Methamphetamine was legally prescribed in injectable form in the US in the 1930-50s as a central nervous stimulant, antidepressant and appetite suppressant (for weight loss).
It became a widely abused prescription drug in the 1960’s, before it became more tightly regulated by the government in the 1970s.
That is when illegal manufacturing and distribution really started to take off in the US.
In the 1980s a new crystalline form of methamphetamine, which could be smoked, found it’s way into the US, and quickly started to replace cocaine as the illicit stimulant of choice among drug users.
Whether snorted, smoked, or injected, methamphetamine rapidly crosses the blood brain barrier where they cause sustained increases in the extracellular concentrations of monoamine neurotransmitters such as dopamine, norepinephrine, and serotonin.
With repeated use in both humans and experimental animal models, methamphetamine depletes the brain’s stores of monoamines, contributing to methamphetamine’s high abuse potential – without the drug, users may have an impaired ability to experience pleasure (anhedonia), slipping into a deep depression
Dopamine and serotonin neurons project widely throughout the brain influence a variety of behaviors and functions. Up to 40% of chronic methamphetamine users have memory loss, impulsive behavior and impaired decision-making. Continued drug abuse can lead to depression and psychosis.
One interesting aspect of chronic methamphetamine psychosis is the delusion of parasitosis or formication – commonly known as “meth mites”, this is a frequent complaint in heavy daily users of methamphetamine, and can lead to self mutilation:
A dream is a succession of images, ideas, emotions, and sensations that occur involuntarily in the mind during REM sleep.
So during REM sleep our subconscious minds are supposed to be active, while we lie unaware with our bodies perfectly still. However, two unusual phenomena can occur during REM sleep:
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1. Lucid dreams
A lucid dream is when a person is aware they are dreaming, and may have some control over their own actions in the dream or even the characters and the environment of the dream.
This is different from simply having a passive memory of a dream, which can sometimes happen if we awake directly from REM sleep.
when a person recognizes he or she is dreaming while in a dreaming state and often manipulates events within the dream.”Read more at: http://phys.org/news202059647.html#jCp
Sound like Inception? It should, the screenplay was inspired by the phenomenon of lucid dreaming:
Click here to listen to a RadioLab podcast about Lucid Dreaming.
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2. REM Sleep Behavior Disorder
REM sleep behavior disorder (RBD) is in a sense the opposite of lucid dreaming. Affected patients lose the motor inhibition that is a typical feature of normal REM sleep, and regain the motor strength to “act out” their unconscious dreams. This is an uncommon disorder, and can be associated with underlying neurodegenerative disorders like Parkinson’s Disease.
So, during REM sleep our conscious minds and bodies are supposed to be switched off, while our subconscious brain performs a scandisk generating passive dreaming. If our conscious brain somehow switches on during this time we experience lucid dreaming. Of our bodies switch on, and we start unconsciously reacting to these dreams we have REM sleep behavior disorder. If both were to happen simultaneously, we’d be awake!
As far as infectious diseases go, prions are a relatively new discovery. While humanity has known about parasites since ancient times, bacteria since the 1660s, and viruses since 1898, the first prion protein was only isolated in 1984. Since then, we’ve gotten to know a little more about these proteins, and we’ve found that its novelty is by no means the most interesting thing about it. hh hh hh hh
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So what are prions?
Prions are basically the misfolded version of a normal protein, PRP or Protease resistant protein. In the vast majority of instances, the body has mechanisms that adequately deal with misshapen proteins. These get tagged for destruction by antibodies or intracellularly by specific molecular signals and lysosomes. However, prions are not your run of the mill abnormal protein. They are resistant to degradation and exhibit the unique characteristic of causing other normal PRP proteins to misfold, which in turn causes even more misfolding. In this sense, prions behave like protein zombies.
And like zombies, they don’t begin their existence as malevolent molecules either. Indeed this is one of the characteristics which differentiate prions from most other infectious agents such as bacteria or viruses, majority of which are inherently disease causing. Studies have shown that normal PRP has functions in sleep, memory, neural development, and possibly the maintenance of the myelin sheath that surrounds neurons. Indeed, a mutation of PRP causes a very rare disease (only 8 cases have been diagnosed as of 2005) called Familial Fatal Insomnia which leads to progressively worse insomnia leading to dementia, hallucinations, and eventually death.
Yes, complete inability to sleep kills.
hh The connection to Alzheimer’s
Until recently, the most notable examples of prion diseases in humans are Creutzfeldt-Jakob disease and Kuru. Although spontaneous CJD does rarely occur, both these diseases are usually caused by ingestion of infected material, ie, eating infected meat (beef) for CJD and cannibalism for Kuru. Both exhibit progressive dementia, memory problems, gait and movement disturbances, and other unusual symptoms like uncontrolled laughter, hallucinations, and personality changes. Pathologically, the disease causes patients’ brains to develop tiny holes, much like a sponge. Thus the name for the disease in cows, Bovine Spongiform Encephalopathy, literally translates “cow spongy brain disease”.
Brain of a CJD patient with multiple “holes”
However, over the past 5 years, research has shown that at least one major protein known to accumulate in Alzheimers disease, amyloid beta, behaves much like prions. Research conducted at UCSF showed that when mice brains are seeded with amyloid beta, after 300 days, the amyloid plaque is found all over the brain, not just the area seeded. A Yale university study in 2009 also showed that prion proteins of CJD interact with amyloid beta in some way to cause the dysfunction in neurons which lead to Alzheimer’s. Although there is no evidence that AD is contagious, it may open up new therapeutic avenues to think of its pathology as like that of prion diseases.
Amyloid plaques and Neurofibrillary tangles in Alzheimer’s disease
How Alzheimer’s spreads in the brain.
Indeed, last year, a British team accidentally stumbled on a discovery that antibodies designed to treat CJD were found to block Alzheimer’s disease. These antibodies, ICSM-35 and ICSM-18, blocked the interaction between the PRP prion and amyloid beta in mice brains, resulting in decreased hippocampal nerve cell disruption. ICSM-18 and ICSM-35 are presently undergoing human trials for the treatment of CJD. With this finding, it’s likely they will be tested for Alzheimer’s as well, and we, for the first time, might have an effective and specific treatment for this disease which affects roughly 20 million people worldwide.
To see just how significant any form of treatment might be, check out the facts and figures provided by http://www.alz.org below:
References:
Jucker M, Walker LC. Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders. 2011:70, 532–540.
Prusiner SB: A unifying role for prions in neurodegenerative diseases. 2012:336, 1511–1513.
When people of think of amnesia, they usually first think of the mysterious stranger in a soap opera, who shows up in town after an accident or traumatic experience, having forgotten their own identity, and the efforts that ensue to uncover the missing information.
Actually, in medical practice this type of “soap opera” amnesia is psychogenic, a so-called psychogenic fugue state, very different from the amnesia seen with organic neurologic disorders like head trauma or stroke.
TGA is a sudden onset of temporary anteriograde amnesia usually lasting lasting 4-12 hours. It is often triggered by an emotional event or sexual intercourse. During the episode, the affected patient is alert and lucid, cognizant of their own identity, but appears perplexed and may ask the same questions repeatedly. The exact cause is unknown. The recurrence rate is low.
More permanent anteriograde amnesia can be caused by:
Korsakoff’s psychosis is caused by thiamine deficiency, usually related to chronic alcoholism. Affected patients have permanent anteriograde amnesia, and so they live in the past, and confabulate (make up details) to fill in the gaps in their memory.
Caused by a disturbance of perception rather than an actual physiological change
– Altered body image (Ex: big buildings look same size as person’s own body)
– Distorted perception of size (micropsia, macropsia)
– Distorted perception of the shape of objects – Loss of spatial perspective (sense of time and space)
– Auditory or tactile hallucinations
AIWS generally affects a younger population and has several associated conditions. Migraine is the classic diseaselinked to AIWS, the distorted sensations can either begin before a migraine (aura or “warning”) or afterwards, and in younger patients can even occur without headache
Certain tests & imaging studies helprule out secondary causes: – urine toxicology screen
– monospot test(for mononucleosis)
–MRI brain – with and without contrast (to look for malignancy)
– EEG(to detect seizures or seizure-like activity)
Sounds scary, right? Well, good news is it’s not as bad as it sounds. Most patients who experience AIWS as children will outgrow the condition as adults. Patients should be monitored for worsening of symptom severity and frequency. If all studies are negative and the patient continues to improve clinically, then further evaluation and/or treatment is not needed. Bestmanagement for future attacks is focused on migraine prophylaxisand lifestyle modifications (healthy diet, regular exercise, adequate sleep).
Posted By Sidra Ghafoor, Drexel University College of Medicine Class of 2013
Charles Bonnet Syndrome affects 10-50% of patients with significant visual loss, who suddenly develop vivid, complex recurrent visual hallucinations, often “lilliputian” hallucinations (where characters or objects are smaller than normal), of faces, people, artoons, animals, or even trees and inanimate objects.
The syndrome is named after Swiss naturalist Charles Bonnet, who in 1769 described this phenomenon in his 89-year-old grandfather, nearly blind from cataracts in both eyes, but claiming to see men, women, birds, carriages, buildings, tapestries, physically impossible circumstances and scaffolding patterns
It is felt by some to be a visual release phenomenon – images generated by regions of the brain deprived of normal sensory input.
There is no known effective treatment, but symptoms usually resolves within a year or 18 months, and most patients are simply reassured to hear it is a normal phenomenon.
Watch a televised lecture by Dr Oliver Sacks entitled “What hallucination reveals about our minds”:
Click here for a link to a review of Dr Sacks’ book “Hallucinations”.
Click here to link an NPR story on Charles Bonnet syndrome entitled “Blind Man ‘Sees'”.
Other causes of Alice in Wonderland Syndrome are:
Neurology Update 