Congress:
ECR24
Poster Number:
C-18300
Type:
EPOS Radiologist (educational)
DOI:
10.26044/ecr2024/C-18300
Authorblock:
A. Gadwal, A. A. Reshmi; Bengaluru/IN
Disclosures:
Aishwarya Gadwal:
Nothing to disclose
Akshay Ashok Reshmi:
Nothing to disclose
Keywords:
CNS, Neuroradiology brain, CT, MR, Diagnostic procedure, Developmental disease, Genetic defects, Metabolic disorders
- The majority of pathological processes result in bilateral lesions, which can exhibit either symmetric or asymmetric characteristics, often displaying distinctive patterns on imaging studies including CT and MR images (Fig 2)
- The diseases involving bilateral basal ganglia in our study included :
- Hyperglycemia : (Fig 3) Non-ketotic hyperglycemia presenting with hemichorea-hemiballismus is characterized by hyperattenuation of the putamen, often involving the caudate nucleus and globus pallidus typically contralateral to patients symptoms. (Fig 4)
- Hypoglycemia : initially causes reduced diffusivity from cell swelling. Hyperattenuation of basal ganglia, hippocampi, subcortical grey matter, and occasionally in white matter. Sparing the thalamus helps distinguish from hypoxia. (Fig 5)
- Hypoxic injury : (Fig 6) On brain MRI, cytotoxic edema manifests as bilateral hyperintensity in the basal ganglia on T2-weighted/FLAIR images, accompanied by hyperintensities in the cortical gray matter.(Fig 7)
- Leigh's syndrome : (Fig 8) Subacute necrotising encephalopathy with characteristic bilateral symmetric hyperintense T2 signals in the putamen and/or brainstem including periaqueductal grey matter.(Fig 9)
- Wilson's disease: (Fig 10) Hepatolenticular degeneration exhibits bilateral symmetric signal changes in basal ganglia, frequently affecting the putamen. Hyperintensity in the midbrain, sparing the red nuclei, part of substantia nigra, and superior colliculi, results in the pathognomic "face of the giant panda" sign. (Fig 11)
- Osmotic myelinosis: Electrolyte imbalances and their correction can lead to central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM), commonly seen in chronically debilitated patients. (Fig 12) EPM is characterized by symmetric T2 hyperintensities in the basal ganglia and thalamus. CPM exhibits a distinct trident-shaped T2 hyperintense area, sparing the corticospinal tracts. (Fig 13)
- Carbon monoxide poisoning: (Fig 14) Most prevalent global cause of human poisoning, resulting from the incomplete combustion of carbon-based fuels. Inhaled carbon monoxide (CO) binds to hemoglobin with a 250-fold greater affinity than oxygen, diminishing oxygen transport capacity and causing tissue hypoxia. (Fig 15)
- Hepatic encephalopathy: (Fig 16) Frequently occurs in the presence of cirrhosis or portal hypertension marked by the distinctive bilateral symmetric hyperintensity in the globus pallidus on T1-weighted images. One of our cases also involved substantia nigra.(Fig 17)
- Wernicke's encephalopathy: (Fig 18) An acute, initially reversible neuropsychiatric condition resulting from a deficiency in vitamin B1 (thiamine), usually characterized by ocular abnormalities, ataxia, and confusion.MRI reveals characteristic symmetric signal changes in the medial thalami, periaqueductal grey matter, quadrigeminal plate, and mammillary bodies.(Fig 19)
- Cryptococcosis: (Fig 20) commonly seen in immunodeficient patients. CT scans may appear normal or show ventriculomegaly only. The pathognomic gelatinous non-enhancing CSF-like pseudocysts are well-defined lesions primarily found in the basal ganglia, varying in size from a few millimeters to several centimeters. (Fig 21)
- PKAN : (Fig 22) Neurodegeneration with brain iron accumulation (NBIA) refers to a collection of inherited neurological disorders marked by the abnormal buildup of iron in the basal ganglia.The "eye of the tiger" sign, indicating a hypointense globus pallidus with a central hyperintensity on T2-weighted images, is nearly diagnostic for pantothenate kinase-associated neurodegeneration (PKAN) accounting for up to 50% of all NBIA cases. (Fig 23)