Neuroprotective Effects Of Cistanche Deserticola: Diagnosis And Treatment Of Parkinson's Disease

Parkinson's disease is a common progressive neurodegenerative disease whose prevalence increases with age. As the population ages and average life expectancy increases, the number of people living with Parkinson's disease is expected to increase in the coming decades. The purpose of this article is to provide clinicians with a practical overview of the initial diagnosis and treatment of Parkinson's disease.

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Diagnosis of Parkinson's disease

While patients with the typical presentations of Parkinson's disease (such as unilateral resting tremor and staggering gait) are easily identified, there are some patients whose diagnosis can be elusive. Patients without tremors may mistakenly attribute their symptoms to another neurological disorder, or generalized slowness and balance disturbances to simple aging. Patients may experience physical symptoms, such as constipation, or orthopedic problems including shoulder pain. Such patients are usually first referred to rheumatology, orthopedic, or psychiatric unit before a diagnosis of Parkinson's disease is suspected. Instead, there are a number of "red flags" that should alert clinicians to possible diagnoses other than Parkinson's disease (Box 1), thus requiring early neurological examination. When a patient presents with one or more red flags, the Parkinson's disease-like symptoms in Table 1 should be considered. While ancillary studies such as neuroimaging can help support the diagnosis and rule out these differential diagnoses, Parkinson's disease remains a clinical diagnosis, and a detailed history and examination are essential to identify the diagnosis.

Parkinson's disease is considered a systemic disorder that affects the gastrointestinal system, in particular, affecting the autonomic nervous system, sleep, and mood in addition to causing motor symptoms. Many non-motor symptoms precede motor symptoms, giving rise to the concept of a prodromal period in Parkinson's disease. Understanding these symptoms aids in early diagnosis and, by recognizing the impact of non-motor performance on disability and quality of life, can aid ineffective treatment.

Motor symptoms

The main manifestation of Parkinson's disease is bradykinesia or slow movement with resting tremor and/or stiffness. Limb bradykinesia is necessary for diagnosis, especially movements that decrease in amplitude with repetition, known as hypokinesia. During the examination, it is important to look for a momentary cessation of reduced range of motion or repetitive finger and toe-tapping motion. The bradykinesia evident on examination included a mask-like face due to reduced spontaneous facial movements, reduced eye blink rate, low voice, and macro writing.

The resting tremor in Parkinson's disease is usually slow (4-6 Hz), most commonly seen in the distal upper extremities and asymmetrical. Assess the upper extremities, preferably with the patient's palms down on the knees, or with the patient's hands hanging by the sides. Ask the patient to do a simple mental test, such as reciting the month of the year backward, which usually causes resting tremors. People with resting tremors are almost certain to have Parkinson's syndrome.

Early gait changes are characterized by a reduction in asymmetric arm swings, but over time, stride lengths become shorter and stride heights decrease, giving the gait a characteristically disorganized gait. Falls are a late feature that occurs within the first year of diagnosis and should be considered for Parkinson's disease-like symptoms.

Non-motor symptoms

Although Parkinson's disease is primarily defined by motor symptoms, extensive but characteristic non-motor symptoms are present in most patients. Often, these non-motor symptoms are the most disturbing to patients and have a greater negative impact on the patient's quality of life than motor symptoms.

Rapid eye movement sleep behavior disorder (RBD) occurs in about one-third of people with Parkinson's disease and can precede motor symptoms by more than a decade. RBD occurs because of failure to paralyze muscles during normal sleep dreaming, resulting in dream-reproduction behaviors including vocalizations, writhing movements, falls from bed, and accidental injury to a partner. Patients are often unaware of RBD while asleep, a symptom that needs to be learned from a partner. Up to 80% of patients with isolated RBD will eventually develop Parkinson's disease. Constipation and hyposmia can further suggest prodromal Parkinson's disease, which may appear more than 10 years before motor symptoms.

Neuropsychiatric symptoms are also common. Anxiety and depression are twice as common as the general population and can occur at any stage of the disease, including prodromal symptoms. Mood disorders are major determinants of health-related quality of life in patients with Parkinson's disease. Apathy, visual hallucinations, and psychiatric symptoms become more common as the disease progresses to an advanced stage. Up to 40 percent of people with Parkinson's disease eventually experience hallucinations, which are usually not threatening, although more disturbing psychiatric symptoms become more common as the disease progresses. Dementia eventually develops in 40% of Parkinson's disease patients and is related to both age and disease duration. Pain is an underrecognized feature that may originate from musculoskeletal, dystonic, neuropathic, or central, and in some cases respond to dopaminergic therapy. Other nonmotor features include excessive daytime sleepiness, fatigue, insomnia, restless legs syndrome, sexual dysfunction, dysphagia, and autonomic dysfunction (including orthostatic dizziness, bladder dysfunction, erectile dysfunction, and hyperhidrosis).

Treatment of Parkinson's disease

As a chronic progressive disease, most patients should be referred to a neurology department for treatment. Treatment of the patient depends on patient preference, the severity of non-motor and motor disability, and associated impairment of quality of life. Other factors affecting the timing of treatment initiation include occupation, age, and the presence of comorbidities. Therefore, in the diagnosis and treatment process, it is necessary to determine which symptoms affect the patient's quality of life and function. In some patients, dyskinesia may be associated with hand tremors, while in others, overall slowness may be the predominant symptom. While some manifestations may not be visible to external examiners, even mild symptoms felt in the dominant hand can produce significant functional impairment and thus affect treatment planning. Dopaminergic therapy has the potential to effectively target these deficits by improving bradykinesia, rigidity, and tremor.

A combination of levodopa with carbidopa or benserazide (both dopa decarboxylase inhibitors that inhibit the peripheral breakdown of levodopa before it reaches the central nervous system) is the most effective therapy for controlling motor symptoms in patients with Parkinson's disease. For people with mild Parkinson's disease, monoamine oxidase-B (MAO-B) inhibitors are a good option because they are well tolerated and given once a day. Oral or patch dopamine agonists are also effective for motor control in mild Parkinson's disease. However, patients should be informed of the risk that dopamine agonists may lead to impulse control disorders, including compulsive gambling, eating, consumption, or excessively sexual behavior. Additionally, dopamine agonists may exacerbate excessive daytime sleepiness and hallucinations. Due to the risk of nausea and dizziness, dopamine agonist therapy should be started gradually (start low and progress slowly). If symptoms are not well controlled after initial treatment with dopamine agonists or MAOB-B inhibitors, levodopa should not be hesitated to add levodopa, which is usually effective at relatively low doses (100 mg three times a day).

Most patients with moderate symptoms of Parkinson's disease respond extremely well to levodopa treatment, usually with an initial dose of 300 mg to 600 mg per day in 3 divided doses (morning, noon, and evening). Elderly patients may not tolerate the initial high dose due to nausea or dizziness; therefore, a slower titration method is recommended. Starting at a dose of 50 mg/day for 3-7 days and gradually increasing the daily dose in 50 mg increments at similar intervals to an initial target dose of 100 mg three times a day is a safe approach. Patients who are unresponsive to levodopa should be referred early to a neurology department for a reassessment of the diagnosis.

Exercise and physical therapy should be considered core components of early treatment and management of Parkinson's disease. Advise patients to strive to maintain their preferred activities, combining aerobic, resistance, active balance, and, if possible, high-intensity interval training. Strategies employed should target specific underlying impairments, with focus areas including gait, balance, transfer, and upper extremity function.

Cistanche Anti-Parkinson's Disease

The main pathological manifestation of Parkinson's disease is the degeneration of dopamine neurons in the substantia nigra, resulting in a decrease in the content of central neurotransmitters, accompanied by abnormalities and imbalances of various neurotransmitters such as acetylcholine and norepinephrine, causing a series of Parkinson's symptoms.

Through mouse experiments, the phenylethanoid extract in Cistanche deserticola can prevent the apoptosis of mouse cerebellar neuron cells;

Echinacea can protect dopamine neurons from oxidative stress damage through its anti-oxidative stress effect, and can also improve the activity and protein level of nerve cells;

Verbasin has an obvious cytoprotective effect on apoptosis in mice.

Conclusion: The active ingredients of Cistanche have a certain significance for drug screening for the treatment of Parkinson's disease.