Parkinson’s disease and Sleep.

May 12, 2009

There could be a connection between Parkinson’s disease and the sleep process.  The symptoms of Parkinson’s disease seem to have a similarity to the physical processes that occur when we are in a deep sleep.  When  we are asleep our gastrointestinal tract slows down. Our urinary system has dulled signals. Our need for swallowing decreases and the signals from our brains that tell our arms and legs what to do changes. Our need to have or control our facial impulses diminish. I think it is related in a basic way to Schizophrenia only because it occurs in the same area of the brain that is in control while we are asleep. Parkinson’s  symptoms occur due to a faulty disconnection from the sleep area of the brain just like a lamp that is only partially plugged into a wall getting flickering symptoms.

Schizophrenics have a disconnection difficulty with the mental aspects of sleep and Parkinson’s  effected people have a disconnection problem with the physical aspects of sleep.

More details can be read here:


* What I think is interesting, is how Parkinsons symptoms seem to be the same as the physical

changes that happen to us during deep sleep.

ie..we dream we are running, but our legs don’t move.

And our gastrointestinal system slows down.

Our urinary system alters.

Our facial expressions while dreaming are flat.


And so Parkinsons and Schizophrenia both seem to me, to be

sleep disorders. Schizophrenia is a dream state while awake, and

Parkinsons is a physical sleep state while awake.


Older antipsychotic medication versus mordern antipsychotic medication and Dopamine re uptake versus Dopamine blocking.

March 27, 2008

Older anti-psychotics work very well for acutely and floridly psychotic people. Modern anti-psychotics seem to be objectively very poor in my opinion at treating acute psychosis. This could be due to the mechanisms of action.

If the process of psychosis involves the flooding of the brain with Dopamine, perhaps the excess Dopamine is being picked up by Dopamine receptors from dormant neighbouring, neuron dopamine receptors. The old fashioned anti-psychotics block re-uptake, therefore preventing the Dopamine from entering dormant neurons. Modern antipsychotics block the Dopamine to slow the flow of Dopamine into the synapse. If there is already a flooded overload of Dopamine, then there is little immediate benefit to be had from Modern Antipsychotics.

Modern anti psychotics probably have a better chance of achieving results in prodromal or mild/emerging psychosis or as a preventative measure in a schizophrenic who is experiencing a remission of symptoms.

Another take is that newer antipsychotics are just not sedating enough and so they don’t increase sleep or REM sleep.  Modern antipsychotics aren’t as sedating.

Emotional Memory Tools, REM Sleep and Psychosis

August 20, 2007

We probably establish pathways, mechanisms or tools for avoiding depression, psychosis, personality disorders, autism and enhancing intelligence inside our brains before we are born; these tools can be enhanced or depleted as we age. Biological susceptibility to depression, psychosis, personality disorders, schizophrenia and autism could be counteracted by strengthening these neurological tools.

A child probably creates emotional memory foundations or tools with the help of the hippocampus, and these foundations serve as protection from mental illness. For example, when frightened a small child might curl up into a fetal position. The fetal position (a tool used during times of stress) is stored in the brain by the hippocampus as a position that produces calming emotions. This position helps the brain to reconnect with pathways that were linked to the sensation of calm felt as a fetus.

It is well known that babies respond well to being wrapped snugly in a way that mimics how they might have felt in the womb. This calming of the child results in lowering cortisol responses which allow the brain to function at a higher level. Stress produces cortisol which may attach to steroid binding sites in the brain, particularly in the hippocampus, which plays a major role in memory.

If a child who is frightened is provided with a new calming experience, verbal or non verbal, a new emotional memory foundation will be learned and stored in the brain with the help of the hippocampus. The new emotional memory foundation is possibly cemented at night during REM sleep.

Towards adolescence the rate of emotional foundations learned from positive human experiences decreases as the comforting from family decreases, so adolescents become more reliant on drawing from their stored emotional memory reserves during times of stress.  Stress and anxiety have been proven to affect memory and make concentration difficult. The emotional memory tools possibly decrease stress, decrease cortisol levels, increase serotonin levels and allows the brain to function with more perceived clarity. These emotional memory tools  are possibly accessed during REM sleep.

For example, healthy adolescents become increasingly emotionally independent from their parents. During sleep, they have dreams that reflect the strong emotions felt during the day. Throughout the dreaming process, the brain accesses emotional tools, for example the soothing feeling from a memory of being physically comforted, laughing or being verbally reassured. This results in a decrease of ‘real’ stress, decreases cortisol, increases serotonin and the adolescent wakes up feeling refreshed and happier.

Individuals likely to experience recurring depression or mental illness have insufficient emotionally soothing memories due to negative experiences, structural neurological deficiencies, lack of sleep, or lack of REM. This limits the storage of positive emotional tools or leads to difficulty accessing stored tools at night.

It is important for parents to let their children experience a range of emotions with positive outcomes as a child. Children surrounded by negativity store destructive memories often resulting in chronic dysthymia and depression. Skewed and maladaptive emotionally soothing memories may encourage personality disorders. If emotionally stored tools are based only on physical/non verbal events, addictive type personalities may result.

Schizophrenics may not be able to access a store of emotionally soothing memories due to poorly functioning neurological systems. This interferes with the formation of emotional tools, resulting in psychosis.

People who suffer from post traumatic stress may experience recurrent nightmares because their brains are unable to find stored memories to match and combat their extreme stressor.

Adults who had anxious parents go to sleep with a calm feeling which gives way to a store of anxiety-laden emotional memory during sleep. As an adult, they wake up with increased anxiety. The same pattern is exhibited with people who had overly critical and negative parents, perhaps culminating in depression.

Infants utilize emotional storage. They register “happy faces”, “sad faces” etc. They also store calming memories during periods of closeness, cuddling and breast feeding. A child completely devoid of human contact will become autistic. They intellectualize all of their soothing.

Autism can also result from infection/physical damage to the hippocampus which possibly hinders adequate laying down of emotional memories. Autistic kids who self soothe with rocking may have this emotionally memory tool stored before birth but they cannot build on this. Head banging may relieve some of the physical discomfort caused by excesses in cortisol and stimulate the release of serotonin.

Allowing children to sort through emotionally stressful issues all by themselves may promote or enhance intellectual ability by stimulating new neural pathways. They can create their own emotional tools using logic and reason, although this should not be relied upon as a sole basis for emotional foundation. An over-reliance on intellectual soothing can posssibly lead to emotional disconnection, culminating in Aspergers-like symptoms.

REM Sleep and Schizophrenia

August 15, 2007

Imagine that REM sleep, a process that occurs in the hippocampus, is like an airline control tower that is trying to organise the landing of airplanes into a busy airport for a short period during the night while you are sleeping. The airplanes represent many scattered emotions and non-concrete information that is spread throughout the perceptual areas of the brain. The landing of the planes is like the collection of random emotional data in the form of impulses , then sorting ,disposing or placing of data into emotional memory banks using previously stored emotional memories to assist the process. Human research supports the function of rapid eye movement (REM) sleep in memory formation. Wagner, Gais, and Born (2001) state “Results are consonant with a supportive function of REM sleep predominating late sleep for the formation of emotional memory in humans.”

Studies with deep electrodes have established that while the EEG of the neocortex is low in voltage during the REM sleep state, “the EEG of the hippocampus is increased in size at a 4-10 Hz (theta) frequency” (Siegel 2000).

Slowing of noradrenergic cells may be responsible for some of the symptoms of sleep deprivation, since norepinephrine release has been shown to increase the “signal to noise ratio” of information processing in a number of brain regions (Hasselmo et al 1997).

I hypothesize that REM sleep helps the brain regulate emotions by altering the sensitivity of D1 and/or D2 receptors. Studies have shown schizophrenics have unusual characteristics of D1 and D2 receptors (Abi-Dargham et al 2002). I suggest that in schizophrenics, REM sleep is unable to successfully carry out it’s task, resulting in an overabundance of emotional- memory-related connections and data. This initially leads to fogginess in higher thinking but ultimately to hallucinations and/or disorganized thoughts. Without proper functioning of REM sleep processes, psychosis occurs. The reason for malfunction would dictate the duration and type of psychosis. i.e. Too much emotional data overloading REM, poor foundation memories needed for sorting. Poor quality fluid and chemical combinations creating difficult pathways for impulses to leave their point of origin and head towards the hippocampus. Perhaps this creates a dream/nightmare state (Psychosis) that exists while awake?

Possible overloading reasons:

  • Sleep deprivation resulting in less REM sleep.
  • Perhaps the REM data could be too much for the REM mechanism to process during stressful times.
  • Ruminations that occur during periods of high anxiety might overload the REM process.
  • Double bind parenting could cause increased emotional stress and result in an ineffective REM process.
  • In schizophrenia and certain types of severe depression, the hippocampus shrinks.
  • Anxiety and depression can lead to psychosis due to an increase or overflow of the REM data sites.
  • Anxiety and wakening during sleep decrease the effective clearing of data sites because there is less REM sleep.
  • It’s commonly known that sleep deprivation causes psychosis, if the Rem mechanism can’t function due to lack of sleep, it overflows [rewrite]. Overloaded REM in a normal individual will spill out onto daytime wakening and perceptions in these circumstances,possibly in the areas they are waiting to be collected from.
  • Poorly functioning REM might result from nightmares which wake the person up and so they never actually continue with an adequate cleansing of the REM sites.

Perhaps hypersomnia during stressful times is an unsuccessful attempt for allowing effective REM sleep in schizophrenics.

Possible reasons for REM mechanism failure:

  • Genetic predisposition to a faulty mechanism.
  • A poorly functioning REM system could also be caused by dehydration, high fructose junk food, coca cola, coffee, cigarettes, poor vitamin intake, low phosphorus levels. Higher levels of nutrients have been shown to affect REM and are linked to better sleep.
  • Some poorly functioning REM mechanisms could be caused by maternal infections during pregnancy, head injury or other illnesses during childhood.
  • Schizophrenia might occur after childhood because the REM takes a while to become overloaded. Perhaps in some cases of high chronic stress or low mood or poor sleep REM data never completely clears so it eventually floods certain areas of the brain, polluting perceptions while the individual is awake .
  • This could explain why prodromal schizophrenics withdraw and become socially autistic, perhaps the cloudiness they complain about is like a polluted stuffiness from over stuffed REM sites that interfere with the processes necessary for the person to take in external information and separate it from their internal overflowing REM data sites.
  • Excessive intake of Junk food, high fructose diets, cola and coffee are common amongst Schizophrenics. Perhaps these diets adversely affect the mechanism or homeostasis required for emptying of the can. It could be as simple as chemical imbalances in the brain resulting in a poorly functioning REM mechanism or flow of impulses.
    • Jin et al, 2005: “Recently, considerable progress has been made in our understanding of the function and regulation of the brain-specific sodium-dependent inorganic phosphate transporter 1 (NPT1), which is found to exist principally in cerebrum and cerebellum. A high phosphate diet caused an increase in serum Pi accompanied by a decrease in calcium, and a decrease in body weight coupled with a decreased relative weight of cerebellum. A study showed the specific radioactivity of the phosphatides was depressed in sleeping as compared with waking animals. These observations suggest that the physiological conditions attributable to environmental, emotional or other determinants can influence shifts in brain metabolism during the sleep-wakefulness cycle.”
  • “Regular coffee and caffeine causes REM sleep to shift to the early part of the night and stages 3 and 4 sleep to shift to the later part” (Karakan et al, 1976)
  • Infection can lead to psychosis. “Sleep deprivation may enable bacterial growth and that sufficient sleep impedes bacterial growth. What’s even more interesting is that di-muramyl peptides created during infection enhance non-REM sleep (but not REM sleep)” (Hobson 1994). It has been shown that even after an individual has recovered from some bacterial infections the ‘dead’ bodies of the tiny bacterium still remain in the brain. This must sometimes impede certain processes or synapsing.

Other possible connections:

  • Siblings of schizophrenics often complain of vivid nightmares.
  • Post traumatic Stress disorder clients complain of terrible nightmares.
  • Antipsychotics Medications that are sedating have a faster acting effect than non-sedating antipsychotics.
  • Some antidepressants can cause psychosis and some antidepressants have been shown to block REM sleep but antidepressants given during the prodromal phase might be beneficial in decrease the workload on the emotional data sorting process.
  • Hypersomnia may be the body’s way to try to empty/sort the REM data, as is sometimes seen in mild depression or prodromal schizophrenia. Sleeping late increases REM (Plihal and Born 1997).
  • It is rare to find a schizophrenic that doesn’t smoke. “Epidemiological investigations indicate that, compared with never smokers, current smokers experience greater difficulty in initiating and maintaining sleep and are generally more dissatisfied with their sleep quality.” (Zhang et al 2006)
  • Could there be a natural steroidal effect that is produced during times of stress that potentiates psychosis by damaging the brain?
  • Perhaps individuals who are tested as genetically susceptible to schizophrenia will be able to put preventative strategies into place by altering their lifestyle.

Interesting Facts:

  • 95% schizophrenic persons smoke cigarettes.
  • Cigarettes interfere with sleep quality.
  • Nicotine patches interfere with sleep quality.
  • Research in the UK links smoking mothers to be with a 20% increase in offspring with psychosis.
  • Anti psychotic medication functions differently when a patient stops smoking.
  • Most schizophrenics drink excessive amounts of caffeine, mostly coffee and coke. In certain areas of the brain, caffeine and nicotine enhance the transmission of dopamine, the main neurotransmitter involved in schizophrenia and the site of anti-psychotic medications. When dopamine rages, it can lead to psychosis.
  • In a sample of 146 patients with schizophrenia from Pennsylvania, the rates of smoking were more than twice as high than the general United States population (59.6% vs. 23.4%). The study participants also reported smoking more cigarettes (24 vs. 13.5) and ingesting more caffeine (471.6mg vs. 254.2mg) at a rate of about ten more cigarettes and two more cups of coffee each day.
  • Caffeine interferes with the sleep process.  One recent study shows that subjects fell asleep more easily when they were not ingesting caffeine, while another other shows that the duration and quality of sleep were improved on non-caffeine days.
  • Schizophrenia is associated with increases in Dopamine whereas Parkinsons disease is associated with decreases in Dopamine.
  • A reduced risk for Parkinson’s disease (PD) among cigarettesmokers has been observed consistently during the past 30 years.Recent evidence suggests that caffeine may also be protective.
  • Poor diets deficient in certain nutrients have been shown to contribute to poor sleep.
  • Schizophrenic persons often have low nutrient diets.  Poor nutrition elevates homocysteine levels.
  • Research recently showed that Normal sleepers, consumed the highest food variety in their diets, and very short sleepers had the least variation in what they ate. A varied diet tends to be a marker for good health since it includes multiple sources of nutrients.
    Read more:
  • There has previously been found that there is a marked elevation of plasma homocysteine in young male schizophrenic patients in hospital. Serum homocysteine levels were studied in 184 consecutively admitted schizophrenic patients and 305 control subjects from an employee screening program. Homocysteine levels were markedly increased in this population of newly admitted schizophrenic patients, especially in young males. Newly admitted male schizophrenic patients have elevated homocysteine levels that cannot be explained on the basis of poor hospital nutrition. Smoking may raise homocysteine by 1–2 μM/L but this is not a large enough effect to explain our findings.
  • Some researchers have already shown a link between folic acid and schizophrenia.
  • Psychosis is usually preceded by high levels of stress.
  • Stress interferes with sleep quality.”The prevalence of insomnia may, in fact, be the result of deteriorating sleep mechanisms associated with increased sensitivity to arousal-producing stress hormones, such as CRH and cortisol.
  • During times of great stress schizophrenic persons display extremely poor sleep habits.
  • The siblings of schizophrenic persons often exhibit strange dreaming phenomena.
  • Schizophrenics often liken there symptoms to dreaming while awake.
  • Schizophrenia often appears during adolescence.
  • Adolescents have marked changes in need for length of sleep and their circadian rhythm changes.
  • Schizophrenics have biological body temperature control problems.
  • Biological body temperature regulation changes when a person is sleeping.
  • Persons abusing barbiturates become psychotic.
  • Barbiturates decrease REM sleep.
  • Heavy marijuana use is linked to psychosis and schizophrenia.
  • During discontinuation of heavy heavy marijuana use, PSG measures of sleep disturbance were detected in heavy marijuana users compared with a drug free control group.
  • New mums have lots of sleepless nights but new research suggests that a lack of sleep could place them at greater risk of suffering from postnatal psychosis.
  • Schizophrenia could simply be a sleep disorder.
  • This is to say there is an underlying belief that the area of the brain which promotes REM sleep, rapid eye movement and dreaming may also be the area that is predominantly supportive of the symptoms that manifest in the schizophrenia patient. In examining dopamine levels at the prefrontal cortex, we find the levels are significantly decreased in individuals who suffer from schizophrenia. Interesting enough, this same decrease in dopamine occurs, temporarily, during our periods of REM sleep and the onset of dreaming phases.
  • First degree relatives of schizophrenic persons often suffer from recurrent nightmares.
  • The contraceptive pill interferes with the absorption of caffeine.
  • Interesting fact, I have never known a schizophrenic to have an acute psychotic episode, while taking contraceptive pills.
  • Difficulties initiating or maintaining sleep are frequently encountered in patients with schizophrenia. Disturbed sleep can be found in 30-80% of schizophrenic patients, depending on the degree of psychotic symptomatology. Measured by polysomnography, reduced sleep efficiency and total sleep time, as well as increased sleep latency, are found in most patients with schizophrenia and appear to be an important part of the pathophysiology of this disorder.
  • Sleep disturbance is as much a part of schizophrenic disorder as it is of affective illness. Research is cited indicating that after REM deprivation, remitted schizophrenics show an abnormally large transient increase in REM sleep and that active schizophrenics have dreams that are more bland and not as well confined to REM sleep as those of normals.


  • Wagner, Gais, and Born (2001): Emotional Memory Formation Is Enhanced across Sleep Intervals with High Amounts of Rapid Eye Movement Sleep. Learning and Memory. Vol. 8, No. 2, pp. 112-119, March/April 2001
  • Siegel, J. M. Brainstem mechanisms generating REM sleep. In: Principals and Practice of Sleep Medicine, Second Edition. Edited by M. K. Kryger, T. Roth, W. C. Dement. New York: Saunders, 2000.
  • Hasselmo, Linster, Patil, Ma, and Cekic. Noradrenergic Suppression of Synaptic Transmission May Influence Cortical Signal-to-Noise Ratio. The Journal of Neurophysiology Vol. 77 No. 6 June 1997, pp. 3326-3339.
  • Abi-Dargham, Mawlawi, Lombardo, Gil, Martinez, Huang, Hwang, Keilp, Kochan, Van Heertum, Gorman, Laruelle.
    Prefrontal Dopamine D1 Receptors and Working Memory in Schizophrenia. The Journal of Neuroscience, May 1, 2002, 22(9):3708-3719
  • Isaac, and Berridge. Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation. Journal of Pharmacology And Experimental Therapeutics. August 27, 2003;
  • Jin, Hwang, Yu, Anderson, Lee, Lee, Prats, Morello, Beck, Jr., Cho. A High Inorganic Phosphate Diet Perturbs Brain Growth, Alters Akt-ERK Signaling, and Results in Changes in Cap-Dependent Translation. December 7, 2005. Toxicological Sciences 2006 90(1):221-229;
  • Karacan, Thornby, Anch, Booth, Williams, Salis. Dose-related sleep disturbances induced by coffee and caffeine. Clin Pharmacol Ther. 1976 Dec;20(6):682-9.
  • Hobson. “Sleep and the Immune System”. In: The Chemistry of Conscious States: How The Brain Changes. Little, Brown 1994.
  • Plihal and Born. Effects of Early and Late Nocturnal Sleep on Declarative and Procedural Memory. The Journal of Cognitive Neuroscience, Vol 9, 534-547, Copyright © 1997 by The MIT Press
  • Zhang, Samet, Caffo, Punjabi. Cigarette Smoking and Nocturnal Sleep Architecture. American Journal of Epidemiology 2006.


Acetylcholine (Ach) – the neurotransmitter in all autonomic ganglia. In other words, it is a chemical that allows neurons to communicate with each other.

Aminergic – Relating to nerve cells or fibres.

Dentate gyrus – Part of the hippocampal formation. It contains granule cells, which project to the pyramidal cells, but mostly to the interneurons of the CA3 subfield of the hippocampus.

Dopamine – dopamine functions as a neurotransmitter, activating the five types of dopamine receptor – D1, D2, D3, D4 and D5, and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra.

EEG topography – using a large number of electrodes to triangulate the source of the electrical activity.

Electroencephalography – the neurophysiologic measurement of the electrical activity of the brain by recording from electrodes placed on the scalp or, in special cases, subdurally or in the cerebral cortex.

Electroencephalogram (EEG) – The resulting traces from Electroencephalography, known as an and represent a summation of post-synaptic potentials from a large number of neurons.

Entorhinal cortex (EC) – Important memory center in the brain. The EC forms the main input to the hippocampus and is responsible for the pre-processing (familiarity) of the input signals.

Hippocampus – has an essential role in the formation of new memories about experienced events (episodic or autobiographical memory).

Medulla oblongata – is the lower portion of the brainstem.

Mesencephalon (or midbrain) – is the middle of three vesicles that arise from the neural tube that forms the brain of developing animals.

Nicotinic acetylcholine receptors (nAChRs) – ionotropic receptors that form ligand gated ion channels in cells’ plasma membranes. Like the other type of acetylcholine receptors, muscarinic acetylcholine receptors (mAChRs), their opening is triggered by the neurotransmitter acetylcholine (ACh), but they are also opened by nicotine.

Noradrenergic – liberating, activated by, or involving norepinephrine in the transmission of nerve impulses

Pons – part of the central nervous system, and relays sensory information between the cerebellum and cerebrum.

Ponto-geniculo-occipital (PGO) spikes – periodically generated during the REM sleep, which are considered to be the main stimuli of dreams. Play an important role in triggering and maintaining rapid eye movement sleep. Similar potentials can be elicited in waking by intense auditory stimulation that elicit orienting

Scalp electrodes – picks up the activity of large groups of neurons

Sensory gating – a process by which the brain adjusts its response to stimuli. It is a largely automatic process. When one stimulus is presented, there is a response. But when it is followed by a second stimulus soon after, the response to the second stimulus is blunted. This is an adaptive mechanism to prevent overstimulation. It helps to focus on a stimulus among a host of other distracing stimuli. The mechanism of sensory gating involves feed-forward and feed-back inhibition of the stimulus perceived. It involves GABA-ergic and α7 nicotinergic receptor-mediated inhibition of the pyramidal neurons in the cornu ammonis (CA3) region of the hippocampus.

Theta rhythms – are one of several characteristic electroencephalogram waveforms associated with various sleep and wakefulness states.