Neurosurgery recall practice
Enable JavaScript for the interactive quiz. The questions are also readable below. Recorded recall sessions come from the source document and are not independently authenticated.
Q93. A patient with a brain tumour receives dexamethasone before surgery. Which effect principally improves tumour-related symptoms?
Recorded recall sessions: September 2017; September 2020
A. Reduction of vasogenic peritumoural oedema
B. Direct eradication of malignant tumour cells
C. Permanent reduction in intracranial tumour volume
D. Stimulation of CSF production
Answer and explanation
A. Reduction of vasogenic peritumoural oedema
Dexamethasone reduces blood–brain barrier permeability and vasogenic oedema surrounding many intracranial tumours, alleviating mass effect and raised-pressure symptoms. It is not routinely appropriate for every intracranial lesion and can affect histological diagnosis of suspected primary CNS lymphoma.
B. Glucocorticoids do not generally provide definitive cytotoxic treatment for most solid brain tumours.
C. Steroids improve surrounding oedema more than removing tumour tissue itself.
D. Would not be the desired mechanism and can worsen intracranial pressure.
- Use the lowest effective dose and taper when appropriate
- Monitor hyperglycaemia and infection risk
- Suspected CNS lymphoma warrants special caution before biopsy
Exam pearl: Dexamethasone treats vasogenic oedema around brain tumours.
Examiner trap: Steroid response should not be mistaken for cure; steroids can obscure a CNS lymphoma biopsy.
Viva extension: What is the difference between vasogenic and cytotoxic cerebral oedema? Barrier leak versus cellular energy-failure swelling.
Q952. A 45-year-old man has progressive morning headache, vomiting and bilateral papilloedema. Urgent brain MRI shows a large frontal mass with substantial vasogenic oedema and midline shift. Which proposed procedure should be avoided because it risks precipitating brain herniation?
Recorded recall sessions: April 2017
A. Neurosurgical assessment
B. Urgent specialist-directed management of raised intracranial pressure
C. Appropriate neuroimaging and airway assessment
D. Diagnostic lumbar puncture
Answer and explanation
D. Diagnostic lumbar puncture
A space-occupying intracranial lesion with mass effect and midline shift creates a dangerous intracranial pressure gradient. Removing CSF by lumbar puncture can precipitate transtentorial or tonsillar herniation. Specialist neurosurgical management and treatment of the underlying lesion take priority.
A. Neurosurgical review is indicated and must not be delayed.
B. Appropriate specialist management of raised ICP is necessary; the precise treatment depends on clinical status and lesion.
C. Imaging and stabilisation are part of safe evaluation.
- Papilloedema plus a suspected mass warrants urgent assessment for intracranial pathology.
- A demonstrated space-occupying lesion with mass effect is a major contraindication to LP.
- Do not confuse isolated papilloedema in other conditions with a demonstrated mass causing midline shift.
- Neurological deterioration, seizures and pupillary abnormalities require urgent escalation.
Exam pearl: Mass lesion with midline shift → avoid lumbar puncture because of herniation risk.
Examiner trap: The original recall could not distinguish glioma from chronic subdural collection without imaging; the new question explicitly supplies MRI.
Viva extension: What is the physiological danger of LP in a large intracranial mass? Rapid change in CSF pressure may exacerbate compartmental pressure gradients and trigger herniation.
Q121. A neonate born at 28 weeks becomes apnoeic and hypotonic on day 2. Cranial ultrasound shows echogenic blood originating at the caudothalamic groove and extending into a lateral ventricle. What is the diagnosis?
Recorded recall sessions: January 2017
A. Subarachnoid haemorrhage
B. Germinal-matrix intraventricular haemorrhage
C. Extradural haematoma
D. Posterior fossa epidural haemorrhage
Answer and explanation
B. Germinal-matrix intraventricular haemorrhage
The highly vascular, fragile subependymal germinal matrix in premature infants is especially vulnerable to haemorrhage. Bleeding begins near the caudothalamic groove and may extend into the ventricles; cranial ultrasonography is the standard bedside screening technique.
A. Blood within the subarachnoid spaces does not classically originate at the caudothalamic groove in a preterm infant.
C. This is an extra-axial collection between the skull and dura, usually trauma-related, rather than a germinal-matrix bleed.
D. This extra-axial posterior fossa lesion would not account for blood arising in the caudothalamic groove and entering a lateral ventricle.
- Risk is highest at very low gestational age and birth weight.
- The caudothalamic groove is the classic site of germinal-matrix haemorrhage.
- Serial cranial ultrasound can detect post-haemorrhagic ventricular dilatation.
- Grade I is confined to the germinal matrix; more extensive haemorrhage enters the ventricles.
Exam pearl: Preterm infant plus caudothalamic-groove echogenicity strongly suggests germinal-matrix haemorrhage.
Examiner trap: The original recall only described a floppy preterm infant; diagnostic ultrasound findings have been added to make the educational question unambiguous.
Viva extension: Which first-line imaging test screens for germinal-matrix haemorrhage? Bedside cranial ultrasonography via the anterior fontanelle.
Q187. A 42-year-old woman reports fatigable ptosis, diplopia and proximal weakness that worsens late in the day. CT reveals an anterior mediastinal mass. Which tumour is classically associated with this syndrome?
Recorded recall sessions: January 2020
A. Bronchial carcinoid
B. Thymoma
C. Pulmonary adenocarcinoma
D. Renal cell carcinoma
Answer and explanation
B. Thymoma
Thymoma has a recognised association with autoimmune myasthenia gravis, in which antibodies interfere with neuromuscular transmission, most commonly at the acetylcholine receptor.
A. Bronchial carcinoids can produce neuroendocrine syndromes but are not the classic mediastinal association with MG.
C. Lung adenocarcinoma is not the classic cause of autoimmune myasthenia gravis.
D. Renal cell carcinoma has other paraneoplastic syndromes but is not typically associated with MG.
- Myasthenic weakness is fatigable and improves with rest.
- Anti-acetylcholine receptor antibodies are common in generalised MG.
- Chest imaging is part of the evaluation for thymoma.
- Lambert–Eaton syndrome is classically associated with small-cell lung cancer, not thymoma.
Exam pearl: Myasthenia gravis + anterior mediastinal mass = consider thymoma.
Examiner trap: Differentiate MG from Lambert–Eaton: MG often has ocular symptoms; Lambert–Eaton often has autonomic features and facilitation.
Viva extension: Which structure is targeted in most MG? The postsynaptic acetylcholine receptor.
Q281. An 18-year-old develops diplopia, dysphagia and descending flaccid paralysis after eating improperly preserved food. Which molecular action of the toxin explains his weakness?
Recorded recall sessions: September 2020
A. Competitive antagonism of postsynaptic nicotinic receptors
B. Inhibition of acetylcholinesterase
C. Cleavage of presynaptic SNARE proteins, preventing acetylcholine release
D. Persistent opening of postsynaptic sodium channels
Answer and explanation
C. Cleavage of presynaptic SNARE proteins, preventing acetylcholine release
Botulinum neurotoxin cleaves proteins required for synaptic vesicle fusion at cholinergic nerve terminals. Acetylcholine release at the neuromuscular junction is blocked, producing flaccid paralysis.
A. This is the mechanism of non-depolarising neuromuscular blockers, not botulinum toxin.
B. Acetylcholinesterase inhibitors increase synaptic acetylcholine rather than prevent its release.
D. This does not explain the presynaptic failure of neurotransmitter release characteristic of botulism.
- Foodborne botulism commonly causes cranial neuropathies followed by descending weakness.
- Sensation and consciousness are usually preserved.
- Antitoxin and respiratory support are time-critical when indicated.
- Tetanus toxin also targets SNARE proteins but acts on inhibitory interneurons, causing spasticity.
Exam pearl: Botulinum blocks ACh release; tetanus blocks inhibitory neurotransmitter release.
Examiner trap: Both toxins act via SNARE cleavage, but their clinical paralysis patterns differ.
Viva extension: Which neurotransmitter is blocked at the motor endplate? Acetylcholine.
Q346. During preparation for carotid endarterectomy, a trainee reviews the internal carotid artery. Which named artery normally arises from its intracranial ophthalmic segment?
Recorded recall sessions: September 2020
A. External carotid artery
B. Middle meningeal artery
C. Posterior inferior cerebellar artery
D. Ophthalmic artery
Answer and explanation
D. Ophthalmic artery
The internal carotid artery enters the skull via the carotid canal and gives off the ophthalmic artery after traversing the cavernous sinus and entering the subarachnoid space. The cervical internal carotid normally has no branches. The ophthalmic artery supplies the orbit and participates in important collateral pathways.
A. The external carotid is a separate terminal branch of the common carotid bifurcation, not an internal carotid branch.
B. The middle meningeal artery usually arises from the maxillary branch of the external carotid.
C. PICA usually arises from the vertebral artery rather than the internal carotid.
- The cervical internal carotid artery has no normal branches.
- The ophthalmic artery enters the orbit through the optic canal with the optic nerve.
- The internal carotid terminates as anterior and middle cerebral arteries.
- The posterior cerebral artery usually arises from the basilar artery, not directly as an ICA terminal branch.
Exam pearl: Internal carotid artery gives off the ophthalmic artery; cervical segment is branchless.
Examiner trap: Posterior communicating artery is an ICA branch, but posterior cerebral artery is usually not.
Viva extension: Which ICA branches contribute to the circle of Willis? Anterior cerebral and posterior communicating arteries.
Q359. A patient with a chronic complete T4 spinal cord injury develops sudden pounding headache, flushing above the lesion and severe hypertension during bladder distension. Injuries at or above which level classically predispose to this syndrome?
Recorded recall sessions: September 2024
A. T12
B. L3
C. T6
D. S2
Answer and explanation
C. T6
Autonomic dysreflexia results from unopposed sympathetic reflexes below a high spinal cord injury, especially at or above T6. Bladder distension and bowel impaction are frequent triggers.
A. Lesions below T6 generally preserve sufficient supraspinal control of the major splanchnic vascular bed to make classic autonomic dysreflexia much less likely.
B. A lumbar lesion is not the typical anatomical substrate for autonomic dysreflexia.
D. Sacral lesions do not usually interrupt descending control of the thoracic splanchnic sympathetic outflow in the required way.
- Acute management: sit upright, monitor BP and remove the trigger promptly.
- Catheter obstruction should be checked without delay.
- Severe persistent hypertension may require short-acting antihypertensive treatment under a protocol.
- It typically becomes a concern after spinal shock resolves, not solely during the initial areflexic phase.
Exam pearl: Autonomic dysreflexia risk is greatest with lesions at or above T6.
Examiner trap: Spinal shock and autonomic dysreflexia are different phases and phenomena.
Viva extension: What are the common triggers? Distended bladder, blocked catheter, bowel impaction or other noxious stimuli below the lesion.
Q402. A woman with Chiari I malformation and a cervical syrinx loses pain and temperature sensation over both shoulders and hands while joint-position sense remains intact. Which fibres are primarily damaged?
Recorded recall sessions: September 2021; 2021 (session not specified)
A. Dorsal-column fibres
B. Lateral corticospinal fibres alone
C. Decussating spinothalamic pain-and-temperature fibres in the anterior white commissure
D. Posterior spinocerebellar tract fibres
Answer and explanation
C. Decussating spinothalamic pain-and-temperature fibres in the anterior white commissure
A central syrinx expands near the central canal and disrupts crossing second-order spinothalamic fibres at the anterior white commissure. This causes segmental, bilateral suspended pain/temperature loss with relative preservation of dorsal-column vibration and proprioception early in disease.
A. Carry vibration, conscious proprioception and discriminative touch; these are initially preserved.
B. Their damage causes upper motor neuron weakness, not isolated suspended pain-temperature loss.
D. Convey unconscious proprioception to the cerebellum rather than conscious pain-temperature sensation.
- Pain-temperature fibres cross within one or two spinal segments.
- A cervical syrinx can produce a cape-like sensory deficit.
- Later expansion may involve anterior horn cells and cause hand wasting.
- Chiari I malformation is associated with syringomyelia.
Exam pearl: Syringomyelia = anterior white commissure damage with suspended pain-temperature loss.
Examiner trap: The sensory level need not match a complete cord transection.
Viva extension: What additional sign develops with anterior horn involvement? Segmental lower motor neuron weakness and wasting.
Q441. After skull-base surgery, a patient develops horizontal diplopia and an inwardly deviated right eye. The right eye cannot abduct, but pupillary responses are intact. Which cranial nerve was injured?
Recorded recall sessions: January 2018
A. Right abducens nerve (CN VI)
B. Right oculomotor nerve (CN III)
C. Right trochlear nerve (CN IV)
D. Right optic nerve (CN II)
Answer and explanation
A. Right abducens nerve (CN VI)
The abducens nerve innervates the lateral rectus muscle. Its palsy prevents abduction and causes convergent strabismus with horizontal diplopia, usually without pupillary dysfunction.
B. A major CN III palsy typically causes impaired adduction/elevation/depression, often ptosis and sometimes pupillary dilatation.
C. CN IV palsy affects the superior oblique and produces vertical/torsional diplopia, especially on downward gaze.
D. CN II injury affects vision and afferent pupillary responses rather than extraocular abduction.
- CN VI supplies lateral rectus.
- CN III supplies all other recti except lateral rectus and also inferior oblique.
- CN IV supplies superior oblique.
- Abducens has a long intracranial course and is vulnerable in raised intracranial pressure.
Exam pearl: Cannot abduct eye = ipsilateral CN VI palsy.
Examiner trap: An eye deviated medially is not necessarily a CN III lesion.
Viva extension: Which muscle abducts the eye? Lateral rectus.
Q442. A 55-year-old develops ataxic dysarthria, intention tremor, gaze-evoked nystagmus and impaired rapid alternating hand movements. Which neuroanatomical system is most strongly implicated?
Recorded recall sessions: January 2018
A. Primary motor cortex alone
B. Cerebellum and its connections
C. Basal ganglia alone
D. Peripheral vestibular labyrinth alone
Answer and explanation
B. Cerebellum and its connections
Dysdiadochokinesia, intention tremor, limb ataxia and gaze-evoked nystagmus are classic cerebellar signs. The specific vascular territory requires additional examination and imaging.
A. Motor cortex lesions primarily cause contralateral weakness and upper motor neuron signs rather than isolated dysmetria.
C. Basal ganglia disease causes hypokinetic or hyperkinetic movement disorders, not the characteristic cluster of cerebellar signs.
D. Peripheral vestibular disorders cause vertigo and nystagmus but do not typically cause dysdiadochokinesia or intention tremor.
- Dysdiadochokinesia means impaired rapid alternating movements.
- Intention tremor worsens when approaching a target.
- Cerebellar hemisphere lesions typically cause ipsilateral limb ataxia.
- Acute cerebellar symptoms require urgent stroke assessment.
Exam pearl: Dysdiadochokinesia + intention tremor = cerebellar dysfunction.
Examiner trap: Do not assign a specific cerebellar artery without a compatible vascular syndrome.
Viva extension: How do you test dysdiadochokinesia? Rapid alternating pronation and supination of the hands.
Q480. During lumbar puncture at L3–L4, the needle produces a transient bloody tap that rapidly clears. Injury to which vascular structure in the vertebral canal is a plausible source?
Recorded recall sessions: January 2020; January 2023
A. Posterior spinal artery
B. Internal vertebral (epidural) venous plexus
C. Anterior spinal artery
D. Basilar artery
Answer and explanation
B. Internal vertebral (epidural) venous plexus
The internal vertebral venous plexus is a valveless network in the epidural space. A traumatic needle pass can injure epidural vessels, producing blood that often clears in successive CSF tubes; this is not by itself proof that intracranial haemorrhage is absent.
A. Posterior spinal arteries supply the cord and are not the usual source of an uncomplicated transient traumatic tap.
C. This vessel runs on the anterior surface of the spinal cord, not normally along the safe lumbar puncture path below the conus.
D. The basilar artery lies intracranially at the ventral pons and cannot be directly injured by a lumbar needle.
- The adult spinal cord typically ends around L1–L2.
- Lumbar puncture is commonly performed at L3–L4 or L4–L5.
- The epidural space contains fat and the internal vertebral venous plexus.
- A traumatic tap and subarachnoid haemorrhage can overlap; interpret with clinical context and appropriate testing.
Exam pearl: Traumatic lumbar puncture may injure epidural veins in the internal vertebral venous plexus.
Examiner trap: Clearing of blood across tubes is suggestive, not a perfect exclusion test for subarachnoid haemorrhage.
Viva extension: What is the landmark for L4? The intercristal line approximately crosses L4 or the L4–L5 space, with anatomical variation.
Q568. A 65-year-old man with atrial fibrillation suddenly develops marked weakness of the right leg with comparatively preserved right arm and facial strength. Brain imaging confirms an acute left hemispheric arterial infarct. Which vascular territory best explains the pattern?
Recorded recall sessions: January 2024
A. Left middle cerebral artery
B. Right anterior cerebral artery
C. Left anterior cerebral artery
D. Right posterior cerebral artery
Answer and explanation
C. Left anterior cerebral artery
The anterior cerebral artery supplies much of the medial frontal and parietal cortex, including the leg region of the primary motor and sensory homunculus. A left ACA infarct causes contralateral (right) leg-predominant weakness; abulia and urinary incontinence may also occur.
A. MCA infarcts typically cause face-and-arm-predominant deficits, often with aphasia in the dominant hemisphere.
B. A right ACA infarct would primarily affect the left leg.
D. PCA infarcts more commonly cause visual field defects from occipital involvement.
- ACA: medial hemispheric surface and lower-limb motor area.
- MCA: lateral hemisphere, face and upper limb.
- PCA: occipital visual cortex.
- Sudden focal weakness requires an emergency stroke pathway and vascular imaging.
Exam pearl: Leg more affected than arm suggests contralateral ACA infarction.
Examiner trap: The side of the cerebral lesion is opposite the weak limb.
Viva extension: Name two additional ACA stroke findings. Abulia and urinary incontinence, especially with medial frontal involvement.
Q574. A 56-year-old man has a right parietal intracerebral mass and develops a left-sided homonymous visual field defect. Which visual pathway structure is most likely involved?
Recorded recall sessions: September 2020; May 2022; September 2024
A. Right optic nerve
B. Right optic radiations
C. Optic chiasm
D. Left retina
Answer and explanation
B. Right optic radiations
A lesion posterior to the optic chiasm produces a contralateral homonymous field defect. The optic radiations traverse the temporal and parietal lobes; right parietal radiation involvement particularly affects the left inferior visual quadrant, although larger lesions may produce a broader homonymous hemianopia.
A. An optic nerve lesion causes ipsilateral monocular visual loss rather than a homonymous deficit.
C. Chiasmal lesions classically produce bitemporal hemianopia.
D. A retinal lesion causes a monocular deficit and would not explain matching left hemifield loss in both eyes.
- Retro-chiasmal lesions cause contralateral homonymous visual loss.
- Temporal Meyer loop injury produces contralateral superior quadrantanopia.
- Parietal optic radiation injury produces contralateral inferior quadrantanopia.
- Occipital cortex injury may cause highly congruous homonymous defects.
Exam pearl: Parietal optic radiations carry the contralateral inferior visual field.
Examiner trap: Do not confuse bitemporal chiasmal loss with homonymous retrochiasmal loss.
Viva extension: Which lesion causes a left superior quadrantanopia? A right temporal lobe lesion affecting Meyer loop.
Q614. A 66-year-old man develops acute vertigo, nystagmus, dysarthria and ipsilateral limb ataxia. He also has dysphagia, ipsilateral facial pain-temperature loss and contralateral body pain-temperature loss. Which arterial territory is most likely involved?
Recorded recall sessions: January 2020
A. Anterior cerebral artery
B. Posterior inferior cerebellar artery
C. Middle cerebral artery
D. Anterior choroidal artery
Answer and explanation
B. Posterior inferior cerebellar artery
PICA territory infarction can involve the lateral medulla and inferior cerebellum, causing a lateral medullary (Wallenberg) pattern: vestibular symptoms, dysphagia, ipsilateral facial and contralateral body sensory deficits, and ataxia.
A. ACA infarction more often causes contralateral leg-predominant weakness and frontal behavioural changes.
C. MCA infarction typically causes face/arm-predominant cortical deficits such as aphasia or neglect.
D. Anterior choroidal infarction classically causes contralateral hemiparesis, hemisensory loss and homonymous hemianopia.
- PICA supplies portions of the inferior cerebellum and lateral medulla.
- Nucleus ambiguus involvement produces dysphagia and hoarseness.
- Spinal trigeminal involvement causes ipsilateral facial pain-temperature loss.
- Spinothalamic involvement causes contralateral body pain-temperature loss.
Exam pearl: Dysphagia plus crossed sensory loss and ataxia suggests PICA/lateral medullary infarction.
Examiner trap: A pure cerebellar syndrome without medullary signs is not sufficient to localise confidently to PICA.
Viva extension: Which cranial nerve nuclei explain dysphagia? Nucleus ambiguus, associated with glossopharyngeal and vagal motor function.
Q853. After an isolated head injury, a 25-year-old patient is assessed before intubation. There is no eye opening to any stimulus, no verbal sound and no motor response to appropriately applied painful stimulation. There is no paralysis or other factor preventing examination. What Glasgow Coma Scale score should be documented?
Recorded recall sessions: not recorded
A. GCS 0 (E0 V0 M0)
B. GCS 6 (E1 V1 M4)
C. GCS 3 (E1 V1 M1)
D. GCS 4 (E1 V1 M2)
Answer and explanation
C. GCS 3 (E1 V1 M1)
The Glasgow Coma Scale assigns a minimum of one point to each of the three components: eye opening E1, verbal V1 and motor M1. Thus a fully unresponsive, assessable patient scores 3/15. Documenting components is preferable to recording only a total; intubation or sedation can render components untestable and must be annotated.
A. No GCS component is scored zero; the minimum total is three.
B. M4 denotes withdrawal from pain, which is absent in this vignette.
D. M2 denotes extensor response to pain, also absent here.
- GCS eye component ranges 1–4.
- GCS verbal component ranges 1–5.
- GCS motor component ranges 1–6.
- Minimum assessable GCS is E1 V1 M1 = 3; maximum is E4 V5 M6 = 15.
Exam pearl: The minimum Glasgow Coma Scale is 3, not 0.
Examiner trap: The original head-injury stem was merged with unrelated splenomegaly choices. This reconstruction uses only the clearly legible GCS clinical fragment.
Viva extension: How do you record GCS in an intubated patient? Document the assessable components and verbal component as not testable rather than assigning a misleading V1.
Q856. A 67-year-old patient has an acute left parietal lobe infarction involving the superior optic radiations. The eyes and pupils are otherwise normal. Which visual-field deficit is most likely?
Recorded recall sessions: May 2022
A. Left inferior homonymous quadrantanopia
B. Bitemporal hemianopia
C. Right superior homonymous quadrantanopia
D. Right inferior homonymous quadrantanopia
Answer and explanation
D. Right inferior homonymous quadrantanopia
Superior optic radiation fibres traverse the parietal lobe and carry information from the contralateral inferior visual field. A left parietal lesion therefore produces a right inferior homonymous quadrantanopia (“pie on the floor”). Temporal Meyer-loop lesions instead produce contralateral superior quadrantanopia.
A. A cerebral hemispheric lesion causes a contralateral, not ipsilateral, homonymous field defect.
B. Bitemporal hemianopia localises to the optic chiasm, classically due to compression of crossing nasal retinal fibres.
C. Superior homonymous quadrantanopia localises more typically to temporal optic radiations (Meyer loop).
- Parietal optic radiations: contralateral inferior quadrantanopia.
- Temporal Meyer loop: contralateral superior quadrantanopia.
- Occipital lesions often produce congruous homonymous hemianopia, sometimes with macular sparing.
- Optic chiasm lesions cause bitemporal visual-field loss.
Exam pearl: PITS: Parietal = Inferior; Temporal = Superior quadrantanopia.
Examiner trap: The source merged visual-pathway teaching notes with unrelated paediatric orthopaedic options. This question uses only the identifiable visual-pathway concept.
Viva extension: What defect results from a left temporal Meyer-loop lesion? Right superior homonymous quadrantanopia.
Q963. A 69-year-old develops sudden bilateral leg weakness and urinary retention after a period of severe hypotension. Examination reveals loss of pinprick and temperature sensation below T10 but preserved vibration and joint-position sense. Which vascular territory is most likely infarcted?
Recorded recall sessions: January 2018
A. Posterior spinal artery territory
B. Anterior spinal artery territory
C. Isolated middle cerebral artery territory
D. Isolated vertebral artery extracranial segment without spinal cord ischaemia
Answer and explanation
B. Anterior spinal artery territory
Anterior spinal artery infarction damages corticospinal and spinothalamic pathways and autonomic tracts, producing weakness, pain/temperature loss and bladder dysfunction. Posterior columns are relatively spared because they are supplied predominantly by the posterior spinal arteries.
A. Posterior spinal arteries supply dorsal columns, so their injury more characteristically impairs vibration and proprioception.
C. An MCA stroke does not typically produce a bilateral spinal sensory level with preserved dorsal-column modalities.
D. This cannot explain the classic bilateral anterior cord syndrome with a thoracic sensory level.
- Anterior spinal artery supplies approximately the anterior two-thirds of the cord.
- Corticospinal injury causes motor weakness; spinothalamic injury impairs pain and temperature.
- Dorsal-column vibration and position sense are relatively preserved.
- The great anterior segmental medullary artery (Adamkiewicz) reinforces lower thoracic/lumbar cord perfusion.
Exam pearl: Anterior cord syndrome: motor and pain/temperature loss with preserved proprioception.
Examiner trap: The original retention-and-paresis recall lacked a sensory level, so anterior spinal versus segmental feeder artery could not be distinguished.
Viva extension: Which examination finding helps separate anterior from posterior cord infarction? Preservation of joint-position and vibration sense favours anterior cord infarction.
Q983. A 59-year-old has a left-sided lesion confined to the optic tract on MRI. Formal perimetry shows loss of the same half of the visual field in both eyes. Which visual-field pattern is expected?
Recorded recall sessions: January 2023
A. Right homonymous hemianopia.
B. Left monocular blindness.
C. Bitemporal hemianopia.
D. Right superior quadrantanopia only.
Answer and explanation
A. Right homonymous hemianopia.
After the optic chiasm, each optic tract carries information from the contralateral visual hemifield. The left optic tract carries the right visual field from both eyes, so its interruption produces right homonymous hemianopia.
B. This localises to the left optic nerve or eye rather than a post-chiasmal tract.
C. Bitemporal loss classically results from chiasmal compression.
D. This is more characteristic of a left temporal optic-radiation (Meyer loop) lesion, not complete tract injury.
- Optic nerve: monocular visual loss.
- Chiasm: often bitemporal field loss.
- Optic tract: contralateral homonymous hemianopia.
- Temporal radiation: contralateral superior quadrantanopia; parietal radiation: inferior quadrantanopia.
Exam pearl: Post-chiasmal lesions cause contralateral homonymous field defects.
Examiner trap: Do not confuse a tract hemianopia with a Meyer-loop quadrantanopia.
Viva extension: What field defect results from a right occipital lesion? Left homonymous hemianopia, often highly congruous.
Q68. What is the classic narrow anatomical site of obstruction producing non-communicating hydrocephalus?
Recorded recall sessions: April 2017; September 2017
A. Foramen magnum
B. Foramen of Luschka
C. Central canal of spinal cord
D. Cerebral aqueduct (aqueduct of Sylvius)
Answer and explanation
D. Cerebral aqueduct (aqueduct of Sylvius)
The aqueduct connects the third and fourth ventricles and is a narrow CSF passage. Aqueductal stenosis produces dilatation of the lateral and third ventricles with a relatively normal fourth ventricle.
A. Not the usual narrow intraventricular CSF bottleneck.
B. A lateral fourth-ventricle outlet, but less characteristically the common aqueductal bottleneck.
C. Not the usual site of ventricular CSF obstruction.
- Hydrocephalus can be obstructive or communicating
- MRI defines ventricular size and obstruction
- Raised intracranial pressure may cause headache, vomiting and papilloedema.
Exam pearl: Aqueductal stenosis enlarges lateral and third ventricles but spares the fourth.
Examiner trap: Do not confuse communicating hydrocephalus with aqueductal stenosis.
Viva extension: Where is CSF mainly produced? Choroid plexus of the ventricles.
Q69. Following cervical hyperextension injury, arm weakness is markedly greater than leg weakness. Which spinal cord syndrome is suggested?
Recorded recall sessions: 2022/2023 (mixed/uncertain session); May 2024
A. Anterior cord syndrome
B. Brown–Séquard syndrome
C. Posterior cord syndrome
D. Central cord syndrome
Answer and explanation
D. Central cord syndrome
Central cord syndrome, often after hyperextension in a stenotic cervical canal, preferentially impairs upper-limb motor function more than lower-limb function. The somatotopic and tract injury pattern is variable in clinical practice.
A. Typically produces motor and pain/temperature loss below injury, with dorsal column sparing.
B. Produces ipsilateral motor/proprioceptive loss and contralateral pain/temperature loss.
C. Primarily affects vibration and joint-position sensation, not upper-limb-predominant motor weakness.
- Bladder disturbance can occur
- CT evaluates bony injury while MRI can assess cord and ligament pathology
- Serial neurological examinations track progression.
Exam pearl: Upper limbs weaker than lower limbs after cervical injury = central cord syndrome.
Examiner trap: Do not assume normal radiographs exclude spinal cord injury.
Viva extension: How is central cord different from Brown–Séquard? It lacks the classic hemicord crossed sensory pattern.
Q92. A patient develops non-communicating hydrocephalus due to obstruction of CSF flow between the third and fourth ventricles. Which narrow passage is blocked?
Recorded recall sessions: April 2021
A. Cerebral aqueduct (of Sylvius)
B. Foramen of Monro
C. Foramen of Luschka
D. Foramen of Magendie
Answer and explanation
A. Cerebral aqueduct (of Sylvius)
The cerebral aqueduct is a narrow midbrain channel connecting the third and fourth ventricles. Aqueductal stenosis is an established cause of obstructive hydrocephalus with dilatation of the lateral and third ventricles.
B. Connects each lateral ventricle with the third ventricle, not the third to the fourth.
C. Allows CSF to leave the fourth ventricle laterally into the subarachnoid compartment.
D. Is the median outlet of the fourth ventricle, not the third–fourth communication.
- CSF is produced mainly by choroid plexus
- The fourth ventricle drains via Luschka and Magendie
- Obstruction location dictates the pattern of ventricular enlargement
Exam pearl: Aqueduct of Sylvius links the third and fourth ventricles.
Examiner trap: Do not confuse the cerebral aqueduct with a fourth-ventricular exit foramen.
Viva extension: Where is the aqueduct located? In the midbrain.
Q333. A 70-year-old man with bronchogenic carcinoma has morning headaches, vomiting and visual blurring. Contrast MRI reveals brain metastases with extensive vasogenic oedema and mass effect. Which medication most rapidly reduces the oedema-related symptoms while definitive treatment is planned?
Recorded recall sessions: January 2016; April 2017; April 2019; September 2020; January 2021; April 2021; September 2021; May 2022; September 2022; January 2023; May 2023; April 2025
A. Carbamazepine
B. Paracetamol
C. Morphine alone
D. Dexamethasone
Answer and explanation
D. Dexamethasone
Dexamethasone is a glucocorticoid used to reduce symptomatic vasogenic oedema surrounding intracranial tumours. It can rapidly improve headache and focal deficits due to mass effect, but it is not definitive cancer treatment. Dose and duration depend on symptom severity, and steroids should be tapered as clinically appropriate.
A. Carbamazepine is an antiseizure medication, not a treatment for tumour-associated vasogenic oedema; routine prophylaxis without seizures is not generally indicated.
B. Paracetamol may help pain but does not reduce tumour-associated cerebral oedema or mass effect.
C. Opioids may relieve pain but cannot treat the underlying oedema and can cloud neurological assessment.
- Symptomatic brain metastasis with vasogenic oedema: consider dexamethasone.
- Asymptomatic metastases without mass effect do not routinely require corticosteroids.
- Coordinate surgery, stereotactic radiotherapy or other oncological treatment.
- Watch for steroid hyperglycaemia, infection, myopathy and gastrointestinal adverse effects.
Exam pearl: Dexamethasone treats symptomatic vasogenic oedema; it does not treat the metastasis itself.
Examiner trap: Do not use prophylactic anticonvulsants automatically in seizure-free brain metastases.
Viva extension: What is the mechanism of raised ICP? Mass effect and blood–brain barrier disruption producing vasogenic oedema.
Q418. An infant has progressive macrocephaly. MRI demonstrates enlargement of both lateral ventricles and the third ventricle, with a normal-sized fourth ventricle. Where is CSF flow most likely obstructed?
Recorded recall sessions: April 2019
A. Foramen of Magendie
B. Cerebral aqueduct (of Sylvius)
C. Foramen of Monro
D. Arachnoid granulations
Answer and explanation
B. Cerebral aqueduct (of Sylvius)
The cerebral aqueduct connects the third to the fourth ventricle. Obstruction dilates the ventricles upstream (lateral and third) while leaving the fourth ventricle relatively normal.
A. An outlet obstruction at the fourth ventricle generally also enlarges the fourth ventricle.
C. A unilateral Monro obstruction usually enlarges the ipsilateral lateral ventricle rather than both lateral and third ventricles.
D. Impaired arachnoid absorption causes communicating hydrocephalus, usually involving all ventricles.
- Aqueductal stenosis is a classic cause of noncommunicating hydrocephalus.
- MRI ventricular pattern helps localise the obstruction.
- The fourth ventricle is downstream of the aqueduct.
- Assess for raised intracranial pressure and neurodevelopmental effects.
Exam pearl: Large lateral + third ventricles with spared fourth = aqueduct obstruction.
Examiner trap: Do not confuse communicating hydrocephalus with focal obstruction of the aqueduct.
Viva extension: Which procedures may be considered? Endoscopic third ventriculostomy in selected patients or CSF diversion by shunt.
Q593. A lumbar puncture is planned for an adult without contraindications. The line connecting the highest points of both iliac crests typically crosses which vertebral level, guiding a safe low lumbar interspace?
Recorded recall sessions: September 2018
A. L1 spinous process
B. T12 vertebral body
C. S1 foramina
D. L4 spinous process or L4–L5 interspace
Answer and explanation
D. L4 spinous process or L4–L5 interspace
Tuffier line (intercristal line) approximates L4 or the L4–L5 interspace. Adult LP is generally performed at L3–L4 or L4–L5, below the usual termination of the spinal cord near L1–L2.
A. L1 is near the conus medullaris and too high for routine LP.
B. T12 is above the adult conus and unsafe for routine LP.
C. S1 foramina are not the usual intercristal landmark.
- Adult conus medullaris usually ends at L1–L2.
- Dural sac extends to approximately S2.
- Tuffier line approximates L4/L4–L5 but varies among patients.
- Assess contraindications, including raised ICP with mass effect and coagulopathy.
Exam pearl: Iliac crest line = approximately L4; LP at L3–4 or L4–5.
Examiner trap: Landmarks are imperfect in obesity or altered anatomy; ultrasound may improve level selection.
Viva extension: Which layers are traversed? Skin, subcutaneous tissue, supraspinous, interspinous, ligamentum flavum, epidural space, dura and arachnoid.
Q775. An intubated woman with aneurysmal subarachnoid haemorrhage develops urine output 450 mL/hour. Serum sodium rises to 155 mmol/L, plasma osmolality is 320 mOsm/kg, urine osmolality is 90 mOsm/kg, and urine output falls with a marked rise in urine osmolality after desmopressin. Which diagnosis best explains these findings?
Recorded recall sessions: January 2016
A. Cerebral salt wasting
B. Syndrome of inappropriate antidiuretic hormone secretion
C. Central arginine-vasopressin deficiency (central diabetes insipidus)
D. Acute tubular necrosis with oliguria
Answer and explanation
C. Central arginine-vasopressin deficiency (central diabetes insipidus)
Central arginine-vasopressin deficiency after hypothalamic-pituitary injury produces high-volume hypotonic urine, hypernatraemia and elevated plasma osmolality. A substantial increase in urine concentration after desmopressin demonstrates renal responsiveness to vasopressin, favouring a central rather than nephrogenic defect.
A. Cerebral salt wasting generally produces renal sodium loss, hypovolaemia and hyponatraemia, not hypernatraemia with maximally dilute urine.
B. SIADH produces inappropriately concentrated urine and usually hyponatraemia, not severe hypotonic polyuria.
D. Acute tubular necrosis does not characteristically show brisk dilute polyuria that responds strongly to desmopressin.
- Central diabetes insipidus is associated with hypotonic polyuria and hypernatraemia.
- Check serum and urine osmolality, urine output, glucose and volume status.
- A major urine-osmolality rise after desmopressin favours central AVP deficiency.
- Manage fluid deficit and sodium correction carefully with specialist input; avoid overly rapid changes.
Exam pearl: SAH plus hypernatraemia, very dilute high-volume urine and desmopressin response points to central DI.
Examiner trap: Do not confuse cerebral salt wasting (typically hyponatraemia) with central DI (often hypernatraemia).
Viva extension: How would nephrogenic DI differ? The kidney responds poorly to desmopressin despite hyperosmolar plasma.
Q122. A man with severe head injury has a mean arterial pressure of 78 mmHg and an intracranial pressure of 18 mmHg. What is his cerebral perfusion pressure?
Recorded recall sessions: May 2022
A. 96 mmHg
B. 78 mmHg
C. 60 mmHg
D. 50 mmHg
Answer and explanation
C. 60 mmHg
Cerebral perfusion pressure (CPP) is the driving pressure for cerebral blood flow and is calculated as CPP = MAP − ICP. Therefore 78 − 18 = 60 mmHg. The Brain Trauma Foundation suggests targeting approximately 60–70 mmHg in severe traumatic brain injury, depending on physiology.
A. This incorrectly adds intracranial pressure to mean arterial pressure.
B. This is mean arterial pressure alone, ignoring the opposing intracranial pressure.
D. This does not follow the CPP calculation from the supplied numbers.
- CPP = MAP − ICP; do not substitute systolic blood pressure for MAP.
- Hypotension and raised ICP can both reduce CPP.
- The BTF recommends treating sustained ICP above 22 mmHg, interpreted with the clinical and imaging context.
- Aggressively driving CPP above 70 mmHg with fluids and vasopressors can increase complications.
Exam pearl: MAP 78 minus ICP 18 gives CPP 60 mmHg.
Examiner trap: The original recall said “mean atrial pressure”; this is a source transcription error repaired to “mean arterial pressure.”
Viva extension: What is the usual severe-TBI CPP target? Approximately 60–70 mmHg, individualised.
Q123. Following head trauma, a patient rapidly deteriorates into coma. The right pupil becomes fixed and dilated, with new left-sided weakness. Which complication best explains the findings?
Recorded recall sessions: January 2017; September 2020; May 2022
A. Communicating hydrocephalus
B. Bilateral papilloedema without herniation
C. Isolated subarachnoid haemorrhage without mass effect
D. Right uncal (transtentorial) herniation
Answer and explanation
D. Right uncal (transtentorial) herniation
A supratentorial mass lesion can displace the medial temporal uncus through the tentorial opening. Compression of the ipsilateral oculomotor nerve produces a dilated, poorly reactive pupil, while compression of descending motor fibres usually causes contralateral weakness. This is an immediate neurosurgical emergency.
A. Hydrocephalus may raise ICP but does not characteristically cause acute lateralised third-nerve compression in this pattern.
B. Papilloedema does not explain a rapidly developing unilateral blown pupil with contralateral weakness.
C. Subarachnoid bleeding can cause deterioration but does not specifically describe the medial temporal displacement producing this pattern.
- A new unilateral fixed dilated pupil after head trauma is an emergency warning sign.
- Prevent hypoxaemia and hypotension while arranging urgent definitive care.
- The pupil is usually ipsilateral to the expanding lesion.
- Kernohan notch phenomenon can produce paradoxical ipsilateral limb weakness.
Exam pearl: Coma plus an ipsilateral blown pupil and contralateral weakness = suspect uncal herniation.
Examiner trap: Papilloedema is not required to diagnose acute brain herniation; it may not develop in time.
Viva extension: Which cranial nerve is compressed? The oculomotor nerve (CN III).
Q125. A patient with an expanding extradural haematoma develops hypertension, bradycardia and irregular respirations. What does this triad most strongly indicate?
Recorded recall sessions: September 2017; January 2020
A. Acute hypovolaemic shock
B. Dangerously raised intracranial pressure with impending brainstem compromise
C. Primary supraventricular tachycardia
D. Isolated peripheral vestibular dysfunction
Answer and explanation
B. Dangerously raised intracranial pressure with impending brainstem compromise
The Cushing response occurs when severe intracranial hypertension threatens cerebral perfusion and brainstem function. Sympathetic activation raises systemic blood pressure; reflex vagal slowing produces bradycardia, while brainstem dysfunction causes abnormal respiration. It is a late, ominous sign.
A. Haemorrhagic shock generally causes hypotension with tachycardia, not hypertension and bradycardia.
C. This would produce a rapid heart rate, not the described bradycardic response.
D. Vestibular disease does not explain the combination of systemic hypertension, bradycardia and abnormal respiration.
- Cushing triad: hypertension, bradycardia and irregular breathing.
- It is a late sign and must not be awaited before treating raised ICP.
- Urgent neuroimaging and neurosurgical management are required when clinically appropriate.
- Avoid hypoxaemia and hypotension because they worsen secondary brain injury.
Exam pearl: Hypertension + bradycardia + irregular respiration after head trauma = Cushing triad.
Examiner trap: The source question ambiguously asked which receptor causes the respiratory pattern; this item instead tests the well-defined clinical syndrome.
Viva extension: What causes bradycardia? Traditionally attributed to a baroreceptor-mediated vagal reflex; direct vagal compression has also been proposed, so the mechanism remains debated.
Q548. A patient with severe head injury rapidly deteriorates from GCS 12 to GCS 3 and develops a unilateral fixed dilated pupil. What is the most immediately concerning intracranial mechanism?
Recorded recall sessions: September 2022
A. Uncal (transtentorial) herniation compressing cranial nerve III
B. Isolated chronic subdural haematoma without mass effect
C. Uncomplicated concussion
D. Small stable intraventricular haemorrhage
Answer and explanation
A. Uncal (transtentorial) herniation compressing cranial nerve III
Expanding supratentorial mass effect can displace the medial temporal lobe through the tentorial notch, compressing the ipsilateral oculomotor nerve and causing a dilated unreactive pupil. This is a neurosurgical emergency associated with brainstem compromise.
B. A chronic subdural collection may cause herniation if sufficiently large, but chronicity alone does not explain the mechanism; the key finding is acute transtentorial mass effect.
C. Concussion does not produce progressive coma with a fixed dilated pupil.
D. A small stable ventricular bleed is not the typical mechanism of a unilateral third-nerve compression syndrome.
- A blown pupil in deteriorating head injury suggests ipsilateral CN III compression.
- Urgent airway protection, neurosurgical consultation and CT are essential.
- Treat raised ICP while preparing definitive management.
- A normal initial scan does not preclude later expanding haemorrhage.
Exam pearl: Falling GCS plus unilateral fixed dilated pupil = suspect herniation until proved otherwise.
Examiner trap: Do not wait for bilateral pupillary changes before escalating care.
Viva extension: Which nerve mediates pupillary constriction? Parasympathetic fibres carried with the oculomotor nerve (CN III).
Q549. A 45-year-old has six weeks of worsening morning headache, vomiting and bilateral papilloedema, without thunderclap onset or recent head injury. Which diagnosis best fits this subacute course?
Recorded recall sessions: not recorded
A. Acute subarachnoid haemorrhage
B. Frontal lobe glioma causing raised intracranial pressure
C. Acute intracerebral haemorrhage
D. Benign positional vertigo
Answer and explanation
B. Frontal lobe glioma causing raised intracranial pressure
A gradually expanding intracranial tumour can elevate intracranial pressure and cause progressive morning headaches, vomiting and papilloedema. Lack of focal neurological signs does not exclude a frontal mass.
A. Subarachnoid haemorrhage usually presents abruptly with a thunderclap headache.
C. Intracerebral haemorrhage typically causes sudden symptoms, often with focal deficits.
D. Benign positional vertigo does not cause papilloedema or progressive raised intracranial pressure.
- Papilloedema indicates raised intracranial pressure, though it is not universally present.
- Progressive morning headache and vomiting are red flags for a space-occupying lesion.
- Urgent neuroimaging is required before considering lumbar puncture.
- Frontal tumours can produce personality or executive-function change.
Exam pearl: Progressive headache with papilloedema warrants urgent brain imaging.
Examiner trap: Never perform routine lumbar puncture before excluding a mass lesion when raised ICP is suspected.
Viva extension: Why can lumbar puncture be dangerous in a patient with mass effect? It may precipitate brain herniation by altering pressure gradients.
Q687. After head trauma, a patient develops a red pulsatile eye, proptosis, chemosis and an audible orbital bruit. Which vascular lesion best explains this constellation?
Recorded recall sessions: April 2026
A. Cavernous sinus thrombosis
B. Carotid-cavernous fistula
C. Optic neuritis
D. Isolated retinal detachment
Answer and explanation
B. Carotid-cavernous fistula
An abnormal communication between the carotid arterial system and cavernous sinus causes arterialisation of orbital venous drainage, leading to pulsatile proptosis, conjunctival chemosis, orbital bruit and raised intraocular pressure. Traumatic direct fistulas are often high flow and require urgent neurovascular and ophthalmic evaluation.
A. Cavernous sinus thrombosis may cause fever, ophthalmoplegia and proptosis but does not characteristically produce a pulsatile orbital bruit.
C. Optic neuritis causes painful visual loss, not an arterialised pulsatile orbit.
D. Retinal detachment presents with flashes, floaters or a curtain-like field defect rather than chemosis and bruit.
- Direct carotid-cavernous fistulas may follow skull-base trauma.
- CN III, IV, V1, V2 and VI are related to the cavernous sinus; VI is particularly vulnerable.
- CTA/MRA may suggest the diagnosis; digital subtraction angiography defines anatomy for treatment.
- Threatened vision or high-flow fistula requires urgent specialist management.
Exam pearl: Pulsatile proptosis + chemosis + orbital bruit = carotid-cavernous fistula.
Examiner trap: Cavernous sinus thrombosis and fistula both cause ocular congestion, but a bruit favours a fistula.
Viva extension: Which cranial nerve runs through the cavernous sinus adjacent to the internal carotid artery? The abducens nerve (CN VI).
Q708. A 25-year-old man deteriorates neurologically after a head injury. CT shows a biconvex extra-axial haematoma measuring 38 mL with 7 mm midline shift. His Glasgow Coma Scale score has fallen from 14 to 9. What is the best definitive management?
Recorded recall sessions: January 2025
A. Routine outpatient review with repeat CT in one week
B. Lumbar puncture to reduce intracranial pressure
C. High-dose steroids as sole treatment
D. Immediate neurosurgical referral for urgent operative evacuation
Answer and explanation
D. Immediate neurosurgical referral for urgent operative evacuation
This is a large, symptomatic acute extradural (epidural) haematoma with mass effect and clinical deterioration. Brain Trauma Foundation guidance recommends surgical evacuation of EDH greater than 30 cm³ regardless of GCS; craniotomy usually allows complete clot evacuation and haemostasis. Airway, haemodynamics and cervical spine protection must be addressed while arranging emergency neurosurgery.
A. Observation is reserved for carefully selected small, thin EDHs with minimal shift and no focal deficit under neurosurgical monitoring.
B. Lumbar puncture is dangerous in the setting of intracranial mass effect and may precipitate herniation.
C. Steroids are not definitive therapy for traumatic extradural bleeding.
- EDH classically appears lentiform/biconvex on CT and is limited by cranial sutures.
- Temporal EDH commonly involves the middle meningeal artery after skull fracture.
- EDH volume greater than 30 cm³ is an operative indication regardless of GCS.
- Small EDH may be observed only under strict neurosurgical criteria and repeat imaging.
- Craniotomy generally provides more complete evacuation than a burr hole alone.
Exam pearl: Deteriorating patient + large biconvex EDH: emergency neurosurgical evacuation.
Examiner trap: A burr hole may be a temporising decompression in exceptional circumstances, but is not the default definitive treatment for a large organised EDH.
Viva extension: Which EDH can be managed nonoperatively? Typically volume under 30 cm³, thickness under 15 mm, shift under 5 mm, GCS above 8 and no focal deficit, with neurosurgical observation and serial CT.
Q820. A 74-year-old man with alcohol dependence has progressive headache, gait disturbance and confusion three weeks after a minor fall. Non-contrast CT shows a crescent-shaped hypodense extra-axial collection extending across suture lines. What is the most likely diagnosis?
Recorded recall sessions: January 2017; April 2026
A. Acute extradural haematoma
B. Aneurysmal subarachnoid haemorrhage
C. Chronic subdural haematoma
D. Cerebellar intraparenchymal haemorrhage
Answer and explanation
C. Chronic subdural haematoma
Chronic subdural blood collects between dura and arachnoid, commonly following tearing of bridging veins in older patients after minor trauma. The crescentic collection may cross sutures and becomes hypodense as blood products age.
A. Extradural haematoma is usually biconvex and limited by suture attachments.
B. Subarachnoid blood typically outlines sulci and basal cisterns rather than a crescentic extra-axial collection.
D. A cerebellar haemorrhage is intraparenchymal in the posterior fossa, not a hemispheric extra-axial crescent.
- Age, cerebral atrophy, alcohol use and antithrombotic drugs increase risk.
- Chronic subdural haematoma may follow seemingly trivial trauma.
- CT density varies with blood age and repeated bleeding.
- Symptomatic collections with mass effect warrant urgent neurosurgical assessment.
Exam pearl: Older patient + delayed confusion + crescentic extra-axial CT collection = chronic subdural.
Examiner trap: Alcohol history alone cannot diagnose a haemorrhage; the original recall lacked diagnostic imaging.
Viva extension: What structure is commonly injured? Bridging veins traversing the subdural compartment.
Q933. A 73-year-old man falls outside a pub and is brought to the emergency department. He is intoxicated and cannot reliably recall whether he lost consciousness. Following appropriate assessment and indicated imaging, there is no intracranial injury. He remains intoxicated and lives alone, with no one available to supervise him. What is the safest disposition?
Recorded recall sessions: January 2023
A. Immediate discharge because the CT is normal
B. Observe until clinically fit and arrange safe supervision before discharge
C. Prescribe antibiotics for the small facial abrasion and discharge
D. Send home alone with verbal reassurance
Answer and explanation
B. Observe until clinically fit and arrange safe supervision before discharge
A normal CT does not override unsafe discharge circumstances. NICE NG232 requires return to baseline consciousness, absence of other admission factors such as intoxication, and appropriate supervision or a risk-based safe alternative. An older patient with an unreliable history also needs head injury imaging criteria assessed before disposition.
A. Normal imaging alone does not establish capacity, safety or adequate home supervision.
C. An abrasion does not determine safe head-injury discharge and antibiotics are not routinely indicated.
D. Verbal reassurance without safe supervision is inadequate in this intoxicated older patient.
- Do not attribute reduced consciousness to alcohol before excluding important traumatic brain injury.
- Age ≥65 with loss of consciousness or amnesia is a NICE CT risk criterion.
- Provide written and verbal head injury advice.
- A responsible adult should ideally supervise for the first 24 hours.
Exam pearl: Normal CT does not equal automatic discharge after head injury.
Examiner trap: Intoxication and living alone are independent safety considerations; a normal scan does not make them disappear.
Viva extension: Viva: What must be satisfied before discharge? GCS 15/baseline, no ongoing clinical concerns, safe supervision, clear return precautions and written advice.
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