Residency · Residency · Neurology

Neuroimaging for the Neurologist: MRI and CT Pattern Recognition

Introduction

Neuroimaging is the neurologist's most powerful diagnostic extension of the clinical examination. The ability to recognize imaging patterns on CT and MRI and correlate them with clinical presentations is a core competency that influences every subspecialty of neurology. This lecture provides a systematic approach to neuroimaging interpretation, emphasizing the patterns that every neurologist must know.

CT Fundamentals

Physics and Image Interpretation

CT measures X-ray attenuation of tissues expressed in Hounsfield units (HU). Key density values to remember are air (-1000 HU), fat (-100 HU), water/CSF (0 HU), gray matter (35-40 HU), white matter (25-30 HU), acute blood (50-70 HU), bone (1000 HU), and calcification (100-300 HU). Structures that are hyperdense (bright) include acute blood, calcification, and bone. Structures that are hypodense (dark) include CSF, edema, infarction, fat, and air.

When CT Is the Study of Choice

CT is preferred for acute hemorrhage detection in the emergency setting, trauma evaluation (fractures, acute epidural/subdural hemorrhage), acute stroke triage (ruling out hemorrhage before thrombolysis), hydrocephalus assessment, bone and skull base pathology, and situations where MRI is contraindicated (pacemaker, metallic implants, claustrophobia). CT angiography (CTA) provides vascular evaluation for large vessel occlusion, aneurysm, and dissection.

Key CT Patterns

The hyperdense MCA sign represents acute thrombus in the middle cerebral artery and is seen in proximal MCA occlusion. Loss of gray-white differentiation is an early sign of ischemic infarction, appearing within 6-12 hours. Epidural hematomas are biconvex (lens-shaped) hyperdense extra-axial collections that do not cross suture lines. Subdural hematomas are crescent-shaped extra-axial collections that cross suture lines and evolve from hyperdense (acute) to isodense (subacute) to hypodense (chronic). Subarachnoid hemorrhage appears as hyperdense blood in the basal cisterns and sulci, with sensitivity of approximately 95% within 6 hours. Hydrocephalus presents with enlarged ventricles and periventricular hypodensity (transependymal CSF flow) suggesting acute obstruction.

MRI Fundamentals

Key Sequences and Their Applications

T1-Weighted Imaging

T1-weighted imaging is the anatomy sequence, providing excellent gray-white differentiation. CSF appears dark, fat appears bright, and subacute blood (methemoglobin) appears bright. Melanin and proteinaceous fluid also appear bright. On post-gadolinium T1, enhancing lesions appear bright, indicating blood-brain barrier breakdown.

T2-Weighted Imaging

T2-weighted imaging is the pathology sequence: most pathological processes (edema, gliosis, demyelination, tumor) appear bright (hyperintense). CSF is also bright, making this sequence useful for assessing periventricular and juxtacortical lesions.

FLAIR (Fluid-Attenuated Inversion Recovery)

FLAIR is a T2-weighted sequence with CSF signal suppressed (CSF appears dark). It is excellent for detecting periventricular lesions, cortical lesions, and subarachnoid pathology. Leptomeningeal enhancement is sometimes better appreciated on post-gadolinium FLAIR than on T1. The hyperintense vessel sign (FLAIR vascular hyperintensity) is seen in slow flow distal to arterial occlusion.

Diffusion-Weighted Imaging (DWI) and ADC Map

DWI detects restricted diffusion, which appears bright on DWI with a corresponding dark signal on the ADC map (true restricted diffusion). Acute ischemic stroke produces restricted diffusion within minutes, making DWI the single most important sequence for stroke diagnosis. Restricted diffusion is also seen in abscess (pus), epidermoid cyst, hypercellular tumor (lymphoma), CJD (cortical ribboning), and toxic leukoencephalopathies. T2 shine-through occurs when a lesion is bright on DWI but also bright on ADC, indicating T2 prolongation rather than true restriction.

Gradient Echo (GRE) / Susceptibility-Weighted Imaging (SWI)

These sequences are exquisitely sensitive to blood products (hemosiderin, deoxyhemoglobin) and calcification. The "blooming" artifact causes hemorrhagic lesions to appear larger than on other sequences. They detect microbleeds, superficial siderosis, cavernous malformations, and vascular malformations. SWI is more sensitive than GRE for detecting microbleeds.

MR Angiography (MRA) and MR Venography (MRV)

MRA (time-of-flight or contrast-enhanced) provides noninvasive evaluation of intracranial and extracranial arteries. MRV evaluates cerebral venous sinuses and is essential for diagnosing cerebral venous sinus thrombosis.

Contrast Enhancement Patterns

Ring enhancement suggests different diagnoses depending on the pattern: abscess produces a smooth, thin, complete ring with restricted diffusion centrally; high-grade glioma shows an irregular, thick, incomplete ring; metastasis may also ring-enhance; and demyelinating lesions characteristically produce an open ring that is incomplete toward the gray matter. Homogeneous enhancement is seen in meningioma, lymphoma, and subacute infarction (gyral enhancement). Leptomeningeal enhancement accompanies meningitis (infectious, carcinomatous, inflammatory) and neurosarcoidosis. Pachymeningeal (dural) enhancement suggests intracranial hypotension, meningioma, or metastatic disease.

Disease-Specific MRI Patterns

Stroke

Acute ischemic stroke produces restricted diffusion in a vascular territory, with DWI becoming positive within minutes. DWI-FLAIR mismatch (DWI positive but FLAIR negative) suggests the infarct is less than 4.5 hours old and is used in wake-up stroke to select patients for thrombolysis. Hemorrhagic transformation produces GRE/SWI signal within the infarct territory.

Multiple Sclerosis

Dawson fingers are periventricular ovoid lesions oriented perpendicular to the ventricles along perivenular white matter. Additional lesions appear in juxtacortical, cortical, infratentorial, and spinal cord locations. Enhancing lesions indicate active inflammation and are typically less than 6 weeks old. The open ring enhancement pattern, where the incomplete ring opens toward the cortex, favors demyelination over tumor or abscess.

Infectious Patterns

Brain abscess presents as a ring-enhancing lesion with restricted diffusion centrally (bright DWI center) and a smooth, thin enhancing wall. HSV encephalitis shows asymmetric medial temporal and insular cortex T2/FLAIR hyperintensity with restricted diffusion. Toxoplasmosis produces multiple ring-enhancing lesions in the basal ganglia and at the corticomedullary junction. PML causes asymmetric white matter lesions without mass effect or enhancement (unless immune reconstitution inflammatory syndrome is present).

Neurodegenerative Patterns

Alzheimer disease shows hippocampal and medial temporal lobe atrophy, with posterior cortical atrophy in the PCA variant. FTD produces frontal and/or anterior temporal atrophy, asymmetric in svPPA. CJD shows cortical ribboning and caudate/putamen signal on DWI. MSA demonstrates cruciform hyperintensity in the pons (the "hot cross bun sign"). PSP produces midbrain atrophy, visible as the "hummingbird sign" on sagittal view and the "morning glory sign" on axial view.

Tumors

Meningioma is a dural-based, homogeneously enhancing, extra-axial mass with a dural tail; it is isointense on T1 and variable on T2. Glioblastoma presents as an irregular ring-enhancing intra-axial mass with central necrosis, surrounding vasogenic edema, and possible hemorrhage. CNS lymphoma appears as a periventricular, homogeneously enhancing lesion with restricted diffusion reflecting hypercellularity; in immunocompetent patients, it typically does not ring-enhance. Metastases present as multiple enhancing lesions at the gray-white junction with disproportionate surrounding edema.

Systematic Approach to Image Interpretation

A systematic approach begins with checking patient information (name, date, clinical indication) and assessing image quality (motion artifact, complete coverage, appropriate sequences). The extra-axial spaces should be evaluated, including the scalp, skull, meninges, ventricles, and cisterns. Brain parenchyma is assessed systematically through the cortex, white matter, deep gray structures, brainstem, and cerebellum. Vascular structures including major arteries and veins should be examined. Enhancement patterns should be evaluated if contrast was given. Comparison with prior imaging assesses interval change. Finally, all findings must be correlated with the clinical presentation, because the image does not make the diagnosis -- the clinician does.

Clinical Pearls

DWI is the single most important MRI sequence for the neurologist, detecting acute ischemic stroke within minutes and being critical for diagnosing abscess (restricted diffusion centrally), CJD (cortical ribboning), and lymphoma. On CT, acute blood is hyperdense (bright); on MRI, the signal characteristics of blood change over time (the "MRI clock"), which helps date hemorrhages. The open ring enhancement pattern (incomplete ring opening toward the cortex) strongly favors demyelination over tumor or abscess and can prevent unnecessary brain biopsies. T2 shine-through on DWI is a common pitfall, and the ADC map should always be checked to confirm true restricted diffusion (dark on ADC equals true restriction). A systematic approach to image interpretation prevents errors of omission, and extra-axial structures, the posterior fossa, and the cervical spine should always be checked on brain MRIs.

References

1. Stable WJ, Gilmore C, Brat DJ. Neuroimaging fundamentals for the practicing neurologist. Continuum (Minneap Minn). 2016;22(5):1547-1571.
2. Schaefer PW, Grant PE, Gonzalez RG. Diffusion-weighted MR imaging of the brain. Radiology. 2000;217(2):331-345.
3. Filippi M, Rocca MA, Ciccarelli O, et al. MRI criteria for the diagnosis of multiple sclerosis: MAGNIMS consensus guidelines. Lancet Neurol. 2016;15(3):292-303.
4. Smirniotopoulos JG, Murphy FM, Rushing EJ, et al. Patterns of contrast enhancement in the brain and meninges. Radiographics. 2007;27(2):525-551.

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