NEURO TO DO

Question 1

STROKE
What vessels can be affected in total anterior circulation syndrome (TACS)?

Answer 1

• ACA, MCA, carotid

Question 2

STROKE
What vessels can be affected in a partial anterior circulation syndrome (PACS)?

Answer 2

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

Question 3

STROKE
What vessels can be affected in a posterior circulation syndrome (POCS)?

Answer 3

• PCA, vertebrobasilar artery or branches

Question 4

STROKE
What vessels can be affected in lacunar syndrome (LACS) and what does that mean?

Answer 4

• Perforating arteries so no higher cortical dysfunction or visual field abnormality, subcortical stroke

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

STROKE
What criteria must be met for a total anterior circulation syndrome (TACS)?

Answer 7

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

Question 8

STROKE
What criteria must be met for a partial anterior circulation syndrome (PACS)?

Answer 8

• 2/3 of the criteria for TACS:
• Hemiplegia (unilateral ± sensory deficit of face, arm leg)
• Homonymous hemianopia
• Higher cerebral dysfunction (dysphasia, visuospatial disturbance)

Question 9

STROKE
What criteria must be met for a posterior circulation syndrome (POCS)?

Answer 9

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

Question 10

STROKE
What criteria must be met for a lacunar syndrome (LACS)?

Answer 10

One of following –
- Pure sensory stroke (thalamus)
- Pure motor stroke (posterior limb of internal capsule)
- Sensori-motor stroke
- Ataxic hemiparesis

Question 11

STROKE
What areas can be affected in lacunar syndrome (LACS)?

Answer 11

• Thalamus, basal ganglia, internal capsule

Question 12

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

Answer 12

• C7–T1
• Elbow trauma or fracture, elbow arthritis

Question 13

NEUROPATHY
What are the motor signs of ulnar neuropathy?

Answer 13

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

Question 14

NEUROPATHY
What are the sensory signs of ulnar neuropathy?

Answer 14

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

Question 15

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

Answer 15

• C5-T1
• Compression against humerus

Question 16

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

Answer 16

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

Question 17

NEUROPATHY
What causes brachial plexus neuropathy?
Presentation?

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

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

Question 21

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

Answer 21

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

Question 22

NEUROPATHY
Roots of the tibial nerve?
Presentation of neuropathy?

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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

Question 27

SPEECH ISSUES What is pseudo? What is pseudobulbar dysarthria?

Answer 27

- Affects UMN - Slow, nasal, effortful 'hot potato' voice

Question 28

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

Answer 28

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

Question 29

SPEECH ISSUES What is bulbar? What is bulbar dysarthria?

Answer 29

- Affects LMN of CN9–12 - Nasal speech due to paralysis of palate

Question 30

STROKE What are some important differentials of stroke?

Answer 30

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

Question 31

STROKE What classification system can be used for strokes?

Answer 31

- Oxford stroke (Bamford) classification

Question 32

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

Answer 32

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

Question 33

TIA What do the scores from ABCD2 mean?

Answer 33

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

Question 34

STROKE What tools can be used to identify stroke?

Answer 34

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

Question 35

STROKE How would an ischaemic stroke appear on CT head?

Answer 35

- 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 36

STROKE How would a haemorrhagic stroke appear on CT head?

Answer 36

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

Question 37

STROKE What are some contraindications to treatment with alteplase?

Answer 37

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

Question 38

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

Answer 38

- 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 39

STROKE What other management is given for ischaemic strokes?

Answer 39

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

Question 40

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

Answer 40

- 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 41

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

Answer 41

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

Question 42

STROKE What is the CHA2DS2-VaSc score

Answer 42

- 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 43

STROKE What is the HAS-BLED score?

Answer 43

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

Question 44

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

Answer 44

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 45

SAH What are the causes of SAH?

Answer 45

- 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 46

SAH What conditions are linked to SAH?

Answer 46

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

Question 47

SAH What are some symptoms of SAH?

Answer 47

- 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 48

SAH What are some signs of SAH?

Answer 48

- 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 49

SAH What is the management of SAH?

Answer 49

- 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 50

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

Answer 50

- 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 51

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

Answer 51

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

Question 52

EDH What is the clinical presentation of EDH?

Answer 52

- 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 53

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

Answer 53

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

Question 54

EDH What are some differentials for EDH?

Answer 54

- Epilepsy, - CO poisoning, - carotid dissection

Question 55

EDH What is the management for EDH?

Answer 55

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

Question 56

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

Answer 56

- 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 57

SDH What is the pathophysiology of a SDH?

Answer 57

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 58

SDH What are the symptoms of SDH?

Answer 58

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

Question 59

SDH What are some signs of SDH?

Answer 59

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

Question 60

SDH What is the management of SDH?

Answer 60

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

Question 61

EPILEPSY Define epilepsy

Answer 61

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

Question 62

EPILEPSY What are the causes of epilepsy?

Answer 62

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

Question 63

EPILEPSY What are some differentials of epilepsy?

Answer 63

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

Question 64

EPILEPSY What investigations would you do in epilepsy?

Answer 64

- 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 65

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

Answer 65

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

Question 66

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

Answer 66

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

Question 67

STATUS EPILEPTICUS What are some causes of status epilepticus?

Answer 67

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

Question 68

STATUS EPILEPTICUS What is the clinical presentation of status epilepticus?

Answer 68

- 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 69

STATUS EPILEPTICUS What are the complications of status epilepticus?

Answer 69

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

Question 70

STATUS EPILEPTICUS What is the initial management for status epilepticus?

Answer 70

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

Question 71

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

Answer 71

- 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 72

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

Answer 72

- 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 73

STATUS EPILEPTICUS What considerations should be made in status epilepticus?

Answer 73

- 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 74

LOC What are the potential causes of LOC?

Answer 74

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

Question 75

LOC How might cardiogenic LOC present/causes?

Answer 75

- 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 76

LOC How might reflex LOC present?

Answer 76

- 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 77

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

Answer 77

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 78

NEAD what is the management of NEAD?

Answer 78

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 79

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

Answer 79

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

Question 80

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

Answer 80

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

Question 81

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

Answer 81

- 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 82

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

Answer 82

● 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 83

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

Answer 83

- 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 84

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

Answer 84

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

Question 85

PARKINSON'S DISEASE What is progressive supranuclear palsy?

Answer 85

- 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 86

PARKINSON'S DISEASE What is multiple system atrophy?

Answer 86

- 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 87

PARKINSON'S DISEASE What is corticobasal degeneration?

Answer 87

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

Question 88

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

Answer 88

DaTscan Functional neuroimaging - PET Can confirm by reaction to levodopa

Question 89

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

Answer 89

- Infections - Falls - Depression - Aspiration pneumonia

Question 90

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

Answer 90

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

Question 91

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

Answer 91

- Autosomal dominant inheritance with 100% penetrance

Question 92

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

Answer 92

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

Question 93

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

Answer 93

- 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 94

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

Answer 94

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

Question 95

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

Answer 95

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

Question 96

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

Answer 96

- 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 97

HEADACHES How does a tension headache present?

Answer 97

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

Question 98

HEADACHES How does a sinusitis headache present?

Answer 98

- 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 99

HEADACHES How does acute glaucoma present?

Answer 99

- 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 100

HEADACHES How can you diagnose cluster headaches?

Answer 100

≥5 classical headaches

Question 101

HEADACHES What is the acute management of cluster headaches?

Answer 101

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

Question 102

HEADACHES What is the management of tension headaches?

Answer 102

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

Question 103

HEADACHES What is the management of sinusitis headache?

Answer 103

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

Question 104

HEADACHES What is the management of acute glaucoma?

Answer 104

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

Question 105

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

Answer 105

- 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 106

TRIGEMINAL NEURALGIA What are the causes of trigeminal neuralgia?

Answer 106

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

Question 107

TRIGEMINAL NEURALGIA What is the clinical presentation of trigeminal neuralgia?

Answer 107

- 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 108

TRIGEMINAL NEURALGIA How would you diagnose trigeminal neuralgia?

Answer 108

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

Question 109

TRIGEMINAL NEURALGIA How would you manage trigeminal neuralgia?

Answer 109

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

Question 110

MIGRAINE What is the pathophysiology of migraines?

Answer 110

- 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 111

MIGRAINE What are the triggers of migraines?

Answer 111

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

Question 112

MIGRAINE Describe the pain of a migraine

Answer 112

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

Question 113

MIGRAINE What is the acute management of migraines?

Answer 113

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

Question 114

MIGRAINE What is the prophylaxis for migarines?

Answer 114

- 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 115

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

Answer 115

- 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 116

MND What is the cause of MND?

Answer 116

- 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 117

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

Answer 117

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

Question 118

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

Answer 118

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

Question 119

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

Answer 119

- 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 120

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

Answer 120

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

Question 121

MND What is the general clinical presentation of MND?

Answer 121

- 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 122

MND What are UMN signs?

Answer 122

Hypertonia or spasticity, brisk reflexes upgoing plantars, muscle wasting

Question 123

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

Answer 123

- 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 124

MND What are some investigations for MND?

Answer 124

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

Question 125

MND What medication may be given in MND?

Answer 125

- 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 126

MULTIPLE SCLEROSIS What is the pathophysiology of MS?

Answer 126

- 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 127

MULTIPLE SCLEROSIS What are some classic sites for MS?

Answer 127

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

Question 128

MULTIPLE SCLEROSIS What is a clinically isolated syndrome?

Answer 128

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

Question 129

MULTIPLE SCLEROSIS What are the 4 types of MS?

Answer 129

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

Question 130

MULTIPLE SCLEROSIS What is relapsing remitting MS?

Answer 130

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

Question 131

MULTIPLE SCLEROSIS What is secondary progressive MS?

Answer 131

Initially RR but now progressive worsening of Sx + incomplete remissions

Question 132

MULTIPLE SCLEROSIS What is the diagnostic criteria for MS?

Answer 132

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

Question 133

MULTIPLE SCLEROSIS What are the symptoms of MS?

Answer 133

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 134

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

Answer 134

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

Question 135

MULTIPLE SCLEROSIS What are some signs of MS?

Answer 135

- 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 136

MULTIPLE SCLEROSIS What is relative afferent pupillary defect?

Answer 136

- 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 137

MULTIPLE SCLEROSIS What is internuclear ophthalmoplegia?

Answer 137

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

Question 138

MULTIPLE SCLEROSIS What are the investigations for MS?

Answer 138

- 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 139

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

Answer 139

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

Question 140

MULTIPLE SCLEROSIS What is the management of MS remissions?

Answer 140

- 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 141

MULTIPLE SCLEROSIS What is the general symptomatic management for MS?

Answer 141

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 142

MENINGITIS What are the bacterial causes of meningitis?

Answer 142

N. meningitidis S. pneumoniae H. influenzae

Question 143

MENINGITIS What are the viral causes of meningitis?

Answer 143

Enterovirus (most common viral) HSV CMV Varicella zoster virus

Question 144

MENINGITIS What are the clinical signs of meningitis?

Answer 144

- 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 145

MENINGITIS What are some differentials of meningitis?

Answer 145

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

Question 146

MENINGITIS What investigations would you do for meningitis?

Answer 146

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 147

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 147

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

Question 148

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 148

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

Question 149

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 149

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

Question 150

MENINGITIS What are some complications following meningitis?

Answer 150

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

Question 151

MENINGITIS What is the management of bacterial meningitis

Answer 151

- 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 152

ENCEPHALITIS What are the viral causes of encephalitis?

Answer 152

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

Question 153

ENCEPHALITIS What is the clinical presentation of encephalitis?

Answer 153

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 154

ENCEPHALITIS What are the differentials of encephalitis

Answer 154

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

Question 155

ENCEPHALITIS What investigations would you do for encephalitis?

Answer 155

- 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 156

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

Answer 156

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

Question 157

ENCEPHALITIS What is the management of encephalitis?

Answer 157

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

Question 158

BRAIN ABSCESS What are the most common causative organisms?

Answer 158

- Staph. aureus + strep. pnuemoniae

Question 159

BRAIN ABSCESS What is the management of brain abscess?

Answer 159

- 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 160

BRAIN DEATH + COMA What is a coma?

Answer 160

Unarousable unresponsiveness

Question 161

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

Answer 161

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 162

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

Answer 162

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

Question 163

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

Answer 163

- 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 164

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

Answer 164

- 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 165

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

Answer 165

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

Question 166

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

Answer 166

- 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 167

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

Answer 167

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

Question 168

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

Answer 168

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

Question 169

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

Answer 169

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

Question 170

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

Answer 170

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

Question 171

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

Answer 171

- 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 172

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

Answer 172

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

Question 173

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

Answer 173

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

Question 174

MYASTHENIA GRAVIS What is the pathophysiology of myasthenia gravis?

Answer 174

- 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 175

MYASTHENIA GRAVIS What is the aetiology of myasthenia gravis?

Answer 175

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

Question 176

MYASTHENIA GRAVIS What is the main symptom of myasthenia gravis?

Answer 176

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

Question 177

MYASTHENIA GRAVIS What will patients with myasthenia gravis struggle with?

Answer 177

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

Question 178

MYASTHENIA GRAVIS What are the signs of myasthenia gravis?

Answer 178

- Ptosis, diplopia (extra-ocular muscle weakness)

Question 179

MYASTHENIA GRAVIS What are some clinical signs of myasthenia gravis?

Answer 179

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

Question 180

MYASTHENIA GRAVIS What antibodies are implicated in myasthenia gravis?

Answer 180

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

Question 181

MYASTHENIA GRAVIS What investigations would you do for myasthenia gravis?

Answer 181

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 182

MYASTHENIC CRISIS What is the main complication of myasthenia gravis?

Answer 182

- Myasthenic crisis

Question 183

MYASTHENIC CRISIS What are the causes of myasthenic crisis?

Answer 183

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

Question 184

MYASTHENIC CRISIS What is the management of myasthenic crisis?

Answer 184

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

Question 185

MYASTHENIA GRAVIS What is the management of myasthenia gravis?

Answer 185

- 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 186

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

Answer 186

- Acute inflammatory demyelinating polyneuropathy which targets Schwann cells

Question 187

GUILLAIN-BARRE What is the pathophysiology of GBS?

Answer 187

- 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 188

GUILLAIN-BARRE What is Miller-Fisher syndrome?

Answer 188

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

Question 189

GUILLAIN-BARRE What are the causes of GBS?

Answer 189

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

Question 190

GUILLAIN-BARRE What is the clinical presentation of GBS?

Answer 190

- 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 191

GUILLAIN-BARRE What are some differentials for GBS?

Answer 191

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

Question 192

GUILLAIN-BARRE What are the investigations for GBS?

Answer 192

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 193

GUILLAIN-BARRE What is the main treatment for GBS?

Answer 193

- 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 194

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

Answer 194

- 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 195

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

Answer 195

- 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 196

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

Answer 196

Personality + intellect change, hemiparesis, expressive dysphasia

Question 197

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

Answer 197

- 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 198

NEUROPATHY What are the peripheral nerve causes of muscle weakness?

Answer 198

- 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 199

NEUROPATHY What is the pathophysiology of mononeuritis multiplex?

Answer 199

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

Question 200

NEUROPATHY What are the causes of peripheral neuropathy?

Answer 200

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

Question 201

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

Answer 201

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

Question 202

NEUROPATHY What is Charcot-Marie-Tooth disease?

Answer 202

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

Question 203

NEUROPATHY What is the generic clinical presentation of mononeuropathy?

Answer 203

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

Question 204

NEUROPATHY What is the generic clinical presentation of peripheral neuropathy?

Answer 204

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

Question 205

NEUROPATHY What is the most common mononeuropathy?

Answer 205

- Carpal tunnel syndrome

Question 206

NEUROPATHY What muscles does the median nerve innervate?

Answer 206

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

Question 207

NEUROPATHY What is the clinical presentation of carpal tunnel syndrome?

Answer 207

- 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 208

NEUROPATHY What investigations can you do for carpal tunnel syndrome?

Answer 208

- 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 209

NEUROPATHY What is the management of carpal tunnel syndrome?

Answer 209

- Splinting - Analgesia - Local steroid injection ± decompression surgery

Question 210

NEUROPATHY What does a CN1 lesion cause?

Answer 210

- Anosmia

Question 211

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 211

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 212

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

Answer 212

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

Question 213

NEUROPATHY What does a CN3 lesion cause?

Answer 213

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

Question 214

NEUROPATHY What does a CN4 lesion cause?

Answer 214

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

Question 215

NEUROPATHY What does a CN5 lesion cause?

Answer 215

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

Question 216

NEUROPATHY What does a CN6 lesion cause?

Answer 216

- Issues abducting eye beyond midline as innervates lateral rectus

Question 217

NEUROPATHY What does a CN7 lesion cause?

Answer 217

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

Question 218

NEUROPATHY What is Bell's palsy?

Answer 218

- 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 219

NEUROPATHY What does a CN8 lesion cause?

Answer 219

- Sensorineural deafness - Tinnitus, vertigo, nystagmus

Question 220

NEUROPATHY What does a CN9/10 lesion cause?

Answer 220

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

Question 221

NEUROPATHY What does a CN11 lesion cause?

Answer 221

- Weakness turning head to contralateral side

Question 222

NEUROPATHY What does a CN12 lesion cause?

Answer 222

- Tongue deviation towards side of lesion

Question 223

NEUROPATHY What are the investigations used in neuropathy?

Answer 223

- 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 224

CORD COMPRESSION What is myelopathy?

Answer 224

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

Question 225

RADICULOPATHY How does radiculopathy present?

Answer 225

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

Question 226

CORD COMPRESSION What are the aetiologies of spinal cord compression?

Answer 226

- 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 227

CORD COMPRESSION What are the symptoms of spinal cord compression?

Answer 227

- 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 228

CORD COMPRESSION What are the signs of spinal cord compression?

Answer 228

- 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 229

CORD COMPRESSION How does degenerative cervical myelopathy present?

Answer 229

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

Question 230

CORD COMPRESSION What are the differentials for spinal cord compression?

Answer 230

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

Question 231

CORD COMPRESSION What are the investigations of spinal cord compression?

Answer 231

- 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 232

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

Answer 232

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

Question 233

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

Answer 233

- 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 234

CORD COMPRESSION What is the management of spinal cord compression?

Answer 234

- 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 235

SPINAL CORD INJURY What is Brown-Sequard syndrome?

Answer 235

- 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 236

ANTERIOR CORD SYNDROME What is anterior cord syndrome?

Answer 236

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

Question 237

SPINAL CORD INJURY What is posterior cord syndrome?

Answer 237

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

Question 238

SPINAL CORD INJURY What is central cord syndrome?

Answer 238

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

Question 239

MYOPATHY What are myopathies?

Answer 239

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

Question 240

MYOPATHY What are the aetiologies of myopathies?

Answer 240

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

Question 241

MYOPATHY How do myopathies present?

Answer 241

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

Question 242

MYOPATHY How does myotonic dystrophy present?

Answer 242

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

Question 243

MYOPATHY What are the investigations for myopathies?

Answer 243

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

Question 244

MYOPATHY What is the management of myopathies?

Answer 244

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

Question 245

MYOPATHY What is the general supportive management of myopathies?

Answer 245

- 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 246

HYDROCEPHALUS What is hydrocephalus?

Answer 246

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

Question 247

HYDROCEPHALUS What is the purpose of CSF?

Answer 247

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

Question 248

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

Answer 248

- 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 249

HYDROCEPHALUS What are the 3 types of hydrocephalus?

Answer 249

- 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 250

HYDROCEPHALUS What are some causes of obstructive hydrocephalus?

Answer 250

Tumour, acute haemorrhages, developmental abnormalities (aqueduct stenosis)

Question 251

HYDROCEPHALUS How does hydrocephalus present?

Answer 251

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

Question 252

HYDROCEPHALUS How does normal pressure hydrocephalus present?

Answer 252

'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 253

HYDROCEPHALUS What are the investigations for hydrocephalus?

Answer 253

- 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 254

HYDROCEPHALUS What is the management of hydrocephalus?

Answer 254

- 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 255

IIH What is idiopathic intracranial hypertension (IIH)?

Answer 255

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

Question 256

IIH What are the causes of IIH?

Answer 256

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

Question 257

IIH What is the clinical presentation of IIH?

Answer 257

- 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 258

IIH What are the investigations for IIH?

Answer 258

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

Question 259

IIH What is the management of IIH?

Answer 259

- #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 260

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

Answer 260

- 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 261

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

Answer 261

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 262

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

Answer 262

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

Question 263

NEURO PHARMACOLOGY What is the mechanism of action of Levodopa?

Answer 263

- 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 264

NEURO PHARMACOLOGY What are the side effects of Levodopa?

Answer 264

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

Question 265

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

Answer 265

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

Question 266

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 266

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

Question 267

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

Answer 267

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

Question 268

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

Answer 268

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

Question 269

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

Answer 269

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

Question 270

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

Answer 270

- 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 271

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

Answer 271

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

Question 272

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

Answer 272

- 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 273

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

Answer 273

- 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 274

ACUTE LABYRINTHITIS What is acute labyrinthitis?

Answer 274

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

Question 275

MENIERE'S DISEASE What is Ménières disease?

Answer 275

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

Question 276

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

Answer 276

- 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 277

STROKE What are the various classifications of strokes?

Answer 277

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

Question 278

SAH What are some risk factors for SAH?

Answer 278

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 279

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

Answer 279

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

Question 280

EDH What causes an EDH?

Answer 280

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

Question 281

EDH What are some complications of EDH?

Answer 281

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

Question 282

SDH what are the risk factors of SDH?

Answer 282

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

Question 283

EPILEPSY Define seizure

Answer 283

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

Question 284

EPILEPSY What is Todd's paresis?

Answer 284

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

Question 285

EPILEPSY What are the 4 main types of generalised seizure?

Answer 285

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

Question 286

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

Answer 286

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

Question 287

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

Answer 287

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

Question 288

NEAD What is NEAD?

Answer 288

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

Question 289

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

Answer 289

- 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 290

TRIGEMINAL NEURALGIA What are some triggers?

Answer 290

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

Question 291

MND What are some complications of MND?

Answer 291

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

Question 292

MULTIPLE SCLEROSIS What is benign MS?

Answer 292

Relapses + Remissions but overall progress will never worsen

Question 293

MULTIPLE SCLEROSIS What is primary progressive MS?

Answer 293

Gradually worsening of disease from point of diagnosis without any RR

Question 294

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

Answer 294

Neck flexion causes electric shock sensation down spine

Question 295

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

Answer 295

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

Question 296

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

Answer 296

- 2 relapses in past 2y

Question 297

MENINGITIS What are the aseptic causes of meningitis?

Answer 297

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

Question 298

ENCEPHALITIS What are the non-viral causes of encephalitis?

Answer 298

Bacterial meningitis TB Malaria Lyme’s disease

Question 299

BRAIN DEATH + COMA What is brain death?

Answer 299

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

Question 300

BRAIN DEATH + COMA What is a persistent vegetative state?

Answer 300

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

Question 301

MYASTHENIA GRAVIS What medications can exacerbate myasthenia gravis?

Answer 301

Abx, CCBs, beta-blockers, lithium + statins

Question 302

BRAIN TUMOURS How do acoustic neuromas present?

Answer 302

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

Question 303

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

Answer 303

Receptive dysphasia, amnesia

Question 304

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

Answer 304

Hemisensory loss, dysphasia

Question 305

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

Answer 305

Contralateral visual defects

Question 306

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

Answer 306

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

Question 307

NEUROPATHY What can cause mononeuritis multiplex?

Answer 307

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

Question 308

RADICULOPATHY What is radiculopathy?

Answer 308

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

Question 309

RADICULOPATHY What is the most common radiculopathy?

Answer 309

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

Question 310

MYOPATHY What are dystrophies?

Answer 310

If they're inherited = dystrophies

Question 311

MYOPATHY How do myopathies compare to neuropathies?

Answer 311

Weakness is proximal in muscle disease (nerves = distal)

Question 312

MENIERE'S DISEASE How does it present?

Answer 312

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 313

MENIERE'S DISEASE What causes it?

Answer 313

Idiopathic, trauma, endo

Question 314

MENIERE'S DISEASE How is it managed?

Answer 314

Bed rest, reassurance

Question 315

ACUTE LABYRINTHITIS How does it present?

Answer 315

- 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 316

ACUTE LABYRINTHITIS What are the causes?

Answer 316

Usually viral, ?vascular lesion

Question 317

CEREBRAL PALSY what are the causes?

Answer 317

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

Question 318

CEREBRAL PALSY what are the symptoms?

Answer 318

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

Question 319

CEREBRAL PALSY what are the investigations?

Answer 319

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

Question 320

CEREBRAL PALSY what is the management?

Answer 320

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

Question 321

BELL'S PALSY what are the causes?

Answer 321

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

Question 322

BELL'S PALSY what is the pathophysiology?

Answer 322

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

Question 323

BELL'S PALSY what are the symptoms?

Answer 323

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

Question 324

BELL'S PALSY what is the management?

Answer 324

- corticosteroid - eye drops - ?antivrials

Question 325

BELL'S PALSY what are the investigations?

Answer 325

- can be clinical diagnosis - ENoG - needle EMG

Question 326

NEUROFIBROMATOSIS what are the clinical signs of NF1?

Answer 326

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

Question 327

NEUROFIBROMATOSIS what are the clincial signs of NF2?

Answer 327

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

Question 328

NEUROFIBROMATOSIS what are the causes of neurofibromatosis 1 and 2?

Answer 328

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

Question 329

NEUROFIBROMATOSIS what is the treatment for NF1 and NF2?

Answer 329

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

Question 330

NARCOLEPSY what are the clinical features?

Answer 330

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

Question 331

NARCOLEPSY what are the investigations?

Answer 331

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

Question 332

NARCOLEPSY what is the management?

Answer 332

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

Question 333

CORD COMPRESSION How is spinal stenosis managed?

Answer 333

MRI + canal decompression surgery

Question 334

CORD COMPRESSION How does spinal stenosis present?

Answer 334

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

Question 335

RADICULOPATHY what are the causes?

Answer 335

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

Question 336

RADICULOPATHY what is the management?

Answer 336

analgesia - amitryptyline, pregabalin, gabapentin physiotherapy surgery in emergencies

Question 337

RADICULOPATHY what is the management?

Answer 337

analgesia - amitryptyline, pregabalin, gabapentin physiotherapy surgery in emergencies

Question 338

WERNICKE-KORSAKOFF SYNDROME what is it?

Answer 338

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

Question 339

WERNICKE-KORSAKOFF SYNDROME what are the clinical signs?

Answer 339

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

Question 340

WERNICKE-KORSAKOFF SYNDROME what is the cause?

Answer 340

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

Question 341

WERNICKE-KORSAKOFF SYNDROME what is the management?

Answer 341

B1 (thiamine) replacement and proper nutrition/hydration

Question 342

MYASTHENIC CRISIS What are the clinical features?

Answer 342

- Resp failure or death

Question 343

MYASTHENIC CRISIS what are the complications?

Answer 343

Resp failure or death

Question 344

CATAPLEXY what is it?

Answer 344

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

Question 345

CATAPLEXY what happens during an attack?

Answer 345

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

Question 346

CATAPLEXY what are the causes?

Answer 346

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

Question 347

CATAPLEXY what is the management?

Answer 347

sodium oxybate tricyclic antidepressants (clomipramine) SSRIs

Question 348

SAH what is the appearance of SAH on CT head?

Answer 348

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

Question 349

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

Answer 349

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

Question 350

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

Answer 350

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

Question 351

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

Answer 351

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

Question 352

EPILEPSY What is the emergency treatment for epilepsy?

Answer 352

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

Question 353

EPILEPSY what is the treatment for generalised myoclonic epilepsy?

Answer 353

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

Question 354

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

Answer 354

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

Question 355

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

Answer 355

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

Question 356

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

Answer 356

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

Question 357

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

Answer 357

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

Question 358

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

Answer 358

Abnormal eye movements Dysarthria Dysphagia Rigidity Ataxia

Question 359

HEADACHES What is the prophylactic management of cluster headaches?

Answer 359

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

Question 360

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

Answer 360

Nausea Photophobia Phonophobia Aura

Question 361

MIGRAINE What is the diagnostic criteria for a migraine?

Answer 361

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 362

MIGRAINE How does triptan work?

Answer 362

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

Question 363

MND does MND affect UMN or LMN?

Answer 363

both UMN and LMN can be affected

Question 364

MND Does MND cause sensory loss or sphincter disturbance?

Answer 364

No (clinical feature of MS)

Question 365

MND What are LMN signs?

Answer 365

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

Question 366

MND What is the diagnostic criteria for MND?

Answer 366

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

Question 367

MULTIPLE SCLEROSIS What are the differential diagnosis’s of MS

Answer 367

SLE Sjogren’s AIDS Syphilis

Question 368

MENINGITIS What are the bacterial causes of meningitis in neonates?

Answer 368

E.coli Group B strep - strep agalactiae

Question 369

MENINGITIS What can cause meningitis in immunocompromised patients?

Answer 369

CMV Cryptococcus TB HIV herpes simplex

Question 370

MENINGITIS Give 4 potential adverse effect of a lumbar puncture

Answer 370

Headache Paraesthesia CSF leak Damage to spinal cord

Question 371

ENCEPHALITIS Name the main triad of symptoms of encephalitis

Answer 371

Fever + headache + altered mental state

Question 372

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

Answer 372

Pregnancy Hypokalaemia Infection Emotion Exercise Drugs

Question 373

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

Answer 373

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

Question 374

NEUROPATHY What is the generic clinical presentation of mononeuritis multiplex?

Answer 374

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

Question 375

NEUROPATHY What is the pathophysiology of carpal tunnel syndrome?

Answer 375

Inflammation of carpal tunnel leads to entrapment of the median nerve

Question 376

NEUROPATHY What are the causes of carpal tunnel syndrome?

Answer 376

Idiopathic but associated with local tumours, DM + RA

Question 377

ANTERIOR CORD SYNDROME what are the causes?

Answer 377

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

Question 378

ANTERIOR CORD SYNDROME what are the symptoms?

Answer 378

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

Question 379

ANTERIOR CORD SYNDROME what are the investigations?

Answer 379

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

Question 380

ANTERIOR CORD SYNDROME what is the treatment?

Answer 380

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

Question 381

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

Answer 381

unilateral damage to the sympathetic chain

Question 382

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

Answer 382

unilateral damage to the sympathetic chain

Question 383

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

Answer 383

stroke, tumours of hypothalamus, spinal cord lesions

Question 384

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

Answer 384

tumours of upper chest cavity, trauma to the neck

Question 385

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

Answer 385

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

Question 386

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

Answer 386

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

Question 387

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

Answer 387

clinical examination MRI - detect lesions

Question 388

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

Answer 388

treat underlying cause

Question 389

BULBAR PALSY what is it?

Answer 389

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 390

BULBAR PALSY what ar ethe causes?

Answer 390

- brainstem tumours and strokes - ALS - GBS

Question 391

BULBAR PALSY what are the causes?

Answer 391

- brainstem tumours and strokes - ALS - GBS

Question 392

BULBAR PALSY what are the symptoms?

Answer 392

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

Question 393

BULBAR PALSY what are the investigations?

Answer 393

MRI lumbar puncture

Question 394

BULBAR PALSY what is the treatment?

Answer 394

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

Question 395

STRABISMUS what is it?

Answer 395

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 396

STRABISMUS what are the causes?

Answer 396

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

Question 397

STRABISMUS what are the symptoms?

Answer 397

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

Question 398

STRABISMUS what are the risk factors?

Answer 398

FHx of strabismus prematurity low birth weight maternal smoking during pregnancy

Question 399

STRABISMUS what are the investigations?

Answer 399

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

Question 400

STRABISMUS what is the management?

Answer 400

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

Question 401

SCIATICA what is it?

Answer 401

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

Question 402

SCIATICA how is the pain from sciatica described?

Answer 402

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

Question 403

SCIATICA what are the risk factors?

Answer 403

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

Question 404

SCIATICA what are the causes?

Answer 404

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

Question 405

SCIATICA what are the symptoms?

Answer 405

- 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 406

SCIATICA what are the investigations?

Answer 406

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

Question 407

SCIATICA what is the management?

Answer 407

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

Question 408

RAISED ICP what are the causes?

Answer 408

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

Question 409

RAISED ICP what are the symptoms?

Answer 409

- 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 410

RAISED ICP what are the investigations?

Answer 410

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

Question 411

RAISED ICP what is the management?

Answer 411

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

Question 412

MYOPATHY what is myotonic dystrophy?

Answer 412

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

Question 413

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

Answer 413

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

Question 414

TIA what are the differential diagnosis’s for a TIA

Answer 414

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

Question 415

TIA what is the ABCD2 score?

Answer 415

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 416

TIA What is the treatment for a TIA?

Answer 416

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 417

HYDROCEPHALUS what are the causes of normal pressure hydrocephalus?

Answer 417

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

Question 418

CHRONIC FATIGUE SYNDROME what is it?

Answer 418

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 419

CHRONIC FATIGUE SYNDROME What are the causes?

Answer 419

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

Question 420

CHRONIC FATIGUE SYNDROME what are the risk factors?

Answer 420

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

Question 421

CHRONIC FATIGUE SYNDROME what are the symptoms?

Answer 421

- 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 422

CHRONIC FATIGUE SYNDROME what are the differentials?

Answer 422

mononucleosis lyme disease MS SLE hypothyroidism fibromyalgia depression sleep disorders

Question 423

CHRONIC FATIGUE SYNDROME what are the investigations?

Answer 423

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

Question 424

CHRONIC FATIGUE SYNDROME what is the management?

Answer 424

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

Question 425

ESSENTIAL TREMOR what is it?

Answer 425

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 426

ESSENTIAL TREMOR what is the presentation?

Answer 426

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

Question 427

ESSENTIAL TREMOR what are the investigations?

Answer 427

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

Question 428

ESSENTIAL TREMOR what is the management?

Answer 428

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

Question 429

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

Answer 429

vertigo hearing loss - worse during attacks tinnitus

Question 430

STROKE what is the primary prevention of strokes?

Answer 430

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

Question 431

STROKE what is the secondary prevention of strokes?

Answer 431

2 weeks of aspirin --> long term clopidogrel

Question 432

SAH give 3 possible complications of a subarachnoid haemorrhage

Answer 432

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

Question 433

SDH what are the differential diagnoses for a subdural haematoma?

Answer 433

stroke dementia CNS masses (tumour vs abscess)

Question 434

EPILEPSY what is the diagnostic criteria for eilespy?

Answer 434

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

Question 435

EPILEPSY how do lamotrigine and carbamazepine work?

Answer 435

Inhibit pre-synaptic Na+ channels so prevent axonal firing

Question 436

EPILEPSY how does sodium valproate work?

Answer 436

Inhibits voltage gated Na+ channels and increases GABA production

Question 437

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

Answer 437

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

Question 438

PARKINSONS DISEASE what is the pathway for dopamine production?

Answer 438

Tyrosine --> L-dopa --> Dopamine

Question 439

HYDROCEPHALUS What are some causes of non-obstructive hydrocephalus?

Answer 439

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

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

DIABETIC NEUROPATHY what is the management of neuropathic pain?

Answer 442

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

Question 443

DIABETIC NEUROPATHY what are the effects on the GI system?

Answer 443

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

Question 444

DIABETIC NEUROPATHY what is the management for gastroparesis?

Answer 444

metoclopramide, domperidone or erythromycin