NEURO

Question 1

STROKE

What is a stroke?

Answer 1

• Clinical syndrome consisting of rapid onset focal neurological deficit lasting >24h or leading to death which is the result of a vascular lesion and is associated with infarction of CNS tissue

Question 2

STROKE

What are the two main causes of stroke and how do they cause a 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

• Cardiac (atherosclerosis, AF, infective endocarditis, structural like ASD, patent foramen ovale, MR, valve replacement)
• Vascular (aortic or vertebral dissection
• Haem (sickle cell, polycythaemia)

Question 4

STROKE

What are the causes of haemorrhagic stroke?

Answer 4

Intracerebral haemorrhage
- Trauma, arteriovenous malformation
- Cerebral amyloid angiopathy due amyloid deposition in arteries
- Small vessel disease due to chronic HTN
SAH (trauma, berry aneurysm, AVM)
Anticoagulants, tumours + substance abuse (secondary causes)

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 strokes?

Answer 6

• HTN = biggest
• CV = hypercholesterolaemia, smoking, AF, IHD
• Previous TIA, carotid artery stenosis
• DM

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?
What are the various components?

Answer 8

• Oxford stroke (Bamford) classification
• Total anterior circulation stroke (TACS)
• Partial anterior circulation stroke (PACS)
• Posterior circulation syndrome (POCS)
• Lacunar syndrome (LACS)

Question 9

STROKE
What vessels can be affected in TACS?
What criteria must be met for a TACS?

Answer 9

• ACA, MCA, carotid
  All three Hs –
• Hemiplegia (unilateral ± sensory deficit of face, arm leg)
• Homonymous hemianopia
• Higher cerebral dysfunction (dysphasia, visuospatial disturbance)

Question 10

STROKE
What vessels can be affected in PACS?
What criteria must be met for a PACS?

Answer 10

• ACA, MCA, carotid (same vessels as TACS)

- 2/3 of the criteria for TACS

Question 11

STROKE
What vessels can be affected in POCS?
What criteria must be met for a POCS?

Answer 11

• PCA, vertebrobasilar artery or branches
  One of the following –
• Cranial nerve palsy + contralateral motor/sensory deficit
• Bilateral motor/sensory deficit
• Conjugate eye movement disorder (e.g. gaze palsy)
• Cerebellar dysfunction (ataxia, nystagmus, vertigo)
• Isolated homonymous hemianopia + cortical blindness

Question 12

STROKE
What vessels can be affected in LACS and what does that mean?
What areas can be affected in LACS?
What criteria must be met for a LACS?

Answer 12

• Perforating arteries so no higher cortical dysfunction or visual field abnormality, subcortical stroke
• Thalamus, basal ganglia, internal capsule
  One of following –
• Pure sensory stroke (thalamus)
• Pure motor stroke (posterior limb of internal capsule)
• Sensori-motor stroke
• Ataxic hemiparesis

Question 13

STROKE

How would an ACA stroke present?

Answer 13

• Contralateral lower limb hemiparesis + loss of sensation

- Gait apraxia (unable to initiate walking)

Question 14

STROKE

How would a MCA stroke present?

Answer 14

• Contralateral upper (± lower) limb weakness + loss of sensation
• Contralateral homonymous hemianopia
• Expressive/receptive dysphasia (Broca’s/Wernicke’s area of dominant hemisphere)
• Dysarthria, facial droop
• Hemineglect syndrome if affecting non-dominant hemisphere
• CLASSIC STROKE*

Question 15

STROKE

How would a PCA stroke present?

Answer 15

• Contralateral homonymous hemianopia with macular sparing
• Visual agnosia (cannot interpret visual information but can see)
• Prosopagnosia (inability to recognise familiar face)
• Cerebellar dysfunction

Question 16

STROKE

How would a brainstem/basilar artery infarct present?

Answer 16

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

Question 17

STROKE
How would lateral medullary/Wallenberg’s syndrome present?
What vessel is implicated?

Answer 17

• Cerebellar: ataxia, nystagmus
• Ipsi: dysphagia, facial numbness + CN palsy
• Contra: limb sensory loss
• Posterior inferior cerebellar artery

Question 18

STROKE
How would lateral pontine syndrome present?
What vessel is implicated?

Answer 18

• Similar to Wallenberg’s but ipsilateral facial paralysis + deafness
• Anterior inferior cerebellar artery

Question 19

STROKE
What is a transient ischaemia attack (TIA)?
What is a crescendo TIA?

Answer 19

• Transient neurological dysfunction secondary to cerebral ischaemia without infarction, usually self-resolving neurological deficit within 24h
• ≥2 TIAs within a week (high risk of stroke)

Question 20

STROKE

What risk assessment tool can be used to calculate a person’s risk of having a stroke within the next 48h?

Answer 20

ABCD2

• Age >60 (1)
• BP >140/90mmHg (1)
• Clinical features (unilateral weakness = 2, speech disturbance = 1)
• Diabetes (1)
• Duration (≥60m = 2, 10–59m = 1)

Question 21

STROKE

What do the scores from ABCD2 mean?

Answer 21

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

Question 22

STROKE

What tools can be used to identify stroke?

Answer 22

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

Question 23

STROKE

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

Answer 23

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

Question 24

STROKE

How would an ischaemic stroke appear on CT head?

Answer 24

• 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 25

STROKE | How would a haemorrhagic stroke appear on CT head?

Answer 25

- Acute = hyperdense - Subacte = isodense - Chronic = hypodense

Question 26

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

Answer 26

- Quick, readily available, can distinguish site affected + if ischaemic or haemorrhagic - Diffusion-weighted MRI head as shows changes within minutes + higher sensitivity for infarcts

Question 27

STROKE | What bloods may be taken in suspected stroke?

Answer 27

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

Question 28

STROKE | What other investigations may you do in stroke?

Answer 28

- 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 29

STROKE | What are some potential complications following a stroke?

Answer 29

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

Question 30

``` STROKE What is the most crucial management for ischaemic strokes? What timeframe? Mechanism of action? Drug? ```

Answer 30

- Thrombolysis with IV tPA (tissue plasminogen activator) - Within 4.5 hours - Converts plasminogen > plasmin so promotes breakdown of fibrin clot - Alteplase (tPA) or can use streptokinase

Question 31

STROKE What must be done after alteplase treatment? What are the benefits of alteplase? What are the risks of alteplase?

Answer 31

- Repeat CT head after 24h to check for haemorrhagic transformation - Improves chance of independence on discharge, benefit decreases with time (time=brain), risk of death same - Haemorrhage (1 in 20), reaction to tPA

Question 32

STROKE | What are some contraindications to treatment with alteplase?

Answer 32

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

Question 33

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

Answer 33

- 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 34

STROKE | What other management is given for ischaemic strokes?

Answer 34

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

Question 35

STROKE | What is the management of a haemorrhagic stroke?

Answer 35

- 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 36

STROKE | What lifestyle advice should be given post-stroke?

Answer 36

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

Question 37

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

Answer 37

- 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 38

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

Answer 38

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

Question 39

STROKE | What is the CHA2DS2-VaSc score

Answer 39

- 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 40

STROKE | What is the HAS-BLED score?

Answer 40

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

Question 41

STROKE What treatment may be considered after a TIA? How would you assess suitability?

Answer 41

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

Question 42

STROKE | Strokes require an MDT approach for rehabilitation. Name some of the members in the stroke MDT and their role

Answer 42

- Nurses (manage meds, NG feeding, prevent pressure sores) - Physio (strength, balance + function training) - OT (functional Ax + home mods) - SALT (swallowing issues, communication rehab) - Dietetics, orthotics, psychology

Question 43

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

Answer 43

- Spontaneous rupture of arteries supplying the brain causes a rapid release of arterial blood into the subarachnoid space, where the CSF is located between pia mater + arachnoid membrane in the meninges - This causes increased ICP + possibly stroke.

Question 44

SAH | What is the most common cause of SAH?

Answer 44

- Saccular/berry aneurysm rupture (80%) - Commonest sites at bifurcations: - Junction of anterior communicating/cerebral arteries - Junction of posterior communicating with internal carotid - Trifurcation of MCA

Question 45

SAH What are some other causes of SAH? What conditions are linked to SAH? What are some risk factors for SAH?

Answer 45

- Congenital arteriovenous malformations (15%), trauma - Polycystic kidneys, coarctation of aorta + Ehlers-Danlos syndrome - Smoking, alcohol misuse, HTN, bleeding disorders, FHx of SAH

Question 46

SAH | What are some symptoms of SAH?

Answer 46

- Sudden onset excruciating headache, often occipital (thunderclap) - Can occur on exertion (weightlifting, sex) - Vomiting, seizures, LOC/collapse, coma/drowsiness which can last for days - Preceding 'sentinel' headache (?small warning leak from offending aneurysm)

Question 47

SAH | What are some signs of SAH?

Answer 47

- Meningism – neck stiffness, photophobia, +ve kernig's (pain/unable to extend leg at knee when it's bent) - Focal neurology (CN III palsy, other CN palsies) - Retinal, subhyaloid + vitreous bleeds on fundoscopy

Question 48

SAH | What are some complications of SAH?

Answer 48

- 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 49

SAH | What is often associated with better outcomes in SAH?

Answer 49

- GCS >12 on arrival

Question 50

SAH | What are some important investigations for SAH?

Answer 50

- CT head gold standard (95% sensitivity on day 1) – white star-shaped lesion as blood fills gyro patterns around brain + ventricles - Lumbar puncture if CT -ve after 12h to allow Hb to break down – xanthochromia (yellow due to bilirubin) confirms - CT angiography to locate aneurysms before surgical procedures

Question 51

SAH | What is the management of SAH?

Answer 51

- Neurosurgery referral ASAP (endovascular coiling vs. surgical clipping which requires craniotomy) - Maintain cerebral perfusion with IV fluids but ensure SBP <160mmHg - PO nimodipine for 3w to reduce vasospasm + prevent morbidity

Question 52

EDH What is the pathophysiology of extra-dural haematoma (EDH)? What is the offending vessel? Any other vessels?

Answer 52

- Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater - Middle meningeal artery - 25% venous if fracture disrupts the venous sinuses

Question 53

EDH What is the ventricles mechanism seen in EDH? What causes an EDH?

Answer 53

- Ventricles get rid of their CSF to prevent the rise in ICP | - Traumatic head injury (typically to temple, just lateral to eye e.g. punch)

Question 54

EDH | What is the natural clinical presentation of EDH?

Answer 54

- May be initial LOC/drowsiness - Slow bleeds lead to lucid interval pattern where pt appears to improve but then rapid decrease in GCS from rising ICP - Signs of increased ICP ± focal neurology develop - Ipsilateral pupil dilation, coma deepens, bilateral limb weakness - Cushing's reflex is a late sign

Question 55

EDH In the natural clinical presentation of EDH... i) what are the signs of ICP ± focal neurology? ii) what is Cushing's reflex?

Answer 55

i) Increasingly severe headache, vomiting, confusion + seizures ± hemiparesis with brisk reflexes + upgoing plantars ii) Bradycardia and increased BP

Question 56

EDH What are some differentials for EDH? What are some complications of EDH?

Answer 56

- Epilepsy, CO poisoning, carotid dissection | - Brainstem compression can cause deep + irregular breathing, death may follow period of coma due to respiratory arrest

Question 57

EDH | What are the investigations for EDH?

Answer 57

Non-contrast CT head – - Hyperdense biconvex haematoma ± midline shift - Haematoma IS limited by cranial sutures as dura mater adheres tightly to skull at cranial sutures Skull XR may show fracture lines crossing course of middle meningeal artery

Question 58

EDH | What investigation is contraindicated in EDH and why?

Answer 58

- 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 59

EDH | What is the management for EDH?

Answer 59

- Neurosurgical transfer for clot evacuation ± ligation of bleeding vessel - IV mannitol if increased ICP (osmotic diuresis)

Question 60

SDH | What is the pathophysiology of subdural haematoma (SDH)?

Answer 60

- 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 61

SDH What causes a SDH? Who are at risk of SDH?

Answer 61

- Often minor trauma, can occur 9m post-incident as venous blood bleeds slowly - Alcoholics + elderly as prone to falls + have atrophic brains making bridging veins stretched so more likely to rupture, also shaken babies

Question 62

SDH | What are the symptoms of SDH?

Answer 62

- Fluctuating level of consciousness (GCS) - Insidious physical/intellectual slowing - Unsteadiness, drowsy - Sx of increased ICP = headache (worse coughing or leaning forward), vomit

Question 63

SDH | What are some signs of SDH?

Answer 63

- Raised ICP, seizures | - Focal neurology occurs later (often >1m after injury) like unequal pupils, hemiparesis

Question 64

SDH | What are the investigations for SDH?

Answer 64

Non-contrast CT head shows crescent/concave shaped haematoma ± midline shift – - Acute/subacute (<14d) = hyperdense (white) - Chronic (>14d) = hypodense (darker) - Acute-on-chronic (rebleed) = both/mixture - Haematoma is NOT limited by cranial sutures

Question 65

SDH | What is the management of SDH?

Answer 65

- Small = clot evacuation via burr hole - Large = craniotomy - IV mannitol if increased ICP (osmotic diuresis)

Question 66

``` EPILEPSY Define... i) epilepsy ii) seizure iii) ictal phase iv) post-ictal phase ```

Answer 66

i) Recurrent tendency to have unprovoked seizures ii) Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain iii) Early phase w/ +ve Sx (excessive/jerky actions) iv) Later phase w/ -ve Sx (weakness, drowsy)

Question 67

EPILEPSY | What are the causes of epilepsy?

Answer 67

- 2/3rd idiopathic, genetics/FHx, alcohol/drugs including withdrawal - Brain injury = trauma, hypoxia, surgery - SOL = tumour, asbcess - Infection = meningitis, encephalitis

Question 68

EPILEPSY | What is a focal/partial seizure?

Answer 68

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

Question 69

``` EPILEPSY What is a... i) simple-partial seizure? ii) complex-partial seizure? iii) secondary generalised seizure? ```

Answer 69

i) Consciousness + awareness is preserved (e.g. foot twitch) ii) Without consciousness or awareness iii) Seizures starts in 1 hemisphere but spreads to both (focal > general)

Question 70

``` EPILEPSY How would a partial seizure present in... i) frontal lobe? ii) temporal lobe? iii) parietal lobe? iv) occipital lobe? ```

Answer 70

i) strange smells, motor movements, Jacksonian march ii) déjà/jamais-vu, automatisms (chewing, lip smacking), hallucinations, aura/sensations, amnesia iii) contralateral altered sensation (tingling, numbness, crawling, electric-shock) iv) flashing lights, eyelid fluttering, eye movements

Question 71

EPILEPSY What is... i) Jacksonian march? ii) Todd's paresis?

Answer 71

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

Question 72

EPILEPSY What is a generalised seizure? What are the 4 main types?

Answer 72

- Activity in both hemispheres, diffuse throughout the brain with bilateral movement abnormalities - Absence seizures, tonic-clonic seizures, myoclonic seizures + atonic (akinetic) seizures/drop attacks

Question 73

EPILEPSY | Explain what an absence seizure is.

Answer 73

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

Question 74

EPILEPSY | Explain what a tonic clonic seizure is.

Answer 74

- 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 75

EPILEPSY | Explain what a myoclonic seizure is.

Answer 75

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

Question 76

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

Answer 76

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

Question 77

EPILEPSY | What are some differentials of epilepsy?

Answer 77

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

Question 78

EPILEPSY | What investigations would you do in epilepsy?

Answer 78

- Mostly clinical Dx, witnessed seizure Hx crucial - Exclude organic causes (FBC, U+Es, LFTs, glucose, ECG) - Electroencephalogram (EEG) often sleep deprived or hyperventilate to provoke - ?Neuroimaging (CT/MRI head) if focal neurology + concerned about SOL

Question 79

EPILEPSY What is the general management in the ictal phase? What are the treatment principles in epilepsy?

Answer 79

- Ensure little harm as possible, maintain airway, do not restrain - Aim for monotherapy, attain maximum tolerated dose before changing or adding drugs, avoid abrupt withdrawal

Question 80

EPILEPSY | Compare the management of generalised seizures and focal seizures

Answer 80

- Generalised 1st line = sodium valproate, 2nd line = lamotrigine, carbamazepine for TC as can exacerbate absent + myoclonic, clonazepam for myoclonic - Focal 1st line = carbamazepine (or lamotrigine), 2nd line = sodium valproate or levetiracetam

Question 81

EPILEPSY What is the management of i) absence seizures? ii) failed AEDs?

Answer 81

i) 1st line = ethosuximide or sodium valproate | ii) Vagal stimulation, surgery (hemispherectomy or non-dominant lobectomy)

Question 82

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

Answer 82

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

Question 83

STATUS EPILEPTICUS | What is status epilepticus?

Answer 83

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

Question 84

STATUS EPILEPTICUS What are some causes of status epilepticus? When might status epilepticus be the first presentation of epilepsy?

Answer 84

- Poor adherence #1 - Infections (meningitis, encephalitis) - Worsening of primary cause of epilepsy (e.g. brain tumour growing) - First presentation in alcohol abuse (most commonly) or acute brain problem (stroke, trauma, infections, hypoglycaemia)

Question 85

STATUS EPILEPTICUS | What is the clinical presentation of status epilepticus?

Answer 85

- Convulsions tend to occur for 2–3m - Followed by slow activity or rest period + then more convulsions - The whole process continues although individual seizures do not

Question 86

STATUS EPILEPTICUS | What are the complications of status epilepticus?

Answer 86

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

Question 87

STATUS EPILEPTICUS | What is the initial management for status epilepticus?

Answer 87

- ABCDE approach (Secure airway, high conc oxygen, assess cardiorespiratory function) - Establish IV access - Measure capillary glucose + correct immediately

Question 88

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

Answer 88

- FBC, U+Es, Ca2+, Mg+, LFTs, INR, AED levels, CK - Blood cultures - Toxicology screen - CT head to rule out organic causes - LP if imaging -ve - EEG useful

Question 89

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

Answer 89

- IV lorazepam 4mg if fitting >5m – repeat after 10m if persists - IV phenytoin (regular ECG/BP), phenobarbital or sodium valproate - No response to step 2 within 30m then anaesthesia + ICU admission as anaesthesia will stop but v dangerous

Question 90

STATUS EPILEPTICUS | What considerations should be made in status epilepticus?

Answer 90

- 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 91

``` LOC What is... i) LOC? ii) syncope? iii) NEAD? ```

Answer 91

i) Partial or complete loss of perception of yourself + surroundings ii) Transient global cerebral hypoperfusion iii) Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges, physical manifestation of psychological distress

Question 92

LOC | What are the potential causes of LOC?

Answer 92

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

Question 93

LOC | How might cardiogenic LOC present/causes?

Answer 93

- 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 94

LOC | How might reflex LOC present?

Answer 94

- 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 95

LOC How might... i) arterial ii) systemic iii) head LOC present?

Answer 95

i) Vertebrobasilar insufficiency (TIA, CVA) ii) Hypoglycaemia iii) Epilepsy, NEAD, anxiety (hyperventilation)

Question 96

LOC | What are some important questions to ask in LOC?

Answer 96

- 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 97

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

Answer 97

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 98

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

Answer 98

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 99

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

Answer 99

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 100

LOC What investigations would you do for LOC? How can NEAD and a true epileptic seizure be differentiated?

Answer 100

- CV + neuro exam - 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 101

LOC What is the driving advice for LOC? What is the management of LOC? Management of NEAD?

Answer 101

- No driving until cause known or until blackout free for 1y - Treat underlying cause - NEAD = 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 102

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

Answer 102

- Progressive loss of dopaminergic neurones from the pars compacta of the substantia nigra leading to decreased levels of dopamine causing an alteration in neural circuits within the basal ganglia which regulates movement

Question 103

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

Answer 103

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

Question 104

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

Answer 104

- 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 105

PARKINSON'S DISEASE | What are some other signs of Parkinson's disease?

Answer 105

- Asymmetrical as Sx on one side always worse - Problems doing up buttons - Smaller writing (micrographia) - Hypomimia

Question 106

PARKINSON'S DISEASE | What are some motor symptoms of Parkinson's disease?

Answer 106

- Insidious onset, reduced arm swing on one side - Tremor worsened by concentration - Progressive fatigue + decrease in amplitude of movements (tap foot on floor + it will start to slow)

Question 107

PARKINSON'S DISEASE | What are some pre-motor symptoms of Parkinson's disease?

Answer 107

- Anosmia (90%, can occur 7y prior to motor Sx) - Depression/anxiety - Sleep disturbance (REM sleep behaviour disorder) + insomnia - Autonomic features – urgency, hypotension, constipation

Question 108

PARKINSON'S DISEASE In terms of tremor, what is... i) intention tremor? ii) resting tremor? iii) postural tremor?

Answer 108

i) Worse at end of movement (past-pointing) indicative of cerebellar issue ii) Tremor seen in Parkinson's disease iii) Anxiety, increased adrenaline, salbutamol, valproate, lithium, benign essential tremor

Question 109

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

Answer 109

- 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 110

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

Answer 110

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

Question 111

PARKINSON'S DISEASE | What is progressive supranuclear palsy?

Answer 111

- 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 112

PARKINSON'S DISEASE | What is multiple system atrophy?

Answer 112

- 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 113

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

Answer 113

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

Question 114

PARKINSON'S DISEASE | What is corticobasal degeneration?

Answer 114

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

Question 115

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

Answer 115

- Clinical Dx - Histological features may show lewy bodies made up of alpha-synuclein + ubiquitin and loss of dopaminergic neurones in the substantia nigra - Idiopathic Parkinson's disease shows normal MRI head + DaTSCAN (used to differentiate from other causes of Parkinsonism)

Question 116

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

Answer 116

- Infections - Falls - Depression - Aspiration pneumonia

Question 117

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

Answer 117

- Lifestyle: education, exercise, physio, MDT - Co-careldopa, co-beneldopa = increase amount of dopamine in CNS - Bromocriptine, cabergoline = dopamine receptor agonist - Entacapone + selegiline = inhibit enzymatic breakdown of dopamine - Anticholinergic amantadine for tremor + overactive bladder - Deep brain stimulation

Question 118

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

Answer 118

- Presence of mutant huntingtin protein causes loss of neurones in striatum (caudate nucleus + putamen) of basal ganglia causing depletion of inhibitory GABA (ACh + dopamine spared) - Reduced GABA = reduced inhibition so dopamine hypersensitivity + increase in dopamine transmission leading to increased stimulation at thalamus + cortex > involuntary movements

Question 119

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

Answer 119

- Autosomal dominant inheritance with 100% penetrance - Trinucleotide expansion repeat of CAG in HTT gene on chromosome 4 - >35 = HD

Question 120

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

Answer 120

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

Question 121

HUNTINGTON'S DISEASE How does Huntington's disease present? What is the life expectancy from Sx onset?

Answer 121

- Chorea (involuntary movements) - Psych (depression, suicide risk, psychotic Sx) - Personality change (irritability) - Cognitive decline (subcortical dementia) - Dysarthria + dysphagia - 15–20y + death mostly respiratory disease

Question 122

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

Answer 122

- 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 123

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

Answer 123

- SSRIs for depression - Antipsychotics (haloperidol), BDZs (diazepam), dopamine-depleting agents (tetrabenazine) may help reduce chorea by blocking dopamine - Risperidone for aggression - MDT input from SALT, OT, physio + psychology - Advanced directive + EOL planning where necessary

Question 124

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

Answer 124

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

Question 125

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 125

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 126

HEADACHES | What are some common causes of headaches and their epidemiology + causes?

Answer 126

- Cluster – 30–50M smokers - Tension – missed meals, stress, dehydration, alcohol, lack of sleep - Med overuse – commonest secondary, often analgesia overuse - Sinusitis – inflammation in ethmoidal, maxillary, frontal or sphenoidal sinuses - Acute glaucoma – elderly, long-sighted people with increased intraocular pressure

Question 127

HEADACHES | How does a cluster headache present?

Answer 127

- 15m–2h - Rapid onset excruciating pain around one eye - Pain unilateral, often nocturnal - Eye may be bloodshot, lid swelling, miosis, ptosis + lacrimation - 'Cluster' of attacks in a day then remission for weeks/months

Question 128

HEADACHES | How does a tension headache present?

Answer 128

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

Question 129

HEADACHES | How does a sinusitis headache present?

Answer 129

- 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 130

HEADACHES | How does acute glaucoma present?

Answer 130

- 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 131

HEADACHES How can you diagnose... i) cluster headaches? ii) tension headaches? iii) medication overuse headaches?

Answer 131

i) ≥5 classical headaches ii) Clinical Dx iii) Present >15d/month, regular use for >3m of >1 symptomatic treatment drugs + headache developed or worsened during drug use

Question 132

HEADACHES | What is the acute and prophylactic management of cluster headaches?

Answer 132

- S/c triptans + high flow 100% oxygen via non-rebreathe mask (about 15m) - Verapamil is first line, avoid triggers (alcohol), short course prednisolone may break cycle during clusters

Question 133

HEADACHES | What is the management of tension headaches?

Answer 133

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

Question 134

HEADACHES | What is the management of medication overuse headache?

Answer 134

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

Question 135

HEADACHES | What is the management of sinusitis headache?

Answer 135

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

Question 136

HEADACHES | What is the management of acute glaucoma?

Answer 136

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

Question 137

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

Answer 137

- 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 138

TRIGEMINAL NEURALGIA What are the causes of trigeminal neuralgia? What is the typical patient? What are some triggers?

Answer 138

- Idiopathic or secondary to tumour or MS - 50y/o asian male - Washing affected area, shaving, eating, talking + dental prostheses

Question 139

TRIGEMINAL NEURALGIA | What is the clinical presentation of trigeminal neuralgia?

Answer 139

- Paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution (knife-like shooting pain with no neuro deficit) - Mostly unilateral, face screws up in pain

Question 140

TRIGEMINAL NEURALGIA | How would you diagnose trigeminal neuralgia?

Answer 140

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

Question 141

TRIGEMINAL NEURALGIA | How would you manage trigeminal neuralgia?

Answer 141

- Carbamazepine 1st line | - If fails, microvascular decompression or stereotactic radiotherapy

Question 142

GIANT CELL ARTERITIS | What is giant cell arteritis (GCA)?

Answer 142

- Systemic vasculitis of the medium + large arteries, typically presents with Sx affecting the temporal arteries

Question 143

GIANT CELL ARTERITIS What is the cause of GCA? Who does GCA typically affect?

Answer 143

- Unknown but strong association with polymyalgia rheumatica - Secondary to SLE, rheumatoid arthritis + HIV - >60y/o + incidence increases with age so exclude in all those >60 + headache

Question 144

GIANT CELL ARTERITIS | What is the general clinical presentation of GCA?

Answer 144

- Severe unilateral headache, often temple or forehead - Scalp tenderness, esp on brushing hair - Blurred/double vision, jaw claudication

Question 145

GIANT CELL ARTERITIS What are the systemic symptoms of GCA? What are the signs of GCA?

Answer 145

- Fever, muscle aches, fatigue, loss of appetite or weight loss - PMR = bilateral shoulder + hip pain, morning stiffness - Tender, thickened/firm, prominent, pulseless temporal arteries

Question 146

GIANT CELL ARTERITIS | What investigations would you do in GCA?

Answer 146

- FBC (normocytic anaemia + thrombocytosis) - LFTs (?raised ALP) - ESR/CRP raised (>60y/o, ESR >60mm/h) - Duplex USS of temporal artery (hypoechoic halo sign) - Temporal artery biopsy (multinucleated giant cells although may be skip lesions)

Question 147

GIANT CELL ARTERITIS | What are some complications of GCA?

Answer 147

- Irreversible painless complete sight loss can rapidly occur due to inflammation + occlusion of the ciliary ± central retinal artery (amaurosis fugax) - Stroke - Later there can be relapses + steroid-related SEs + aortitis > aneurysm + dissection

Question 148

GIANT CELL ARTERITIS | What medications would you prescribe in GCA?

Answer 148

- Stat high dose (60mg) prednisolone + continue until Sx resolve then slowly wean (may take 2y) - Aspirin 75mg OD to reduce vision loss + stroke risk - Omeprazole for gastric protection whilst on steroids - Alendronate with calcium + cholecalciferol supplements for osteoporosis prevention due to steroids

Question 149

GIANT CELL ARTERITIS | What referrals should you make for GCA?

Answer 149

- Vascular surgeons > temporal artery biopsy - Rheumatology > specialist diagnosis + management - Ophthalmology > emergency same day appt if visual Sx

Question 150

MIGRAINE | What is the pathophysiology of migraines?

Answer 150

- 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 151

MIGRAINE What is the aetiology of migraines? How long do they last for and who are they more common in?

Answer 151

``` CHOCOLATE – - Chocolate - Hangovers - Orgasms - Cheese/caffeine - Oral contraceptives - Lie-ins - Alcohol - Travel - Exercise 4–72h, F>M ```

Question 152

MIGRAINE | What are the stages of migraine?

Answer 152

- 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 153

MIGRAINE | What are the 4 main types of migraine?

Answer 153

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

Question 154

MIGRAINE | How does a migraine without aura present?

Answer 154

- Unilateral, pulsatile + throbbing, mod–severe pain, physical activity worsens - Photophobia ± phonophobia, N+V

Question 155

MIGRAINE | How does a migraine with aura present?

Answer 155

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 156

MIGRAINE How does a... i) silent migraine ii) hemiplegic migraine present?

Answer 156

i) Migraine with aura but no headache | ii) Can mimic a stroke with typical migraine Sx, sudden/gradual onset, hemiplegia, ataxia + changes in consciousness

Question 157

MIGRAINE | What investigations would you do in migraine?

Answer 157

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

Question 158

MIGRAINE | What is the acute management of migraines?

Answer 158

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

Question 159

MIGRAINE | What is the prophylaxis for migarines?

Answer 159

- 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 160

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

Answer 160

- 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 161

MND | What is the cause of MND?

Answer 161

- 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 162

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

Answer 162

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

Question 163

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

Answer 163

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

Question 164

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

Answer 164

- 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 165

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

Answer 165

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

Question 166

MND | What is the general clinical presentation of MND?

Answer 166

- Insidious + progressive muscle weakness affecting limbs, trunk, face + speech - Often first noticed in upper limbs, may be fatigue when exercising - May have stumbling spastic gait, weak grip + clumsiness - Dysarthria, dysphagia, emotional lability in pseudobulbar palsy - NO SENSORY SYMPTOMS

Question 167

MND What are... i) UMN signs? ii) LMN signs?

Answer 167

i) Hypertonia or spasticity, brisk reflexes + upgoing plantars, muscle wasting ii) Hypotonia + muscle wasting, reduced reflexes, fasciculations (particularly tongue)

Question 168

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

Answer 168

- 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 169

MND | What are some investigations for MND?

Answer 169

- Clinical Dx with El-Escorial diagnostic criteria for ALS (definite = UMN/LMN signs in 3 regions) - Nerve conduction studies (muscle denervation) + electromyography (spontaneous fibrillation potentials) - Increased creatinine kinase (muscle breakdown) - MRI head/spinal cord to exclude structural causes - Lumbar puncture to exclude inflammatory causes

Question 170

MND What are some complications of MND? How rapidly does MND progress?

Answer 170

- UTI, pneumonia + respiratory failure (common cause of death), constipation, pressure sores - Half of patients die <3y from onset, monitor FVC closely for respiratory distress as most die from bulbar palsy respiratory failure

Question 171

MND | What medication may be given in MND?

Answer 171

- Riluzole – Na+ blocker inhibits glutamate release | - Not curative but aims to increase survival by 2–3m + increase their time before needing ventilation

Question 172

MND | What MDT management is given for MND?

Answer 172

- 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 173

MULTIPLE SCLEROSIS | What is the physiology of myelin?

Answer 173

- Myelin covers axons of neurones + helps electrical impulses move faster along the axon - Schwann cells myelinate peripheral nerves, oligodendrocytes myelinate CNS nerves

Question 174

MULTIPLE SCLEROSIS | What is multiple sclerosis (MS)?

Answer 174

- Chronic + progressive autoimmune inflammatory disorder due to T-cell mediated immune response affecting the CNS

Question 175

MULTIPLE SCLEROSIS | What is the pathophysiology of MS?

Answer 175

- 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 176

MULTIPLE SCLEROSIS | What are some classic sites for MS?

Answer 176

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

Question 177

MULTIPLE SCLEROSIS What is the aetiology of MS? What is the epidemiology of MS?

Answer 177

- Unknown as autoimmune but influenced by genes, EBV, lifestyle factors such as low vitamin D, smoking + obesity - Commonly presents in young females living further away from equator

Question 178

MULTIPLE SCLEROSIS | What is a clinically isolated syndrome?

Answer 178

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

Question 179

MULTIPLE SCLEROSIS | What are the 4 types of MS?

Answer 179

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

Question 180

MULTIPLE SCLEROSIS | What is relapsing remitting MS?

Answer 180

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

Question 181

MULTIPLE SCLEROSIS What is... i) secondary progressive MS? ii) primary progressive MS? iii) benign MS?

Answer 181

i) Initially RR but now progressive worsening of Sx + incomplete remissions ii) Gradually worsening of disease from point of diagnosis without any RR iii) Relapses + Remissions but overall progress will never worsen

Question 182

MULTIPLE SCLEROSIS | What is the diagnostic criteria for MS?

Answer 182

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

Question 183

MULTIPLE SCLEROSIS | What are the symptoms of MS?

Answer 183

DEMYELINATION – - Diplopia (CN VI) - Eye movement pain (optic neuritis, v common) - Motor weakness - nYstagmus - Elevated temp worsens - Lhermitte's sign - Intention tremor - Neuropathic pain - Ataxia - Talking slurred (dysarthria) - Impotence - Overactive bladder - Numbness

Question 184

MULTIPLE SCLEROSIS In terms of the symptoms of MS, what is meant by... i) motor weakness? ii) elevated temp worsens? iii) Lhermitte's sign?

Answer 184

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower ii) Uhthoff's phenomenon iii) Neck flexion causes electric shock sensation down spine

Question 185

MULTIPLE SCLEROSIS | What are some signs of MS?

Answer 185

- 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 186

MULTIPLE SCLEROSIS | What is relative afferent pupillary defect?

Answer 186

- 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 187

MULTIPLE SCLEROSIS | What is internuclear ophthalmoplegia?

Answer 187

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

Question 188

MULTIPLE SCLEROSIS | What are the investigations for MS?

Answer 188

- 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 189

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

Answer 189

- IV methylprednisolone | - Shortens acute relapses but no overall effect on prognosis

Question 190

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

Answer 190

- First line = beta-interferons (1b) to decrease # relapses + lesions on MRI but SEs = depression, flu Sx + miscarriage - 2 relapses in past 2y - Second line = monoclonal antibody like natalizumab, dimethyl fumarate

Question 191

MULTIPLE SCLEROSIS | What is the general symptomatic management for MS?

Answer 191

- Spasticity = baclofen or gabapentin - Fatigue = amantadine or CBT + Exercise - Neuropathic pain = gabapentin or amitriptyline - Lifestyle = smoking cessation, avoid stress

Question 192

MENINGITIS What is meningitis? How does it occur? What can cause it?

Answer 192

- Inflammation of the meninges which line the brain + spinal cord - Microorganisms can reach the meninges either by direct extension from ears, nasopharynx or via blood - Infection (bacterial, viral, TB) or aseptic (autoimmune, reactive)

Question 193

MENINGITIS | What are the bacterial causes of meningitis?

Answer 193

- Strep pneumoniae (pneumococcal) most common – gram +ve cocci chain - N. meningitidis (meningococcal) – gram -ve diplococci, more serious - Group B strep in neonates (contracted during birth via vagina) - TB

Question 194

MENINGITIS What are the... i) viral ii) aseptic causes of meningitis?

Answer 194

i) Enteroviruses #1 (Coxsackie virus), HSV + varicella zoster virus ii) MS. HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis

Question 195

MENINGITIS What are the symptoms of meningitis? How does viral + TB present?

Answer 195

- Fever, headache, vomiting, drowsiness. - Meningism = neck stiffness + photophobia - Later = seizures, focal neurology, decreased GCS - Viral = benign + self-limiting, no rash but blurred vision or headache - TB = long Hx + vague Sx with meningism later

Question 196

MENINGITIS | What are the clinical signs of meningitis?

Answer 196

- 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 197

MENINGITIS | What are some differentials of meningitis?

Answer 197

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

Question 198

MENINGITIS | What investigations would you do for meningitis?

Answer 198

- Blood cultures + serology (before LP + Abx unless undesirable delay) - FBC, U+Es, LFTs, CRP, blood glucose - CT head if other signs like papilloedema - Lumbar puncture for MC&S with protein, cell count, glucose + viral PCR

Question 199

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 199

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

Question 200

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 200

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

Question 201

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 201

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

Question 202

MENINGITIS | When is a lumbar puncture contraindicated in meningitis?

Answer 202

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

Question 203

MENINGITIS | What are some complications following meningitis?

Answer 203

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

Question 204

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 204

- IM benzylpenicillin

Question 205

MENINGITIS | What is the management of bacterial meningitis

Answer 205

- 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 206

MENINGITIS | What is the management of viral meningitis?

Answer 206

- Supportive therapy mainly | - IV aciclovir for HSV

Question 207

MENINGITIS | What prevention can be given for meningitis?

Answer 207

- Childhood vaccination schedule | - All close contacts should receive PO ciprofloxacin (or rifampicin) prophylaxis if <7d exposure since onset

Question 208

MENINGITIS | Who must you notify about cases of meningitis?

Answer 208

- Public Health England immediately as notifiable disease

Question 209

ENCEPHALITIS | What is encephalitis?

Answer 209

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

Question 210

ENCEPHALITIS What are the... i) viral ii) non-viral causes of encephalitis?

Answer 210

i) Most commonly – HSV, HIV, CMV/EBV, measles, mumps, rabies, tick-borne encephalitis ii) Any bacterial meningitis, TB, malaria, listeria, lyme disease, legionella

Question 211

ENCEPHALITIS | What is the clinical presentation of encephalitis?

Answer 211

- Headache + altered mental state (confusion, behavioural changes, bizarre) - Reduced GCS compared to meningitis - Focal neurological deficit (hemiparesis, dysphasia) - Preceded by infectious prodrome (fever, rash, meningeal signs) - ?Hx of travel or animal bite

Question 212

ENCEPHALITIS | What are the differentials of encephalitis

Answer 212

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

Question 213

ENCEPHALITIS | What investigations would you do for encephalitis?

Answer 213

- Blood culture + serology for viral PCR - CT head - LP for MC&S with protein, cell count, glucose + viral PCR - EEG may aid Dx

Question 214

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

Answer 214

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

Question 215

ENCEPHALITIS | What is the management of encephalitis?

Answer 215

- Start aciclovir within 30m of pt arriving if suspected - Supportive therapy in HDU/ICU if needed - Symptomatic treatment such as phenytoin for seizures

Question 216

BRAIN ABSCESS What is a brain abscess? What are the most common causative organisms?

Answer 216

- Pus-filled swelling in the brain | - Staph. aureus + strep. pnuemoniae

Question 217

BRAIN ABSCESS | What are the aetiologies of brain abscesses?

Answer 217

- 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 218

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

Answer 218

- Fever, headache (raised ICP Sx) + focal neurology are the classic triad - If in critical area (motor cortex) will present earlier - Often have considerable mass effect in brain + raised ICP common

Question 219

BRAIN ABSCESS | What are the investigations for brain abscess?

Answer 219

- CT head shows ring-enhancing lesion ± surrounding oedema | - LP is contraindicated due to raised ICP

Question 220

BRAIN ABSCESS | What is the management of brain abscess?

Answer 220

- CT guided aspiration via burr hole or craniotomy + abscess cavity debridement - Craniotomy usually if no response to aspiration or if reoccurs - Abx with IV ceftriaxone + metronidazole, ICP Mx with dexamethasone

Question 221

BRAIN DEATH + COMA What is... i) coma? ii) persistent vegetative state? iii) brain death?

Answer 221

i) Unarousable unresponsiveness ii) State of wakefulness with sleep-wake cycles but no detectable awareness iii) Irreversible cessation of all brain function, usually from widespread injury to brain indicated by lack of brainstem signs

Question 222

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

Answer 222

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

Question 223

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

Answer 223

- 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 224

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

Answer 224

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 225

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

Answer 225

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

Question 226

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

Answer 226

- 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 227

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

Answer 227

- 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 228

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

Answer 228

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

Question 229

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

Answer 229

- 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 230

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

Answer 230

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

Question 231

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

Answer 231

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

Question 232

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

Answer 232

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

Question 233

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

Answer 233

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

Question 234

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

Answer 234

- 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 235

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

Answer 235

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

Question 236

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

Answer 236

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

Question 237

MYASTHENIA GRAVIS | What is myasthenia gravis?

Answer 237

- Autoimmune disorder against acetylcholine receptors in the neuromuscular junction

Question 238

MYASTHENIA GRAVIS | What is the pathophysiology of myasthenia gravis?

Answer 238

- 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 239

MYASTHENIA GRAVIS | What is the aetiology of myasthenia gravis?

Answer 239

- Associated with autoimmune disease (RA, SLE) - If <40y: F>M, thymic hyperplasia - If >60y: M>F, thymoma

Question 240

MYASTHENIA GRAVIS What is the main symptom of myasthenia gravis? What is the natural course of myasthenia gravis?

Answer 240

- Fatiguable weakness of muscles which improves with rest - Affects ocular, bulbar + proximal limb muscles - Dysphagia + dysarthria (bulbar) - Eventually leads to atrophy - Fluctuating relapsing + remitting pattern

Question 241

MYASTHENIA GRAVIS | What will patients with myasthenia gravis struggle with?

Answer 241

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

Question 242

MYASTHENIA GRAVIS What are the signs of myasthenia gravis? What can exacerbate myasthenia gravis?

Answer 242

- Ptosis, diplopia (extra-ocular muscle weakness) | - Abx, CCBs, beta-blockers, lithium + statins

Question 243

MYASTHENIA GRAVIS | What are some clinical signs of myasthenia gravis?

Answer 243

- Repeated blinking = ptosis | - Repeated abduction of one arm 20x + compare to other side

Question 244

MYASTHENIA GRAVIS | What antibodies are implicated in myasthenia gravis?

Answer 244

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

Question 245

MYASTHENIA GRAVIS | What other investigations would you do for myasthenia gravis?

Answer 245

- Tensilon/edrophonium test = cholinesterase enzymes > increased ACh in NMJ so briefly relieves weakness - Electromyogram shows decremental muscle response to repeated nerve stimulation - CT/MRI chest for thymoma

Question 246

MYASTHENIA GRAVIS What is the main complication of myasthenia gravis? What happens? What may occur?

Answer 246

- Myasthenic crisis - Acute exacerbation of Sx with severe muscle weakness incl. resp muscles leading to difficult breathing, speaking, intercostal recessions, tiredness + trouble swallowing - Resp failure or death

Question 247

MYASTHENIA GRAVIS | What are the causes of myasthenic crisis?

Answer 247

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

Question 248

MYASTHENIA GRAVIS | What is the management of myasthenic crisis?

Answer 248

- Urgent review by neurologists + anaesthetists - Monitor breathing with serial FVC measurements - NIV, BiPAP or intubation + ventilation - Immunomodulatory therapies (IVIg or plasmapheresis)

Question 249

MYASTHENIA GRAVIS | What is the management of myasthenia gravis?

Answer 249

- Acetylcholinesterase inhibitors like pyridostigmine or rivastigmine - Immunosuppression with prednisolone (acute) or azathioprine to suppress antibody production - Thymectomy if thymoma or anti-AChR +ve disease - Plasmapheresis for severe relapsing cases

Question 250

LAMBERT-EATON | What is Lambert-Eaton myasthenic syndrome?

Answer 250

- Progressive muscle weakness with increased use as a result of damage to the neuromuscular junction. - Very similar to myasthenia gravis

Question 251

LAMBERT-EATON | What is the pathophysiology of Lambert-Eaton myasthenic syndrome?

Answer 251

- Typically seen in those with small cell lung cancer - Antibodies produced by immune system against voltage gated Ca2+ channels in SCLC cells also target + damage those at the pre-synaptic terminals of the NMJ responsible for releasing ACh - Channels destroyed = less ACh bind to receptors so less muscle contraction

Question 252

LAMBERT-EATON | What is the clinical presentation of Lambert-Eaton myasthenic syndrome?

Answer 252

- Main difference is repeated use of muscle IMPROVES fatigue - Proximal muscles affected causing proximal muscle weakness (hairs, stairs, chairs) - Limb girdle weakness so lower limbs affected first - Autonomic involvement (dry mouth, constipation, impotence) - Hyporeflexia - Diplopia + resp muscle involvement is rare (gait before eye signs)

Question 253

LAMBERT-EATON | What are the investigations for Lambert-Eaton myasthenic syndrome?

Answer 253

- Autoantibodies against voltage gated Ca2+ channels - Tensilon test response is not as noticeable - EMG shows incremental muscle response to repeated nerve stimulation - CT chest for SCLC

Question 254

LAMBERT-EATON | What is the management of Lambert-Eaton myasthenic syndrome?

Answer 254

- 3,4-diaminopyridine like amifampridine which allows more ACh release at NMJ - Immunosuppression with prednisolone, azathioprine - IVIg (Screen for IgA deficiency to avoid anaphylaxis) or plasmapheresis may be useful too

Question 255

LAMBERT-EATON | What is the mechanism of action of amifampridine?

Answer 255

- Blocks voltage gated K+ channels in presynaptic cells which prolongs depolarisation of cell membrane + assists Ca2+ channels

Question 256

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

Answer 256

- Acute inflammatory demyelinating polyneuropathy which targets Schwann cells

Question 257

GUILLAIN-BARRE | What is the pathophysiology of GBS?

Answer 257

- 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 258

GUILLAIN-BARRE | What is Miller-Fisher syndrome?

Answer 258

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

Question 259

GUILLAIN-BARRE | What is the aetiology of GBS?

Answer 259

- Often triggered by preceding illness 4w before symptoms | - Campylobacter jejuni (v common), CMV, EBV

Question 260

GUILLAIN-BARRE | What is the clinical presentation of GBS?

Answer 260

- Acute symmetrical, progressive, ascending muscle weakness. - Peripheral neuropathy or neuropathic pain - Absent tendon reflexes early in disease - Back or leg pain is very common in initial stages - Proximal muscles (trunk, resp) more affected + cranial nerves (esp. VII) - Autonomic – urinary retention, diarrhoea, sweating, BP changes

Question 261

GUILLAIN-BARRE | What are some differentials for GBS?

Answer 261

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

Question 262

GUILLAIN-BARRE | What are the investigations for GBS?

Answer 262

- Clinical usually - Nerve conduction studies = slowing of motor conduction velocity (demyelination) - LP CSF shows raised protein with normal WCC + glucose - Monitor FVC 4h for ?resp involvement

Question 263

GUILLAIN-BARRE | What is the prognosis of GBS?

Answer 263

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

Question 264

GUILLAIN-BARRE | What is the main treatment for GBS?

Answer 264

- IVIg reduces duration + severity of paralysis but C/I if IgA deficiency as would cause anaphylaxis - Plasma exchange - Intubation, ventilation + ICU admission in severe cases in resp failure

Question 265

GUILLAIN-BARRE | What is the supportive therapy for GBS?

Answer 265

- VTE prophylaxis with heparin - Physio to prevent contractures - NG or PEG feeding if swallowing issues

Question 266

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

Answer 266

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

Question 267

BRAIN TUMOURS | Give 4 examples of different brain tumours

Answer 267

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

Question 268

BRAIN TUMOURS What are gliomas? Give some examples

Answer 268

- 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 269

BRAIN TUMOURS | What are meningiomas?

Answer 269

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

Question 270

BRAIN TUMOURS | What are pituitary tumours?

Answer 270

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

Question 271

BRAIN TUMOURS What are acoustic neuromas? What are they associated with? How do they present?

Answer 271

- Tumours of Schwann cells that occur around cerebellopontine angle surrounding the auditory nerve that innervates inner ear - Slow growing but eventually grow large enough to produce Sx - Usually unilateral, bilateral associated with neurofibromatosis type 2 - Classic Sx = hearing loss, tinnitus, balance issues, decreased facial sensation

Question 272

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

Answer 272

- 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 273

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

Answer 273

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

Question 274

BRAIN TUMOURS What focal signs would you get if the tumour was located in... i) frontal lobe? ii) temporal lobe? iii) parietal lobe? iv) occipital lobe? v) cerebellum?

Answer 274

i) Personality + intellect change, hemiparesis, expressive dysphasia ii) Receptive dysphasia, amnesia iii) Hemisensory loss, dysphasia iv) Contralateral visual defects v) Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia (DANISH)

Question 275

BRAIN TUMOURS | What are some symptoms of raised ICP?

Answer 275

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

Question 276

BRAIN TUMOURS | What investigations would you perform for brain tumours?

Answer 276

- 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 277

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

Answer 277

- 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 278

BRAIN TUMOURS | What other management is there for brain tumours?

Answer 278

- 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 279

NEUROPATHY | What is a neuropathy?

Answer 279

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

Question 280

NEUROPATHY | What are the peripheral nerve causes of muscle weakness?

Answer 280

- 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 281

NEUROPATHY What is the pathophysiology of mononeuritis multiplex? What can cause mononeuritis multiplex?

Answer 281

- Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit - Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis

Question 282

NEUROPATHY | What are the causes of peripheral neuropathy?

Answer 282

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

Question 283

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

Answer 283

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

Question 284

NEUROPATHY | What is Charcot-Marie-Tooth disease?

Answer 284

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

Question 285

NEUROPATHY What is the generic clinical presentation of... i) mononeuropathy? ii) mononeuritis multiplex?

Answer 285

i) Individual nerve deficits in isolation, mostly upper limb nerves affected at compression points ii) Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy

Question 286

NEUROPATHY | What is the generic clinical presentation of peripheral neuropathy?

Answer 286

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

Question 287

NEUROPATHY What is the most common mononeuropathy? What is the pathophysiology? What is the aetiology?

Answer 287

- Carpal tunnel syndrome - Inflammation of carpal tunnel leads to entrapment of the median nerve - Idiopathic but associated with local tumours, DM + RA

Question 288

NEUROPATHY | What muscles does the median nerve innervate?

Answer 288

LLOAF – - Lateral lumbricals x2 - Opponens pollicis - Abductor pollicis brevis - Flexor pollicis brevis

Question 289

NEUROPATHY | What is the clinical presentation of carpal tunnel syndrome?

Answer 289

- Aching pain in hand + arm (especially at night) - Paraesthesia in radial 3.5 digits relieved by dangling hand over edge of bed + shaking (wake + shake) - Difficulty with precision grip - Sensory loss (radial 3.5 digits palmar + fingertips dorsally) - Wasting of thenar eminence (APB, FPB + OP)

Question 290

NEUROPATHY | What investigations can you do for carpal tunnel syndrome?

Answer 290

- Phalen's test = inverse prayer sign, can only maximally flex wrist for 1m - Tinel's test = tapping on nerve at wrist induces tingling - Nerve conduction studies

Question 291

NEUROPATHY | What is the management of carpal tunnel syndrome?

Answer 291

- Splinting - Analgesia - Local steroid injection ± decompression surgery

Question 292

NEUROPATHY Roots of the ulnar nerve? What causes ulnar neuropathy?

Answer 292

- C7–T1 | - Elbow trauma or fracture, elbow arthritis

Question 293

NEUROPATHY | What are the motor signs of ulnar neuropathy?

Answer 293

Weakness/wasting of – - Interossei (can't do good luck sign) - Medial lumbricals (claw hand) - Hypothenar eminence - +ve Froment's sign when grip paper between thumb + index finger

Question 294

NEUROPATHY | What is Froment's sign?

Answer 294

- Weak adductor pollicis (usually keeps IPJ straight) means flexor pollicis longus compensates, manifesting as thumb hyperflexion (pinching paper)

Question 295

NEUROPATHY | What are the sensory signs of ulnar neuropathy?

Answer 295

- Sensory loss 1.5 fingers ulnar side on dorsal + palmar aspects

Question 296

NEUROPATHY Roots of the radial nerve? What causes radial neuropathy?

Answer 296

- C5-T1 | - Compression against humerus

Question 297

NEUROPATHY What are the motor signs of radial neuropathy? What are the sensory signs?

Answer 297

- Wrist + finger drop (weak extension), can't open first | - Below fingertips on radial 3.5 fingers dorsally, part of thenar eminence

Question 298

NEUROPATHY What causes brachial plexus neuropathy? Presentation?

Answer 298

- Trauma, radiotherapy or heavy rucksack | - Pain, paraesthesia + weakness in affected arm in variable distribution

Question 299

NEUROPATHY Roots of phrenic nerve? Causes of neuropathy? Presentation?

Answer 299

- C3–5 - Lung cancer, myeloma, thymoma - Orthopnoea with raised hemidiaphragm on CXR

Question 300

NEUROPATHY Roots of lateral cutaneous nerve of the thigh? Causes of neuropathy? Presentation?

Answer 300

- L2–L3 - Entrapment under inguinal ligament - Meralgia paraesthetica = antero-lateral burning thigh pain

Question 301

NEUROPATHY Roots of sciatic nerve? Causes of neuropathy? Presentation?

Answer 301

- L4–S3 - Pelvic tumours or pelvic/femoral # - M = foot drop, S = loss below the knee laterally

Question 302

NEUROPATHY Roots of common peroneal nerve? Causes of neuropathy? Presentation?

Answer 302

- L4–S1 - Damaged as winds round fibular head by trauma or sitting cross-legged (classic after night out) - M = foot drop, weak ankle dorsiflexion + eversion with high steppage gait, S = loss over dorsal foot

Question 303

NEUROPATHY Roots of the tibial nerve? Presentation of neuropathy?

Answer 303

- L4–S3 | - M = weak ankle plantar flexion, inversion + toe flexion, S = loss over sole of foot

Question 304

NEUROPATHY | What does a CN1 lesion cause?

Answer 304

- Anosmia

Question 305

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 305

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 306

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

Answer 306

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

Question 307

NEUROPATHY | What does a CN3 lesion cause?

Answer 307

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

Question 308

NEUROPATHY | What does a CN4 lesion cause?

Answer 308

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

Question 309

NEUROPATHY | What does a CN5 lesion cause?

Answer 309

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

Question 310

NEUROPATHY | What does a CN6 lesion cause?

Answer 310

- Issues abducting eye beyond midline as innervates lateral rectus

Question 311

NEUROPATHY | What does a CN7 lesion cause?

Answer 311

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

Question 312

NEUROPATHY | What is Bell's palsy?

Answer 312

- 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 313

NEUROPATHY | What does a CN8 lesion cause?

Answer 313

- Sensorineural deafness | - Tinnitus, vertigo, nystagmus

Question 314

NEUROPATHY | What does a CN9/10 lesion cause?

Answer 314

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

Question 315

NEUROPATHY | What does a CN11 lesion cause?

Answer 315

- Weakness turning head to contralateral side

Question 316

NEUROPATHY | What does a CN12 lesion cause?

Answer 316

- Tongue deviation towards side of lesion

Question 317

NEUROPATHY | What are the investigations used in neuropathy?

Answer 317

- 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 318

NEUROPATHY | What is the management of neuropathy?

Answer 318

- 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 319

CORD COMPRESSION What is... i) myelopathy? ii) radiculopathy?

Answer 319

i) Injury to the spinal cord due to severe compression resulting in UMN signs + specific symptoms based on compression ii) Sx caused by pinching of a nerve root as they exit the spinal cord

Question 320

CORD COMPRESSION How does radiculopathy present? What is the most common radiculopathy?

Answer 320

- Sharp, shooting pain within distribution of nerve, weakness + loss of sensation - Sciatica (L5) = lower back pain that travels to buttocks + down back of thigh to calf

Question 321

CORD COMPRESSION | What are the aetiologies of spinal cord compression?

Answer 321

- 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 322

CORD COMPRESSION | What are the symptoms of spinal cord compression?

Answer 322

- Weakness of legs with UMN signs (contralateral spasticity + hyperreflexia) - Sudden/progressive onset weakness = emergency - Sensory loss below certain level - Numbness/tingling may have stabbing pain - Bladder + anal sphincter involvement is a later manifestation (hesitancy, frequency, painless retention)

Question 323

CORD COMPRESSION | What are the signs of spinal cord compression?

Answer 323

- 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 324

CORD COMPRESSION | How does degenerative cervical myelopathy present?

Answer 324

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

Question 325

CORD COMPRESSION | What are the differentials for spinal cord compression?

Answer 325

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

Question 326

CORD COMPRESSION | What are the investigations of spinal cord compression?

Answer 326

- 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 327

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

Answer 327

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

Question 328

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

Answer 328

- 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 329

CORD COMPRESSION What is spinal stenosis? How does it present? How is it managed?

Answer 329

- Narrowing of lower spinal canal - Spinal claudication > pain in buttocks/legs when walking, pain eased by bending forward as canal opens, negative straight leg raise - MRI + canal decompression surgery

Question 330

CORD COMPRESSION | What is the management of spinal cord compression?

Answer 330

- 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 331

SPINAL CORD INJURY | What is Brown-Sequard syndrome?

Answer 331

- 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 332

SPINAL CORD INJURY | What is anterior cord syndrome?

Answer 332

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

Question 333

SPINAL CORD INJURY | What is posterior cord syndrome?

Answer 333

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

Question 334

SPINAL CORD INJURY | What is central cord syndrome?

Answer 334

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

Question 335

MYOPATHY What are myopathies? What are dystrophies? How do they compare to neuropathies?

Answer 335

- Neuromuscular disorders where the primary Sx is muscle weakness due to dysfunction of muscle fibres - If they're inherited = dystrophies - Weakness is proximal in muscle disease (nerves = distal)

Question 336

MYOPATHY | What are the aetiologies of myopathies?

Answer 336

- Inflammatory = polymyositis, dermatomyositis (associated with interstitial lung disease) - Inherited = Duchenne, Becker's muscular dystrophy, myotonic dystrophy or rare = fascioscapulohumeral muscular dystrophy (FSHD), mitochondrial - Endo = Cushing's, thyrotoxicosis - Drugs = alcohol, statins

Question 337

MYOPATHY | How do myopathies present?

Answer 337

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

Question 338

MYOPATHY | How does myotonic dystrophy present?

Answer 338

- DM1 = (DMPK gene on C19) = distal weakness more prominent - DM2 = (ZNF9 gene on C3) = proximal weakness more prominent. - May have cataracts, testicular atrophy, cardiac lesions (heart block, cardiomyopathy), DM

Question 339

MYOPATHY How does... i) polymyositis ii) dermatomyositis iii) FSHD iv) mitochondrial issues present?

Answer 339

i) Proximal muscle weakness ± pain, Raynaud's, dysphagia, dysphonia ii) Photosensitive, macular rash over back + shoulder iii) Facial weakness iv) Eye movement disorders

Question 340

MYOPATHY | What are the investigations for myopathies?

Answer 340

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

Question 341

MYOPATHY | What is the management of myopathies?

Answer 341

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

Question 342

MYOPATHY | What is the general supportive management of myopathies?

Answer 342

- 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 343

HYDROCEPHALUS | What is hydrocephalus?

Answer 343

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

Question 344

HYDROCEPHALUS | What is the purpose of CSF?

Answer 344

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

Question 345

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

Answer 345

- 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 346

HYDROCEPHALUS | What are the 3 types of hydrocephalus?

Answer 346

- 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 347

HYDROCEPHALUS What are some causes of... i) obstructive ii) non-obstructive hydrocephalus?

Answer 347

i) Tumour, acute haemorrhages, developmental abnormalities (aqueduct stenosis) ii) Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage) or increased CSF production (choroid plexus tumour) but very rare

Question 348

HYDROCEPHALUS | How does hydrocephalus present?

Answer 348

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

Question 349

HYDROCEPHALUS | How does normal pressure hydrocephalus present?

Answer 349

'Wet, wacky, wobbly' – - Urinary incontinence, dementia + abnormal gait (apraxia) - Sx come on gradually + similar to Alzheimer's so difficult to diagnose

Question 350

HYDROCEPHALUS | What are the investigations for hydrocephalus?

Answer 350

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

Question 351

HYDROCEPHALUS | What is the management of hydrocephalus?

Answer 351

- Ventriculoperitoneal shunt = surgically implanted into brain to drain excess fluid (may become blocked or infected) - Endoscopic third ventriculostomy = hole made in floor of 3rd ventricle to allow trapped CSF to escape to be reabsorbed

Question 352

IIH | What is idiopathic intracranial hypertension (IIH)?

Answer 352

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

Question 353

IIH | What are the causes of IIH?

Answer 353

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

Question 354

IIH | What is the clinical presentation of IIH?

Answer 354

- Presents as if mass but none found - Signs of raised ICP (headache, papilloedema + enlarged blind spot) - Blurred vision, narrowed visual fields ± diplopia - Consciousness + cognition preserved

Question 355

IIH | What are the investigations for IIH?

Answer 355

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

Question 356

IIH | What is the management of IIH?

Answer 356

- #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 357

DVS THROMBOSIS What is dural venous sinus thrombosis (DVS thrombosis)? What can it lead to? What causes it?

Answer 357

- Blood clot in the dural venous sinuses which drain blood from the brain. - Cerebral infarction (stroke) but less commonly than arterial - Thrombophilias, pregnancy, polycythaemia, sickle cell

Question 358

DVS THROMBOSIS | What is the clinical presentation of DVS thrombosis?

Answer 358

- Headaches (sudden onset), N+V, abnormal vision - Sagittal sinus thrombosis (mostly) = seizures + hemiplegia - Lateral sinus thrombosis = CN6+7 palsies - Cavernous sinus thrombosis = periorbital oedema, ophthalmoplegia (CN 6 usually before 3 + 4), hyperaesthesia to upper face + eye pain (CN 5)

Question 359

DVS THROMBOSIS | What structures run through the cavernous sinus?

Answer 359

- CN3, 4, CN 5 (V1+V2) + ICA

Question 360

DVS THROMBOSIS What are the investigations for DVS thrombosis? What is the management?

Answer 360

- CT head of superior sagittal sinus thrombosis can show classic empty delta sign - CT/MRI venogram may visualise clot - Anticoagulation with LMWH

Question 361

ABNORMAL GAIT What is an ataxic gait? What causes it? What side is deficit?

Answer 361

- Wide based, falls, cannot walk heel-to-toe, worse in dark or eyes closed - Cerebellar issues (MS, posterior fossa tumour, alcohol, POCS) - Ipsilateral as cerebellar fibres decussate twice

Question 362

ABNORMAL GAIT What is an important differential of ataxic gait? How can they be differentiated?

Answer 362

- Proprioception issues (sensory neuropathies, inner ear problem affecting vestibular system - Normal walking when eyes open but issues when eyes closed = proprioceptive, constant issues = cerebellar

Question 363

ABNORMAL GAIT What is a circumduction or spastic or hemiplegic gait? When is it seen?

Answer 363

- Stiff gait, circumduction of legs ± scuffing of toe of shoes, asymmetrical with affected side flexion in upper limb, extension in lower - Stroke, haemorrhage, UMN lesion

Question 364

ABNORMAL GAIT What is an apraxic gait? What causes it?

Answer 364

- Pathognomonic "gluing to floor" on attempting to walk, short + shuffling steps, freezing, wide based unsteady gait + falls - Normal pressure hydrocephalus, multi-infarct states, Alzheimer's

Question 365

ABNORMAL GAIT What is a waddling gait? What causes it?

Answer 365

- Body/hip swings or drips side-side as hard to balance when walking - Proximal muscle weakness in pelvic girdle (myopathies, DDH)

Question 366

SPEECH ISSUES What is dysphasia? What is it seen in?

Answer 366

- Impairment of language caused by brain damage (area affected dictates type) - Stroke

Question 367

SPEECH ISSUES What are the features of Broca's dysphasia? What area is affected?

Answer 367

- Expressive dysphasia so reading + writing impaired, malformed words + non-fluent speech BUT comprehension intact (can follow commands) - Frontal lobe of dominant hemisphere (often left)

Question 368

SPEECH ISSUES What are the features of Wernicke's dysphasia? What area is affected?

Answer 368

- Receptive dysphasia so cannot respond to requests (comprehension issues) BUT fluent speech production (albeit replies inappropriate) - Temporal lobe dominant hemisphere

Question 369

SPEECH ISSUES What is dysarthria? What is it seen in?

Answer 369

- Difficulty in speech articulation due to weakness of speech-related musculature so slurred - Cerebellar disease, stroke, pseudobulbar palsy (MND), bulbar palsy (GBS, MND)

Question 370

``` SPEECH ISSUES What is pseudo? What is bulbar? What is pseudobulbar dysarthria? What is bulbar dysarthria? ```

Answer 370

- Affects UMN - Affects LMN of CN9–12 - Slow, nasal, effortful 'hot potato' voice - Nasal speech due to paralysis of palate

Question 371

SPEECH ISSUES What is dysphonia? What is it seen in?

Answer 371

- Difficulty in speech volume due to weakness of resp muscles or vocal cords - MG, GBS, Parkinson's (mixed dysphonia + dysarthria)

Question 372

UNILATERAL VISION LOSS | What are vascular causes of unilateral vision loss?

Answer 372

- Amaurosis fugax/central retinal artery occlusion - Central retinal vein occlusion - Anterior ischaemic optic neuropathy - Vitreous haemorrhage - GCA - Occipital lobe stroke

Question 373

UNILATERAL VISION LOSS Explain the process of... i) central retinal artery occlusion. ii) central retinal vein occlusion. iii) anterior ischaemic optic neuropathy. iv) vitreous haemorrhage.

Answer 373

i) Branch of ophthalmic artery which supplies whole retina blocked ii) Dilatation of branch veins (backflow) as central vein occluded iii) Ischaemia of posterior choroidal artery that supplies head of optic nerve, can be arteritic (think GCA) iv) Blood leaks into vitreous humour between lens + retina preventing light travelling lens>retina (assoc. with diabetic retinopathy, CRVO, macular degeneration)

Question 374

UNILATERAL VISION LOSS | What are some non-vascular causes of unilateral vision loss

Answer 374

- Optic neuritis - Retinal detachment - Acute angle closure glaucoma

Question 375

UNILATERAL VISION LOSS Explain the process of... i) optic neuritis. ii) retinal detachment. iii) acute angle closure glaucoma.

Answer 375

i) Inflammation of optic nerve caused by MS, infection (lyme, syphilis, HIV), B12 deficiency or arteritis ii) Retina pulled away from underlying surface (flashers/floaters with decrease in vision) iii) Drainage of aqueous humour suddenly occluded leading to rise in intraocular pressure

Question 376

UNILATERAL VISION LOSS What causes... i) painless ii) painful iii) generic unilateral vision loss?

Answer 376

i) Central retinal artery occlusion + central retinal vein occlusion ii) Optic neuritis, acute angle closure glaucoma iii) Retinal detachment + vitreous haemorrhage

Question 377

UNILATERAL VISION LOSS How does... i) CRAO ii) optic neuritis iii) acute angle closure glaucoma iv) retinal detachment v) vitreous haemorrhage present?

Answer 377

i) Amaurosis fugax (like pulling curtain over eyes) ii) Reduced visual acuity over few days (cloudy vision), painful eye movements, heat exacerbation, RAPD + dyschromatopsia iii) Painful red eye, N+V iv) Flashes/floaters, decrease in vision, 'curtain' over part of vision v) Flashes/floaters, decrease in vision, red 'tinge'

Question 378

UNILATERAL VISION LOSS What are the findings on fundoscopy for... i) CRAO? ii) CRVO? iii) optic neuritis?

Answer 378

i) Cherry red spot in macula (different blood supply), pale optic disc ii) Cotton wool spots, multiple retinal haemorrhages iii) Pale optic disc

Question 379

UNILATERAL VISION LOSS | What other investigations would you do in unilateral vision loss and what for?

Answer 379

- ESR/CRP (GCA) - Fluorescein angiography (CRVO) - Tonometry (measure intraocular pressure for glaucoma) - Ocular USS (vitreous haemorrhage/retinal detachment)

Question 380

UNILATERAL VISION LOSS | What is the management of acute angle closure glaucoma?

Answer 380

- Bright room - Pilocarpine (constricts pupil) - Timolol drops with laser or surgical intervention

Question 381

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

Answer 381

- 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 382

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

Answer 382

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 383

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

Answer 383

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

Question 384

NEURO PHARMACOLOGY | What is the mechanism of action of Levodopa?

Answer 384

- 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 385

NEURO PHARMACOLOGY | What are the side effects of Levodopa?

Answer 385

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

Question 386

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

Answer 386

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

Question 387

``` 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 387

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

Question 388

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

Answer 388

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

Question 389

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

Answer 389

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

Question 390

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

Answer 390

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

Question 391

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

Answer 391

- 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 392

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

Answer 392

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

Question 393

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

Answer 393

- 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 394

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

Answer 394

- 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 395

DIZZINESS/VERTIGO What is acute labyrinthitis? How does it present? What are the causes?

Answer 395

- Inflammation of labyrinth + damage to vestibular + auditory end organs - Abrupt onset severe vertigo, N+V, may have hearing loss or tinnitus + nystagmus towards side opposite to lesion - Severe vertigo subsides in days, full recovery 3-4w - Usually viral, ?vascular lesion

Question 396

``` DIZZINESS/VERTIGO What is Ménières disease? How does it present? What causes it? How is it managed? ```

Answer 396

- Increased pressure in endolymphatic system due to increased volume of inner ear. - Recurrent attacks in clusters of vertigo lasting >20m, fluctuating/perm sensorineural hearing loss (uni/bilateral), tinnitus + sense of fullness or pressure in one or both ears - Idiopathic, trauma, endo - Bed rest, reassurance

Question 397

DIZZINESS/VERTIGO | How does traumatic damage present?

Answer 397

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

Question 398

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

Answer 398

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

Question 399

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

Answer 399

- 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 400

MOVEMENT ISSUES What is ballismus? What is it caused by?

Answer 400

- Severe movement disorder with spontaneous involuntary movements, muscular weakness + incoordination of movements or proximal extremities (aka chorea but worse, can be hemi). - Vascular issue with subthalamic nucleus like thalamic stroke