Movement Disorders Phenomenology: An Office-Based Approach

By Steven J. Frucht and Pichet Termsarasab

​This book presents a comprehensive, practical approach to the evaluation of movement disorders using phenomenological basic principles, new discoveries in phenomenological research, and core values of outpatient neurology.
Movement Disorders Phenomenology begins with an overview of phenomenology and common approaches to movement disorder patients. Subsequent chapters then accurately and concisely relay information on major hypokinetic disorders such as atypical Parkinsonism, idiopathic Parkinson’s disease, cortical myoclonus, and complex motor tics. Expertly written text is further supplemented by patient vignettes at the beginning of select chapter that focus the reader's attention and highlight the urgency of the problem. These high quality videos aid in the astute clinical diagnosis of many movement disorders that are still largely dependent on visual pattern recognition in the clinic. The book closes with a timely discussion on the role of genetics in movement disorders.
Written for the practicing physician, Movement Disorders Phenomenology is an indispensable reference for neurology residents, general neurologists, movement disorders fellows and clinicians, and to any clinician who encounters and evaluates patients in the outpatient arena.

• Language: English
• Publisher: Springer
• Release date: Mar 12, 2020
• ISBN: 9783030369750

Book preview

© Springer Nature Switzerland AG 2020

S. J. Frucht, P. TermsarasabMovement Disorders Phenomenologyhttps://doi.org/10.1007/978-3-030-36975-0_1

1. What Is Phenomenology and Why Should We Care?

Steven J. Frucht¹   and Pichet Termsarasab²

(1)

Division of Movement Disorders, New York University Grossman School of Medicine, The Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders, NYU Langone Health, New York, NY, USA

(2)

Division of Neurology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand

Steven J. Frucht (Corresponding author)

Email: [e-mail]

Keywords

PhenomenologyParkinson’s diseaseMyoclonusTicsChoreaTremorDystonia

The word phenomenology derives from the Greek phainomenon, i.e., that which appears, and logos, to study. Movement disorder phenomenology is thus the study of that which appears, specifically the study of normal and abnormal movement and motor control. Movement disorders differ from other subspecialty areas in neurology. Movement disorders encompass both the central and peripheral nervous systems, while most specialties confine themselves to one or the other (e.g., peripheral in neuromuscular neurology, cortical and subcortical in behavioral neurology). Movement disorders encompass hundreds of diagnoses and disease mechanisms, and any disorder that produces an excess of movement (hyperkinetic) or deficiency of movement (hypokinetic) is included in the field. The requisite body of neurology to apply the moniker movement disorder expert is continuously expanding, and for these and other reasons, it is unlikely that movement disorders will ever be an ACGME-accredited specialty. Neurology may be the crown jewel of medicine, but for those attracted to our field, movement disorders is our hope diamond.

Observation and careful documentation lie at the heart of movement disorders. Meticulous documentation of the history and examination dates to the nineteenth century, in the tradition of Bell, Darwin, Gowers, Hammond, Duchenne, Charcot, Weir Mitchell, and Dana. Movement disorders benefited tremendously from the development of cinematography and film. Muybridge’s studies of horses and men in action, von Economo’s description of postencephalitic patients, Cotzias’ movies of manganese parkinsonism, and Irving Cooper’s surgical films of postencephalitic parkinsonism and dystonia form a natural extension of the photographic tradition of the mid-nineteenth century. By the middle third of the twentieth century, investigators such as Denny-Brown, Critchley, Bender, Purdon-Martin, and others extended the techniques of observational neurology to experimental intervention and physiology. Movement disorders as a recognized subspecialty began with the introduction of levodopa in the late 1960s. Oliver Sacks, Donald Calne, George Cotzias, and Melvin Yahr demonstrated the dramatic and sometimes problematic nature of the miraculous new drug [1–3], and the field of movement disorders was born.

The twenty-first century field of clinical movement disorders reflects the profound influence of two individuals, Stanley Fahn and C David Marsden [4, 5]. Over a period of 25 years, they developed movement disorders as a subspecialty, including organizing the Movement Disorder Society and associated journal, training fellows and pursuing research, and defining the importance of phenomenology. Movement disorder phenomenology breaks with the classic neurology cannon that prizes localization before differential diagnosis. In movement disorders, the principal question is not where is the lesion?, but rather, what is the phenomenology? Differential diagnosis, work-up, and treatment depend on phenomenology (e.g., dystonia vs. tremor vs. chorea vs. parkinsonism) rather than localization. Phenomenology also offers a powerful window into disease mechanism. Features of the history and examination link diseases that might not seem related at first glance, suggesting common pathophysiology and potential treatments. Phenomenology also focuses on patients’ experiences and the impact of illness on quality of life. For example, freezing of gait in parkinsonism, sensory tricks in dystonia, complex motor tics, visual hallucinations in Lewy body disease, and alcohol-responsive vocal tremor cannot be replicated in animal models. To study them and to try to treat them, one must study patients. As expressed by C David Marsden, patients with movement disorders are experiments of nature, presenting to the treating physician an opportunity and responsibility to try to design novel treatment strategies that relieve suffering and improve quality of life (personal communication).

Movement disorder diagnoses are classically divided into three categories: hypokinetic movement disorders (parkinsonism and related disorders); the five major hyperkinetic disorders (myoclonus, tics, chorea, tremor, and dystonia); and a large group of diverse movement disorders including ataxia, tardive syndromes, peripheral movement disorders, paroxysmal movement disorders, stereotypies, athetosis, and others.

The hypokinetic movement disorders (Parkinson’s disease, atypical parkinsonism (progressive supranuclear palsy, multiple system atrophy, corticobasal syndrome, Lewy body disease)) and secondary forms of parkinsonism are linked by the presence of the cardinal features of parkinsonism: bradykinesia; cogwheeling; tremor; and postural impairment. Patients with atypical parkinsonism display additional features that are important clues to diagnosis. The differential diagnosis of parkinsonism (hypokinetic disorders) appears in Table 1.1

Table 1.1

Differential diagnosis of the major hypokinetic movement disorders

aTypically parkinsonism appears in the late stages of the diseases

The five major hyperkinetic movement disorders in order of decreasing speed of movement include myoclonus, tics, chorea, tremor, and dystonia. Myoclonus, tics, and chorea comprise the three movement disorders with jerks. Myoclonus is brief, shock-like, unpredictable, and impossible to imitate. Tics are either simple (brief) or complex (longer and patterned), typically preceded by an urge and followed by a sense of relief once performed. Chorea is flowing, random, and unpredictable. Myoclonus cannot be suppressed, and attempts to dampen it usually paradoxically worsen its severity. Tics are classically suppressible, often allowing patients the opportunity to inhibit them in classrooms or meetings and to release them at a later time. Patients may be unaware of chorea, but most patients with chorea can at least partially suppress involuntary movements if they concentrate. Tremor is defined by a rhythmic oscillation of a body part around an axis. Dystonia is the slowest hyperkinetic disorder, with sustained and repetitive movements that often result in sustained postures. The phenomenology of each hyperkinetic movement disorder will be covered in Chaps. 5, 6, 7, 8, and 9. With the exception of rare forms of myoclonus, all hyperkinetic movement disorders disappear in sleep. Figure 1.1 displays the major hyperkinetic movement disorders, referencing their speed and amplitude of movements.

../images/466194_1_En_1_Chapter/466194_1_En_1_Fig1_HTML.png

Fig. 1.1

Speed and amplitude of hyperkinetic movement disorders

The differential diagnosis of myoclonus appears in Table 1.2. The etiology of myoclonus varies depending on where the patient is encountered. In the hospital, myoclonus is common in the intensive care unit, on the transplant service, in the dialysis suite, and on the oncology ward. Toxic, metabolic, and structural causes are the usual culprits. The reason for consult is almost never myoclonus, but almost always tremor. In the outpatient setting, genetic forms of myoclonus (myoclonus-dystonia and the various progressive myoclonic epilepsies) and myoclonus accompanying neurodegenerative diseases (Alzheimer’s disease, corticobasal syndrome) usually trigger the referral.

Table 1.2

Differential diagnosis of myoclonus

The differential diagnosis of tics (Table 1.3) is relatively straightforward. Secondary causes of tics are exceptionally uncommon.

Table 1.3

Differential diagnosis of tics

The differential diagnosis of chorea is extremely broad (Table 1.4). The phenomenology of chorea is unhelpful in guiding the work-up. Chorea is uncommon in hospital and is also infrequent in outpatient clinics except for Huntington’s disease referral centers. Elucidating the cause of chorea often requires broader laboratory investigations than any other hyperkinetic movement disorder.

Table 1.4

Differential diagnosis of chorea

The differential diagnosis of tremor appears in Table 1.5. Most consults for tremor in hospital turn out to be myoclonus. In the outpatient arena, tremor is the most common reason for referral to a movement disorder neurologist, usually due to Parkinson’s disease or essential tremor.

Table 1.5

Differential diagnosis of tremor

The differential diagnosis of dystonia appears in Table 1.6. Dystonia is nearly exclusively seen in the outpatient clinic. The classification scheme reflects the traditional rubric for evaluating dystonia diagnosis, rather than the revised modern criteria that are mainly used for research. Most patients seen in outpatient clinics have isolated focal dystonia.

Table 1.6

Differential diagnosis of dystonia

aIn the juvenile Westphal variant, patients present with parkinsonism and can have dystonia and seizures.

Ataxia is a frequent cause for referral to the movement disorder clinic. The phenomenology of ataxia is reviewed in Chap. 10, and the differential diagnosis appears in Table 1.7

Table 1.7

Differential diagnosis of ataxia (also see Tables 10.​5, 10.​6, and 10.​7)

Movement disorders also include a wide range of conditions that do not fit neatly into one category. A partial list of these disorders appears in Table 1.8

Table 1.8

Various unusual movement disorders

Notes

Notes

References

1.

Yahr MD, Duvoisin RC, Schear MJ, Barrett RE, Hoehn MM. Treatment of parkinsonism with levodopa. Arch Neurol. 1969;21(4):343–54. https://​doi.​org/​10.​1001/​archneur.​1969.​00480160015001.CrossrefPubMed

2.

Santos-Lobato BL, Tumas V. Harbinger of storm: influence of Oliver Sacks on levodopa therapy in early 1970s. Arq Neuropsiquiatr. 2016;74(8):687–9. https://​doi.​org/​10.​1590/​0004-282X20160095.CrossrefPubMed

3.

Calne DB, Stern GM, Laurence DR, Sharkey J, Armitage P. L-dopa in postencephalitic parkinsonism. Lancet. 1969;1(7598):744–6. https://​doi.​org/​10.​1016/​s0140-6736(69)91751-6.CrossrefPubMed

4.

Fahn S. Professor C. David Marsden. JAMA Neurol. 1999;56(1):119–20. https://​doi.​org/​10.​1001/​archneur.​56.​1.​119.Crossref

5.

Jankovic J, Bressman S, Dauer W, Kang UJ. Clinical and scientific perspectives on movement disorders: Stanley Fahn’s contributions. Mov Disord. 2015;30(14):1862–9. https://​doi.​org/​10.​1002/​mds.​26445.CrossrefPubMed

© Springer Nature Switzerland AG 2020

S. J. Frucht, P. TermsarasabMovement Disorders Phenomenologyhttps://doi.org/10.1007/978-3-030-36975-0_2

2. The Approach to the Movement Disorders Patient

Steven J. Frucht¹   and Pichet Termsarasab²

(1)

Division of Movement Disorders, New York University Grossman School of Medicine, The Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders, NYU Langone Health, New York, NY, USA

(2)

Division of Neurology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand

Steven J. Frucht (Corresponding author)

Email: [e-mail]

Keywords

Movement disorderPhenomenology

Several comments may help guide the clinician in evaluating patients in the outpatient arena.

In virtually all other subspecialty fields of neurology, the evaluation and management of patients hinges on the results of ancillary testing. For example, in stroke the Doppler and imaging studies determine the cause; in epilepsy, the EEG; in neuromuscular disease, the EMG and muscle biopsy; in peripheral neurology, the nerve conduction studies, serologies, and nerve biopsy; in sleep medicine, the sleep study; and in memory disorders, the neuropsychological evaluation and specialized imaging studies. Headache medicine depends critically on the history to define various headache syndromes, but the neurologic exam is almost always normal. In comparison, movement disorders are unique among neurology subspecialty fields. The history and examination are indispensable, and these two elements complement one another in the evaluation of the patient. Imaging and genetic testing may be needed to confirm the diagnosis, but the clinical evaluation still holds primary place. History and examination also allow rational decision-making when following patients long term to assess the results of treatment. Performed correctly, modern movement disorder neurology employs late nineteenth- and early twentieth-century clinical skills using twenty-first-century understanding of genetics and pathophysiology.

Most chapters of this book focus on three areas: the history of phenomenology; the phenomenology of the movement disorders history; and the phenomenology of the movement disorders examination. The movement disorders history and exam provide complimentary and independent clues to the diagnosis. As in general neurology, the movement disorders history possesses high sensitivity but only modest specificity. For example, a history of festination or imbalance with forward leaning posture is highly sensitive for parkinsonism but does not distinguish between Parkinson’s disease and other forms of parkinsonism. In contrast, the movement disorders examination is only modestly sensitive but is highly specific. For example, patients with very early Parkinson’s disease may display very subtle signs, trace bradykinesia, intermittent tremor, and slight decreased arm swing. However, when these signs coalesce in a single patient, they powerfully influence the ultimate diagnosis. Thus, the movement disorders history and examination complement one another, marrying strengths and weaknesses (high sensitivity and modest specificity for history; modest specificity and high sensitivity for exam).

Several general principles guide the neurologist in taking a detailed movement disorders history. We believe that the history should ideally be taken with pen and paper in hand, facing the patient and family, with the computer safely hidden in the corner of the room [1]. Patients should be asked to relay their story (why are you here?), and the experienced clinician learns not to interrupt for at least 45 seconds. Features of the history should be gleaned from the patient and their family (if present). Disparities between the patient’s experience of illness and the family’s perception may be profoundly important. Time is a critical element in the movement disorders history, influencing the differential diagnosis of parkinsonism and hyperkinetic movement disorders. Medication exposure and family history are also relevant. The experienced clinician distrusts the cavalier negative response to queries in these domains, digging deeply to uncover evidence that may be overlooked or even purposefully hidden.

The movement disorders examination should be tailored to the individual patient and likely diagnosis. However, a standard movement disorders exam is a good starting point for the evaluation of most patients in the office (Table 2.1). Communicating the results of the history and examination is the most important part of the office visit. Patients and families may be anxious and unable to fully process or remember the details of the office visit. A diagnosis of Parkinson’s disease, progressive supranuclear palsy, or Huntington’s disease has a profound impact on patients and their families. Allowing patients time to process the diagnosis and to ask questions in a supported manner helps guide them to a nuanced understanding of the complexity of illness and its implications for the patient, family, and caregiving network.

Table 2.1

Features of the standard movement disorders examination

Once the examiner arrives at a principal diagnosis, certain examination techniques can be employed to elaborate each diagnosis (Table 2.2).

Table 2.2

Specific features of the tailored movement disorders exam

Notes

Notes

Reference

1.

Toll E. A piece of my mind. The cost of technology. JAMA. 2012;307(23):2497–8. https://​doi.​org/​10.​1001/​jama.​2012.​4946.CrossrefPubMed

© Springer Nature Switzerland AG 2020

S. J. Frucht, P. TermsarasabMovement Disorders Phenomenologyhttps://doi.org/10.1007/978-3-030-36975-0_3

3. Typical Parkinson’s Disease Phenomenology

Steven J. Frucht¹   and Pichet Termsarasab²

(1)

Division of Movement Disorders, New York University Grossman School of Medicine, The Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders, NYU Langone Health, New York, NY, USA

(2)

Division of Neurology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand

Steven J. Frucht (Corresponding author)

Email: [e-mail]

Supplementary Information

The online version contains supplementary material available at https://​doi.​org/​10.​1007/​978-3-030-36975-0_​3. The videos can be accessed individually by clicking the DOI link in the accompanying figure caption or by scanning this link with the SN More Media App.

Keywords

Parkinson’s diseaseTremorRigidityBradykinesiaPostural impairment

Historical Review of Parkinson’s Disease Phenomenology

Parkinson’s Disease Phenomenology Prior to 1817

Parkinson’s disease (PD) was described in 5000 BC as kampavata in Ayurvedic medicine. In several Ayurvedic treatises, including Caraka Samhita and Madhava Nidana among others [1], the clinical features of PD included movement difficulty, sialorrhea, love of solitude (apathy or depression), somnolence, and eye staring. Treatment with the tropical legume Mucuna pruriens was used in Ayurvedic medicine (Fig. 3.1). Later, levodopa was found to be an active compound of this legume [2]. In Ancient Chinese medicine, symptoms suggestive of PD were described in the Huang di neijingsu wen (the Yellow Emperor’s Internal Classic; Huang di = the Yellow Emperor), the oldest Chinese medical text in 500 BC, including tremor, stiffness, limitation of movement, and postural disturbance [3].

../images/466194_1_En_3_Chapter/466194_1_En_3_Fig1_HTML.jpg

Fig. 3.1

Mucuna pruriens. (a)Mucuna pruriens inflorescence. (From Agong1. Wikimedia Creative Commons [Attribution-Share Alike 3.0 Unported license. https://​commons.​wikimedia.​org/​wiki/​File:​Mucuna_​pruriens_​flower.​jpg].) (b) Mucuna pruriens seeds. (From Tracey Slotta @ USDA-NRCS PLANTS Database [Public domain])

Between 169 and 180 AD, Galen (Aelius Galenus) described the difference between tremor and palpitation [4]. In tremor, the entire part of the body shook up and downward with intended movements due to weakness of the force that supports and moves the body. Tremor was provoked by lack of nourishment, stomach and cardiac diseases, decreased vital force, violent chills, or by carrying heavy objects. In contrast, palpitation referred to movements at rest involving a part of the body due to defective muscle and nerve, provoked by cold, winter, drunkenness, cold food, fear, aging, or sickness.

In his Essay on the Shaking Palsy, James Parkinson referenced Juncker and Sylvius de la Boë’s descriptions of tremor [5]. Juncker classified tremor into active and passive tremor, the former caused by sudden affections such as terror and anger, the latter advanced age and palsy. Sylvius de la Boë divided tremor into rest tremor (Tremor Coactus) and action tremor, as did the Frenchman Sauvages. James Parkinson referred to Tremor Coactus of Sauvages [in Tremor Coactus], the tremulous parts leap, and as it were vibrate, even when supported: whilst every other tremor, he observes, ceases when the voluntary extrusion for moving the limbs stops, or the part is supported, but returns when we will the limb to move; whence, he states, tremor is distinguished from every other kind of spasm.

The clinical features of festination described in An Essay on the Shaking Palsy referred to a previously described term, scelotyrbe festinans, by Sylvius de la Boë, a peculiar species of scelotyrbe, in which the patient’s, whilst wishing to walk in the ordinary mode, forced to run.

An early description by Leonardo da Vinci may also represent the phenomenology of PD [6, 7]:

This appears clearly in paralytics… who move that trembling limbs such as the head or the hands without permission of the soul; which soul with all its power cannot prevent these limbs from trembling.

James Parkinson’s Phenomenology of PD

James Parkinson (1755–1824) was a true man of science—a surgeon, geologist, paleontologist, apothecary, and politician [8]. His 1817 pamphlet, An Essay on the Shaking Palsy, defined the illness that was named for him by Charcot. Parkinson described six cases of shaking palsy or paralysis agitans: one (Case I) followed by himself throughout the course of the disease, two (Cases II and III) casually met in the street, one (Case IV) seen in the office for another reason (thoracic abscess), and two (Cases V and VI) from observation alone [5]. He may have been influenced by John Hunter’s lecture which he attended in 1785 describing one patient with clinical features similar to PD [9].

Of the four cardinal features of PD, Parkinson vividly described rest tremor and postural instability. Bradykinesia may be indirectly implied from his description; however he did not clearly distinguish bradykinesia from weakness, i.e., extrapyramidal from pyramidal symptoms. He also described several non-motor features including constipation, urinary dysfunction, sleep disturbance, and motor features such as festination, speech impairment, and drooling of saliva. Although he stated that the senses and intellects being uninjured, this likely reflects his limited exposure to milder patients earlier in the disease course.

True PD phenomenology begins with Parkinson’s original description [5]:

Rest Tremor

It is also necessary to bear in mind, that this affection [palpitation] is distinguishable from tremor, by the agitation, in the former [palpitation of the limbs; Palmos of Galen; Tremor Coactus of de la Boë], occurring whilst the affected part is supported and unemployed, and being even checked by the adoption of voluntary motion; whilst in the latter [tremor], the tremor is induced immediately on drinking the parts into action. Thus, an artist, afflicted with the malady here treated of, whilst his hand and arm is palpitating strongly, will seize his pencil, and the motions will be suspended, allowing him to use it for short periods; but in tremor, if the hand be quite free from the affection, should the pain of pencil be taken up, the trembling immediately commences. In contrast to PD, the artist with action tremor described above was likely afflicted with essential tremor.

Postural Instability

[Case III]: He was entirely unable to walk; the body being so bowed, and the head thrown so forward, as to up oblige him to go on a continued run, and to employ his stick every five or six steps to force him more into an upright posture, by projecting the point of it with great force against the pavement. This clearly describes the flexed or stooped posture of PD.

Festination

[Case V]… One of the characteristic symptoms of this malady, the inability for motion, except in a running pace, appeared to exist in an extraordinary degree. It seemed to be necessary that the gentleman should be supported by his attendant, standing before him with a hand placed on each shoulder, until by gently swaying backward and forward, he had placed himself in an equipoise; when, giving the word, he would start in a running pace, the attendance sliding from before him and running forward, being ready to receive him and prevent his falling, after his having run about twenty paces. Parkinson used the term scelotyrbe festinans, undoubtedly referring to festinating gait of progressive reduction of stride length, typically after starting walking for some distance, producing a picture of walking as if running.

Bradykinesia

Hitherto the patient will have experienced but little inconvenience; and befriended by the strong influence of habitual endurance, would perhaps seldom think of his being the subject of disease, except when reminded of it but the unsteadiness of his hand, whilst writing or employing himself in any nice or kind of manipulation. But as the disease proceeds, similar employment sign accomplished with considerable difficulty, the hand failing to answer with exactness to the dictates of the will...At this period, the patient experiences much inconvenience, which unhappily is found daily to increase. The submission of the limbs to the directions of the will and hardly ever be obtained in the performance of the most ordinary offices of life.

Parkinson elegantly described impairment of the limbs in performing tasks, using terms such as lessened muscular power or weakness, and he did not differentiate between pyramidal and extrapyramidal signs. Interestingly he described in Chap. 5 that …; since the disease depends not on general weakness, but merely on the interruption of the flow of the nerve influence to the affected parts.

In addition to describing the clinical features of PD, Parkinson also beautifully delineated the typical age at onset (50s to 70s years in his series) and the natural history of the disease: So slight and nearly imperceptible are the first inroads of this malady, and so extremely slow this is a progress, that it rarely happens, that the patient can form any recollection of the precise period of its commencement…These symptoms [weakness and trembling] gradually increase in the part first affected; and at a certain period, but seldom in less than twelve months or more, ….

Asymmetric involvement at onset and the pattern of progression of tremor from one limb to the other was also described: Thus assuming one of the hands and arms to be first attacked, the other, at this period becomes similarly affected. After a few more months the patient is found to be less strict than usual…Commencing, for instance in one arm, the wearisome agitation is bourne until beyond sufferance, when by suddenly changing the posture it is a time stopped in that limb, to commence, generally, in less than a minute in one of the legs, or in the arm of the other side.

[Case VI]… he first perceived weakness in the left hand and arm, and soon after found the trembling commence. In about three years afterwards the right arm became affected in a similar manner: And soon afterwards the convulsive motions affected her whole body… In about three years from that time the legs became affected. Although rest tremor typically spreads from one arm or hand to the contralateral side, rigidity and bradykinesia are typically already present in the ipsilateral leg at the onset, rather than the contralateral arm. In addition, he proposed to divide PD in two stages, and suggested to intervene in the earliest stage for successful treatment: ... It seldom happens that the agitation extends beyond the arms within the first two years; which period, therefore, if we will be disposed to define the disease into stages, might be said to comprise the first stage. In this period, it is very probable, that remedial means might be employed with success…

Other Features

The slops with which he is attempted to be fed, with the saliva, are continually trickling from the mouth. The power of articulation is lost. The urine and fæces are passed involuntarily; and at the last, constant sleepiness, with slight delirium, and other marks of extreme exhaustion, announce the wished-for-release. Parkinson recognized the importance of non-motor features, including sialorrhea, speech impairment, bowel and urinary incontinence, hypersomnolence, neuropsychiatric features, psychosis, and fatigue.

Parkinson’s Disease Phenomenology in the Last 200 Years

James Parkinson’s work was not well known during his lifetime. Sanders made a comment that succeeding authors have, in general, simply quoted it, or have… overlooked the disease altogether [10, 11]. The next major advance in PD phenomenology was made by Jean-Martin Charcot (1825–1893), the leading neurologist of his time at the Hôpital Universitaire Pitié-Salpêtrière (or the Salpêtrière Hospital). He admired James Parkinson’s work, encouraged his pupils to read it, and named the disease after him. Charcot added several crucial points to