Parkinson’s disease is a degenerative disorder of the central nervous system, causing Parkinson dementia symptoms indicative of subcortical dementia. Early symptoms of Parkinson’s disease include rigidity, tremor, involuntary shaking of arms and legs, and slowing of movements, especially walking. Later symptoms involving the dementia signs of PD exhibit varying degrees of difficulty regarding:
- Selective attention
- Abstract thinking
- Planning and reasoning
- Recalling encoded information (riding a bicycle or unlocking a door)
- Impulse control (the patient may develop hypersexuality, crave enormous amounts of food or becoming addicted to gambling)
- Depression, anxiety and apathy
Behavioral changes affect Parkinson’s patients more often than cognitive issues, although Parkinson’s dementia can produce delusions and/or hallucinations due to dopaminergic excess in the brain.
What is Dopamine?
This chemical is solely produced by dopaminergic neurons existing in the brain’s substantia nigra region and is one of several dozen different types of brain cells. However, they are the only kind of brain cell involved in Parkinson’s disease that does not reproduce. Because of this inability to perpetuate, dopaminergic neurons suffer irreversible and substantial reductions in their number when struck with Parkinson’s-type progressive dementia.
Muscle contraction is controlled by five dopamine receptors–receptor one and five are stimulatory and two, three, and four are inhibitory. Complementing dopamine is another important brain chemical called acetylcholine, which also regulates muscle contraction through five cholinergic receptors.
Number one, three and five cholinergic receptors are stimulatory; two and four are inhibitory. When someone suffers from PDD (Parkinson’s disease dementia) and associated Parkinson’s dementia signs, it is a deficiency in number two, three and four dopamine receptors rather than too much acetylcholine affecting number one, three and five Ach receptors that causes the disease.
Normal muscle functioning occurs when a balance exists between inhibitory and stimulatory signals regulated by these receptors that exist on the surface of nerve cells. When receptors do not receive enough dopamine but Ach receptors continue receiving the same amount of acetylcholine, Parkinson’s dementia signs slowly begin to overwhelm the patient, along with motor symptoms that eventually leave the affected individual unable to walk or initiate independent movement.
More on Parkinson Dementia Symptoms…
When degeneration of the brain areas underneath the cerebral cortex occurs as it does in Parkinson’s, this type of dementia is called subcortical dementia. Symptoms of subcortical dementia include most of the signs of Alzheimer’s dementia–memory and speech problems, irrationality, memory problems and depression.
Certain brain structures, such as the basal ganglia, are especially damaged in subcortical dementia, which causes severe difficulties with controlling voluntary movements. Huntington’s disease is another example of a neurodegenerative disorder producing subcortical dementia and difficulties regulating muscle control.
Late-stage Parkinson’s dementia signs include:
- Mask-like, expressionless face caused by extremely rigid muscles
- Shuffling, rapid gait (festination)
- Stooped or crooked posture
- Severely slowed movements (bradykinesia)
- Inability to speak or swallow
Parkinson’s Dementia Medications
Levodopa, or L-dopa, a dopamine agonist may alleviate motor problems early in the disease. Although L-dopa is usually effective at the onset of Parkinson’s, the progressively dramatic loss of dopaminergic neurons eventually overrides the ability of the drug to relieve muscle tremors and rigidity.
Moreover, the longer Parkinson’s patients take L-dopa, the better chance that they will develop a disorder called dyskinesia, which makes the patient experience uncontrollable writhing movements.
Patients are sometimes helped by rehabilitation therapy, deep brain stimulation or surgery in the most advanced Parkinson’s cases where medication is no longer effective Other therapies currently being researched are stem cell transplants and gene therapy but have yet to be implemented successfully in the treatment of Parkinson’s.
In response to treatment dementia associated with Parkinson’s disease is managed with the Excelon patch or capsules containing rivastigmine, the same ingredient contained in the patch. However, only mild to moderate Parkinson’s dementia signs are treatable with this FDA-approved medication. Severe symptoms require alternative and more aggressive therapies.
Several theories that have been formulated using the results of many research studies regarding the cause or causes of Parkinson’s disease include:
- Genetic abnormalities
- Environmental toxins that may attack and damage dopaminergic neurons (carbon monoxide, manganese and some pesticides)
- Oxidative stress enacted by free radicals
- Strong antipsychotic medications designed to relieve symptoms of schizophrenia and psychosis
Doctors specializing in neurodegenerative diseases speculate that Parkinson’s may develop because of a combination of one or more of these factors.
Receiving a correct diagnosis and initiating a treatment plan at the initial onset of Parkinson’s dementia signs is the best way to slow the progression of muscle rigidity and cognitive impairments. In addition, many Parkinson’s patients live semi-independently for many years following a diagnosis but may eventually deteriorate to a point where 24-hour care is necessary.
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