Parkinson's Disease -
Symptoms and Causes
Symptoms and Causes
Parkinson's disease is a common, debilitating, neurodegenerative disorder
characterized by neuronal loss within the basal ganglia and insufficient levels of
the neurotransmitter dopamine. It was first described as "the shaking palsy" by
Dr. James Parkinson in 1817. [F]
In the normal brain, some nerve cells produce the chemical dopamine, which
transmits signals within the brain to produce smooth movement of muscles. 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. Symptoms include [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
Sep;62(9):1679-84.
characterized by neuronal loss within the basal ganglia and insufficient levels of
the neurotransmitter dopamine. It was first described as "the shaking palsy" by
Dr. James Parkinson in 1817. [F]
In the normal brain, some nerve cells produce the chemical dopamine, which
transmits signals within the brain to produce smooth movement of muscles. 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. Symptoms include [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
Sep;62(9):1679-84.
Popular
Supplements
Acetyl-L Carnitine
Acidophilus
Bladderwrack
Bilberry
Chromium
CLA
Cod Liver Oil
Coenzyme Q
Colostrum
Dandelion
EGCG
Echinacea
Eleuthero
Ellagic Acid
Eve. Primrose Oil
Fish Oil
Flaxseed
Garlic
Ginger
Ginseng
Ginkgo Biloba
Glucosamine
Gotu Kola
Guar Gum
Hyaluronic acid
Lecithin
Lycopene
Milk Thistle
Nattokinase
Passion Flower
Probiotics
Policosanol /
Polycosanol
Pycnogenol
Reishi / Lingzhi
Resveratrol
Rhodiola
Royal Jelly
Stevia
Whey
Xylitol
Supplements
Acetyl-L Carnitine
Acidophilus
Bladderwrack
Bilberry
Chromium
CLA
Cod Liver Oil
Coenzyme Q
Colostrum
Dandelion
EGCG
Echinacea
Eleuthero
Ellagic Acid
Eve. Primrose Oil
Fish Oil
Flaxseed
Garlic
Ginger
Ginseng
Ginkgo Biloba
Glucosamine
Gotu Kola
Guar Gum
Hyaluronic acid
Lecithin
Lycopene
Milk Thistle
Nattokinase
Passion Flower
Probiotics
Policosanol /
Polycosanol
Pycnogenol
Reishi / Lingzhi
Resveratrol
Rhodiola
Royal Jelly
Stevia
Whey
Xylitol
Discuss with your doctor before taking any alternative medicine. This article is for reference only, it is not a medical advice. All rights
reserved. Do not copy this article to other website or blog.
reserved. Do not copy this article to other website or blog.
 | |  | |  | |  | |  | |  | |  |
