Follow-up on Your Patient: You immediately suspect that [George] has Parkinson disease because of his shuffling gait and unilateral resting tremor. Your examination reveal[ed no] cogwheel rigidity in [his]upper [left] extremity. [He reported micrographia and dysphonia]. His cognitive testing is normal. You tell [him he] has Parkinson’s disease and discuss starting treatment with levodopa-carbidopa. […] He agrees and begins treatment immediately. One month later in follow-up [he] reports that the medication has helped [him] immensely. [He] has been able to continue working much as [he] has become accustomed to. You arrange to see [him] on a regular basis to monitor [his] symptoms and medication.
What is ”Off” Time in Parkinson’s Disease
Opqrst
https://en.wikipedia.org/wiki/OPQRST
Dopamine agonists act directly on the dopamine receptors and mimic dopamine’s effect.[1] Dopamine agonists have two subclasses: ergoline and non-ergoline agonists. Both subclasses target dopamine D2-type receptors. Types of ergoline agonists are cabergoline and bromocriptine and examples of non-ergoline agonists are pramipexole, ropinirole and rotigotine
parkinsons-treatment-29399.com
https://en.m.wikipedia.org/wiki/Swallowing
https://en.m.wikipedia.org/wiki/Parkinson%27s_disease_dementia
https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/diagnosis-treatment/drc-20376062
>> Alpha-synuclein clumps are a hallmark sign of Parkinson’s disease. The test accurately identified people with Parkinson’s disease 87.7% of the time. ..The test is called an alpha-synuclein seed amplification assay.
Levodopa, the most effective Parkinson’s disease medicine, is a natural chemical that passes into the brain and is converted to dopamine.
https://en.wikipedia.org/wiki/Substantia_nigra
The substantia nigra is an important player in brain function, in particular, in eye movement, motor planning, reward-seeking, learning, and addiction.!!!!
Pars compacta /SNpc : Parkinson’s disease is characterized by the death of dopaminergic neurons in this region.[1]
There’s also Cannabinoidergic, or cannabinergic, means “working on the endocannabinoid neurotransmitters“. As with terms such as dopaminergic and serotonergic, related proteins and cellular components involved endocannabinoid signaling, such as the cannabinoid (CB1) receptor, as well as exogenous compounds, such as phytocannabinoids or other cannabinoids which modulate the activity of endocannabinoid system, can be described as cannabinoidergic.[1]
https://en.m.wikipedia.org/wiki/Basal_ganglia
Degeneration of pigmented neurons in this region [SN] is the principal pathology that underlies Parkinson’s disease and this depigmentation can be visualized in vivo with Neuromelanin MRI.[9]
https://en.m.wikipedia.org/wiki/Cannabinoid
CBN is thought to interact with other kinds of neurotransmission (e.g., dopaminergic, serotonergic, cholinergic, and noradrenergic).
https://www.instagram.com/reel/CxONyjHrjDA/?igshid=MzRlODBiNWFlZA==
the current opinion in pharmacology is that dopamine instead confers motivational salience;[6][7][8]
The blood–brain barrier (BBB) is a highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and the central nervous system, thus protecting the brain from harmful or unwanted substances in the blood.[1]
l-DOPA crosses the protective blood–brain barrier, whereas dopamine itself cannot.[7]
To bypass these effects, it is standard clinical practice to coadminister (with l-DOPA) a peripheral DOPA decarboxylase inhibitor (DDCI) such as carbidopa (medicines containing carbidopa
In work that earned him a Nobel Prize in 2000, Swedish scientist Arvid Carlsson first showed in the 1950s that administering l-DOPA to animals with drug-induced (reserpine) Parkinsonian symptoms caused a reduction in the intensity of the animals’ symptoms.
https://en.m.wikipedia.org/wiki/Neuropsychopharmacology
As a consequence, high levels of dopamine lead to high levels of motor activity and impulsive behavior; low levels of dopamine lead to torpor and slowed reactions.[50]
Recent advances have demonstrated that glial cells, specifically microglia and astroglia, are involved in several neurodegenerative diseases including Amyotrophic lateral sclerosis (ALS), Epilepsy, Parkinson’s disease (PD), Alzheimer’s disease (AD), and ..