Author: geoplotsadmin

Diazepam, first marketed as Valium, is a medicine of the benzodiazepine family that acts as an anxiolytic.[10] It is commonly used to treat a range of conditions, including anxiety, seizures, alcohol withdrawal syndrome, muscle spasms, insomnia, and restless legs syndrome.[10] It may also be used to cause memory loss during certain medical procedures.[11][12] It can be taken orally (by mouth), as a suppository inserted into the rectum, intramuscularly (injected into muscle), intravenously (injection into a vein) or used as a nasal spray.[6][12] When injected intravenously, effects begin in one to five minutes and last up to an hour.[12] Orally, effects begin after 15 to 60 minutes.[13

Gabapentin is recommended as a first-line treatment for chronic neuropathic pain by various medical authorities.[7][8][26][27] This is a general recommendation applicable to all neuropathic pain syndromes except for trigeminal neuralgia, where it may be used as a second- or third-line agent.[8][27]

https://en.m.wikipedia.org/wiki/Trigeminal_neuralgia

Gabapentin is effective in treating sleep disorders such as insomnia and restless legs syndrome that are the result of an underlying illness, but comes with some risk of discontinuation and withdrawal symptoms after prolonged use at higher doses.[34]

Zhittya believes that this same drug that proved efficacious in the heart, could treat Parkinson’s disease, where recent evidence has demonstrated that a lack of blood flow to parts of the brain could be the initiating cause of Parkinson’s disease. < angiogenesis 

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Human Connectome Project |  Mapping the human brain connectivity

Human Connectome Project |  Mapping the human brain connectivity

We’re more curious about ourselves than we are about each other

What part of the brain deals with honour and revenge?

Criiminology and neurology, what a combo!

REM sleep is procesing the previous day’s events, laying down tracks of memory.

 Caelun non animum mutant qui trans mare currunt

https://www.latin-is-simple.com/en/vocabulary/phrase/253/

1000101=69

The hypothalamus is responsible for regulating certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes certain neurohormones, called releasing hormones or hypothalamic hormones, and these in turn stimulate or inhibit the secretion of hormones from the pituitary gland. The hypothalamus controls body temperature, hunger, important aspects of parenting and maternal attachment behaviours, thirst,[3] fatigue, sleep, and circadian rhythms ( <Wiki)       

The subthalamus is located ventral to the thalamus, medial to the internal capsule and lateral to the hypothalamus. It is a region formed by several grey matter nuclei and their associated white matter structures, namely:[3]

• The subthalamic nucleus, whose neurons contain glutamate and have excitatory effects over neurons of globus pallidus and substantia nigra  < Wiki

 

 Zen-Brain Reflections: Reviewing Recent Developments in Meditation and States of Consciousness Hardcover – February 1, 2006

by James H. Austin (Author) 

A sequel to the popular Zen and the Brain further explores pivotal points of intersection in Zen Buddhism, neuroscience, and consciousness, arriving at a new synthesis of information from both neuroscience research and Zen studies.

This sequel to the widely read Zen and the Brain continues James Austin’s explorations into the key interrelationships between Zen Buddhism and brain research. In Zen-Brain Reflections, Austin, a clinical neurologist, researcher, and Zen practitioner, examines the evolving psychological processes and brain changes associated with the path of long-range meditative training. Austin draws not only on the latest neuroscience research and new neuroimaging studies but also on Zen literature and his personal experience with alternate states of consciousness.

Zen-Brain Reflections takes up where the earlier book left off. It addresses such questions as: how do placebos and acupuncture change the brain? Can neuroimaging studies localize the sites where our notions of self arise? How can the latest brain imaging methods monitor meditators more effectively? How do long years of meditative training plus brief enlightened states produce pivotal transformations in the physiology of the brain? In many chapters testable hypotheses suggest ways to correlate normal brain functions and meditative training with the phenomena of extraordinary states of consciousness.

After briefly introducing the topic of Zen and describing recent research into meditation, Austin reviews the latest studies on the amygdala, frontotemporal interactions, and paralimbic extensions of the limbic system. He then explores different states of consciousness, both the early superficial absorptions and the later, major “peak experiences.” This discussion begins with the states called kensho and satori and includes a fresh analysis of their several different expressions of “oneness.” He points beyond the still more advanced states toward that rare ongoing stage of enlightenment that is manifest as “sage wisdom.”

Finally, with reference to a delayed “moonlight” phase of kensho, Austin envisions novel links between migraines and metaphors, moonlight and mysticism. The Zen perspective on the self and consciousness is an ancient one. Readers will discover how relevant Zen is to the neurosciences, and how each field can illuminate the other. < Amazon blurb  

Why does Parkinson’s dopamine depletion affect movement and not so much or so visibly learning and reward mechanisms?

Deep and beautiful. The reward prediction error hypothesis of dopamine – ScienceDirect

Twenty-Five Lessons from Computational Neuromodulation – ScienceDirect

 Access options for healthcare and patients

https://en.m.wikipedia.org/wiki/Dopamine

 The substantia nigra is a small midbrain area that forms a component of the basal ganglia. This has two parts—an input area called the pars compacta and an output area the pars reticulata. The dopaminergic neurons are found mainly in the pars compacta (cell group A8) and nearby (group A9).[42] In humans, the projection of dopaminergic neurons from the substantia nigra pars compacta to the dorsal striatum, termed the nigrostriatal pathway, plays a significant role in the control of motor function and in learning new motor skills.[44] These neurons are especially vulnerable to damage, and when a large number of them die, the result is a parkinsonian syndrome.[45] < wiki

https://en.m.wikipedia.org/wiki/Hypophonia

Levodopa is the mainstay of pharmacologic therapy for PD, although other agents are indicated for monotherapy or in combination with levodopa. These include traditional and newer dopamine agonists, amantadine, anticholinergics, selegiline, and an emerging class of agents called COMT inhibitors. < https://pubmed.ncbi.nlm.nih.gov/9597979/

 The main problem for most patients after prolonged treatment with L-dopa is the longterm L-dopa syndrome. Fluctuations and dyskinesias are usually the principal complaint in younger, and neuropsychiatric symptoms in older, patients <  https://pubmed.ncbi.nlm.nih.gov/9426870/ 

Benign tremulous parkinsonism (BTP) is a tremor dominant syndrome characterized by mild, levodopa-resistant parkinsonism with limited disability or progression.<  https://pubmed.ncbi.nlm.nih.gov/24019787/

Recent genetic discoveries support this idea because mutations in a few genes (α-synuclein, LRRK2, tau) can cause partially overlapping pathologies <  https://pubmed.ncbi.nlm.nih.gov/29151060/

 For most of human history, Parkinson has been a rare disorder. However, demography and the by-products of industrialization have now created a Parkinson pandemic that will require heightened activism, focused planning, and novel approaches.  <       https://pubmed.ncbi.nlm.nih.gov/30584159/

Camptocormia https://en.wikipedia.org/wiki/Camptocormia#Neurological_origin

Chocolate : Clinical observations amongst in-patients with PD in Dresden suggested an increased chocolate consumption. We speculated that due to its high content of biogenic amines chocolate may partially substitute the dopaminergic system and may improve PD symptoms <  https://link.springer.com/article/10.1007/s00702-022-02509-1

Thinking like a neurologist

Hickam’s dictum, the idea that a patient’s symptoms might be due to multiple lesions or diseases, becomes more likely with advancing age.

Pace + Localization = Syndrome

Syndrome + Context = Differential Diagnosis

  

   

The spirit of our times seems to urge us that we should let it all hang out. I don’t know about that as a general policy but I have posted this piece on a recent diagnosis of my own which I invite the curious or the merely morbid to read:

Diagnosis

I’m in the early stages of real Parkinson’s (PD), not Atypical Parkinsonian Syndrome (APS), many symptoms of which overlap with Parkinson’s and deploy a different, sometimes faster moving array of many of the same disabilities. No, I suffer from the classic variety of this neurodegenerative, idiopathic affliction, one which responds well to dopamine surrogates, at least initially. As the euphemism goes, one based on the model of “enslaved person” as opposed to “slave”, I am a PWP, a person with Parkinson’s.   

To be precise, I am not in  early onset phase, just the early stages. Typically, Parkinson’s  begins around 60, and the average life expectancy following diagnosis is 7–15 years.  Since I’m 78, this means I could live till 85-93, give or take….

I’m hoping that I belong in this category: “Individuals with mild motor-predominant Parkinson disease (49%-53% of individuals with Parkinson disease) have mild symptoms, a good response to dopaminergic medications (eg, carbidopa-levodopa, dopamine agonists), and slower disease progression.” < https://jamanetwork.com/journals/jama/article-abstract/276074

Imminent death is the lot of all 78 year olds, especially males. We are collectively entering the end game, not many chits are left to play. It follows that a diagnosis of PD can be enlightening. It further focuses attention on the facts of life and dying, on how to live (out) the time remaining.

Once diagnosed, I bought and have devoured a copy of Neuroscience for Dummies. I realized, as only a humanist dummy can, how much science there is which is worth knowing. Now there’s so little time in which to learn.

***

Here are two succinct webpages on PD:

https://www.narayanahealth.org/blog/parkinsons-disease/amp/

https://www.narayanahealth.org/blog/what-is-parkinsons-disease/amp/

 

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

https://www.fepblue.org/-/media/FEPBlue-Sitecore-10-Media/PDFs/October%20Policies/Pharm-Replace/560039%20Nourianz%20istradefylline.pdf

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

Hypokinesia

Parkinson’s disease

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://www.mayoclinic.org/drugs-supplements/carbidopa-and-levodopa-oral-route/before-using/drg-20095211    

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 ..