead still innervated - forehead sparing - Bell’s palsy = both forehead and lower face are affected on one side

Question 437

PARKINSON'S DISEASE Define Parkinson’s disease

Answer 437

Degenerative movement disorder caused by a reduction in dopamine in the pars compacta of the substantia nigra

Question 438

PARKINSON'S DISEASE Would you describe the symptoms of Parkinson’s disease as symmetrical or asymmetrical?

Answer 438

Asymmetrical = One side is always worse than the other

Question 439

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

Answer 439

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

Question 440

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

Answer 440

Deep brain stimulation of the sub-thalamic nucleus Surgical ablation of overactive basal ganglia circuits

Question 441

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

Answer 441

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

Question 442

HUNTINGTON'S DISEASE what are the signs of Huntington's disease?

Answer 442

Abnormal eye movements Dysarthria Dysphagia Rigidity Ataxia

Question 443

HEADACHES What is the prophylactic management of cluster headaches?

Answer 443

1st line = Verapamil - avoid triggers (alcohol) - short course prednisolone may break cycle during clusters

Question 444

HEADACHES What is the most common type of secondary headache?

Answer 444

Medication overuse headache - episodic headache becomes daily chronic headache

Question 445

MIGRAINE What other symptoms may a patient with a migraine experience other than pain?

Answer 445

Nausea Photophobia Phonophobia Aura

Question 446

MIGRAINE What is a prodrome for migraines?

Answer 446

Precedes migraine by hours-days yawning food cravings changes in sleep, appetite or mood

Question 447

MIGRAINE what is a migraine aura?

Answer 447

Precedes migraine attacks and can be a variety of symptoms - Visual = lines, dots, zig-zags - somatosensory = paraesthesia, pins and needles Dysphagia Ataxia

Question 448

MIGRAINE what is a migraine aura?

Answer 448

Precedes migraine attacks and can be a variety of symptoms - Visual = lines, dots, zig-zags - somatosensory = paraesthesia, pins and needles Dysphagia Ataxia

Question 449

MIGRAINE What is the diagnostic criteria for a migraine?

Answer 449

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

Question 450

MIGRAINE How does triptan work?

Answer 450

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

Question 451

MND does MND affect UMN or LMN?

Answer 451

both UMN and LMN can be affected

Question 452

MND does MND affect eye movement?

Answer 452

Never affects eye movements (clinical feature of myasthenia gravis)

Question 453

MND Does MND cause sensory loss or sphincter disturbance?

Answer 453

No (clinical feature of MS)

Question 454

MND What are LMN signs?

Answer 454

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

Question 455

MND What is the diagnostic criteria for MND?

Answer 455

LMN + UMN signs in 3 regions El Escorial criteria Presences of LMN and UMN degeneration and progressive history Absence of other disease processes

Question 456

MULTIPLE SCLEROSIS what is MS?

Answer 456

A chronic autoimmune, T-cell mediated inflammatory condition of the CNS characterised by multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years

Question 457

MULTIPLE SCLEROSIS What are the differential diagnosis’s of MS

Answer 457

SLE Sjogren’s AIDS Syphilis

Question 458

MENINGITIS What are the bacterial causes of meningitis in neonates?

Answer 458

E.coli Group B strep - strep agalactiae

Question 459

MENINGITIS What can cause meningitis in immunocompromised patients?

Answer 459

CMV Cryptococcus TB HIV herpes simplex

Question 460

MENINGITIS How would you describe the rash associated with meningococcal sepsis?

Answer 460

Petechial non-blanching rash

Question 461

MENINGITIS What can be given as prophylaxis against meningitis?

Answer 461

IV CIPROFLOXACIN (all ages and pregnancy) and IV RIFAMPICIN (all ages but NOT pregnancy)

Question 462

MENINGITIS Give 4 potential adverse effect of a lumbar puncture

Answer 462

Headache Paraesthesia CSF leak Damage to spinal cord

Question 463

ENCEPHALITIS In what group of people is encephalitis common?

Answer 463

Immunocompromised the infections are most frequent in children and elderly

Question 464

ENCEPHALITIS Name the main triad of symptoms of encephalitis

Answer 464

Fever + headache + altered mental state

Question 465

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

Answer 465

Pregnancy Hypokalaemia Infection Emotion Exercise Drugs

Question 466

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

Answer 466

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

Question 467

NEUROPATHY What is the generic clinical presentation of mononeuritis multiplex?

Answer 467

Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy

Question 468

NEUROPATHY What is the pathophysiology of carpal tunnel syndrome?

Answer 468

Inflammation of carpal tunnel leads to entrapment of the median nerve

Question 469

NEUROPATHY What are the causes of carpal tunnel syndrome?

Answer 469

Idiopathic but associated with local tumours, DM + RA

Question 470

ANTERIOR CORD SYNDROME what are the causes?

Answer 470

- iatrogenic - thoracic and thoracoabdominal AA repair - aortic dissection - atherothrombotic disease - emboli - vasculitis

Question 471

ANTERIOR CORD SYNDROME what are the symptoms?

Answer 471

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

Question 472

ANTERIOR CORD SYNDROME what are the investigations?

Answer 472

MRI - 'owls eyes' hyperintensities in anterior horns lumbar puncture, CSF testing, blood and urine to rule out other causes

Question 473

ANTERIOR CORD SYNDROME what is the treatment?

Answer 473

- IV fluids to increase intravascular volume - vasopressor medications to increase systemic vascular resistance - lumbar drain to remove CSF symptomatic management - mechanical ventilation - catheterisation

Question 474

HORNER'S SYNDROME what is the pathophysiology of horner’s syndrome?

Answer 474

unilateral damage to the sympathetic chain

Question 475

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

Answer 475

Stroke Syringomyelia MS tumour encephalitis anhidrosis to face, arm and trunk

Question 476

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

Answer 476

Pancoast's tumour thyroidectomy trauma cervical rib anhidrosis of face

Question 477

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

Answer 477

carotid artery dissection carotid aneurysm cavernous sinus thrombosis cluster headache no anhidrosis

Question 478

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

Answer 478

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

Question 479

HORNER'S SYNDROME what are the investigations for horner’s syndrome?

Answer 479

clinical examination MRI - detect lesions

Question 480

HORNER'S SYNDROME what is the treatment for horner’s syndrome?

Answer 480

treat underlying cause

Question 481

BULBAR PALSY what is it?

Answer 481

refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself CN 9, 10, 11 and 12

Question 482

BULBAR PALSY what are the causes?

Answer 482

- brainstem tumours and strokes - ALS - GBS

Question 483

BULBAR PALSY what are the symptoms?

Answer 483

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

Question 484

BULBAR PALSY what are the investigations?

Answer 484

MRI lumbar puncture

Question 485

BULBAR PALSY what is the treatment?

Answer 485

- no known treatment - drooling = riluzole - feeding tube - SaLT - help chewing

Question 486

STRABISMUS what is it?

Answer 486

where there is misalignment of the visual axes of the eyes; it may be latent or manifest and, if manifest, it may be constant or intermittent

Question 487

STRABISMUS what are the causes?

Answer 487

- congenital - graves (restricted eye movement) - myasthenia gravis - intra-cranial process (mass, raised ICP, CNS infarction, inflammation of CNS)

Question 488

STRABISMUS what are the symptoms?

Answer 488

- diplopia - eye misalignment - amblyopia (decreased vision in an anatomically normal eye) - abnormal eye movements - visual confusion - asthenopia (ocular discomfort)

Question 489

STRABISMUS what are the risk factors?

Answer 489

FHx of strabismus prematurity low birth weight maternal smoking during pregnancy

Question 490

STRABISMUS what are the investigations?

Answer 490

- cover test - simultaneous prism and cover test (SPCT) - uncover test (UCT) - alternate prism cover test (APCT) - Hirschberg test - Krimsky test

Question 491

STRABISMUS what is the management?

Answer 491

definitive treatment = extraocular muscle surgery correction of refractive errors treatment of amblyopia - eye patch treatment for diplopia - patch, prisms, high prescription, orthoptic exercises

Question 492

SCIATICA what is it?

Answer 492

nerve pain from an injury or irritation to sciatic nerve which originates in buttock/gluteal region

Question 493

SCIATICA how is the pain from sciatica described?

Answer 493

- burning - electric - stabbing can be constant or it can come and go worse when sat down usually unilateral

Question 494

SCIATICA what are the risk factors?

Answer 494

- previous injury - overweight - lack of core strength - physically demanding job - diabetes - osteoarthritis - inactivity - smoking

Question 495

SCIATICA what are the causes?

Answer 495

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

Question 496

SCIATICA what are the symptoms?

Answer 496

- moderate pain in lower back, buttock and leg - numbness/weakness in lower back, buttock, leg or feet - pain gets worse with movement - pins and needles in legs, toes, or feet - loss of bladder or bowel control (due to cauda equina)

Question 497

SCIATICA what are the investigations?

Answer 497

- physical exam - straight leg raises - spinal x-ray - MRI/CT - nerve conduction velocity - electromyography - myelogram

Question 498

SCIATICA what is the management?

Answer 498

- apply ice/hot packs - over the counter medications - NSAIDs - aspirin - paracetamol - prescription medications - muscle relaxants (cyclobenzaprine) - tricyclic antidepressants (amitryptyline) - gabapentin/pregabalin - physical therapy

Question 499

RAISED ICP what are the causes?

Answer 499

- tumour - abscess - haemorrhage - hydrocephalus - strokes that cause brain swelling

Question 500

RAISED ICP what are the symptoms?

Answer 500

SYMPTOMS - headache - nausea + vomiting - confusion SIGNS - papilloedema - altered consciousness - blown pupil - HTN - bradycardia - irregular respirations * cushing's triad = HTN, bradycardia + irregular respirations

Question 501

RAISED ICP what are the investigations?

Answer 501

- 1st line = CT head - fundoscopy to consider - lumbar puncture (contraindicated in raised ICP) - ICP monitoring

Question 502

RAISED ICP what is the management?

Answer 502

TREAT UNDERLYING CAUSE - antibiotics (CEFTRIAXONE) - ventriculo-peritoneal (VP) shunts - surgery REDUCING ICP - elevate head - mannitol - dexamethasone (CI in TBI or haemorrhage) - hyperventilation - surgical decompression

Question 503

RAISED ICP what is the prognosis for brain herniation?

Answer 503

high chance of brain damage/death

Question 504

MYOPATHY what is myotonic dystrophy?

Answer 504

autosomal dominant genetic condition causing progressive muscle weakness most common form of muscular dystrophy to occur in adults

Question 505

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

Answer 505

type 1 - DMPK gene mutation on chromosome 19 type 2 = ZNF9 gene on chromosome 3

Question 506

TIA What are the causes of a transient ischaemia attack (TIA)?

Answer 506

- Artherothromboembolism of the carotid - main cause (can hear carotid bruit) - Cardioembolism - in AF, after MI, valve disease/prosthetic valve - Hyperviscosity - polycythaemia, sickle cell, high WBCC - hypoperfusion - postural hypotension, decreased flow

Question 507

TIA what is the pathophysiology of TIA?

Answer 507

Cerebral ischaemia due to lack of O2 and nutrients –> cerebral dysfunction without infarction (no irreversible cell death) symptoms are maximal at onset -> usually last 5-15 mine (<24hrs)

Question 508

TIA what are the signs of a carotid TIA?

Answer 508

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

Question 509

TIA what are the signs of a vertebrobasilar TIA?

Answer 509

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

Question 510

TIA what are the differential diagnosis’s for a TIA

Answer 510

Migraine aura Epilepsy Hypoglycaemia Hyperventilation retinal bleed syncope - due to arrhythmia

Question 511

TIA What investigations would you do in someone who you suspect to have a TIA?

Answer 511

- ECG (to rule out AF) - Bloods (HbA1c, lipids, clotting screen) - TIA clinic (within 24hrs) - at TIA clinic, other imaging such as diffusion weighted MRI head + carotid doppler can be arranged to consider - CT head (only indicated to rule out other pathology) - echocardiogram (rule out septal defect)

Question 512

TIA what is the ABCD2 score?

Answer 512

Assesses risk of stoke in the next 7 days for those who have had a TIA *no longer recommended by NICE

Question 513

TIA What is the acute treatment for a TIA?

Answer 513

- aspirin 300mg - refer to specialist within 24hrs

Question 514

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

Answer 514

- 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

Question 515

HYDROCEPHALUS what are the causes of normal pressure hydrocephalus?

Answer 515

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue - injury - bleeding - infection - brain tumour - brain surgery

Question 516

CHRONIC FATIGUE SYNDROME what is it?

Answer 516

It is a disorder characterized by extreme fatigue or tiredness that doesn’t go away with rest and can’t be explained by an underlying medical condition.

Question 517

CHRONIC FATIGUE SYNDROME What are the causes?

Answer 517

unknown - could be: - viruses (EBV, rubella, RRV) - a weakened immune system - stress - hormonal imbalances

Question 518

CHRONIC FATIGUE SYNDROME what are the risk factors?

Answer 518

- sex (female) - existing anxiety/depression - middle age - allergies - stress - environmental factors

Question 519

CHRONIC FATIGUE SYNDROME what are the clinical features?

Answer 519

FATIGUE - new + specific onset - persistent and/or recurrent - unexplained by other conditions - has resulted in substantial reduction in activity - characterised by post-exertional malaise and/or fatigue SLEEP DISTURBANCE MUSCLE OR JOINT PAIN (without inflammation) PALPITATIONS (in absence of cardiac disease) HEADACHES COGNITIVE DYSFUNCTION (difficulty concentrating) PAINFUL LYMPH NODES (without pathological enlargement)

Question 520

CHRONIC FATIGUE SYNDROME what are the differentials?

Answer 520

mononucleosis lyme disease MS SLE hypothyroidism fibromyalgia depression sleep disorders

Question 521

CHRONIC FATIGUE SYNDROME what is the diagnostic criteria?

Answer 521

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

Question 522

CHRONIC FATIGUE SYNDROME what are the investigations?

Answer 522

- FBC (rule out anaemia) - CRP/ESR (rule out inflammatory cause) - TFTs (rule out hypothyroidism) - LFTS (rule out chronic liver disease) - U&Es (rule out chronic kidney disease) - blood glucose or HbA1c (rule out DM) - coeliac serology (rule out coeliac)

Question 523

CHRONIC FATIGUE SYNDROME what is the management?

Answer 523

1st line - education - rest strategies - graded exercise therapy - CBT 2nd line - referral to pain management clinic - low dose TCA e.g. amitriptyline

Question 524

ESSENTIAL TREMOR what is it?

Answer 524

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms usually absent at rest and present during posture and intentional movements. it can also involve the voice, head and jaw

Question 525

ESSENTIAL TREMOR what is the presentation?

Answer 525

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)

Question 526

ESSENTIAL TREMOR what are the investigations?

Answer 526

clinical diagnosis - bilateral tremor with normal muscle tone and speed of movement other investigations to rule out other causes: - bloods: U&Es, LFTs, TFTs - urinalysis - imaging: MRI head, SPECT (dAT) scan

Question 527

ESSENTIAL TREMOR what is the management?

Answer 527

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

Question 528

STROKE what is the primary prevention of strokes?

Answer 528

Risk factor modifcaiton - Antihypertensives for HTN - Statins for hyperlipiaemia - Smoking cessation - Control DM - AF treatment = warfarin/NOAC's

Question 529

STROKE what is the secondary prevention of strokes?

Answer 529

2 weeks of aspirin --> long term clopidogrel

Question 530

STROKE what non-pharmaceutical treatment options are there for people after a stroke?

Answer 530

1. Specialised stroke units 2. Swallowing and feeding help 3. Phsyio and OT 4. Neurorehab - physio + speech therapy

Question 531

SAH give 3 possible complications of a subarachnoid haemorrhage

Answer 531

1. Rebleeding (common = death) 2. Cerebral ischaemia 3. Hydrocephalus 4. Hyponatraemia

Question 532

SDH what are the differential diagnoses for a subdural haematoma?

Answer 532

stroke dementia CNS masses (tumour vs abscess)

Question 533

EPILEPSY what is the diagnostic criteria for eilespy?

Answer 533

At least 2 or more unprovoked seizures occurring >24 hours apart One unprovoked seizure + probability of future seizures Epileptic syndrome diagnosis

Question 534

EPILEPSY what are the investigations?

Answer 534

BEDSIDE - urinalysis - capillary blood glucose - ECG BLOODS - FBC, U&Es, bone profile, magnesium, inflammatory markers, toxicology screen IMAGING - CT head - MRI head - EEG

Question 535

EPILEPSY how do lamotrigine and carbamazepine work?

Answer 535

Inhibit pre-synaptic Na+ channels so prevent axonal firing

Question 536

EPILEPSY how does sodium valproate work?

Answer 536

Inhibits voltage gated Na+ channels and increases GABA production

Question 537

EPLILEPSY give 4 potential side effects of anti-epileptic drugs (AEDs)

Answer 537

1. Cognitive disturbances 2. Heart disease 3. Drug interactions 4. Teratogenic

Question 538

PARKINSONS DISEASE what is the pathway for dopamine production?

Answer 538

Tyrosine --> L-dopa --> Dopamine

Question 539

HYDROCEPHALUS What are some causes of non-obstructive hydrocephalus?

Answer 539

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

Question 540

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 540

- Obstructive (non-communicating) - Non-obstructive (communicating) - Normal pressure

Question 541

HYDROCEPHALUS What is the pathophysiology of obstructive (non-communicating) hydrocephalus?

Answer 541

due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction

Question 542

HYDROCEPHALUS What is the pathophysiology of non-obstructive (communicating) hydrocephalus?

Answer 542

due to an imbalance of CSF production absorption

Question 543

DIABETIC NEUROPATHY what is the distribution of sensory loss?

Answer 543

glove and stocking - usually lower legs are affected first

Question 544

DIABETIC NEUROPATHY what is the management of neuropathic pain?

Answer 544

- 1st line = amitriptyline, duloxetine, gabapentin or pregabalin (if one doesn't work try another) - tramadol for rescue therapy - topical capsaicin

Question 545

DIABETIC NEUROPATHY what are the effects on the GI system?

Answer 545

- gastroparesis - chronic diarrhoea (particularly at night) - GORD

Question 546

DIABETIC NEUROPATHY what is the management for gastroparesis?

Answer 546

metoclopramide, domperidone or erythromycin

Question 547

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 547

- Obstructive (non-communicating) = structural pathology blocking flow of CSF with dilatation superior to site of obstruction - Non-obstructive (communicating) = imbalance of CSF production/absorption - Normal pressure = unknown, can develop after head injury or stroke, >60s

Question 548

BRAIN METASTASES what is it?

Answer 548

when cancer spreads from primary location to the brain through haematogenous spread

Question 549

BRAIN METASTASES where are they located?

Answer 549

in adults - 80% = supratentorial - 20% = infratentorial (15% in cerebellum, 5% in brainstem) in children - 45-60% = infratentorial

Question 550

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

Answer 550

- lung cancer - breast cancer - melanoma - colorectal cancer - renal cell carcinoma

Question 551

BRAIN METASTASES what are the clinical features?

Answer 551

SYMPTOMS - headache (worsened by lying flat, at night + early morning) - nausea + vomiting - reduced consciousness - seizures - blurred vision SIGNS - focal neuro signs (determined by location) - signs of raised ICP (papilloedema) - cushing's triad (HTN, bradycardia + irregular resps) - hemiparesis - CN palsies (abducens (CN VI) = most common)

Question 552

BRAIN METASTASES what are the investigations?

Answer 552

- MRI brain (gold standard) - CT brain to consider - PET scan

Question 553

BRAIN METASTASES what is the management?

Answer 553

- corticosteroids (DEXAMETHASONE) - radiotherapy - stereotactic radiosurgery - surgery - chemotherapy - targeted therapies

Question 554

BRAIN METASTASES what are the complications?

Answer 554

- raised ICP - neurological deficits (hemiparesis, aphasia, visual field defects) - seizures - neurocognitive deficits

Question 555

VASOVAGAL SYNCOPE what are the clinical features?

Answer 555

PRE-SYNCOPE - trigger (e.g. prolonged standing) - sweating - warmth - nausea - lightheadedness - diminished vision or hearing - pallor - hyperventilation - palpitations SYNCOPE - rapid onset LOC - usually lasts seconds with spontaneous + complete recovery

Question 556

VASOVAGAL SYNCOPE what are the investigations?

Answer 556

can be clinical diagnosis to consider - lying + standing BP - ECG (assess for cardiac cause) - FBC (check for anaemia) - glucose (check for hypoglycaemia) - B-hCG - tilt table

Question 557

VASOVAGAL SYNCOPE what is the management?

Answer 557

1st line - reassurance - education - tilt training - counterpressure manoeuvres (leg crossing, arm tensing) 2nd line - medications = midodrine, fludrocortisone

Question 558

MONONEUROPATHY what are the nerve roots for median nerve?

Answer 558

C5-T1

Question 559

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

Answer 559

- 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)

Question 560

MONONEUROPATHY what are the investigations for carpal tunnel syndrome?

Answer 560

tinels test phalens test

Question 561

MONONEUROPATHY what is the management of carpal tunnel syndrome?

Answer 561

- wrist splints - corticosteroid injections - surgical decompression (flexor retinaculum decompression)

Question 562

MONONEUROPATHY what are the nerve roots for the ulnar nerve?

Answer 562

C8-T1

Question 563

MONONEUROPATHY what are the clinical features of ulnar neuropathy?

Answer 563

- 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

Question 564

MONONEUROPATHY what are the investigations for ulnar neuropathy

Answer 564

froments test - pinch paper between thumb + index finger

Question 565

MONONEUROPATHY what are the nerve roots for the radial nerve?

Answer 565

C5-T1

Question 566

MONONEUROPATHY what are the clinical features of radial neuropathy?

Answer 566

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

Question 567

MONONEUROPATHY what are the nerve roots of the axillary nerve?

Answer 567

C5-6

Question 568

MONONEUROPATHY what are the clinical features of axillary neuropathy?

Answer 568

sensory loss over lateral shoulder

Question 569

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

Answer 569

L4-S2

Question 570

MONONEUROPATHY what are the clinical features of common peroneal neuropathy?

Answer 570

- foot drop (weakness of dorsiflexion) - sensory loss over dorsum of foot + lateral shin

Question 571

MONONEUROPATHY what are the nerve roots of the tibial nerve?

Answer 571

L4-S3

Question 572

MONONEUROPATHY what are the clinical features of tibial neuropathy?

Answer 572

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

Question 573

MONONEUROPATHY what is meralgia parasthetica?

Answer 573

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

Question 574

MONONEUROPATHY what are the investigations for mononeuropathies?

Answer 574

nerve conduction studies EMG to consider - x-rays