Parkinson's disease

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Related to Parkinson's disease: Alzheimer's disease, dopamine

Parkinson's disease

a slowly progressive disease usually occurring in later life, characterized pathologically by degeneration within the nuclear masses of the extrapyramidal system, and clinically by a masklike face (parkinson's facies), a characteristic tremor of resting muscles, a slowing of voluntary movements, a festinating gait, peculiar posture, and muscular weakness. Called also paralysis agitans and shaking palsy. When the symptom complex occurs secondarily to another disorder, the condition is called parkinsonism.
Symptoms. Parkinson's disease usually appears gradually and progresses slowly. At first the victim may be troubled by “resting tremors” of the hands and feet that diminish or disappear when the patient begins to move. Hypokinesia (reduced movement) is the most disabling feature of Parkinson's disease. A minor feeling of sluggishness may progress to inability to get up from a chair or even change position in bed. However, once the patient gets into motion, prolonged walking is possible. The gait is shuffling and festinating as the person attempts to regain his center of gravity. Rigidity of muscles in the arms, legs, and face is due to an increase in the tone of skeletal muscles. Loss of mobility in the face produces the characteristic masklike expression. Parkinson's disease does not adversely affect mental capacity.
Treatment. In general, treatment is symptomatic, supportive, and palliative. Most patients require lifelong management consisting of drug therapy, supportive psychotherapy, physical therapy, and rarely, surgical intervention. Newer forms of treatment now give hope for freedom from the progressive disability that once was almost inevitable. The biochemical basis of parkinsonism is a loss or inhibition of dopamine activity in the corpus striatum, resulting from degeneration of the dopaminergic nigrostriatal pathway. Normally, the two opposing neurotransmitters in this structure, dopamine and acetylcholine, are in balance. When dopamine is depleted, the functional overactivity of acetylcholine produces the symptoms of parkinsonism.

In patients with mild symptoms and little functional impairment, some relief from symptoms can be obtained with anticholinergic agents, such as trihexyphenidyl (Artane), or with antihistamines with anticholinergic properties, such as diphenhydramine (Benadryl). These drugs block the muscarinic effects of acetylcholine in the central nervous system. Tricyclic antidepressants, such as imipramine or amitriptyline, are also effective; they block the reuptake of dopamine from nerve synapses and also have anticholinergic effects.

In patients with more severe symptoms and difficulty with routine daily activities, it is necessary to augment the dopamine level in the brain. This is done by administering levodopa, which crosses the blood-brain barrier and is converted to dopamine by decarboxylation. This reaction also occurs in the peripheral tissues, and the dopamine produced may cause side effects such as cardiac stimulation (tachycardia and arrhythmias) and also nausea and vomiting. A newer drug called Sinemet, which combines carbidopa with levodopa, is now being used to counteract the undesirable effects that may occur when levodopa is used alone. Carbidopa inhibits production of dopamine outside the brain, thus allowing more effective relief of symptoms. A disadvantage to the combination drug is that in some patients it may have only a limited span of effectiveness; therefore, it is usually reserved for more severe cases.

Patients receiving levodopa alone or in combination with carbidopa require nutritional counseling because dietary habits can greatly affect the action of the drug. Protein intake requires special attention because levodopa, an amino acid, must compete with the dietary amino acids for transport through the intestinal epithelium and across the blood-brain barrier. Alcohol intake also must be limited because in large amounts it can antagonize the effects of dopamine. Although the newer combined form of medication offers relief to many persons with Parkinson's disease, it must be given with caution and under continued supervision. Fewer than 10 per cent of patients with Parkinson's fail to respond to some combination of individual drugs.
Patient Care. Since these patients' mental outlook and motivation can affect the extent to which they can successfully cope with their disability, it is important that they receive psychological support. They should know the nature of the disease affecting them and be given realistic hopes for forestalling or preventing its more serious effects.

Some benefits can be derived from physical therapy in the form of applications of heat and massage to alleviate muscle cramps and relieve the tension headaches that often accompany rigidity of the cervical muscles. The patient also is instructed in simple exercises to perform at home. Although depression often accompanies the physical limitations of Parkinson's disease, much psychological benefit can be derived from maintaining mobility and observing social and emotional ties. Patients can be taught to initiate walking by leaning forward to stimulate intact walking reflexes. Family members will need help in dealing with the patient's slowness of speech and communication difficulties. Some minor changes in the home, such as railings and support bars, can encourage independent movement.

Parkinson's disease

(pär′kĭn-sənz) also

Parkinson disease

A progressive disease of the central nervous system, associated with the destruction of brain cells that produce dopamine and characterized by muscle tremors, muscle rigidity or stiffness, abnormally slow movement, and impaired balance and coordination. It usually affects people over the age of 50. Also called paralysis agitans.

Parkinson's disease

Etymology: James Parkinson
a slowly progressive degenerative neurological disorder characterized by resting tremor, pill rolling of the fingers, a masklike facies, shuffling gait, forward flexion of the trunk, loss of postural reflexes, and muscle rigidity and weakness. It is usually an idiopathic disease of people over 60 years of age; it may occur in younger people, however, especially after acute encephalitis or carbon monoxide or metallic poisoning, particularly by reserpine or phenothiazine drugs. Typical pathological changes are destruction of neurons in basal ganglia; loss of pigmented cells in the substantia nigra; and depletion of dopamine in the caudate nucleus, putamen, and pallidum, structures in the neostriatum that normally contain high levels of the neurotransmitter dopamine. Signs and symptoms of Parkinson's disease, which include resting tremor, bradykinesias, drooling, increased appetite, intolerance to heat, oily skin, emotional instability, and defective judgment, are increased by fatigue, excitement, and frustration. Palliative and symptomatic treatment of the disease focuses on correcting the imbalance between depleted dopamine and abundant acetylcholine in the striatum because dopamine normally appears to inhibit excitatory cholinergic activity in this brain area. Levodopa, a dopamine precursor that crosses the blood-brain barrier, may be used, but many patients experience side effects, such as nausea, vomiting, insomnia, orthostatic hypotension, and mental confusion. Carbidopa-levodopa, which contains an inhibitor of the enzyme dopa decarboxylase, limits peripheral metabolism of levodopa and thus causes fewer side effects. Anticholinergic drugs, such as benztropine mesylate, biperiden, procyclidine, and trihexyphenidyl, may be used as therapeutic agents but often cause ataxia, blurred vision, constipation, dryness of the mouth, mental disturbances, slurred speech, and urinary urgency or retention. Amantadine hydrochloride, an antiviral drug with antiparkinsonian activity, promotes the accumulation of dopamine in extracellular or synaptic sites, but the therapeutic effectiveness may not last more than 3 months in some patients; side effects, such as mental confusion, visual disturbances, and seizures, occur infrequently. Also called paralysis agitans. parkinsonian, adj.
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Parkinson's disease: depigmented substantia nigra

Parkinson's disease

Paralysis agitans Neurology A condition characterized by tremors and rigidity followed by inhibition of voluntary movement, a shuffling gait due to neuronal degeneration in the basal ganglia–substantia nigra and corpus striatum, focal ↓ of dopamine production and eventually severe mental deterioration Clinical Older subjects with static tremor, plastic rigidity of trunk and extremities, bradykinesia, masklike facies, progressive stoop, slow monotonous voice, slow shuffling gait, often accompanied by autonomic dysfunction–hypersalivation, sweating, rapid, coarse tremor, pill-rolling movements, cogwheel rigidity, drooling, akinesia Management l-Dopa is effective in early PD, as it is transported to the brain and converted into dopamine, but with time, loses efficacy, clozapine; 'brain-graft' surgery was disappointing; fetal nerve graft–mesencephalic dopamine neurons from 8-9 wk fetuses–may be more effective; deprenyl, an MAOI that blocks conversion of MPTP to MPP+; PD may be prevented by 3+ cups of coffee/day. See BDNF, Clozapine, Fetal-brain tissue grafting, MPTP, Unified Parkinson's Disease Rating Scale.

Parkinson's disease

A SYNDROME featuring involuntary tremor of the hands with ‘pill-rolling’ finger movements, muscle rigidity and slowness of movements. The face becomes mask-like, the speech slow and the voice quiet and monotonous. Hand-writing becomes minute. There is difficulty in starting to walk and a tendency for the body to incline forwards. Steps are short and tottering, as if the affected person were falling forwards. Cognitive loss and psychiatric changes may occur. Parkinson's disease affects about 1 person in 100 over age 60 and becomes progressively more common with advancing age. It is due to brain changes in the area of the connections between the SUBSTANTIA NIGRA and the CORPUS STRIATUM, with loss of pigment and dopamine-producing cells. There are intraneuronal Lewy bodies. It may be a side effect of certain drugs, such as various phenothiazine or designer drugs or the effects of various poisons such as carbon monoxide. It may be caused by brain tumours, ENCEPHALITIS and repeated head injuries, as from boxing. In 2% of cases there is a mutation in the gene LRRK2 that codes for the protein dardarin, and this mutation is present in 5% of familial cases and 7% of autosomal dominant disease. Most cases remain idiopathic. Treatment is by dopamine replacement using the drug levodopa and other drugs which stimulate dopamine receptors in the brain. Deep brain electrical stimulation by an implanted device delivering very short pulses up to 185 times per second greatly reduces tremor and rigidity. Unilateral pallidotomy may be useful in some cases. The status of fetal cell implantation treatment remains uncertain. Also known as paralysis agitans. (James Parkinson, 1755–1824, London physician).

Parkinson's disease

a debilitating, neurological disorder, that results from the degeneration of NERVE CELLS in the region of the BRAIN controlling movement. Limb tremor, particularly when the body is at rest, is an initial symptom of the disease.

Parkinson's disease

A slowly progressive disease that destroys nerve cells in the basal ganglia and thus causes loss of dopamine, a chemical that aids in transmission of nerve signals (neurotransmitter). Parkinson's is characterized by shaking in resting muscles, a stooping posture, slurred speech, muscular stiffness, and weakness.
Parkinson's disease; parkinsonism; paralysis agitans; shaking palsy neurological syndrome of unknown cause associated with degenerative changes of basal ganglia (loss of pars compacta cells within the substantia nigra, the appearance of eosinophilic inclusion bodies [Lewy bodies] and decreased dopamine levels); affects 1% of older people; also associated with long-term head trauma (i.e. so-called ‘punch-drunk’ syndrome of boxers) or certain antipsychotic drugs (e.g. perazine, phenothiazines, butyrophenones and depot preparations); characterized by insidious onset of rhythmical muscular tremors at rest (pill-rolling tremor; 4–6 Hz), paucity and slowness of movement (hypokinesia, bradykinesia) and generalized rigidity (cogwheel and lead-pipe rigidity), festinant gait, stooped posture, mask-like facies and eventual progressive dementia

Patient discussion about Parkinson's disease

Q. What to expect from a Parkinson's patient? My 70 year old father has been diagnosed with Parkinson's. What will he be like from now on, what to expect?

A. Some of the symptoms of Parkinson's disease are:
• Trembling of hands, arms, legs, jaw and face
• Stiffness of the arms, legs and trunk
• Slowness of movement
• Poor balance and coordination
The symptoms usually get worse with time and then people with the disease may have trouble walking, talking or doing simple tasks.

Q. what is the latest on parkinson?

A. the "National Institute of Neurological Disorders and Stroke" keeps an article on "what's new in Parkinson research" and they update it every now and then. i have to say that the last one is from 2005, but it has some interesting things you might wanna know...:

and the "National Parkinson Foundation" also keeps their readers updated and have a jornal you may find useful things in:

Q. How do you tell between temporal shaky hands and parkinson disease? My dear granpa's hands are being a bit shaky lately. I was wondering if I should worry about Parkinson's disease or is it most likely to be something else? How to tell? are there other symptoms for Parkinson's?? Any help...

A. The tremor (shaking body parts) of Parkinson disease appears during rest of the limb and disappears or weakens during active movement. Additionally, Parkinson's disease cause walking problems and slow movements.

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More discussions about Parkinson's disease
References in periodicals archive ?
Neurogenic orthostatic hypotension (NOH) occurs within the context of a disease process characterized by nervous system lesions, such as in Parkinson's disease (Figueroa et al.
Usually people who develop Parkinson's disease are 60 and older.
DNA mutations resulting in the production of a specific enzyme called glucocerebrosidase (GBA) have been linked to a five-fold greater risk of developing Parkinson's disease; however, only 30 percent of individuals with this mutation have been shown to develop Parkinson's disease by the age of 80.
These studies show posterior rather than anterior cortical involvement in Parkinson's disease dementia versus Parkinson's disease alone," Dr.
Environmental antecedents of young-onset Parkinson's disease.
But in many parts of South Wales there is no-one employed as a Parkinson's disease nurse specialist and many people miss out.
This study hasn't yet proven unequivocally that coenzyme Q10 will slow the progression of Parkinson's disease," says study co-author Clifford W.
The person diagnosed with Parkinson's disease has to travel many novel and personally uncharted waters in the course of the illness.
Parkinson's disease has a complex relationship to dementia and depression, as well as to the medications used to treat the motor components of the illness.
Parkinson's disease with depression: A possible subgroup of idiopathic Parkinsonism.
FINLAND: A Finnish study of same-sex twins born before 1958 and still alive in 1975 has concluded that Parkinson's disease is caused by environmental rather than hereditary factors.
com/research/88l8xd/global) has announced the addition of the "Global Parkinson's Disease Epidemiology and Patient Flow Analysis - 2012" report to their offering.

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