This section serves as an introduction to the basic anatomy of the brain, head, neck, and spine. Brain anatomy is complex, and a complete discussion is beyond the scope of this text.

The human brain can be roughly divided into the cerebrum, thalamus, brain stem, and cerebellum. The cerebrum is comprised of the cerebral cortex, basal ganglia, and limbic system. The brain stem includes the midbrain, pons, and medulla. The cerebellum is composed of the cerebellar hemispheres and vermis.

Figures 3.1 to 3.10 illustrate the structures and blood vessels of the brain, head, neck, and spine.

MR (magnetic resonance) is the cornerstone of modern imaging of the brain and spinal cord. Images are obtained by taking advantage of resonance properties of nuclei under the influence of an external magnetic field. Some basic sequences that the reader should become familiar with are shown in Figs. 3.11 to 3.13.

PATIENT PRESENTATION

A 72-year-old male presents to the emergency department with acute onset of focal sensory loss and right arm weakness.

CLINICAL SUSPICION

Acute ischemic stroke

IMAGING MODALITY OF CHOICE

Noncontrast CT of the head to evaluate for hemorrhage and early ischemic changes. Advantages: fast and readily available, high sensitivity for presence of hemorrhage.

FINDINGS

Cerebral infarcts are the leading cause of disability and fourth leading cause of death in the United States. Patients with acute cerebral ischemia/infarct usually present with sudden-onset neurologic deficit (weakness, sensory loss, aphasia). Risk factors include diabetes, hypertension, smoking, and hyperlipidemia. It is important to realize that the value in CT is not to diagnose an acute ischemic infarct. The role of CT is to exclude hemorrhage, exclude nonischemic pathologies (masses, infections, vascular malformations), and evaluate the volume of infarcted territory. In the setting of cerebral infarcts, the infarcted territory results in contralateral symptomatology.

CT

• 
  

  Usually normal in the hyperacute phase

  
  
• 
  

  Hyperdense vessel representing acute thrombus (low sensitivity, high specificity) (Fig. C1.1)

  
  
• 
  

  Loss of gray matter–white matter differentiation

  
  
  
  
  • 
    

    “Insular ribbon” sign: swelling and blurring of normal gray-white differentiation within the insular cortex

    
    
  • 
    

    Obscured lentiform nucleus

  
  
• 
  

  Parenchymal hypodensity resulting from early cytotoxic edema (Fig. C1.2)

  
  
• 
  

  Gyral swelling with sulcal effacement

  
  

  Additional CT examinations that may be performed:

  
  
• 
  

  CT angiography: useful in localizing area of arterial stenosis or occlusion

  
  
• 
  

  CT perfusion: useful in identification of penumbra (brain at risk), which may help stratify patients for therapeutic intervention

MRI

• 
  

  Highly sensitive to diagnose acute infarcts within minutes of onset.

  
  
• 
  

  Areas of acute ischemia restrict free diffusion of water, resulting in elevated signal on DWI images and decreased ADC values (Fig. C1.3).

  
  
• 
  

  Limitations of MRI in the emergency setting include difficulty to transport and monitor unstable patients, longer scan times, limited availability, and contraindications in certain patients (pacemakers, intraocular metallic foreign bodies).

Intravenous treatment of acute ischemic stroke with r-TPA can be considered if it is less than 4.5 hours since symptom onset, there is no CT evidence of hemorrhage, and the infarct does not involve more than one-third of the MCA distribution. Intra-arterial treatment with r-TPA can be considered up to 6 hours after symptom onset.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

• 
  

  Acute hemorrhagic infarct

  
  
• 
  

  Neoplasm

  
  
• 
  

  Encephalitis

  
  
• 
  

  Todd’s paralysis

Imaging Differential

• 
  

  Hyperdense vessel: high hematocrit, atherosclerosis.

  
  
• 
  

  Parenchymal hypodensity: infiltrating neoplasm, encephalitis/cerebritis, encephalomalacia, dural venous thrombosis with venous congestion and edema.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 59-year-old hypertensive male presents to the emergency department with headache and acute sensory deficit.

CLINICAL SUSPICION

Hypertensive hemorrhagic stroke

IMAGING MODALITY OF CHOICE

CT head without contrast to evaluate for presence of hemorrhage (Fig. C2.1). Advantages: fast and readily available, high sensitivity for presence of hemorrhage.

FINDINGS

Chronic hypertension results in damage to small perforating arteries leading to fibrinoid necrosis and vessel fragility. Hemorrhagic strokes account for only 10% of all strokes (the majority are ischemic) and are associated with a higher mortality rate. Patients with hypertension have a fourfold increased risk of intracranial hemorrhage. The most common locations include the basal ganglia/external capsule, thalamus, brain stem, and cerebellum; however, approximately 10% are lobar. Initially, there may be little mass effect or surrounding edema; however, this often develops in the first couple of days leading to patient deterioration. As treatment differs markedly from ischemic stroke, prompt diagnosis is essential.

CT

• 
  

  Round or oval hyperdense lesion in the brain parenchyma on noncontrast CT with predilection for certain locations as described earlier.

  
  
• 
  

  Other evidence of hypertensive cerebrovascular disease including chronic lacunar infarcts, multiple subacute/chronic microbleeds, and microvascular white matter changes.

MR

Hemorrhage on MR has varied imaging characteristics (Table C2.1, Figs. C2.2 and C2.3):

• 
  

  Gradient echo sequences may show several hypointense foci secondary to microbleeds. It is important to note that this is also commonly seen in cerebral amyloid angiopathy (disorder of vascular amyloid deposition leading to multiple bleeds).

  
  
• 
  

  No/mild peripheral contrast enhancement.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

• 
  

  Ischemic stroke

  
  
• 
  

  Neoplasm

  
  
• 
  

  Encephalitis/meningitis

Imaging Differential

• 
  

  Hemorrhagic transformation of an ischemic infarct

  
  
• 
  

  Cerebral amyloid angiopathy

  
  
• 
  

  Underlying neoplasm or vascular lesion

  
  
• 
  

  Cocaine abuse

  
  
• 
  

  Coagulopathy

  
  
• 
  

  Venous thrombosis

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

Patient presents to the emergency department after hitting his head in a car accident.

CLINICAL SUSPICION

Traumatic intracranial extra-axial hemorrhage

IMAGING MODALITY OF CHOICE

CT head without contrast. Advantages: fast and readily available, high sensitivity for presence of hemorrhage.

FINDINGS

Injuries involving the central nervous system are the leading cause of death in trauma patients. Intracranial hemorrhage is often seen in patients with moderate to severe head trauma. Acute hemorrhage is usually hyperdense on noncontrast CT images. In some instances the hemorrhage may have low density due to severe anemia, DIC, and hyperacute active bleeding, making its detection more difficult. There are several types of extra-axial hemorrhage based on location, as shown in Fig. C3.1.

Epidural Hematoma (EDH)

The epidural space is a potential space between the inner table of the skull and the dura mater. CT shows a hyperdense biconvex extra-axial collection (Figs. C3.2 and C3.3). It does not cross suture lines due to firm attachment of the dura to the suture but may cross the midline. Bleeding most commonly results from tearing of the middle meningeal artery from calvarial fracture, secondary to trauma. Most epidural hematomas are found in the temporal and parietal regions. They may also be found in the posterior fossa secondary to a venous sinus tear. Approximately half of patients will have a lucid interval after the insult.

Subdural Hematoma (SDH)

Collection of blood in the space between the dura mater and the arachnoid layer. CT shows a hyperdense crescentic extra-axial collection (Fig. C3.4). It can cross suture lines but does not cross the midline. Bleeding results from tearing of bridging cortical veins as a result of rotational motion of the brain with respect to the fixed venous structures. This most commonly occurs over the cerebral convexities. Subdural hematomas are often secondary to trauma but can occur secondary to minor trauma in elderly patients and patients on anticoagulation.

Subarachnoid Hemorrhage (SAH)

CT shows hyperdensity in the subarachnoid space (Fig. C3.5); 4 different patterns may be seen.

• 
  

  Adjacent to intraparenchymal or extraparenchymal hematomas: common in severe head trauma.

  
  
• 
  

  Overlying the cerebral hemispheres in isolation: common in mild and moderate head trauma.

  
  
• 
  

  Extensive hemorrhage within the basal cisterns and subarachnoid space: often seen in the setting of nontraumatic subarachnoid hemorrhage from ruptured aneurysm or arteriovenous malformation (AVM). It can also occur from traumatic arterial dissection, sometimes with concomitant skull base fracture.

  
  
• 
  

  Nontraumatic perimesencephalic hemorrhage: focal small hemorrhage in the interpeduncular cistern can be seen in patients presenting with headache without aneurysm. It usually results in no long-term clinical sequelae.

It is critical to evaluate patients with SAH for an intracranial aneurysm, regardless of a history of head trauma. A ruptured aneurysm may have been the precipitating event prior to the incident leading to the head trauma.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

Epidural hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, diffuse axonal injury (DAI), and concussion.

Imaging Differential

• 
  

  Epidural hemorrhage: subdural hemorhhage, abscess, tumor, inflammatory lesion, extramedullary hematopoiesis.

  
  
• 
  

  Subdural hemorrhage: EDH, subdural hygroma, pachymeningitis (thickened dura), tumor.

  
  
• 
  

  Subarachnoid hemorrhage: exudates in the subarachnoid space, serpentine calcifications from cortical laminar necrosis, arteriovenous malformation, Sturge-Weber syndrome, racemous neurocysticercosis.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

An unconscious trauma patient presents to the emergency department and has a normal noncontrast head CT.

CLINICAL SUSPICION

Diffuse axonal injury (traumatic brain injury)

IMAGING MODALITY OF CHOICE

MRI brain without contrast. Advantages: excellent contrast between normal and edematous brain parenchyma, highly sensitive for small hemorrhages due to susceptibility of blood products.

FINDINGS

Diffuse axonal injury (DAI) is a shearing/stress injury caused by rotational acceleration/deceleration movements of the head. Brain tissues of different densities accelerate/decelerate at varying speeds, and particularly in regions where these tissues intersect the axons get stretched, resulting in damage. Small white matter vessels may also tear, resulting in petechial hemorrhages. Injuries are most commonly nonhemorrhagic, but hemorrhagic lesions also occur. Initial noncontrast CT is usually normal.

MRI

Multiple bilateral punctate to 1.5 cm round or ovoid foci with the long axis parallel to fiber bundles.

• 
  

  Nonhemorrhagic foci: bright on T2-weighted and FLAIR sequences.

  
  
• 
  

  Hemorrhagic foci: bright on T1, dark on T2, bright on FLAIR, and very dark on gradient echo images (due to susceptibility from blood products). GRE is the most sensitive sequence.

  
  
• 
  

  DWI may show areas of restricted diffusion (bright signal).

Lesions are found in characteristic locations with increasing order of injury severity:

1. 
   

   Gray-white matter junction, typically in the frontal and temporal lobes, and cerebral white matter (Figs. C4.1 and C4.2).

   
   
2. 
   

   Corpus callosum, most common in the splenium.

   
   
3. 
   

   Dorsal upper brain stem and cerebellum.

   
   
4. 
   

   Additional less common locations: deep gray matter, internal/external capsule, tegmentum, and fornix. Lesion burden on MRI may predict the degree of potential neurological recovery.

Additional MRI sequences can be performed such as diffusion tensor imaging and MR spectroscopy, which can be helpful in cases in which conventional MR imaging is inconclusive.

CT

• 
  

  May show punctate areas of high density (hemorrhage) surrounded by a collar of low-density edema.

  
  
• 
  

  Usually underestimates the extent of the disease.

DAI should be considered if the patient’s symptoms are disproportionate to the imaging findings. DAI carries a poor prognosis, and patients may remain in a persistent vegetative state.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

EDH, SDH, SAH

Imaging Differential

• 
  

  Multifocal nonhemorrhagic lesions: age-related lesions (leukoaraiosis and lacunes), demyelinating disease, Marchiafava-Bignami syndrome (corpus callosum lesions).

  
  
• 
  

  Multifocal hemorrhagic lesions: cerebral amyloid angiopathy, chronic hypertension, cavernous malformations, hemorrhagic metastases.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 24-year-old pregnant female presents to her physician with elevated blood pressure and sudden onset of headache and visual disturbance.

CLINICAL SUSPICION

Posterior reversible encephalopathy syndrome (PRES)

IMAGING MODALITY OF CHOICE

MRI head with and without contrast (include DWI). Advantages: T2/FLAIR images are sensitive for edema.

FINDINGS

Bilateral, symmetric, patchy abnormalities classically involving the subcortical white matter of the occipital and parietal lobes. It may also extend to the cortex and involve the temporal and frontal lobes, pons, and cerebellum.

CT

Hypodensity in the subcortical white matter of the occipital and parietal lobes (Figs. C5.1 and C5.2).

MRI

• 
  

  T2-weighted image/FLAIR: high signal intensity in the affected areas.

  
  
• 
  

  T1-weighted image: corresponding low signal intensity.

  
  
• 
  

  DWI-ADC map: areas of DWI abnormality without ADC correlation are more common, but irreversible ischemia (high DWI signal with decreased ADC signal) may occur.

  
  
• 
  

  Enhancement can be seen but is not a common finding.

  
  
• 
  

  MR perfusion: may show decreased relative cerebral blood volume, decreased cerebral blood flow, and increased mean transit time.

  
  
• 
  

  Areas of hemorrhage are seen in approximately 15% of patients.

Angiography (MRA or Conventional)

May demonstrate a vasculopathy type pattern with areas of vessel irregularity, consistent with vasoconstriction/vasodilation.

The underlying etiology of PRES is thought to be the inability of the posterior circulation to autoregulate in response to acute changes in blood pressure. This results in vascular damage and breakdown of the blood-brain barrier leading to vasogenic edema. Symptoms include headache, confusion, seizures, and loss of vision. Interestingly, hypertension is absent in approximately 25% of patients with PRES, alluding to alternative underlying mechanisms of the disease. With prompt diagnosis and treatment of the underlying cause, PRES is usually reversible; in some instances it may progress to infarction.

PRES may be caused by hypertension, preeclampsia/eclampsia, immunosuppressive drugs, chemotherapy (tacrolimus and cyclosporine), sepsis, renal disease, autoimmune diseases, cryoglobulinemia, and hemolytic-uremic syndrome.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

• 
  

  Primary headache/migraine

  
  
• 
  

  Preeclampsia/eclampsia not associated with PRES

  
  
• 
  

  Venous sinus thrombosis

  
  
• 
  

  Intraparenchymal hemorrhage

Imaging Differential

• 
  

  Acute ischemic infarct

  
  
• 
  

  Status epilepticus

  
  
• 
  

  Metabolic abnormalities

  
  
• 
  

  Gliomatosis cerebr

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 28-year-old female presents with sudden onset of severe headache, confusion, and right extremity weakness.

CLINICAL SUSPICION

Intracranial hemorrhage, possibly from vascular malformation

IMAGING MODALITY OF CHOICE

CT head without contrast in the acute setting followed by CTA or MRA. Definitive diagnosis/characterization performed with catheter angiography. Advantages: fast and readily available, high sensitivity for presence of hemorrhage.

FINDINGS

Arteriovenous malformations are abnormal connections/networks of blood vessels that result in arteriovenous shunting of blood, bypassing blood supply to the brain tissue (Fig. C6.1A,B). They are characterized by an enlarged feeding artery/arteries leading to a nidus of entangled abnormal vessels (no true capillary bed) and early drainage into enlarged draining veins (Fig. C6.2). In the acute setting, noncontrast head CT is the imaging modality of choice.

CT

• 
  

  Intraparenchymal hematoma if ruptured. Can also result in intraventricular or subarachnoid hemorrhage.

  
  
• 
  

  If unruptured, hyperdense serpentine mass lesion.

  
  
• 
  

  Curvilinear or speckled calcifications may be seen.

  
  
• 
  

  Surrounding hypodensity of gliosis (chronic ischemia or previous hemorrhage).

CTA/MRA

• 
  

  Intensely enhancing curvilinear structures on CTA, curvilinear flow voids on MRI.

  
  
• 
  

  Dilated feeding arteries and draining veins; veins typically larger than arteries.

  
  
• 
  

  Intranidal aneurysms (found more than 50% of the time).

Catheter angiography provides dynamic information showing the arterial supply and venous drainage of the lesion.

Pitfalls in diagnosis can occur with small lesions, location near a major dural venous sinus, and due to compression from acute hematoma (repeat angiogram is warranted if initial study is normal).

AVMs can be classified using the Spetzler-Martin grading system in order to predict operative outcomes as shown in Table C6.1 (graded 1 to 5 by adding the points in each category).

Grades 1 and 2 are treated with surgical resection; Grade 3 lesions receive multimodality treatment (microsurgery/endovascular/radiosurgery); Grades 4 and 5 are not treated, with the exception of recurrent hemorrhages, progressive neurological deficits, steal-related symptoms, and AVM-related aneurysms. Imaging features that are associated with a risk of future hemorrhage include prior hemorrhage (low signal intensity on gradient echo sequence), intranidal aneurysms, venous stasis or ectasia, deep venous drainage, single venous drainage, and deep or posterior fossa locations. Imaging features associated with risk of nonhemorrhagic neurological deficits include high-flow shunt, venous congestion or outflow obstruction, long pial course of draining vein, perifocal or perinidal gliosis, mass effect or hydrocephalus, and arterial steal.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

CVA, underlying neoplasm, amyloid angiopathy

Imaging Differential

Hypertensive bleed, other vascular lesions (cavernous hemangioma), intratumoral hemorrhage, dural sinus thrombosis with hemorrhagic infarct, mycotic aneurysm, drug abuse.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 53-year-old female with history of hypertension presenting with complaints of intermittent headache. Patient recalls having been diagnosed with benign tumor many years ago.

CLINICAL SUSPICION

Meningioma

IMAGING MODALITY OF CHOICE

In the acute setting, noncontrast CT is obtained to exclude intracranial hemorrhage. MRI is preferred for evaluation of intracranial neoplasms as it provides greater sensitivity, superior parenchymal detail, and better tissue contrast.

FINDINGS

Meningiomas are tumors that arise from the meninges and as a result are extra-axial. While most meningiomas are benign (WHO Grade 1), atypical (WHO Grade 2) and malignant meningiomas (WHO Grade 3) can rarely be seen.

CT

• 
  

  Hyperdense extra-axial mass on noncontrast CT (Fig. C7.1)

  
  
• 
  

  20% to 25% are calcified

  
  
• 
  

  Hyperostosis (thickening) of the adjacent calvarium

  
  
• 
  

  Avidly enhance, with enhancement of a dural tail

MRI

• 
  

  T1: isointense to hypointense to cerebral cortex; may be heterogeneous due to cystic degeneration and/or hemorrhage (Fig. C7.2).

  
  
• 
  

  T2: variable, large lesions can be associated with edema within the subjacent brain parenchyma; visualization of a CSF cleft between mass and adjacent brain parenchyma is helpful in diagnosis of an extra-axial mass.

  
  
• 
  

  T1+C: avid enhancement with enhancement of a dural tail (Fig. C7.3).

DIFFERENTIAL DIAGNOSIS

Clinical Differential

While most patients with typical meningioma are asymptomatic, patients with larger lesions may present with varied symptoms based upon the location of the lesion. Parasagittal lesions may present with seizures and weakness; basisphenoid/diaphragm sella lesions with visual defects, and cavernous sinus lesions with cranial nerve palsies.

Imaging Differential

• 
  

  Metastasis: Dural-based metastasis can mimic meningiomas; however, patients usually have a known primary tumor and may have other sites of metastatic disease.

  
  
• 
  

  Granuloma: Meningeal involvement from sarcoid or TB can mimic meningioma; however, these patients often have signs/symptoms of disease elsewhere in the body.

  
  
• 
  

  Lymphoma: Extra-axial areas of lymphomatous involvement are usually multifocal and present in patients with known history of lymphoma. Lesions demonstrate hypointensity on T2 images due to hypercellularity.

  
  
• 
  

  Hemangiopericytoma: Can mimic meningioma; however, calcification and hyperostosis are usually absent. Enhancement is usually more heterogeneous.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 48-year-old male presents to his physician with new-onset seizures.

CLINICAL SUSPICION

High-grade glioma / glioblastoma multiforme (GBM)

IMAGING MODALITY OF CHOICE

MRI brain with and without contrast. Advantages: MRI is preferred for evaluation of intracranial neoplasms as it provides greater sensitivity, superior parenchymal detail, and better tissue contrast. Diffusion weighted imaging, perfusion imaging, and MR spectroscopy may be helpful in evaluation of intracranial neoplasms.

FINDINGS

While most intra-axial neoplasms are metastatic, glioblastoma multiforme (WHO grade 4 tumor) accounts for approximately 25% of all intra-axial neoplasms. It is a highly malignant infiltrating astrocytoma with a poor prognosis (10%-15% two-year survival). These tumors can occur anywhere but most commonly arise, in decreasing order of frequency, in the temporal, parietal, and frontal lobes. GBMs can either be a primary tumor (arising de novo) or a secondary tumor (resulting from dedifferentiation of a lower grade astrocytoma).

MRI

• 
  

  T1: usually heterogeneously isointense to hypointense. Heterogeneity results from internal necrosis; some cases present with hemorrhage.

  
  
• 
  

  T2/FLAIR: heterogneously hyperintense with surrounding edema/infiltrative tumor (Fig. C8.1).

  
  
• 
  

  T1+C: variable. Typically there is an irregular rind of enhancement surrounding a central area of necrosis (Fig. C8.2).

The tumor frequently crosses the midline to the contralateral hemisphere by direct extension through the corpus callosum, anterior commisure, or posterior commisure (“butterfly” tumor). It is important to realize that microscopic infiltration of tumor beyond the borders of imaging abnormality. Increased relative cerebral blood volume (rCBV) can be seen on perfusion studies and has been shown to correlate with the histological grade (higher rCBV = higher histological grade). The presence of lactic acid on MR spectroscopy and the presence of intratumoral hemorrhage have also been linked to higher-grade tumors.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

• 
  

  Medication/drug related seizures, CVA, metabolic disorder, meningitis/encephalitis, posttraumatic, autoimmune/degenerative diseases, neoplasm.

Imaging Differential

• 
  

  Metastasis.

  
  
• 
  

  Ring-enhancing lesions: abscess, demyelinating disease, resolving hematoma, subacute cerebral infarction, radiation necrosis.

  
  
• 
  

  Corpus callosum lesions: lymphoma, multiple sclerosis.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

Patient presents to the emergency department with seizure and has a history of AIDS.

CLINICAL SUSPICION

Opportunistic infection versus neoplasm

IMAGING MODALITY OF CHOICE

MRI brain with and without contrast. Advantages: MRI is preferred for evaluation of intracranial infections or neoplasms as it provides greater sensitivity, superior parenchymal detail, and better tissue contrast.

FINDINGS

The vast majority of primary CNS lymphoma is non-Hodgkins lymphoma and usually occurs in immunocompromised individuals. These lesions are mostly supratentorial in location (above the tentorium cerebelli) and commonly involve the periventricular white matter and deep gray matter. CNS lymphoma may spread along the ventricular lining (subependymal) and cross the midline. It usually presents with multiple lesions that are less than 2 cm in size. Primary CNS lymphoma in immunocompetent patients is less often seen and usually has a later onset.

CT

• 
  

  High-density mass/masses typically periventricular in location on noncontrast exam with variable enhancement.

  
  
• 
  

  Central necrosis may be present; hemorrhage rarely present.

MR

• 
  

  T1: isointense or hypointense lesions (Fig. C9.1).

  
  
• 
  

  T2/FLAIR: variable; approximately half will be isointense or slightly hypointense owing to tumor cellularity. Increased T2/FLAIR signal surrounding lesions representing edema.

  
  
• 
  

  T1+C: variable, usually solid or ring enhancement (Fig. C9.2).

  
  
• 
  

  DWI: mildly restricted diffusion due to high cellularity.

An alternative diagnosis found in AIDS patients that must be differentiated from lymphoma (due to similar imaging characteristics) is toxoplasmosis (Table C9.1). Toxoplasmosis is the most common cause of focal lesions in AIDS patients.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

HIV encephalitis, other CNS infections (toxoplasmosis, CMV, PML, aspergillosis, cryptococcus, TB), alcohol withdrawal, drug toxicity, CVA, hemorrhage, metabolic disorders.

Imaging Differential

• 
  

  Diffuse/patchy WM abnormalities in AIDS: HIV encephalitis, PML, CMV.

  
  
• 
  

  Focal/multifocal brain lesions in AIDS: toxoplasmosis, lymphoma, tuberculoma, fungal, abscess.

REFERENCES AND SUGGESTED READING

PATIENT PRESENTATION

A 5-year-old female presents to the clinic with several-week history of increasing ataxia and 3-day history of nausea/vomiting.

CLINICAL SUSPICION

Brain tumor

IMAGING MODALITY OF CHOICE