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[Striatonigral degeneration]
1Department of Neurology, Teikyo University School of Medicine.
Nihon Rinsho. Japanese Journal of Clinical Medicine
|January 1, 1997
Summary
Striatonigral degeneration (SND), a form of multiple system atrophy (MSA), presents parkinsonian symptoms and is difficult to distinguish from Parkinson's disease (PD). SND shows reduced brain glucose metabolism and poor Levodopa response, unlike PD.
Area of Science:
- Neuroscience
- Neuropathology
- Radiology
Context:
- Striatonigral degeneration (SND) is a sporadic, middle-aged onset neurodegenerative disease.
- SND is pathologically characterized by neuronal loss and gliosis in the striatum and substantia nigra.
- Clinically, SND often presents with dominant parkinsonian symptoms, mimicking idiopathic Parkinson's disease (PD).
Purpose:
- To differentiate Striatonigral degeneration (SND) from idiopathic Parkinson's disease (PD).
- To highlight key pathological and imaging features of SND.
- To discuss the implications for diagnosis and treatment.
Summary:
- Pathologically, SND involves neuron cell loss and gliosis primarily in the striatum (putamen) and substantia nigra.
- MRI T2-weighted imaging may reveal putaminal hypointensity and slit-like hyperintensity in the outer putamen.
- PET scans show decreased striatal glucose utilization in SND, contrasting with normal utilization in PD. Striatal dopamine D1 and D2 receptors are reduced, leading to a poor or absent response to Levodopa.
Impact:
- Improved diagnostic accuracy for SND, distinguishing it from PD.
- Understanding the neurochemical deficits in SND, particularly dopamine receptor reduction.
- Informing therapeutic strategies by highlighting the limited efficacy of Levodopa in SND.