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Brain Reserve in a Case of Cognitive Resilience to Severe Leukoaraiosis
- Dana M. Szeles, Nicholas J. Milano, Hunter J. Moss, Maria Vittoria Spampinato, Jens H. Jensen, Andreana Benitez
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- Journal:
- Journal of the International Neuropsychological Society / Volume 27 / Issue 1 / January 2021
- Published online by Cambridge University Press:
- 16 June 2020, pp. 99-108
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Objective:
Leukoaraiosis, or white matter rarefaction, is a common imaging finding in aging and is presumed to reflect vascular disease. When severe in presentation, potential congenital or acquired etiologies are investigated, prompting referral for neuropsychological evaluation in addition to neuroimaging. T2-weighted imaging is the most common magnetic resonance imaging (MRI) approach to identifying white matter disease. However, more advanced diffusion MRI techniques may provide additional insight into mechanisms that influence the abnormal T2 signal, especially when clinical presentations are discrepant with imaging findings.
Method:We present a case of a 74-year-old woman with severe leukoaraoisis. She was examined by a neurologist, neuropsychologist, and rheumatologist, and completed conventional (T1, T2-FLAIR) MRI, diffusion tensor imaging (DTI), and advanced single-shell, high b-value diffusion MRI (i.e., fiber ball imaging [FBI]).
Results:The patient was found to have few neurological signs, no significant cognitive impairment, a negative workup for leukoencephalopathy, and a positive antibody for Sjogren’s disease for which her degree of leukoaraiosis would be highly atypical. Tractography results indicate intact axonal architecture that was better resolved using FBI rather than DTI.
Conclusions:This case illustrates exceptional cognitive resilience in the face of severe leukoaraiosis and the potential for advanced diffusion MRI to identify brain reserve.
13 - Global Cerebral Anoxia in Mature Brain
- from Section 1 - Bilateral Predominantly Symmetric Abnormalities
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC, Zoran Rumboldt, Medical University of South Carolina
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
- Print publication:
- 08 November 2012, pp 27-28
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Summary
Specific Imaging Findings
Global cerebral anoxia (hypoxic-ischemic injury, HII) findings vary depending on the duration and severity of insult, brain maturity, and type and timing of imaging studies with different presentations in premature neonates, full-term neonates, and older children and adults. In all three scenarios the lesions are bilateral and predominantly symmetrical. The spectrum of mild to severe findings in mature brains on non-contrast CT are: (1) poor differentiation of the cortical gray matter from subcortical white matter with sulcal effacement, predominantly affecting the arterial boundary zones; (2) loss of deep gray and white matter definition; (3) relative hyperdensity of the subarachnoid space (pseudosubarachnoid hemorrhage); (4) relatively hyperdense cerebellum (bright cerebellum); (5) hypodense brainstem; and (6) herniations. MRI shows hyperintense T2 (and low T1) signal of the affected areas, especially cortical, when CT findings may be absent. Diffusion MRI is the most sensitive technique with bright lesions on DWI and low ADC values involving deep gray matter, cortex, and cerebellum in the early stages. Periro-landic and deep gray matter involvement is observed in term neo-nates. Profound HII in older children and adults affects the deep gray matter nuclei, cortices, hippocampi, and cerebellum. Areas of reduced diffusion shift from the gray matter to the white matter in the subacute phase, when laminar enhancement of the cortex and patchy enhancement of the deep gray matter may be present on post-contrast images. This is followed by T1 bright cortical laminar necrosis in the late subacute phase and cortical atrophy and progressive white matter changes in the chronic stage.
90 - Frontotemporal Lobar Degeneration
- from Section 3 - Parenchymal Defects or Abnormal Volume
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 185-186
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Summary
Specific Imaging Findings
The role of imaging in the evaluation of frontotemporal lobar degeneration (FTLD) is to exclude other forms of dementia such as Alzheimer disease and vascular dementia. FTLD typically shows selective atrophy of the anterior temporal and frontal lobes with relatively preserved occipital and parietal lobes. The involvement is often asymmetric, with the dominant hemisphere more severely affected. Diffuse brain atrophy may also be observed. FDG-PET in FTLD demonstrates decreased glucose uptake in the frontal and temporal cortices.
Pertinent Clinical Information
FTLD is the second most common type of dementia in individuals under 65 years of age with a prevalence of 15 per 100 000 in the 45–64 year age range. It is a primary neurodegenerative disease characterized by the development of progressive behavioral change, executive dysfunction and language deficits with relatively preserved memory in the early stages. FTLD comprises three clinical subtypes: (1) frontotemporal dementia (FTD, also known as Pick's disease) or the frontal variant, the most common form, characterized by early personality changes such as apathy and indifference, impulsive behaviors and disinhibition, and poor judgment; (2) semantic dementia (SD) characterized by early loss of word meaning but fluent speech; (3) progressive nonfluent aphasia (PNFA) characterized by loss of speech fluency with anomia (primary progressive aphasia). The differential diagnosis between AD and FTLD can be difficult in the early stages and the clinical overlap between these conditions highlights the importance of neuroimaging, along with neuropsychological testing.
161 - Oligodendroglioma
- from Section 6 - Primarily Intra-Axial Masses
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
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- 05 August 2013
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- 08 November 2012, pp 333-334
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Summary
Specific Imaging Findings
Oligodendrogliomas are usually well-demarcated supratentorial lesions that arise from the gray matter, most commonly in the frontal lobes. The typical CT findings include the presence of clumped and nodular calcification within a hypodense to isodense mass involving the cortex. Cystic changes commonly occur, while intratumoral hemorrhages are rare. Oligodendrogliomas are usually T1 hypointense and T2 hyperintense cortical-based lesions with mild mass effect, and areas of signal loss/susceptibility artifact on T2* sequences, caused by calcifications, may be found. Development of new areas of contrast enhancement and edema have been traditionally considered signs of anaplastic transformation in gliomas; however, contrast enhancement has shown very poor accuracy in differentiating anaplastic from lowgrade oligodendroglial tumors. Also, increased relative cerebral blood volume (rCBV) on contrast-enhanced T2* MR perfusion studies, a marker for rapid progression and poor outcome in patients with gliomas, may be found in some low-grade oligodendrogliomas. Increase in tumor size within 6 months appears to be the best prognosticator of rapid tumor progression and poor outcome, better than the high initial tumor volume or high rCBV. Signal heterogeneity, irregular borders, and high rCBV of the tumors are suggestive of the 1p/19q deletion, which is associated with a better treatment response.
103 - Polymicrogyria
- from Section 4 - Abnormalities Without Significant Mass Effect
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 213-214
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Summary
Specific Imaging Findings
Polymicrogyria is characterized by an irregular cortical surface, apparent thickening of the cortex, “stippled” gray–white matter junction, and a greater than expected number of abnormally small gyri, usually without T2 signal abnormality in the myelinated brain. High-resolution images reveal that the cortical ribbon itself is thin, and the apparent thickening results from juxtaposition of the small folds. The perisylvian cortex is the site most commonly affected by polymicrogyria; however, any region of the cortical mantle can be involved. Cortical involvement can be restricted to a single focus or it can affect extended areas, as seen in cases of uni- or bilateral, symmetrical or asymmetrical, diffuse polymicrogyria. The imaging appearances of polymicrogyric cortex can be heterogeneous, ranging from multiple abnormal small gyri to a relatively smooth cortical surface and an overall coarse appearance. Diffuse coarse polymicrogyria can have the appearance of cortical palisades. The sulcation pattern is aberrant, without a recognizable pattern. Sulci may be shallow or deeply indent the parenchyma. Polymicrogyria may be associated with schizencephaly, corpus callosum dysgenesis, cerebellar hypoplasia, periventricular and subcortical heterotopias. An imaging protocol including volumetric T1-weighted images with thin sections (< 1.5 mm) and reconstruction in the three orthogonal planes is optimal for evaluation of these abnormalities.
26 - Radiation- and Chemotherapy-Induced Leukoencephalopathy
- from Section 1 - Bilateral Predominantly Symmetric Abnormalities
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 53-54
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Summary
Specific Imaging Findings
Radiation-induced leukoencephalopathy presents with rapidly progressive, symmetric CT hypodensities and T2 hyperintensities in the periventricular and deep white matter, initially with sparing of the corpus callosum and subcortical arcuate fibers. Over time, lesions increase in size and coalesce leading to a confluent pattern with smooth peripheral margins. Concurrent cerebral atrophy may develop and rapidly progress. The affected white matter is of increased diffusivity on ADC maps and gradual decrease of rCBV on perfusion imaging may be observed. Pediatric patients may develop a mineralizing microangiopathy months or years following radiation or more commonly combined chemoradiation, with large calcifications within the affected white matter. Symptomatic reversible methotrexate toxicity shows T2 hyperintense areas in the supratentorial and cerebellar cortex and subcortical white matter in addition to deep white matter changes. Chemotherapy with or without radiotherapy, typically including intrathecal methotrexate, may lead to disseminated necrotizing leukoencephalopathy, characterized by rapidly progressive confluent white matter T2 hyperintensity and T1 hypointensity with internal hemorrhages and corresponding ill-defined areas of enhancement, which can evolve into circular necrotic lesions.
Pertinent Clinical Information
Radiation-induced delayed encephalopathy is a common and serious irreversible condition characterized by neurocognitive deterioration ranging from mild impairment to dementia. Known risk factors include combined radiation and chemotherapy, diabetes, hypertension, and advanced age. It is particularly common following whole-brain radiotherapy (WBRT), which can induce cognitive dysfunction in up to 50% of long-term survivors. Preexisting leukoaraiosis appears to be a predisposing factor for developing further leukoencephalopathy after WBRT.
44 - Craniopharyngioma
- from Section 2 - Sellar, Perisellar and Midline Lesions
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 91-92
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Summary
Specific Imaging Findings
The appearance of pediatric craniopharyngiomas is typical: they occupy the suprasellar cistern, have a cystic component and are partially calcified in 90% of cases. Multiple cysts with varying signal intensities are characteristic. Cystic components are typically hyperintense and less commonly isointense to the CSF on T1- weighted images. Fluid-debris levels may be present within the cysts. Solid components have variable signal intensities and they usually enhance with contrast. Enhancement may be minimal and limited to the cyst wall. Compression on the third ventricle is a common feature, which may be accompanied by obstructive hydrocephalus. Optic tract edema is commonly seen in craniopharyngiomas; however, it may occasionally be present in other parasellar tumors. Solid craniopharyngiomas are more common in adults and less frequently contain calcifications.
Pertinent Clinical Information
Patients commonly present with symptoms of increased intracranial pressure, including headache, nausea, vomiting, and symptoms of optic chiasm compression. The most common endocrine abnormality in children consists of growth disturbance, in about 80% of cases. Patients may also present with global hypopituitarism, hyperprolactinemia, or diabetes insipidus.
Differential Diagnosis
Pituitary Macroadenoma (41)
• originates from the sella
• usually isointense with brain and shows solid, frequently delayed, enhancement
• calcifications are rare
Rathke's cleft cyst (38)
• a single ovoid cyst without enhancing nodules, wall enhancement absent to minimal
• calcifications are uncommon, thin and peripheral
• intracystic nodules of low T2 signal may be present
202 - Craniopharyngioma
- from Section 7 - Intracranial Calcifications
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
- Print publication:
- 08 November 2012, pp 407-408
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57 - Joubert Syndrome
- from Section 2 - Sellar, Perisellar and Midline Lesions
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 117-118
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Summary
Specific Imaging Findings
The molar tooth sign on axial brain MRI or CT images is pathognomonic of Joubert syndrome (JS). This sign results from the combination of marked hypoplasia or aplasia of the cerebellar vermis, a narrow isthmus (the area of the midbrain caudal to the inferior colliculi and immediately above the pons), a triangular shaped or “umbrella-shaped” mid-fourth ventricle and a “batwing” appearance of the superior fourth ventricle. The key finding are thickened, elongated and horizontally oriented superior cerebellar peduncles (SCP) with a very deep interpeduncular fossa. In JS patients older than 30 months the absence of SCP decussation can be identified on a mid-sagittal T1WI as a lack of the rounded low signal-intensity area at the level of the pontomesencephalic junction, representing the SCP decussation. Diffusion-tensor MR imaging and fiber tractography have been employed to demonstrate the abnormal morphology and aberrant course of the SCP and corticospinal tract. Associated abnormalities may include migration disorders (such as heterotopia), callosal dysgenesis, ventriculomegaly, and cephaloceles.
Pertinent Clinical Information
JS is a rare, autosomal recessive disorder with a distinctive hindbrain malformation. The molar tooth sign was first described in JS; however, it is present in numerous other rare syndromes that are partially overlapping with JS and characterized by abnormalities outside of the CNS in addition to the brainstem and cerebellar findings [e.g. Joubert–polymicrogyria syndrome, Dekaban–Arima syndrome, COACH (Cerebellar vermis hypoplasia, Oligophrenia, Ataxia, Coloboma, and Hepatic fibrosis) syndrome, Varadi–Papp syndrome, Senior–Löchen syndrome].
32 - Posterior Reversible Encephalopathy Syndrome (PRES, Hypertensive Encephalopathy)
- from Section 1 - Bilateral Predominantly Symmetric Abnormalities
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC, Zoran Rumboldt, Medical University of South Carolina
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
- Print publication:
- 08 November 2012, pp 65-66
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Summary
Specific Imaging Findings
Posterior Reversible Encephalopathy Syndrome (PRES) usually shows characteristic bilateral, predominantly symmetric, patchy areas of hyperintense T2 signal in the subcortical regions of the parietal and occipital lobes. Cortex may also be involved, while mass effect is absent to minimal. In addition to the primary parietal- occipital pattern, patchy bilateral T2 hyperintensities are also found in holohemispheric and superior frontal patterns, and may be present in the cerebellum, basal ganglia, and brainstem. There is characteristically increased diffusion on ADC maps corresponding to vasogenic edema, while contrast enhancement is absent to minimal, usually leptomeningeal. Hemorrhage, either subarachnoid or parenchymal, is associated with vasogenic edema in a minority of patients. Areas of reduced diffusion are found in some cases, likely representing infarction. More prominent cases of PRES are visible on CT as ill-defined foci of subcortical low attenuation. Vascular studies commonly show evidence of vasculopathy with irregular and beaded appearance of distal intracranial arteries, which is, similar to other imaging findings, typically reversible. Findings on perfusion studies can span from decreased to increased cerebral blood flow, which may depend on the timing, underlying etiology, and brain area.
Pertinent Clinical Information
The most common presentations include headache, altered mentation, nausea, and visual disturbances. Symptoms may develop acutely or over several days and may lead to generalized seizures and coma. Various conditions place patients at risk of PRES, the most common are pre-eclampsia/eclampsia, hypertensive crisis, following transplantation, autoimmune diseases, infection/sepsis/shock, and after cancer chemotherapy.
122 - Moyamoya
- from Section 4 - Abnormalities Without Significant Mass Effect
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 251-252
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Summary
Specific Imaging Findings
In the earliest stages the typical vascular imaging features of moyamoya are narrowing of the terminal internal carotid arteries (ICAs) and proximal anterior and middle cerebral arteries, followed by development of abnormal dilated lenticulostriate and thalamoperforator collaterals with appearance similar to a “puff of smoke” (Moyamoya in Japanese), and in the late stages transdural and transosseous external-to-internal carotid artery collaterals. Aneurysms of the basilar artery tip and posterior communicating artery may also be found. The flow-voids in the ICAs, middle, and anterior cerebral arteries appear decreased, with prominent flow-voids in the region of the basal ganglia and thalami from Moyamoya collateral vessels, best seen on T2WI. The “ivy sign”, consisting of hyperintensity on FLAIR images along the cerebral sulci and leptomeningeal enhancement on post-contrast T1WI appears characteristic for Moyamoya. Pial collateral vessel engorgement in the attempt to compensate for the decreased perfusion pressure is responsible for this appearance.
Pertinent Clinical Information
Moyamoya disease and syndrome generally manifests with symptoms of brain ischemia or hemorrhage, seizures, and headache from dilated transdural collaterals. Intracranial hemorrhage, due either to bleeding from fragile collaterals or aneurysms, is more common in adults. Major neurologic deficits, personality changes and cognitive impairments are frequent. The natural history of the disease is variable with progression, either slow or fulminant, observed in the majority of untreated cases. A six-vessel cerebral angiography, including evaluation of the external carotid arteries (ECAs), is necessary to accurately stage the disease.
89 - Alzheimer Disease
- from Section 3 - Parenchymal Defects or Abnormal Volume
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 183-184
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Summary
Specific Imaging Findings
The role of imaging in the evaluation of Alzheimer disease (AD) is to exclude other forms of dementia and identify early cases of AD which could benefit from treatment. Morphometric and metabolic measurements of the mesial temporal regions are the best imaging biomarkers for early diagnosis. In the appropriate clinical setting the diagnostic accuracy of MRI in the diagnosis of AD is approximately 87%. Typical MR findings consist of temporal and parietal cortical volume loss with prominent hippocampal atrophy. Angled coronal images perpendicular to the long axis of the hippocampus best show atrophy of the hippocampi and parahippocampal gyri with enlargement of the parahippocampal fissures.
Fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) findings in the AD brain include decreased glucose uptake in the temporal and parietal lobes with sparing of the occipital and frontal lobes, while the posterior cingulate is typically affected first. FDG PET helps differentiate AD from other forms of dementia, such as vascular dementia and frontotemporal dementia, although advanced Parkinson's disease may present with a regional metabolic pattern not distinguishable from AD.
Pertinent Clinical Information
The diagnosis of AD is based on the criteria of the National Institute of Neurological and Communicative Disorders and Stroke – AD and Related Disorders Association. These standards require: insidious onset; gradual progression of memory impairment; deficits of recent memory in the early stages; impairment of orientation, judgment, problem-solving, community and home living, and personal care present later on.
37 - Spontaneous Intracranial Hypotension
- from Section 1 - Bilateral Predominantly Symmetric Abnormalities
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 75-76
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Summary
Specific Imaging Findings
Spontaneous Intracranial Hypotension (SIH) typically presents with a “sagging brain” imaging appearance with downward displacement of the brain stem and cerebellar tonsils, loss of the basal cisterns, flattened brainstem, bowing of the optic chiasm over the sella, pituitary hyperemia, and effacement of the ventricles and sulci. Diffuse pachymeningeal thickening is bright on FLAIR images with characteristic contrast enhancement, although absent in some cases. Subdural hygromas or less commonly hematomas can also be found. Clinical improvement is not always accompanied by prompt resolution of the MRI findings. Spinal MRI and CT myelography can demonstrate extra-dural fluid collections indicating the location of the CSF leak. MRI may also show meningeal enhancement and dilation of the internal vertebral venous plexi, especially at C1–C2 level. High T2 signal intensity between the spinous processes of C1 and C2 is highly characteristic for SIH.
Pertinent Clinical Information
SIH is a clinical syndrome in which low CSF volume results in orthostatic headache, occurring within 15 min after a change from supine to standing position, and improvement or resolution after lying down. The headache may be diffuse or localized, most commonly to the occipital and suboccipital regions. Associated symptoms in severe cases include nausea, vomiting, photophobia, vertigo, tinnitus, visual loss, diplopia, and even coma. It can occur following a minor trauma, strenuous exercise, sexual activity, or a bout of sneezing or coughing.
1 - Hepatic Encephalopathy
- from Section 1 - Bilateral Predominantly Symmetric Abnormalities
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
- Published online:
- 05 August 2013
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- 08 November 2012, pp 3-4
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Summary
Specific Imaging Findings
Classic brain MR imaging finding in patients with hepatic encephalopathy (HE) is bilateral symmetric globus pallidus hyperintensity on T1-weighted images. When more prominent, high T1 signal is also present in substantia nigra, subthalamic nucleus, tectum, and cerebellar denatate nucleus, with no corresponding findings on T2-weighted images or on CT. Additional MRI findings include diffuse white matter T2 hyperintensity involving predominantly the hemispheric corticospinal tract and focal bright T2 lesions in subcortical hemispheric white matter. MR spectroscopy obtained with short echo time shows depletion of myo-inositol. Myo/Cr ratios are decreased not only in cirrhotic patients with clinical or subclinical encephalopathy, but also in individuals without encephalopathy. Increased levels of glutamine/ glutamate have also been observed, particularly in severe cases. All these MR imaging findings – bright T1 lesions, white matter T2 hyperintensity, and MRS abnormalities – tend to improve and return to normal with restoration of liver function, such as following a successful liver transplantation. Characteristic MRI appearance of acute hyperammonemic encephalopathy appears to be bilateral symmetric cortical T2 hyperintensity involving the insula and cingulate gyrus, best seen on FLAIR and DWI.
Pertinent Clinical Information
HE includes a spectrum of neuropsychiatric abnormalities occurring in patients with liver dysfunction. Most cases are associated with cirrhosis and portal hypertension or portal-systemic shunts. It is a reversible metabolic encephalopathy, characterized by personality changes and shortened attention span, anxiety and depression, motor incoordination, and flapping tremor of the hands (asterixis). In severe cases, coma and death may occur.
87 - Benign External Hydrocephalus
- from Section 3 - Parenchymal Defects or Abnormal Volume
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
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- 05 August 2013
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- 08 November 2012, pp 179-180
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Summary
Specific Imaging Findings
Benign external hydrocephalus (BEH) is characterized by an increased amount of fluid in the subarachnoid spaces (SAS), with density and signal intensity following CSF, typically in the bilateral frontal regions and along the interhemispheric fissure. Enlarged SAS follow the contour of gyri and appear symmetric between the two hemispheres. Additional imaging features include widening of the suprasellar cistern and normal to slightly increased ventricular size. The distance between the frontal gyri and the skull and between the mesial frontal gyri and the anterior interhemispheric fissure measures more than 5 mm. MRI or Doppler ultrasound can confirm the presence of transversing leptomeningeal vessels within the extra-axial collections. MRI can rule out associated chronic subdural hematomas or hygromas.
Pertinent Clinical Information
Increased head circumference above the 95th percentile, full fontanelles, and frontal bossing are the most common clinical findings. Patients are usually referred for imaging when the head size has rapidly increased over the course of months. A family history of macrocephaly is often present. BEH is usually diagnosed between 3 and 8 months of age and is more common in male infants. Transient gross motor delay can be observed and is usually attributed to the added head weight in the macrocephalic infant. Otherwise BEH is usually not associated with developmental delay or neurological deficit. Once the diagnosis of BEH is established, clinical follow-up is required to confirm normal development and no treatment is necessary. In selected cases, follow-up imaging at 18–24 months of age can be considered and should show resolution of the abnormality.
154 - Therapy-Induced Cerebral Necrosis (Radiation Necrosis)
- from Section 6 - Primarily Intra-Axial Masses
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- By Maria Vittoria Spampinato, Department of Radiology and Radiological Science, Charleston, SC, Zoran Rumboldt, Medical University of South Carolina
- Edited by Zoran Rumboldt, Medical University of South Carolina, Mauricio Castillo, University of North Carolina, Chapel Hill, Benjamin Huang, University of North Carolina, Chapel Hill, Andrea Rossi
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- Book:
- Brain Imaging with MRI and CT
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- 05 August 2013
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- 08 November 2012, pp 319-320
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Summary
Specific Imaging Findings
Therapy-induced (radiation) cerebral necrosis (TCN) cannot be reliably differentiated from residual/progressive malignancy on CT or conventional MR imaging. TCN appears as an enhancing mass with surrounding vasogenic edema, frequently increasing in size on serial examinations. Internal irregular linear areas of high T1 signal may be found. Typical patterns of contrast enhancement include internal localized specks of bright signal within necrotic areas (“Swiss cheese/soap bubble” – presumably due to contrast leakage into the cavity) and ill-defined feathery peripheral enhancement (“spreading wavefront”). Edema is limited to the white matter without infiltrative gray matter involvement. On perfusion imaging TCN characteristically shows very low relative cerebral blood volume (rCBV), in contrast to malignant neoplasms. The perfusion signal intensity–time curve shows substantially lower signal recovery than in gliomas, reflecting the high degree of contrast leakage within TCN. Necrosis shows higher signal on ADC maps, compared to relatively low ADC values of viable neoplasms. TCN is characterized by decrease of all metabolites on MR spectroscopy and a dominant very high level of lipids, known as “death peak”.
Pertinent Clinical Information
TCN is a serious complication of radiation therapy for intracranial tumors and non-neoplastic conditions. It also occurs following treatment of extracranial diseases, most notably nasopharyngeal carcinoma. Development of TCN is related to the method of radiation delivery, total dose, fraction size, treatment volume, patient age, and administration of chemotherapy. The changes occur from several months to years after treatment, more frequently following high-dose local radiation, such as radiosurgery or brachytherapy.