NEURO

Question 1

STROKE
What is a stroke?

Answer 1

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

poor blood flow to the brain causes cell death

Question 2

STROKE
What are the two main classifications of stroke?

Answer 2

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

Question 3

STROKE
What are the causes of ischaemic strokes?

Answer 3

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

Question 4

STROKE
What are the causes of haemorrhagic stroke?

Answer 4

Bleeding from the brain vasculature

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

Question 5

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

Answer 5

• Charcot-Bouchard aneurysms most often in the basal ganglia

Question 6

STROKE
What are the risk factors for ischaemic strokes?

Answer 6

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

Question 7

STROKE
What are some important differentials of stroke?

Answer 7

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

Question 8

STROKE
What classification system can be used for strokes?

Answer 8

• Oxford stroke (Bamford) classification

Question 9

STROKE
What are the various classifications of strokes?

Answer 9

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

Question 10

STROKE
How would an ACA stroke present?

Answer 10

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

Question 11

STROKE
How would a MCA stroke present?

Answer 11

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

Question 12

STROKE
How would a PCA stroke present?

Answer 12

visual issues

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

Question 13

STROKE
How would a brainstem/basilar artery infarct present?

Answer 13

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

Question 14

STROKE
What tools can be used to identify stroke?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

STROKE
How would an ischaemic stroke appear on CT head?

Answer 16

• 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 17

STROKE
How would a haemorrhagic stroke appear on CT head?

Answer 17

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

Question 18

STROKE
What are the pros of CT head imaging?

Answer 18

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

Question 19

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

Answer 19

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

Question 20

STROKE
What bloods may be taken in suspected stroke?

Answer 20

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

Question 21

STROKE
What other investigations may you do in stroke?

Answer 21

• 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 22

STROKE
What are some potential complications following a stroke?

Answer 22

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

Question 23

STROKE
What is the treatment for an ischaemic stroke?

Answer 23

Immediate management:

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

Antiplatelet therapy

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

Anticoagulation (e.g. warfarin) for AF

thrombolysis

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

mechanical thromboectomy
- endovascular removal of thrombus

Question 24

STROKE
What is the timeframe for thrombolysis for ischaemic strokes?

Answer 24

• Within 4.5 hours of the onset of symptoms

Question 25

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

Answer 25

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

Question 26

STROKE What must be done after alteplase treatment?

Answer 26

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

Question 27

STROKE What are the benefits of alteplase?

Answer 27

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

Question 28

STROKE What are the risks of alteplase?

Answer 28

- Haemorrhage (1 in 20), reaction to tPA

Question 29

STROKE What are some contraindications to treatment with alteplase?

Answer 29

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

Question 30

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

Answer 30

- 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 31

STROKE What other management is given for ischaemic strokes?

Answer 31

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

Question 32

STROKE What is the management of a haemorrhagic stroke?

Answer 32

- 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 33

STROKE What lifestyle advice should be given post-stroke?

Answer 33

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

Question 34

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

Answer 34

- 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 35

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

Answer 35

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

Question 36

STROKE What is the CHA2DS2-VaSc score

Answer 36

- 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 37

STROKE What is the HAS-BLED score?

Answer 37

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

Question 38

STROKE what is the primary prevention of strokes?

Answer 38

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

Question 39

STROKE what is the secondary prevention of strokes?

Answer 39

2 weeks of aspirin --> long term clopidogrel

Question 40

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

Answer 40

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

Question 41

TIA What is a transient ischaemia attack (TIA)?

Answer 41

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

Question 42

TIA what are the signs of a carotid TIA?

Answer 42

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

Question 43

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

Answer 43

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

Question 44

TIA what is the pathophysiology of TIA?

Answer 44

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

Question 45

TIA What is a crescendo TIA?

Answer 45

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

Question 46

TIA what are the signs of a vertebrobasilar TIA?

Answer 46

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

Question 47

TIA what are the differential diagnosis’s for a TIA

Answer 47

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

Question 48

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

Answer 48

first line = diffusion weighted MRI or CT second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found) Bloods FBC - look for polycythaemia ESR - raised in vasculitis U&Es, glucose ECG echocardiogram

Question 49

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

Answer 49

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

Question 50

TIA what is the ABCD2 score?

Answer 50

Assesses risk of stoke in the next 7 days for those who have had a TIA age BP clinical features - unilateral weakness, speech disturbance duration of TIA presence of diabetes mellitus

Question 51

TIA What do the scores from ABCD2 mean?

Answer 51

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

Question 52

TIA What is the treatment for a TIA?

Answer 52

immediate treatment = aspirin 300mg and refer to specialist within 24hrs control CV risk factors BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN) smoking cessation statin - SIMVASTATIN no driving for 1 month antiplatelet therapy - ASPIRIN 75mg daily (With Dipyridamole) or - CLOPIDOGREL daily anticoagulation (e.g. WARFARIN) for patients with AF carotid endarterectomy if >70% carotid stenosis reduces stroke/TIA risk by 75%

Question 53

TIA What treatment may be considered after a TIA?

Answer 53

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

Question 54

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

Answer 54

- Carotid doppler USS

Question 55

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

Answer 55

1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death 2. raised ICP - fast flowing arterial blood is pumped into the cranial space 3. space occupying lesion - puts pressure on the brain 4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus 5. vasospasm - bleeding irritates other vessels -> ischaemic injury

Question 56

SAH What are the causes of SAH?

Answer 56

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

Question 57

SAH What conditions are linked to SAH?

Answer 57

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

Question 58

SAH What are some risk factors for SAH?

Answer 58

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

Question 59

SAH What are some symptoms of SAH?

Answer 59

- sudden onset excruciating headache - thunderclap, worst headache, typically occipital - sentinel headache - before main rupture, sign of warning leak - nausea - vomiting - collapse - loss of/depressed consciousness - seizures - vision changes - coma - can last for days

Question 60

SAH What are some signs of SAH?

Answer 60

- signs of meningeal irritation 1. Kernig’s sign (can’t straighten leg past 135 degrees) 2. neck stiffness 3. Brudzinski’s sign (Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed) - retinal, subhyaloid and vitreous bleeds - worse prognosis - with/without papilloedema - neurological signs - e.g. 3rd nerve palsy - increased BP

Question 61

SAH What are some complications of SAH?

Answer 61

- 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 62

SAH What is often associated with better outcomes in SAH?

Answer 62

- GCS >12 on arrival

Question 63

SAH What are the investigations for SAH?

Answer 63

1. urgent Head CT = star pattern (diagnostic) 2. Lumbar Puncture = xanthochromia -> RBC breakdown (only if normal ICP and after 12 hrs) 3. MR/CT angiography - to establish source of bleeding

Question 64

SAH what is the appearance of SAH on CT head?

Answer 64

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

Question 65

SAH What is the management of SAH?

Answer 65

- NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia - surgery = endovascular coiling - IV fluids - maintain cerebral perfusion - ventricular drainage for hydrocephalus

Question 66

SAH give 3 possible complications of a subarachnoid haemorrhage

Answer 66

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

Question 67

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

Answer 67

- Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater over minutes to hours After a lucid interval there is: - rapid rise in ICP pressure on the brain - midline shift - tentorial herniation - coning

Question 68

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

Answer 68

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

Question 69

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

Answer 69

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

Question 70

EDH What causes an EDH?

Answer 70

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

Question 71

EDH What is the clinical presentation of EDH?

Answer 71

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

Question 72

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

Answer 72

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

Question 73

EDH what is Cushing's reflex?

Answer 73

Bradycardia and increased BP

Question 74

EDH What are some differentials for EDH?

Answer 74

- Epilepsy, - CO poisoning, - carotid dissection

Question 75

EDH What are some complications of EDH?

Answer 75

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

Question 76

EDH What are the investigations for EDH?

Answer 76

Non-contrast CT head Skull x-ray - may show fracture lines LP is contraindicated

Question 77

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

Answer 77

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

Question 78

EDH What investigation is contraindicated in EDH and why?

Answer 78

- 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 79

EDH What is the management for EDH?

Answer 79

STABILISE PATIENT URGENT SURGERY clot evacuation ligation of bleeding vessel IV MANNITOL - to reduce ICP airway care - intubation and ventilation

Question 80

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

Answer 80

- 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 81

SDH What is the pathophysiology of a SDH?

Answer 81

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

Question 82

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

Answer 82

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

Question 83

SDH what are the risk factors of SDH?

Answer 83

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

Question 84

SDH What are the symptoms of SDH?

Answer 84

- Fluctuating GCS - Headache - Confusion - may fluctuate - Drowsiness - physical and intellectual slowing - personality change - unsteadiness

Question 85

SDH What are some signs of SDH?

Answer 85

- raised ICP - seizures - localising neurological signs (unequal pupils, hemiparesis)

Question 86

SDH what are the differential diagnoses for a subdural haematoma?

Answer 86

stroke dementia CNS masses (tumour vs abscess)

Question 87

SDH What are the investigations for SDH?

Answer 87

Non-contrast CT head MRI scan

Question 88

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

Answer 88

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

Question 89

SDH What is the management of SDH?

Answer 89

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

Question 90

EPILEPSY Define epilepsy

Answer 90

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

Question 91

EPILEPSY Define seizure

Answer 91

Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain

Question 92

EPILEPSY Define ictal phase

Answer 92

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

Question 93

EPILEPSY Define post-ictal phase

Answer 93

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

Question 94

EPILEPSY What are the causes of epilepsy?

Answer 94

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

Question 95

EPILEPSY What is a focal/partial seizure?

Answer 95

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

Question 96

EPILEPSY What is a simple-partial seizure?

Answer 96

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

Question 97

EPILEPSY What is a complex-partial seizure?

Answer 97

Without consciousness or awareness

Question 98

EPILEPSY What is a secondary generalised seizure?

Answer 98

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

Question 99

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

Answer 99

strange smells, motor movements, Jacksonian march

Question 100

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

Answer 100

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

Question 101

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

Answer 101

contralateral altered sensation (tingling, numbness, crawling, electric-shock)

Question 102

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

Answer 102

flashing lights, eyelid fluttering, eye movements

Question 103

EPILEPSY What is Jacksonian march?

Answer 103

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

Question 104

EPILEPSY What is Todd's paresis?

Answer 104

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

Question 105

EPILEPSY What is a generalised seizure?

Answer 105

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

Question 106

EPILEPSY What are the 4 main types of generalised seizure?

Answer 106

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

Question 107

EPILEPSY Explain what an absence seizure is.

Answer 107

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

Question 108

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

Answer 108

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 109

EPILEPSY Explain what a tonic clonic seizure is.

Answer 109

- 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 110

EPILEPSY Explain what a myoclonic seizure is.

Answer 110

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

Question 111

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

Answer 111

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

Question 112

EPILEPSY What are some differentials of epilepsy?

Answer 112

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

Question 113

EPILEPSY What investigations would you do in epilepsy?

Answer 113

- Mostly clinical Dx, witnessed seizure Hx crucial Electroencephalogram (EEG) = supports diagnosis MRI/ CT head = rule out space-occupying lesions Bloods FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose = rule out metabolic disturbances Genetic testing If suspected genetic cause -> juvenile myoclonic epilepsy

Question 114

EPILEPSY what is the diagnostic criteria for eilespy?

Answer 114

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

Question 115

EPILEPSY What is the emergency treatment for epilepsy?

Answer 115

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

Question 116

EPILEPSY What is the general management in the ictal phase?

Answer 116

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

Question 117

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

Answer 117

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

Question 118

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

Answer 118

Sodium Valproate for Males & women unable to childbear, Lamotrigine to females of childbearing potential

Question 119

EPILEPSY what is the treatment for generalised myoclonic epilepsy?

Answer 119

Sodium Valproate for Males & women unable to childbear, Levetiracetam/Topiramate to females of childbearing potential

Question 120

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

Answer 120

Sodium Valproate for Males & women unable to childbear, Ethosuximide to females of childbearing potential

Question 121

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

Answer 121

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

Question 122

EPILEPSY how do lamotrigine and carbamazepine work?

Answer 122

Inhibit pre-synaptic Na+ channels so prevent axonal firing

Question 123

EPILEPSY how does sodium valproate work?

Answer 123

Inhibits voltage gated Na+ channels and increases GABA production

Question 124

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

Answer 124

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

Question 125

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

Answer 125

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

Question 126

STATUS EPILEPTICUS What is status epilepticus?

Answer 126

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

Question 127

STATUS EPILEPTICUS What are some causes of status epilepticus?

Answer 127

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

Question 128

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

Answer 128

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

Question 129

STATUS EPILEPTICUS What is the clinical presentation of status epilepticus?

Answer 129

- 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 130

STATUS EPILEPTICUS What are the complications of status epilepticus?

Answer 130

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

Question 131

STATUS EPILEPTICUS What is the initial management for status epilepticus?

Answer 131

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

Question 132

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

Answer 132

- 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 133

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

Answer 133

- 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 134

STATUS EPILEPTICUS What considerations should be made in status epilepticus?

Answer 134

- 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 135

LOC What is LOC?

Answer 135

Partial or complete loss of perception of yourself + surroundings

Question 136

LOC What are the potential causes of LOC?

Answer 136

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

Question 137

LOC How might cardiogenic LOC present/causes?

Answer 137

- 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 138

LOC How might reflex LOC present?

Answer 138

- 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 139

LOC What are some important questions to ask in LOC?

Answer 139

- 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 140

SYNCOPE What is syncope?

Answer 140

Transient global cerebral hypoperfusion

Question 141

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

Answer 141

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 142

NEAD What is NEAD?

Answer 142

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

Question 143

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

Answer 143

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 144

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

Answer 144

- 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 145

NEAD what is the management of NEAD?

Answer 145

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 146

PARKINSON'S DISEASE Define Parkinson’s disease

Answer 146

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

Question 147

PARKINSONS DISEASE what is the pathway for dopamine production?

Answer 147

Tyrosine --> L-dopa --> Dopamine

Question 148

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

Answer 148

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

Question 149

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

Answer 149

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

Question 150

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

Answer 150

Anticholinergics can precipitate confusion

Question 151

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

Answer 151

- 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 152

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

Answer 152

● Often an insidious onset impaired dexterity, fixed facial expressions, foot drag ● Common associated symptoms: dementia, depression, urinary frequency, constipation, sleep disturbances - Smaller writing (micrographia) - Hypomimia

Question 153

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

Answer 153

Asymmetrical = One side is always worse than the other

Question 154

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

Answer 154

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

Question 155

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

Answer 155

Tremor seen in Parkinson's disease

Question 156

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

Answer 156

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

Question 157

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

Answer 157

- 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 158

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

Answer 158

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

Question 159

PARKINSON'S DISEASE What is progressive supranuclear palsy?

Answer 159

- 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 160

PARKINSON'S DISEASE What is multiple system atrophy?

Answer 160

- 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 161

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

Answer 161

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

Question 162

PARKINSON'S DISEASE What is corticobasal degeneration?

Answer 162

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

Question 163

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

Answer 163

DaTscan Functional neuroimaging - PET Can confirm by reaction to levodopa

Question 164

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

Answer 164

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

Question 165

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

Answer 165

- Infections - Falls - Depression - Aspiration pneumonia

Question 166

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

Answer 166

- Lifestyle: education, exercise, physio, MDT young onset + fit - Dopamine agonist (ropinirole) - MAO-B inhibitor (rasagiline) - L-DOPA (co-careldopa) frail + co-morbidities - L-DOPA (co-careldopa) - MAO-B inhibitor (rasagiline)

Question 167

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

Answer 167

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

Question 168

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

Answer 168

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

Question 169

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

Answer 169

- Autosomal dominant inheritance with 100% penetrance

Question 170

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

Answer 170

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

Question 171

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

Answer 171

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

Question 172

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

Answer 172

● Main sign is hyperkinesia ● Characterised by: ○ Chorea, dystonia, and incoordination ● Psychiatric issues ● Depression ● Cognitive impairment, behavioural difficulties ● Irritability, agitation, anxiety

Question 173

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

Answer 173

Abnormal eye movements Dysarthria Dysphagia Rigidity Ataxia

Question 174

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

Answer 174

15–20y + death mostly respiratory disease

Question 175

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

Answer 175

- 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 176

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

Answer 176

poor prognosis - no treatment ● Benzodiazepines/valproic acid - chorea ● SSRIs = depression ● Haloperidol = psychosis

Question 177

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

Answer 177

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

Question 178

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 178

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 179

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

Answer 179

- 15m–3h - Rapid onset excruciating pain around one eye - Pain is unilateral, often nocturnal - Eye may be bloodshot, lid swelling, miosis, ptosis + lacrimation - 'Cluster' of attacks in a day then remission for weeks/months

Question 180

HEADACHES How can you diagnose cluster headaches?

Answer 180

≥5 classical headaches

Question 181

HEADACHES What is the acute management of cluster headaches?

Answer 181

- S/c triptans - 15L 100% oxygen via non-rebreathe mask for 15 minutes

Question 182

HEADACHES What is the prophylactic management of cluster headaches?

Answer 182

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

Question 183

HEADACHES How does a tension headache present?

Answer 183

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

Question 184

HEADACHES How can you diagnose tension headaches?

Answer 184

Clinical Dx

Question 185

HEADACHES What is the management of tension headaches?

Answer 185

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

Question 186

HEADACHES How does a sinusitis headache present?

Answer 186

- 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 187

HEADACHES What is the management of sinusitis headache?

Answer 187

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

Question 188

HEADACHES How does acute glaucoma present?

Answer 188

- 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 189

HEADACHES What is the management of acute glaucoma?

Answer 189

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

Question 190

HEADACHES What is the most common type of secondary headache?

Answer 190

Medication overuse headache - episodic headache becomes daily chronic headache

Question 191

HEADACHES How can you diagnose medication overuse headaches?

Answer 191

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

Question 192

HEADACHES What is the management of medication overuse headache?

Answer 192

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

Question 193

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

Answer 193

- 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 194

TRIGEMINAL NEURALGIA What are the causes of trigeminal neuralgia?

Answer 194

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

Question 195

TRIGEMINAL NEURALGIA What is the epidemiology?

Answer 195

peak age = 50-60yrs women > men

Question 196

TRIGEMINAL NEURALGIA What are some triggers?

Answer 196

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

Question 197

TRIGEMINAL NEURALGIA What is the clinical presentation of trigeminal neuralgia?

Answer 197

- 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 198

TRIGEMINAL NEURALGIA How would you diagnose trigeminal neuralgia?

Answer 198

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

Question 199

TRIGEMINAL NEURALGIA How would you manage trigeminal neuralgia?

Answer 199

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

Question 200

MIGRAINE What is the pathophysiology of migraines?

Answer 200

- 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 201

MIGRAINE What are the triggers of migraines?

Answer 201

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

Question 202

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

Answer 202

4–72h, F>M

Question 203

MIGRAINE What are the stages of migraine?

Answer 203

- 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 204

MIGRAINE What is a prodrome for migraines?

Answer 204

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

Question 205

MIGRAINE what is a migraine aura?

Answer 205

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

Question 206

MIGRAINE what is a migraine aura?

Answer 206

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

Question 207

MIGRAINE What are the 4 main types of migraine?

Answer 207

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

Question 208

MIGRAINE Describe the pain of a migraine

Answer 208

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

Question 209

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

Answer 209

Nausea Photophobia Phonophobia Aura

Question 210

MIGRAINE How does a migraine with aura present?

Answer 210

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 211

MIGRAINE What investigations would you do in migraine?

Answer 211

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

Question 212

MIGRAINE What is the diagnostic criteria for a migraine?

Answer 212

classified as with or without aura at least 2 of: unilateral pain (usually 4-72hrs) throbbing-type pain moderate > severe intensity motion sensitivity plus at least 1 of: - nausea/vomiting -photophobia/phonophobia there must also be a normal examination and no attributable cause

Question 213

MIGRAINE What is the acute management of migraines?

Answer 213

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

Question 214

MIGRAINE How does triptan work?

Answer 214

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

Question 215

MIGRAINE What is the prophylaxis for migarines?

Answer 215

- 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 216

MND does MND affect UMN or LMN?

Answer 216

both UMN and LMN can be affected

Question 217

MND does MND affect eye movement?

Answer 217

Never affects eye movements (clinical feature of myasthenia gravis)

Question 218

MND Does MND cause sensory loss or sphincter disturbance?

Answer 218

No (clinical feature of MS)

Question 219

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

Answer 219

- 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 220

MND What is the cause of MND?

Answer 220

- 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 221

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

Answer 221

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

Question 222

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

Answer 222

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

Question 223

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

Answer 223

- 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 224

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

Answer 224

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

Question 225

MND What is the general clinical presentation of MND?

Answer 225

- 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 226

MND What are UMN signs?

Answer 226

Hypertonia or spasticity, brisk reflexes upgoing plantars, muscle wasting

Question 227

MND What are LMN signs?

Answer 227

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

Question 228

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

Answer 228

- 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 229

MND What are some investigations for MND?

Answer 229

Head/spine MRI Blood tests = muscle enzymes, autoantibodies Nerve conduction studies EMG Lumbar Puncture

Question 230

MND What is the diagnostic criteria for MND?

Answer 230

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

Question 231

MND How rapidly does MND progress?

Answer 231

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

Question 232

MND What are some complications of MND?

Answer 232

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

Question 233

MND What medication may be given in MND?

Answer 233

- RILUZOLE – Na+ blocker inhibits glutamate release - Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE - Dysphagia: NG tube - Spasms: ORAL BACLOFEN - Non-invasive ventilation - Analgesia e.g. NSAIDs - DICLOFENAC

Question 234

MND What MDT management is given for MND?

Answer 234

- 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 235

MULTIPLE SCLEROSIS what is MS?

Answer 235

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

Question 236

MULTIPLE SCLEROSIS What is the pathophysiology of MS?

Answer 236

- 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 237

MULTIPLE SCLEROSIS What are some classic sites for MS?

Answer 237

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

Question 238

MULTIPLE SCLEROSIS What is the aetiology of MS?

Answer 238

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

Question 239

MULTIPLE SCLEROSIS What is the epidemiology of MS?

Answer 239

Commonly presents in young females living further away from equator

Question 240

MULTIPLE SCLEROSIS What is a clinically isolated syndrome?

Answer 240

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

Question 241

MULTIPLE SCLEROSIS What are the 4 types of MS?

Answer 241

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

Question 242

MULTIPLE SCLEROSIS What is relapsing remitting MS?

Answer 242

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

Question 243

MULTIPLE SCLEROSIS What is secondary progressive MS?

Answer 243

Initially RR but now progressive worsening of Sx + incomplete remissions

Question 244

MULTIPLE SCLEROSIS What is primary progressive MS?

Answer 244

Gradually worsening of disease from point of diagnosis without any RR

Question 245

MULTIPLE SCLEROSIS What is benign MS?

Answer 245

Relapses + Remissions but overall progress will never worsen

Question 246

MULTIPLE SCLEROSIS What is the diagnostic criteria for MS?

Answer 246

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

Question 247

MULTIPLE SCLEROSIS What are the symptoms of MS?

Answer 247

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 248

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

Answer 248

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

Question 249

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

Answer 249

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

Question 250

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

Answer 250

Neck flexion causes electric shock sensation down spine

Question 251

MULTIPLE SCLEROSIS What are some signs of MS?

Answer 251

- 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 252

MULTIPLE SCLEROSIS What is relative afferent pupillary defect?

Answer 252

- 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 253

MULTIPLE SCLEROSIS What is internuclear ophthalmoplegia?

Answer 253

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

Question 254

MULTIPLE SCLEROSIS What are the differential diagnosis’s of MS

Answer 254

SLE Sjogren’s AIDS Syphilis

Question 255

MULTIPLE SCLEROSIS What are the investigations for MS?

Answer 255

- 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 256

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

Answer 256

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

Question 257

MULTIPLE SCLEROSIS What is the management of MS remissions?

Answer 257

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

Question 258

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

Answer 258

- 2 relapses in past 2y

Question 259

MULTIPLE SCLEROSIS What is the general symptomatic management for MS?

Answer 259

Spasticity - BACLOFEN (GABA analogue, reduces Ca2+ influx) - TIZANIDINE (alpha-2 agonist) - BOTOX INJECTION (reduces ACh in neuromuscular junction) urinary incontinence = catheterisation incontinence - DOXAZOSIN (anti-cholinergic alpha blocker drugs

Question 260

MENINGITIS What is meningitis?

Answer 260

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

Question 261

MENINGITIS How does it occur?

Answer 261

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

Question 262

MENINGITIS What are the bacterial causes of meningitis?

Answer 262

N. meningitidis S. pneumoniae H. influenzae

Question 263

MENINGITIS What are the bacterial causes of meningitis in neonates?

Answer 263

E.coli Group B strep - strep agalactiae

Question 264

MENINGITIS What are the viral causes of meningitis?

Answer 264

Enterovirus (most common viral) HSV CMV Varicella zoster virus

Question 265

MENINGITIS What can cause meningitis in immunocompromised patients?

Answer 265

CMV Cryptococcus TB HIV herpes simplex

Question 266

MENINGITIS What are the aseptic causes of meningitis?

Answer 266

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

Question 267

MENINGITIS What are the symptoms of meningitis?

Answer 267

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

Question 268

MENINGITIS How does viral meningitis present?

Answer 268

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

Question 269

MENINGITIS What are the clinical signs of meningitis?

Answer 269

- 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 270

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

Answer 270

Petechial non-blanching rash

Question 271

MENINGITIS What are some differentials of meningitis?

Answer 271

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

Question 272

MENINGITIS What investigations would you do for meningitis?

Answer 272

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

Question 273

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 273

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

Question 274

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 274

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

Question 275

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 275

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

Question 276

MENINGITIS When is a lumbar puncture contraindicated in meningitis?

Answer 276

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

Question 277

MENINGITIS What are some complications following meningitis?

Answer 277

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

Question 278

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 278

- IM benzylpenicillin

Question 279

MENINGITIS What is the management of bacterial meningitis

Answer 279

- 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 280

MENINGITIS What is the management of viral meningitis?

Answer 280

- Supportive therapy mainly - IV aciclovir for HSV

Question 281

MENINGITIS What can be given as prophylaxis against meningitis?

Answer 281

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

Question 282

MENINGITIS Who must you notify about cases of meningitis?

Answer 282

- Public Health England immediately as notifiable disease

Question 283

MENINGITIS Give 4 potential adverse effect of a lumbar puncture

Answer 283

Headache Paraesthesia CSF leak Damage to spinal cord

Question 284

ENCEPHALITIS What is encephalitis?

Answer 284

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

Question 285

ENCEPHALITIS In what group of people is encephalitis common?

Answer 285

Immunocompromised the infections are most frequent in children and elderly

Question 286

ENCEPHALITIS What are the viral causes of encephalitis?

Answer 286

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

Question 287

ENCEPHALITIS What are the non-viral causes of encephalitis?

Answer 287

Bacterial meningitis TB Malaria Lyme’s disease

Question 288

ENCEPHALITIS Name the main triad of symptoms of encephalitis

Answer 288

Fever + headache + altered mental state

Question 289

ENCEPHALITIS What is the clinical presentation of encephalitis?

Answer 289

begins with features of viral infection: - fever, headaches, myalgia, fatigue, nausea progresses to: personality & behavioural changes decreased consciousness, confusion, drowsiness focal neurological deficit - hemiparesis, dysphagia seizures raised ICP and midline shift coma

Question 290

ENCEPHALITIS What are the differentials of encephalitis

Answer 290

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

Question 291

ENCEPHALITIS What investigations would you do for encephalitis?

Answer 291

- Blood culture + CSF serology for viral PCR MRI - shows areas of inflammation, may be midline shifting EEG - periodic sharp and slow wave complexes lumbar puncture

Question 292

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

Answer 292

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

Question 293

ENCEPHALITIS What is the management of encephalitis?

Answer 293

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

Question 294

BRAIN ABSCESS What are the most common causative organisms?

Answer 294

- Staph. aureus + strep. pnuemoniae

Question 295

BRAIN ABSCESS What is a brain abscess?

Answer 295

- Pus-filled swelling in the brain

Question 296

BRAIN ABSCESS What are the aetiologies of brain abscesses?

Answer 296

- 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 297

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

Answer 297

- 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 298

BRAIN ABSCESS What are the investigations for brain abscess?

Answer 298

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

Question 299

BRAIN ABSCESS What is the management of brain abscess?

Answer 299

- 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 300

BRAIN DEATH + COMA What is a coma?

Answer 300

Unarousable unresponsiveness

Question 301

BRAIN DEATH + COMA What is a persistent vegetative state?

Answer 301

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

Question 302

BRAIN DEATH + COMA What is brain death?

Answer 302

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

Question 303

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

Answer 303

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

Question 304

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

Answer 304

- 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 305

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

Answer 305

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 306

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

Answer 306

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

Question 307

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

Answer 307

- 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 308

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

Answer 308

- 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 309

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

Answer 309

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

Question 310

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

Answer 310

- 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 311

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

Answer 311

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

Question 312

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

Answer 312

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

Question 313

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

Answer 313

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

Question 314

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

Answer 314

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

Question 315

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

Answer 315

- 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 316

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

Answer 316

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

Question 317

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

Answer 317

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

Question 318

MYASTHENIA GRAVIS What is myasthenia gravis?

Answer 318

- Autoimmune disorder against acetylcholine receptors in the neuromuscular junction

Question 319

MYASTHENIA GRAVIS What is the pathophysiology of myasthenia gravis?

Answer 319

- 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 320

MYASTHENIA GRAVIS What is the aetiology of myasthenia gravis?

Answer 320

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

Question 321

MYASTHENIA GRAVIS What is the main symptom of myasthenia gravis?

Answer 321

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

Question 322

MYASTHENIA GRAVIS What is the natural course of myasthenia gravis?

Answer 322

- Eventually leads to atrophy - Fluctuating relapsing + remitting pattern

Question 323

MYASTHENIA GRAVIS What will patients with myasthenia gravis struggle with?

Answer 323

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

Question 324

MYASTHENIA GRAVIS What are the signs of myasthenia gravis?

Answer 324

- Ptosis, diplopia (extra-ocular muscle weakness)

Question 325

MYASTHENIA GRAVIS What medications can exacerbate myasthenia gravis?

Answer 325

Abx, CCBs, beta-blockers, lithium + statins

Question 326

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

Answer 326

Pregnancy Hypokalaemia Infection Emotion Exercise Drugs

Question 327

MYASTHENIA GRAVIS What are some clinical signs of myasthenia gravis?

Answer 327

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

Question 328

MYASTHENIA GRAVIS What antibodies are implicated in myasthenia gravis?

Answer 328

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

Question 329

MYASTHENIA GRAVIS What investigations would you do for myasthenia gravis?

Answer 329

mostly clinical examination positive tensilon test anti-AChR antibodies TFTs EMG CT of thymus crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis

Question 330

MYASTHENIC CRISIS What is the main complication of myasthenia gravis?

Answer 330

- Myasthenic crisis

Question 331

MYASTHENIC CRISIS What are the clinical features?

Answer 331

- Resp failure or death

Question 332

MYASTHENIC CRISIS what are the complications?

Answer 332

Resp failure or death

Question 333

MYASTHENIC CRISIS What are the causes of myasthenic crisis?

Answer 333

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

Question 334

MYASTHENIC CRISIS What is the management of myasthenic crisis?

Answer 334

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

Question 335

MYASTHENIA GRAVIS What is the management of myasthenia gravis?

Answer 335

- 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 336

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

Answer 336

- Acute inflammatory demyelinating polyneuropathy which targets Schwann cells

Question 337

GUILLAIN-BARRE What is the pathophysiology of GBS?

Answer 337

- 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 338

GUILLAIN-BARRE What is Miller-Fisher syndrome?

Answer 338

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

Question 339

GUILLAIN-BARRE What are the causes of GBS?

Answer 339

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

Question 340

GUILLAIN-BARRE What is the clinical presentation of GBS?

Answer 340

- 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 341

GUILLAIN-BARRE What are some differentials for GBS?

Answer 341

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

Question 342

GUILLAIN-BARRE What are the investigations for GBS?

Answer 342

Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation) bloods - FBC, U&E, LFT, TFT Spirometry = respiratory involvement ECG

Question 343

GUILLAIN-BARRE What is the prognosis of GBS?

Answer 343

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

Question 344

GUILLAIN-BARRE What is the main treatment for GBS?

Answer 344

- 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 345

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

Answer 345

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

Question 346

GUILLAIN-BARRE What is the supportive therapy for GBS?

Answer 346

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

Question 347

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

Answer 347

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

Question 348

BRAIN TUMOURS Give 4 examples of different brain tumours

Answer 348

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

Question 349

BRAIN TUMOURS What are gliomas? Give some examples

Answer 349

- 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 350

BRAIN TUMOURS What are meningiomas?

Answer 350

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

Question 351

BRAIN TUMOURS What are pituitary tumours?

Answer 351

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

Question 352

BRAIN TUMOURS What are acoustic neuromas? What are they associated with?

Answer 352

- 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

Question 353

BRAIN TUMOURS How do acoustic neuromas present?

Answer 353

Classic Sx = hearing loss, tinnitus, balance issues, decreased facial sensation

Question 354

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

Answer 354

- 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 355

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

Answer 355

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

Question 356

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

Answer 356

Personality + intellect change, hemiparesis, expressive dysphasia

Question 357

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

Answer 357

Receptive dysphasia, amnesia

Question 358

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

Answer 358

Hemisensory loss, dysphasia

Question 359

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

Answer 359

Contralateral visual defects

Question 360

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

Answer 360

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

Question 361

BRAIN TUMOURS What are some symptoms of raised ICP?

Answer 361

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

Question 362

BRAIN TUMOURS What investigations would you perform for brain tumours?

Answer 362

- 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 363

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

Answer 363

- 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 364

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

Answer 364

- 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 365

NEUROPATHY What is a neuropathy?

Answer 365

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

Question 366

NEUROPATHY What are the peripheral nerve causes of muscle weakness?

Answer 366

- 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 367

NEUROPATHY What is the pathophysiology of mononeuritis multiplex?

Answer 367

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

Question 368

NEUROPATHY What can cause mononeuritis multiplex?

Answer 368

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

Question 369

NEUROPATHY What are the causes of peripheral neuropathy?

Answer 369

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

Question 370

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

Answer 370

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

Question 371

NEUROPATHY What is Charcot-Marie-Tooth disease?

Answer 371

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

Question 372

NEUROPATHY What is the generic clinical presentation of mononeuropathy?

Answer 372

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

Question 373

NEUROPATHY What is the generic clinical presentation of mononeuritis multiplex?

Answer 373

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

Question 374

NEUROPATHY What is the generic clinical presentation of peripheral neuropathy?

Answer 374

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

Question 375

NEUROPATHY What is the most common mononeuropathy?

Answer 375

- Carpal tunnel syndrome

Question 376

NEUROPATHY What is the pathophysiology of carpal tunnel syndrome?

Answer 376

Inflammation of carpal tunnel leads to entrapment of the median nerve

Question 377

NEUROPATHY What are the causes of carpal tunnel syndrome?

Answer 377

Idiopathic but associated with local tumours, DM + RA

Question 378

NEUROPATHY What muscles does the median nerve innervate?

Answer 378

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

Question 379

NEUROPATHY What is the clinical presentation of carpal tunnel syndrome?

Answer 379

- 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 380

NEUROPATHY What investigations can you do for carpal tunnel syndrome?

Answer 380

- 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 381

NEUROPATHY What is the management of carpal tunnel syndrome?

Answer 381

- Splinting - Analgesia - Local steroid injection ± decompression surgery

Question 382

NEUROPATHY What does a CN1 lesion cause?

Answer 382

- Anosmia

Question 383

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 383

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 384

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

Answer 384

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

Question 385

NEUROPATHY What does a CN3 lesion cause?

Answer 385

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

Question 386

NEUROPATHY What does a CN4 lesion cause?

Answer 386

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

Question 387

NEUROPATHY What does a CN5 lesion cause?

Answer 387

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

Question 388

NEUROPATHY What does a CN6 lesion cause?

Answer 388

- Issues abducting eye beyond midline as innervates lateral rectus

Question 389

NEUROPATHY What does a CN7 lesion cause?

Answer 389

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

Question 390

NEUROPATHY What is Bell's palsy?

Answer 390

- 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 391

NEUROPATHY What does a CN8 lesion cause?

Answer 391

- Sensorineural deafness - Tinnitus, vertigo, nystagmus

Question 392

NEUROPATHY What does a CN9/10 lesion cause?

Answer 392

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

Question 393

NEUROPATHY What does a CN11 lesion cause?

Answer 393

- Weakness turning head to contralateral side

Question 394

NEUROPATHY What does a CN12 lesion cause?

Answer 394

- Tongue deviation towards side of lesion

Question 395

NEUROPATHY What are the investigations used in neuropathy?

Answer 395

- 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 396

NEUROPATHY What is the management of neuropathy?

Answer 396

- 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 397

CORD COMPRESSION What is myelopathy?

Answer 397

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

Question 398

RADICULOPATHY What is radiculopathy?

Answer 398

Sx caused by pinching of a nerve root as they exit the spinal cord

Question 399

RADICULOPATHY How does radiculopathy present?

Answer 399

- Sharp, shooting pain within distribution of nerve, weakness + loss of sensation

Question 400

RADICULOPATHY what are the causes?

Answer 400

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

Question 401

RADICULOPATHY what is the management?

Answer 401

analgesia - amitryptyline, pregabalin, gabapentin physiotherapy surgery in emergencies

Question 402

RADICULOPATHY What is the most common radiculopathy?

Answer 402

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

Question 403

CORD COMPRESSION What are the aetiologies of spinal cord compression?

Answer 403

- 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 404

CORD COMPRESSION What are the symptoms of spinal cord compression?

Answer 404

- 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 405

CORD COMPRESSION What are the signs of spinal cord compression?

Answer 405

- 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 406

CORD COMPRESSION How does degenerative cervical myelopathy present?

Answer 406

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

Question 407

CORD COMPRESSION What are the differentials for spinal cord compression?

Answer 407

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

Question 408

CORD COMPRESSION What are the investigations of spinal cord compression?

Answer 408

- 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 409

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

Answer 409

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

Question 410

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

Answer 410

- 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 411

CORD COMPRESSION What is spinal stenosis?

Answer 411

- Narrowing of lower spinal canal almost always due to degeneration

Question 412

CORD COMPRESSION How does spinal stenosis present?

Answer 412

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

Question 413

CORD COMPRESSION How is spinal stenosis managed?

Answer 413

MRI + canal decompression surgery

Question 414

CORD COMPRESSION What is the management of spinal cord compression?

Answer 414

- 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 415

SPINAL CORD INJURY What is Brown-Sequard syndrome?

Answer 415

- 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 416

ANTERIOR CORD SYNDROME What is anterior cord syndrome?

Answer 416

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

Question 417

ANTERIOR CORD SYNDROME what are the causes?

Answer 417

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

Question 418

ANTERIOR CORD SYNDROME what are the symptoms?

Answer 418

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

Question 419

ANTERIOR CORD SYNDROME what are the investigations?

Answer 419

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

Question 420

ANTERIOR CORD SYNDROME what is the treatment?

Answer 420

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

Question 421

SPINAL CORD INJURY What is posterior cord syndrome?

Answer 421

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

Question 422

SPINAL CORD INJURY What is central cord syndrome?

Answer 422

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

Question 423

MYOPATHY What are myopathies?

Answer 423

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

Question 424

MYOPATHY What are dystrophies?

Answer 424

If they're inherited = dystrophies

Question 425

MYOPATHY How do myopathies compare to neuropathies?

Answer 425

Weakness is proximal in muscle disease (nerves = distal)

Question 426

MYOPATHY What are the aetiologies of myopathies?

Answer 426

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

Question 427

MYOPATHY How do myopathies present?

Answer 427

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

Question 428

MYOPATHY what is myotonic dystrophy?

Answer 428

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

Question 429

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

Answer 429

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

Question 430

MYOPATHY How does myotonic dystrophy present?

Answer 430

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

Question 431

MYOPATHY What are the investigations for myopathies?

Answer 431

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

Question 432

MYOPATHY What is the management of myopathies?

Answer 432

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

Question 433

MYOPATHY What is the general supportive management of myopathies?

Answer 433

- 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 434

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 434

- 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 435

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 435

- 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 436

HYDROCEPHALUS What is hydrocephalus?

Answer 436

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

Question 437

HYDROCEPHALUS What is the purpose of CSF?

Answer 437

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

Question 438

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

Answer 438

- 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 439

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 439

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

Question 440

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

Answer 440

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

Question 441

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

Answer 441

due to an imbalance of CSF production absorption

Question 442

HYDROCEPHALUS What are some causes of obstructive hydrocephalus?

Answer 442

Tumour, acute haemorrhages, developmental abnormalities (aqueduct stenosis)

Question 443

HYDROCEPHALUS What are some causes of non-obstructive hydrocephalus?

Answer 443

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

Question 444

HYDROCEPHALUS How does hydrocephalus present?

Answer 444

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

Question 445

HYDROCEPHALUS what are the causes of normal pressure hydrocephalus?

Answer 445

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

Question 446

HYDROCEPHALUS How does normal pressure hydrocephalus present?

Answer 446

'Wet, wacky, wobbly' – - Urinary incontinence, dementia + abnormal gait (apraxia) Trouble walking (feels like the feet are stuck to the ground) Poor balance Falling Changes in the way you walk Forgetfulness and confusion Mood changes Depression Difficulty responding to questions Loss of bladder control - Sx come on gradually + similar to Alzheimer's so difficult to diagnose

Question 447

HYDROCEPHALUS What are the investigations for hydrocephalus?

Answer 447

- 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 448

HYDROCEPHALUS What is the management of hydrocephalus?

Answer 448

- An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside - 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 449

IIH What is idiopathic intracranial hypertension (IIH)?

Answer 449

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

Question 450

IIH What are the causes of IIH?

Answer 450

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

Question 451

IIH What is the clinical presentation of IIH?

Answer 451

- 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 452

IIH What are the investigations for IIH?

Answer 452

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

Question 453

IIH What is the management of IIH?

Answer 453

- #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 454

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

Answer 454

- 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 455

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

Answer 455

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 456

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

Answer 456

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

Question 457

NEURO PHARMACOLOGY What is the mechanism of action of Levodopa?

Answer 457

- 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 458

NEURO PHARMACOLOGY What are the side effects of Levodopa?

Answer 458

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

Question 459

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

Answer 459

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

Question 460

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 460

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

Question 461

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

Answer 461

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

Question 462

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

Answer 462

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

Question 463

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

Answer 463

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

Question 464

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

Answer 464

- 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 465

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

Answer 465

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

Question 466

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

Answer 466

- 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 467

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

Answer 467

- 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 468

ACUTE LABYRINTHITIS What is acute labyrinthitis?

Answer 468

- Inflammation of labyrinth + damage to vestibular + auditory end organs

Question 469

ACUTE LABYRINTHITIS How does it present?

Answer 469

- 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

Question 470

ACUTE LABYRINTHITIS What are the causes?

Answer 470

Usually viral, ?vascular lesion

Question 471

MENIERE'S DISEASE What is Ménières disease?

Answer 471

- Increased pressure in endolymphatic system due to increased volume of inner ear.

Question 472

MENIERE'S DISEASE How does it present?

Answer 472

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

Question 473

MENIERE'S DISEASE what is the classical triad of symptoms?

Answer 473

vertigo hearing loss - worse during attacks tinnitus

Question 474

MENIERE'S DISEASE What causes it?

Answer 474

Idiopathic, trauma, endo

Question 475

MENIERE'S DISEASE How is it managed?

Answer 475

Bed rest, reassurance

Question 476

DIZZINESS/VERTIGO How does traumatic damage present?

Answer 476

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

Question 477

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

Answer 477

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

Question 478

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

Answer 478

- 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 479

SHINGLES what is the cause of shingles?

Answer 479

reactivation of herpes varicella zoster virus

Question 480

SHINGLES what are the risk factors for shingles?

Answer 480

- increasing age - immunocompromised - HIV, hodgkins lymphoma, bone marrow transplants

Question 481

SHINGLES what is the pathophysiology of shingles?

Answer 481

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

Question 482

SHINGLES what is the clinical presentation?

Answer 482

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

Question 483

SHINGLES how is it diagnosed?

Answer 483

clinical diagnosis

Question 484

SHINGLES what is the management?

Answer 484

- acyclovir - analgesia for pain

Question 485

SHINGLES what are the complications?

Answer 485

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

Question 486

CEREBELLAR DISEASE what are the signs of cerebellar dysfunction?

Answer 486

DANISH dysdiadochokinesia ataxia nystagmus intention tremor slurred speech hypotonia

Question 487

CEREBRAL PALSY what are the causes?

Answer 487

- antenatal = prematurity, multiple births, TORCH - perinatal = asphyxia during delivery - postnatal = hyperbilirubinaemia, neonatal sepsis, resp distress, meningitis, head injuries, seizures

Question 488

CEREBRAL PALSY what are the symptoms?

Answer 488

- delay in motor/speech/cognitive development - retention of primitive reflexes - spasticity/clonus - toe walking/knee hyperextension - scissoring - crouched gait - contractures

Question 489

CEREBRAL PALSY what are the investigations?

Answer 489

MRI brain - periventricular leukomalacia, congenital malformation, stroke or haemorrhage

Question 490

CEREBRAL PALSY what is the management?

Answer 490

- OT, physio and speech therapy - orthoses - adaptive equipment

Question 491

BELL'S PALSY what are the causes?

Answer 491

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

Question 492

BELL'S PALSY what is the pathophysiology?

Answer 492

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

Question 493

BELL'S PALSY what are the symptoms?

Answer 493

unilateral LMN facial weakness altered taste post auricular pain - pain behind ears

Question 494

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

Answer 494

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

Question 495

BELL'S PALSY what is the management?

Answer 495

- corticosteroid - eye drops - ?antivrials

Question 496

BELL'S PALSY what are the investigations?

Answer 496

- can be clinical diagnosis - ENoG - needle EMG

Question 497

NEUROFIBROMATOSIS what are the clinical signs of NF1?

Answer 497

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

Question 498

NEUROFIBROMATOSIS what are the clincial signs of NF2?

Answer 498

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

Question 499

NEUROFIBROMATOSIS what are the causes of neurofibromatosis 1 and 2?

Answer 499

NF1 = neurofibromin 1 (autosomal dominant) NF2 = neurofibromin 2 (autosomal dominant)

Question 500

NEUROFIBROMATOSIS what is the treatment for NF1 and NF2?

Answer 500

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

Question 501

NARCOLEPSY what are the clinical features?

Answer 501

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

Question 502

NARCOLEPSY what are the investigations?

Answer 502

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

Question 503

NARCOLEPSY what is the management?

Answer 503

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

Question 504

RADICULOPATHY what is the management?

Answer 504

analgesia - amitryptyline, pregabalin, gabapentin physiotherapy surgery in emergencies

Question 505

WERNICKE-KORSAKOFF SYNDROME what is it?

Answer 505

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

Question 506

WERNICKE-KORSAKOFF SYNDROME what are the clinical signs?

Answer 506

- mental confusion/amnesia - vision problems - coma - tremor - ataxia - hypothermia - low blood pressure

Question 507

WERNICKE-KORSAKOFF SYNDROME what is the cause?

Answer 507

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

Question 508

WERNICKE-KORSAKOFF SYNDROME what is the management?

Answer 508

B1 (thiamine) replacement and proper nutrition/hydration

Question 509

CATAPLEXY what is it?

Answer 509

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

Question 510

CATAPLEXY what happens during an attack?

Answer 510

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

Question 511

CATAPLEXY what are the causes?

Answer 511

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

Question 512

CATAPLEXY what is the management?

Answer 512

sodium oxybate tricyclic antidepressants (clomipramine) SSRIs

Question 513

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

Answer 513

unilateral damage to the sympathetic chain

Question 514

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

Answer 514

unilateral damage to the sympathetic chain

Question 515

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

Answer 515

stroke, tumours of hypothalamus, spinal cord lesions

Question 516

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

Answer 516

tumours of upper chest cavity, trauma to the neck

Question 517

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

Answer 517

lesions to carotid artery, middle ear infections, injury to base of the skull

Question 518

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

Answer 518

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

Question 519

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

Answer 519

clinical examination MRI - detect lesions

Question 520

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

Answer 520

treat underlying cause

Question 521

BULBAR PALSY what is it?

Answer 521

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

Question 522

BULBAR PALSY what ar ethe causes?

Answer 522

- brainstem tumours and strokes - ALS - GBS

Question 523

BULBAR PALSY what are the causes?

Answer 523

- brainstem tumours and strokes - ALS - GBS

Question 524

BULBAR PALSY what are the symptoms?

Answer 524

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

Question 525

BULBAR PALSY what are the investigations?

Answer 525

MRI lumbar puncture

Question 526

BULBAR PALSY what is the treatment?

Answer 526

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

Question 527

STRABISMUS what is it?

Answer 527

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

Question 528

STRABISMUS what are the causes?

Answer 528

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

Question 529

STRABISMUS what are the symptoms?

Answer 529

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

Question 530

STRABISMUS what are the risk factors?

Answer 530

FHx of strabismus prematurity low birth weight maternal smoking during pregnancy

Question 531

STRABISMUS what are the investigations?

Answer 531

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

Question 532

STRABISMUS what is the management?

Answer 532

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

Question 533

SCIATICA what is it?

Answer 533

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

Question 534

SCIATICA how is the pain from sciatica described?

Answer 534

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

Question 535

SCIATICA what are the risk factors?

Answer 535

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

Question 536

SCIATICA what are the causes?

Answer 536

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

Question 537

SCIATICA what are the symptoms?

Answer 537

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

Question 538

SCIATICA what are the investigations?

Answer 538

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

Question 539

SCIATICA what is the management?

Answer 539

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

Question 540

RAISED ICP what are the causes?

Answer 540

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

Question 541

RAISED ICP what are the symptoms?

Answer 541

- high BP - irregular or slow pulse - severe headache - weakness - cardiac arrest - LOC, coma - loss of brainstem reflexes (blinking, gagging, pupils reacting to light) - respiratory arrest - dilated pupils + no movement in one/both eyes

Question 542

RAISED ICP what are the investigations?

Answer 542

- x-ray of skull + neck - head CT - MRI head - blood tests

Question 543

RAISED ICP what is the management?

Answer 543

- drain to remove CSF - mannitol to reduce swelling - intubation - surgery to remove part of skull

Question 544

RAISED ICP what is the prognosis for brain herniation?

Answer 544

high chance of brain damage/death

Question 545

CHRONIC FATIGUE SYNDROME what is it?

Answer 545

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

Question 546

CHRONIC FATIGUE SYNDROME What are the causes?

Answer 546

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

Question 547

CHRONIC FATIGUE SYNDROME what are the risk factors?

Answer 547

- sex (female) - genetic predisposition - allergies - stress - environmental factors

Question 548

CHRONIC FATIGUE SYNDROME what are the symptoms?

Answer 548

- severe fatigue that interferes with daily life for >6 months - sleep problems - feeling unrefreshed after night's sleep - chronic insomnia - memory loss - reduced concentration - orthostatic intolerance - muscle pain - frequent headaches - multi-joint pain without redness or swelling - frequent sore throat

Question 549

CHRONIC FATIGUE SYNDROME what are the differentials?

Answer 549

mononucleosis lyme disease MS SLE hypothyroidism fibromyalgia depression sleep disorders

Question 550

CHRONIC FATIGUE SYNDROME what are the investigations?

Answer 550

rule out all other causes - bloods - FBC, U+Es, CRP, ESR, TFTs

Question 551

CHRONIC FATIGUE SYNDROME what is the management?

Answer 551

no cure - pacing activities - reduce caffeine, nicotine and alcohol - create sleep routine - antidepressant medications - complementary/alternative medicines

Question 552

ESSENTIAL TREMOR what is it?

Answer 552

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms (69% of patients) that is usually absent at rest and present during posture and intentional movements. it can also involve the voice, head and jaw

Question 553

ESSENTIAL TREMOR what is the presentation?

Answer 553

- slowly progressive - difficulties with writing, eating, drinking, dressing - tremor only present with movement

Question 554

ESSENTIAL TREMOR what are the investigations?

Answer 554

clinical diagnosis - bilateral tremor with normal muscle tone and speed of movement

Question 555

ESSENTIAL TREMOR what is the management?

Answer 555

- medication - propranolol, primidone - deep brain stimulation - focused ultrasound thalamotomy with MRI guidance

Question 556

MENIERE'S DISEASE what is it?

Answer 556

It is an auditory disease characterised by an episodic sudden onset of vertigo, low-frequency hearing loss (in the early stages of the disorder), low-frequency roaring tinnitus, and sensation of fullness in the affected ear

Question 557

MENIERE'S DISEASE what are the investigations?

Answer 557

pure tone air and bone conduction with masking speech audiometry tympanometry oto-acoustic emissions (OAE)

Question 558

MENIERE'S DISEASE what is the management?

Answer 558

- dietary changes - salt restriction, limit caffeine, alcohol, smoking - reduce stress - audiological counselling - endolymphatic sac surgery - vestibular nerve section - labyrinthectomy

Question 559

DIABETIC NEUROPATHY what is the distribution of sensory loss?

Answer 559

glove and stocking - usually lower legs are affected first

Question 560

DIABETIC NEUROPATHY what is the management of neuropathic pain?

Answer 560

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

Question 561

DIABETIC NEUROPATHY what are the effects on the GI system?

Answer 561

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

Question 562

DIABETIC NEUROPATHY what is the management for gastroparesis?

Answer 562

metoclopramide, domperidone or erythromycin