Appreciating that films can influence audiences’ political imaginations and expectations, this chapter looks at first lady characters in feature length presidential movies released during the Clinton, Bush, and Obama administrations. Hillary Clinton, Laura Bush, and Michelle Obama were all politically active, setting new standards as presidential advisors, campaign fundraisers, and policy advocates. Presidential movies partially reflected this change, though historic gender constraints on women characters endured. These movies set an affirming wife-husband relationship as a prerequisite for first ladies to exercise political influence. Still, the films presented those relationships as alliances between politically knowledgeable and engaged individuals. That depiction was not extended to first ladies’ interactions with other decision-makers, which were rare and seldom successful. As a result, while presidential movies present their audiences with politically knowledgeable first ladies, these films do not yet encourage ticket holders to recognize these women as actually exercising political influence.

Non-invasive brain stimulation (NIBS) is a powerful and typically painless technique to stimulate the human brain. Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) with different stimulus modes and parameters are well used patterns of NIBS. Long-term potentiation or long-term depression (LTP and LTD)-like effects can be induced by NIBS. NIBS with practical interventional protocols produces various forms of cortical plasticity and its application has promise for PD treatment. Many clinical trials have shown that rTMS and tDCS with established guidelines are safe, and the interventional protocols using these techniques produce modest therapeutic effects in the patients. Multiple sessions using combinations of different patterns of NIBS and with other therapeutic methods may be more effective for the patient than a single type of intervention. Disease-modifying therapies with long-term effects and development of treatment with benefit beyond conventional therapy in clinical practice using NIBS in PD are theoretically possible and deserve further physiologic studies and clinical trials with large sample size.

Conservation is a fundamental feature of true ruin-mindedness, but the early attempts to preserve the ruins of Rome were unsuccessful until the tourism of the eighteenth century made it clear that there was an economic benefit to the preservation and attractive presentation of the city’s ruins. Once this was appreciated, care for the preservation of the ruins from further damage and decay became an issue. Towards the end of that century, soil and rubble were removed from the bases of a number of the more significant ruins, and steps were taken to isolate them so as to protect them from harm, an innovative measure. Rome took the lead in guarding the heritage of its built environment. But since no one had ever tried to protect a building out of doors before, novel means of preservation and even of conservation and rebuilding were devised to ensure that the ruins looked their best for visitors and for posterity. Further projects of excavation were undertaken by the French and the Kingdom of Italy in the nineteenth century, and in the twentieth century the ruins were furbished up for propaganda purposes by the Fascist regime.

Clinical diagnosis of movement disorders can be challenging, especially in the early stages of the disease. Therapy and prognosis of the disorders differ markedly, and early diagnosis is desirable. Structural imaging and complementary nuclear imaging can detect characteristic changes in diseases and present an objective, reproducible opportunity to confirm the suspected diagnosis, sometimes before the disease reaches its clinical full-blown stage. Differential diagnoses may also be excluded. After an introduction of the imaging methods, we present structural changes of a typical Parkinson syndrome as seen in sporadic Parkinson’s disease and some familial mono-/oligo-/polygenic and intermediate genetic variants, such as the "swallow tail sign." Characteristic features of atypical parkinsonian syndromes (MSA, PSP, CBD and vascular parkinsonism) are also presented and extended to include nuclear medicine aspects. Imaging features are classified in terms of their importance for diagnosis and differential diagnosis. Image examples are given to illustrate the features and the most important features and differential diagnoses are summarized and presented in tables.

This chapter deals with the pharmacotherapy of motor clinical hallmarks in Parkinson’s disease (PD), plus other PD and/or its intervention-related signs and symptoms. The treatment of PD-related non-dopaminergic symptoms such as mainly autonomic, neuropsychiatric and sleep–wake disorders are extensively dealt with in other chapters, so the pharmacotherapy of these disorders are only be discussed briefly. Autonomic non-motor fluctuations comprise cardiovascular (orthostatic hypotension), urogenital (detrusor over- and underactivity-related problems, e.g., urgency, frequency, nocturia, hesitation and straining), and gastrointestinal manifestations (sialorrhea, dysphagia, delayed gastric emptying, constipation). Depression and (mild) cognitive impairment are the most important mainly direct PD-related neuropsychiatric disorders, whereas impulse control disorders, as well as dementia and psychosis, are frequently seen as dopaminomimetic adverse events. Sleep–wake disorders with parasomnias are also characteristic non-motor symptoms in PD. The tailored pharmacologic strategies in these non-dopaminergic symptoms are discussed in detail.

Hereditary cerebellar ataxia (HA) are a heterogeneous group of disorders characterized by the presence of slowly progressive gait ataxia, dysarthria and other cerebellar signs. Detailed clinical history and neurologic as well as systemic examination are key to accurate diagnosis and hierarchical diagnostic investigations. The initial diagnostic evaluation of patients with HA should include a detailed assessment to rule out acquired treatable etiologies. If such a detailed screening is inconclusive, investigations should be directed towards hereditary causes of cerebellar ataxias. Early diagnosis and treatment can lead to favorable outcomes. Disease-specific therapies have emerged for various cerebellar ataxia syndromes including hereditary ones. Despite these advances, management of the majority of HA remains symptomatic. Moreover, there are no US FDA-approved medications for HAs to date. However, there are a few progressive HA conditions that can improve with disease-specific treatment, particularly if initiated early in the disease course. Here, we discuss various hereditary cerebellar ataxia syndromes that are amenable to disease-specific/targeted treatment.

Tremor is clinically defined by an involuntary rhythmic oscillatory movement of a body part. The most recent 2-axis classification scheme describes a clinical tremor syndrome in axis 1, mainly relying on tremor characteristics (body distribution, activation condition, tremor frequency, regularity, amplitude) and associated signs (isolated versus combined tremor syndromes). Based on further diagnostic tests (blood analysis, imaging, neurophysiology, genetic testing) the etiology is then described in axis 2, which may be acquired, genetic or idiopathic. The most common axis 1 isolated tremor syndromes are essential tremor and enhanced physiologic tremor, characterized by bilateral action tremor of the arms. Combined tremor syndromes relate to the accompanying neurologic sign or are described phenomenologically. These tremor syndromes relate to hyperoscillatory states of distinct networks, with the so-called cerebellar network playing a central role. Depending on the degree of disturbance as well as the additional involvement of other networks, specific tremor phenotypes emerge.

Sleep-related movement disorders and disturbances of motor control cover a broad range of conditions with a negative impact on an individual’s quality of sleep and daily functioning: (1) sleep-related movement disorders (e.g., periodic limb movements in sleep, restless limbs/legs syndrome, sleep-related leg cramps, sleep-related bruxism, sleep-related rhythmic movement disorder); (2) sleep-related disturbances of motor control, including (2a) parasomnias, such as RBD, sleepwalking, sleep-related eating disorder, sleep terror, sleep paralysis, (2b) sleep-related epileptic syndromes, such as nocturnal epilepsy with simple motor manifestations, nocturnal epilepsy with complex motor manifestations (sleep-related hypermotor epilepsy), and (2c) sleep-related dissociative disorders/psychogenic non-epileptic seizures. This chapter is designed to be a resource for clinicians, sleep specialists, and researchers, offering a comprehensive overview on the distinct features and characteristics; epidemiologic aspects; underlying pathophysiologic mechanisms; diagnostic criteria; and available treatment/management options of sleep-related movement disorders and sleep-related disturbances of motor control.

Paroxysmal movement disorders are a heterogeneous group of syndromes that produce recurrent attacks of involuntary movements without loss of consciousness as their common feature. In this chapter a very short historical overview is given before discussing the current classification and diagnostic criteria of the three main types of paroxysmal movement disorders: paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia and paroxysmal exercise–induced dyskinesia. During the past two decades, a rapidly growing number of genes that cause paroxysmal movement disorders have been reported. This also challenges the current classification because many genetic forms of paroxysmal dyskinesia can be caused by mutations of the same gene. Nevertheless, a first clinical description and classification appears to be reasonable and important. The chapter also describes the episodic ataxias, along with their genetic background, as well as the non-genetic causes of paroxysmal movement disorders, which include vascular, structural, infectious, inflammatory and metabolic causes. The last part of the chapter deals with a proposed approach to a patient with paroxysmal dyskinesia in daily practice.

The second chapter accounts for the steady ruination of Rome despite attempts at maintenance of the built environment in late antiquity. Fire, earthquake and flood were the chief agents of destruction. Repairs were always needed but became increasingly rare thanks to depopulation and diminishing public revenue. The shift of secular power to Constantinople and the gradual decay of paganism in the face of buoyant Christianity did the public buildings of Rome, especially the temples and places of entertainment, no favours. Stone from such structures began to be recycled for repairs or for the adornment of new buildings, such as churches. Depopulation emptied large sectors of the city within the Aurelian walls, and the abandoned sites were turned into farms and vineyards.

Tremor, which is defined as an oscillatory and rhythmic movement of a body part, is the most common movement disorder worldwide. The most frequent tremor syndromes are tremor in Parkinson’s disease, essential tremor, and dystonic tremor syndromes, whereas Holmes tremor, orthostatic tremor, and palatal tremor are less common in clinical practice. The pathophysiology of tremor consists of enhanced oscillatory activity in brain circuits, which are ofen modulated by tremor-related afferent signals from the periphery. The cerebello-thalamo-cortical circuit and the basal ganglia play a key role in most neurologic tremor disorders, but with different roles in each disorder. Here we review the pathophysiology of tremor, focusing both on neuronal mechanisms that promote oscillations (automaticity and synchrony) and circuit-level mechanisms that drive and maintain pathologic oscillations.

Chorea is a state of excessive, spontaneous movements, irregularly timed, non-repetitive, randomly distributed, and abrupt in character. The severity of movements may vary from restlessness with mild intermittent exaggeration of gesture and expression, fidgeting movements of the hands, and dance-like gait to a continuous flow of disabling violent movements. The pathogenesis of chorea is mainly related to striatal dysfunction. The classification of the causes of choreatic dyskinesias is complex and involves many clinical entities, both hereditary and acquired. The severity of chorea can be reduced by antipsychotics, tetrabenazine or benzodiazepines.

Lewy body disease is a common cause of neurodegenerative dementia. The clinical syndrome of dementia with Lewy bodies (DLB) has specific diagnostic, care and management needs, is underrecognized in clinical practice, and often mistaken for Alzheimer’s disease. It may only be identified at autopsy. It typically has a worse prognosis after diagnosis than Alzheimer’s disease. Early, accurate identification is important; improving this at clinical and prodromal stages may assist effective management and reduce patient and caregiver burden. The characteristic clinical features must be recognized: parkinsonism, RBD, fluctuating attention and cognition, complex visual hallucinations. In clinically equivocal cases, diagnosis may be supported by biomarkers specific to Lewy body disease: dopaminergic imaging, cardiac sympathetic imaging, polysomnography. A pattern of cognitive impairment not typical of Alzheimer’s disease may also be seen, with implications for cognitive symptom screening. Screening may be aided by seeking other symptoms of Lewy body disease (hypolfaction, autonomic symptoms, hallucinations other than visual), and other neuropsychiatric symptoms (delusions and mood changes).

Behavior is considered the response to internal and external stimuli. Both the basal ganglia as well as the cerebellum process internal (homeostatic) and external (environmental) cortical information in order to orchestrate adequately adapted behavior and send this processed information via the thalamus back to the cortex for final execution through motor neurons and neuromuscular structures. The basal ganglia arrange for the appropriate selection of behavioral fragments (response selection) out of the available pool of learned standard behaviors, and define their magnitude, while the cerebellum together with the sensory, visual, and vestibular organs deal with their coordination, that is, the exact timing of muscle actions so that the body can move smoothly. The final execution of these movements is enabled by upper/lower motor neurons and neuromuscular structures.

Corticobasal degeneration (CBD) is a neurodegenerative disease characterized by abnormal aggregation of hyperphosphorylated 4R-tau in cortical and subcortical areas of the brain. It is associated with various clinical phenotypes, such as the characteristic clinical phenotype corticobasal syndrome (CBS), which manifests with asymmetric akinetic–rigid, poorly levodopa-responsive parkinsonism, and cerebral cortical dysfunction. Other associated phenotypes are progressive supranuclear palsy (PSP) syndrome, frontotemporal dementia, Alzheimer’s disease (AD)-like dementia, and non-fluent/agrammatic variant of primary progressive aphasia. Precise use of terminology is critical for a common understanding in discussions of clinical phenotype, attempted clinical diagnosis of CBD with its many presenting phenotypes, and accurate pathologic diagnosis (which can only be made neuropathologically). Diagnosis of probable or possible CBS and the other CBD-associated syndromes is based on the presence of certain clinical features. Pathologic and neuroimaging findings and currently available biological markers are discussed. Treatment for CBD and CBS is symptomatic and supportive at present.

Autoimmune movement disorders, although relatively rare, are not to be missed because of the treatment implications. There is a broad clinical spectrum, but recognition of some characteristic forms, or associated red flags or other clues, can point to the diagnosis. This chapter covers the clinical spectrum of primary neurologic or systemic autoimmune disease presenting or mainly manifesting as a movement disorder, and addresses the underlying immune-pathophysiologic aspects.

This chapter uses the lens of feminine rhetorical style to examine how gendered expectations affect first ladies’ public speeches and how their rhetorical styles evolved over time. Selected speeches of first ladies from Eleanor Roosevelt to Melania Trump are analyzed and five recurring themes are reviewed. These include the discussion of feminine topics such as family and childcare and envisioning women’s role in society, addressing masculine issues such as war and politics through feminine rhetoric, connecting with audiences as peers, use of personal narratives, and use of expert sources and statistics. The chapter concludes that first ladies’ addresses are usually delivered within the bounds of stereotypical gendered expectations, though subtle deviations can be found depending on the first lady’s public image, her professional experience, and the popular opinion of the times. The analysis of first ladies’ rhetorical styles helps us better understand their evolving role in US politics.

True ruin-mindedness begins with the poet Petrarch, the subject along with his successors of the fourth chapter. He was the first person we know of who visited Rome with the intention of seeing the ruins. Thanks to his unrivalled knowledge of Latin literature, he viewed the ruins as ‘sites of memory’, complementary to and made comprehensible by the texts of Roman poets and historians. For Petrarch and his successors, the ruins became an essential part of the historical and cultural heritage of the ancient Romans, a material complement to the history of Livy and the poetry of Virgil. Such complementarity was crucial to endowing the ruins with some context and meaning; they were not just piles of broken rubble but a valuable part of the Roman cultural achievement as a whole. Petrarch’s enthusiasm was infectious and it can be claimed that he initiated two new disciplines, urban topography and antiquarianism, the subjects of the next two chapters, 5 and 6. From this point on, progression will be largely chronological, as the sentiment of ruin-mindedness is developed and enlarged.