Basal ganglia and thalamus signal abnormalities occur in a wide variety of conditions. Ischemia/hypoxia, metabolic disorders and toxins, particularly those that affect the respiratory chain, have a predilection for affecting the basal ganglia as they are highly metabolically active.
They can be thought of in terms of the specific signal abnormality or according to the underlying disease processes.
Signal intensity changes
Although there is significant overlap between some of these lists they are discussed separately.
- increased T2 signal in the basal ganglia (usually also results in decreased T1 signal)
- decreased T2 signal in the basal ganglia
- increased T1 signal in the basal ganglia
- restricted diffusion in the basal ganglia
- calcification in the basal ganglia
- neurodegenerative/metabolic (A-Z)
- acquired hepatocerebral degeneration
- autoimmune encephalitis (e.g. anti-D2 dopamine antibodies)
- Creutzfeldt-Jakob disease
- extrapontine myelinolysis (osmotic demyelination)
- Fahr disease
- focal areas of signal intensity in neurofibromatosis type 1
- Huntington disease
- methylmalonic acidemia
- mitochondrial diseases: e.g. Leigh disease
- neurodegeneration with brain iron accumulation (NBIA) (e.g. PKAN)
- Wilson disease