One thing clear to me from reading research articles over the last few years on PSP is that even though the Queen Square Brain Bank doesn’t have the number of brains that Mayo Jax has, QSBB does loads more research and publishes more based on what they do have.
This (mostly) British research is about hyposmia (poor sense of smell) in PSP.
Researchers gave 36 patients with PSP who had scored more than 18 on the MMSE the University of Pennsylvania Smell Identification Test (UPSIT). 140 patients with PD and 126 controls were also tested.
PSPers had worse sense of smell than controls but better sense of smell than those with PD.
“For patients with PSP, UPSIT scores correlated with MMSE but not disease duration…”
Though people may have PSP pathology in regions of the brain responsible for smell, their sense of smell may not be affected. “The brains of six of the patients with PSP were examined postmortem and all revealed neurofibrillary tangles and tau accumulation in the rhinencephalon, although only three had hyposmia.”
“Further prospective studies including patients with early PSP and PSP-P with postmortem confirmation might help clarify if smell tests could be useful when the differential diagnosis lies between PD and PSP.”
Robin
Research Article
Hyposmia in progressive supranuclear palsy
Movement Disorders, Published Online: 5 Mar 2010
ABSTRACT
Previous studies suggested that olfaction is normal in progressive supranuclear palsy (PSP). We applied the University of Pennsylvania Smell Identification Test (UPSIT) to 36 patients with PSP who scored more than 18 on the Mini Mental State Examination (MMSE), 140 patients with nondemented Parkinson’s disease (PD) and 126 controls. Mean UPSIT scores in PSP were lower than in controls (P < 0.001) but higher than in PD (P < 0.001) after adjusting for age, gender, and smoking history. For patients with PSP, UPSIT scores correlated with MMSE (r = 0.44, P = 0.006) but not disease duration (P = 0.6), motor subscale of the Unified Parkinson’s Disease Rating Scale (P = 0.2), or Frontal Assessment Battery (P = 0.5). The brains of six of the patients with PSP were examined postmortem and all revealed neurofibrillary tangles and tau accumulation in the rhinencephalon, although only three had hyposmia. Further prospective studies including patients with early PSP and PSP-P with postmortem confirmation might help clarify if smell tests could be useful when the differential diagnosis lies between PD and PSP.
Authors:
Laura Silveira-Moriyama, MD 1, Graham Hughes, MD 2, Alistair Church, MD 3, Hilary Ayling, MSc 4, David R. Williams, MD, PhD 1 5, Aviva Petrie, MSc, CStat 6, Janice Holton, MD, PhD 1 4, Tamas Revesz, MD 4, Ann Kingsbury, PhD 1, Huw R. Morris, MD, PhD 7, David J. Burn, MD 2, Andrew J. Lees, MD 1 4 *
1Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, United Kingdom
2Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, United Kingdom
3Department of Neurology, Royal Gwent Hospital, Newport, Gwent, United Kingdom
4Queen Square Brain Bank, UCL Institute of Neurology, London, United Kingdom
5Department of Neurology, Faculty of Medicine (Neurosciences), Monash University (Alfred Hospital Campus), Melbourne, Australia
6Biostatistics Unit, UCL Eastman Dental Institute, London, United Kingdom
7Department of Neurology, Cardiff University School of Medicine, Cardiff University, Cardiff, United Kingdom
This abstract isn’t available yet on PubMed but is available on the publisher’s website.
http://www3.interscience.wiley.com/jour … 0/abstract