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Bilateral Thalamic Lesions

Bilateral Thalamic Lesions

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AJR:192, February 2009 W53
presentation is variable. Wernicke encephal-opathy is a medical emergency managedwith IV thiamine. T2-weighted MR imagesmay show symmetric high signal intensity inthe mamillary bodies, medial aspects o thethalami, tectal plate, periaqueductal graymatter, and dorsal medulla [4]. Contrast en-hancement is variable. Thiamine is an os-motic gradient regulator, and deciency candisrupt the blood–brain barrier, resulting incontrast enhancement [5]. Wernicke enceph-alopathy can have reduced diusion (Fig. 2)owing to ischemia-like changes in the thala-mi that should be dierentiated rom truevenous and arterial inarction [6].
Osmotic Myelinolysis
Osmotic myelinolysis accompanies rapidshits in serum osmolality; the classic settingis the rapid correction o hyponatremia [7].The classic lesion involves the central pons(central pontine myelinolysis). Other lesionsaect the basal ganglia, thalami, and whitematter (extrapontine myelinolysis). Acute T2hyperintensity and T1 hypointensity occur inthe aected regions. Contrast enhancementis uncommon, and reduced diusion may beseen [8] (Fig. 3).
Fabry Disease
Fabry disease is an X-linked disorder o glycosphingolipid metabolism leading toaccumulation o glycosphingolipids in thevascular endothelium, perithelium, smooth-muscle cells, heart, and brain that results inmyocardial ischemia and stroke [9]. On T2-weighted images, lesions o high signal in-tensity due to the vasculopathy may be seen
Bilateral Thalamic Lesions
Alice B. Smith
 James G. Smirniotopoulos
 Elisabeth J. Rushing
Steven J. Goldstein
Smith AB, Smirniotopoulos JG, Rushing EJ,Goldstein SJ
Department o Radiology and Radiological Sciences,Uniormed Services University, 4301 Jones Bridge Rd.,Bethesda MD 20814. Address correspondence to A. B.Smith (alsmith@usuhs.mil).
Department o Radiologic Pathology, Armed ForcesInstitute o Pathology, Washington, DC.
Department o Neuropathology and OphthalmicPathology, Armed Forces Institute o Pathology,Washington, DC.
Department o Radiology, University o KentuckyCollege o Medicine, Lexington, KY.
Neuroradiology/Head and Neck Imaging • Pictorial Essay
This article is available or CME credit. See www.arrs.org or more inormation.
This is a Web exclusive article.
2009; 192:W53–W620361–803X/09/1922–W53© American Roentgen Ray Society
ilateral thalamic lesions are un-common. These paired lesionshave a limited dierential diag-nosis that includes metabolic andtoxic processes, inection, vascular lesions,and neoplasia. The dierential diagnosis canbe urther narrowed with the patient history,imaging characteristics, and presence or ab-sence o lesions outside the thalami.
Primary Neoplasm
Bilateral thalamic glioma is a rare neo-plasm, usually a diuse low-grade astrocy-toma (World Health Organization grade II),that occurs in both children and adults [1].Bilateral thalamic glioma has a poor progno-sis due to the location o the lesions [2]. Chil-dren typically have signs o increased intra-cranial pressure and movement disorders.Adults experience mental deterioration [1].Typically, expansion o both thalami is ac-companied by abnormal hyperintensity onT2-weighted images and hypointensity onT1-weighted images that is not associatedwith contrast enhancement. Hydrocephalusdepends on the degree o mass eect. Diu-sion is normal (Fig. 1).
Metabolic and Toxic Disorders
Many metabolic and toxic processes a-ect both thalami simultaneously.
Wernicke Encephalopathy 
Wernicke encephalopathy results rom adeciency o vitamin B
and is requently as-sociated with alcohol abuse [3]. The classicclinical triad is ataxia, altered consciousness,and abnormal eye movements; however, the
bilateral thalamic, metabolic brain disorders,prion disease, viral encephalitisDOI:10.2214/AJR.08.1585Received July 24, 2008; accepted ater revisionAugust 29, 2008.
The purpose o this study was to present the neuroimaging ndings anddierential diagnosis o bilateral thalamic lesions.
The limited dierential diagnosis o bilateral thalamic lesions can beurther narrowed with knowledge o the specic imaging characteristics o the lesions incombination with the patient history.
Smith et al.Bilateral Thalamic LesionsNeuroradiology/Head and Neck ImagingPictorial Essay
W54 AJR:192, February 2009
Smith et al.
in the deep white and gray matter. T1 hyperin-tensity in the pulvinar is a common and sensi-tive nding [10]. Pulvinar hypointensity maybe seen on T2-weighted images but not con-sistently (Fig. 4). The cause o these changesin signal intensity is undetermined [9].
Fahr Disease
Fahr disease is a rare disease o unknowncausation. It is characterized clinically byneuropsychiatric abnormalities and parkin-sonian or choreoathetotic movement disor-der. Extensive bilateral calcication o thedeep gray matter is present and most re-quently involves the globus pallidus (Fig. 5).Other areas o involvement include the puta-men, caudate nuclei, thalami, and dentatenuclei [11]. Calcium–phosphorus metabo-lism is normal in these patients [11]. The T1and T2 signal intensity in the calcied re-gions varies with disease stage and calcica-tion [11]. The dierential diagnosis o theseparenchymal calcications includes endo-crinologic disorders such as hyperparathy-roidism, hypoparathyroidism, and pseudo-hypoparathyroidism.
Wilson Disease
Wilson disease is an autosomal recessiveinborn error o copper metabolism. Patientshave cirrhosis, corneal Kayser-Fleischer rings,and degeneration o the basal ganglia. I thepatient is not treated, the disease is progres-sive and atal. MR images show symmetricT2 hyperintensity o the deep gray matter:putamina, globus pallidi, caudate nuclei, andthe thalami. T1 signal intensity in the basalganglia and thalami is usually reduced, butT1 signal intensity may increase owing to theparamagnetic eects o copper [12]. Contrastenhancement does not occur (Fig. 6). Evi-dence o restricted diusion may be seen onearly images and is ollowed by return to nor-mal diusivity ater necrosis and spongiormdegeneration have occurred [13].
Leigh Disease
Leigh disease is a genetically heterogeneousmitochondrial disorder in which progressiveneurodegeneration leads to respiratory ailureand death in childhood. Patients have elevatedlevels o lactate in the CSF, serum, and urine.On T2-weighted images hyperintensity maybe seen in the involved regions, most requent-ly the basal ganglia, diencephalon, brainstem,thalami, and dentate nuclei [14]. MR spectros-copy reveals a decreased level o 
-acetylaspartate with elevated choline and lactate lev-els [15]. Contrast enhancement is uncommon(Fig. 7). In the acute phase, reduced diusionmay be seen.
Many viral orms o encephalitis involvethe thalami, including West Nile encephali-tis, Japanese encephalitis, Murray Valley en-cephalitis, Eastern equine encephalitis, andrabies. West Nile encephalitis is a single-strand RNA virus o the favivirus amilytransmitted to humans rom birds by culicinemosquitoes. It has been a summer seasonalepidemic in the United States since 1999.West Nile encephalitis causes bilateral T2hyperintensity in both thalami, the basalganglia, and the midbrain. Sulcal T2 hyper-intensity has also been reported, suggestingleptomeningeal infammation [16] (Fig. 8).Contrast enhancement is variable. Reduceddiusion has been reported, most oten inthe posterior limb o the internal capsule,corona radiata, and subcortical white matter[16].Creutzeldt-Jakob disease (CJD) is a rareneurodegenerative disease caused by the ac-cumulation o prion proteins in neurons. Per-sons with CJD experience rapidly progressivedementia. The disease is classied into threetypes. Most common (
85% o cases) is thesporadic orm, o which no cause has beenidentied. The amilial orm accounts or ap-proximately 15% o cases, and the inectious(variant CJD) or iatrogenic orm is least com-mon, making up less than 1% o cases. Imag-ing may reveal T2 prolongation and reduceddiusion in the basal ganglia, thalami, andcortex (cortical ribboning) [17] (Fig. 9).There is no contrast enhancement. Diusecortical atrophy occurs late in the course.A key imaging nding in variant CJD isthe pulvinar sign—high T2 signal intensityin the pulvinar (Fig. 10). This sign has a sen-sitivity o 68–90% or variant CJD and wasonce considered pathognomonic o variantCJD; however, it can also occur in sporadicCJD [18, 19]. The hockey stick sign (sym-metric pulvinar and dorsomedial hyperinten-sity) is characteristic o variant CJD [18].Cortical ribbon hyperintensity is rarely seenin variant CJD (Fig. 11).
Vascular Occlusion
Bilateral thalamic arterial inarcts are un-common. The thalami are supplied by bothanterior (anteroinerior thalami) and poste-rior (medial thalami) circulation, but severalvariations occur. Top o the basilar syndromeresults in inarcts o the superior cerebellarand posterior cerebral artery territories (Fig.12). The artery o Percheron, a variant, is asolitary arterial trunk arising rom the proxi-mal segment o the posterior cerebral arteryand supplying the paramedian thalami androstral midbrain bilaterally. Occlusion causesbilateral thalamic inarction.Deep venous thrombosis typically resultsin bilateral symmetric involvement o thethalami and occasionally the basal ganglia.The causes include pregnancy, oral contra-ceptives, inection, trauma, and dehydration,but the cause is undetermined in 20–25% o patients [20]. An abnormally hyperdensevein may be seen on CT scans, and corre-sponding T1 hyperintensity rom clot in thesinuses may be seen on MR images. CT andMR venography show no areas o contrastenhancement or signal intensity in the deepvenous sinuses. Diusion-weighted imagingmay show heterogeneous signal intensity[21]. Patchy contrast enhancement may beseen (Fig. 13).Mild to moderate cerebral hypotensioncauses refex shunting o blood rom the an-terior to the posterior circulation to preservethe brainstem, basal ganglia, and cerebel-lum. Severe reduction in blood fow exceedsthis mechanism, and protective shunting o blood no longer occurs. The result is damageto the deep cerebral nuclei, brainstem, andmost active regions o the cerebral cortex[22]. Diusion-weighted MRI is the earliestimaging technique to have abnormal nd-ings [22] (Fig. 14).Posterior reversible encephalopathy syn-drome (Fig. 15) is a disorder o cerebral vas-cular autoregulation. The multiple causes,which are oten but not always associatedwith hypertension [23], include glomerulone-phritis, preeclampsia and eclampsia, anddrug toxicity (cyclosporin). Symptoms in-clude headache, seizures, and visual distur-bance. CT and MRI typically show symmet-ric areas o vasogenic edema predominantlyinvolving the posterior circulation. Localizedmass eect, hemorrhage, and subtle enhance-ment are uncommon. Diusion-weightedMRI ndings usually are normal, but occa-sionally reduced diusion occurs, suggestingthe presence o cytotoxic edema [24].
Bilateral thalamic lesions have a variety o causes, and knowledge o the associated im-aging ndings can help narrow the dieren-tial diagnosis.
AJR:192, February 2009 W55
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Fig. 1—
52-year-old woman with bilateral thalamic glioma.
Axial T2-weighted MR image shows hyperintensity and bilateral diuse enlargement o thalami resulting in hydrocephalus due to mass eect.
Axial T1-weighted gadolinium-enhanced MR image shows bilateral low signal intensity within thalami and no associated contrast enhancement.
Apparent diusion coecient map shows high signal intensity in both thalami.

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