CNS Imaging
Neuroimaging looks intimidating because the anatomy is unfamiliar and the sequences have names that mean nothing until explained. Two questions organise nearly all of it.
Is there blood, and how old is it? Acute blood is bright on CT because clotted haemoglobin is dense, and CT answers this within minutes, which is why it remains the first study in almost every neurological emergency. MRI is far better at everything else, including at dating blood, because haemoglobin degradation products have distinctive magnetic properties.
What shape is the collection? Shape reveals which layer the blood is in, and that determines the vessel, the cause and the operation.
A third principle governs modality selection. CT is fast, available and unmatched for acute blood, bone and gross mass effect. MRI is unmatched for the posterior fossa, the spinal cord, early infarction, white matter and everything subtle.
1. Reading a CT Head
Blood, calcification and bone are bright. Cerebrospinal fluid, fat, air and oedema are dark. Grey and white matter differ slightly, and loss of that difference is itself a sign.
The systematic questions are worth asking in order.
Is there blood, and where? Is there a shift of midline structures? Are the ventricles enlarged or effaced? Is the grey-white differentiation preserved? Are the basal cisterns open?
Effaced basal cisterns indicate raised intracranial pressure and impending herniation, and this is the finding that most often changes immediate management.
Loss of grey-white differentiation is the earliest sign of infarction on CT, and it appears before any established low density.
2. Shape Tells You the Layer
| Bleed | Shape | Vessel | Crosses sutures | Crosses midline |
|---|---|---|---|---|
| Extradural | Biconvex lens | Middle meningeal artery | No | Yes |
| Subdural | Crescent | Bridging veins | Yes | No |
| Subarachnoid | Fills sulci and cisterns | Aneurysm, usually berry | Not applicable | Not applicable |
| Intraparenchymal | Within brain substance | Small perforating vessels | Not applicable | Not applicable |
The reasoning behind the shapes is more useful than the table.
Extradural blood is limited by sutures, where the dura is firmly attached to the skull, so it cannot cross them and instead pushes inward as a lens. It can cross the midline because it lies outside the dura, and the falx is a fold of dura.
Subdural blood lies inside the dura, so it spreads freely across sutures over the convexity, but it cannot cross the midline because the falx is in the way. It forms a crescent following the brain surface.
The classical extradural history is a lucid interval, with brief loss of consciousness, apparent recovery, then deterioration as arterial bleeding accumulates.
Subdural haematoma is a disease of the elderly and of alcohol dependence, because brain atrophy stretches the bridging veins, so minor trauma tears them and the history of injury may be absent.
An isodense subdural is the trap. At around one to three weeks the blood becomes the same density as brain, so a large collection can be nearly invisible, and the clues are effacement of sulci, midline shift and loss of grey-white differentiation at the margin.
3. Subarachnoid Haemorrhage
Blood in the subarachnoid space fills sulci and basal cisterns, and the presentation is a sudden severe headache reaching maximum intensity within seconds.
CT sensitivity is highest in the first hours and falls with time, approaching very high sensitivity within six hours of onset and declining steadily thereafter as blood is cleared.
A negative CT beyond six hours does not exclude the diagnosis, and lumbar puncture is performed after an interval of about twelve hours, looking for xanthochromia, the yellow discolouration produced by bilirubin from broken-down haemoglobin.
Xanthochromia distinguishes true subarachnoid haemorrhage from a traumatic tap, because it requires time for haemoglobin to be metabolised in vivo and cannot be produced by needle trauma.
CT angiography identifies the aneurysm, which most often arises at branch points on the circle of Willis, particularly the anterior communicating artery, the posterior communicating artery and the middle cerebral bifurcation. A posterior communicating artery aneurysm classically presents with a painful third nerve palsy in which the pupil is involved, because the parasympathetic fibres run superficially in the nerve and are compressed first.
4. Stroke Imaging
The first question in acute stroke is not what type but whether there is blood, because that determines whether thrombolysis is possible.
Non-contrast CT is performed first to exclude haemorrhage. It is poor at showing early infarction, which is acceptable because it is not being asked to.
Early CT signs of infarction, when present, are loss of grey-white differentiation, insular ribbon loss, sulcal effacement and the hyperdense artery sign, which is thrombus within a vessel.
MRI diffusion-weighted imaging detects infarction within minutes, far earlier than CT, because cytotoxic oedema restricts water movement almost immediately after energy failure.
The diffusion-perfusion mismatch identifies salvageable tissue. Tissue that is underperfused but not yet restricted on diffusion imaging is the ischaemic penumbra, and its presence is what justifies intervention beyond conventional time windows.
CT angiography identifies large vessel occlusion, which is the finding that selects patients for mechanical thrombectomy.
Territory identifies the vessel. Middle cerebral artery infarction produces contralateral face and arm weakness with aphasia if dominant. Anterior cerebral artery infarction affects the leg disproportionately. Posterior cerebral artery infarction produces homonymous hemianopia.
5. Mass Lesions
Contrast enhancement indicates breakdown of the blood-brain barrier, which is why it identifies tumour, abscess, inflammation and infarct after several days.
Ring enhancement has a limited differential and is examined repeatedly: metastasis, high-grade glioma, abscess, tuberculoma, toxoplasmosis, and resolving haematoma.
Diffusion-weighted imaging separates abscess from tumour, because the viscous pus in an abscess restricts diffusion and appears bright, while the necrotic centre of a tumour does not.
Ring enhancement in India carries a different prior probability from Western practice, because tuberculoma and neurocysticercosis are common.
Neurocysticercosis is the commonest cause of adult-onset seizures in much of India. Its appearances follow the parasite's life cycle: a vesicular cyst with a visible scolex, then a colloidal stage with ring enhancement and surrounding oedema as the parasite dies, then a granular nodular stage, and finally a calcified nodule.
The scolex within a cyst is close to pathognomonic, and it is best seen on MRI.
6. MRI Sequences Without the Jargon
Sequences are easier to hold if each is understood as answering one question rather than as a name to memorise.
T1 shows anatomy. Fat is bright and water is dark, so the brain looks the way an anatomist expects. It is the sequence on which gadolinium enhancement is assessed.
T2 shows pathology. Water is bright, and since almost every pathological process involves increased water content, lesions stand out. The difficulty is that cerebrospinal fluid is also bright and can obscure lesions beside it.
FLAIR is T2 with the cerebrospinal fluid signal suppressed, which is why periventricular and cortical lesions become conspicuous. It is the workhorse sequence for demyelination and for subtle cortical abnormality.
Diffusion-weighted imaging shows restricted water movement, which occurs in cytotoxic oedema within minutes of infarction, and also in the viscous contents of an abscess and in highly cellular tumours such as lymphoma.
Gradient echo and susceptibility-weighted sequences show blood products, because haemosiderin distorts the local magnetic field. They detect microbleeds and old haemorrhage that every other sequence misses.
The one rule that prevents errors
A bright lesion on diffusion-weighted imaging must be checked against the apparent diffusion coefficient map. True restriction is bright on diffusion and dark on the coefficient map. A lesion bright on both is showing T2 shine-through rather than genuine restriction, which is a common source of overcalled infarcts.
7. Hydrocephalus, Herniation and the Spine
Hydrocephalus
The useful division is by where the obstruction lies.
Communicating hydrocephalus results from failure of absorption at the arachnoid granulations, typically after subarachnoid haemorrhage or meningitis, and all ventricles enlarge.
Non-communicating or obstructive hydrocephalus results from a block within the ventricular system, and the pattern of dilatation localises the block, since ventricles proximal to the obstruction dilate while those distal do not. Aqueduct stenosis dilates the lateral and third ventricles while sparing the fourth.
Normal pressure hydrocephalus produces ventricular enlargement out of proportion to sulcal atrophy, with the clinical triad of gait apraxia, urinary incontinence and cognitive decline, and gait is the feature most likely to improve after shunting.
Herniation
Uncal herniation compresses the third nerve, producing an ipsilateral fixed dilated pupil, and then the midbrain.
Subfalcine herniation pushes the cingulate gyrus under the falx and can compress the anterior cerebral artery.
Tonsillar herniation through the foramen magnum compresses the medulla and is the reason lumbar puncture is avoided where raised pressure with a mass effect is suspected.
Spinal imaging
MRI is the only modality that shows the cord directly, and it is the investigation for cord compression, myelopathy, syringomyelia and demyelination.
Suspected cord compression is an emergency, and whole-spine MRI is performed rather than imaging only the clinically suspected level, because compression is multilevel in a significant proportion of malignant cases.
CT remains superior for bony detail, fracture assessment and instrumentation, and CT myelography is used where MRI is contraindicated.
8. Choosing Between CT and MRI
| Situation | Preferred | Reason |
|---|---|---|
| Acute head trauma | CT | Fast, shows blood and fracture |
| Suspected acute stroke | CT first | Excludes haemorrhage before thrombolysis |
| Posterior fossa or brainstem | MRI | CT is degraded by beam-hardening artefact from bone |
| Spinal cord | MRI | Only modality showing cord directly |
| Early infarction | MRI diffusion | Detects within minutes |
| Seizure, first presentation | MRI | Detects hippocampal sclerosis and cortical lesions |
| Multiple sclerosis | MRI | Demyelinating plaques are invisible on CT |
| Bone detail or acute blood | CT | Superior for both |
MRI is contraindicated or hazardous with certain implants, notably older pacemakers, cochlear implants and intraocular metallic foreign bodies, and a patient with a history of metalwork requires an orbital radiograph before entering the scanner, since a ferromagnetic fragment can move and blind them. MRI is also impractical in an unstable or agitated patient, because acquisition takes far longer than CT and the patient is largely inaccessible inside the bore.
9. Worked Examples
Example 1. A young man is struck on the temple, loses consciousness briefly, recovers and talks normally, then deteriorates an hour later. CT shows a biconvex hyperdense collection that does not cross the coronal suture. Diagnose and explain the shape.
Extradural haematoma, almost always from a torn middle meningeal artery beneath a temporal bone fracture.
The lucid interval is characteristic and is explained by the mechanism. The initial concussion causes brief loss of consciousness, from which the patient recovers, while arterial bleeding accumulates in the extradural space. Once the volume is sufficient to raise intracranial pressure, consciousness deteriorates again, and the interval between the two can be an hour or several.
The biconvex shape follows from anatomy. The dura is firmly adherent to the inner table of the skull at the sutures, so extradural blood cannot spread past them and instead strips the dura inward, producing a lens shape. It can cross the midline, because the falx is itself a fold of dura and the blood lies superficial to it.
This is a neurosurgical emergency, and outcome is excellent if evacuated promptly, which is why the lucid interval must not be mistaken for recovery.
Example 2. An 80-year-old on warfarin has become confused over three weeks. CT shows effaced sulci on the right with 5 mm midline shift but no obvious collection. What has happened?
An isodense subdural haematoma. Between roughly one and three weeks the haemoglobin in a subdural collection degrades to the point where its attenuation matches that of brain, so the collection becomes nearly invisible on a non-contrast CT.
The secondary signs are what reveal it: effacement of cortical sulci on the affected side, midline shift with no visible cause, ventricular compression, and displacement of the grey-white junction away from the inner table.
The clinical setting fits precisely. Cerebral atrophy in an elderly patient stretches the bridging veins so that trivial or forgotten trauma tears them, and anticoagulation both increases the chance of bleeding and prolongs it. Symptoms are insidious, with confusion, unsteadiness and headache rather than a dramatic presentation.
MRI resolves the diagnosis where CT is equivocal, since blood remains conspicuous on MRI at all ages, and bilateral collections are particularly easy to miss on CT because the midline shift cancels out.
Example 3. A patient has a sudden severe headache eight hours ago. CT is normal. What next, and why?
Lumbar puncture, timed appropriately, because a normal CT at this point does not exclude subarachnoid haemorrhage.
CT sensitivity for subarachnoid blood is very high within the first six hours of onset but declines progressively thereafter, as blood is diluted and cleared from the cerebrospinal fluid. At eight hours the negative predictive value is no longer sufficient to discharge a patient with a thunderclap headache.
The lumbar puncture is deliberately delayed to around twelve hours from onset, because that is the time needed for haemoglobin released into the cerebrospinal fluid to be metabolised to bilirubin, producing xanthochromia.
Xanthochromia is what distinguishes true haemorrhage from a traumatic tap, since a traumatic tap introduces fresh blood that has had no time to be metabolised. A falling red cell count across sequential bottles supports a traumatic tap but is less reliable than xanthochromia. If subarachnoid haemorrhage is confirmed, CT angiography follows to identify the aneurysm.
Example 4. A patient in India presents with a first seizure. MRI shows a small cystic lesion with an eccentric bright dot inside it. What is this?
Neurocysticercosis, in the vesicular stage, and the eccentric bright dot is the scolex of the larva.
The appearance is close to pathognomonic, and it is one of the few situations in neuroimaging where a single finding establishes a parasitic diagnosis without tissue.
Neurocysticercosis is the commonest cause of adult-onset seizures in much of India, so the pretest probability is high, unlike in most Western settings where a ring-enhancing lesion would prompt a search for metastasis.
Recognising the stage matters for management. In the vesicular stage the larva is alive and the surrounding brain is quiet. As the parasite dies it enters the colloidal stage, the host mounts an inflammatory response, and the lesion develops ring enhancement with surrounding oedema, which is when seizures typically occur. It then involutes through a granular nodular stage to a calcified nodule.
Treatment combines antiepileptic drugs, corticosteroids to control the inflammatory response, and antiparasitic therapy in selected patients, since killing live cysts provokes inflammation and can worsen symptoms if given without steroid cover.
Example 5. A patient with a ring-enhancing lesion has restricted diffusion in its centre. What does this indicate, and why?
An abscess rather than a necrotic tumour.
Diffusion-weighted imaging measures the freedom with which water molecules move. Pus is thick and cellular, containing inflammatory cells, bacteria, proteins and debris, and that viscosity impedes water movement, so the abscess cavity shows restricted diffusion and appears bright with a corresponding dark signal on the apparent diffusion coefficient map.
The necrotic centre of a high-grade glioma or metastasis contains liquefied tissue with far lower viscosity, so water moves relatively freely and diffusion is not restricted.
This single sequence therefore separates two entities that can look identical on contrast-enhanced imaging, and it does so quickly and without additional contrast.
The practical importance is that management diverges completely. An abscess requires drainage and prolonged antibiotics with a search for the source, whereas a tumour requires biopsy, oncological staging and a quite different operation.
Summary
Ask whether there is blood and how old it is, then what shape it takes.
CT is fast and unmatched for acute blood, bone and gross mass effect.
MRI is superior for posterior fossa, cord, early infarction and white matter.
Effaced basal cisterns indicate raised intracranial pressure.
Loss of grey-white differentiation is the earliest CT sign of infarction.
Extradural blood is biconvex, cannot cross sutures, and can cross the midline.
Subdural blood is crescentic, crosses sutures, and cannot cross the midline.
The lucid interval belongs to extradural haematoma.
Subdural haematoma follows atrophy and stretched bridging veins in the elderly.
An isodense subdural is revealed by effaced sulci and unexplained midline shift.
CT sensitivity for subarachnoid haemorrhage is highest within six hours and falls thereafter.
Lumbar puncture is delayed to about twelve hours to detect xanthochromia.
Xanthochromia distinguishes true haemorrhage from a traumatic tap.
Non-contrast CT in acute stroke is performed to exclude blood, not to find infarct.
Diffusion-weighted MRI detects infarction within minutes.
The diffusion-perfusion mismatch identifies salvageable penumbra.
CT angiography identifies large vessel occlusion for thrombectomy.
Ring enhancement includes metastasis, glioma, abscess, tuberculoma and toxoplasmosis.
Restricted diffusion in the centre indicates abscess rather than tumour.
Neurocysticercosis with a visible scolex is close to pathognomonic and is a leading cause of adult seizures in India.
