Thursday, November 30, 2006

Chemobrain is real:

Researches have found out that the phenomenon of 'chemobrain'- a feeling reported by cancer patients of forgetfulness, confusion and disorientation after chemotherapy is not really imagined by the ailing patient. A team of medical investigators in Japan found the condition indeed is genuine and substantially affects cognition.

"The phrase "chemo brain" has come to be used by cancer survivors to describe
changes in memory, attention, concentration, and abilities to perform various
mental tasks that are associated with receiving chemotherapy treatments for
cancer. In neurology the effects are referred to as cognitive deficits or
declining neuropsychological functioning."

They have also found out the structural changes discovered are essentially reversible after some period of time. This means that after certain forms of chemotherapy, some patients could go into a "chemobrain type syndrome mode" for some time and then 'cognitively return' back to normal in time.

"They found that at one-year, patients treated with chemotherapy had smaller
volumes in cognitively sensitive areas, such as the prefrontal, parahippocampal
and cingulate gyri, and precuneus regions. However, at three-years post-surgery
there was no volume differences. That there were no differences between cancer
patients and healthy controls at any time point demonstrates that there is no
observable cancer-effect in cognitive deficits."

There is a growing hypothesis that the powerful drugs used to fight cancer are capable of diffusing through the blood-brain barrier, a protective sheath that keeps most harmful substances out of the brain. Many chemo drugs are made up of molecules small enough to breach the barrier it is thought. The publishers of this study have not made it clear that the breach of the blood-brain barrier could be the reason behind the structural changes seen in brain MRI before and after chemotherapy.

The study is published in the 1 January 2007 issue of CANCER, a peer-reviewed journal of the American Cancer Society. The following link give you a little more detail.

Not very ecstatic news:

Yes, they seem to have done yet another study on something that is obvious to most of us, but this one proves that using MDMA (3,4-methylenedioxy-N-methylamphetamine), most commonly known by the street names Ecstasy, E, X, or XTC just one time (even the first time) can damage the users brain leading to memory loss (in verbal memory retention tests), indications of subtle changes in cell architecture and decreased blood flow in some brain regions.

"We found a decrease in blood circulation in some areas of the brain in
young adults who just started to use ecstasy," said Maartje de Win, M.D.,
radiology resident at the Academic Medical Center at the University of Amsterdam in the Netherlands. "In addition, we found a relative decrease in verbal memory
performance in ecstasy users compared to non-users."

It is fairly well known that long-term or heavy ecstasy use can damage serotonergic neurons and cause depression, anxiety, confusion, difficulty sleeping and decrease in memory. However, no previous studies have looked at the effects of low doses of the drug on first-time users.

This means that even one time use of this drug is strictly a no-no if you want to look after your brain...

Read more here.

Wednesday, November 29, 2006

A million years hence and the brain in the vat:

I was browsing through an online Photoshop art contest and I came upon the category called "Humans In One Million Years". I looked at this one picture and immediately thought of the following lines by Rama (V.S. RAMACHANDRAN, a neuroscientist, is professor and director, Center for Brain and Cognition UCSD).
You can browse all of the entries under the category here or browse the entire collection here

Lets advance to a point of time where we know everything there is to know about the intricate circuitry and functioning of the human brain. With this knowledge, it would be possible for a neuroscientist to isolate your brain in a vat of nutrients and keep it alive and healthy indefinitely.

Utilizing thousands of electrodes and appropriate patterns of electrical stimulation, the scientist makes your brain think and feel that it's experiencing actual life events. The simulation is perfect and includes a sense of time and planning for the future. The brain doesn't know that its experiences, its entire life, are not real.

Further assume that the scientist can make your brain "think" and experience being a combination of Einstein, Mark Spitz, Bill Gates, Hugh Heffner, and Gandhi, while at the same time preserving your own deeply personal memories and identity (there's nothing in contemporary brain science that forbids such a scenario). The mad neuroscientist then gives you a choice. You can either be this incredible, deliriously happy being floating forever in the vat or be your real self, more or less like you are now (for the sake of argument we will further assume that you are basically a happy and contended person, not a starving pheasant). Which of the two would you pick?

The complete text of Rama’s article is here with some comments…

Hope you enjoy this...

Monday, November 27, 2006

Painting post with a little deviation into visual consciousness:

At first glance, this one seems to be a little more like an abstract portraiture. When I asked for comments on this picture, I got comments ranging from "It looks like the Lord Ganesh with his elephant trunks splayed all over" to "all I see splotches of bluish black paint". After that I told them to take about 10 steps backwards and then step sideways the painting such that you are looking at the painting from your left. They then said that the face of a man with an intense expression emerged from the solid blocks of paint on the canvas.
I know that the human brain 'fills in' a lot of detail for our visual senses when we look at an image. This is the reason why some people did not recognize this image immediately. Their brains were trying to piece together familiar image representations but could not find any from their memory repertoire - but as soon as the face emerges from the canvas through a little coaching, the brain fills in any additional details (please see details in a paper linked at the bottom of this post) that are required to make it look like a face and not see splotches any more.
See if you see the face in this painting...
This oil is titled 'Self - Portrait I' and was done about three months back and is 36 inches wide and 48 inches tall.

The following paper is an excellent review of visual consciousness (Highly recommended).
Just a reminder:

Just as we were carving up our turkeys and putting on the finishing touches to our Thanksgiving meals on Thursday last week, bombs carved up and put finishing touches on about 150 human beings and injured another 200 over in Iraq (all this happened in a single city - of course scores of people died in other areas also...). The stated reason for the war was that we were going in to find weapons of mass destruction.

Wednesday, November 22, 2006

Baylor College of Medicine cases:

I refer to this site sometime when I get bored with the usual and they have some pretty good neurology cases with complete differential diagnosis, discussion and references.
This months case seems a bit dicey and am not even too sure if this is a dyed in wool neurology case or a case of edema in the lower extremities caused by too much of sedentary activities (the patient is a computer programmer)...
Read on more about this case here. They will post the diagnosis over the month end.

Tuesday, November 21, 2006

Painting Post:

This one is titled 'Lady With Branch'. I liked the fact that this painting was accentuated by dabbing appropriate amounts of paints against a bare white canvas enhancing the silhouette of the figure... I did not fill in the bare portions of the canvas at the end. Just decided to leave it the way it was...
Painting Post:

The following is an oil I did entitled 'Mugshots on grilled cheese sandwiches - new trends in religiosity'. I completed this in about a month early this year.
Again, like most of my paintings, this one is 48 inches long and 36 inches wide. This is meant to be a commentary on the current trend of finding religious icons in grilled cheese sandwiches and selling the same on e-bay for thousands of dollars... What were the seller and buyer thinking? Reminds me of a fad that happened about 10 years ago in India when stone idols of Ganesha (a Hindu god) suddenly started drinking milk from devotees cups... This sure is an opium for the masses...
Still waters STILL run deep:

Beneath thin veneers of cultivated sensibility lies raging undercurrents of pent up bigotry held in check by social pressures and lawsuits. OK, what am I spouting here now???
I am a big fan of the 'Kramer' character in the 'Seinfeld' show, but a recent tirade by Mr. Michael Richards onstage that both forth in full resplendence his innate feelings towards ingrained dispositional representations of skin color is worth mentioning here. The video of the incident is even more shocking and it really shows what a lot of ordinary (looking) folks around us have on their minds and how it all comes spewing out when they are pushed just little bit. In this case all that was required to trigger this amazing dispensation was a heckler in the crowd.

Monday, November 20, 2006

Out of Body experiences triggered by electrical simulation of the angular gyrus

Yet another notch for science. We have all read about mystical sounding abnormal 'out of body' experiences where people seem to inhabit a non-corporeal self and seem to look down upon their own bodies from a position outside their body. Rational explanation for a lot of this could not be unearthed and it was thought that either these people were faking it or these people were closer to some superior force. Some people were just waiting for a rational scientific explanation. Looks like the people who were waiting just got it...

Dr. Olaf Blanke, a neurologist at the École Polytechnique Fédérale de Lausanne in Switzerland reported in the Sept. 21 issue of Nature magazine of cases of women who sensed a shadow person behind her on electrical simulation to certain parts of the brain.

As we know the angular gyrus in the temporal parietal junction forms one of the higher association areas for senses like vision, sound and touch. Located behind the somatosensory strip and ventral to the primary visual areas with inputs from the speech and sound areas, it is possible that this area could provide a representation for our 'self' in a rudimentary form (in the same sense as one gets a feeling for a 'phantom limb'). On electrical simulation to this area, people have reported seeing or feeling detached from the corporeal self and have also found to experience intriguing behavior.

"There is nothing mystical about these ghostly experiences, said Peter Brugger, a neuroscientist at University Hospital in Zurich, who was not involved in the experiments but is an expert on phantom limbs, the sensation of still feeling a limb that has been amputated, and other mind-bending phenomena.

“The research shows that the self can be detached from the body and can live a phantom existence on its own, as in an out-of-body experience, or it can be felt outside of personal space, as in a sense of a presence,” Dr. Brugger said. "

The woman replied that she had a weird sensation that another person was lying beneath her on the bed. The figure, she said, felt like a “shadow” that did not speak or move; it was young, more like a man than a woman, and it wanted to interfere with her.
When the current was turned off, the woman stopped looking to the right, and said the strange presence had gone away. Each time he reapplied the current, she once again turned her head to try to see the shadow figure.

When the woman sat up, leaned forward and hugged her knees, she said that she felt as if the shadow man was also sitting and that he was clasping her in his arms. She said it felt unpleasant. When she held a card in her right hand, she reported that the shadow figure tried to take it from her. “He doesn’t want me to read,” she said.

Because the presence closely mimicked the patient’s body posture and position, the doctor performing the test concluded that the patient was experiencing an unusual perception of her own body, as a double. But for reasons that scientists have not been able to explain, he said, she did not recognize that it was her own body she was sensing

Read on more here.

Painting Post:
Finally I managed to photograph some of my oils over the weekend and am planning on slowly posting them up here.. I am not the greatest at photography. I laid out the painting on a wooden deck on our backyard and took a snapshot (tried my best to not take the wooden rafters, but in a couple of cases they do show through)...

The following was an oil I did entitled 'Yearning - A tribute to Leonardo'. I completed this in about a month in November of last year.
The painting is about 48 inches long and 36 inches wide.

Friday, November 17, 2006

An imaginary journey up Jack’s ventricles

As I attempt to continue my armchair explorations into neurology, I am slowly realizing that unless I have a good idea of the various neural substrates and their spatial existence within our heads, it may be very difficult for me to understand where the structures are in the first place and secondly, how they are interconnected. With this in mind, I modified an elegantly laid out thought experiment in one of the books that I was reading (Neuroanatomy through Clinical Cases by Hal Blumental from Yale) and thought that you might enjoy this piece.

(It might be useful to use this diagram as a guide as you go through your journey)

It is basically a thought experiment where I am a scuba diver with a powerful flashlight on a mission to find the hippocampus (that elusive organ that is supposed to orchestrate our short and long term memories. The same thought experiment allows me to miniaturize myself such that I would be able to pass myself though a syringe used for a lumbar puncture on one of my close friend Jack who has volunteered to sit through my explorations. Included in my survival kit is also a miniature copy of Grey’s anatomy that will help me navigate my way through some of those tough sounding Latin named structures that I am going to encounter along the way – hey, we all need a Rand McNally’s when we go on a long exciting trip, don’t we? So here goes…

OK, that minitaturization hurt a little, but I was happy to pass easily through the lumbar puncture syringe into the subarachnoid space of Jack’s lumbar cistern passing through the skin, subcutaneous tissues, the hard interspinous ligament, through the tough dura mater and finally into the cerebrospinal fluid in the subarachnoid space. As soon as I was released into the cerebrospinal fluid, I stretched my legs and hands and looked around me to try and learn what was going on… Instinctively I notice that I was placed above the vertebral body S1 between L3 and L4. I also notice that I am bounded internally by the pia mater and externally by the arachnoid. As I start to swim in the cerebrospinal fluid, I start to notice a lot of wispy spiderweb like protrusions called the arachnoid trabecula from the outer arachnoid wall that seem to swim and sway in the cerebrospinal fluid and some of them even reach out and touch the pia mater. Carefully avoiding the spiderweb like protrusions, I use my flippers to swim upwards a little bit. I look up and I see wondrous rope like filaments descending all around I am somehow reminded of a horse’s tail. The tail seems to sway in the cerebrospinal fluid all the way into the lumbar cistern. I understand that I am looking at the cauda equina. Looking upwards and in front of me, I see a gleaming whitish pink tube like organ through the translucent pia and look at the conus medullaris portion of the spinal cord. I swim around the cord a little bit trying my best to avoid all of the horse tail like strings and see some of the nerve roots entering and exiting the spinal cord. The ones entering the spinal cord seem to be sensory nerves from the dorsal side (Jack’s back side) and motor nerves seem to be exiting on the ventral side of the whitish cord.

I make my way up, swimming against the flow of the cerebrospinal fluid for quite a while until I see a large opening up above me. It seems to be about the level of Jack’s mouth and realize that I am looking at the foramen magnum (a large ring shaped entrance to the cranial cavity). It is a bit foreboding as I seem to be heading into a large chamber of some sort and realize that this is the Cisterna Magna. I look up and see the ventral aspects of the cerebellum that looks like grayish pink structure with lots of little goose bumps all over… Below me I see that the spinal cord has given way to become the medulla. I also realize that the reticular formation forms some part of the floor beneath me if I stand here… I swim around the whitish pink cord and am fascinated by looking at the pons on the opposite side. I also seem to have fallen into the Pontine cistern on the other side. I quickly extricate myself from the Pontine cistern and come back to the cisterna magna and notice that there is another ventricular structure around me to either side. On either side of me, I can see the lateral foramina of Luschka. In fact I can slide down the walls of this foramen, but decide against it as I have more interesting things up there and let’s not forget, I am in search of the hippocampus. I decide to swim up against the dorsal side of the medulla and as soon as I come up a little above the cerebellum I notice the midline foramen of Megendie. The cerebellum still stretches on above me… a pulsating greyish mass that seems to be busy calculating coordination, gait and other higher motor functions. Without stopping at the foramen of Megendie, I decide to keep swimming upstairs… The force of the cerebrospinal fluid seems to be especially strong now and I force myself upward and notice that I have entered a large cavity and realize that this is the fourth ventricle that I am in…. I stop swimming and slowly land on the ventral floor of the fourth ventricle. Rostrally, I see the pons up ahead and caudally, I see the medulla. You must realize that I am standing perpendicular to Jack’s upright posture. (if I wanted to shoot out of his body, I would come head first out of the lower portion of his head at this time – just to give you a visual of where I was) Dorsally, the roof seems to be the cerebellum, with the large cerebellar peduncles on either side. I look at the miniature copy of the Grey’s anatomy that I am carrying and notice that the floor is also called the rhomboid fossa (containing important structures like the facial colliculus and the sulcus limitans). Parts of the floor rostrally also seem to be colored bluish grey and on looking it up is the locus ceruleus, which owes its color to an underlying patch of deeply pigmented nerve cells, termed the substantia ferruginea. I turn my headlight again rostrally and put it on high beam and realize that now I have come to a very narrow passage that I doubt that I will be able to cross. I start swimming upwards and with great difficulty clamber my way through a narrow tunnel called the cerebral aqueduct of Sylvius. The rush of the cerebrospinal fluid at this portion is really strong and I had to use all of my energy in staying my course at this point in time. I swam some of the way and walked some of the way as the tunnel seems to gradually slope with an upward trajectory. I also notice that there is a substantial grey matter at this point in time and slowly understand that I am crossing the periaqueductal grey portion of the midbrain (an important descending pathway which can be instrumental in inhibiting pain signals from the spinal cord). Clambering out of the tunnel, I thought that I could relax for a bit, but I seem to be immediately pulled down and start to sink to the depths of another cavity – the third ventricle. As I am traveling down the third ventricle, I look to my left and right and notice that I first pass the walls of the thalamus and then the walls of the hypothalamus. The third ventricle seem be bounded by the thalamus and hypothalamus on the left and the right. I also notice that the two thalami seem to be joined tighter at the interthalamic adhesion midway along the third ventricle.

At this point I stop swimming, look up and notice two parallel white arches running along the roof of the ventricle and realize that I am looking at parts of the fornix running over me. This is really exciting! I also notice that there is a profusion of capillary like vessels separated from the subarachnoid space by pia mater. Liquid seems to be filtering through ependymal cells (a type of neuroglia) from blood to become the cerebrospinal fluid that I am swimming in. I now realize that I was seeing this all along my way except along the narrow walls of the cerebral aqueduct, but only now did I begin to notice this. Looks like the cerebrospinal fluid is being made all along the ventricular system. I look behind me and notice the pineal and the suprapineal recesses on the caudal end of the third ventricle. I decide not to go the caudal end, but I seem to have two ways to go forward or rostrally, I can either swim upwards entering one of the two narrow tunnels that I see there or I can swim forward (rostrally) the third ventricle and see if there is anything out there that will lead me to the hippocampus. I first decide to swim straight ahead (rostrally). No luck. I seem to have come up against a dead end of some sort, but I notice that I can touch the supra optic recess (above the optic chiasma – where Jack’s optic nerves birfucate), and the infundibular recess (above the pituitary stalk). I know that the hypophysis is somewhere at the end of the infundibular recess, but I have other things to do… I also notice that walls of the hypothalamus extend all its way down here also. Well, now that I have had no luck, I decide to swim back up and squeeze myself through the tunnel to my right. On consulting Grey’s I find that I am entering the right foramen of Monro. Just as I am entering this new tunnel, I pause and look around me and I notice that I am standing on the anterior commissure (a bundle of white fibers, connecting the two cerebral hemispheres across the middle line) with my left hand up on the fornix and my right hand on the walls of the thalamus. I swim my way up this passage and find myself in a larger chamber – in fact one of the largest chamber that I have been in so far. Well, this is it – it is the right lateral ventricle. I start to swim forward in this cavity to find my way around a little better and I reach the rostral or anterior end of the lateral ventricle. This is called the anterior horn. Looking up, I see a bunch of white fibers running in close formation and recognize that as the corpus callosum – that great highway of fibers that connect the two hemispheres. I also realize that I am deep in the frontal lobes of Jack’s head. The floor here seems to be the head of the caudate nucleus.

I then decide to turn all the way around and swim to the other ends of this great chamber and realize that in reality this big cavity is made of three large horns, the anterior or the frontal horn that I just ran into, the posterior or the occipital horn and the inferior or temporal horn located lower down in the temporal lobes. I am sure that I will be able to find the hippocampal structures somewhere here. As I swim back I feel like I am being sucked into the foramen on Monro and have to swim quite strong against the current of the cerebrospinal fluid that is draining into the third ventricle. I seem to be in the body of the lateral ventricle now… I look to my right and see a translucent wall of membrane called the septum pellucidum. The septum pellucidum is located in the midline of the brain, between the two cerebral hemispheres. It is attached superiorly (above), anteriorly (in front), and inferiorly (below) to the corpus callosum, the large collection of nerve fibers that connect the two hemispheres. Inferiorly and posteriorly (in back), it is attached to the anterior part of the fornix. I shine my headlight through the septum pellucidum and look into the further reaches of Jack’s left lateral ventricle. To my left, I see a huge grey mass bulging into the walls of the lateral ventricle and realize that this is the body of the caudate nucleus. I also notice that I am able to make out the outlines of part of the thalamus, the choroids plexus and the fornix from my vantage point in the body of the lateral ventricle. I decide to keep swimming forward and presently find myself in the posterior horn of the lateral ventricle. Now I am in close proximity of the occipital lobe but still no sign of the hippocampus. I still notice that on looking up, I can see the great fibers of the corpus callosum running silently overhead carrying all of that important information between the hemispheres. I reach a dead end here also and then turn right around and am planning on heading back home when I lose my step and fall headlong into a long curvy descending passageway down and slowly realize that I am falling down the steep slope of the temporal horn of the lateral ventricle.

Luckily I do not hurt myself and manage to gather myself and stand up and look around. Upwards I see nothing but the white of the sky and realize that I am staring at Jack’s right cerebral hemisphere inside the temporal lobe – the seat of his higher thinking and memory. Anteriorly, along the median, I see the stria terminalis. The stria terminalis extends from the region of the interventricular foramen to the temporal horn of the lateral ventricle, carrying fibers from the amygdala to the septal, hypothalamic, and thalamic areas of the brain. It also carries fibers projecting from these areas back to the amygdala. It participates in anxiety and stress responses. I also notice that I can see the tail of the caudate nucleus upfront. I turn my head caudally and notice the amydaliod nucleus towards the terminal end of the inferior horn. OK, now where is the hippocampus. I look down and cannot seem to believe my eye.. There in a row I recognize the fimbria (a prominent band of white fibers along the medial edge of the hippocampus) the hippocampus itself and the collateral eminence (elevation along the floor of the posterior part of the temporal horn of the lateral ventricle, lateral to the hippocampus caused by the deep collateral sulcus). I realize at this point that I am standing on the hippocampus!!!!

Now I need to find the shortest way out – but that is another story.

Wednesday, November 15, 2006

Nanotechnology promises new hope for Glioblastoma multiforme (a deadly brain cancer):

Glioblastoma multiforme (GBM) is the most aggressive form of the primary brain tumors known collectively as gliomas. These tumors arise from the supporting, glial (Glial cells provide physical and chemical support for neurons and make up about 90 percent of all the cells in the brain) cells of the brain during childhood and in adults. These growths do not spread throughout the body like other forms of cancer, but cause symptoms by invading the brain. Untreated, GMB’s are rapidly lethal and kill in about a year.

This is also known as "octopus tumors" because of the manner in which tendrils of malignant cells can extend into surrounding healthy brain tissue. As the term "multiforme" suggests, malignant cells can take on a wide variety of different shapes, making detection difficult until the tumors become quite large.

The area of the brain first involved by the tumor influences the first symptoms of GBMs. Progressive weakness, speech or visual loss occurs when "eloquent" brain regions are involved. More "silent" areas of the brain allow the tumors to become large before symptoms arise. In this case increased pressure in the head produces headache and rarely, visual loss from swelling of the optic nerves. The tumors also can irritate the brain, causing epileptic seizures. Rarely, spontaneous hemorrhage into the tumor yields a stroke syndrome, with the sudden development of a neurological deficit.

The tumor can be imaged by contrast-enhanced MRI scan. Progressive growth of the lesion on serial MR scans differentiates tumor from stroke. A PET scan showing increased uptake of glucose can also help separate a diagnosis of tumor from stroke. An open or needle biopsy provides tissue for microscopic diagnosis.

Striking some 18,000 new victims in the United States every year, the disease is always fatal, usually within six months of onset. Surgery and conventional radiation therapies may prolong life for up to a year, but cannot stop the tumors from continuing to spread throughout the brain. There are anticancer drugs that show promise against glioblastoma multiforme tumors, but getting these drugs past the blood-brain barrier has proven to be a major challenge.

A collaboration of researchers from the Lawrence Berkeley National Laboratory and the Children's Hospital of Oakland Research Institute (CHORI) have demonstrated, through in vitro studies, the potential for nanosized synthetic particles of low density lipoprotein, or LDL, to be used as a safe and effective means of delivering anticancer drugs to glioblastoma multiforme tumors.

The research team have now identified LDL receptors on glioblastoma multiforme tumor cells that can serve as specific molecular targets. In addition as the LDL receptors are sparse in normal human brain tissue but elevated on the tumor cells, the synthetic nano-LDLs can deliver drugs to the glioblastoma multiforme tumors while sparing healthy cells.

Read on more about this exciting new application where technology and neuroscience come together at

The related paper is here.

Tuesday, November 14, 2006

The mystery that is Morgellons disease: is it really a neuropsychiatric disorder disguised by dermatologic symptoms?

With the recent news reports on Morgellons disease, I got to thinking about this poorly understood disease. There is really nothing known about Morgellons, but I am surprised that most of the research into this disease is conducted from a dermatological standpoint. Sure, this is a skin related disorder with most, if not all, symptoms being dermatologic. However, many doctors believe that this is actually a neuropsychiatric disorder in origin.

The following is a great article on this topic.
So what are your thoughts?
Dyslexia or 'difficulty with lexicon' IS a genetic disorder and NOT because the person is un-intelligent :

This could be news that is a little dated, but the following paper from Haiying Meng, Jeffrey Gruen et. al. of the Yale University School of Medicine talks about the isolation of a gene that is responsible for dyslexia in human beings. Dyslexia or 'difficulty with lexicon' is a neurological disorder that effects between 5-17% of the population of the United States (depending upon the diagnostic criteria used). Usually when children of the age of 10 or 11 fail to develop the necessary markers with respect to reading or writing, they are labeled unintelligent. It is clear that they are as intelligent as the rest of us. Now it has been proved that dyslexia is caused due to a missing nucleotide (also called a single nucleotide polymorphism or SNPs as they are called in genetic parlance) in the DCD2 gene. The DCD2 gene is also known to be highly active in areas of the temporal cortex that are thought to be used a lot in reading and writing. People who inherit variations in this gene use less efficient methods to master skills like reading and writing (leading to the rest of us labeling the child/person un-intelligent). It is also thought that the less efficient methods that the brain uses to compensate for the deficiency produced by the SNP leads to a different rewiring of the brain during the most plastic stages of an individuals life (the first 10-12 years of life). This means that if the implicated gene can be identified in babies early on, then they can be put on specifically structured training programs that will take advantage of a infant brain's inherent plasticity to re-rewire itself in order to expose better reading and writing skills. As we know the plasticity of the brain reduces (but never dies) as the individual grows older, therefore the key here would be to get the kid into a training program as soon as the generic insufficiency is detected.

My view is that much more research will be needed in the following areas though -
  • Content of training programs to make the brain rewire
  • Proof that the rewiring does indeed result in better reading and writing skills.
I am sure that Professor Jeffrey and his team have this and a lot more of stuff like this on their brains...
Side effects of antidepressants that seem to help diabetics :

Research from Eli Lilly suggests that Serotonin-norepinephrine reuptake inhibitor (SNRIs), a medication which selectively inhibits the reuptake of both serotonin and norepinephrine and used mainly as an antidepressant has very significant advantages in alleviating diabetic peripheral neuropathy . High levels of sugar in patient's blood over long periods of time could lead to complications involving multiple parts of the body. One additional complication that diabetic patients deal with, is pain in the peripheries (the hands and legs). This happens because of damage to nerves resulting in a)loss of sensation b)tingling pain or sharp pain (depending upon the type/extent/morphology of nerve damage) - more commonly referred to in medical fields as neuropathy. In their paper ( Duloxetine vs. placebo in patients with painful diabetic neuropathy), authors Goldstein et. al. demonstrate that Cymbalta® (duloxetine) at the rate of 60 or 120 mg/day showed a 50% reduction in pain for peripheral neuropathies in diabetic patients. They also show that this medication does not work against numbness or tingling pain or work towards any meaningful regeneration of nerves, rather it just reduces the pain in peripheral organs and extremities. The authors do not do a great job in explaining hoiw it does this though… (or maybe I have not done a great job of understanding it...) As a side note, Cymbalta® (duloxetine) is also approved for major depressive disorder and is believed to work by enhancing the effectiveness of two chemicals, serotonin and norepinephrine, which are involved in regulation of emotion and pain in the brain.
Let there be light and there was ....

The optic nerve conveys the sensory information gathered by the retina of the eyes to the visual cortex in the brain through a pretty complicated pathway. Now what happens when part of the optic nerve has degenerated or atrophied due to diseases like glaucoma (Early signs of glaucoma occurs when passages that filter and exchange fluid within the eye are blocked, internal fluid eye pressure to increase. If left untreated, the increased pressure can cause permanent damage to the optic nerve) or due to other genetic causes. The optic nerve axons do not have the power to automatically regenerate and repair itself after an injury of this nature.

Researchers at the Benowitz lab at Harvard Medical School (Drs. Steven Leon and Yuqin Yin) discovered that producing an inflammatory reaction in the eye causes macrophages to secrete proteins (hereinafter referred to as MDPs or Macrophage Derived Proteins) that enable retinal ganglion cells (RGCs) to survive axon damage and regenerate their axons through the optic nerve.

"Dr. Yin developed a cell culture model of the adult retina and discovered that axon regeneration requires 3 components: a low molecular weight factor that is constitutively present in the eye, elevated intracellular cAMP, and a protein that is secreted by macrophages.

"They found out that the carbohydrate mannose helps fulfill the low molecular weight criteria. They also found that an MDP called oncomodulin displays a high affinity for binding to cell surface receptors on RGCs. When this was delivered through slow release microspheres that elevated intracellular cAMP in RGCs, the end result seems to be dramatic axon regeneration of a mature optic nerve (of course this is a mouse model, but we seem to be fairly successful at replicating things like this onto humans). This has a lot of implications to people who have chronic blindness as a result of optic nerve damage following glaucoma based elevated eye pressure. From ""

"When oncomodulin was added to retinal nerve cells in a Petri dish, with known growth-promoting factors already present, axon growth nearly doubled. No other growth factor was as potent. In live rats with optic-nerve injury, oncomodulin released from tiny sustained-release capsules increased nerve regeneration 5- to 7-fold when given along with a drug that helps cells respond to oncomodulin. Yin, Benowitz and colleagues also showed that oncomodulin switches on a variety of genes associated with axon growth. Benowitz, the study's senior investigator, believes ncomodulin could someday prove useful in reversing optic-nerve damage caused by glaucoma, tumors or traumatic injury. In addition, the lab has shown that oncomodulin works on at least one other type of nerve cell, and now plans to test whether it also works on the types of brain cells that would be relevant to treating conditions like stroke and spinal cord injury.

Please see a pdf handout at the following site:
Papers from my master’s thesis published:

I finished my masters about seven years ago from Penn State. Over the weekend on a whimsical note, I was doing a cursory search on the internet for any references to the work I had done as part of my masters.
I had not expected to get any results whatsoever - but I was pleasantly surprised to see the following seven papers published in the journals and cnoference proceedings and thought I should share this with you...

Maybe I should have pursued on... (who knows?)

"Love-wave-based ice sensor"
Sunil Gangadaran, Vasundara V. Varadan, Vijay K. Varadan, K. A. Jose, and Massood Z. Atashbar
The Pennsylvania State Univ. (USA) Proceedings of SPIE -- Volume 3673 Smart Structures and Materials 1999: Smart Electronics and MEMS, July 1999, pp. 287-293
This paper has a better abstract here.

Love wave surface acoustic wave sensor for ice detection on aircraft.”
Vasundara V. Varadan, Sunil Gangadharan, and Vijay K. Varadan
The Journal of the Acoustical Society of America -- October 1999 -- Volume 106, Issue 4, p. 2269

"Wireless IDT ice sensor"
Jose, K.A.; Sunil, Gangadharan.; Varadan, V.K.; Varadan, V.V.,
Microwave Symposium Digest, 2002 IEEE MTT-S International, Volume: 2, 2002, 655pp.

"Wireless surface acoustic wave based humidity sensor"
M.Z. Atashbar, S. Gangadharan, V.K. Varadan, V.V. Varadan and R. Hollinger
SPIE's International Symposium on Micromachining and Microfabrication, 20-23 Sept., Santa Clara, USA, Proceedings of SPIE Vol. 3876 (1999).

"Wireless surface acoustic wave ice sensor"
K. A. Jose, S. Gangadharan, V. V. Varadan, and V. K. Varadan
212 Earth-Eng. Sci. Bldg., Penn State Univ., University Park, PA 16801
The Journal of the Acoustical Society of America -- November 2000 -- Volume 108, Issue 5, p. 2599

Perturbation theory for attenuation of a surface acoustic wave employed in my thesis also gets mention here. (Section 7 in the paper and reference 28)

I found the following conference papers also that I had worked on...

-V.K. Varadan, V.V. Varadan, S.Gangadharan, J.A. Kollakompil, and M.Z. Atahsbar
“Strain based SAW Accelerometer”
SPIE’s 6th Annual International Symposium on Smart Structures and Material, California USA, 1-5th March (1999).

-V.K. Varadan, V.V. Varadan, S. Gangadharan, J.A. Kollakompil, and M.Z. Atahsbar
“Love-wave ice sensor”
SPIE’s 6th Annual International Symposium on Smart Structures and Material, California USA, SPIE Proceedings Vol. 3673, pp. 287-295, 1-5th March (1999).
Virtual Reality phantom limb eases pain for amputees...

It was bound to happen sooner or later. After mirror therapy (citation below) to treat phantom limbs, it seems that they have finally perfected a technique to treat this condition using virtual reality...
Read on more at

From the Glaxo Wellcome page I got this information that explains the malady a little better..

"Phantom limb pain – pain appearing to come from where an amputated limb used to be – is often excruciating and almost impossible to treat.After amputation of a limb, an amputee continues to have an awareness of it and to experience sensations from it. These phantom limb sensations are also present in children born without a limb, suggesting that perception of our limbs is 'hard-wired' into our brain and that sensations from the limbs become mapped onto these brain networks as we develop.

If phantom limb sensations are normal then so too, alas, is phantom limb pain. This occurs in a majority of those who lose their limbs. In fact, limbs do not need to be lost; it also occurs in conditions in which the brain is disconnected from the body, such as peripheral nerve injuries and after spinal cord injury, when an area becomes insentient (and usually paralysed).

"Evidence that stimulation of the motor cortex (the area that controls movement) can reduce phantom limb pain has been around for some time. Perhaps more surprising was a trial by Ramachandran and Rogers-Ramachandran . They asked people with amputations of the arm and phantom limb pain to place their arms inside a mirror box so that they saw their remaining arm mirror-reversed to look like their amputated one. When they moved their remaining arm in the box they were 'fooled' into thinking they were moving their amputated one, and their pain was reduced. Although this has proved less effective in some subsequent trials, it did suggest that phantom limb pain might reflect a loss of motor control to the limb, as well as loss of sensory input from it.

More recently the mirror box has been used with some success in pain that is not due to sensory loss. In fact, a box may not be required. In phantom limb pain due to a peripheral nerve injury (brachial plexopathy), the authors have shown that merely training patients to imagine their paralysed arms moving in relation to a moving arm on a screen in front of them can relieve phantom limb pain.

Tuesday, November 07, 2006

The Macaca's might:
I am sitting up watching the results and there is a chance that the macaca senator might make it...
Sorry to keep bringing up politics here, but wins like this will be a significant setback to this great country from achieving intelluctual progress as fast as we could expect and limit equality...
Still praying...

Sunday, November 05, 2006

Pathological laughter or crying (PLC)

I am always fascinated by behaviours that seem to be outwardly strange and dubbed by people as 'off their rockers', but have an explanation that involve a very logical interplay between various neurological substrates. PLC (Pathological laughter or crying) is one of them. I ran into this just as I was about to dump one more of the endless journals that my wife gets (this one was proceedings of the Mayo Institute) and that is when I happened to eye an article on uncontrolled laughter/crying... I decided to read on and did some more poking around on the web and I wanted to point out to this eminently readable paper at this location. Seems to be a very good logical explanation for this seemingly crazy behaviour... Please read if you get a chance. I will post more on this after I read up a bit more...

Wednesday, November 01, 2006

Scoop on the macaca senator
Not too sure if you read my previous post about a senator from Virginia who casually insulted an Indian reporter by calling him a 'macaca'.. Well, here is the rest of the story about this senator:

-He keeps a Confederate Flag in his office
-He opposed martin Luther King’s birthday
-He keeps a noose in his office (is it to remind him of lynchings - not too sure)
-He has signed into law “Confederate Day” without once mentioning slavery...

It also seems like he just cant get out of the eyes of the press. This morning on metro NY (a free newspaper in NYC), I saw a couple of photograps of his staff heckling a web reporter out of a campaign stop he had made and it sure looked ugly.

Read on more here here and here...