Neil Diamond, aged 82, is finally coming to terms with his Parkinson’s diagnosis. Initially disclosed in 2018, along with his retirement from touring, the singer-songwriter revealed in a forthcoming CBS Sunday Morning interview that he spent two years in denial after receiving the diagnosis from his doctor.
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Neil Diamond Diagnosis
During his 50 Year Anniversary World Tour in January 2018, Diamond received his Parkinson’s Disease (PD) diagnosis. Although he no longer believes he can continue touring, he has persisted in prioritizing his health with the hope of returning to the stage.
Speaking to the Associated Press, he shared, “Well, I’m doing pretty well. I’m active.
I take my meds. I do my workouts. I’m in pretty good shape. I’m feeling good. I want to stay productive … I just can’t do the traveling that I once did, but I have my wife there supporting me (and) friends.”
Acknowledging the challenges, Diamond remains optimistic, stating, “It does have its challenges, but I’m feeling good and I feel very positive about it. I’m feeling better every day. [I’m] just dealing with it as best I can, and just keep the music coming.”
Expressing his aspirations, Diamond hopes to undertake a residency in the future: “Well, I feel I can do it. I want to do it,” he said. “It’s just a matter of resting up, finding the time, preparing, and then just doing the show.”
Parkinson’s Disease
PD falls within a category of conditions known as motor system disorders, which induce unintended or uncontrollable movements of the body. Its impact on the central nervous system is both chronic and progressive.
As nerve cells (neurons) in various brain regions deteriorate or perish, individuals may experience movement issues, tremors, stiffness in limbs or the trunk, and impaired balance.
These symptoms may exacerbate, leading to difficulties in walking, speaking, or carrying out simple tasks.
In the U.S., PD ranks as the second-most prevalent neurodegenerative disorder following Alzheimer’s disease.
While most PD diagnoses occur in individuals aged 60 years and above, a notable 5%-10% are diagnosed before reaching the age of 50.
Though approximately 500,000 Americans receive a PD diagnosis, the true figure is likely higher due to underdiagnosis or misdiagnosis. Some experts estimate that up to 1 million Americans may be living with PD.
Causes of Parkinson’s Disease
Although various brain regions are impacted, the most prevalent symptoms arise from the decline of neurons in the substantia nigra. Typically, these neurons produce dopamine, facilitating smooth, purposeful movement by transmitting signals to the corpus striatum, a key brain relay station. Diminished dopamine levels lead to irregular nerve firing patterns.
Studies reveal that most Parkinson’s patients have lost 60%-80% or more of the dopamine-producing cells in the substantia nigra by symptom onset.
Additionally, individuals with PD experience a reduction in nerve endings that generate the neurotransmitter norepinephrine, which regulates autonomic functions like heart rate and blood pressure.
This loss may contribute to non-motor symptoms such as fatigue and blood pressure irregularities.
The affected brain cells of PD patients harbor Lewy bodies, which are deposits of the protein alpha-synuclein. Despite ongoing research, the reasons for Lewy body formation and their role in the disease remain unclear.
Some theories propose that malfunctioning protein disposal mechanisms lead to harmful protein accumulation and subsequent cell death.
Others suggest that Lewy bodies may form in an attempt to shield cells from the toxicity of smaller protein aggregates.
Genetics play a role in PD, with several genetic mutations, including those in the alpha-synuclein gene, linked to the disorder. Environmental factors also contribute, as exposure to certain toxins can induce parkinsonian symptoms in susceptible individuals.
Additionally, mitochondrial abnormalities are implicated in PD development, as they generate free radicals that harm cellular components, leading to oxidative stress. Mutations affecting mitochondrial function have been identified as PD causes.
Symptoms of Parkinson’s Disease
PD’s impact on the central nervous system is both chronic and progressive. By the time PD is diagnosed, it usually has advanced to a stage where individuals struggle to control their body movements due to tremors, bradykinesia (slowed movement and reflexes), limb or trunk stiffness, and impaired balance.
These symptoms can escalate, making walking, talking, swallowing, and completing simple tasks challenging.
Alongside motor symptoms, non-motor symptoms such as cognitive decline, mood disturbances, sleep disturbances, and constipation significantly affect quality of life, requiring tailored symptom management.
Some non-motor symptoms like reduced sense of smell (hyposmia), REM sleep behavior disorder (acting out dreams), and constipation typically precede motor symptoms by several years.
Others, like cognitive decline, often emerge after motor symptoms appear.
Although dementia eventually develops in many PD patients, the time from movement symptom onset to dementia onset varies widely.
Dementia often prompts PD patients to transition from independent living to long-term care facilities.
Parkinson’s Disease Treatment
Several categories of medications are used to treat PD. The first category comprises drugs that elevate dopamine levels in the brain.
The primary medications for PD are dopamine precursors, such as levodopa, which penetrate the blood-brain barrier and convert into dopamine.
Alternatively, other drugs mimic dopamine or hinder its breakdown.
Another category of PD medications targets different neurotransmitters in the body to alleviate certain symptoms.
For instance, anticholinergic drugs disrupt the production or absorption of the neurotransmitter acetylcholine, effectively reducing tremors.
The third category of PD medications encompasses drugs that assist in managing the non-motor symptoms of the disease, those symptoms unrelated to movement. For instance, individuals experiencing PD-related depression may receive antidepressants.
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