T1 Hypointense, T2 Hyperintense Parenchymal Lesions



T1 Hypointense, T2 Hyperintense Parenchymal Lesions


Anne G. Osborn, MD, FACR



DIFFERENTIAL DIAGNOSIS


Common



  • Enlarged Perivascular Spaces


  • Arteriolosclerosis


  • Chronic Hypertensive Encephalopathy


  • Cerebral Amyloid Angiopathy


  • Lacunar Infarction


  • Demyelinating Disease



    • Multiple Sclerosis


    • ADEM


    • Susac Syndrome


  • Encephalomalacia



    • Post-Traumatic


    • Post-Ischemic


  • Neurocysticercosis


  • Cerebral Contusion


  • Diffuse Axonal Injury (DAI)


Less Common



  • Primary Brain Tumor



    • Diffuse Astrocytoma, Low Grade


    • Anaplastic Astrocytoma


    • Glioblastoma Multiforme


    • Oligodendroglioma


    • Gliomatosis Cerebri


  • Metastases, Parenchymal


  • Abscess


  • Cerebral Amyloid Disease


  • Encephalitis



    • Herpes Encephalitis


    • Encephalitis (Miscellaneous)


  • Cerebritis


  • Vasculitis


  • Neurofibromatosis Type 1


  • Tuberous Sclerosis Complex


Rare but Important



  • Neurosarcoid


  • Radiation and Chemotherapy


  • Inherited Leukodystrophies (Many)


ESSENTIAL INFORMATION


Key Differential Diagnosis Issues



  • Very broad differential diagnosis


  • Most parenchymal masses, benign or malignant, are hypointense on T1-, hyperintense on T2WI


  • Look for presence/absence of mass effect, enhancement, blooming on T2* GRE/SWI, diffusion restriction, etc., to help narrow differential diagnosis


  • Location generally less helpful (some exceptions like herpes encephalitis, NF1, TSC, enlarged PVSs)


Helpful Clues for Common Diagnoses



  • Enlarged Perivascular Spaces



    • All locations, all ages but most common in basal ganglia/around anterior commissure, in midbrain, dentate nuclei, hemispheric white matter


    • Contain interstitial fluid; follow CSF signal on all sequences


    • May cause focal mass effect (expanded gyri, occasionally cause aqueductal obstruction)


    • May look bizarre, mimic neoplasm but spare cortex, do not enhance


  • Arteriolosclerosis



    • Small vessel ischemic changes (“microvascular disease”)


    • Scattered or confluent white matter/basal ganglia hypointensities on T1WI, hyperintense on T2WI


    • No enhancement


    • Patients generally older, often hypertensive


  • Chronic Hypertensive Encephalopathy



    • Look for confluent lesions around atria of lateral ventricles


    • Do T2* (GRE or SWI) to look for microbleeds (central > peripheral)


  • Cerebral Amyloid Angiopathy



    • Elderly normotensive demented patients


    • Hemorrhages of different age, peripheral microbleeds on T2*


  • Demyelinating Disease



    • MS > > ADEM



      • History of viral illness, recent immunization suggests ADEM


    • Susac Syndrome



      • Rare; often mistaken for MS!


      • Young to early middle-aged females


      • Progressive encephalopathy, sensorineural hearing loss, visual symptoms


      • “Holes” in middle of corpus callosum


Helpful Clues for Less Common Diagnoses



  • Primary Brain Tumor



    • Most primary brain neoplasms typically hypointense on T1WI, hyperintense on T2WI; may be difficult to distinguish neoplastic from nonneoplastic etiologies




      • DWI helpful (neoplasms generally don’t restrict; ischemia/infarction, infection typically do)


      • MRS helpful in some cases (↑ Cho)


    • Presence/absence/pattern of enhancement helpful but often nonspecific


    • Tend to be infiltrative rather than discrete, round masses


  • Metastases, Parenchymal



    • Tend to be round rather than infiltrative


    • Gray-white junction common location


    • Almost always enhance (ring, punctate, solid)


    • May cause multifocal white matter hyperintensities, mimic “small vessel disease”


    • Difficult to detect or differentiate from vascular disease without contrast


  • Abscess



    • Early cerebritis stage can be difficult to distinguish from ischemia, neoplasm


    • Late cerebritis to late capsule stages show ring enhancement


    • DWI restriction at all stages typical


    • MRS often shows lactate, amino acid peaks


  • Cerebral Amyloid Disease



    • Can be multifocal, diffuse (amyloid angiopathy)



      • Do T2* (GRE/SWI) to detect microbleeds


      • Peripheral > central (basal ganglia)


    • Lobar (hemorrhages of different ages)


    • Mass-like (“amyloidoma” rare)


  • Herpes Encephalitis



    • Affects limbic system



      • Temporal lobes, insular cortex


      • Cingulate gyrus, subfrontal cortex


    • Look for “sequential bilaterality” in temporal lobes


    • Preferentially involves cortex


    • FLAIR, DWI most sensitive for early detection


    • Hemorrhage with T1 shortening in late acute/subacute stages


  • Vasculitis



    • Can be primary CNS or secondary to systemic disorder


    • Combination of cortical/subcortical, basal ganglia disease suggestive


    • Punctate/linear enhancement common


  • Neurofibromatosis Type 1



    • Foci of abnormal signal intensity best seen on T2WI, FLAIR


    • Hypointensities on T1WI less common; basal ganglia may have hyperintensity


    • Typically represent myelin vacuolization, not demyelination; are transient (rarely seen in adults)


    • No enhancement; if present, suggests possibility of astrocytoma (usually pilocytic)


  • Tuberous Sclerosis Complex

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Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on T1 Hypointense, T2 Hyperintense Parenchymal Lesions

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