History of Parkinson's disease

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First page of James Parkinson's classical Essay on the Shaking Palsy Parkinson, An Essay on the Shaking Palsy (edit).png
First page of James Parkinson's classical Essay on the Shaking Palsy

The history of Parkinson's disease expands from 1817, when British apothecary James Parkinson published An Essay on the Shaking Palsy, to modern times. Before Parkinson's descriptions, others had already described features of the disease that would bear his name, while the 20th century greatly improved knowledge of the disease and its treatments. [1] PD was then known as paralysis agitans (shaking palsy in English). The term "Parkinson's disease" was coined in 1865 by William Sanders and later popularized by French neurologist Jean-Martin Charcot. [2]

Contents

Early descriptions

Several early sources describe symptoms resembling those of PD. [3] An Egyptian papyrus from the 12th century B.C. mentions a king drooling with age and the Bible contains a number of references to tremor. [2] [3] An Ayurvedic medical treatise from the 10th century B.C. describes a disease that evolves with tremor, lack of movement, drooling and other symptoms of PD. Moreover, this disease was treated with remedies derived from the mucuna family, which is rich in L-DOPA. [3] Galen wrote about a disease that almost certainly was PD, describing tremors that occur only at rest, postural changes and paralysis. [3] [4]

After Galen there are no known references unambiguously related to PD until the 17th century. [3] In this and the following century several authors wrote about elements of the disease, preceding the description by Parkinson. Franciscus Sylvius, like Galen, distinguished tremor at rest from other tremors, while Johannes Baptiste Sagar and Hieronymus David Gaubius described festination, a term for the characteristic gait of PD. [3] [4] [5] John Hunter provided a thorough description of the disease, which may have given Parkinson the idea of collecting and describing patients with "paralysis agitans". [3] [6] Finally, Auguste François Chomel in his pathology treatise, which was contemporary to Parkinson's essay, included several descriptions of abnormal movements and rigidity matching those seen in PD. [3]

19th century

Charcot1893.jpg
A 1893 photograph of Jean-Martin Charcot made contributions to the understanding of PD and proposed its name honoring James Parkinson
Person with Parkinson disease BW.jpg
An individual with (advanced) Parkinson's disease, drawings by William Richard Gowers, published in 1886 [7] [8]

In 1817, James Parkinson published his essay reporting six cases of what he called paralysis agitans. [2] An Essay on the Shaking Palsy described the characteristic resting tremor, abnormal posture and gait, paralysis and diminished muscle strength, and the way that the disease progresses over time. [2] [9] He also acknowledged the contributions of many of the previously mentioned authors to the understanding of PD. [2] Although the article was later considered the seminal work on the disease, it received little attention over the forty years that followed. [9] Furthermore, the term paralysis agitans was at times applied to any condition with a loss of motor activity accompanied by seizures. Indeed, the term 'paralysis' alone included both motor and sensory deficits. [10] Noting this, William Sanders proposed in 1865 that the term Parkinsons Disease be used for the onset of symptoms in older people; it had been variously designated paralysis agitans festinia, - senilis or parkinsonii. [11]

Neurologists who made further additions to the knowledge of the disease include Trousseau, Gowers, Kinnier Wilson and Erb, and most notably Charcot, whose studies between 1868 and 1881 were a landmark in the understanding of the disease. [2] Among other advances he made the distinction between rigidity, weakness and bradykinesia. [2] He also championed the renaming of the disease in honor of Parkinson. [2]

20th century and beyond

The first speculations concerning the anatomical substrate of PD were made 80 years after Parkinson's essay, when Édouard Brissaud proposed that it had its origin in the subthalamus or cerebral peduncle and might be caused by an ischemic lesion. [2] In 1912 Frederic Lewy described a pathologic finding in affected brains, later named "Lewy bodies". [2] In 1919 Konstantin Tretiakoff reported that the substantia nigra was the main cerebral structure affected, but this finding was not widely accepted until it was confirmed by further studies published by Rolf Hassler in 1938. [2] The underlying biochemical changes in the brain were identified in the 1950s, due largely to the work of Arvid Carlsson on the neurotransmitter dopamine and Oleh Hornykiewicz on its role on PD. Carlsson was eventually awarded a Nobel Prize for this work. [12]

Alice Lazzarini et al pinpointed a genetic component to PD in 1994. [13] [14] Years earlier, the neurology clinic at Robert Wood Johnson Medical School (RWJMS) had located a family of Italian origin that encompassed at least five generations of more than 400 individuals and at least 60 members with PD, [15] and traced their ancestors to the small village of Contursi, Italy. [15] In 1995, the RWJMS team joined with the National Center for Human Genome Research at the National Institutes of Health to take advantage of the laboratory resources available from the NIH [16] in an effort to locate the gene causing PD in the Contursi family. [15] The team reported the first Parkinson disease-causing mutation (PARK1) in the brain protein, alpha-synuclein. [16] [17] [18] [19] [20] [21] Within days of the publication of the PARK1 findings, alpha-synuclein was discovered to be the major component of Lewy bodies within brain cells of PD patients; according to the UMDNJ magazine, "This discovery changed the direction of research into PD by providing scientists with an entirely new protein whose manufacture, function or breakdown could be the key to the disease." [16] [22] Synuclein proteins being the main component of Lewy bodies was discovered in 1997 by Spillantini, Trojanowski, Goedert and others. [23] Mutations in the parkin gene in autosomal recessive juvenile parkinsonism were discovered in 1998 and finally, between 2002 and 2005, DJ-1 gene mutations, PINK1 gene mutations and the most common mutations in the LRRK2 gene were identified in Japanese and European families. [24] [25] The pathological staging in Parkinson's disease was described by Heiko Braak in 2003. [26]

History of treatments

The positive albeit modest effects on tremor of anticholinergic alkaloids obtained from the plant of the belladonna were described during 19th century by Charcot, Erb and others. Modern surgery for tremor, consisting of the lesioning of some of the basal ganglia structures was first tried in 1939 and was improved over the following 20 years. [4] Before this date surgery consisted in lesioning the corticospinal pathway with paralysis instead of tremor as result. Anticholinergics and surgery were the only treatments until the arrival of levodopa, which reduced their use dramatically. [4] [27] Levodopa was first synthesized in 1911 by Casimir Funk, but it received little attention until the mid 20th century. [12] It entered clinical practice in 1967, and the first large study reporting improvements in people with Parkinson's disease resulting from treatment with levodopa was published in 1968. Levodopa brought about a revolution in the management of PD. [12] [28] By the late 1980s deep brain stimulation introduced by Alim-Louis Benabid and colleagues at Grenoble, France, emerged as a possible treatment and it was approved for clinical use by the FDA in 1997. [29]

Related Research Articles

<span class="mw-page-title-main">Parkinsonism</span> Medical condition

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. These are the four motor symptoms found in Parkinson's disease (PD) – after which it is named – dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD.

<span class="mw-page-title-main">Dementia with Lewy bodies</span> Type of progressive dementia

Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described by Kenji Kosaka in 1976.

<span class="mw-page-title-main">Lewy body</span> Spherical inclusion commonly found in damaged neurons

Lewy bodies are the inclusion bodies – abnormal aggregations of protein – that develop inside nerve cells affected by Parkinson's disease (PD), the Lewy body dementias, and some other disorders. They are also seen in cases of multiple system atrophy, particularly the parkinsonian variant (MSA-P).

<span class="mw-page-title-main">Multiple system atrophy</span> Neurodegenerative disorder

Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by autonomic dysfunction, tremors, slow movement, muscle rigidity, and postural instability and ataxia. This is caused by progressive degeneration of neurons in several parts of the brain including the basal ganglia, inferior olivary nucleus, and cerebellum.

Parkinson-plus syndromes (PPS) are a group of neurodegenerative diseases featuring the classical features of Parkinson's disease with additional features that distinguish them from simple idiopathic Parkinson's disease (PD). Parkinson-plus syndromes are either inherited genetically or occur sporadically.

In the management of Parkinson's disease, due to the chronic nature of Parkinson's disease (PD), a broad-based program is needed that includes patient and family education, support-group services, general wellness maintenance, exercise, and nutrition. At present, no cure for the disease is known, but medications or surgery can provide relief from the symptoms.

<span class="mw-page-title-main">Konstantin Tretiakoff</span> Russian neurologist

Konstantin Nikolaevitch Tretiakoff was a Russian neuropathologist. He was born in Fergana, Uzbekistan, as a son of military physician, who was member of Pierre Bonvalot's first Pamir expedition. He studied medicine in L'Assistance Publique des Hopitaux de Paris. He received his doctorate in 1919. In his thesis, he described degeneration of the substantia nigra associated with paralysis agitans. Tretiakof was first to link this anatomic structure with parkinsonism. Between 1922 and 1926 Tretiakoff worked at the Hospício de Juquery, near the city of São Paulo, Brazil. In 1931, he was appointed Chairman at the new Department of Neuropathology at the Medical Institute in Saratov, USSR, where he spent the rest of his life.

<span class="mw-page-title-main">Dopamine dysregulation syndrome</span> Medical condition

Dopamine dysregulation syndrome (DDS) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It typically occurs in people with Parkinson's disease (PD) who have taken dopamine agonist medications for an extended period of time. It is characterized by problems such as addiction to medication, gambling, or sexual behavior.

<span class="mw-page-title-main">Parkinson's disease</span> Long-term degenerative neurological disorder

Parkinson's disease (PD), or simply Parkinson's, is a chronic degenerative disorder of the central nervous system that affects both the motor system and non-motor systems. The symptoms usually emerge slowly, and as the disease progresses, non-motor symptoms become more common. Early symptoms are tremor, rigidity, slowness of movement, and difficulty with walking. Problems may also arise with cognition, behaviour, sleep, and sensory systems. Parkinson's disease dementia is common in advanced stages.

Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis.

<span class="mw-page-title-main">Kufor–Rakeb syndrome</span> Medical condition

Kufor–Rakeb syndrome (KRS) is an autosomal recessive disorder of juvenile onset also known as Parkinson disease-9 (PARK9). It is named after Kufr Rakeb in Irbid, Jordan. Kufor–Rakeb syndrome was first identified in this region in Jordan with a Jordanian couple's 5 children who had rigidity, mask-like face, and bradykinesia. The disease was first described in 1994 by Najim Al-Din et al. The OMIM number is 606693.

<span class="mw-page-title-main">Braak staging</span> Classification of disease severity

Braak staging refers to two methods used to classify the degree of pathology in Parkinson's disease and Alzheimer's disease. These methods are used both in research and for the clinical diagnosis of these diseases and are obtained by performing an autopsy of the brain.

Parkinson's disease (PD) is a degenerative disorder of the central nervous system. Most people with PD have idiopathic Parkinson's disease. A small proportion of cases, however, can be attributed to known genetic factors. Other factors such as environmental toxins, herbicides, pesticides, and fungicides, have been associated with the risk of developing PD, but no causal relationships have been proven.

Gene therapy in Parkinson's disease consists of the creation of new cells that produce a specific neurotransmitter (dopamine), protect the neural system, or the modification of genes that are related to the disease. Then these cells are transplanted to a patient with the disease. There are different kinds of treatments that focus on reducing the symptoms of the disease but currently there is no cure.

<span class="mw-page-title-main">Alice Lazzarini</span> Scientist, author and researcher

Alice M. Lazzarini is a scientist, author and researcher on neurogenetic disorders, including Huntington's disease and Parkinson's disease. She is an assistant professor of Neurology at Rutgers Robert Wood Johnson Medical School, where her work helped establish the genetic basis of Parkinson's. Later in life, she was diagnosed with Parkinson's—the very disease she had spent decades researching.

<span class="mw-page-title-main">Synucleinopathy</span> Medical condition

Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of aggregates of alpha-synuclein protein in neurons, nerve fibres or glial cells. There are three main types of synucleinopathy: Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Other rare disorders, such as various neuroaxonal dystrophies, also have α-synuclein pathologies. Additionally, autopsy studies have shown that around 6% of sporadic Alzheimer's Disease exhibit α-synuclein positive Lewy pathology, and are sub-classed as Alzheimer's Disease with Amygdalar Restricted Lewy Bodies (AD/ALB).

Parkinson's disease dementia (PDD) is dementia that is associated with Parkinson's disease (PD). Together with dementia with Lewy bodies (DLB), it is one of the Lewy body dementias characterized by abnormal deposits of Lewy bodies in the brain.

<span class="mw-page-title-main">Animal models of Parkinson's disease</span> Models used in Parkinsons disease research

Animal models of Parkinson's disease are essential in the research field and widely used to study Parkinson's disease. Parkinson's disease is a neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of the dopamine neurons in the brain, results in motor dysfunction, ultimately causing the four cardinal symptoms of PD: tremor, rigidity, postural instability, and bradykinesia. It is the second most prevalent neurodegenerative disease, following Alzheimer's disease. It is estimated that nearly one million people could be living with PD in the United States.

<span class="mw-page-title-main">Parkinson's disease in South Asians</span>

Epidemiological studies have shown lower age-related prevalence of Parkinson's disease in South Asians, with the rate of prevalence being around 52.7 per 100,000 as compared to a higher prevalence rate observed in populations with European origin, 108-257 per 100,000. Additionally, several studies have seen a higher prevalence of in women which contrasts with global data that observes a overall higher prevalence seen in men. Compared to most of the rest of the world, the South Asian countries seem to be on the lower end of PD prevalence. However, this is not to say that PD is not of concern in these countries. Over the past couple of years, the rate of Parkinson's has gone up in South Asia meaning that it is of high importance to study this pathological disease in these populations.

Parkinson's disease (PD), the second most common neurodegenerative disease after Alzheimer's disease, affects 1% of people over 60 years of age. In the past three decades, the number of PD cases has doubled globally from 2.5 million in 1990 to 6.1 million in 2016. As of 2022, there are ~10 million PD cases globally. In the United States, the estimated prevalence of PD by 2030 is estimated will be ~1.24 million. These numbers are expected to increase as life expectancy and the age of the general population increase. PD is considered to be a multisystem and multifactorial disease, where many factors, such as the environment, gut, lifestyle and genetics, play a significant role in the onset and progression of the disease.

References

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  29. ↑ Coffey RJ (March 2009). "Deep brain stimulation devices: a brief technical history and review". Artificial Organs. 33 (3): 208–20. doi:10.1111/j.1525-1594.2008.00620.x. PMID   18684199.
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