bigiotteria louis vuitton Abnormalities of the basal ganglia and thalami in adults
All JournalsSeveral diseases may cause non specific MR signal abnormalities of the bilateral basal ganglia and thalami. As such, diagnosis of the underlying etiology may be difficult to achieve at imaging. In this review, we will present interpretative guidelines based on clinical data (mode of presentation, previous history, clinical symptoms, and evolution) and imaging data (type of signal abnormalities, location of lesions, and associated abnormalities). The main categories of diseases causing MR signal abnormalities of the bilateral basal ganglia and thalami in adults are reviewed: toxic, metabolic, vascular, tumoral, infectious and inflammatory diseases.
To cite the present paper, use exclusively the following reference. F Brami Zylberberg, E Méary, C Oppenheim, MP Gobin Metteil, D Delvat, I de Montauzan Rivière, et al. Atteintes bilatérales des noyaux gris de l’adulte. J Radio 2005;86:281 93.
The basal ganglia correspond to subcortical masses of gray matter located near the ventricles. Telencephalic in origin, they include the neostriatum represented by the caudate nucleus and putamen, the globus pallidus, the claustrum, and amygdaloid complex with connections to the thalamus (diencephalic in origin), subthalamic nucleus and substantia nigra. The lentiform nucleus corresponds to the putamen and globus pallidus.
The presence of signal abnormality at MRI involving the bilateral basal ganglia is a diagnostic challenge because the differential diagnosis is extensive and the imaging findings seldom are specific. Diagnosis thus relies on a review of clinical and imaging features. The purpose of this paper is to propose interpretative guidelines and review the main categories of diseases causing signal abnormalities of the basal ganglia.
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While the presence of abnormal signal intensity in the bilateral basal ganglia at MR imaging may be an incidental finding it more frequently is symptomatic and the mode of clinical presentation is important for differential diagnosis (tableI). A careful review of systems and personal and family history is needed to assess for underlying factors including: alcohol abuse, malnutrition, vascular risk factors, intoxication or poisoning, professional exposure, inherited or familial diseases
Clinical symptoms are variable, but characteristic clinical presentations include: dementia with preferential attention and memory deficits is seen in patients with bilateral thalamic involvement; involvement of the striatum may lead to movement disorders including choreic syndrome; Parkinson’s syndromes occur with involvement of the striatonigral system. Headache, nausea, vomiting and abdominal pain are suggestive of intoxication or poisoning. Early diagnosis with diffusion weighted MRI. Nervenarzt 2001;72:632 5.
The signal of the basal ganglia is nearly isointense to cortex on conventional spin echo T1W and T2W images and FLAIR images. The globus pallidus is slightly hypointense relative to the putamen. With increasing age, the following signal modifications may occur. On MRI, VR spaces are isointense to cerebrospinal fluid. Sometimes, calcifications may be T1W hyperintense [3Dell LA, Brown MS, Orrison WW, Eckel CG, Matwiyoff NA. Physiologic intracranial calcification with hyperintensity on MR imaging: Case report and experimental model. AJNR Am J Neuroradiol 1988;9:1145 8.
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Hepatic encephalopathy, resulting from hepatocellular disease, is secondary to the accumulation of toxic substances normally metabolized by the liver (ammonia, manganese). Clinical manifestations include extrapyramidal signs, neurobehavioral symptoms and alertness deficits including coma. Manganese toxicity, also seen with total parenteral nutrition, causes the basal ganglia to appear T1W hyperintense on spin echo T1W images [4Vymazal J, Babis M, Brooks RA, Filip K, Dezortova M, Hrncarkova H, et al. T1 and T2 alterations in the brains of patients with hepatic cirrhosis. AJNR Am J Neuroradiol 1996;17:333 6. The association with T1W hyperintensity of the adenohypophysis is pathognomonic of manganese toxicity [5Dietemann JL, Reimund JM, Diniz RL, Reis M Jr, Baumann R, Neugroschl C, et al. High signal in the adenohypophysis on T1 weighted images presumably due to manganese deposits in patients on long term parenteral nutrition. Neuroradiology 1998;40:793 6. In patients with hepatic encephalopathy, basal ganglia signal abnormalities are associated with other findings of chronic alcoholism including frontoparietal and cerebellar atrophy secondary to direct toxicity from ethanol.
Due to a deficiency in thiamine or vitamin B1, this disease occurs in patients with severe denutrition. Chronic alcoholism is not necessary. Early diagnosis and The classical clinical presentation is a triad of ataxia, ophthalmoplegia, and mental confusion. On MRI during the acute phase, T2W and FLAIR hyperintensity involves the medial thalami, periaqueductal gray matter and mammillary bodies (fig.3). Isolated enhancement of the mammillary bodies may be the only detectable abnormality [6Lenz V, Vargas MI, Bin JF, Bogorin A, Grebici Guessoum M, Jacques C, et al. Value of MRI findings in Gayet Wernicke encephalopathy. J Neuroradiol 2002;29:153 60. Extrapontine myelinolysis of the basal ganglia without central pontine myelinolysis. Clin Neuropathol 1996;15:96 100. Clinical features include rapid onset of quadriplegia with pseudobulbar syndrome. The lesions are nonspecific and very rarely hemorrhagic. The basal ganglia and thalami are preferentially involved. On MRI, they are characterized by T2W hyperintensity and T1W hypointensity corresponding to demyelination at the acute phase and gliosis at the chronic phase. Diagnosis relies on clinical features. The association of central pontine myelinolysis with its characteristic trident shaped appearance is suggestive.
Methanol toxicity (formic acid)
Clinical symptoms include a sensation of drunkenness, headache, nausea without or with vomiting, abdominal pain, and blurred vision. Symptoms usually develop within 24 hours after ingestion. MRI (fig.4) shows bilateral hemorrhagic striatal necrosis, more conspicuous on gradient echo T2W images [10Hsu HH, Chen CY, Chen FH, Lee CC, Chou TY, Zimmerman RA. Optic atrophy and cerebral infarcts caused by methanol intoxication: MRI. Neuroradiology 1997;39:192 4.