الفهرس 
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Abstract
This study aimed to study the role of Magnetic Resonance Imaging in the evaluation of bilateral basal ganglia lesions. It was conducted upon forty patients having definite or suspicious basal ganglia lesions.
All the patients were subjected to full history taking and thorough clinical examination. Magnetic resonance imaging was performed on 1.5 T MR System using a standard head coil. Imaging included conventional MRI and advanced MRI if needed.
Many diseases present as basal ganglia abnormalities.MRI allows the detection of basal ganglia injury.
Knowledge of patient age, onset and clinical course of the disease with MRI is a powerful tool to establish the diagnosis.
The basal ganglia lesions were identified on the T1WI, T2WI and FLAIR. Then determine being unilateral or bilateral. Unilateral as: in Rasmussen encephalitis, diabetes with hemi chorea/hemi ballism and infarction, or more frequently bilateral in many pathologic conditions.
Bilateral lesions then classified according to the onset of the clinical presentations into acute and chronic, acute onset as in icteric encephalopathy, toxic (CO- calmepam, unknown), toxoplasma infection, Leigh disease, extra pontine osmotic myelinolysis, venous thrombosis, global ischemia, HIE and ischemia. chronic onset in hepatic failure, endocrine abnormality hypopituitarism, Hallervorden -Spatz syndrome, Huntington disease, Virchow Robin spaces, glutaric acidemia type I, lymphoma and metastasis.
Basal ganglia lesions also classified according to age into pediatric age group and adult group. The pediatric age group are HIE, venous thrombosis, Leigh disease, extra pontine osmotic demyelination, glutaric acidemia type I, endocrine abnormality (hypo pituitarism.), icteric encephalopathy, Huntington disease and Hallervorden -spatz syndrome. The adult group are HIE, global ischemia, ischemia, hepatic failure, Vichow Robin spaces, toxoplasma infection, toxic causes and neoplastic (lymphoma and metastasis.).
Laboratory and histo-pathological correlation confirm the diagnosis. These include serologic studies or immunoassays for toxoplasmosis; and determination of serum sugar levels for hypoglycemia and hyperglycemia; serum sodium levels and osmolality for osmotic myelinolysis; lactate levels in the serum and CSF ,serum lactate pyruvate ratio for Leigh disease, metabolic acidosis for global ischemia, HIE and venous thrombosis and toxic causes ,elevated carboxy haemoglobin level and metabolic acidosis for CO poisoning, elevated serum ammonia and liver enzymes for hepatic failure and histo-pathological correlation for confirmation of lymphoma and metastasis.
Bilateral lesions then classified according to the symmetry of the basal ganglia nuclei affection. Asymmetrical affection noted in limited lesions as in lacunar ischemic infarct, toxoplasma infection, dilated Virchow Robin spaces and neoplastic lesions (metastasis and lymphoma.).Symmetric lesions frequently noted with predominance of the metabolic causes (HIE, global ischemia, Leigh disease, icteric encephalopathy, chronic hepatic disease, glutaric acidemia type I, extra pontine osmotic myelinolysis and endocrine abnormality).Toxic causes (CO poisoning, calmepam toxicity, unknown substance) and degenerative causes in (Hallervorden-Spatz syndrome and Huntington disease.).