@article{3101249,
    title = "What do patients with scans without evidence of dopaminergic deficit (SWEDD) have? New evidence and continuing controversies",
    author = "Erro, R. and Schneider, S.A. and Stamelou, M. and Quinn, N.P. and Bhatia, K.P.",
    journal = "JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY",
    year = "2016",
    volume = "87",
    number = "3",
    pages = "319-323",
    publisher = "BMJ Publishing Group",
    doi = "10.1136/jnnp-2014-310256",
    keywords = "levodopa, clinical feature;  diagnostic error;  differential diagnosis;  dopaminergic system;  dystonia;  essential tremor;  evidence based medicine;  human;  molecular imaging;  neuroimaging;  Parkinson disease;  predictive value;  priority journal;  radiological parameters;  Review;  scans without evidence for dopaminergic deficit;  diagnostic error;  dopaminergic nerve cell;  functional neuroimaging;  Parkinson disease;  pathology;  positron emission tomography;  single photon emission computer tomography, Diagnostic Errors;  Dopaminergic Neurons;  Functional Neuroimaging;  Humans;  Parkinson Disease;  Positron-Emission Tomography;  Tomography, Emission-Computed, Single-Photon",
    abstract = "The term SWEDD (scans without evidence for dopaminergic deficit) refers to the absence, rather than the presence, of an imaging abnormality in patients clinically presumed to have Parkinson's disease (PD). However, such a term has since been widely used in the medical literature, even as a diagnostic label. While many authors have suggested that different disorders of PD lookalikes may account for a proportion of SWEDD cases, others have claimed that some of them may have a benign subtype of PD. Thus, there has been ensuing controversy and confusion and the use of this term continues without clarity of what it represents. We have systematically reviewed all the studies involving patients with SWEDD with the aim of shedding light on what these patients actually have. It becomes clear from this systematic review that while most 'SWEDD' cases are due to a clinical misdiagnosis of PD, there exists a small proportion of patients with SWEDD who may have PD on the basis of a positive levodopa response, clinical progression, imaging and/or genetic evidence. The latter challenge the seemingly incontrovertible relationship between dopaminergic tracer binding and the diagnosis of nigrostriatal parkinsonism, particularly PD. Patients with SWEDD are unlikely to reflect a single clinical entity and we suggest that the term SWEDD should be abandoned."
}