MRI Brain

Magnetic resonance imaging (MRI) of the brain uses a strong static magnetic field (1.5 or 3 tesla), radiofrequency pulses and magnetic field gradients. It produces multiplanar images of the brain, meninges, cranial nerves, skull base and intracranial vessels without ionising radiation.

A routine study takes 20 to 45 minutes. It includes axial T1-weighted, T2-weighted and fluid attenuated inversion recovery (FLAIR) sequences, diffusion weighted imaging with an apparent diffusion coefficient map, and susceptibility weighted or gradient echo T2*-weighted imaging. Coronal and sagittal sequences are added as needed.

Gadolinium based contrast (0.1 mmol each kg, or 0.05 to 0.1 mmol each kg for macrocyclic agents) is given for tumour, infection, inflammation, demyelination activity and vascular lesions, with post-contrast T1-weighted imaging in three planes.

Additional sequences include time-of-flight or contrast MR angiography, MR venography, perfusion, spectroscopy and high resolution thin section imaging of the pituitary, internal auditory canals, hippocampus, and orbits.

MRI is the reference test for most brain disorders.

It detects acute ischaemic stroke on diffusion weighted imaging within minutes of onset with a sensitivity of about 95 to 99% (against 40 to 60% for early CT). It shows multiple sclerosis lesions with a sensitivity of over 95%. It identifies small tumours, metastases, encephalitis, posterior fossa lesions, and congenital malformations that CT misses.

The lifetime risk of stroke is about 1 in 4 adults. Multiple sclerosis affects about 2.8 million people worldwide. Brain tumours affect 20 to 25 in 100 000 people yearly (metastases outnumber primary tumours), and epilepsy affects about 50 million people.

Indications. Acute stroke and transient ischaemic attack (diffusion weighted imaging, angiography). Headache with red flags (thunderclap, progressive, new in older adults, with neurological signs or raised pressure). New seizures or epilepsy (hippocampal sclerosis, cortical dysplasia, tumours).

Suspected demyelinating disease (multiple sclerosis, neuromyelitis optica, acute disseminated encephalomyelitis). Brain tumours (diagnosis, surgical planning, response to treatment) and metastases screening. Infection (encephalitis, abscess, meningitis complications, progressive multifocal leukoencephalopathy).

Dementia and cognitive decline (pattern of atrophy, vascular disease, normal pressure hydrocephalus, prion disease). Movement disorders. Hydrocephalus and shunt assessment.

Cranial neuropathies, visual loss, and pituitary or skull base disease. Congenital malformations and developmental delay in children, hypoxic ischaemic injury in neonates. Head trauma with neurological deficit not explained by CT (diffuse axonal injury).

Vascular malformations, aneurysm follow up and venous thrombosis. Psychiatric presentations with atypical features. Not for uncomplicated headache or migraine without red flags. Not as a first test in acute head trauma or suspected acute haemorrhage when CT is faster and adequate.

Contraindications and precautions. Strict screening for ferromagnetic implants and devices:

• Cardiac pacemakers and defibrillators (unless certified conditional and managed with the device team).
• Cochlear implants (conditional models only).
• Intracranial aneurysm clips (non-conditional).
• Metallic intraocular foreign bodies, neurostimulators, and insulin pumps.

Most modern joint replacements, stents, sternal wires and dental work are safe.

Claustrophobia (sedation, open or wide bore scanners). Pregnancy: MRI without gadolinium is acceptable at any stage if needed; avoid gadolinium unless essential.

Gadolinium: severe renal impairment (estimated glomerular filtration rate under 30 mL each minute) carries a risk of nephrogenic systemic fibrosis with linear agents. Group II macrocyclic agents are therefore used at the lowest dose, or contrast is avoided. Other concerns are previous allergic reaction and the small risk of gadolinium deposition in the brain, of uncertain significance.

Sedation or general anaesthesia for young children and uncooperative patients. Hearing protection, monitoring of unconscious patients with compatible equipment, and metal free clothing are required. Tattoos with metallic pigments and some transdermal patches heat (burns).

Preparation and technique. Screening form, removal of metal objects, and a gown. The patient lies supine with the head in a dedicated coil (8 to 64 channel), and earplugs or headphones are used. A cannula is placed if contrast is needed.

Sequences are chosen for the question:

• Stroke: diffusion, FLAIR, susceptibility, angiography (10 to 15 minutes).
• Multiple sclerosis: 3D FLAIR, T2, pre- and post-contrast T1, sagittal views for callosal lesions.
• Epilepsy: thin section coronal T2 and FLAIR perpendicular to the hippocampal axis, 3D T1.
• Tumour: pre- and post-contrast T1, perfusion, spectroscopy.
• Pituitary or cranial nerve: high resolution thin slices.

Motion correction and parallel imaging shorten acquisition. A radiologist plans the sequences and monitors the examination.

Normal appearances. Grey matter is intermediate on T1 (darker than white matter) and brighter than white matter on T2 in adults; white matter is bright on T1 and dark on T2. Myelination is complete by about 2 years. CSF is dark on T1 and FLAIR and bright on T2.

The ventricles and sulci are symmetrical and proportional to age. There is no restricted diffusion, no abnormal enhancement (the choroid plexus, pituitary, pineal, and venous sinuses enhance normally), and no susceptibility blooming except physiological calcification and iron in the basal ganglia in older people. The flow voids in the major arteries and venous sinuses are present on T2.

Perivascular spaces and a few small punctate white matter lesions are common in older adults.

Interpretation.

• Acute ischaemic stroke: restricted diffusion (bright on diffusion weighted imaging, dark on the apparent diffusion coefficient map) within minutes, FLAIR hyperintensity appearing after 3 to 6 hours (a diffusion-FLAIR mismatch indicates onset within about 4.5 hours), vessel occlusion on angiography, and perfusion deficit.
• Chronic infarct is encephalomalacia with gliosis. Lacunar infarcts and white matter small vessel disease appear as periventricular and subcortical T2/FLAIR hyperintensities.
• Haemorrhage: acute (deoxyhaemoglobin: dark on T2), subacute (methaemoglobin: bright on T1), and chronic (haemosiderin rim: dark on susceptibility).
• Other haemorrhage findings: microbleeds (small foci of susceptibility signal) in hypertension and amyloid angiopathy (lobar, cortical subcortical); cavernoma ("popcorn" lesion with a haemosiderin rim); and subarachnoid blood on FLAIR.
• Multiple sclerosis: ovoid periventricular lesions perpendicular to the ventricles, juxtacortical, infratentorial and spinal cord lesions. Acute lesions show enhancement (ring or open ring) and restricted diffusion, and chronic lesions are black holes on T1.
• Dissemination in space and time is shown by lesions in different locations and a mix of enhancing and non-enhancing lesions, or new lesions on follow up.
• Neuromyelitis optica spectrum disorder: optic nerve, long cord and area postrema lesions. Acute disseminated encephalomyelitis: large bilateral multifocal lesions after infection.
• Tumours, glioma: infiltrative T2/FLAIR hyperintensity, enhancement and necrosis in high grade, increased perfusion, choline peak with reduced N-acetylaspartate.
• Tumours, metastases: multiple enhancing lesions at the grey white junction with oedema. Lymphoma: homogeneous enhancement, restricted diffusion, periventricular.
• Tumours, others: meningioma (extra-axial, dural tail, avid homogeneous enhancement), schwannoma (cerebellopontine angle, internal auditory canal extension, "ice cream cone"), pituitary adenoma, medulloblastoma, ependymoma, and hemangioblastoma (cyst with mural nodule).
• Infection, abscess: ring enhancing lesion with central restricted diffusion. Encephalitis (herpes simplex): medial temporal and insular T2 hyperintensity with restricted diffusion and haemorrhage.
• Infection, meninges: meningitis (leptomeningeal enhancement), ventriculitis (ependymal enhancement and debris), tuberculoma and tuberculous meningitis (basal enhancement, hydrocephalus, infarcts).
• Infection, others: toxoplasmosis, cryptococcosis, neurocysticercosis (cyst with scolex, calcified nodule), progressive multifocal leukoencephalopathy (asymmetric subcortical white matter lesions without mass effect), and prion disease (cortical and basal ganglia restricted diffusion).
• Dementia and neurodegeneration: global and regional atrophy (hippocampal atrophy in Alzheimer disease, frontotemporal atrophy in frontotemporal dementia, midbrain atrophy "hummingbird sign" in progressive supranuclear palsy), vascular changes, superficial siderosis.
• Normal pressure hydrocephalus: ventriculomegaly out of proportion to sulci, flow void in the aqueduct.
• Epilepsy: hippocampal sclerosis (atrophy and T2/FLAIR hyperintensity of the hippocampus), focal cortical dysplasia (cortical thickening, blurred grey white junction), tumours (ganglioglioma, dysembryoplastic neuroepithelial tumour), malformations of cortical development (heterotopia, polymicrogyria, lissencephaly), tuberous sclerosis, and Sturge-Weber syndrome.
• Hydrocephalus and CSF disorders: enlarged ventricles with transependymal oedema, aqueduct stenosis, Chiari malformation (tonsillar descent over 5 mm), arachnoid cyst, and intracranial hypotension (pachymeningeal enhancement, brain sag).
• Vascular lesions: aneurysm, arteriovenous malformation (nidus with flow voids), developmental venous anomaly, dural arteriovenous fistula, venous sinus thrombosis (absent flow void and thrombus signal, with venous infarcts), vasculitis (multifocal infarcts, vessel wall enhancement), and reversible cerebral vasoconstriction.
• Posterior reversible encephalopathy syndrome: bilateral posterior vasogenic oedema in hypertension, eclampsia and immunosuppression.
• Metabolic and toxic: Wernicke encephalopathy (symmetric thalamic, mamillary body and periaqueductal lesions), hypoxic ischaemic injury (basal ganglia, cortex, watershed lesions), osmotic demyelination (central pontine hyperintensity), carbon monoxide (globus pallidus), and leukodystrophies in children.
• Trauma: diffuse axonal injury (small susceptibility foci at the grey white junction, corpus callosum and brainstem, with restricted diffusion), contusions, and subdural collections.
• Congenital: corpus callosum agenesis, Dandy-Walker spectrum, holoprosencephaly, hypoxic injury in neonates (basal ganglia and thalamus), and delayed myelination.
• Incidental: pineal and arachnoid cysts, non-specific white matter lesions, developmental venous anomalies, and small meningiomas, most needing no action.

Critical values and findings needing immediate action.

• Acute infarct on diffusion weighted imaging within the treatment window or with vessel occlusion: immediate stroke team contact for thrombolysis or thrombectomy.
• Haemorrhage with mass effect, herniation, or hydrocephalus: immediate neurosurgical review.
• Mass lesion with oedema and midline shift: steroid, urgent neurosurgical and oncology review.
• Brain abscess, empyema, or ventriculitis: immediate antibiotics and drainage.
• Herpes encephalitis pattern: start aciclovir immediately without waiting for cerebrospinal fluid results.
• Cerebral venous sinus thrombosis: anticoagulation after specialist review.
• Pituitary apoplexy or optic chiasm compression with visual loss: urgent neurosurgical and endocrine care.
• Cord compression or spinal lesion seen on the sagittal views: emergency spine imaging.
• Posterior reversible encephalopathy: control blood pressure, treat eclampsia.
• Intracranial aneurysm with subarachnoid blood: neurointerventional or neurosurgical referral.

Limitations and artefacts.

• Patient motion is the commonest cause of degraded images; children, confused or agitated patients need sedation or rapid sequences.
• Metal implants (dental work, clips, shunt valves) cause susceptibility artefacts that distort adjacent brain. Some shunt valves change setting in the magnetic field and need checking after scanning.
• Diffusion weighted imaging is not perfectly specific: restricted diffusion occurs in abscess, lymphoma, hypercellular tumours, seizures, hypoglycaemia, demyelination and prion disease. The clinical context is essential.
• Very early (under 1 hour) or small brainstem infarcts can be diffusion negative in 1 to 3% of cases.
• Flow artefacts, pulsation of CSF, and magnetic susceptibility near the skull base can mimic lesions (FLAIR artefacts in the basal cisterns).
• MRI cannot show acute bone injury, calcification and fine fractures well. CT is better for acute skull trauma, haemorrhage in the first hours, and bone detail.
• Contrast enhancement requires correct timing, and non-enhancing infiltrative tumour is underestimated. Enhancement can be absent in early abscess or encephalitis.
• Gadolinium agents may accumulate in tissue, and risks in renal failure and pregnancy must be weighed.
• Long scan times and noise limit emergency use, and access is restricted in many places.
• Incidental findings are common (about 2 to 3% of adults have a significant incidental finding), leading to anxiety and further tests.
• Normal MRI does not exclude all causes of symptoms, such as migraine, functional disorders and many neurodegenerative diseases early on.

Special groups.

• Children: sedation or anaesthesia under 6 to 7 years; sequences are adapted to myelination stage; use of MRI in suspected non-accidental injury and neonatal encephalopathy.
• Pregnant patients: MRI without gadolinium is safe and preferred over CT for most brain indications.
• Patients with implanted devices: check the manufacturer's conditions and involve the device team.
• Older adults: small vessel disease and atrophy are common and must be matched to symptoms.
• Patients with renal impairment: macrocyclic gadolinium at low dose, or non-contrast sequences.
• Patients with claustrophobia: preparation, open scanner, sedation.
• Immunocompromised patients: low threshold for contrast MRI for opportunistic infection and lymphoma.
• Regions: neurocysticercosis, tuberculous meningitis, cerebral malaria, HIV-related conditions, stroke at young age, and hydrocephalus in children are common.
• MRI is available in few centres with long waiting times. CT is the main tool, and MRI is reserved for problems that CT cannot answer.

Follow up tests. CT head for acute haemorrhage or bone detail, MR angiography and venography, CT angiography, digital subtraction angiography, cerebrospinal fluid analysis (cell count, protein, glucose, oligoclonal bands, polymerase chain reaction, cytology), electroencephalography, visual evoked potentials and optical coherence tomography in demyelination,

blood tests (full blood count, inflammatory markers, glucose, electrolytes, vitamin B12, thyroid function, autoimmune and paraneoplastic antibodies, HIV, syphilis serology), PET or SPECT for epilepsy and dementia, neuropsychological testing, genetic tests in leukodystrophies, repeat MRI at set intervals for tumours, demyelination and incidental lesions, and referral to neurology, neurosurgery,

neuro oncology, epilepsy or memory services.