There is a special type of PET scan — fluorodeoxyglucose PET (FDG-PET) — that tests for glucose metabolism in the brain. Such scans are only available at large medical research institutions, such as UCSF or Stanford. There have been FDG-PET studies in the past comparing progressive supranuclear palsy (PSP) and Parkinson’s Disease patients.
This German study takes the research a step further and looks at two different types of PSP. In this study, 11 patients with the Richardson’s syndrome (RS) form of PSP, 8 patients with the parkinsonism form of PSP (PSP-P), 12 patients with Parkinson’s Disease, and 10 controls underwent an FDG-PET. They found that different areas in the brain were affected in each of the PSP patient groups — thalamus and frontal lobe for RS and putamen for PSP-P.
For those who may be new to our PSP support group, let me briefly give the primary symptoms of these two most common types of PSP:
* RS, or “classic PSP”: early onset of postural instability and falls, supranuclear vertical gaze palsy and cognitive dysfunction
* PSP-P: asymmetric onset, tremor, a moderate initial therapeutic response to levodopa, and frequently confused with Parkinson’s disease
If you’d like to read more about the two most common types of PSP, see this post from 2005:
Using this German study, we can correlate some of these primary symptoms of the two types of PSP with the FDG-PET findings:
* Reduced neurotransmitter activity levels in the thalamus are associated with falls and postural instability, and those with RS have a high frequency of falls.
* Reduced activity in the frontal lobe is associated with cognitive dysfunction, which occurs in those with RS. (RS patients “have an increased risk for dementia.”)
* And the putamen is associated with parkinsonism symptoms, such as those seen in PSP-P. Frontal metabolism was normal for PSP-P patients.
The authors state that the “putamen/thalamus ratio may be a useful parameter in clinical differential diagnosis of these PSP subgroups.” This is potentially helpful for distinguishing PSP-P from PD (Parkinson’s Disease) because these two diseases are hard to differentiate in the early stages.
Limitations of this study are the small sample size and the lack of pathological confirmation of the diagnoses. I’ve copied the abstract below.
Movement Disorders. 2012 Jan;27(1):151-5.
Fluorodeoxyglucose positron emission tomography in Richardson’s syndrome and progressive supranuclear palsy-parkinsonism.
Srulijes K, Reimold M, Liscic RM, Bauer S, Dietzel E, Liepelt-Scarfone I, Berg D, Maetzler W.
Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.
We hypothesized that postural instability and cognitive decline in patients with Richardson’s syndrome could be a consequence of reduced thalamic and frontal metabolism. Severe Parkinsonian signs in patients with progressive supranuclear palsy-parkinsonism may be reflected by alterations in putaminal metabolism.
Eleven patients with Richardson’s syndrome, 8 patients with progressive supranuclear palsy-parkinsonism, 12 with Parkinson’s disease, and 10 controls underwent clinical assessment and fluorodeoxyglucose positron emission tomography (PET).
Richardson’s syndrome patients showed pronounced thalamic hypometabolism, and patients with progressive supranuclear palsy-parkinsonism pronounced putaminal hypometabolism, compared to all other investigated groups. The putamen/thalamus uptake ratio differentiated progressive supranuclear palsy-parkinsonism from Richardson’s syndrome (area under the curve 5 0.86) and from Parkinson’s disease (area under the curve 5 0.80) with acceptable accuracy. Frontal hypometabolism was predominantly found in Richardson’s syndrome patients.
Richardson’s syndrome, progressive supranuclear palsy-parkinsonism and Parkinson’s disease showed different metabolic patterns in fluorodeoxyglucose PET.
PubMed ID#: #22359740 (see https://www.ncbi.nlm.nih.gov/pubmed/?term=22359740 for this abstract only)