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Neuroradiology Case of the Week

Case 143

Alisa Johnson, Jeevak Almast, MD, Loris Cedeno, MD,
and PL Westesson MD, DDS, PhD

Clinical Presentation: The patient is a 54-year-old female who was grocery shopping and noticed left-sided weakness and language deficits which persisted until she came to the ED one hour later.  There is clinical suspicion for cerebral vascular injury.

Radiological Findings: CT findings noted a loss of the gray/white matter interface throughout much of the left frontal and parietal lobes in the MCA distribution.  There is effacement of the cortical sulci throughout the left hemisphere.  The left middle cerebral artery demonstrated increased attenuation in the region of the M2 segment (Figs. 1A & B).
     In addition a large low attenuation right enhancing mass lesion within the left frontal lobe with a focus of increased signal intensity centrally which may represent a small amount of hemorrhage.  Moderate amount of surrounding edema and compression of the anterior horn of the right lateral ventricle (Figs. 1A & B).
     On CT angiogram there is an abrupt occlusion of the left middle cerebral artery at approximately the origin of the M2 segment and displacement of the mass lesion in the left frontal lobe (Figs. 2 & 3).

    MRI recommended for further evaluation:  The mass demonstrated low T1 signal with peripheral enhancement (Fig. 4) and high T2 signal (Fig. 5).  Diffusion weighted images demonstrate increased signal intensity in the left MCA distribution consistent with a large infarct (Fig. 6). Perfusion weighted imaging demonstrated increased perfusion in the periphery of the mass and decreased signal within the mass consistent with necrosis (Fig. 7).

Clinical Discussion:

     Glioblastoma multiformes, also known as grade IV astrocytomas, are the most common and most malignant adult primary brain neoplasm, representing 15-20% of primary CNS neoplasms. They usually occur in patients > 50 years old but can occur at any age. GBMs represent approximately half of all astrocytomas [1].
     Clinically the presentation of GBM varies depending on the location and size of the lesion. GBM can invade and compress brain parenchyma and cause an increase of intracranial pressure through restricting cerebrospinal fluid outflow, resulting in hydrocephalus. Typically GBM present with seizures and hemiparesis but depending on the variables mentioned above; they can also present with other focal Neurologic deficits or strokelike syndromes [1].
     GBMs have a poor prognosis with a median postoperative survival of 8 to 12 months and a 5 year recurrence-free survival rate of <5% [2].

     Acute infarct: One of the first steps with a patient with a suspected stroke is to ascertain if it is an ischemic or hemorrhagic stroke. The presence of headache and vomiting favor the diagnosis of intracerebral hemorrhage or subarachnoid hemorrhage compared with a thromboembolic stroke, while the abrupt onset of impaired cerebral function without focal symptoms favors the diagnosis of SAH. These are helpful but imperfect ways of determining if the patient has an ischemic or hemorrhagic stroke; therefore, it is essential that the patient is evaluated with noncontrast CT imaging for intracranial hemorrhage so that in the absence of an ICH, thrombolytic therapies can be considered. Thrombolytic therapies are most effective when used shortly after the onset of symptoms to restore blood flow and salvage ischemic brain parenchyma [3].
     Incidence of new stroke is approximately 160 cases per 100,000 population per year. Cerebral infarct is the third most common cause of death in the United States with a mortality rate between 15 and 35% with each episode. The risk of stroke increases with age, hypertension, the presence of a carotid bruit, diabetes, smoking, atrial fibrillation, obesity, hyperlipidemia and elevated homocysteine level. Most ischemic strokes are caused by thromboembolic disease originating from atherosclerotic plaques. 90% of all extracranial carotid lesions are due to atherosclerosis primarily from the carotid bulb. Approximately 75% of all cerebral infarctions involve the territory of the MCA as it has in the patient presented here [4].

Neuroimaging Discussion:

     Glioblastoma multiformes: The typical location for a GBM is in the deep cerebral white matter especially in the frontal or temporal lobes. Bihemispheric tumors that extend through the corpus callosum are common resulting in the “butterfly” type GBM. Classic findings in GBM are a nodular rim of enhancement with a large amount of surrounding edema and mass effect. CT scans typically show low density regions that reflect necrosis or cyst formation in 95% of cases (4). Peripheral edema is common and surrounds the tumor, extending into the white matter tracts. Hemorrhage of different ages is common but calcifications are uncommon. Following contrast administration, CT often shows a thick irregular rim enhancement.
      On MRI, T1WI demonstrates a mass that is hypointense with a poorly delineated mixed signal mass with cyst formation or necrosis and a thick irregular wall. GBM are often very vascular tumors, which will demonstrate flow voids and hemorrhages of different ages. A hyperintense mass is seen on T2WI and FLAIR usually with a striking amount of edema.

     Acute infarct: As mentioned above, CT is the first step in imaging a patient suspected to have an infarct to rule out hemorrhage. Hemorrhage appears hyperdense on CT. Once hemorrhage has been ruled out, we begin to look for signs of ischemia. Hyperacute ischemic infarcts (< 12 hours) have normal CT findings 50-60% of the time (4). Once an ischemic infarct is 12-24 hours old it becomes more evident on CT imaging and is considered an acute infarct. Acute signs of MCA infarct include hyperdense MCA on noncontrast CT (25%-50%), “disappearing” lentiform nucleus, and loss of insular cortex [4]. It is important to be aware that ischemic strokes can have “hemorrhagic transformation” in 15%-45% of cases usually occurring between 24-48 hours after initial onset of symptoms [1].
     MRI is more sensitive to ischemic stroke than CT and can detect signs of infarct in the hyperacute stage of a stroke (<12 hours). Intravascular enhancement can be seen as early as two hours after the stroke. On T1WI early cortical swelling and hypointensity with loss of gray white junction are seen. On T2WI early cortical swelling and hyperintensity are seen in the affected brain. FLAIR is very sensitive and may be positive with a hyperintense signal when other imaging is negative. T2 gradient (T2 GRE) can show thrombosed vessel as arterial “blooming” from clot susceptibility. DWI demonstrates hyperintense restriction from cytotoxic edema. It is good to cross reference the ADC map as there will be a low signal on ADC maps with the same geographic area of ischemia. MRA may demonstrate major vessel occlusions, stenosis, and collateral status. MR spectrography will show elevated lactate and decreased NAA. Perfusion MRI is helpful in that it increases accuracy of conventional MR from 70-80% to 95% and helps define the tissue that has possible reversible damage if treatment is pursued. The “at risk” tissue is defined by the “penumbra” which is the tissue that is negative on DWI but positive on PWI, the DWI/PWI mismatch [1].

References:

1. Osborn AG. Diagnostic Imaging: Brain. 1st ed. Amirsys Inc: Altona, 2004.
2. Grossman, R., Yousem, D. Neuroradiology, The Requisites. 2nd ed. Elsevier Inc. Philadelphia, 2003.
3. Arnold, Jeffrey L. Acute ischemic stroke. EMedicine. March 2005.
4. Castillo, M. The Core Curriculum: Neuroradiology.  Lippincott Williams & Wilkins, Philadelphia: 2002.