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Letter to the Editor
T1 hyperintensity in the pulvinar: A pathognomonic sign of Fabry disease?
Hiperintensidad pulvinar en T1: ¿un signo patognomónico de enfermedad de Fabry?
J.A. Matías-Guiua,
Corresponding author
jordimatiasguiu@hotmail.com

Corresponding author.
, M. Yusb, M. Jorquerab, J. Porta-Etessama
a Servicio de Neurología, Instituto de Neurociencias, Hospital Clínico San Carlos, Madrid, Spain
b Servicio de Radiología, Hospital Clínico San Carlos, Madrid, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Fabry disease is an X-linked disorder of lysosomal metabolism that causes glycosphingolipid deposits in different tissues&#44; with vascular endothelium being particularly susceptible&#46; Clinical manifestations vary depending on the patient&#39;s age at onset&#59; they include skin lesions&#44; acroparesthesia&#44; pain episodes&#44; anhidrosis&#44; corneal opacity&#44; hearing loss&#44; and others&#46; However&#44; its vascular complications in the kidneys&#44; heart&#44; and brain are severe&#44; especially in late-onset cases or in patients with longer histories of the disease&#46; Although other types of neurological manifestations may be present&#44; cerebrovascular problems are particularly frequent and serious&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> Doctors consider Fabry disease in the differential diagnosis of strokes of undetermined causes&#44; and these strokes are most commonly linked to the vertebrobasilar territory&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Early diagnosis of this disease is important&#44; given the availability and usage recommendations for enzyme replacement therapy with recombinant acid alpha-glucosidase&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> For example&#44; researchers have described that hyperintensities in both pulvinar nuclei in a T1-weighted MRI sequence may be a pathognomonic sign for Fabry disease&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We present the case of a patient with ischaemic stroke and bilateral pulvinar hyperintensities whose enzyme analysis was negative for Fabry disease&#46; This 64-year-old man with hypertension and dyslipidaemia experienced sudden-onset dizziness and instability together with loss of lower limb strength and impaired enunciation&#46; Neurological examination observed right hemiparesis which abated over the next few hours&#46; Cranial CT revealed hyperintensities in both pulvinar nuclei &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; A T2-weighted MRI also showed a hyperintense lesion in the left hemi-pons with restricted diffusion&#59; findings are compatible with a recent infarct&#46; In the T1-weighted sagittal sequence&#44; we also observed hyperintensity restricted to both pulvinar nuclei &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; Hyperintense lesions in the subcortical and periventricular white matter are also apparent in the T2-weighted sequence&#46; There were no clinical signs or symptoms that would indicate Fabry disease&#44; and the patient had no family history of the entity&#46; Spectrofluorimetric determination of acid alpha-glucosidase in blood showed an activity level of 100&#37;&#46; We also ruled out other causes of calcification in the basal ganglia by measuring calcium&#44; parathyroid hormone&#44; glucose&#44; and ammonia&#59; HIV serology was also tested&#46; It is therefore possible to state that pulvinar hyperintensity in this case may be secondary to small-vessel impairment due to arterial hypertension&#46; Furthermore&#44; pulvinar hyperintensity was secondary to calcifications at this location according to CT and MRI&#59; similar findings have also been demonstrated in studies of Fabry disease&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">To the best of our knowledge&#44; this is the first reported case in which T1-weighted images of pulvinar hyperintensity are not linked to Fabry disease&#46; Two other case studies have questioned whether the sign is really pathognomonic&#59; in both&#44; however&#44; hyperintensity was not limited to the pulvinar nucleus and also affected the lenticular nucleus&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> The frequency of this radiological sign in patient series with Fabry disease<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#8211;6</span></a> has been estimated at 25&#37; in men&#44; but exceptionally rare in women&#46; For this reason&#44; theories suggest that this pattern could be related to the lower enzymatic activity in men&#44; which would result in the formation of vascular microcalcifications&#46; Presence of the sign has been correlated to age and severity of kidney disease&#44; but not to the appearance of ischaemic stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The case we present confirms that T1-weighted images of bilateral pulvinar hyperintensity secondary to calcification are not pathognomonic for Fabry disease&#46; Researchers require further studies to evaluate the frequency of this sign&#44; and its association with Fabry disease&#44; in populations not previously diagnosed with Fabry disease&#46; This will help us ascertain the diagnostic utility of this radiological sign in establishing ischaemic stroke aetiology&#46;</p></span>"
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ISSN: 21735808
Original language: English
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