Parkinson's disease: chameleons and mimics

Abstract

Parkinson's disease (PD) is a common neurodegenerative condition that usually presents with symptoms related to asymmetric bradykinesia, resting tremor, rigidity and postural instability. Making the correct diagnosis can be challenging as many conditions-including tremor, gait and atypical parkinsonian disorders-can mimic PD. PD can present with unanticipated motor and non-motor symptoms, and so can masquerade as a number of rheumatological, neurological, sleep and mood disorders. Careful clinical assessment, informed by well-validated diagnostic criteria, is important in the initial diagnostic formulation. In uncertain or ambiguous cases, follow-up with monitoring of the treatment response usually gives the correct diagnosis, as validated in postmortem follow-up studies. 'Premotor' PD-a range of non-motor symptoms, particularly sleep disorders and constipation, which can occur up to 20 years before PD motor onset-is common. The presence of non-motor features in early disease sometimes supports the diagnosis of PD. Here we give an overview of the diagnosis of PD and its most important chameleons and mimics, and review the recent advances in structural and functional imaging in parkinsonism.

Shoulder arthroplasty in patients with Parkinson's disease is associated with increased complications

“…3,15,29 In addition, difficulties with balance and a higher rate of falls further increase their risk and likely explain the findings in the current study. 2,7,23,29 Existing literature on postoperative stiffness after arthroplasty in patients with PD demonstrates variable results. In a case series of 3 patients with PD, Dunn et al 4 noted a mean active forward flexion of only 40 .…”

Neuroimaging of Parkinson's disease: Expanding views

“…antipsychotic medications, amphetamine) (Ham et al, 2015), traumatic brain injury (Bhidayasiri et al, 2012), and toxins such as Mn (Criswell et al, 2011), etc. (Ali & Morris, 2014). Current validation of a diagnosis of PD is based on neuropathological findings.…”

An order in Lewy body disorders: Retrograde degeneration in hyperbranching axons as a fundamental structural template accounting for focal/multifocal Lewy body disease

“…This hierarchal pattern led to a hypothesis that αS lesions start at the lower brainstem and spread upward along neuroanatomical connections as claimed by Del Tredici and Braak, now conceptualized as “the Braak's scheme” . On the other hand, accumulating evidence suggests that there are some exceptional cases not in conformity with this unified scheme . Anyway, this attractive hypothesis prompted neuroscientists to perform experimental inoculation of “seeds” or focal expression of relevant proteins into animal brains or nerves, expecting that subsequent lesion spread “like prion” may replicate what is going on in the human brain with PD/DLB .…”

“…Probably, the propensity to develop LBs may be higher at the lower brainstem, while its variability frequently hampers stereotypic recognition of PD/DLB. This paradigm shift prompted clinicians to redefine PD or DLB by taking clinicopathological diversities of these disorders into account . Probably, it is now necessary to redefine the clinicopathological framework of LBD so that their diversity is appropriately integrated in the diagnostic criteria.…”