A History of Movement Disorders PDF
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This chapter provides a brief history of human movement disorders, tracing the evolution of understanding and treatment from ancient times to the present. It highlights the contributions of different cultures and medical traditions, including Ayurvedic medicine and ancient Greek thought.
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**Chapter 2** **A Very Brief History of Human Movement Disorders** **Learning Objectives for Chapter 2** 1. 2. 3. 4. 5. Across history, the descriptions, understanding and treatment of neurological disorders have slowly evolved. This slow progress was influenced by trial and error, oral tr...
**Chapter 2** **A Very Brief History of Human Movement Disorders** **Learning Objectives for Chapter 2** 1. 2. 3. 4. 5. Across history, the descriptions, understanding and treatment of neurological disorders have slowly evolved. This slow progress was influenced by trial and error, oral tradition, religion, region, culture, and science. Of course, early descriptions were also influenced by superstition and mythology. One wonders, however, that when societies flourished and then crumbled did, they just leave behind the mere vestiges of their art, science, and philosophy? Perhaps these "remnants" were based on historically sound practices. Practices and treatments that were simply scrambled over time by being orally handed down generation after generation. As they say, history becomes legend and legend becomes mythology. From this perspective, new civilizations like Sisyphus, repeatedly rebuild the same wheel, and repeatedly push the same rock up the same hill and suffer the same consequences. Varied diagnostic interpretations and perspectives each time evolve into similar early clinical practice. Despite uncertainty in interpreting antiquity, early observations around diagnosis, prognosis and ensuing medicinal treatments were found to be on target (Stern 2013). As there are hundreds of neurologically based movement disorders that humans suffer from after a brief tour of ancient history we will focus on the histories of essential tremor, Parkinson's disease, Huntington's disease, and epilepsy. **Ancient Thoughts Concerning Behaviour, the Brain, and Medicine** From an historical perspective only recently have people recognized the role of the brain in controlling behaviour. When Pharaoh's were mummified 2000 - 3000 years B.C. five important organs were preserved. Those organs were the liver, lungs, stomach, intestines and heart. All these organs were considered necessary to ensure the Pharaoh's continued existence in the afterlife. The brain however was sucked out through the nostrils and thrown away. Many ancient Greeks like Aristotle believed that the brain was an organ simply meant to cool the blood. As with the Egyptians the brain was not considered much of an asset. In the Bible neither the Old Testament nor New Testament mentions the brain. However, the Bible mentions the heart, liver, stomach, and bowels as the seat of passion, courage, and pity. The heart is also where Aristotle about 400 BC located mental capacities as in kind-hearted, openhearted, or fainthearted. Herophilus advanced knowledge as a Greek physician by dissecting bodies of both people and animals. He traced nerves from muscles and skin into the spinal cord and noted that each region of the body is connected to separate nerves about 400 BC. (Breedlove and Watson 2017; Stern 2013). Obvious disorders of movement, no matter which organ caused them, in ancient times did attract 'clinical' attention. However, the interpretation of ancient texts, continued to remain obscure in many ways. Original Sanskrit texts and some early printed books especially ones printed before the 1500s reveal the contributions of Ayurvedic medicine (5000--3000 BC). History Diseases were categorized into three living things: **vata** (psychomotor or life force), pitta (metabolic), and kapha (growth). Imbalance of vata gave rise to neurological disorders, which were further divided into **kampa** (motor tremor), stambha (motor stiffness), and **vishada** (emotional depression correlated with slowness of movement). These three living things could be mixed and compounded. Thus, **kampavata** indicated shaking palsy. An imbalance of vata was believed to cause neurological disorders such as tremor, stiffness, and depression. Among the prescribed traditional medications were atmaghupta seed (Mucuna pruriens), containing levodopa, from plants like Aswagandha Root. All were solanaceous alkaloids like **Atropa belladonna** (Kumar & Clark, 2009). Some well-known solanaceous alkaloids included: **Nicotine**, Solanine, Capsaicin, **Atropine**, and **Scopolamine**). These were not introduced into European medicine until the nineteenth century, when they were used by a pupil of **Charcot** for the symptomatic treatment of Parkinson's disease. The **Moon Plant** was used as a sedative for recurring mania and attributed incorrectly to lunar movements. Interestingly in modern times many still believe that there are more hospitalizations and crimes committed during full moons. This drug was rediscovered during World War II by Nathaniel Kline, who introduced it to America as the first effective medication for chronic schizophrenia (Banerjee, 2002). Sustained use of this plant caused **drug-induced parkinsonism**, providing evidence that dopamine was a brain-based neurotransmitter (Hornykiewicz, 2006). **Early Mesopotamian and Chinese Medicine and Others** (From Stern 2013) Early Mesopotamian literature from the first half of the second millennium includes precise descriptions, such as an early diagnosis and prognosis of Parkinson's disease (Nemet-Nejat, 1998). Evidence from the second millennium BC indicates that early Chinese society had medicine men comparable to North Asian shamans. Extensive disease catalogues, like the Imperial Grace Formulary (992 AD), provided prescriptions for roughly a thousand disorders (Unschuld, 1985). Chinese medicine viewed health (ch'i) as a balance between [yin and yang] and hypothesized the cause disease as unbalance such as undisciplined emotions and uncontrolled dietary factors (Bowers, 2006). Around 500 BC, excessive undisciplined emotions were recognized causes of disease (psychosomatic?). The conditions of health were partly inborn (genomic?), and partly due to food and drink (nutrigenic and across generations epigenetic?) The clinical features and prognosis of rabies were also set out in 556 BC "... when a mad dog bites someone, the patient becomes manic... but if he remains well for 100 days he will remain safe... (5)." The 2000-year-old ceramic sculptures of the Moche civilization of Peru picture many diseases and deformities. Martinez-Castrillo et al. have argued that the horizontally tensed lips and pronounced nasolabial folds of one such sculpture represents the first depiction of Meige syndrome.[(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0012) (Newby et al. 2017)] This speculation is given some support from the attention of the Moche to individual differences in their sculpture, with various facial disfigurements that appear to portray cutaneous leishmaniasis, ritual mutilation, and cleft lip.[(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0013) (Newby et al. 2017)] **Sources from the Ancient Greek World and Beyond** From (Newby et al. 2017) References to spasmodic cervical conditions in the writings of ancient world physicians are obscure. Hippocrates' (430 BC) "*traxhlos sklhros"* means "a stiff and painful neck," a fatal sign when accompanied by "contraction of the jaws, a powerful throbbing of the jugular vessels, and contraction of the tendons."[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0003), [](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0004) Hippocrates may have been referring to tetanus or meningitis caused neck stiffness rather than torticollis. Celsus later used the term "*rigor cervicis"* in a similar context.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0005) Celsus also described a rigor of the sinews, *rigore nervorum*, that "draws down the head to the shoulder-blades, now the chin to the chest, now stretches out the neck straight and immobile."[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0006) Pliny the Elder, who was not a physician, made mention of *rigor cervicis*, along with a number of suggested remedies for softening (*mollitur*) the neck.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0007) The abnormal neck posture seen in some statues of Alexander the Great has prompted the suggestion that he had ocular torticollis.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0008) This is probably an over-interpretation, since not all statues depict this posture, and texts describing his appearance are ambiguous in their original languages.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0009) Plutarch claimed that the sculptor Lysippus had "accurately observed" Alexander\'s neck, which "was bent slightly to the left."[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0010) Plutarch wrote this centuries after Alexander\'s death, and it is not clear on what source he based his assertion.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0011) Centuries later medical records of cervical dystonia, by Swiss physician Felix Platerus (1536--1614), described "a kind of spasm in which the head was turned to the left side."[(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0026)] Samuel Kinnier Wilson (1878--1937) used this verse by the poet and dramatist Paul Scarron (1610--1660) as an epigraph to his textbook chapter on torticollis: - *Mon pauvre corps est raccourci* (My poor body is shortened) - *Et j\'ai la tête sur l\'oreille (*And I have my head on my ear) - *Mais cela me sied à merveille* (But it suits me marvelously) - *Et parmi les torticollis* (And among the stiff-necked) - *Je passe pour des plus jolis* (I pass for one of the prettiest)[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0027), [](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0028) Scarron\'s postures resemble dystonic torticollis. While some paintings and engravings show the poet with his head inclined forward and to the right, there are portraits with a leftward tilt, suggesting variable muscle overactivity. (From Newby et al. 2017) A medieval set of painted figures from El Burgo de Osma cathedral in Spain look as if they had cervical dystonic postures, with heads tilted to the left and pained facial expressions [1(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0009)] .Usually there is difficulty in differentiating damage leading to dystonic muscular torticollis (muscular contraction without voluntary control) from congenital muscular torticollis. Indeed, the muscular form might have been because of poor obstetric care. Certain medieval texts record postures that are consistent with muscular torticollis. Vesalius and Piccolomini distinguished subcortical nuclei from cortex and white matter in the 16th century. In the mid-19th-century the localization of function concerning movement disorders was focused on the striatum. Thomas Willis, in his *Cerebri Anatome* (1664), introduced much of the present nomenclature of the basal ganglia, while advances in anatomy and microscopy continued to reveal clinical and pathological links (Finger, 2001). In 1911 when Hermann Oppenheim introduced the term **dystonia** (abnormal tone in any tissue), the movement disorder lacked a unifying descriptor. Words like **epilepsy**, **apoplexy**, and **palsy** were present from ancient times, however, references to dystonia were much harder to locate historically. Torticollis was the exception. There were difficulties distinguishing different types of dystonia i.e. dystonic torticollis from congenital muscular torticollis. It was only after Charcot\'s contributions to clinical neuroscience that various forms of generalized and focal dystonia were delineated. However, dystonia were categorized as *neuroses*: Neurosis is a term for a psychological condition i.e. without an identifiable neuroanatomical cause. Psychoanalytic models of dystonia were based on Freud\'s unconscious mind. An unconscious mind that caused physical symptoms and this view prevailed for a time. During the 1970s, theories went back toward organic causation. Of course, when asked the question Nature or Nurture the answer is always both. It was only in the late-20th century that an organic framework was firmly established with the identification of genetic mutations in some families with dystonia and with the demonstration that the basal ganglia were often damaged contralateral to acquired hemidystonia. There is still much to be understood and theorized concerning organic and functional dystonia. More flexible biopsychosocial frameworks are needed to address diagnostic and therapeutic procedures. Focal and segmental forms of dystonia, including writer\'s cramp, other occupational dystonias, and torticollis, were also recognized in the 19th century. See below: 1\. Writer\'s Cramp (Focal Upper Limb Dystonia): the earliest medical report of occupational disturbance of writing was from Italian physician Beradino Ramazzini (1633--1714) in 1713. Beradino was more focused on muscular fatigue than spasm.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0039) The disorder as we now recognize it was originally described by Charles Bell (1774--1842), who encountered an epidemic of writer\'s cramp in clerks of the British Civil Service in 1830 (scriviner's palsy).[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0040) Guillaume-Benjamin Duchenne (1806--1875) was the first to distinguish occupational spasm (*spasme fonctionnel*) from occupational muscle paralysis (*paralysie musculaire fonctionnelle*).[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0041) Both Later outbreaks in telegraphists and typists were regarded as hysterical manifestations in emotionally vulnerable individuals. In the latter half of the 19th century, these types of disorders were referred to as "craft palsies," "occupational neuroses," or "professional impotence." (See below) 1\. The first descriptions of **musician\'s dystonia**, from Romberg in 1853 and Bianchi in 1878, were of task-specific flexion of the digits in a pianist and a flautist.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0044), [](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0045) 2\. **Myoclonus**: In 1903, Lundborg proposed a classification of myoclonus that remains in use, with primary (essential), **epileptic**, and secondary or symptomatic categories. 3\. **Startle syndromes**: Early descriptions of pathologic startle syndromes included Beard\'s description of the jumping Frenchmen of Maine (1878) and Hammond\'s description of miryachit (1884), both of which may have had psychological origins. In contrast, the \"**startle disease**\" was described in the late 1950s and early 1960s. The genetic forms were later found to result from various mutations affecting **glycine synapses**. 4\. **Tics**: Tic disorders were described by Itard (1825) and Trousseau (1873), and gained recognition in the late 19th century after Charcot presented cases before his classroom audiences. Although Gilles de la Tourette\'s and Charcot initially considered tic disorders and startle syndromes to be similar these disorders were later recognized as distinct. **Galen and Medieval Medicine and Beyond** (From Newby 2017) In the Western world, Claudius Galen (129--216 AD), a Greek polymath, dominated medical science for over a thousand years until refuted by figures like Maimonides, Vesalius, and William Harvey. Galen\'s dissections and extensive writings, later translated into Arabic, documented his clinical experience and rational approach to medicine (Nutton, 2004). The early scientific enlightenment in Europe saw medieval physicians rediscover Greek heritage through Syriac manuscripts, leading to the integration of Greek, Roman, Arabic, and medieval concepts. Many of his thoughts about trauma were no doubt influenced by his experience as a physician to the Roman school of gladiators. From these sources, classical notions of movement disorders are clearly documented. Galen recognized involuntary tremor, tremor associated with stiffness, and the influence of temperature. Amongst several listed causes, he distinguished those related to poor nutrition, those occurring in the mentally retarded, ocular tremor, and those related to psychiatric states including depression, and clearly separated the shaking of epilepsy (Stren 2012). **Choreoathetosis**, a combination of involuntary twisting and writhing movements was historically described in the Middle Ages, as possibly both an organic and a psychological disorder of motor control. Paracelcus introduced the concept of chorea as an organic medical condition in the 16th century. Sydenham\'s description of childhood chorea (1686) was followed by recognition in the 19th and 20th centuries of Alexa what is a sequel of group A streptococcal fare reveling giant exists a type of chorea that followed rheumatic fever. By the 1930s, rheumatic fever was categorized as a sequel of group A streptococcal pharyngitis, which could be effectively prevented with sulfonamides. **Athetosis**, the slow involuntary movement of hands and feet normally seen in children was described by Hammond (1871). Hammond later linked these movements to a malignant growth in the corpus striatum. Athetosis has been described as part of a continuum between chorea and dystonia. (From Lanska, 2010) Descriptions of a variety of tremors were delineated from Galen\'s definition in the 2nd century; to Galileo\'s physiologic tremor in 1610. Huntington\'s classic description of adult-onset hereditary chorea (1872) was followed a full century later by demonstration that Huntington\'s disease is caused by an unstable CAG trinucleotide repeat expansion in the Huntington disease gene on chromosome 4; this triggered a surge in research, development of various animal models, and numerous important discoveries of cell function and disease pathogenesis. More on this history in the Huntington's Chapter. The general population read about various forms of movement disorders from great literary works like Charles Dickens' *David Copperfield* (1850). Dickens had inserted several possible examples of dystonia---the repeated use of the epithet "writhing" for the malevolent Uriah Heep; and the vain Mr. Sharp, who is described as "carrying his head on one side, as if it were a little too heavy for him." Mr. Creakle, young David\'s harsh and dictatorial headmaster, "had no voice, but spoke in a whisper," suggesting spasmodic dysphonia.[](https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0061) In line with Victorian views these grotesque physical attributes were used to call attention to unattractive features of their inner selves. Something Sigmund Freud may have used in his psychoanalytic theory. **Moving Toward the 20^th^ Century Beyond** The separation of involuntary movements during action and at rest in the 17th and 18^th^ centuries came next. The description of **Parkinson\'s disease** by James Parkinson, stated that the rest tremor of Parkinson\'s disease was different than the intention tremor seen in **multiple sclerosis** as described by Charcot. Some familial tremors reported by Dana and others in the late 19th century; were demonstrated to be an **autosomal dominant essential tremor** in the mid-20th century. Pathologic changes in Parkinson\'s disease were recognized as damage to in substantia nigra by Blocq and Marinescu in the late 19th century, and around 1920 Trértiakoff established that **Lewy bodies** in the substantia nigra were a pathologic hallmark while the Vogts emphasized additional pathologic changes in the striatum. (From Lanska 2010) It was only in the mid-1960s that a **nigrostriatal dopaminergic pathway** was demonstrated and found to be critical to movement pathogenesis. Early treatment approaches with **anticholinergic** medications or crude neurosurgical ablation procedures were eclipsed in the 1960s by the advent of **L-DOPA** therapy due to the work of Carlsson and colleagues. Progress in understanding and treating Parkinson\'s disease included recognition of **neuroleptic-induced parkinsonism** beginning in the 1950s, development of **dopamine agonists** and elaboration of **different dopamine receptors that began in the 1960s**. Of interest in the 1980's electrographic experiments at the University of Calgary reported two types of sinusoidal electrographic activities in the hippocampi of rodents. The two types were movement related and non-movement related. Type I theta rhythm recorded from the dentate gyrus of the hippocampus involved conscious purposeful voluntary ongoing movement that was not affected by anticholinergic drugs. Type II theta rhythm recorded from the dentate gyrus of the hippocampus was generated during the planning, selection, and deselection of purposeful movements and this wave form was eliminated by IP injections of anticholinergic drugs. It was noted at the time that anticholinergic drugs like atropine sulfide interfered with memory and slowed down motor reaction speeds. A third hippocampal waveform termed large amplitude irregular activity (LIA) was also produced in the hippocampus, during when the animal grooms or performs other automatic behaviours. (Sainsbury and Montoya, 1984; Montoya and Sainsbury, 1985; Sainsbury et al., 1987; Montoya at al., 1989). (From Lanska 2010) The discovery of **MPTP-induced parkinsonism occurred in 1982** and subsequent development of **experimental models of MPTP-induced parkinsonism were subsequently developed**. Since the 1980s, stereotactic neurosurgical ablation procedures such as stereotactic pallidotomy (in humans) for the control of tremor were attempted. Substantia nigra electrolytic or neurotoxic ablations (in the animal model of Parkinson's disease) were revisited and augmented by the implanting of stem cells to regrow areas of damaged brain sites. Stem cell implantation did restore lost function in the animal model (Montoya et al. 1990; Montoya et al. 1991). Since 1990, rare genetic forms of Parkinson\'s disease were discovered, which accelerated progress in understanding pathogenesis, and established roles for **alpha synuclein** and the **ubiquitin-proteasome proteolytic system**. Separation of atypical forms of parkinsonism (e.g. **Wilson\'s disease, multisystem atrophy, progressive supranuclear palsy, and corticobasal degeneration**) from Parkinson\'s disease in the 20th century also led to important discoveries of basal ganglia function, and in the case of Wilson\'s disease to recognition of **genetic mutations** and effective treatments. The relationship between a lesion of the subthalamic nucleus and contralateral hemiballismus was first convincingly demonstrated by Martin in 1927. This led 20 years later to development of an animal model by Whittier and Mettler, who produced experimental hemichorea-hemiballismus in monkeys by lesioning the contralateral subthalamic nucleus. Since the late 1980s, the neurochemistry and neurophysiology of the subthalamic nucleus have been substantially revisited and revised with the demonstration that the subthalamic nucleus is not fundamentally inhibitory but instead provides excitatory glutaminergic inputs to the globus pallidus, and with this the idea that the subthalamic nucleus serves a role in both hyperkinetic (Huntington like) and hypokinetic (Parkinson like) movement disorders. In the last two centuries, neuroscientists and clinicians have contributed greatly to our understanding of basal ganglia anatomy and physiology, as well as to movement disorder semiology, pathophysiology, treatment, and prevention. The development of animal models, and the increasing use of genetic and molecular biological techniques will lead to further advances in the coming years. To sum up, even with a basic understanding of the nomenclature, it can be hard for the modern reader to catch sight of the historical traces of any disease. Even movement disorders that had a visible presence in past societies lack clarity in written accounts until a framework of knowledge is created around a diagnostic label. For instance, the shaking palsy was common and easily observable but was poorly recognized before James Parkinson (1755--1824) made sense of the fragmentary classifications of tremor in 1817. The term dystonia was not introduced until 1911, when Hermann Oppenheim (1858--1919) described the sustained spasm of dystonia deformans.(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0001) Athetosis (without fixed posture) was first used just 40 years earlier for more dynamic movements that would satisfy a modern definition of hemidystonia.(https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mdc3.12493#mdc312493-bib-0002) Enlightened approaches to the natural sciences relied on observation and classification as keys to new knowledge. Illnesses could be separated into "types" according to their symptoms, visible manifestations, and chronology. During the late 19th and early 20th century, a body of knowledge about dystonia was being assembled, two intellectual undercurrents shaped the development of modern neurology. With his *Clinical Anatomical Method* Jean-Martin Charcot (1825--1893) created a separation of "organic" disorders, which could be matched to structural changes in the nervous system, to "functional" disorders (Psychgenic), which could not. His career hastened the dichotomy of neurology and psychiatry. The second influence was Sigmund Freud\'s (1856--1939) theories about early life experiences and resultant psychic distresses that could be transformed into physical sensory-motor symptoms. These two perspectives were applied to dystonia, which for many years occupied a shared space between neurology and psychiatry a space which remains even today. With the creation of new diagnostic classifications, nomenclature, and taxonomies the rise of sub-specializations in movement disorders during the 1970s blossomed and brought new approaches to the study of dystonia. However, the stereotypic presentations of the anxiously ruminating woman with spasmodic torticollis; or the fastidious clerical worker, worn down by years of occupational penmanship, who develops writer\'s cramp---suggested a blurring in these disorders along the physical and psychological demarcations. **Conclusion** The evolution of understanding and treating neurological disorders is a testament to humanity\'s journey from ancient and often mystical interpretations to the inductive scientific method. This journey helped develop modern neurology and neurosurgery, highlighting the intricate interplay between ancient wisdom and contemporary scientific methodology. It has been demonstrated that the initiation, selection, inhibition, and the execution of movements depends on a fine-tuned feedback circuit and that there must be a balance between excitatory and inhibitory actions in the CNS. This is as evident in the spinal cord, where specific neuronal networks called **central pattern generators** (CPGs) determine their execution, as it is in the motor cortex, basal ganglia, and cerebellum, where movements are **initiated**, but more importantly many other movements are **deselected and inhibited**. Overall performance is continually **monitored and optimized** via 1000's of neural feedback loops that transect and connect with dozens of related brain nuclei. At all levels many different neural chemicals are involved, however, GABA's role as an **inhibitor** is crucial. It is not surprising that movement disorders can be caused by GABAergic dysfunction or that GABA receptors are strategic targets for drugs used to treat various pathological conditions. **Critical Thinking Box 1 Chapter 2** (See Appendix I for other critical thinking strategies) From an indigenous critical thinking perspective, the history of the categorization of neurological disorders is a slow process that begins with **examining the evidence** (see below from appendix I). **Examine the evidence:** A First Nation story tells of a wise elder who was always examining the evidence and looking for clues to make the best decisions. He believed in relying on facts and evidence, rather than simply trusting what people said. **Bridge**: In a similar fashion evidence-based science is empirical that is... measuring things you can touch, see, and measure. Another First Nation story that examines the evidence is the Haida story of Raven and the Box of Daylight. In this story, Raven, a trickster god, was sent to retrieve the box of daylight from its hiding place. Upon arriving, Raven found a large house with many doors, each one guarded by a creature that could only be convinced to help by evidence and logical reasoning. After providing evidence to each creature, Raven was eventually able to convince them to move and retrieve the box of daylight. This story is a reminder to examine the evidence and use logic before deciding. **Bridge**: Psychology is the marriage of Philosophy (logical reasoning) and Physiology (evidence based) biology. This pattern holds true across cultures and time. **Post Formal Thought Box 1 Chapter 2** (See Appendix II for Other Post Formal Thoughts) Hence the term **sophistry:** [subtle](http://click.reference.com/click/nn1ov4?clksite=dict&clkpage=dic&clkld=0&clkorgn=0&clkord=0&clkmod=1clk&clkitem=subtle&clkdest=http%3A%2F%2Fdictionary.reference.com%2Fbrowse%2Fsubtle), tricky (if you will), a superficially plausible, but generally fallacious method of reasoning or simply... a false argument. Sophistry had its pretentious origins in Middle English and French circa the 1300's. /In social terms, sophistication is or can be "intellectual snobbery.\" Early on Philosophers in England correctly regarded sophistication as decadent, prideful, and deceptive. It remained as such until the aristocrats beat it out of the then free thinkers in the 1800's. Why is this rather picayune point so important to science? It is because obtaining a PhD in Science means having a Doctor of Philosophy in your chosen scientific discipline. I feel that scientists overly pride themselves in their sophistication, and in getting their "materialistic snob on." I feel they do this rather than admitting what they don't know why something happened or indeed how it happened. Indeed, they fail to appreciate the limitations of their compartmentalized and limited inductive science. Not to put too fine a point on it, but as we shall see, science would not know the truth if truth ran it over in a Mac truck. It is obvious that in an infinite universe there will always be much more that we do not know compared to what we suppose we do know. Further the things that we think we know in this space-time within our own small **Goldilocks Zone**, may not be accurate outside our current gravitational field. In addition, even within our Goldilocks Zone as time passes as it does, even what we think we know theoretically is subject to being proven wrong or subject at least to major modifications. The final point is that people tend to be persuaded by the eloquence of the argument and not by the complexities of the universe or the evidence thereof. In the end look at the evidence you have, and then consider the fact that you will never completely understand the complexities of our infinite, fractal, and **Created** **Multiverse**. Then make your best guess. Major References Used 1. Lanska, D. J. (2009). The history of movement disorders. In *Handbook of Clinical Neurology* (Vol. 95, pp. 501--546). [[https://doi.org/10.1016/S0072-9752(08)02133-7]](https://doi.org/10.1016/S0072-9752(08)02133-7) 2. Munts, A. G., & Koehler, P. J. (2010). How psychogenic is dystonia? Views from past to present. *Brain, 133*(Pt 5), 1552--1564. 3. Newby, R. E., Thorpe, D. E., Kempster, P. A., & Alty, J. E. (2017). A history of dystonia: Ancient to modern. *Movement Disorders Clinical Practice, 4*(3), 1--6. [[https://doi.org/10.1002/mdc3.12493]](https://doi.org/10.1002/mdc3.12493)