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.
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.
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