Medical School · Year 4 · Radiology · includes a quiz and discussion video
Neuroimaging
Year 4: Radiology Elective
Learning Objectives
By the end of this seminar, students will be able to:
- Apply a systematic approach to head CT interpretation including window settings, normal anatomy, and recognition of common pathologic findings
- Identify and differentiate intracranial hemorrhage patterns including epidural, subdural, subarachnoid, and intraparenchymal hemorrhage on CT
- Recognize imaging findings of acute ischemic stroke on CT and MRI and understand the role of CT angiography and perfusion imaging in treatment decisions
- Evaluate brain tumors using MRI sequences and distinguish intra-axial from extra-axial masses based on characteristic imaging features
- Interpret spine imaging for disc herniation, spinal stenosis, and cord pathology and select appropriate modalities for specific clinical scenarios
- Apply neuroimaging appropriately in emergency settings including stroke, trauma, and acute neurological deficits
I. Head CT Fundamentals
Computed tomography window and level settings optimize visualization of different intracranial structures by adjusting the displayed range of Hounsfield units. Brain windows using a width of approximately eighty and level of forty provide optimal differentiation between gray and white matter and detection of most parenchymal abnormalities. Bone windows with wide width settings of two thousand or greater demonstrate skull fractures, skull base anatomy, and mastoid air cells. Subdural windows with narrow width settings of one hundred fifty to two hundred enhance detection of thin extra-axial blood collections. Stroke windows with even narrower settings of thirty to forty maximize contrast between normal and ischemic brain parenchyma.
Normal head CT anatomy demonstrates characteristic attenuation values for different intracranial structures. Gray matter measures approximately thirty-five to forty Hounsfield units and appears slightly hyperdense compared to white matter, which measures twenty-five to thirty units. Cerebrospinal fluid measures zero to ten units and appears hypodense in the ventricles and sulci. The ventricles should be symmetric and of normal size for age, and the sulci should be of uniform depth bilaterally. The major cerebral structures including the basal ganglia, thalami, internal capsules, and brainstem should be symmetric with normal attenuation.
Systematic head CT review ensures thorough evaluation and minimizes the risk of missed findings in emergency settings. The scalp is examined for swelling that may indicate the site of trauma. The skull is evaluated for fractures on bone windows, paying particular attention to the skull base. Extra-axial spaces are assessed for epidural and subdural collections. The brain parenchyma is evaluated for masses, areas of abnormal attenuation, and loss of gray-white differentiation. The ventricles are assessed for size, symmetry, and evidence of hydrocephalus. Midline structures are examined for shift indicating mass effect.
Reference density values guide interpretation of CT findings and facilitate recognition of acute pathology. Acute hemorrhage measures fifty to seventy Hounsfield units, appearing hyperdense or white compared to surrounding brain. Subacute hemorrhage becomes isodense to brain over one to three weeks, then hypodense as it evolves to chronic hematoma. Calcification measures greater than one hundred units and appears intensely hyperdense. Fat measures approximately negative fifty to negative one hundred units, appearing hypodense. Familiarity with these values enables recognition of abnormalities even when they are subtle.
<image>Panel A: Normal head CT on brain windows demonstrating gray-white matter differentiation, symmetric ventricles, and normal sulci. Panel B: The same image on bone windows optimizing visualization of skull and mastoid structures. Panel C: Subdural window settings demonstrating a thin subdural hematoma that is less apparent on standard brain windows. Panel D: Reference image showing expected attenuation values for various intracranial structures.</image>
II. Intracranial Hemorrhage
Epidural hematoma results from arterial bleeding, most commonly from laceration of the middle meningeal artery, and represents a neurosurgical emergency. The classic CT appearance is a biconvex or lens-shaped hyperdense collection between the skull and dura that does not cross cranial sutures because the dura is firmly attached at these locations. The underlying brain is compressed, and significant epidural hematomas produce midline shift. Clinical presentation classically includes a lucid interval following head trauma before deterioration due to hematoma expansion. Prompt surgical evacuation is required to prevent herniation and death.
Subdural hematoma arises from tearing of bridging veins that traverse the subdural space and is commonly seen in elderly patients and those with brain atrophy or coagulopathy. The characteristic CT appearance is a crescent-shaped collection that conforms to the brain surface and can cross suture lines because it is deep to the dura. Acute subdural hematoma is hyperdense, evolving through isodense at one to three weeks to hypodense in the chronic phase. Mixed-density subdural hematoma may indicate acute bleeding into a chronic collection or rebleeding from membrane formation. Large subdural hematomas with mass effect require surgical drainage, while smaller collections may be managed conservatively.
Subarachnoid hemorrhage fills the cerebrospinal fluid spaces with blood and most commonly results from aneurysm rupture in non-traumatic cases. CT demonstrates high-attenuation material within the subarachnoid spaces, including the basal cisterns, sylvian fissures, and cortical sulci. The distribution of blood may suggest the aneurysm location, with anterior communicating artery aneurysms bleeding into the interhemispheric fissure and middle cerebral artery aneurysms into the ipsilateral sylvian fissure. CT angiography is performed immediately to identify the causative aneurysm. Complications include rebleeding, vasospasm leading to delayed cerebral ischemia, and hydrocephalus from impaired cerebrospinal fluid circulation.
Intraparenchymal hemorrhage occurs within the brain substance itself and has various etiologies that influence location and imaging appearance. Hypertensive hemorrhage typically occurs in the basal ganglia, thalamus, pons, and cerebellum, where small penetrating vessels are susceptible to rupture. Cerebral amyloid angiopathy causes lobar hemorrhages in elderly patients, often with evidence of prior hemorrhages. Hemorrhagic transformation of ischemic stroke produces blood within an area of infarction. Hemorrhage into tumors, particularly metastases and high-grade primary tumors, may present as spontaneous intracerebral bleeding. Traumatic hemorrhage includes contusions at sites of brain contact with bone and diffuse axonal injury affecting white matter tracts.
<image>Panel A: Epidural hematoma with classic biconvex shape, mass effect, and adjacent skull fracture. Panel B: Acute subdural hematoma with crescent shape extending along the cerebral convexity with midline shift. Panel C: Subarachnoid hemorrhage with blood in the basal cisterns and sylvian fissures. Panel D: Hypertensive intraparenchymal hemorrhage centered in the left basal ganglia with surrounding edema.</image>
III. Acute Stroke Imaging
Non-contrast head CT serves as the initial imaging study in acute stroke to exclude hemorrhage and evaluate for early ischemic changes. The hyperdense artery sign represents acute thrombus within a major vessel, most commonly the middle cerebral artery, appearing as increased attenuation compared to the normal contralateral vessel. Loss of gray-white matter differentiation in the affected territory indicates cytotoxic edema from early infarction. The insular ribbon sign describes loss of distinction between the insular cortex and adjacent structures in middle cerebral artery occlusion. Sulcal effacement from brain swelling may be present even when other findings are subtle.
CT angiography is performed immediately following non-contrast CT to identify large vessel occlusion that may be amenable to mechanical thrombectomy. The examination covers the vasculature from the aortic arch through the circle of Willis to map the site and extent of occlusion. Large vessel occlusion is defined as thrombus within the internal carotid artery or proximal middle or anterior cerebral arteries. CT angiography also assesses collateral circulation, which influences outcome and treatment decisions. Carotid stenosis or dissection causing stroke may be identified as the embolic source or mechanism of infarction.
CT perfusion imaging provides quantitative maps that distinguish irreversibly infarcted tissue from potentially salvageable ischemic penumbra. Cerebral blood flow represents the volume of blood moving through brain tissue per unit time and is severely reduced in the infarct core. Cerebral blood volume is maintained by autoregulation in the penumbra but reduced in the core. Mean transit time is prolonged in both core and penumbra, making it sensitive for detecting ischemia. The mismatch between core defined by reduced blood flow and total hypoperfused territory identifies the penumbra that may be salvaged by reperfusion therapy.
MRI provides the most sensitive detection of acute ischemic stroke and additional characterization of stroke etiology and extent. Diffusion-weighted imaging detects restricted water motion in cytotoxic edema within minutes of stroke onset, appearing as bright signal in the affected territory. The apparent diffusion coefficient map confirms true restricted diffusion by demonstrating corresponding dark signal. FLAIR hyperintensity develops after approximately four to six hours and helps date the infarct. MR angiography demonstrates vessel occlusion and may be combined with perfusion imaging for comprehensive stroke evaluation when MRI is feasible in the acute setting.
<image>Panel A: Non-contrast head CT showing hyperdense MCA sign indicating acute thrombus and loss of insular ribbon. Panel B: CT angiography demonstrating left M1 segment occlusion with absent distal flow. Panel C: CT perfusion maps showing mismatch between small core and larger hypoperfused territory representing salvageable penumbra. Panel D: Diffusion-weighted MRI with bright signal in left MCA territory confirming acute infarct.</image>
IV. Brain MRI Sequences
Basic MRI sequences provide complementary information about brain anatomy and pathology through different tissue contrast mechanisms. T1-weighted images demonstrate excellent anatomic detail with bright fat signal, intermediate gray and white matter that can be differentiated, and dark cerebrospinal fluid. T2-weighted images highlight pathology by demonstrating bright signal in tissues with high water content including edema, inflammation, and many tumors, with cerebrospinal fluid also appearing bright. Fluid-attenuated inversion recovery sequences suppress the signal from cerebrospinal fluid while maintaining T2 contrast, enabling detection of periventricular lesions and subtle cortical abnormalities. Diffusion-weighted imaging detects restricted water motion and is essential for acute stroke and abscess diagnosis.
Advanced MRI sequences and techniques extend diagnostic capability for specific clinical questions. Gradient echo and susceptibility-weighted imaging are exquisitely sensitive for blood products and calcification, which cause local magnetic field inhomogeneities. T1-weighted post-gadolinium images demonstrate enhancement in lesions with disrupted blood-brain barrier or increased vascularity. MR angiography provides non-invasive visualization of intracranial and cervical vessels using time-of-flight or contrast-enhanced techniques. MR spectroscopy measures metabolite concentrations within tissues, with elevated choline suggesting increased cell turnover and decreased N-acetylaspartate indicating neuronal loss.
Signal characteristics on different sequences enable tissue identification and lesion characterization. Acute blood products are typically isointense or hypointense on T1 and hypointense on T2 due to deoxyhemoglobin. Subacute blood becomes T1 bright from methemoglobin formation, initially with T2 dark signal that becomes bright as cells lyse. Edema appears dark on T1 and bright on T2. Fat is bright on both T1 and T2 on standard sequences but can be suppressed with fat-saturation or short tau inversion recovery techniques. Calcification is typically dark on all sequences due to low proton density and susceptibility effects.
Enhancement patterns on post-gadolinium imaging provide diagnostic information about lesion pathophysiology and narrow differential diagnoses. Ring enhancement with a regular thin rim suggests abscess, while irregular thick ring enhancement is more typical of high-grade glioma or metastasis. Homogeneous enhancement characterizes meningioma, lymphoma, and some metastases. Irregular enhancement within a mass suggests tumor heterogeneity and higher grade. Leptomeningeal enhancement coating the brain surface indicates meningitis or leptomeningeal carcinomatosis. Enhancement of previously non-enhancing lesions on follow-up imaging may indicate transformation or progression.
<image>Panel A: T1-weighted image demonstrating normal brain anatomy with gray-white differentiation and intermediate signal parenchyma. Panel B: T2-weighted image of the same level showing bright CSF and subtle periventricular hyperintensity. Panel C: FLAIR image with CSF suppression making periventricular white matter lesions conspicuous. Panel D: Gradient echo sequence demonstrating susceptibility artifact from prior hemorrhage appearing as dark signal foci.</image>
V. Brain Tumors
Intra-axial tumors arise within the brain parenchyma and produce characteristic imaging patterns that suggest specific diagnoses. Glioblastoma, the most common primary malignant brain tumor in adults, typically appears as an irregularly enhancing mass with central necrosis, surrounding edema, and mass effect. Low-grade gliomas demonstrate T2 hyperintensity without significant enhancement or mass effect and may be difficult to distinguish from other causes of white matter signal abnormality. Metastases typically occur at the gray-white junction, are often multiple, and demonstrate surrounding edema disproportionate to lesion size. Primary CNS lymphoma appears as a homogeneously enhancing periventricular mass, characteristically demonstrating restricted diffusion and less surrounding edema than other tumors of similar size.
Extra-axial tumors arise from structures outside the brain parenchyma and can be distinguished from intra-axial lesions by their imaging features. Meningiomas arise from arachnoid cap cells and appear as dural-based homogeneously enhancing masses with a characteristic dural tail of enhancement extending from the mass. They may contain calcification and cause hyperostosis of adjacent bone. Vestibular schwannomas arise from the vestibular nerve and appear as enhancing masses centered on the internal auditory canal, often with a characteristic ice cream cone appearance. Pituitary adenomas arise within the sella and may extend superiorly to compress the optic chiasm, laterally into the cavernous sinus, or inferiorly into the sphenoid sinus.
Distinguishing primary brain tumors from metastases has important treatment implications and relies on several imaging features. Metastases are typically multiple and located at the gray-white junction where emboli lodge, while primary gliomas are usually solitary and infiltrative. The degree of edema relative to enhancing tumor is often greater with metastases than with primary tumors. Metastases tend to have well-defined margins, while gliomas demonstrate infiltrative spread into adjacent brain. Imaging elsewhere in the body may reveal a primary malignancy, and clinical history of known cancer supports metastatic disease.
Advanced imaging techniques assist in tumor characterization and treatment planning. MR perfusion demonstrates elevated relative cerebral blood volume in high-grade tumors, helping distinguish glioblastoma from low-grade glioma and tumor recurrence from treatment effect. MR spectroscopy shows elevated choline and decreased N-acetylaspartate in tumors, with specific metabolite patterns suggesting particular tumor types. Functional MRI maps eloquent cortex involved in motor, language, and visual function to guide surgical planning. Diffusion tensor imaging demonstrates white matter tract displacement or invasion by tumor.
<image>Panel A: Glioblastoma with ring enhancement, central necrosis, and surrounding edema in the right temporal lobe. Panel B: Multiple enhancing metastases at the gray-white junction with surrounding vasogenic edema. Panel C: Homogeneously enhancing meningioma with dural tail along the falx cerebri. Panel D: Pituitary macroadenoma extending superiorly from the sella with compression of the optic chiasm.</image>
VI. Infection and Inflammation
Brain abscess appears as a ring-enhancing lesion with characteristic imaging features that distinguish it from neoplastic processes. The enhancing rim is typically thin, smooth, and complete, thinner along the medial ventricular aspect due to relatively decreased blood supply. Restricted diffusion within the abscess cavity is a key differentiating feature, appearing bright on diffusion-weighted imaging with corresponding low apparent diffusion coefficient values. The surrounding vasogenic edema may be extensive and produce significant mass effect. Abscesses typically occur at the gray-white junction where emboli lodge and may be multiple in the setting of hematogenous dissemination.
Meningitis is diagnosed primarily by clinical presentation and cerebrospinal fluid analysis, though imaging plays an important role in detecting complications. Contrast-enhanced MRI may demonstrate leptomeningeal enhancement coating the brain surface and extending into the sulci. Complications detectable on imaging include hydrocephalus from impaired cerebrospinal fluid circulation, subdural empyema, cerebral infarction from vasculitis, and ventriculitis with ependymal enhancement. CT may be performed before lumbar puncture to exclude mass lesions that could predispose to herniation, though this practice is increasingly questioned for patients without clinical signs of elevated intracranial pressure.
Encephalitis produces characteristic imaging patterns that vary by etiology and provide clues to the causative agent. Herpes simplex encephalitis demonstrates bilateral but often asymmetric temporal lobe involvement with T2 hyperintensity, swelling, and often hemorrhage. Autoimmune limbic encephalitis affects the mesial temporal lobes and is associated with specific antibodies including anti-NMDA receptor and anti-LGI1. HIV encephalopathy produces white matter atrophy and diffuse hyperintensity. Progressive multifocal leukoencephalopathy in immunocompromised patients demonstrates white matter lesions without significant enhancement or mass effect.
Demyelinating diseases produce characteristic patterns on MRI that enable diagnosis and monitoring of disease activity. Multiple sclerosis demonstrates periventricular white matter lesions oriented perpendicular to the ventricles, termed Dawson fingers, along with lesions in the corpus callosum, brainstem, and spinal cord. Active lesions enhance following gadolinium administration, often with incomplete ring enhancement that opens toward the cortex. Acute disseminated encephalomyelitis produces large, multifocal, bilateral white matter lesions that enhance simultaneously, distinguishing it from the temporal dissemination of multiple sclerosis. Neuromyelitis optica spectrum disorder affects the optic nerves and spinal cord with longitudinally extensive lesions spanning three or more vertebral segments.
<image>Panel A: Brain abscess with smooth thin ring enhancement and bright signal on diffusion-weighted imaging. Panel B: Leptomeningeal enhancement on post-contrast FLAIR in bacterial meningitis. Panel C: Herpes simplex encephalitis with bilateral temporal lobe T2 hyperintensity and swelling. Panel D: Multiple sclerosis with periventricular white matter lesions including Dawson fingers.</image>
VII. Spine Imaging
Modality selection for spine imaging depends on the clinical question, with MRI serving as the primary modality for evaluating disc disease, cord pathology, and soft tissue abnormalities. CT provides superior evaluation of osseous structures and is the preferred modality for assessing spinal fractures and post-surgical hardware. Plain radiographs offer initial assessment of alignment, degenerative changes, and obvious fractures but lack sensitivity for soft tissue pathology. CT myelography provides an alternative when MRI is contraindicated and offers excellent visualization of nerve root compression through contrast within the thecal sac.
Disc pathology is characterized by specific terminology that describes the relationship between displaced disc material and the annular margin. Disc bulge represents diffuse extension of disc material beyond the vertebral body margin involving more than fifty percent of the disc circumference. Disc protrusion is a focal displacement where the base of the displaced material at the disc space is wider than the apex. Disc extrusion describes focal displacement where the apex is wider than the base, indicating material has migrated through a defect in the annulus. Disc sequestration indicates a fragment of disc material has separated from the parent disc.
Spinal stenosis may occur at central, lateral recess, or foraminal levels and produces characteristic symptoms of neurogenic claudication or radiculopathy. Central stenosis results from combination of disc bulging, facet hypertrophy, and ligamentum flavum thickening that narrows the central canal. Lateral recess stenosis occurs between the thecal sac and the pedicle, compressing the traversing nerve root before it exits the foramen. Foraminal stenosis narrows the neural foramen through which the exiting nerve root passes, caused by foraminal disc herniation, osteophytes, or facet hypertrophy. MRI provides excellent visualization of the degree of canal and foraminal narrowing and nerve root compression.
Spinal cord pathology produces characteristic MRI findings that require urgent evaluation when cord compression is present. Cord compression from any cause, including disc herniation, tumor, or epidural abscess, requires urgent imaging and often emergent intervention to prevent permanent neurological deficit. Myelopathy produces T2 hyperintensity within the cord representing edema or gliosis, which may progress to cord atrophy in chronic cases. Syringomyelia appears as a CSF-signal cavity within the cord parenchyma and may be associated with Chiari malformation or prior trauma. Intramedullary tumors, including ependymoma and astrocytoma, expand the cord and demonstrate enhancement.
<image>Panel A: Sagittal T2-weighted MRI showing disc herniation at L4-L5 with compression of the thecal sac. Panel B: Axial image at the same level demonstrating central and lateral recess stenosis with nerve root compression. Panel C: Cervical spine MRI showing cord compression with T2 hyperintensity indicating myelopathy. Panel D: Syringomyelia with CSF-signal cavity extending through multiple thoracic cord segments.</image>
VIII. Head and Neck Imaging
Sinus imaging evaluates for inflammatory disease, tumors, and complications of sinusitis that may extend beyond the sinus cavities. Acute sinusitis demonstrates mucosal thickening and air-fluid levels within the affected sinuses and is usually diagnosed clinically without imaging. Chronic sinusitis produces mucosal thickening, polypoid changes, and opacification that may require CT for surgical planning. Complications of sinusitis including orbital cellulitis, subperiosteal abscess, and intracranial extension require urgent imaging and may necessitate surgical drainage. Sinonasal tumors produce bone destruction and extension beyond the sinus walls, distinguishing them from inflammatory disease.
Temporal bone imaging with CT provides detailed evaluation of the ossicles, otic capsule, and mastoid air cells. Cholesteatoma appears as a soft tissue mass eroding bone in the middle ear or mastoid, with characteristic locations in the pars flaccida or pars tensa. Chronic otitis media produces mastoid opacification and may be associated with ossicular erosion or tympanic membrane perforation. Temporal bone fractures are classified as longitudinal, transverse, or mixed based on orientation relative to the petrous pyramid. Otic capsule involvement in temporal bone fracture carries risk of sensorineural hearing loss and is an important finding to communicate.
Neck masses are localized by compartment to generate an appropriate differential diagnosis based on the structures present in each location. Thyroid nodules are evaluated with ultrasound and categorized using standardized reporting systems to guide biopsy decisions. Lateral neck masses include lymphadenopathy from various causes, branchial cleft cysts arising from embryologic remnants, and salivary gland lesions. Midline neck masses include thyroglossal duct cysts, which move with swallowing and tongue protrusion. Parotid masses are most commonly pleomorphic adenomas, which appear as well-defined enhancing lesions, though Warthin tumor and malignant tumors also occur.
Cerebrovascular imaging evaluates the carotid and vertebral arteries for stenosis, dissection, and other vascular pathology. CT angiography provides rapid evaluation of the cervical and intracranial vessels and has largely replaced conventional angiography for diagnostic purposes. Carotid stenosis is graded using the NASCET criteria based on the ratio of residual lumen to normal distal internal carotid artery diameter. Arterial dissection appears as narrowing of the arterial lumen with crescent of mural hematoma and may demonstrate the classic string sign of irregular narrowing. Doppler ultrasound serves as a screening and surveillance modality for carotid disease, with CT or MR angiography for comprehensive evaluation.
<image>Panel A: CT demonstrating opacification of the left maxillary sinus with air-fluid level indicating acute sinusitis. Panel B: Temporal bone CT showing middle ear cholesteatoma with erosion of the scutum. Panel C: Ultrasound of thyroid nodule with suspicious features requiring fine needle aspiration. Panel D: CT angiography demonstrating high-grade carotid stenosis with ulcerated atherosclerotic plaque.</image>
IX. Pediatric Neuroimaging
Modality selection in pediatric neuroimaging prioritizes minimizing radiation exposure while maintaining diagnostic accuracy. Ultrasound through the open anterior fontanelle provides excellent evaluation of neonatal brain anatomy and pathology without radiation or sedation. MRI offers superior soft tissue contrast without ionizing radiation but often requires sedation in young children. CT is reserved for trauma, emergent indications where rapid imaging is necessary, and evaluation of osseous abnormalities. When CT is required, pediatric protocols with reduced radiation parameters should be employed.
Congenital brain malformations produce characteristic imaging appearances that enable specific diagnosis. Chiari I malformation demonstrates cerebellar tonsillar descent greater than five millimeters below the foramen magnum, often associated with syringomyelia. Chiari II malformation occurs in the setting of myelomeningocele and features a small posterior fossa, tectal beaking, and extensive supratentorial abnormalities. Dandy-Walker malformation demonstrates a large posterior fossa cyst communicating with the fourth ventricle and absence or hypoplasia of the cerebellar vermis. Corpus callosum agenesis may be complete or partial and is recognized by characteristic ventricular configuration and absence of the normal midline white matter structure.
Hydrocephalus in children may be congenital or acquired and is classified as communicating or non-communicating based on the site of cerebrospinal fluid flow obstruction. Non-communicating hydrocephalus results from obstruction within the ventricular system, such as aqueductal stenosis, which produces selective dilation of the lateral and third ventricles. Communicating hydrocephalus results from impaired absorption at the arachnoid granulations and produces uniform ventricular dilation. Imaging features suggesting hydrocephalus requiring treatment include transependymal edema, thinning of the corpus callosum, and progressive ventricular enlargement. Shunt evaluation is commonly performed to assess for malfunction when patients present with symptoms of elevated intracranial pressure.
Non-accidental trauma produces characteristic imaging findings that should raise concern for child abuse and prompt appropriate evaluation and reporting. Subdural hematomas of different ages indicate recurrent injury and are highly suspicious for abuse, particularly in infants without history of accidental trauma. Complex skull fractures, multiple fractures, or fractures inconsistent with reported mechanism raise concern for non-accidental injury. Diffuse axonal injury from shaking produces white matter injury at gray-white junctions and in the corpus callosum. Retinal hemorrhages detected on ophthalmologic examination support the diagnosis of abusive head trauma.
<image>Panel A: Cranial ultrasound in a neonate demonstrating normal ventricles and periventricular white matter. Panel B: Chiari I malformation on sagittal MRI with cerebellar tonsillar descent and associated syringomyelia. Panel C: Hydrocephalus with dilated lateral and third ventricles and transependymal edema. Panel D: Subdural hematomas of different densities indicating different ages concerning for non-accidental trauma.</image>
X. Emergent Neuroimaging
Indications for emergent head CT include acute stroke requiring time-sensitive treatment decisions, head trauma to exclude intracranial hemorrhage, sudden severe headache concerning for subarachnoid hemorrhage, and new focal neurological deficit or altered consciousness requiring rapid diagnosis. CT is preferred in the emergency setting due to rapid acquisition, wide availability, and ability to exclude hemorrhage and other surgical emergencies. The examination should be performed immediately upon patient arrival, with results communicated directly to the treating team.
Acute stroke imaging follows a standardized protocol designed to identify candidates for thrombolysis and mechanical thrombectomy within narrow time windows. Non-contrast CT is obtained first to exclude hemorrhage, which would contraindicate thrombolytic therapy. CT angiography is performed immediately after to identify large vessel occlusion amenable to thrombectomy. CT perfusion may be added in selected patients to identify salvageable penumbra that could benefit from intervention beyond standard time windows. The door-to-imaging goal is typically less than twenty-five minutes to enable treatment decisions within appropriate time limits.
MRI is the urgent imaging modality of choice for specific neurological emergencies where CT would be insufficiently sensitive. Suspected spinal cord compression from any cause requires urgent MRI to evaluate the degree of compression and guide treatment decisions. Brain abscess evaluation benefits from MRI with diffusion imaging to distinguish abscess from necrotic tumor. Encephalitis produces characteristic MRI findings that enable diagnosis when clinical presentation is suggestive. Pituitary apoplexy with visual compromise requires urgent MRI to evaluate the extent of hemorrhage and mass effect on the optic chiasm.
Communication of emergent neuroimaging findings follows established protocols to ensure timely notification of the responsible clinical team. Large vessel occlusion in the setting of acute stroke requires immediate notification of the stroke team to enable rapid intervention. Expanding hematoma or signs of herniation demand immediate neurosurgical consultation. Any finding requiring emergent intervention must be communicated directly by verbal contact with documentation in the medical record. Systematic communication protocols, including callbacks and tracking of critical results, ensure that urgent findings are not lost in the transition from imaging to treatment.
<image>Panel A: Acute stroke CT protocol workflow from door arrival through perfusion imaging and treatment decision. Panel B: Large vessel occlusion on CT angiography requiring immediate stroke team notification for thrombectomy consideration. Panel C: Epidural hematoma with midline shift requiring emergent neurosurgical decompression. Panel D: Spinal cord compression on MRI requiring urgent surgical evaluation.</image>
Summary
Head CT interpretation follows a systematic approach using appropriate window settings to evaluate scalp, skull, extra-axial spaces, brain parenchyma, ventricles, and midline. Normal anatomy demonstrates characteristic attenuation values with gray matter slightly hyperdense to white matter and CSF hypodense. Acute hemorrhage appears hyperdense at fifty to seventy Hounsfield units and evolves through isodense to hypodense phases over weeks.
Intracranial hemorrhage patterns provide diagnostic information about etiology and guide management. Epidural hematoma is biconvex, arterial, and does not cross sutures. Subdural hematoma is crescent-shaped, venous, and crosses sutures. Subarachnoid hemorrhage fills CSF spaces and requires CT angiography to identify causative aneurysm. Intraparenchymal hemorrhage location suggests etiology, with basal ganglia suggesting hypertension and lobar suggesting amyloid angiopathy.
Acute stroke imaging identifies candidates for thrombolysis and thrombectomy through rapid CT, CT angiography, and perfusion imaging. MRI with diffusion-weighted imaging provides the most sensitive detection of acute ischemia. Brain tumors are characterized by location, enhancement pattern, and advanced imaging features. Intra-axial tumors include gliomas, metastases, and lymphoma, while extra-axial tumors include meningioma and schwannoma.
Spine imaging with MRI evaluates disc disease, stenosis, and cord pathology. Emergent MRI is required for suspected cord compression. Pediatric neuroimaging minimizes radiation through use of ultrasound and MRI when possible. Emergent neuroimaging requires systematic protocols for rapid acquisition and communication of critical findings.
Key Terms
DWI: Diffusion-weighted imaging, an MRI sequence detecting restricted water motion that appears bright in acute ischemic stroke and abscess.
FLAIR: Fluid-attenuated inversion recovery, an MRI sequence that suppresses CSF signal while maintaining T2 contrast, making periventricular and cortical lesions conspicuous.
LVO: Large vessel occlusion, thrombus within the internal carotid artery or proximal cerebral arteries that may be amenable to mechanical thrombectomy.
Penumbra: Ischemic brain tissue surrounding the infarct core that maintains blood volume through collateral flow and may be salvaged by timely reperfusion.
Dawson Fingers: Periventricular white matter lesions oriented perpendicular to the ventricles, characteristic of multiple sclerosis.
Dural Tail: Extension of enhancement along the dura from a meningioma, a characteristic imaging sign of this extra-axial tumor.
Cord Compression: Narrowing of the spinal canal with deformation of the spinal cord, an emergency requiring urgent MRI and often emergent intervention.
Midline Shift: Displacement of midline structures from their normal position, indicating mass effect that may progress to herniation if untreated.
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