Can we recover from Parkinson's Disease? How to slow down the progress of Parkinson's
Before we discuss how to slow down Parkinson's Desease, we first need to know what it is.

Parkinson's disease is a common, debilitating, neurodegenerative disorder characterized by neuronal loss within the
basal ganglia and insufficient levels of the neurotransmitter dopamine. [F] Parkinson's disease may happen to anyone
of us. In a healthy body, some of our nerve cells in the brain produce a chemical called dopamine, dopamine transmits
signals within the brain to produce smooth movement of muscles. While, in Parkinson's patients, 80 percent or more of
these dopamine-producing cells are damaged, dead, or otherwise degenerated. This causes the nerve cells to fire
wildly, leaving patients unable to control their movements. People diagnosed with Parkinson's Disease may have
symptoms like: [i] resting tremor, or trembling in hands, arms, legs, jaw, and face, [ii] rigidity, or stiffness of limbs and
trunk,  [iii] bradykinesia, or slowness of voluntary movement and [iv] postural disturbances, instability or impaired
balance and coordination. [6]

Motor Symptoms

The motor symptoms of Parkinson's disease are predominantly due to progressive degeneration of nigral
dopaminergic neurons. In most cases there is a substantial asymmetry of clinical symptoms from disease onset, which
occurs in sporadic and in hereditary forms of the disease. [5]

Low frequency rest tremor is one of the cardinal signs of Parkinson's disease. There is evidence that neural
oscillations and synchronization play a central role in the generation of the disease. However, Parkinsonian tremor is
not strictly correlated with the synchronous oscillations in the basal ganglia networks. Rather, abnormal basal ganglia
output enforces abnormal thalamo-cortical processing leading to akinesia. [4]

In advanced stage of Parkinson's disease, patients may experience freezing of gait. Freezing of gait (FOG) is a
disabling episodic gait disturbance. Freezing of gait typically lasts a few seconds and is associated with a unique
sensation: the patient feels that his feet are glued to the ground, causing him to remain in place despite making a
concerted effort to overcome the motor block and move forward. However, stress, anxiety, depression and cognitively
challenging situations are also associated with freezing of gait. [2]

The disease is related to basal ganglia, substantia nigra, globus pallidus, thalamus and cerebellum of the brain. [F]
Basal ganglia affects normal movement and walking; substantia nigra is the type of basal ganglia that produce the
neurotransmitter dopamine, which sends messages that control muscles. The globus pallidus is part of a larger
structure connected to the substantia nigra affecting movement, balance and walking. The thalamus serves as a relay
station for brain impulses, and the cerebellum affects muscle coordination.

Though full-blown Parkinson's can be crippling or disabling, experts say early symptoms of the disease may be so
subtle and gradual that patients sometimes ignore them or attribute them to the effects of aging. At first, patients may
feel overly tired, "down in the dumps," or a little shaky. Their speech may become soft and they may become irritable
for no reason. Movements may be stiff, unsteady, or unusually slow. In the early stage of the disease, the absence of
biomarkers leads to imprecise diagnosis or even misdiagnoses. [6] Inexperienced doctors may diagnose the problem
as arthritis. [F]

Non-motor Symptoms

Though Parkinson's disease is a progressive disease that usually affects the motor system, it is also associated with a
non-motor symptom complex. The non-motor symptoms include dribbling saliva, constipation, depression, rapid eye
movement behavior disorder, sleep disorders, apathy, hallucinations, and dementia. [1,7] Recent evidence suggests
that non-motor symptoms may be markers of a preclinical stage of Parkinson's disease. [7]

Several cognitive deficits can also be observed in non-demented patients with Parkinson's disease during their history.
The core symptom in the cognitive deficits in Parkinson's disease is the executive dysfunction. Executive dysfunction is
related to abnormalities in the dorsolateral prefrontal circuit which largely passes through the caudate nucleus. [8]

Associated Diseases

Patients suffered from Parkinson's disease always have mood disorders, and have a negative impact on disability and
quality of life. [3]

Treatments for Parkinson's disease

Levodopa remains the most effective agent for relief of motor symptoms, but long-term levodopa use is associated
with development of motor complications, including severe dyskinesias. For this reason, some doctors prefer selegiline
or a dopamine agonist as initial therapy. Carbidopa/levodopa (with or without a COMT inhibitor) may alsobe needed
for relief of motor symptoms. When medical therapy can no longer provide adequate symptom control, doctor may
suggest surgical intervention. [1]

More about Parkinson's Disease
Parkinson's Disease - Supplements
Parkinson's Disease - Herbs
Parkinson's Disease - Side Effects of Drugs
Parkinson's Disease - Symptoms

[1] Brunton S. A comprehensive approach to Parkinson's disease. How to manage fluctuating motor and nonmotor
symptoms. Postgrad Med. 2006 Jun-Jul;119(1):55-64. [2] Giladi N, et al, The role of mental function in the
pathogenesis of freezing of gait in Parkinson's disease. J Neurol Sci. 2006 Oct 25;248(1-2):173-6. Epub 2006 Jun 14.
[3] Marsh L, et al, Provisional diagnostic criteria for depression in Parkinson's disease: report of an NINDS/NIMH Work
Group. Mov Disord. 2006 Feb;21(2):148-58. [4] Rivlin-Etzion M, et al, Basal ganglia oscillations and pathophysiology
of movement disorders. Curr Opin Neurobiol. 2006 Dec;16(6):629-37. Epub 2006 Nov 3. [5] Djaldetti R, et al, The
mystery of motor asymmetry in Parkinson's disease. Lancet Neurol. 2006 Sep;5(9):796-802. [6] Sethi KD. Clinical
aspects of Parkinson disease. Curr Opin Neurol. 2002 Aug;15(4):457-60. [7] Chaudhuri KR, et al, The non-motor
symptom complex of Parkinson's disease: a comprehensive assessment is essential. Curr Neurol Neurosci Rep. 2005
Jul;5(4):275-83. [8] Kanazawa A. The cognitive dysfunction in Parkinson's disease Nippon Rinsho. 2004
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