Abstract
The term scans without evidence of dopaminergic deficit (SWEDD) can be associated with any patient diagnosed at first with Parkinson’s disease but with a negative dopamine transporter-single photon emission computed tomography (DaTSPECT), which does not confirm the presynaptic dopaminergic deficiency. Therefore, an alternative diagnosis should be sought to support parkinsonism as a clinical diagnosis. Parkinsonism is a well-known manifestation of frontotemporal lobar degeneration (FTLD), particularly frequent in those with positive DaTSPECT. Here, we reinforce previous observations that parkinsonism can be present in FTLD patients with negative DaTSPECT and therefore, FTLD may account for a percentage of patients with SWEDD. We gather the clinical observations supporting this hypothesis and describe a case report illustrating this idea. Studies suggest the result of DaTSPECT in FTLD may depend on the neuropathology and clinical subtype. However, most studies do not provide a clinical description of the clinical subtype or pathological features making the association between subtypes of FTLD and DaTSPECT results impossible at the moment. Further studies correlating clinical, neuropsychological, neuroimaging, genetic, and pathology findings are needed to better understand parkinsonism in FTLD.
Highlights
Parkinson’s disease (PD) is a common neurodegenerative disorder
The active ingredient of [123I]FP-CIT SPECT is a cocaine analog, 123I-nortropane, labeled: N-u-fluoropropyl 2b-carbomethoxy-3b-(4-iodophenyl), referred to as: ([123I]ioflupane). It binds to striatal presy naptic dopamine transporter (DaT) in animals and humans and helps visualize indirectly these neurons with SPECT
Patients with scans without evidence of dopaminergic deficit (SWEDD) can present motor features similar to those which are dopamine-deficient (PD), previous longitudinal research suggests that patients with SWEDD do not demonstrate the progression of motor symptoms [20] and continue to have normal DaTSPECTs for up to 4 years after they are initially identified [19, 21, 22]
Summary
Parkinson’s disease (PD) is a common neurodegenerative disorder. It is characterized by progressive degeneration of dopaminergic neurons in the pars compacta of the substantia nigra and the loss of nerve terminals in the basal ganglia structures [1, 2]. Patients with SWEDD can present motor features similar to those which are dopamine-deficient (PD), previous longitudinal research suggests that patients with SWEDD do not demonstrate the progression of motor symptoms [20] and continue to have normal DaTSPECTs for up to 4 years after they are initially identified [19, 21, 22]. In a 5-year follow-up study of 16 patients with SWEDD, only 2 patients demonstrated reduced dopamine uptake on DaTSPECTs, while 14 remained classified as SWEDD [11] These studies seem to indicate that individuals with SWEDD have a distinctly different disorder than dopamine-deficient PDs [14, 15, 18, 22]. We present a case report illustrating this possibility and discuss the clinical, neuropsychological, genetics, and neuroimaging findings supporting the observation that FTLD is behind some cases of SWEDD
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