This chapter discusses the clinical approach to a patient with a movement disorder, based on the phenomenology of that particular disorder. It summarizes the definitions of the most prevalent movement disorders and highlights particular clinical aspects that may help narrow down the differential diagnosis.

A core purpose of South Africa’s Constitution was to modify private orderings growing out of Apartheid’s legacy of racism. Hence, the South African framers, and specifically those representing the African National Congress (ANC), had strong reason to adopt some version of horizontal application. While republican elements occur in some of the ANC’s early thought on private actors’ duties, such discourses featured less when the party had to find consensus with representatives of the Nationalist Party while negotiating the Interim Constitution. A strong formalist streak in the legal culture, concerns about preserving property rights, and the incentives of institutions such as the Supreme Court of Appeal all cut against the practice of horizontal application. Ultimately, the constitutional framers provided for both direct and indirect horizontal application in the Final Constitution. The ANC’s vision was thus fixed in this feature, and subsequent cases further cemented a break from prior orderings. Republican discourses ensued in cases involving horizontal application and perhaps most clearly in issues striking at the heart of the old Apartheid regime, such as housing and education.

Continuous dopaminergic stimulation aims to avoid fluctuations in plasma levels of antiparkinsonian drugs in Parkinson’s disease. There are limited possibilities for translating this concept into practice with standard oral therapies: subcutaneous infusions of apomorphine (and in the near future most probably also of levodopa) and intestinal infusions of levodopa/carbidopa (LD/CD). Both allow the maintenance of stable drug levels in blood and hence a sustained stimulation of dopamine receptors. The magnitude of the effect is more or less similar between techniques, with a reduction in OFF time, an improvement in ON time, and at least for infusions of LD/CD, documented reduction in dyskinesias. The effect is apparently greater with the intestinal and subcutaneous levodopa infusions given that they were compared with oral LD/CD in their pivotal studies whereas apomorphine was compared with placebo. As of yet, subcutaneous apomorphine and intestinal LD/CD infusions are positioned at the same level of efficacy as surgical treatment of PD and are alternatives for the treatment of patients with motor fluctuations not controlled with conventional treatment.

People with Parkinson’s disease (PD) often suffer from various non-motor symptoms, including manifestations of autonomic dysfunction. The latter encompass cardiovascular, urogenital, gastrointestinal manifestations, sexual dysfunction and thermoregulatory disturbances. Autonomic manifestations can be an intrinsic aspect of PD, resulting from degeneration of parasympathetic and sympathetic pathways, or can be secondary to comorbidity or medication intake. As autonomic dysfunction is prevalent and often troublesome, identification and appropriate treatment are relevant steps in the management of people with Parkinson’s disease. Some manifestations of this autonomic dysfunction may precede the onset of PD motor features by many years, and might be considered biomarkers of this disease. A variety of non-pharmacologic and pharmacologic treatments have been investigated for the treatment of autonomic dysfunction in PD, but a limited evidence base is available so far.

This chapter reviews the K-theory functors due to Segal and Elmendorf–Mandell. These are also called infinite loop space machines because they produce connective spectra from permutative categories and multicategories. Each is constructed as a composite of other functors, via certain diagram categories, that we describe.

Multiple system atrophy (MSA) is an adult-onset, rapidly progressive, rare, neurodegenerative disorder characterized by an abnormal accumulation of α-synuclein (αSYN) in oligodendrocytes associated with multifocal neuronal degeneration. Further synucleionopathies include Parkinson disease (PD) and dementia with Lewy bodies (DLB). Clinically, the disease is characterized by poorly L-dopa-responsive parkinsonism and/or cerebellar ataxia accompanied by autonomic failure. This chapter provides an update of clinical symptomatology, diagnosis and, especially, disease-modifying and symptomatic treatment.

Electronic media use by first ladies dates to the 1930s when Lou Hoover delivered her first radio address. The development of radio and television—and later social media—placed a greater emphasis on image and personality, giving first ladies the opportunity to be heard as well as seen, and in some cases offering them more control over their messaging. This chapter looks at several notable examples of how first ladies strategically used—and in some cases misused—electronic media to shape their public image, support their husband’s programs, and advocate for their own causes.

The complexity of movement disorders poses challenges for clinical management and research. Functional imaging with PET or SPECT allows in-vivo assessment of the molecular underpinnings of movement disorders, and biomarkers can aid clinical decision making and understanding of pathophysiology, or determine patient eligibility and endpoints in clinical trials. Imaging targets traditionally include functional processes at the molecular level, typically neurotransmitter systems or brain metabolism, and more recently abnormal protein accumulation, a pathologic hallmark of neurodegenerative diseases. Functional neuroimaging provides complementary information to structural neuroimaging (e.g. anatomic MRI), as molecular/functional changes can present in the absence of, prior to, or alongside structural brain changes. Movement disorder specialists should be aware of the indications, advantages and limitations of molecular functional imaging. An overview is given of functional molecular imaging in movement disorders, covering methodologic background information, typical molecular changes in common movement disorders, and emerging topics with potential for greater future importance.

Gait and balance are fundamental human abilities. When assessing a patient, a certain phenomenologic gait pattern is identified based on characteristic signs that we relate to anatomic systems (topo-diagnosis). According to their functional complexity, these systems can be categorized into lower-level systems (bones, muscles, nerves); intermediate-level systems (basal ganglia, cerebellum, sensory systems); and higher-level systems (cortex–basal ganglia loops). In a second step, we relate this to an underlying etiology, giving rise to a two-axis diagnosis. Gait examination can show direct stepping disturbances as well as indirect, i.e., compensatory changes mainly related to dysbalance (e.g., broad-based gait). The most common disorders include the “ataxias,” related to disturbances of the cerebellum or the sensory systems; basal ganglia gait disorders with parkinsonian or hyperkinetic phenomenology; and higher-level gait disorders, related to disturbances within the cortex–basal ganglia loops, which lead to inappropriate selection and organization of gait and balance programs, resulting in impaired stepping (with freezing of gait) and balance.

PSP was identified in 1963 by Richardson, Steele and Olszewski, as an “unusual syndrome” characterized by axial rigidity, bradykinesia, postural instability with falls, cognitive deficits, and supranuclear vertical gaze palsy, with uniform tau pathology predominating in the neurons of the pallido-nigro-luysian axis. The classical view is that tau protein and neuropil thread accumulation appears mainly in the subthalamic nucleus, red nucleus, substantia nigra, pontine tegmentum, striatum, oculomotor nucleus, medulla, and dentate nucleus, but there is growing evidence that cortical tau pathology is also common. Tau pathology uniformly predominates in the neurons of the pallido-nigro-luysian axis, but clinical PSP subtypes confirmed differential distribution patterns of neuronal, astroglial, and oligodendroglial tau pathologies both in total tau load and cell-type specific vulnerability patterns of brain regions, suggesting distinct dynamics or circuit-specific segregation of propagation of tau pathologies with accumulation of brainstem neurofibrillary tangles. Here, the novel clinicopathologic classification of PSP syndromes with specifically underlying neuropathology is discussed.