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Signs and symptoms of Parkinson's disease are varied. Parkinson's disease affects movement, producing motor symptoms. [1] Non-motor symptoms, which include dysautonomia, cognitive and neurobehavioral problems, and sensory and sleep difficulties, are also common. [1] When other diseases mimic Parkinson's disease, they are categorized as parkinsonism.
Four motor symptoms are considered cardinal signs in PD: slowness of movement (bradykinesia), tremor, rigidity, and postural instability. [1] Typical for PD is an initial asymmetric distribution of these symptoms, where in the course of the disease, a gradual progression to bilateral symptoms develops, although some asymmetry usually persists. Other motor symptoms include gait and posture disturbances such as decreased arm swing, a forward-flexed posture, and the use of small steps when walking; speech and swallowing disturbances; and other symptoms such as a mask-like facial expression or small handwriting are examples of the range of common motor problems that can appear. [1]
Four motor signs are considered cardinal in PD: tremor, rigidity, bradykinesia, and postural instability (also referred to as parkinsonism). [1]
... immobile patients who become excited may be able to make quick movements such as catching a ball (or may be able to suddenly run if someone screams "fire"). This phenomenon (kinesia paradoxica) suggests that patients with PD have intact motor programmes, but have difficulties accessing them without an external trigger, such as a loud noise, marching music, or a visual cue requiring them to step over an obstacle. [1]
Other motor symptoms include:
Mood problem | Prevalence |
---|---|
Depression | 58% |
Apathy | 54% |
Anxiety | 49% |
Parkinson's disease causes neuropsychiatric disturbances, which mainly include cognitive disorders, mood disorders, and behavior problems, and can be as disabling as motor symptoms. [1]
Since L-Dopa, the widely used drug in Parkinson's disease treatment, is decarboxylated by aromatic L-amino acid decarboxylase (AADC), which is found in both dopaminergic and serotonergic neurons, it is possible for serotonergic neurons to convert L-Dopa into dopamine and generate excessive neuronal death by creating reactive oxygen species and quinoproteins. The association of serotonin with mood and cognition may explain some of the side-effects observed in patients treated with L-Dopa due to serotonin deficit. [9] [10]
In most cases, motor symptoms predominate at early PD stages, while cognitive disturbances (such as mild cognitive impairment or dementia) emerge later. [11] The onset of parkinsonism in PD relative to dementia is used as an arbitrary criterion to clinically distinguish Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) using a 'one-year rule'. [11] Dementia onset within 12-months of or at the same time as motor dysfunctions qualified as DLB, whereas in PDD, parkinsonism had to precede dementia by at least one year. [11]
Cognitive disturbances occur even in the initial stages of the disease in some cases. [12] A very high proportion of patients have mild cognitive impairment as the disease advances. [1] Most common deficits in nondemented patients are:
Deficits tend to aggravate with time, developing in many cases into dementia. A person with PD has a six-fold increased risk of developing it, [1] and the overall rate in people with the disease is around 30%. [12] Moreover, prevalence of dementia increases in relation to disease duration, going up to 80%. [12] Dementia has been associated with a reduced quality of life in patients and caregivers, increased mortality, and a higher probability of moving to a nursing home. [12]
Cognitive problems and dementia are usually accompanied by behavior and mood alterations, although these kinds of changes are also more common in those patients without cognitive impairment than in the general population. Most frequent mood difficulties include: [1]
Obsessive–compulsive behaviors (also known as impulse-control disorders) such as craving, binge eating, hypersexuality, pathological gambling, punding, or others, can also appear in PD, and have been related to a dopamine dysregulation syndrome associated with the medications for the disease. [1]
Psychotic symptoms are common in PD, generally associated with dopamine therapy. Symptoms of psychosis, or impaired reality testing, are either hallucinations, typically visual, less commonly auditory, and rarely in other domains including tactile, gustatory, or olfactory, or delusions, that is, irrational beliefs. Hallucinations are generally stereotyped and without emotional content. Initially, patients usually have insight so that the hallucinations are benign in terms of their immediate impact, but have poor prognostic implications, with increased risk of dementia, worsened psychotic symptoms, and mortality. Delusions occur in about 5-10% of treated patients, and are considerably more disruptive, being paranoid in nature, of spousal infidelity or family abandonment. Psychosis is an independent risk factor for nursing-home placement. [23]
Hallucinations can occur in parkinsonian syndromes for a variety of reasons. An overlap exists between PD and dementia with Lewy bodies, so that where Lewy bodies are present in the visual cortex, hallucinations may result. Hallucinations can also be brought about by excessive dopaminergic stimulation. Most hallucinations are visual in nature, often formed as familiar people or animals, and are generally not threatening in nature. Some patients find them comforting; however, their caregivers often find this part of the disease most disturbing, and the occurrence of hallucinations is a major risk factor for hospitalisation. Treatment options consist of modifying the dosage of dopaminergic drugs taken each day, adding an antipsychotic drug such as quetiapine, or offering caregivers a psychosocial intervention to help them cope with the hallucinations.
Sleep problems can be worsened by medications for PD, but they are a core feature of the disease. [1] Sleep dysfunction in PD has significant negative impacts on both patient and carer quality of life. [24] Some common symptoms are:
Parkinson's Disease causes constipation and gastric dysmotility that is severe enough to endanger comfort and even health. [26] A factor in this is the appearance of Lewy bodies and Lewy neurites even before these affect the functioning of the substantia nigra in the neurons in the enteric nervous system that control gut functions. [27]
PD is related to different ophthalmological abnormalities produced by the neurological changes. [1] [28] Among them are:
Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. Both hypokinetic as well as hyperkinetic features are displayed by Parkinsonism. 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.
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 on autopsy by Kenji Kosaka in 1976, and he named the condition several years later.
Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by tremors, slow movement, muscle rigidity, and postural instability, autonomic dysfunction 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.
Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. The condition leads to symptoms including loss of balance, slowing of movement, difficulty moving the eyes, and cognitive impairment. PSP may be mistaken for other types of neurodegeneration such as Parkinson's disease, frontotemporal dementia and Alzheimer's disease. The cause of the condition is uncertain, but involves the accumulation of tau protein within the brain. Medications such as levodopa and amantadine may be useful in some cases.
Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.
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.
Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. CBD symptoms typically begin in people from 50 to 70 years of age, and typical survival before death is eight years. It is characterized by marked disorders in movement and cognition, and is classified as one of the Parkinson plus syndromes. Diagnosis is difficult, as symptoms are often similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and dementia with Lewy bodies, and a definitive diagnosis of CBD can only be made upon neuropathologic examination.
Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.
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.
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is an autosomal dominant neurodegenerative tauopathy and Parkinson plus syndrome. FTDP-17 is caused by mutations in the MAPT gene located on the q arm of chromosome 17, and has three cardinal features: behavioral and personality changes, cognitive impairment, and motor symptoms. FTDP-17 was defined during the International Consensus Conference in Ann Arbor, Michigan, in 1996.
Dopamine-responsive dystonia (DRD) also known as Segawa syndrome (SS), is a genetic movement disorder which usually manifests itself during early childhood at around ages 5–8 years.
Parkinson's disease (PD), or simply Parkinson's, is a long-term neurodegenerative disease of mainly the central nervous system that affects both the motor and non-motor systems of the body. The symptoms usually emerge slowly, and as the disease progresses, non-motor symptoms become more common. Usual symptoms include tremors, slowness of movement, rigidity, and difficulty with balance, collectively known as parkinsonism. Parkinson's disease dementia, falls and neuropsychiatric problems such as sleep abnormalities, psychosis, mood swings, or behavioral changes may arise in advanced stages as well.
The Pacific Udall Center was established in 2009 as a new Morris K. Udall Center of Excellence for Parkinson's Disease Research. It is one of nine Udall Centers across the U.S. that honor former Utah Congressman Morris Udall with a "multidisciplinary research approach to elucidate the fundamental causes of PD [Parkinson's Disease] as well as to improve the diagnosis and treatment of patients with Parkinson's and related neurodegenerative disorders." The Pacific Udall Center is a collaboration among Stanford University, the University of Washington, the VA Puget Sound Health Care System, Oregon Health & Science University, and the Portland VA Medical Center. It is funded by a grant from the National Institute of Neurological Disorders and Stroke.
Parkinsonian gait is the type of gait exhibited by patients with Parkinson's disease (PD). It is often described by people with Parkinson's as feeling like being stuck in place, when initiating a step or turning, and can increase the risk of falling. This disorder is caused by a deficiency of dopamine in the basal ganglia circuit leading to motor deficits. Gait is one of the most affected motor characteristics of this disorder although symptoms of Parkinson's disease are varied.
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.
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. PD was then known as paralysis agitans. The term "Parkinson's disease" was coined in 1865 by William Sanders and later popularized by French neurologist Jean-Martin Charcot.
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.
Gait variability seen in Parkinson's Disorders arise due to cortical changes induced by pathophysiology of the disease process. Gait rehabilitation is focused to harness the adapted connections involved actively to control these variations during the disease progression. Gait variabilities seen are attributed to the defective inputs from the Basal Ganglia. However, there is altered activation of other cortical areas that support the deficient control to bring about a movement and maintain some functional mobility.
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.
Rapid eye movement sleep behaviour disorder and Parkinson's disease is rapid eye movement sleep behavior disorder (RBD) that is associated with Parkinson's disease. RBC is linked genetically and neuropathologically to α- synuclein, a presynaptic neuronal protein that exerts deleterious effects on neighbouring proteins, leading to neuronal death. This pathology is linked to numerous other neurodegenerative disorders, such as Lewy body dementias, and collectively these disorders are known as synucleinopathies. Numerous reports over the past few years have stated the frequent association of synucleinopathies with REM sleep behaviour disorder (RBD). In particular, the frequent association of RBD with Parkinson's. In the general population the incidence of RBD is around 0.5%, compared to the prevalence of RBD in PD patients, which has been reported to be between 38% and 60%. The diagnosis and symptom onset of RBD typically precedes the onset of motor or cognitive symptoms of PD by a number of years, typically ranging anywhere from 2 to 15 years prior. Hence, this link could provide an important window of opportunity in the implementation of therapies and treatments, that could prevent or slow the onset of PD.