1
Q
Main indications for awake craniotomy?
A
Brain tumour excision, epilepsy surgery, DBS, AVMs/mycotic aneurysms.
2
Q
Two key advantages of awake craniotomy?
A
Maximises lesion removal with improved survival, shorter hospitalisation time
3
Q
Absolute contraindications?
A
Patient refusal, inability to cooperate, inability to remain still.
4
Q
Relative contraindications?
A
Severe anxiety, LD/young age, chronic cough/OSA, inability to lie flat.
5
Q
Two surgical contraindications?
A
Highly vascular lesion, significant dural involvement, low occipital lesion.
6
Q
Which nerves are blocked in a scalp block?
A
Supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, greater/lesser occipital, great auricular.
7
Q
Two main anaesthetic techniques?
A
Asleep–awake–asleep, sedation with scalp block.
8
Q
Advantages of dexmedetomidine?
A
Analgesic, minimal resp depression, minimal ICP effect, sedative/anxiolytic.
9
Q
Disadvantage of dexmedetomidine?
A
Bradycardia, hypotension, user unfamiliarity.
10
Q
How do you manage an intra-op seizure?
A
Stop procedure, irrigate with cold saline, rapid A–E, give midazolam 2–5 mg IV or propofol 10–30 mg IV.
11
Q
Effect of seizure-terminating drugs on mapping?
A
Benzos suppress epileptiform discharges, propofol variably alters cortical excitability.
12
Q
Four specific complications of awake craniotomy?
A
Anxiety/distress, venous air embolism, ineffective LA, new focal neurological deficit.
13
Q
Key intra-op anaesthetic goals?
A
Maximise comfort, prevent N&V, maintain haemodynamic stability, use short-acting drugs.
14
Q
Post-op care priorities?
A
Neuro-HDU admission, monitor for haematoma/seizures/deficits, multimodal analgesia, psychological support.
15
Q
List three presenting features of SAH.
A
Sudden occipital headache, reduced consciousness, focal neurology, seizures, cardiac arrest, meningism.
16
Q
List three genetic conditions increasing risk of intracranial aneurysm
A
DPKD, Ehlers–Danlos IV, Marfan’s, hereditary haemorrhagic telangiectasia.
17
Q
List three modifiable risk factors for aneurysm bleeding.
A
Hypertension, smoking, cocaine use, alcohol, trauma, arteriosclerosis, aneurysm size.
18
Q
What systolic BP range is acceptable in acute SAH?
A
19
Q
List three neurological complications of acute SAH.
A
Re-bleeding, vasospasm/ischemia, hydrocephalus, seizures, cerebral oedema, death.
20
Q
Role of nimodipine after SAH.
A
Reduces risk of delayed cerebral ischaemia/vasospasm.
21
Q
Three complications of endovascular coiling.
A
Vascular access bleeding/infection/pseudoaneurysm, intracranial vessel injury, aneurysm rupture, thromboembolism, incomplete coiling.
22
Q
Key goals during induction for aneurysm surgery.
A
Smooth, haemodynamically stable, avoid ↑BP/↑ICP, avoid coughing/straining.
23
Q
Key goals at emergence in aneurysm surgery.
A
Smooth, avoid coughing/straining, consider delayed extubation.
24
Q
Arterial supply to the spinal cord?
A
1 anterior spinal artery (ant 2/3, vertebral), 2 posterior spinal arteries (post 1/3, vertebral), segmental arteries (vertebral, deep cervical, intercostal, aortic, pelvic).
25
How does anaesthesia affect IONM?
NMBD abolish MEP/EMG → avoid after intubation; volatiles ↓ amplitude → use TIVA; ketamine ↑ amplitude; alpha-2 agonists ↓ amplitude.
26
Physiological strategies to reduce neuro injury in cervical spine surgery?
Avoid hypoxia/hypercapnia, maintain MAP, replace blood loss, maintain acid–base balance, maintain normothermia.
27
Three complications of cervical spinal injury?
Cord/root injury, airway compromise from haematoma, infection (discitis/abscess/meningitis), CSF leak, injury to oesophagus/trachea/vessels/nerves.
28
Six complications of GA in prone?
Airway: accidental extubation, oedema Resp: ↓lung expansion if abdomen compressed CVS: IVC compression, loss of IV access Neuro: abnormal neck position → drainage issues, peripheral nerve injury Skin/MSK: pressure sores (face, breast, genitalia, femoral triangle) GI: reflux, eye irritation from regurgitation
29
Types of spinal cord monitoring?
SSEP, MEP, EMG, EEG, wake-up test.
30
Anaesthetic considerations with spinal cord monitoring?
TIVA, avoid NMBD, ≤0.5 MAC volatile if used, avoid N₂O.
31
Drugs that influence IONM signals?
Ketamine ↑ signals; alpha-2 agonists ↓ MEP.
32
MAP targets in spine surgery?
≥65–75 mmHg generally; ≥80–90 if myelopathy, cord injury, or signal loss.
33
How to minimise blood loss in long spinal fusion?
TXA, free abdomen, TIVA, controlled hypotension (if safe), cell salvage, ANH, viscoelastic-guided transfusion, maintain Ca²⁺/temp/pH.
34
Why does poor prone positioning ↑ blood loss?
Abdominal/IVC compression → ↑epidural venous pressure → more bleeding.
35
What is POVL and risk factors?
Peri-operative visual loss (ischemic optic neuropathy/CRAO). Risks: long surgery, large blood loss, anaemia, hypotension, oedema, large crystalloids, obesity, male sex, Wilson frame, eye pressure.
36
How is traumatic brain injury classified by GCS?
A: Mild 13–15, Moderate 9–12, Severe ≤8.
37
What must be excluded before assessing GCS in TBI?
A: Reversible causes (e.g. intoxication, metabolic disturbance, hypoglycaemia).
38
What is primary brain injury?
Direct mechanical disruption at impact.
39
What is secondary brain injury?
Delayed damage from raised ICP, ischaemia, oedema, excitotoxicity, inflammation.
40
Components of the Glasgow Coma Scale?
A: Eye (E/4), Verbal (V/5), Motor (M/6).
41
Symptoms of raised ICP?
Headache, vomiting, visual disturbance.
42
Signs of raised ICP?
Papilloedema, CN VI palsy, pupillary dilation, abnormal posturing, focal neurology, irregular respiration.
43
What is Cushing’s triad?
Hypertension, bradycardia, irregular breathing → late sign of herniation.
44
Normal ICP in adults and treatment threshold?
10–15 mmHg normal, treat if ≥22 mmHg.
45
CT head indications in TBI (immediate)?
GCS <13 on arrival or <15 at 2h, open/depressed skull fracture, basal skull signs, seizure, focal deficit, vomiting, amnesia >30 min.
46
Additional CT indications if LOC/amnesia present?
Age >65, anticoagulation, dangerous mechanism, coagulopathy.
47
ndications for intubation in TBI?
GCS ≤8, motor drop ≥2, absent reflexes, PaO₂ <13, PaCO₂ >6, PaCO₂ <4 from hyperventilation, facial trauma, bleeding, seizures.
48
Specific targets in TBI (oxygenation)?
SaO₂ >97%, PaO₂ >11–13 kPa.
49
Specific targets in TBI (ventilation)?
PaCO₂ 4.5–5.0 kPa, hyperventilation (4.0–4.5) only if herniation.
50
Specific targets in TBI (circulation)?
MAP >80 mmHg, CPP ≥60 mmHg.
51
Other key ICU targets in TBI?
Head up 15–30°, Na⁺ <155, osmolality <320, temp <37.5 °C, glucose 6–10 mmol/L, DVT prophylaxis.
52
Step 1 in raised ICP management?
Optimise ABC, sedation, gases, position, normothermia.
53
Step 2 in raised ICP management?
Osmotic therapy (mannitol 0.25–1 g/kg, hypertonic saline 3% 2 ml/kg or 5% 1–2 ml/kg q4–6h).
54
Step 3 in raised ICP management?
Hyperventilation to PaCO₂ 4.0–4.5 temporarily for herniation only.
55
Contraindication to mannitol?
Hypovolaemia.
56
Gold standard for ICP monitoring?
Intraventricular catheter (allows CSF drainage).
57
Indications for ICP monitoring?
Severe TBI + abnormal CT, or severe TBI + normal CT if ≥2 of: age >40, motor posturing, SBP <90.
58
Equation for cerebral perfusion pressure (CPP)?
CPP = MAP – ICP.
59
Osmotic therapy doses for ICP control?
Mannitol 0.25–1 g/kg; hypertonic saline 3% 2 ml/kg or 5% 1–2 ml/kg q4–6h (max 8 ml/kg/day).
60
Definition of stroke?
Sudden onset focal neurological deficit of vascular origin, lasting >24 h or causing death.
61
Types of stroke?
Ischaemic (~85%) and haemorrhagic (~15%)
62
NICE first-line imaging for suspected stroke?
Non-enhanced CT brain within 24 h; add CTA if thrombectomy considered; CTP if >6 h.
63
Eligibility for IV thrombolysis (alteplase)?
Onset <4.5 h, no contraindications, BP <185/110.
64
Mechanism of alteplase?
tPA activates plasminogen → plasmin → clot breakdown.
65
First-line antiplatelet in ischaemic stroke?
Aspirin 300 mg within 24 h, then 75 mg daily.
66
Indication for anticoagulation post-stroke?
Cerebral venous sinus thrombosis or cardioembolic stroke (after initial delay).
67
Indications for thrombectomy?
Large vessel occlusion, <6 h from onset, up to 24 h with favourable perfusion imaging.
68
Indications for carotid endarterectomy?
Symptomatic stenosis 50–99% after TIA/non-disabling stroke, within 2 weeks.
69
What is hyperperfusion syndrome?
Headache, seizures, focal deficits post-CEA; reduced risk with BP <160/100.
70
General BP limits in acute stroke?
SBP <200, DBP <110
71
BP targets if thrombolysis candidate
<185/110 mmHg.
72
Indications for decompressive hemicraniectomy?
Age ≤60, MCA infarct >50%, NIHSS >15, ↓consciousness.
73
Post-stroke PaO₂ and PaCO₂ targets?
PaO₂ >13 kPa, PaCO₂ 4.5–5.0 kPa.
74
Key elements of secondary prevention?
Antiplatelet, statin, BP control, anticoagulation if AF, lifestyle modification, carotid surgery if indicated.
75
Normal adult CSF volume?
150 ml.
76
Where is CSF absorbed?
Arachnoid granulations → dural venous sinuses.
77
Four non-congenital causes of hydrocephalus?
SAH, meningitis, tumour, IVH, colloid cyst.
78
Three clinical features of raised ICP?
Headache, vomiting, impaired consciousness.
79
Classic triad of normal pressure hydrocephalus?
Gait disturbance, cognitive decline, urinary incontinence.
80
How to zero an EVD?
Align burette to Foramen of Monro (external auditory meatus in supine).
81
Four complications of an EVD?
Haemorrhage, infection, over-drainage, blockage/malposition.
82
Four anaesthetic considerations in a patient with a VP/VA shunt?
83
Assess ICP, avoid pressure on shunt site, avoid IJV cannulation (VA), minimise laparoscopy duration.
84
How does ICP affect CSF production/absorption?
Production relatively constant, but absorption ↑ with higher ICP.
85
Communicating hydrocephalus cause?
Impaired absorption (e.g. SAH, meningitis).
86
Non-communicating hydrocephalus cause?
Obstruction (e.g. tumour, aqueduct stenosis).
87
Four complications of EVD?
Haemorrhage, infection, over-drainage, catheter blockage/displacement.
88
Major risk factors for PDPH?
Young, female, pregnancy, low BMI, large/traumatic needle, multiple attempts.
89
Define epilepsy.
Disorder of the brain characterised by a predisposition to generate abnormal synchronous neuronal activity, clinically observed as seizures.
90
Define convulsive status epilepticus (SE).
A generalised tonic–clonic seizure lasting >5 minutes, or ≥2 seizures without recovery between.
91
Mechanism of AEDs?
Enhance inhibitory synapses (↑ GABA) + inhibit excitatory synapses (↓ glutamate, Na⁺/Ca²⁺).
92
Common perioperative causes of seizures?
Hypoxia, hypocapnia, hypoglycaemia, hyponatraemia, hypocalcaemia, drug withdrawal, local anaesthetic toxicity.
93
Key investigations in SE?
ABG, glucose, Ca²⁺, Mg²⁺, U&E, LFT, FBC, clotting, AED levels, toxicology, microbiology, LP if indicated.
94
Name complications of prolonged convulsive SE.
CNS excitotoxic injury Hyperthermia Aspiration, pulmonary oedema
95
First-line drug therapy in SE (0–5 min)?
IV lorazepam 0.1 mg/kg (max 4 mg; repeat once after 10 min).
96
Second-line drug therapy in SE (15–30 min)?
IV levetiracetam 60 mg/kg OR sodium valproate 40 mg/kg OR phenytoin/fosphenytoin 20 mg/kg.
97
Third-line (refractory SE >30–60 min)?
General anaesthesia (propofol, thiopental, midazolam, ketamine) ± phenobarbital. ICU + EEG monitoring.
98
Which drugs should be avoided/cautioned in epilepsy?
Ketamine (low dose pro-convulsant), Etomidate (myoclonus), Enflurane (seizures), Tramadol (↓ seizure threshold)
99
Outline stepwise management of a 27 y/o in convulsive SE.
ABC: airway, O₂, IV access, monitoring, glucose ± thiamine. First line: lorazepam 0.1 mg/kg IV. Second line: levetiracetam 60 mg/kg OR valproate 40 mg/kg OR phenytoin 20 mg/kg. Third line: GA with propofol/thiopental/midazolam/ketamine ± phenobarbital.
100
What is the underlying pathophysiology of Parkinson’s disease (simple)?
Loss of dopaminergic neurons in the substantia nigra pars compacta → ↓ dopamine in the striatum → imbalance with acetylcholine → impaired movement (bradykinesia, rigidity, tremor).
101
Which motor features define Parkinson’s disease?
Bradykinesia, rigidity, resting tremor, postural instability.
102
Name three non-motor features of Parkinson’s disease.
Autonomic dysfunction (orthostatic hypotension, constipation), psychiatric/cognitive symptoms (depression, dementia, psychosis), sleep disturbance.
103
What are the key airway and respiratory issues in PD patients
↑ risk of OSA, poor secretion clearance (aspiration, atelectasis), restrictive lung defect, respiratory muscle bradykinesia, fixed cervical spine deformity (difficult airway).
104
Name the first-line drug for PD and why it is combined with another drug.
Levodopa – converted to dopamine in CNS. Always combined with a peripheral decarboxylase inhibitor (carbidopa/benserazide) to reduce peripheral metabolism and side effects
105
Name two classes of PD drugs that reduce dopamine breakdown.
MAO-B inhibitors (e.g. selegiline, rasagiline).
106
Give examples of dopamine agonists used in PD.
Pramipexole, ropinirole, rotigotine (transdermal patch), apomorphine (subcutaneous infusion).
107
What is Parkinsonism–Hyperpyrexia Syndrome (PHS)?
Life-threatening condition caused by sudden withdrawal of PD drugs. Features: severe rigidity, hyperthermia, altered mental state, autonomic instability, raised CK.
108
How is PHS managed?
Reinstitute dopaminergic therapy urgently, supportive care (IV fluids, cooling, benzodiazepines, ICU). Sometimes dantrolene or bromocriptine.
109
Which antiemetics should be avoided in PD and why?
Metoclopramide, prochlorperazine, droperidol — all are antidopaminergic and worsen symptoms.
110
Which antiemetics are safe in PD?
Ondansetron and domperidone.
111
What are the autonomic features of PD relevant to anaesthesia?
Orthostatic hypotension, sweating abnormalities, bowel/bladder dysfunction, labile BP under anaesthesia.
112
hat is the underlying pathology in Myasthenia Gravis?
IgG autoantibodies against post-synaptic nicotinic ACh receptors at the NMJ → ↓ functional receptors → fatigable weakness.
113
Which muscles are most often affected early in MG?
Ocular muscles (ptosis, diplopia).
114
Why does MG cause fatigable weakness?
With repeated stimulation, less ACh is available; fewer receptors remain to depolarise muscle → contraction fails.
115
What are the key bulbar and respiratory risks in MG?
Dysphagia, dysarthria, aspiration, and respiratory muscle weakness → risk of myasthenic crisis.
116
How is MG diagnosed?
Antibody testing, neurophysiology (decremental response), ice-pack test, historically Tensilon test.
117
What drugs are used to treat MG?
Pyridostigmine (cholinesterase inhibitor), steroids, immunosuppressants, plasma exchange/IVIG, thymectomy.
118
How do MG patients respond to suxamethonium and non-depolarising NMBs?
Resistant to suxamethonium, very sensitive to non-depolarising NMB
119
What is a myasthenic crisis?
Acute weakness of bulbar/respiratory muscles → ventilatory failure. Triggers: infection, drugs, surgery, pregnancy, temperature changes
120
Which drugs worsen MG?
Aminoglycosides, magnesium, β-blockers, anti-arrhythmics, some anaesthetic agents.
121
What is the underlying pathology in LEMS?
IgG autoantibodies against pre-synaptic voltage-gated Ca²⁺ channels → impaired ACh release.
122
How does weakness in LEMS differ from MG?
Improves with exercise (due to Ca²⁺ build-up → ↑ ACh release).
123
What is the typical tumour association with LEMS?
Small cell lung carcinoma (SCLC).
124
What additional symptoms are common in LEMS but not MG?
Autonomic features: dry mouth, constipation, impotence.
125
What happens to reflexes in LEMS?
Reflexes are reduced/absent, but may return after exercise.
126
How do LEMS patients respond to suxamethonium and non-depolarising NMBs
Sensitive to both depolarising and non-depolarising agents.
127
What type of disease is Multiple Sclerosis?
Chronic, immune-mediated, demyelinating disease of the CNS.
128
What is the pathophysiology of MS?
Autoimmune attack on oligodendrocytes → demyelination and axonal loss → impaired saltatory conduction.
129
Which part of the nervous system is affected in MS?
CNS only (brain, spinal cord, optic nerves) — not the peripheral nervous system.
130
What are common presenting symptoms of MS?
Optic neuritis (visual loss, painful eye movement), sensory disturbance, limb weakness, ataxia, diplopia.
131
Name three common non-motor symptoms of MS.
Bladder dysfunction, constipation, fatigue, cognitive decline, depression
132
How is MS diagnosed?
McDonald criteria: dissemination in time and space. MRI shows T2 hyperintense plaques; CSF with oligoclonal bands.
133
What are the main types of MS?
Relapsing–remitting (most common), secondary progressive, primary progressive.
134
What is the treatment of an acute MS relapse?
High-dose corticosteroids.
135
Why should hyperthermia be avoided in MS patients perioperatively
Heat can worsen conduction block in demyelinated axons and precipitate relapse.
136
How do MS patients respond to suxamethonium?
Risk of severe hyperkalaemia (due to upregulation of extrajunctional ACh receptors) → avoid.
137
How do MS patients respond to non-depolarising neuromuscular blockers?
Variable, often increased sensitivity and prolonged block → careful titration and neuromuscular monitoring required.
138
What perioperative factors increase the risk of MS relapse?
Infection, stress, surgery, hyperthermia.
139
List three perioperative concerns in a patient with advanced MS.
Respiratory weakness, autonomic dysfunction (BP lability), urinary retention, risk of VTE if immobile, sensitivity to sedatives/opioids.
140
Which motor neurons are affected in motor neuron disease?
141
What clinical feature distinguishes MND from MS?
MND does not involve sensory symptoms; MS often does.
142
What are bulbar symptoms in MND?
Dysarthria, dysphagia, tongue wasting and fasciculations.
143
What is the typical pattern of weakness in GBS?
Ascending symmetrical weakness starting in the legs.
144
What is the classic cerebrospinal fluid finding in GBS?
Albuminocytologic dissociation (↑ protein, normal WCC).
145
Which preceding infection is most commonly associated with GBS?
Campylobacter jejuni.
146
What is the main risk to life in GBS?
Respiratory muscle weakness → respiratory failure.
147
What are the two main disease-modifying treatments?
IV immunoglobulin and plasma exchange.
148
What is the pathophysiological defect in myasthenia gravis?
Autoantibodies against postsynaptic acetylcholine receptors.
149
What is the hallmark clinical feature of MG?
Fluctuating weakness that worsens with exertion and improves with rest.
150
Which muscles are most commonly involved early in MG?
Extraocular muscles → ptosis and diplopia.
151
Which neoplasm is associated with MG?
Thymoma.
152
What are the mainstays of symptomatic treatment?
Acetylcholinesterase inhibitors (e.g., pyridostigmine).
153
What is the underlying antibody in LEMS?
Antibodies against presynaptic voltage-gated calcium channels.
154
Which malignancy is most commonly associated with LEMS?
Small-cell lung carcinoma.
155
How does muscle weakness in LEMS typically present?
Proximal limb weakness, improving with repeated activity.
156
What is the pathophysiology of MS?
Autoimmune demyelination within the CNS.
157
Name two classic presenting features of MS.
Optic neuritis (painful vision loss) and sensory disturbances.
158
What is the inheritance pattern of Duchenne muscular dystrophy?
X-linked recessive.
159
What is the molecular defect in Duchenne MD?
Absence of dystrophin protein.
160
What is the most common cause of death in Duchenne muscular dystrophy?
Cardiomyopathy or respiratory failure.
161
Three neurological features to assess pre-op Posterior cranial surgery (sitting case):
• Raised ICP (↓GCS, headache, vomiting) • Bulbar/cranial nerve function (airway protection) • Cerebellar function (gait, posture, coordination).
162
Two other suitable positions
prone; lateral/park bench; supine with head turned.
163
Absolute contraindications to sitting:
ventriculo-atrial shunt; right-to-left intracardiac shunt.
164
Three complications due to sitting position:
Airway – macroglossia/ETT displacement/jugular obstruction; CVS – VAE, hypotension from venous pooling; Neuro – quadriplegia/cord ischaemia, peripheral nerve injury, pneumocephalus.
165
Most sensitive non-invasive monitor for VAE:
precordial Doppler.
166
Immediate VAE steps (4 to quote):
Flood wound with saline & cover with wet packs. Lower head; apply PEEP; give IV fluids. 100% O₂, stop N₂O.Aspirate RA via central line if present; left-lateral/Trendelenburg; chest compressions and inotropes if severe
167
What are the 3 determinants of ICP?
Brain, blood, and CSF (Monro–Kellie doctrine).
168
In TBI, what is the ICP treatment threshold and CPP target?
Treat if ICP >22 mmHg; aim CPP 60–70 mmHg.
169
Name 3 secondary insults that must be avoided in raised ICP.
Hypoglycaemia, hyperthermia, seizures (also hypoxia/hypotension).
170
How does hyperventilation reduce ICP and what is the safe PaCO₂ target?
↓ PaCO₂ → cerebral vasoconstriction → ↓ CBF and ICP. Target 4.5–5.0 kPa (rescue 4.0–4.5 kPa).
171
Which osmotic agents are used to reduce ICP?
Hypertonic saline (3%, 2–5 mL/kg) or mannitol (0.25–1 g/kg)
172
How can collateral perfusion be improved in acute arterial occlusion?
Control BP, reduce ICP; post-dural opening → brief hypotension (MAP 50–60 mmHg); adenosine 0.3–0.4 mg/kg for temporary flow arrest.
173
Name 2 causes of haemorrhagic vascular emergencies.
Aneurysm rupture, vessel dissection.
174
How is intraoperative vasospasm treated?
Intra-arterial vasodilators, mechanical thrombectomy, or stent/device retrieval.
175
What type of surgery is at highest risk for VAE?
Sitting craniotomy (posterior fossa) and spinal surgery.
176
What are 3 intraoperative signs of VAE?
Sudden ↓ETCO₂, hypotension/tachyarrhythmia, mill-wheel murmur.
177
List 3 immediate steps if VAE occurs.
Flood surgical field with saline, 100% O₂ and stop N₂O, aspirate air from RA catheter if present.
FRCA
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