NEURO Flashcards

Question 1

Q

STROKE

What is a stroke?

Answer

A

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

Question 2

Q

STROKE

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

Answer

A

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

Question 3

Q

STROKE

What are the causes of ischaemic strokes?

Answer

A

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

Question 4

Q

STROKE

What are the causes of haemorrhagic stroke?

Answer

A

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

Question 5

Q

STROKE

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

Answer

A

Charcot-Bouchard aneurysms most often in the basal ganglia

Question 6

Q

STROKE

What are the risk factors for strokes?

Answer

A

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

Question 7

Q

STROKE

What are some important differentials of stroke?

Answer

A

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

Question 8

Q

STROKE
What classification system can be used for strokes?
What are the various components?

Answer

A

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

Question 9

Q

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

Answer

A

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

Question 10

Q

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

Answer

A

ACA, MCA, carotid (same vessels as TACS)

- 2/3 of the criteria for TACS

Question 11

Q

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

Answer

A

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

Question 12

Q

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

Answer

A

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

Question 13

Q

STROKE

How would an ACA stroke present?

Answer

A

Contralateral lower limb hemiparesis + loss of sensation

- Gait apraxia (unable to initiate walking)

Question 14

Q

STROKE

How would a MCA stroke present?

Answer

A

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

Question 15

Q

STROKE

How would a PCA stroke present?

Answer

A

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

Question 16

Q

STROKE

How would a brainstem/basilar artery infarct present?

Answer

A

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

Question 17

Q

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

Answer

A

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

Question 18

Q

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

Answer

A

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

Question 19

Q

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

Answer

A

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

Question 20

Q

STROKE

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

Answer

A

ABCD2

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

Question 21

Q

STROKE

What do the scores from ABCD2 mean?

Answer

A

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

Question 22

Q

STROKE

What tools can be used to identify stroke?

Answer

A

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

Question 23

Q

STROKE

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

Answer

A

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

Question 24

Q

STROKE

How would an ischaemic stroke appear on CT head?

Answer

A

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

Question 25

Q

STROKE

How would a haemorrhagic stroke appear on CT head?

Answer

A

Acute = hyperdense
Subacte = isodense
Chronic = hypodense

Question 26

Q

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

Answer

A

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

Question 27

Q

STROKE

What bloods may be taken in suspected stroke?

Answer

A

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

Question 28

Q

STROKE

What other investigations may you do in stroke?

Answer

A

ECG 72h tape to look for paroxysmal AF, MI.
ECHO to check for endocarditis or CHD
CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis

Question 29

Q

STROKE

What are some potential complications following a stroke?

Answer

A

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

Question 30

Q

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

Answer

A

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

Question 31

Q

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

Answer

A

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

Question 32

Q

STROKE

What are some contraindications to treatment with alteplase?

Answer

A

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

Question 33

Q

STROKE

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

Answer

A

Thrombectomy (mechanical retrieval of clot)
Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue

Question 34

Q

STROKE

What other management is given for ischaemic strokes?

Answer

A

Control BP

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

Question 35

Q

STROKE

What is the management of a haemorrhagic stroke?

Answer

A

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

Question 36

Q

STROKE

What lifestyle advice should be given post-stroke?

Answer

A

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

Question 37

Q

STROKE

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

Answer

A

Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
Anticoagulation if have AF but wait 2w post-stroke
Manage co-morbidities (HTN, DM)
Cholesterol >3.5mmol/L diet + 80mg atorvastatin
VTE assessment + monitor for infection

Question 38

Q

STROKE

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

Answer

A

CHA2DS2-VaSc (risk of stroke due to AF)

- HAS-BLED (risk of serious bleeding)

Question 39

Q

STROKE

What is the CHA2DS2-VaSc score

Answer

A

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

Question 40

Q

STROKE

What is the HAS-BLED score?

Answer

A

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

Question 41

Q

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

Answer

A

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

Question 42

Q

STROKE

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

Answer

A

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

Question 43

Q

SAH

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

Answer

A

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

Question 44

Q

SAH

What is the most common cause of SAH?

Answer

A

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

Question 45

Q

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

Answer

A

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

Question 46

Q

SAH

What are some symptoms of SAH?

Answer

A

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

Question 47

Q

SAH

What are some signs of SAH?

Answer

A

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

Question 48

Q

SAH

What are some complications of SAH?

Answer

A

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

Question 49

Q

SAH

What is often associated with better outcomes in SAH?

Answer

A

GCS >12 on arrival

Question 50

Q

SAH

What are some important investigations for SAH?

Answer

A

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

Question 51

Q

SAH

What is the management of SAH?

Answer

A

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

Question 52

Q

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

Answer

A

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

Question 53

Q

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

Answer

A

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

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

Question 54

Q

EDH

What is the natural clinical presentation of EDH?

Answer

A

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

Question 55

Q

EDH
In the natural clinical presentation of EDH…

i) what are the signs of ICP ± focal neurology?
ii) what is Cushing’s reflex?

Answer

A

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

Question 56

Q

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

Answer

A

Epilepsy, CO poisoning, carotid dissection

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

Question 57

Q

EDH

What are the investigations for EDH?

Answer

A

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

Question 58

Q

EDH

What investigation is contraindicated in EDH and why?

Answer

A

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

Question 59

Q

EDH

What is the management for EDH?

Answer

A

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

Question 60

Q

SDH

What is the pathophysiology of subdural haematoma (SDH)?

Answer

A

Rupture of a vein running from hemisphere to the sagittal sinus of the dural venous sinuses (bridging veins) that’s beneath the dura leading to haematoma between arachnoid + dura mater

Question 61

Q

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

Answer

A

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

Question 62

Q

SDH

What are the symptoms of SDH?

Answer

A

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

Question 63

Q

SDH

What are some signs of SDH?

Answer

A

Raised ICP, seizures

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

Question 64

Q

SDH

What are the investigations for SDH?

Answer

A

Non-contrast CT head shows crescent/concave shaped haematoma ± midline shift –

Acute/subacute (<14d) = hyperdense (white)
Chronic (>14d) = hypodense (darker)
Acute-on-chronic (rebleed) = both/mixture
Haematoma is NOT limited by cranial sutures

Answer 65

A

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

Answer 66

A

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

Answer 67

A

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

Answer 68

A

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

Answer 69

A

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

Answer 70

A

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

Answer 71

A

i) Starts on one side of body then “marches” over a few seconds to affect larger parts of body like entire hand, foot or facial muscles + may generalise
ii) Focal weakness in a part or all of the body after a seizure

Answer 72

A

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

Answer 73

A

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

Answer 74

A

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

Answer 75

A

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

Answer 76

A

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

Answer 77

A

Cardiac = postural or cardiogenic syncope

- Non-epileptic attack disorder, hypoglycaemia, TIA

Answer 78

A

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

Answer 79

A

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

Answer 80

A

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

Answer 81

A

i) 1st line = ethosuximide or sodium valproate

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

Answer 82

A

Cannot drive for 6m following seizure + must inform DVLA

- Established epilepsy must be seizure free for 12m before driving

Answer 83

A

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

Answer 84

A

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

Answer 85

A

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

Answer 86

A

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

Answer 87

A

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

Answer 88

A

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

Answer 89

A

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

Answer 90

A

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

Answer 91

A

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

Answer 92

A

CRASH

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

Answer 93

A

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*

Answer 94

A

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)

Answer 95

A

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

Answer 96

A

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

Answer 97

A

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

Answer 98

A

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

Answer 99

A

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

Answer 100

A

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

Answer 101

A

No driving until cause known or until blackout free for 1y
Treat underlying cause
NEAD = correct Dx vital, speak to pt, reassure them, wait for seizure to pass, CBT, avoid AEDs as can be fatal if mistreated excessively (respiratory depression)

Answer 102

A

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

Answer 103

A

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

Answer 104

A

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)

Answer 105

A

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

Answer 106

A

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

Answer 107

A

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

Answer 108

A

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

Answer 109

A

Asymmetrical vs symmetrical
4–6Hz vs 5–8Hz
Worse at rest vs improves at rest
Improves with intentional movement vs worse with intentional movement
No change with alcohol vs improves with alcohol (also Rx = propranolol)
Parkinson’s vs. autosomal dominant condition

Answer 110

A

Parkinson’s plus syndromes –

Progressive supranuclear palsy
Multiple system atrophy
Lewy Body dementia
Corticobasal degeneration

Answer 111

A

Early falls, cognitive decline or both sides being equally affected
Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
Impaired vertical gaze (down worse = issues reading or descending stairs)
Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes

Answer 112

A

Neurones in multiple systems in the brain degenerate
Degeneration in basal ganglia > Parkinsonism
Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction

Answer 113

A

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

Answer 114

A

Early myoclonic jerks, gait apraxia, agnosia + alien limb

Answer 115

A

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

Answer 116

A

Infections
Falls
Depression
Aspiration pneumonia

Answer 117

A

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

Answer 118

A

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

Answer 119

A

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

Answer 120

A

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

Answer 121

A

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

Answer 122

A

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

Answer 123

A

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

Answer 124

A

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

Answer 125

A

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

Answer 126

A

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

Answer 127

A

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

Answer 128

A

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

Answer 129

A

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

Answer 130

A

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

Answer 131

A

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

Answer 132

A

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

Answer 133

A

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

Answer 134

A

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

Answer 135

A

Nasal irrigation w/ saline

- Prolonged Sx with steroid nasal spray

Answer 136

A

Immediate expert help + IV acetazolamide (carbonic anhydrase inhibitor)

Answer 137

A

Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly

Answer 138

A

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

Answer 139

A

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

Answer 140

A

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

Answer 141

A

Carbamazepine 1st line

- If fails, microvascular decompression or stereotactic radiotherapy

Answer 142

A

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

Answer 143

A

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

Answer 144

A

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

Answer 145

A

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

Answer 146

A

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

Answer 147

A

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

Answer 148

A

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

Answer 149

A

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

Answer 150

A

Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex

Answer 151

A

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

Answer 152

A

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

Answer 153

A

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

Answer 154

A

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

Answer 155

A

Same as without but –

Sparks/zig-zag lines in vision, blurred vision or loss of different visual fields
Aura usually unilateral + lasts up to 60m before headache

Answer 156

A

i) Migraine with aura but no headache

ii) Can mimic a stroke with typical migraine Sx, sudden/gradual onset, hemiplegia, ataxia + changes in consciousness

Answer 157

A

Mostly clinical Dx

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

Answer 158

A

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

Answer 159

A

Propranolol or topiramate are first line
Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
Also, amitriptyline, botulinum toxin or acupuncture.
400mg OD of riboflavin (B2) may help
NOT gabapentin
Avoid indentified triggers (?headache diary)

Answer 160

A

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

Answer 161

A

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

Answer 162

A

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

Answer 163

A

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

Answer 164

A

Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
Primarily affects muscles of talking, chewing, tongue palsy + swallowing
Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations

Answer 165

A

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

Answer 166

A

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

Answer 167

A

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

Answer 168

A

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

Answer 169

A

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

Answer 170

A

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

Answer 171

A

Riluzole – Na+ blocker inhibits glutamate release

- Not curative but aims to increase survival by 2–3m + increase their time before needing ventilation

Answer 172

A

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

Answer 173

A

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

Answer 174

A

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

Answer 175

A

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

Answer 176

A

Periventricular white matter lesions

- Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles

Answer 177

A

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

Answer 178

A

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

Answer 179

A

Relapsing remitting (most common)
Secondary progressive
Primary progressive
Benign

Answer 180

A

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

Answer 181

A

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

Answer 182

A

McDonald criteria –

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

Answer 183

A

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

Answer 184

A

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

Answer 185

A

UMN = spastic paraparesis, brisk reflexes, hypertonia
Sensory = loss of sensation, cerebellar signs
Relative afferent pupillary defect
Internuclear ophthalmoplegia
Optic atrophy (pale optic disc) in chronic MS

Answer 186

A

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

Answer 187

A

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

Answer 188

A

MRI head + spinal cord to show demyelination plaques = diagnostic
Lumbar puncture may show oligoclonal bands of IgG on CSF electrophoresis
Evoked potentials = delayed visual, auditory + somatosensory potentials

Answer 189

A

IV methylprednisolone

- Shortens acute relapses but no overall effect on prognosis

Answer 190

A

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

Answer 191

A

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

Answer 192

A

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

Answer 193

A

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

Answer 194

A

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

Answer 195

A

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

Answer 196

A

Meningism
+ve Kernig’s = pain or unable to extend leg at knee when it’s bent
+ve Brudzinski = involuntary flexion of hips + knees when neck flexed
Non-blanching purpuric rash = later sign in meningococcal septicaemia

Answer 197

A

Malaria
Encephalitis
SAH
Septicaemia
Tetanus
Dengue fever

Answer 198

A

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

Answer 199

A

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

Answer 200

A

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

Answer 201

A

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

Answer 202

A

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

Answer 203

A

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

Answer 204

A

IM benzylpenicillin

Answer 205

A

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

Answer 206

A

Supportive therapy mainly

- IV aciclovir for HSV

Answer 207

A

Childhood vaccination schedule

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

Answer 208

A

Public Health England immediately as notifiable disease

Answer 209

A

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

Answer 210

A

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

Answer 211

A

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

Answer 212

A

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

Answer 213

A

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

Answer 214

A

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

Answer 215

A

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

Answer 216

A

Pus-filled swelling in the brain

- Staph. aureus + strep. pnuemoniae

Answer 217

A

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

Answer 218

A

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

Answer 219

A

CT head shows ring-enhancing lesion ± surrounding oedema

- LP is contraindicated due to raised ICP

Answer 220

A

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

Answer 221

A

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

Answer 222

A

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

Answer 223

A

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

Answer 224

A

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

Answer 225

A

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

Answer 226

A

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

Answer 227

A

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

Answer 228

A

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

Answer 229

A

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

Answer 230

A

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

Answer 231

A

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

Answer 232

A

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

Answer 233

A

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

Answer 234

A

Decerebrate posturing – arms + legs extended, head extension, plantar flexion, internal rotation, pt rigid with teeth clenched
Indicates brainstem damage + so lesions in cerebellum or midbrain

Answer 235

A

Uncal (transtentorial) or tonsillar brain herniation ‘coning’

Answer 236

A

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

Answer 237

A

Autoimmune disorder against acetylcholine receptors in the neuromuscular junction

Answer 238

A

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

Answer 239

A

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

Answer 240

A

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

Answer 241

A

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

Answer 242

A

Ptosis, diplopia (extra-ocular muscle weakness)

- Abx, CCBs, beta-blockers, lithium + statins

Answer 243

A

Repeated blinking = ptosis

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

Answer 244

A

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

Answer 245

A

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

Answer 246

A

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

Answer 247

A

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

Answer 248

A

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

Answer 249

A

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

Answer 250

A

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

Answer 251

A

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

Answer 252

A

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

Answer 253

A

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

Answer 254

A

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

Answer 255

A

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

Answer 256

A

Acute inflammatory demyelinating polyneuropathy which targets Schwann cells

Answer 257

A

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

Answer 258

A

GBS variant which affects CNS + eye muscles

- Characterised by ophthalmoplegia + ataxia

Answer 259

A

Often triggered by preceding illness 4w before symptoms

- Campylobacter jejuni (v common), CMV, EBV

Answer 260

A

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

Answer 261

A

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

Answer 262

A

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

Answer 263

A

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

Answer 264

A

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

Answer 265

A

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

Answer 266

A

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

Answer 267

A

Gliomas
Meningiomas
Pituitary tumours
Acoustic neuromas (vestibular Schwannomas)

Answer 268

A

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

Answer 269

A

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

Answer 270

A

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

Answer 271

A

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

Answer 272

A

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)

Answer 273

A

Mass effect of tumour + surrounding cerebral oedema as it grows

Answer 274

A

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

Answer 275

A

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

Answer 276

A

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

Answer 277

A

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

Answer 278

A

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

Answer 279

A

Dysfunction/disease of the nerves typically causing weakness or numbness

Answer 280

A

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

Answer 281

A

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

Answer 282

A

ABCDE –

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

Answer 283

A

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

Answer 284

A

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

Answer 285

A

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

Answer 286

A

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

Answer 287

A

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

Answer 288

A

LLOAF –

Lateral lumbricals x2
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis

Answer 289

A

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)

Answer 290

A

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

Answer 291

A

Splinting
Analgesia
Local steroid injection ± decompression surgery

Answer 292

A

C7–T1

- Elbow trauma or fracture, elbow arthritis

Answer 293

A

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

Answer 294

A

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

Answer 295

A

Sensory loss 1.5 fingers ulnar side on dorsal + palmar aspects

Answer 296

A

C5-T1

- Compression against humerus

Answer 297

A

Wrist + finger drop (weak extension), can’t open first

- Below fingertips on radial 3.5 fingers dorsally, part of thenar eminence

Answer 298

A

Trauma, radiotherapy or heavy rucksack

- Pain, paraesthesia + weakness in affected arm in variable distribution

Answer 299

A

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

Answer 300

A

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

Answer 301

A

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

Answer 302

A

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

Answer 303

A

L4–S3

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

Answer 304

A

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

Answer 305

A

Parietal lobe
Temporal lobe
PITS – Parietal Inferior Temporal Superior

Answer 306

A

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

Answer 307

A

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

Answer 308

A

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

Answer 309

A

Issues abducting eye beyond midline as innervates lateral rectus

Answer 310

A

Face, ear, taste, tear –

Muscles of expression
Stapedius
Anterior 2/3rd tongue
Parasympathetic fibres to lacrimal + salivary glands

Answer 311

A

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

Answer 312

A

Sensorineural deafness

- Tinnitus, vertigo, nystagmus

Answer 313

A

Swallow, gag + cough issues

- Uvula deviated away from side of lesion

Answer 314

A

Weakness turning head to contralateral side

Answer 315

A

Tongue deviation towards side of lesion

Answer 316

A

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

Answer 317

A

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

Answer 318

A

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

Answer 319

A

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

Answer 320

A

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

Answer 321

A

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)

Answer 322

A

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

Answer 323

A

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

Answer 324

A

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

Answer 325

A

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

Answer 326

A

Cauda equina syndrome

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

Answer 327

A

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

Answer 328

A

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

Answer 329

A

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

Answer 330

A

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

Answer 331

A

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

Answer 332

A

Trauma or posterior spinal artery occlusion

- Loss of fine touch, proprioception + vibration (DCML)

Answer 333

A

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

Answer 334

A

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

Answer 335

A

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

Answer 336

A

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

Answer 337

A

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

Answer 338

A

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

Answer 339

A

CRP/ESR, creatinine kinase elevated

- Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy

Answer 340

A

Remove causative agent (statins, steroids)

- Immunosuppression (steroids, azathioprine) if inflammatory cause.

Answer 341

A

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

Answer 342

A

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

Answer 343

A

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

Answer 344

A

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

Answer 345

A

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

Answer 346

A

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

Answer 347

A

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

Answer 348

A

‘Wet, wacky, wobbly’ –

Urinary incontinence, dementia + abnormal gait (apraxia)
Sx come on gradually + similar to Alzheimer’s so difficult to diagnose

Answer 349

A

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)

Answer 350

A

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

Answer 351

A

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

Answer 352

A

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

Answer 353

A

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

Answer 354

A

Routine bloods + CT head to exclude organic causes

- LP to exclude infection = increased opening pressure (can be therapeutic)

Answer 355

A

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

Answer 356

A

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

Answer 357

A

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

Answer 358

A

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

Answer 359

A

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

Answer 360

A

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

Answer 361

A

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

Answer 362

A

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

Answer 363

A

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

Answer 364

A

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

Answer 365

A

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

Answer 366

A

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

Answer 367

A

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

Answer 368

A

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

Answer 369

A

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

Answer 370

A

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

Answer 371

A

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

Answer 372

A

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

Answer 373

A

Optic neuritis
Retinal detachment
Acute angle closure glaucoma

Answer 374

A

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

Answer 375

A

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

Answer 376

A

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

Answer 377

A

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

Answer 378

A

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

Answer 379

A

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

Answer 380

A

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

Answer 381

A

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

Answer 382

A

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

Answer 383

A

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

Answer 384

A

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

Answer 385

A

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

Answer 386

A

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

Answer 387

A

Pulmonary retroperitoneal + cardiac fibrosis

- Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)

Answer 388

A

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

Answer 389

A

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

Answer 390

A

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

Answer 391

A

Dizziness, dry mouth, sleepy, nausea

- C/I in CVD

Answer 392

A

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

Answer 393

A

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

Answer 394

A

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

Answer 395

A

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

Answer 396

A

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

Answer 397

A

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

Answer 398

A

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

Answer 399

A

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

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