What is Parkinson's disease > Health and Wellness.

Parkinson's disease: disease of the central nervous system

Parkinson's disease or Parkinson's (PRK) is a chronic and degenerative disease of the central nervous system that affects an area of the brain called the basal ganglia, whose function is to act as a support system in the production and control of movements, both voluntary and involuntary.
Parkinson's develops a so insidious, slow, generally between 55 and 60, although the lower age limit for the disease is 35 years. Evolution is progressive, although variable. It is not a deadly disease, but it is still incurable.
Causes of the Parkinson's disease
In an area of the brain called the substantia nigra, there are a number of neurons (nerve cells) in a darker color than the rest, whose function is to produce and secrete a very important substance for the control of movements: dopamine.
In the "gateway" to these basal ganglia, which is called core striated (EST), receptors that dopamine acts are. When the dopamine receptors have been activated, produce a series of biochemical changes that allow the proper connection with the rest of the components of the basal ganglia, regulating the activity of the same. This complex function only takes out correctly when there is a perfect balance between all the components involved.
When this process occurs properly, the individual is able to keep under control voluntary movements that is say, those who "want to do"-, but also allows you to maintain inhibited involuntary movements--those who "don't want to" carry out-, and thus prevent their emergence.
When develops parkinson, black neurons responsible for the release of dopamine degenerate and, consequently, stop producing the neurotransmitter, or make it less. When this occurs, the regulation of basal ganglia is not adequate, and other components and substances of the nodes do not work in the required manner, resulting in a lack of control of movements: voluntary movements do not carry out in the desired shape, resulting in the appearance of one of the most striking signs of Parkinson's: hypokinesia (decrease of voluntary movements).
Some of the symptoms that occur in this disease are intensified by the presence of acetylcholine, a neurotransmitter antagonist to dopamine which intensifies their effects by reducing the level of this.

Symptoms of Parkinson's disease

The symptoms of Parkinson's, they include:

• Hypokinesia: due to the decrease in dopamine. Slowness of voluntary and automatic movements. Lack of facial expression. Slow writing and small (micrograph). Clumsiness in handling objects.
• Tremors: slow and rhythmic. Predominate in resting State and decrease when performing a voluntary movement. It is a symptom not necessarily all parkinson's patients, experiencing them although his presence is very important, since the diagnosis of Parkinson's disease is very difficult when there is trembling.
• Muscle stiffness: resistance to move extremities, muscle hypertonia. Referred to as 'cogwheel' stiff because, although the Member presents resistance to be moved from one point resistance disappears and the movement is easy. Is it due to the lack of dopamine to allow exaggerated action of another substance contrary to this, acetylcholine, which stimulates the muscles and difficulty in movement.
• Posture abnormalities: inclination of the trunk and the head forward. Elbows and knees are as cramped.
• Walking abnormalities: gait is slow, with a tendency to drag your feet, and alternating with short (accelerating) with difficulty and quick steps to stop. Parkinson's patient suffers episodes of lock in which feet appear to be stuck to the ground, as if they were frozen or magnetized.
• Disorder of balance: altered reflexes, easy to fall.

Other symptoms of Parkinson's disease that does not affect the movement

While it is true that the symptoms and signs related to the movement, posture, and balance are the most frequent and easy to identify, they aren't the only ones who a person diagnosed Parkinson's disease can develop:

• Depression and anxiety: many diagnosed parkinson's patients may develop depression or anxiety, as well as sudden mood changes.
• Cognitive disorders: loss of memory, confusion, difficulty concentrating.
• Decrease in some senses, such as smell.
• Dull pain and discomfort in the extremities.
• Sleep disorders: daytime sleepiness and frequent NAPs. The hypokinesia and rigidity can make it difficult on the nocturnal sleep, especially when it comes to getting out of bed, turn on or change their stance.
• Fatigue.
• Gastrointestinal problems.

Many of these disorders are due to degeneration of the basal ganglia function can end up affecting structures located near the brain.
One of these structures is the brain stem, where the thalamus, which regulates important functions as some of the senses and the nerve sensations that reach the brain (thalamus is known as the door of consciousness). Other structures that regulate the smell, breathing movements, the functions of the heart or blood vessels can also be affected: the bulb and extrusion.

Risk factors for Parkinson's disease

The cause which causes Parkinson's is not known, but it is accepted that there is a confluence of factors (multifactorial) that can help to trigger the disease.
Some of these risk factors for Parkinson's disease are:

• Positive family history (genetic component).
• Male: women are less likely to develop the disease.
• Head injury: trauma, shock in head (boxers Parkinsonism).
• Exposure to pesticides.
• Consumption of drinking water and rural residence.

Other risk factors linked to Parkinson's disease less frequently are the consumption of coffee, smoking, use of nonsteroidal anti-inflammatory drugs (ibuprofen, naproxen, indomethacin...) and hormone replacement therapy in postmenopausal women.

Types of Parkinson's

There are several types of Parkinson's. The main difference is the cause of the outbreak of the disease, since the most important characteristics are common to all types, regardless of the cause.
The most common forms of the disease can be classified into:

Primary Parkinson

Primary Parkinson's disease is one that is purchased outright. It is not caused by a chemical or other pathology. Various types of primary Parkinson's can be distinguished:

• Family or genetic. Quite rare.
• Idiopathic or sporadically. It has genetic basis. It is the most frequent.
• Associated with other neurodegenerative process: Alzheimer's disease with Parkinsonism; atrophy or degeneration of other basal ganglia-related structures...
• Genetic disorders that can cause manifestations of Parkinson's time: Wilson disease (a disease of the metabolism of copper of genetic origin, which makes this accumulate in the Central nervous system, liver and other organs); Huntington's disease...
• Other disorders: of vascular origin (in the blood vessels that feed the basal ganglia, the substantia nigra, striatum core); Hydrocephalus; cerebral palsy.

Secondary Parkinson

Secondary Parkinson's is the one who is motivated by another disease, drugs or toxic:

• Repeated head trauma: as you develop some boxers, because the blows received repeatedly.
• Diseases infectious or post-infectious: as neurosyphilis (is the moment in which syphilis affect the brain); or Parkinson's that can develop in the period of time after an encephalitis (infection of the brain).
• Metabolic diseases.
• Drug-induced Parkinsonism: it is very important, since possibly the most frequent reason for development of symptoms of secondary Parkinsonism is the consumption of certain drugs, whether they are by prescription as for self-medication. There are several medications that can cause the appearance of these signs and symptoms. But, usually, the symptoms go away when you stop taking the medication that is producing them. Among the drugs that can cause parkinson: some antipsychotics and Neuroleptics (medications used for certain mental illnesses); some antiemetics (for vomiting), such as metoclopramide; Alpha-methyldopa (for hypertension); (for bipolar disorder) Lithium Carbonate; valproic acid (an antiepileptic)... It is necessary to always consult your doctor or pharmacist if you suspect that any medication is causing symptoms or signs of parkinsonism.
• Toxin-induced Parkinsonism: cyanide, methanol and carbon monoxide.

Diagnosis of Parkinson's disease

In the absence of any type of marker that is say, something that can be seen in an analysis - to serve for the diagnosis, Parkinson's disease is diagnosed through clinical manifestations. In general, can be a pretty successful diagnosis when a patient presents, at least two of the three core symptoms of Parkinson's disease: hypokinesia, resting tremor and rigidity. It is very important that the tremor is at rest and that disappears when making a move, as there are other pathologies of the nervous system that do not have tremor at rest, but this appears to try to carry out the movement.
Family medical history and physical examination should be thorough, because, although it is not the most frequent form, Parkinson's may have a genetic inheritance (familial Parkinsonism). Approximately 5% of diagnosed cases of Parkinson's are due to genetic form. Elsewhere, although the causes may be different, it seems clear that there are certain genetic factors (genetic vulnerability), to interact with the environment, predisposes the individual to develop some type of Parkinson's (see causes).
The doctor may carry out exploratory testing of the head, such as a magnetic resonance image, to rule out other possible causes for the symptoms, such as Hydrocephalus (or accumulation of fluid in the brain, which increases its pressure and decreases the operation), cerebral vascular diseases or injuries caused by mass, as tumors. Also other tests may be performed to confirm the degeneration of nigral - mostly in the less frequent forms of Parkinson's - and thus, the diagnosis of the disease.

Treatment of Parkinson's disease

Treatment for Parkinson's is intended to address one or more therapeutic fronts, aiming to raise levels of dopamine in striatum core nodes, either providing dopamine missing, through the administration of substances that activate dopamine receptors (but non-dopamine), or delaying possible degradation of low dopamine that remains in the area.
Therapy for Parkinson's disease does not cure the disease (remember that it is degenerative), but it is proven that the quality of life of the patients improved significantly when they adhere to treatment and followed it regularly. However, approximately 5-10% of patients will not respond effectively to the treatment. In addition, not all treatments are suitable for all types of Parkinson's. The doctor will decide the most effective treatment depending on the shape of Parkinson's who has been diagnosed.

Medication to treat Parkinson's disease

Almost all drugs used in the treatment of Parkinson's disease experience side effects. In general, establishing a specialist treatment and usually does not start until the symptoms affect significantly the work of everyday life. The following are the main drugs used to counter the effects of Parkinson's disease.

Therapy with levodopa and enzyme inhibitors of DOPA-decarboxylase

Levodopa is a dopamine precursor amino acid. When administered, brain metabolizes it, turning it into dopamine, which is the diminished neurotransmitter. But outside the brain, the body also has enzymes that are responsible for turning this levodopa into dopamine. Enzymes are small molecules of the family of proteins that catalyze reactions. These enzymes to metabolize the levodopa to dopamine, do not allow that it reaches the brain and the lymph nodes. Therefore levodopa is given together with inhibitors of enzymes, thus allowing the levodopa to reach the brain and, once there, transform into dopamine.
The main adverse effects come from the conversion of levodopa to dopamine in the body, but outside of the brain. These adverse effects are nausea, vomiting, cardiovascular effects, and abnormal movements, especially in the area of the face and mouth. But as a result of the introduction of the inhibitors of the enzymes in the treatment, reduced the intensity of these adverse effects, which can also be avoided with other medications.
Other complications that may appear are psychiatric disorders, largely due to the accumulation of dopamine in the brain, since not only dopamine will act at the level of the nodes, but in many other areas, making these symptoms. Where this happens, the doctor can consider decreasing the dose or stop the therapy with levodopa; or add other medications that control symptoms (antipsychotics).
Eventually, therapy with levodopa may lose some of its effectiveness, appearing a phenomenon by which the doses given increasingly last less time you enable and, therefore, reappear (phenomenon of end-of-dose) and phenomenon on/off symptoms. The effective duration of levodopa-therapy is 5 to 7 years. After this period of time, they can begin to appear the phenomena described.

Therapy with dopamine agonists

The objective of this group of drugs is to act as if they are dopamine, i.e. activating receptors where dopamine binds. But they are not dopamine, which effects occur to a lesser extent adverse associated with abnormal movements. However, these agonists seem to be more related to adverse psychiatric or, at least, are more frequent.
Some of these drugs are: bromocriptine, pergolide, lisuride, amantadine (which is also used to treat severe cases of flu), apomorphine (also used in erectile dysfunction cases and in cases of poisoning, since it induces vomiting), pramipexole and ropinirole.
A new drug, with the peculiarity that is administered in the form of patch is available. He is rotigotine, and it works by the same mechanism, but it is much more easy to use.

Inhibitors of other enzymes (Mao-B inhibitors and ICOMT)

Fairly used, especially when the levodopa begins to show signs of exhaustion, allowing you to raise levels of dopamine by inhibiting the enzymes that degrade it (unlike inhibitors used with levodopa, who were responsible for inhibiting the enzymes that turn outside the brain, levodopa into dopamine).
Some examples: entocapona (ICOMT) and selegiline (Mao-B).

Central anticholinergic

By decreasing dopamine, acetylcholine (a neurotransmitter contrary to it) produces more intense effects, interact with their receptors more easily (among them, enhances rigidity and it can be related with the tremor at rest). There is a real increase of acetylcholine, but the lack of dopamine causes seem to increase the level of the transmitter.
These drugs (biperiden, trihexyphenidyl, procyclidine) decrease the action of acetylcholine receptors and, thus, help control the dopamine, especially rigidity anti-competitive effects.
On the other hand, they present many unwanted and annoying effects such as dryness of mouth, constipation, blurred vision... and in some cases may appear mental confusion, since we are preventing acetylcholine to act on their receivers.

Power for parkinson's patients

Patients with Parkinson's, in principle, do not have nutritional needs different from healthy people, except those who have both diabetes, cholesterol or high triglycerides, some kind of gastrointestinal pathology such as celiac disease or intolerance to lactose, among others. But present certain difficulties arising from its pathology (whether by make it difficult for chewing, swallowing, producing saliva, loss of appetite, constipation or any other), they do need to pay special attention when it comes to feed them.
The main objective is to get that these limitations are not reflected in their nutritional status, trying to find a varied and balanced diet that provides them the nutrients they need. An inadequate diet can encourage the emergence of other conditions such as: infections (and delayed healing), muscle weakness (worsened by the hypokinesia of Parkinson's), ulcers on the skin of the patient if it stays too long in bed...
Parkinson's, is also a condition that presents a high energy requirement, since the resting tremor that you consume large amounts of energy. A good intake will prevent unwanted weight losses. In addition, a proper diet may soften somewhat adverse effects of therapy (constipation and nausea), since the drug absorption in the intestine when food contains is slower.
However, it should be recalled that levodopa, by its nature, is a drug that when administered with protein-rich foods, may be less effective. In the event that the patient or caregiver noticed a worsening of symptoms, will have to readjust the amount of ingested protein.
We must not forget that if the disease is advanced, it will be advisable to manage the food into small pieces; and that it is preferable to take small portions of food, spread throughout the day and were composed of various nutrients, which will facilitate the intake without affecting the nutritional balance.
Of course, any undue weight loss must always be commented with the doctor.

Published for educational purposes