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.
The debate regarding the use of marijuana medically and recreationally is ongoing in the United States.
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.
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.
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.”
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!
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.
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.
Jean-Martin Charcot (1825-1893) is regarded by most scholars to be the founder of modern neurology.
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.
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. <br/l>
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:
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.
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.
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?
We know that the strongest risk factor for developing dementia is old age.
However, we also know that dementia is not an inevitable consequence of old age.
Why do some older adults get dementia and others don’t?
Instead of looking for dementia risk factors, some researchers have turned the tables on this question, and looking at things that might be protective, reduce the likelihood of age related dementia.
This could translate into activities or behaviors anyone could use to lower their dementia risk.
The investigators designed a game called NeuroRacer in which the player drives a virtual car along a track and must respond to the appearance of specific road signs by pressing a button. The trick is that the player has to attend to one type of sign only, ignore the others, and continue “driving” all the while. Then, as the participants learned the game and improved their scores, the game gets harder and harder.
The study had 46 participants, aged 60-85, engage in 12 hours of the training over the course of a month. During that time, they vastly improved their performance, and at the end of that study they played just as well as 20-year olds. Furthermore, these gains in brain function persisted for more than 6-months, and more importantly weren’t limited to gaming – study participants also showed improved attention and working memory.
However, this study does demonstrate that older adults can still re-shape their brain connections, and also re-affirms that the old adage, if you don’t use it you lose it, also includes brain function!
Maybe it’s time to start playing chess or BrainAge regularly?
D-Lactate Encephalopathy and Periodic Ataxia
Posted by Michael Twomey, Drexel MSIV, Class of 2014
Remember that pain in your side during a long hard workout? That’s the buildup of lactic acid or L-lactate which is a way for your body to burn energy when it there isn’t much oxygen around (like when you think it’s a good idea to run 5 miles). This feeling, although uncomfortable, won’t make you loopy–it’s twin brother, however, has no such qualms.
D-lactate is just like normal old lactic acid, only completely different. In fact, it is the mirror image of the molecule that causes us such grief. For those of us who have forgotten organic chemistry, or would rather walk on broken glass than take such a torturous class, think
of it like a pair of gloves. L-lactate would be your left hand glove and D-lactate the right. They look like the same darn thing from a distance (made out of the same leather and thread, and stuffing), but no matter how you rotate them, you could never get them to match up.
Our bodies happen to be finicky. Like the 7 year old fussy eater we all know and (hopefully still) love, the human body can only make and break down L-lactate. Thus, under factory settings, we all have an undetectable level of D-lactate in our blood. Bacteria, however, are wired a bit differently (shocking, I know). Some can take the same sugars that we eat, turn them into D-lactate, and when those buggers are in your intestinal system–this form of lactic acid can enter our blood stream.
Lactobacilli (the bad guys)
It just so happens that high levels of D-lactate effects the brain just as much as it does the rest of our bodies. We aren’t exactly sure the why or how this compound acts on our central nervous system, but it can cause anything from making you unbalanced to putting a patient in a delirious state. Case reports show symptoms of sleepiness, hallucinations, clumsiness, blurred vision, disorientation, dizziness, lethargy, excessive irritability, and abusive behavior. All of which can last up to a few days! The gait can be very unsteady (ataxic) during each episode, and this syndrome is one of the causes of “periodic ataxia”.
To make the diagnosis these patients also had an elevated amount of acid in their blood (something normal Lactic Acid can do as well) and high levels of D-lactate.
So can you blame the next time you trip over the doormat on bacteria? Probably not.
Fortunately the only reports of this syndrome have been found in people with extensive small intestine surgery. It turns out that the bacteria who can make D-lactate tend to live in our large intestine where they almost never see large amounts of sugar. Normally our small intestine is long enough to absorb all of those nutrients and leaving them to digest your Mexican meal instead. People with short bowel syndrome, however, should be aware of this possibility and eat appropriately. Otherwise having meals high in simple sugars could cause you to end up in the hospital with some strange behaviors and a nice long course of antibiotics!
There are already more than 5 million affected patients, and Alzheimer’s is now the 6th leading cause of death in the US.
Caregivers spend an average of 70 to 100 hours per week providing care to an affected family member.
Alzheimer’s patients cope better in familiar surroundings. They get worse more quickly when socially isolated. It is more cost effective to keep affected patients at home for as long as possible, avoiding expensive residential care.
However, many caregivers need to go to work, and cannot be at home with their affected family member 24/7.
New programs using robots to provide social contact and even supervision for Alzheimer’s patients on their own at home may provide a cost effective solution to this problem.
Scotland’s National Health Service is putting robots into the rural homes of some dementia patients in a pilot scheme to help them to continue to live independently.
A relative or carer – potentially hundreds of miles away – can drive the machine around the house to check that everything is all right. The pair can also have a chat through a two-way video call system.
The robots are about 5ft tall, on wheels and have a TV screen instead of a head.
A relative or carer can connect to the robot with a computer from any location. Their face will appear on the screen allowing them to chat to the other person.
The operator can also drive the robot around the house to check that medication is being taken and that food is being eaten.
Ongoing studies are showing that robots can provide affordable personalized cognitive stimulation, motivation and companionship to dementia patients, and potentially keep them living independently longer.
Neurology Update 