Recent study links marijuana use to structural brain changes

 

 

Post  prepared by Amanda Baker, Drexel University College of Medicine Class of 2014

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A study recently published in the Journal of Neuroscience by Harvard researchers have linked casual marijuana use to structural changes in distinct areas of the brain.

These areas, the nucleus accumbens and amygdala, and are largely involved in recognition of reward, motivation, fear, and memory.  In this study, the brain scans of 20 young adult casual marijuana users were compared to those of 20 young adult non-users.

While the results clearly demonstrated significant structural differences between the two groups, the structural changes have not been correlated with consequences in mental or physical functioning.  In other words, researchers aren’t entirely sure of the impact of these brain changes.

 

Casual marijuana use may damage your brain

The debate regarding the use of marijuana medically and recreationally is ongoing in the United States.

Although the Drug Enforcement Administration(DEA) categorizes this drug as Schedule I, “with currently no accepted medical use and a high potential for abuse”, many argue that there is, in fact, much benefit to medical marijuana, especially in comparison to other sedating pain medications.

This is reflected in 21 state laws which have legalized medical marijuana to varying degrees.

Last summer, Dr. Sanjay Gupta completed a documentary “Weed” highlighting the benefit of medical marijuana:

However, some states such as Washington and Colorado, have gone one step further by legalizing marijuana for both recreational and medical use.

Given the ongoing research on the effects of marijuana, perhaps this new study will call into question continued legalization of the most widely used recreational drug in America.

 

Click here to find out more.

 

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Cabin Fever

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Cabin fever  is a state of restlessness, depression and irritability brought on by an extended stay in a confined space or a remote and isolated area.

The term was first used to describe early U.S. settlers who experienced long winters snowed in alone in their log cabins – a well known example is the Montana winter of 1886-7 when snow fell every day from November through the end of February, cattle froze in place on the range, and ranchers ran short on coal, flour and wood.

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In 1915, polar explorer Sir Ernest Shackleton and his men made camp on a drifting ice floe in the so-called voyage of endurance for three months after their ship sank. The 28 men lived in crowded tents. Shackleton later wrote: “Day by day goes by, much the same as one another, We work; we talk; we eat.  …  The two subjects of most interest  …  our rate of drift and the weather.”

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The term has also applied to mental illness occurring on long oceanic voyages, after passengers and crew have endured long trips in small, cramped quarters below the deck of a ship

The mental anguish of cabin fever will often end in violence.  In 1959 a Russian at a Soviet Antarctic base murdered a colleague with an axe after losing a game of chess.  Following this, the Soviet authorities prohibited cosmonauts from playing chess!

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Probably the best known case of Cabin Fever affected author Jack Torrence in Stephen King’s novel and film, The Shining, while snow bound with his family in an old hotel.

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As the winter progresses, Jack becomes more and more unhinged, until he finally attempts to kill his wife and child.

What do you do if you think you are getting Cabin Fever (aside from trying to kill your wife an family)?  ……………  Get Out of the House if you can – for exposure to daylight exercise.  Maintain Normal Eating Patterns – try not to overindulge in junk food or skip meals altogether.  Set Goals – set daily and weekly goals, and track your progress toward completion.  Use Your Brain – although TV is a distraction, it is also relatively mindless, stimulating your mind can help keep you moving forward and reduce feelings of isolation and helplessness.

A New Spin on The “Founder” of Neurology

Jean-Martin Charcot (1825-1893) is regarded by most scholars to be the founder of modern neurology.

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Known to be an excellent clinical teacjer, he was a professor at the University of Paris for 33 years and was  associated with Paris’s Salpêtrière Hospital that lasted throughout his life, ultimately becomiwas known as an excellent medical teacher, and he attracted students from all over Europe. His focus turned to neurology, and he is called by some the founder of modern neurology.

Charcot took an interest in hysteria, a mental disorder with physical manifestations, which he believed to be the result of an inherited weak neurological system, set off by a traumatic event like an accident

He learned the technique of hypnosis to evaluate these patients, and very quickly became a master of the relatively new “science.”

He believed that a hypnotized state was very similar to a bout of hysteria, and so he hypnotized his patients in order to induce and study their symptoms.

Charcot’s work also included other aspects of neurology – he was first to describe the degeneration of ligaments and joint surfaces due to lack of use or control, now called Charcot’s joint. He discovered the importance of small arteries in cerebral hemorrhage.  He described hereditary motor and sensory neuropathy.

He died in 1893 in Morvan, France.

The new movie focuses on his relationship with one hysterical patient named Agustine,

Click here to find out more about this.

CJD – A downward spiral of depression into dementia and death

Post prepared by Dr Mariam Kemal, PGY-3 (Internal medicine), Monmouth Medical Center

Case History:

This 66 year old female had been living alone independently.  However, her neighbors became concerned when she had seemed more withdrawn than usual for about a month, and then stopped going out of the house and paying her utility bills.  Ultimately, one of them  noticed a dead cat in the house, and immediately called patient’s son who lived out-of- state, and he requested that she be admitted hospital.  At the time of her initial evaluation, she was depressed and had a urinary tract infection.  She was treated for the infection, and when she expressed suicidal ideation she was transferred to the psychiatric unit. While she was on the psychiatric unit she developed slurred speech, right arm clumsiness and and unsteady gait.   She was transferred back to the medical service and underwent a diagnostic evaluation.   Her brain MRI showed diffusion restriction in left putamen and caudate nucleus. Her EEG was also abnormal.  Her spinal fluid was ultimately positive for presence of Protein 14-3-3, indicating Creutzfeldt –Jacob disease.  She has progressed to a very debilitated state in just two week – Her speech was limited to a few intermittent slurred words, she was not able to walk and had diffuse myoclonic jerks. She was transferred to hospice.  Her brain was sent for autopsy to The National Prion Disease Pathology Surveillance Center which confirmed the presence of abnormal protease resistant prion protein (PrPSc), commonly identified as PrP 27-30, confirming the diagnosis of sporadic Creutzfeldt-Jacob disease.
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What is Creutzfeldt-Jakob disease?

Creutzfeldt-Jakob disease (“CJD”) is a rare brain disorder that causes rapidly progressive dementia with muscle twitching, leading to death within several months.

CJD usually affects older adults.


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It is caused by abnormal proteins called “prions” that infect the brain.

“Classic” CJD has been transmitted by infected organs during transplant surgery.

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“Variant” CJD (“mad cow disease”) has been transmitted by infected beef.

In addition to dementia and myoclonus, many CJD patients also exhibit behavioral change (including depression), balance problems, and sleep disturbance.

It is the presence of these unusual clinical features, and the rapid rate of clinical deterioration, that distinguish CJD from other dementias like Alzheimer’s disease.

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How is Creutzfeldt-Jakob disease diagnosed?

MRI imaging of the brain can show characteristic findings:

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The electroencephalogram (EEG) can show periodic complexes:

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The spinal fluid can show the 14-3-3 protein.

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However, a brain biopsy demonstrating spongiform change is still necessary to confirm the diagnosis in many cases:

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How is Creutzfeldt-Jakob disease treated?

Sadly, there are no treatments that can stop or cure the disease, and all affected patients die within several months.

Lytico-Bodig Syndrome, You Might Get it From Eating Bats

Posted by Daniel Rubio, Drexel University College of Medicine Class of 2014

“A man” obsessing over “bats”…

“A man” eating “bats”…


The patients above are displaying symptoms resulting from a disease known as Lytico-Bodig Syndrome (LBS), a neurologic disease resembling amyotrophic lateral sclerosis (ALS/Lou Gehrig’s Disease), Parkinson’s disease, and Alzheimer’s disease.  The country with the greatest number affected is the US territory of Guam.  In fact, between the 1940-1960 it was the leading cause of death among the Chamorro people, a tribe found on the island of Guam.  The afflicted were usually between the ages of 25-40 years of age.

What’s up with the bats?

Although yet to be proven, it is believed that the high incidence of LBS is due to the consumption of fruit bat, a cultural delicacy on the island.  These fruit bats feed on specific fruits containing high concentrations of an altered amino acid called beta-N-methylamino-L-alanine (BMAA). BMAA is a known neurotoxin and is believed to be the cause of LBS.  BMAA is a protein building block that is incorporated into neuronal proteins to produce an abnormal form that creates clumps with neurons resulting in their dysfunction and death.

I don’t eat bat though?

I addition to the high concentrations found in the fruit bats on the island of Guam, multiple sources have been proposed leading to BMAA exposure within the United States.  Certain bacteria in fresh and salt waters produce BMAA; and, fish and crustaceans will concentrate BMAA within their tissues when they consume the bacteria as part of their normal diet.  It is believed that human consumption of fish and crustaceans in at-risk areas might increase the incidence of neurodegenerative diseases, like Alzheimer’s, Parkinson’s, and Lou Gehrig’s.  This association has been seen in many areas within the United States, especially around the gulf regions and around large bodies of water.  Click here for more details about this.

Am I more lytico or bodig?

Presenting symptoms exist along the continuum of lytico-bodig.  Patients on the lytico spectrum present more like ALS/Lou Gehrig’s disease.  These patients have muscle wasting/atrophy and accompanying weakness, paralysis of mouth and tongue, and an inability to swallow resulting in choking to death.  Over time, paralysis involves the breathing muscles requiring mechanical ventilation to help the patient breath and to prevent choking on secretions.  Lytico patients remain aware of their deterioration.  The form of LBS is fatal in all cases.

On the other end of the spectrum, patients with bodig presentations look more like Parkinson’s disease and Alzheimer’s disease patients.  Bodig patients present with “freezing” with progressive immobility with loss of starting purposeful movement and loss of spontaneous movement.  Progressive dementia with loss of speech and irrational behavior, including violence and rapid fluctuations in mood, are common.  Over time, patients are left in stiff and immobile postures with inability to speak and swallow.

How would I know if I had LBS?

Currently Lytico-Bodig syndrome is diagnosed based upon appropriate history and physical exam by a neurologist.  Definite LBS is declared in post-mortem autopsy.  However, there is research being done to develop rapid tests using cerebral spinal fluid analysis.

What can I do if I have LBS?

Treatment is mainly supportive as is based upon symptoms present, whether it’s Parkinson’s, Alzheimer’s, ALS, or a combination of the three spectrums of diseases.   The more the symptoms resemble Lytico, the greater the mortality: in patients with predominantly lytico-type symptoms the disease is practically 100% fatal.

Synesthesia: Boy that word tastes good, huh?

Posted by Deepak H. Singh, MS IV Drexel University College of Medicine

Putting my intense desire to describe the mauve affect of a patient, or the loud shirt that a colleague is wearing aside, synesthesia is a fascinating phenomenon in which two or more senses in certain individuals are overlapped, meaning that the experience of both senses is connected in someway.

This has been described in terms of various different senses including forms such as grapheme-color synesthesia in which letters and numbers are perceived as colors, chromesthesia in which sounds are perceived as color, or lexical-gustatory synesthesia in which individual words are perceived as taste sensations in the mouth as alluded to in the title of this blog post.

Click here to find out more about word-taste synesthesia from the BBC.

Some notable supposed synesthetes to perhaps pique your interest are inventor Nikola Tesla, Muscians Eddie Van Halen, Billy Joel, Pharell Williams, and Actor Geoffrey Rush, among others.

This condition has long perplexed neuroscientists who are only touching the surface of the unique neural pathways that may account for the various experiences described by synesthetes.

One school of thought that has gained some traction is the concept of cross-activation, which is made possible by a failure of the physiological process of “synaptic pruning” that occurs in all of our brains during the initial developmental stages.  Synaptic pruning refers to a series of regulatory processes during which various axonal networks that were functional in one stage of development are outcompeted and subsequently eliminated as other synaptic connections become more frequently used as maturation occurs. In synesthetes  it is hypothesized that certain of these connections fail to regress leading to atypical connections between two sensory regions of the brain, thereby opening the door for some pretty vivid sensorial experiences. This, however, has only really held up for sensory regions directly adjacent to one another, as was demonstrated by fMRI studies showing significant brain activity in both the auditory cortex and the fusiform gyrus (responsible for color perception) in synesthetes while no such congruous activity was seen in age-matched controls. Similarly, in one study on lexical-gustatory synesthesia, the lateral sulcus (responsible for taste processing) was activated simultaneously with the auditory cortex in synesthetes.

Another prevailing hypothesis is the concept of “disinhibited feedback“. Normally, signals are travelling in both directions between the primary sensory regions of the brain and those that are involved in organizing that information, and feedback (both positive and negative) is constantly occurring to reconcile all of the different sensory input. If this balance were disrupted, however, it would be possible for signals encountered in the later stage of processing to influence those that were encountered earlier, resulting in the overlapping sensations that are perceived by synesthetes. This, too, may make more sense of the case reports in which individuals with temporal lobe epilepsy or individuals who have just experienced head trauma or stroke to “acquire” a synesthesia-like experience due to some disruption in those pathways, though no concrete studies have been done to test that theory.

Perhaps we’ll never know what is truly occurring at a neuroanatomical level that causes such a curious phenotype. In the meantime, looking at the accomplished list of puported “sufferers” of this condition, it may be worthwhile to pose the following question: which came first the synesthesia or the visionary?