Name : Dr.Bulabai Karpagam MD,FRCR
Family : Bulabai desai
Affiliation :DR.B.Karpagam,Assistant Professor,SRM medical college Hospital and Research Institute, Kattankulathu
Academic Degree : MD,FRCR
Resident : M.S.Hemhnath
Gender : Female
Age : 53
A 53yrs female patient came with complaints of mild weakness of left upper and lower limbs of few hours with no abnormal movement. Past history known case of diabetic mellitus type ll for the past 25 yrs on irregular follow up . CBG was 480 mg/dl on time of admission. Rest of the biochemical investigations are normal.
Figure 1 -- On axial T1 weighed image shows hyperintense signal in the right basal ganglia region. Figure 2 – On flair series reveals mild hyperintesity at corresponding region . Figure 3 – On T2 series basal ganglia do not reveal altered signal. Figure 4 - On diffusion weighed series the lesion shows no diffusion restriction.
For lesion appearing hyperintense on T1 series are as follows- pysiological calcification, manganese toxicity, disorders of calcium metabolism and chronic liver diseases and these conditions are usually bilateral and based upon there clinical history they can be differentiated. Hypoxic brain injury may be unilateral but they shows diffusion restriction on early imagining. Basal ganglia bleed can be differentiated either with CT or GRE series. In our case bleed was excluded by these study series.
Non Ketotic Hyperglycemic Encephalopathy .
Discussion (Related Text)
Abstract Hemichorea- hemiballism is the prime manifestation of non ketotic hyperglycemic encephalopathy with MRI imaging finding of lateralizing / asymmetric basal ganglia lesion (hyperintense on T1 ).The presence of this finding highly suggestive of non ketotic hyperglycemia, after excluding hemorrhage. We present an unusual case of a patient presenting with vague stroke like symptom, laboratory analysis revealed nonketotic hyperglycemia and neurologic exam failed to elicit any finding of movement disorder. As far we know this is second published case of a patient with typical neuro imaging manifestation of non ketotic hyperglycaemia without assosicated hemichorea and hemiballismus. This finding suggest that radiologist should be alert to the possibility of non ketotic hyperglycemia in patient with basal ganglia lesion even in the absences of a movement disorder. DISCUSSION Nonketotic hyperglycemia affects patients with poorly controlled diabetes mellitus who classically present with the clinical finding of HC-HB . This is a rare condition with the largest published case series consisting of only 53 patients. The majority of reported cases have involved Asians, with a female to male ratio of 1.76. This condition is thought to occur most frequently in the elderly, most commonly in the seventh decade . In the radiology literature, nonketotic hyperglycemia has been associated with a characteristic appearance of unilateral or asymmetric lesions of the BG which are typically contralateral to the side of the patient's presenting symptoms. The most commonly described MRI findings associated with nonketotic hyperglycemia include high signal intensity BG lesions on T1-weighted brain MRI on the side contralateral to patient symptoms. The T2-weighted findings are much more variable with the majority of BG lesions described as either hypo-intense or iso-intense to background normal BG. Relatively little has been published regarding nonketotic hyperglycemia and findings on DWI . A small case series and case report have demonstrated mild to moderate restricted diffusion corresponding to the T1-weighted hyperintense BG lesions . Diffusion restricted signal denotes cytotoxic edema and also depends upon the period of evaluation after symptom. On follow-up MRI, Oh et al reported the resolution of T1 signal abnormalities in 19 of 22 patients presenting with nonketotic hyperglycemia, suggesting that the neuroimaging findings of nonketotic hyperglycemia are usually reversible with appropriate treatment . The etiology of the hyperintense signal observed on T1-weighted imaging has been attributed to hyperosmolar state. The most widely promoted hypothesis ascribes the T1 hyperintensity to the protein hydration layer in the cytoplasm of swollen gemistocytes . Supporting this hypothesis, Shan et al. reported that a biopsy of a hyperintense putaminal lesion demonstrated abundant gemistocytes in a fragment of brain tissue. The another
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