Band heterotopia

CASE 1 (7-month-old)






CASE 2 (Pre-adolescent)






Findings

Case 1: Axial and coronal T2-weighted images of the brain in a 7-month-old girl with seizures demonstrate a band of isointense signal within the subcortical white matter, characteristic of band heterotopia.
Case 2: Axial and coronal T1-weighted images demonstrate band heterotopia, better seen in this preadolescent girl due to completion of myelination.


Diagnosis: Band heterotopia


Band heterotopia is a rare neuronal migration anomaly which manifests as homogenous bands of gray matter are interposed between the lateral ventricles and cortical mantle with normal appearing white matter on either side. The overlying cortex may be normal, pachygyric, or display a simplified gyral pattern with short gyri and shallow sulci. At least six morphologically distinct subtypes have been described. Band heterotopias represent a subset of gray matter heterotopia which also includes subependymal and subcortical heterotopia subtypes.

Band heterotopia typically affects female patients as a result of an X-linked dominant inheritance pattern secondary to abnormal function of the doublecortin (DCX) gene (Xp22.3-p23) or less frequently the LIS1 (17p13.3) gene. Male patients can be affected due to sporadic mutations of these genes (41 reported cases in the literature by D’Agostino, et al in 2002). The rate of detectable mutations involving DCX or LIS1 in male patients (42%) is lower than the rate of 85% described in female patients. Dysmorphic features described in patients with band heterotopia include microcephaly (most common), wide nasal bridge, high arched palate, and short stature.

The clinical presentation of band heterotopia can range from normal to nearly normal intelligence and mild developmental delay to frank mental retardation. Seizures are often also present and may begin in the first decade, ranging from partial to generalized or multiple seizure types. The discovery of the underlying brain malformation is due to the onset of seizures in 65% of patients. Eventually 95% of patients with band heterotopias will develop epilepsy. Seizures associated with band heterotopia are often refractory to medical therapy, and surgical therapies such as callosotomy may be performed in these patients. In the series of 30 male patients published in 2002, 46% of patients were refractory to medical therapy and experienced up to 20-30 seizures daily despite trails of multiple therapeutic regimens. Affected male patients tend to have either mild or severe symptoms, whereas, female patients tend to have symptoms within the mild to moderate range of the spectrum from minimal cognitive impairment to severe mental retardation. Posterior involvement, in particular the partial posterior and intermediate posterior subtypes, occur more commonly in male patients. Frontal and diffuse subtypes are more often present in affected female patients.

Chloroma of epidural space

Additional clinical history: Acute leukemia.


Findings

Large anterior epidural mass extending from posterior clinoid to the cervicothoracic junction measuring approx. 6x3x1.5 cm with mass effect on the anterior pons, medulla, and upper cervical cord. No post-contrast imaging obtained.

Differential diagnosis: Epidural mass
- Metastatic disease
- Lymphoma
- Leukemia/chloroma
- Chordoma
- Osteomyelitis/epidural abscess
- Epidural hematoma
- Primary tumor such as neurofibroma/schwannoma


Diagnosis: Chloroma of epidural space


Key points

AKA granulocytic sarcoma, extramedullary myeloblastoma.
Most commonly occurs in the setting of AML.
Can also occur in setting of chronic myelogenous leukemia and other myeloproliferative disorders.
These tumors can involve any part of the body, either concurrently or sequentially.

Imaging characteristics:
- NECT: Isodense or hyper dense to brain or muscle
- MR: Hypo intense or Iso intense on T1-weighted MR images, heterogeneously Iso intense or hyper intense on T2-weighted MR images
- MR+C: Enhance homogeneously after injection of contrast medium

Paraspinal and intraspinal lesions are also thought to arise from perivenous arachnoid spread of leukemic cells. Uncommonly, spinal involvement by granulocytic sarcoma may cause compression of the spinal cord, cauda equina, or nerve roots

Basilar dolichoectasia determining a vascular loop compression syndrome

Findings

Figure 1, Figure 2, Figure 3, Figure 4, and Figure 5: Axial high resolution T2 fiesta images show a dilated and tortuous basilar artery which extends into the left cerebellopontine angle. The visualized inner ear structures are normal.
Figure 6: The basilar artery appears to contact the left trigeminal nerve at the root-exit zone.


Diagnosis: Basilar dolichoectasia


Trigeminal neuralgia is a clinical syndrome composed of paroxysmal facial pain usually confined to the maxillary (V2) and/or mandibular (V3) branches of the trigeminal nerve. Occasionally the opthalmic division (V1) is also affected. This syndrome is more common in patients over the age of 65, with no gender specificity.

VLCS is a recognized cause of trigeminal neuralgia. The offending vessel courses into the anterior cerebellopontine cistern with subsequent irritation of the 5th cranial nerve at the preganglionic root entry zone (REnZ). Additional causes of trigeminal neuralgia include anuersysms, AVMs, and tumors of the cerebello-pontine angle. Demyelinating disorders such as multiple sclerosis are also described as a potential cause.

Thin section high resolution T2 MRI of the CPA/IAC allows the best visualization of the vascular loop. These images also show the anatomic course of the 5th cranial nerve from the root entry zone into meckel’s cave. The imaging protocol should include whole brain T2/FLAIR to exclude additional etiologies such as multiple sclerosis. Axial and coronal T1 of the brainstem with gadolinium enhancement is also helpful to look for cranial neuritis, perineural tumor, and cisternal tumor such as an epidermoid, schwanomma, or meningioma.

Lateral medullary syndrome (Wallenberg syndrome)

Findings

Axial FLAIR (Figure 1 and Figure 2) and T2-weighted (Figure 3 and Figure 4) images demonstrate mild signal hyperintensity in region of the left lateral and posterior medulla PICA territory.
Axial DWI (Figure 5 and Figure 6) and matching ADC maps (Figure 7 and Figure 8) demonstrate true restricted diffusion in the left lateral and posterior medulla PICA suggestive of cytotoxic edema fort an acute infarction.
3D TOF posterior circulation MIP projection (Figure 9) demonstrates absence of a normal left PICA. It's possibile to see the right PICA for comparison, arising from the distal right intracranial vertebral artery. There is also a mild narrowing of the basilar artery. It's possibile also to appreciate bith the superior cerebellar arteries.


Diagnosis: Lateral medullary syndrome (Wallenberg syndrome)


Adolf Wallenberg (November 10, 1862-1949) was a German internist and neurologist who first described the clinical manifestations (1895) and the autopsy findings (1901) in occlusions of the arteria cerebelli posterior inferior (Wallenberg syndrome).

Lateral medullary syndrome is characterized by sensory deficits affecting the trunk and extremities on the opposite side of the infarct and sensory, and motor deficits affecting the face and cranial nerves on the same side with the infarct. Other clinical symptoms and findings include ataxia, facial pain, vertigo, nystagmus, diplopia, Horner syndrome, and dysphagia. The cause of this syndrome is secondary to occlusion of the PICA near its origin. Similar symptoms may be produced by vertebral artery occlusion near the origin of the PICA.

Afflicted persons can have dysphagia resulting from involvement of the nucleus ambiguus and slurred speech (dysphonia and dysarthria). Damage to the spinal trigeminal nucleus causes absence of pain on the ipsilateral side of the face as well as an absent corneal reflex. The spinothalamic tract can be damaged, resulting in loss of pain and temperature sensation to the opposite side of the body. Damage to the cerebellum can cause ataxia. Damage to the hypothalamospinal fibers disrupts sympathetic nervous system relay and gives symptoms analogous to Horner syndrome (ptosis, anhidrosis, and miosis).

In older patients, the most common cause of posterior circulation ischemia is thromboembolic disease resulting from accelerated atheromatous disease or embolic disease from a cardiac source. In young patients with posterior fossa ischemia, in addition to embolic disease, the diagnosis of arterial dissection should also be considered.
Wallenberg syndrome synonyms: dorsolateral medullary syndrome, lateral bulbar syndrome, lateral medullary infarction syndrome, and PICA syndrome.

Subdural empyema

Findings

A large left middle cranial fossa subdural empyema is demonstrated, with a relatively thin rim of enhancement. Internally, there is a large quantity of debris. There is mass effect, with a modest midline shift and effacement of the left lateral ventricle. Inflammatory changes are demonstrated in the left temporal bone which is likely the source of the abscess. There is diffusion restriction, not marked, consistent with abscess. There is extensive dural enhancement, along with considerable surrounding edema.

Differential diagnosis:
- Subdural empyema
- Chronic subdural hematoma
- Subdural effusion
- Subdural hygroma
- Dural metastasis


Diagnosis: Large left middle cranial fossa subdural empyema; left mastoiditis


Key points

Loculated collection of pus in subdural space
Best diagnostic clue: Extra-axial collection with contrast enhancing rim
Supratentorial typical
Infratentorial (up to 10%), often associated with mastoiditis
Crescentic typical; may be lens shaped on coronal images
CT demonstrates extra-axial collection, iso-to hyper dense to CSF on noncontrasted CT; shows strong peripheral enhancement with contrast
Best imaging tool: MR with DWI to demonstrate presence, nature, extent and complications
T1W image shows:
Extra-axial collection hyper intense to CSF
Crescentic extra-axial collection
T2WI demonstrates a lesion that is Iso-to hyper intense to CSF,
FLAIR shows a crescentic fluid collection which is hyper intense to CSF, underlying brain may be hyper intense
DWI shows restricted diffusion (increased signal intensity); Differentiates subdural empyema from subdural effusions
T1WI post contrast shows:
Prominent enhancement at margin related to granulomatous tissue and inflammation
Encapsulating membranes enhance strongly, may be loculated with internal fibrous strands
May see enhancement of adjacent brain parenchyma
MRV may show venous thrombosis seen as a lack of flow
CT may miss small collections
Complications include cerebritis and brain abscess, cortical vein and dural sinus thrombosis, and cerebral edema
Subdural empyema is much more common than epidural empyema
In older children, adults: Related to paranasal sinus disease (>2/3), in infants and young children it can be a complication of bacterial meningitis
Most common signs/symptoms include fever, headaches, meningismus, sinusitis, cerebritis
Sinus or ear infection in > 75% of cases
Confused with meningitis which may lead to delayed diagnosis
Can occur at any age
Rare, yet high mortality rate.
If subdural or epidural abscess is discovered, look also for sinusitis, otomastoiditis, dural sinus thrombosis and brain abscess
Progresses rapidly, neurosurgical emergency
Surgical drainage via wide craniotomy is gold standard

Benign perimesencephalic SAH

Findings

Figure 1, Figure 2, and Figure 3: Axial CT images of the brain demonstrate SAH in the premedullary, prepontine, suprasellar, and interpeduncular cisterns.
Other figures (not shown): Representative images from a 4-vessel cerebral angiogram demonstrate no evidence of aneurysm or vascular malformation.


Diagnosis: Benign perimesencephalic SAH


Trauma and aneurysm are the two most common causes of SAH. At least 80% of cases of atraumatic SAH are caused by rupture of an intracranial aneurysm. When SAH is present, many clinicians request CT or MR angiography in order to quickly and non-invasively diagnose aneurysm. If an aneurysm is not detected with one of these modalities, conventional cerebral angiography (the gold standard for exclusion of aneurysm) is necessary. If the initial angiogram is negative, a second cerebral angiogram, typically performed 1-3 weeks after the first, is mandatory. This is because occasionally an aneurysm will be missed on the initial angiogram due to spasm or partial/complete thrombosis. The diagnosis of non-aneurysmal SAH can be applied to patients who have two consecutive negative technically adequate 4-vessel cerebral angiograms. Additionally, many clinicians request MRI of the spine to exclude the possibility of spinal AVM as a source for SAH.

The classic variety of non-aneurysmal SAH is known as benign perimesencephalic SAH or pretruncal nonaneurysmal SAH. As the name implies, the hemorrhage is situated around the midbrain and anterior to the brainstem in the ambient, interpeduncular, and prepontine cisterns. The term “benign” refers to the fact that after recovery from the initial episode, there is no increased risk of repeat hemorrhage. Cerebral vasospasm is less likely in these patients, but does occur. Hydrocephalus also remains a possibility during the acute phase. Although not clearly understood, one proposed mechanism of benign perimesencephalic SAH is rupture of the venous plexus anterior to the pons (the anterior pontomesencephalic plexus). This is postulated to occur as a result of increased venous pressure from strenuous activities such as exercise. Intramural hematoma of the basilar artery and rupture of a basilar perforating artery have also been suggested as alternate hypotheses.

Although benign perimesencephalic SAH has been known as a distinct clinical entity for some time, patients may present with non-aneurysmal SAH in an atypical distribution (non-perimesencephalic). In some of these patients, the total volume of hemorrhage is increased such that blood is present throughout the basal cisterns and extends over the cerebral convexities. In other patients, the hemorrhage is confined to the convexities, quadrigeminal cistern, or other atypical locations. In today’s case, Patient #1 presented with the classic variety of benign perimesencephalic SAH. Patient #2 presented with atypical non-aneurysmal SAH. Both patients recovered, and have had no repeat episodes of hemorrhage to date.

Possible causes of SAH:
- Trauma
- Aneurysm
- AVM
- Vasculitis
- Dural AV fistula
- Extension from intraparenchymal hemorrhage
- Dural venous sinus thrombosis
- Infection
- Neoplasm
- Idiopathic

Lumbar disc extrusion with a wrapped disc

Findings

There is a left central disc extrusion at L5-S1 that causes mild to moderate left lateral recess narrowing and nerve root displacement without nerve root compression. At this level there is also contrast enhancement traversing the left laminectomy defect and encasing the disc extrusion, consistent with a wrapped disc. There is enhancement in the left lateral recess, suggesting post-operative fibrosis.

Differential diagnosis:
- Wrapped disc
- Peridural fibrosis
- Epidural abscess
- Epidural metastasis
- Nerve sheath tumor
- Disc pseudobulge
- Intervertebral disc protrusion
- Intervertebral disc extrusion
- Recurrent intervertebral disc herniation


Diagnosis: Lumbar disc extrusion with a wrapped disc


Key points: "Wrapped" disc


Disc herniation (protrusion, extrusion, or fragment) may be caused by trauma, repetitive or acute, and are a common source of pain and subsequent back surgery in the general population. In the acute phase, the herniated disc stimulates a fibrovascular response. A "wrapped disc" is the focal herniation (protrusion, extrusion, or fragment) that is encased in vascular scar tissue stimulated by this response and is evident by enhancement on contrast-enhanced T1-weighted images.

Asymptomatic or low back pain and/or radiculopathy are most common in the lumbar spine at L4-L5 and L5-S1. A wrapped disc is a post-surgical sequela, particularly following surgery for spinal stenosis in which the surgical procedure is more extensive, involving a laminectomy and a medial facetectomy.

Best imaging modality: MR (sequences: sagittal and axial T2WI and T1WI, as well as contrast-enhanced axial and sagittal T1WI)
Other imaging modalities: CT, myelography


Imaging findings

MR: Anterior extradural mass contiguous with the disc space extending into the spinal canal
*Contrast-enhanced T1WI: Peripheral enhancement surrounding the disc herniation or fragment with/without central canal, lateral recess, or foraminal stenosis and cord or nerve root impingement. (*most helpful MR sequence)
Non-enhanced T1WI: Isointense to parent disc
T2WI: Iso- to hyper intense to parent disc
General disc hypointensity and height loss at the level of the herniation, as well as postoperative changes (laminectomy defects, etc), degenerative facet disease, and osteophytes, are common associated findings.
CT:
Non-contrast CT: An anterior extradural soft tissue mass that may displace the nerve root / indent the thecal sac
Contrast-enhanced CT: Mild peripheral enhancement of the disc herniation/fragment
Myelography: An extradural mass that indents the thecal sac and nerve root sleeves
Imaging findings of other common differential diagnoses
Peridural fibrosis: Scar within epidural space after lumbar surgery that infiltrates epidural fat, causing homogeneous enhancement that diffusely surrounds the thecal sac and nerve root; increased in T2 signal relative to adjacent disc herniation
Epidural abscess: A distinct fluid collection in the epidural space with peripheral enhancement on post-contrast images, often associated with findings of diskitis
Epidural metastasis: Elongated (cranial-caudal orientation) enhancing mass with osseous involvement and may demonstrate paravertebral extension
Nerve sheath tumor: Avid enhancement surrounding the nerve root, some of which are in a "dumbbell" shape
Disc pseudobulge: Smooth generalized extension of the disc margin without a focal defect due to "uncovering" of disc related to spondylolisthesis
Intervertebral disc protrusion: Anterior extradural mass contiguous with disc space and triangular in shape with broader base than apex; no enhancement
Intervertebral disc extrusion: Anterior extradural mass contiguous with disc space by a "neck," in which this herniated disc material then widens in the epidural space
Recurrent intervertebral disc herniation: Extradural mass contiguous with intervertebral disc margin, demonstrating enhancement peripherally but without central enhancement
Treatment
Conservative: Anti-inflammatory and pain medications, avoid trauma
Surgical: Repeat surgery to remove herniated disc (protrusion, extrusion, fragment)

Pseudotumor cerebri - Idiopathic Intracranial Hypertension (IIH)

Findings

T2W axial MRI (Figure 1) shows signs of increased ICP, but only increased fluid within the optic nerve sheaths, flattening of the posterior orbit, and a partially empty sella.
The 3D TOF MRV Towne and RPO projections (Figure 2 and Figure 3) show bilateral, right greater than left, focal transverse-sigmoid venous sinus junction narrowing’s. It is not a normal MRV given the pt’s history, with more explanation in the discussion. There is no aneurysm or collection of collateral blood vessels seen in these images.

The AP and lateral (Figure 4 and Figure 5) venous phase carotid arteriogram shows long segment stenosis at transverse-sigmoid venous sinus junction distal to the vein of Labbé. Pre procedure venography showed a venous pressure gradient across this lesion of 17 mmH2O with 37 mmH2O on transverse sinus side and 15 mmH2O on internal jugular vein side.

AP and lateral (Figure 6 and Figure 7) venous phase carotid arteriogram shows long segment stenosis at transverse-sigmoid venous sinus junction with a balloon crossing the gradient lesion.


Diagnosis: Pseudotumor cerebri - Idiopathic Intracranial Hypertension (IIH)


Pseudotumor cerebri is defined by typical clinical symptoms which occur in the setting of elevated “idiopathic” ICP and a normal composition of CSF. Classic clinical symptoms include diffuse recalcitrant headaches, vision changes (including vision loss), and hearing changes (e.g., tinnitus), and the disease is typically seen in obese women who are 20-50 years of age. Papilledema is the most common physical exam finding, but visual loss and sixth nerve palsy are also seen. Other symptoms include disabling headaches and blindness. LP opening pressure is greater than 25 cm H2O. Brain computed tomography (CT) and magnetic resonance imaging (MRI) are typically normal, however, the following suggestive non-pathognomonic findings are frequently present:

– Cerebral venous sinus stenoses
– Flattening of the bilateral posterior sclera
– Partially or fully empty sella; enlargement of the chiasmatic recess of the 3rd ventricle
– Distension of perioptic nerve subarachnoid space
– Intraocular protrusion of the optic nerve head
– Orbital optic nerve vertical tortuosity

Treatment for pseudotumor cerebri typically includes medical management with acetazolamide and pain control for headaches. Furosemide and corticosteroids have been used, as well. Surgical interventions to treat pseudotumor cerebri include lumboperitoneal shunt (LPS) and ventriculoperitoneal shunt (VPS), which often produce immediate results, however, eventual return of pseudotumor symptoms occur in approximately 50% within three years. Optic nerve sheath fenestration is also used to treat vision changes, with variable headache relief. Dominant transverse/sigmoid venous sinus angioplasty and stenting are relatively new methods for the treatment of pseudotumor cerebri for those who have significant dural sinus stenosis. Given that 80% of intracranial vascular compliance is provided from the venous vasculature, reduction of pressure in the sinuses reduces CSF pressure. Better results are achieved in patients with documented high pressure gradients, and greater efficacy is seen with regard to arrest of visual loss (>90%) than with headache relief (~50%). Long-term results are lacking. however.

In this case, cerebral angiography demonstrated bilateral high-grade transverse/sigmoid sinus stenoses distal to vein of Labbe insertions. Selective catheterization of the right transverse sinus revealed an estimated 80% narrowing to a luminal diameter of 1mm, and a pressure gradient across the stenosis of 13 mmHg (normal <5 mmHg). The contralateral sinus was smaller, but distally stenotic. A stent was placed across the right sided stenosis.
The patient was placed on antiplatelet medication to preserve stent patency immediately after the procedure. She had no headaches after the procedure and demonstrated objective visual improvement at her one- and six-week follow-up examinations.

Intracranial pseudotumor (Tolosa-Hunt syndrome)

Findings

Increased CSF signal demonstrated by T2 hyper intensity within the right optic sheath. Nodular enhancement at the superior aspect of the right optic nerve at the orbital apex, which extends with prominent nodular enhancement posteriorly along the dural reflection of the right cavernous sinus. Asymmetric dilatation of the right superior ophthalmic vein.

Differential diagnosis:
- Meningitis
- Sarcoidosis
- En plaque meningioma
- Meningeal metastases
- Meningeal Non-Hodgkin's lymphoma
- Tolosa-Hunt syndrome


Diagnosis: Intracranial pseudotumor (Tolosa-Hunt syndrome)


Discussion

Intracranial pseudotumor (Tolosa-Hunt syndrome) is a part of a spectrum of "quasineoplastic" lesions that demonstrate orbital, intracranial, or pulmonary involvement, and include such other disorders as plasma cell granuloma and hypertrophic cranial pachymeningitis. It is a chronic granulomatous disease of unknown origin, which has been hypothesized to represent a low grade fibrosarcoma of inflammatory cells versus an autoimmune phenomenon. While Tolosa-Hunt syndrome is rare, orbital pseudotumor is the third most common ophthalmic disorder, and encompasses 5-8% of all orbital masses. Histologically, the lesions of Tolosa-Hunt demonstrate mixed lymphocytic and plasma cell infiltrate, with a variable degree of fibrosis. Lesions favor the cavernous sinus and basal meninges, although falcine and tentorial lesions have been described.

Patients with intracranial lesions are more frequently young adults, who present initially with chronic headaches or cranial nerve palsies. Patients with orbital involvement are more frequently middle-aged, and may present with painful proptosis and vision loss . Symptoms may be intractable, leading to severe disability. Untreated or unresponsive disease may progress to death. First-line treatment is invariably high-dose steroids, with radiotherapy or surgical resection reserved for patients with incomplete response to steroids .


Radiologic Overview of the diagnosis

The imaging hallmarks of Tolosa-Hunt syndrome are characterized by an enhancing, infiltrating meningeal mass, which favors the cavernous sinus or basal meninges, although falcine and tentorial involvement has been described . Focal meningeal thickening may range from just a few millimeters to a greater than 2 cm rind. With intracranial pseudotumor, orbital involvement is spared more than 90% of the time. Tolosa-Hunt remains a diagnosis of exclusion, once meningitis, en plaque meningioma, and meningeal metastases are ruled out.

The imaging modality of choice for imaging patients with Tolosa-Hunt remains MRI, although useful information may be gleaned from other modalities. On non-contrast enhanced CT (NECT), there are no specific findings to suggest the diagnosis; however, this modality may be of some value in differentiating the lesion from en plaque meningioma. On contrast enhanced CT (CECT), salient imaging findings include enhancing, thickened meninges or a curvilinear appearance of a single meningeal region. As aforementioned, MRI remains the primary modality for diagnosis of Tolosa-Hunt syndrome, and each sequence may provide critical information required to make the diagnosis. On T1WI, one may find focal thickening of the meninges that is isointense to gray matter. On T2WI, lesions are characterized as iso- to hypo intense regions of focal meningeal thickening, which may be more hypo intense as they become more fibrotic. FLAIR is of little help in making the diagnosis, but it is unlikely to demonstrate focal brain edema underlying the lesion . Contrast enhanced T1WI is the single most valuable sequence for evaluation of Tolosa-Hunt syndrome, and is characterized by diffusely enhancing region of meningeal thickening, which may range from a few millimeters to greater than 2 cm in some cases. Diffuse boney infiltrates may be appreciated on fat saturated contrast enhanced T1 sequence. While angiography is not considered a primary modality, severe disease may result in carotid artery narrowing, thus MRA may be a useful adjunct in the appropriate clinical setting.

The appropriate differential diagnosis of Tolosa-Hunt syndrome includes meningitis, sarcoidosis, en plaque meningioma, meningeal metastases, and meningeal Non-Hodgkin's lymphoma.

Hypertensive intracranial hemorrhage

Findings

Axial CT of the head shows a large hyper dense focus with peripheral hypo density in the left frontal lobe, causing sulcal effacement at the frontal cortex but no significant midline shift. Surrounding rim of low density represents edema (image 1). Unenhanced MRI of the brain shows an the same mass-like focus in the left frontal lobe, which has an isointense center with a hyper intense rim (image 2). Post gadolinium-enhanced T1 image of the brain shows no internal enhancement of this lesion (image 3).


Differential diagnosis:
- Hypertensive intracranial hemorrhage
- Ruptured arteriovenous malformation (AVM)
- Hemorrhagic intracranial mass
- Posttraumatic cerebral contusion


Diagnosis: Hypertensive intracranial hemorrhage


Acute blood appears hyper dense of unenhanced head CT.
Without a history of trauma, intraparenchymal brain hemorrhage on head CT could represent a hemorrhagic mass, a ruptured AVM, or a hemorrhagic brain tumor (primary or metastatic).
MRI with and without contrast is the best diagnostic tool for determining if a mass lesion is present, and for evaluating the age of the intracranial hemorrhage.
Acute blood products on T1 appear hypo intense to isointense (image 2), whereas subacute and chronic hematoma are hyper intense.
Neoplasms should enhance on post contrast T1. The lack of enhancement in this patient on post contrast T1 excludes neoplasm (image 3).