Neuropathic Pain And Brain Inflammation

Today's post from medicaldaily.com (see link below) is an important one for neuropathy patients, who have trouble explaining the parameters of their pain to doctors, who then have to prescribe the appropriate pain medication. It's not their fault: neuropathic pain is notoriously difficult to quantify and the clichéd scales of 1 to 10, rarely reflect the true nature of nerve pain. This article talks about a breakthrough which in the future will be able to much more accurately match the medication to the extent of the pain. It will be measured by means of brain scans which will measure the neural inflammation in the area of the brain responsible for pain signals. Medicine prescription will become less a question of 'suck it and see' and more based on accurate levels of pain, which can only be a good thing for neuropathy patients who often end up as guinea pigs in the search for pain relief.

Chronic Pain Patients Show Patterns Of Brain Inflammation, Setting Stage For Objective Pain Scale
Jan 12, 2015 02:59 PM By Chris Weller


One day scientists may be able to figure out which pain pills you should take based on nothing but a brain scan. Intel Free Press, CC BY-SA 2.0

“On a scale of 1 to 10, how bad is the pain?”

That question has been asked in a variety of settings for an equally colorful range of afflictions. That’s because doctors, despite 76 million Americans having had suffered from chronic pain at one point or another, don’t yet have a standardized scale for measuring pain — after all, what registers as a 6 for you may be a 9 for someone with a lower threshold. Now, a new study finds that a standardized scale may be within reach, and neuroinflammation, of all things, is here to help.

Researchers from Massachusetts General Hospital collected data on 44 subjects, 19 with chronic lower back pain and 25 who were pain-free. Specifically, they performed scans on the brain’s thalamus, a region that, among other things, is responsible for signaling pain. Using a drug that shows up in contrast on the scan when it binds with a particular protein — known as a translocator protein (TSPO) — they could see how chronic pain correlates to inflammation in the brain, which the protein illuminates in the thalamus.

The findings are significant because they offer a future of health care that doesn’t have to rely on questionable data. Unlike physicians, who can look at high blood pressure and cholesterol levels to assess a patient’s risk for disease, people who study pain have had to trust murky self-reports to go in one direction or another. Now, the findings suggest a new approach, in which doctors can enjoy a solid footing for making complex decisions about pain — all from a helpful batch of brain cells.

“Demonstrating glial activation in chronic pain suggests that these cells may be a therapeutic target, and the consistency with which we found glial activation in chronic pain patients suggests that our results may be an important step toward developing biomarkers for pain conditions,” said Marco Loggia, of the MGH-based Martinos Center for Biomedical Imaging, in a statement. The inflammation was so starkly evident in the scans that Loggia could pick apart the control group from the pain group just by looking at them, he added.

Images created by averaging PET scan data from chronic pain patients (left) and healthy controls (right) reveal higher levels of inflammation-associated translocator protein (orange/red) in the thalamus and other brain regions of chronic pain patients. Marco Loggia, PhD, Martinos Center for Biomedical Imaging, Massachusetts General Hospital

What really interested the investigators was the relationship between TSPO and pain levels. It wasn’t the case that higher pain showed more protein activation. In fact, it was just the opposite.

“While upregulation of TSPO is a marker of glial activation, which is an inflammatory state,” Loggia said, “animal studies have suggested that the protein actually limits the magnitude of glial response after its initiation and promotes the return to a pain-free, pre-injury status.”

This means that people with more pain may actually be expressing less TSPO, sort of as a way to "calm down" the inflammation site, as Loggia explains. "While larger studies would be needed to further support this interpretation, this evidence suggests that drugs called TSPO agonists, which intensify the action of TSPO, may benefit pain patients by helping to limit glial activation."

Up next for the research team is narrowing the focus of glial activation studies. They want to understand how certain forms of pain, like fibromyalgia and rheumatoid arthritis, produce a similar response in the brain. It may be the case, for instance, that each type of pain generates a "glial signature." One day, patients may be able to take different drugs according to the inflammation seen solely in their brain scans.

Source: Loggia M, Chonde D, Akeju O, et al. Evidence for brain glial activation in chronic pain patients. Brain. 2015.

http://www.medicaldaily.com/chronic-pain-patients-show-patterns-brain-inflammation-setting-stage-objective-pain-317374

COPPER ON THE BRAIN AT REST

In recent years it has been established that copper plays an essential role in the health of the human brain. Improper copper oxidation has been linked to several neurological disorders including Alzheimer's, Parkinson's, Menkes' and Wilson's. Copper has also been identified as a critical ingredient in the enzymes that activate the brain's neurotransmitters in response to stimuli. Now a new study by researchers with the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) has shown that proper copper levels are also essential to the health of the brain at rest.

"Using new molecular imaging techniques, we've identified copper as a dynamic modulator of spontaneous activity of developing neural circuits, which is the baseline activity of neurons without active stimuli, kind of like when you sleep or daydream, that allows circuits to rest and adapt," says Chris Chang, a faculty chemist with Berkeley Lab's Chemical Sciences Division who led this study. "Traditionally, copper has been regarded as a static metabolic cofactor that must be buried within enzymes to protect against the generation of reactive oxygen species and subsequent free radical damage. We've shown that dynamic and loosely bound pools of copper can also modulate neural activity and are essential for the normal development of synapses and circuits."

Chang , who also holds appointments with the University of California (UC) Berkeley's Chemistry Department and the Howard Hughes Medical Institute (HHMI), is the corresponding author of a paper that describes this study in the Proceedings of the National Academy of Sciences (PNAS). The paper is titled "Copper is an endogenous modulator of neural circuit spontaneous activity." Co-authors are Sheel Dodani, Alana Firl, Jefferson Chan, Christine Nam, Allegra Aron, Carl Onak, Karla Ramos-Torres, Jaeho Paek, Corey Webster and Marla Feller.

Although the human brain accounts for only two-percent of total body mass, it consumes 20-percent of the oxygen taken in through respiration. This high demand for oxygen and oxidative metabolism has resulted in the brain harboring the body's highest levels of copper, as well as iron and zinc. Over the past few years, Chang and his research group at UC Berkeley have developed a series of fluorescent probes for molecular imaging of copper in the brain.

"A lack of methods for monitoring dynamic changes in copper in whole living organisms has made it difficult to determine the complex relationships between copper status and various stages of health and disease," Chang said. "We've been designing fluorescent probes that can map the movement of copper in live cells, tissue or even model organisms, such as mice and zebra fish."

For this latest study, Chang and his group developed a fluorescent probe called Copper Fluor-3 (CF3) that can be used for one- and two-photon imaging of copper ions. This new probe allowed them to explore the potential contributions to cell signaling of loosely bound forms of copper in hippocampal neurons and retinal tissue.

"CF3 is a more hydrophilic probe compared to others we have made, so it gives more even staining and is suitable for both cells and tissue," Chang says. "It allows us to utilize both confocal and two-photon imaging methods when we use it along with a matching control dye (Ctrl-CF3) that lacks sensitivity to copper."

With the combination of CF3 and Ctrl-CF3, Chang and his group showed that neurons and neural tissue maintain stores of loosely bound copper that can be attenuated by chelation to create what is called a "labile copper pool." Targeted disruption of these labile copper pools by acute chelation or genetic knockdown of the copper ion channel known as CTR1 (for copper transporter 1) alters spontaneous neural activity in developing hippocampal and retinal circuits.

"We demonstrated that the addition of the copper chelator bathocuproine disulfonate (BCS) modulates copper signaling which translates into modulation of neural activity," Chang says. "Acute copper chelation as a result of additional BCS in dissociated hippocampal cultures and intact developing retinal tissue removed the copper which resulted in too much spontaneous activity."

The results of this study suggest that the mismanagement of copper in the brain that has been linked to Wilson's, Alzheimer's and other neurological disorders can also contribute to misregulation of signaling in cell−to-cell communications.

"Our results hold therapeutic implications in that whether a patient needs copper supplements or copper chelators depends on how much copper is present and where in the brain it is located," Chang says. "These findings also highlight the continuing need to develop molecular imaging probes as pilot screening tools to help uncover unique and unexplored metal biology in living systems."

CHANGES IN EYE CAN PREDICT CHANGES IN BRAIN

Researchers at the Gladstone Institutes and University of California, San Francisco have shown that a loss of cells in the retina is one of the earliest signs of frontotemporal dementia (FTD) in people with a genetic risk for the disorder -- even before any changes appear in their behavior.

Published in the Journal of Experimental Medicine, the researchers, led by Gladstone investigator Li Gan, PhD and UCSF associate professor of neurology Ari Green, MD, studied a group of individuals who had a certain genetic mutation that is known to result in FTD. They discovered that before any cognitive signs of dementia were present, these individuals showed a significant thinning of the retina compared with people who did not have the gene mutation.

"This finding suggests that the retina acts as a type of 'window to the brain,'" said Dr. Gan. "Retinal degeneration was detectable in mutation carriers prior to the onset of cognitive symptoms, establishing retinal thinning as one of the earliest observable signs of familial FTD. This means that retinal thinning could be an easily measured outcome for clinical trials."

Although it is located in the eye, the retina is made up of neurons with direct connections to the brain. This means that studying the retina is one of the easiest and most accessible ways to examine and track changes in neurons.

Lead author Michael Ward, MD, PhD, a postdoctoral fellow at the Gladstone Institutes and assistant professor of neurology at UCSF, explained, "The retina may be used as a model to study the development of FTD in neurons. If we follow these patients over time, we may be able to correlate a decline in retinal thickness with disease progression. In addition, we may be able to track the effectiveness of a treatment through a simple eye examination."

The researchers also discovered new mechanisms by which cell death occurs in FTD. As with most complex neurological disorders, there are several changes in the brain that contribute to the development of FTD. In the inherited form researched in the current study, this includes a deficiency of the protein progranulin, which is tied to the mislocalization of another crucial protein, TDP-43, from the nucleus of the cell out to the cytoplasm.

However, the relationship between neurodegeneration, progranulin, and TDP-43 was previously unclear. In follow-up studies using a genetic mouse model of FTD, the scientists were able to investigate this connection for the first time in neurons from the retina. They identified a depletion of TDP-43 from the cell nuclei before any signs of neurodegeneration occurred, signifying that this loss may be a direct cause of the cell death associated with FTD.

TDP-43 levels were shown to be regulated by a third cellular protein called Ran. By increasing expression of Ran, the researchers were able to elevate TDP-43 levels in the nucleus of progranulin-deficient neurons and prevent their death.

"With these findings," said Dr. Gan, "we now not only know that retinal thinning can act as a pre-symptomatic marker of dementia, but we've also gained an understanding into the underlying mechanisms of frontotemporal dementia that could potentially lead to novel therapeutic targets."

IMPACT OF VIOLENT MEDIA ON THE BRAIN DEPENDS ON EACH INDIVIDUALS BRAIN CIRCUITRY

With the longstanding debate over whether violent movies cause real world violence as a backstop, a study published in PLOS One found that each person's reaction to violent images depends on that individual's brain circuitry, and on how aggressive they were to begin with.

The study, which was led by researchers at the Icahn School of Medicine at Mount Sinai and the NIH Intramural Program, featured brain scans which revealed that both watching and not watching violent images caused different brain activity in people with different aggression levels. The findings may have implications for intervention programs that seek to reduce aggressive behavior starting in childhood.

"Our aim was to investigate what is going on in the brains of people when they watch violent movies," said lead investigator Nelly Alia-Klein, PhD, Associate Professor of Neuroscience and Psychiatry at the Friedman Brain Institute and Icahn School of Medicine at Mount Sinai. "We hypothesized that if people have aggressive traits to begin with, they will process violent media in a very different way as compared to non-aggressive people, a theory supported by these findings."

After answering a questionnaire, a group of 54 men were split by the research team into two groups -- one with individuals possessing aggressive traits, including a history of physical assault, and a second group without these tendencies. The participants' brains were then scanned as they watched a succession of violent scenes (shootings and street fights) on day one, emotional, but non-violent scenes (people interacting during a natural disaster) on day two, and nothing on day three.

The scans measured the subjects' brain metabolic activity, a marker of brain function. Participants also had their blood pressure taken every 5 minutes, and were asked how they were feeling at 15 minute intervals.

Investigators discovered that during mind wandering, when no movies were presented, the participants with aggressive traits had unusually high brain activity in a network of regions that are known to be active when not doing anything in particular. This suggests that participants with aggressive traits have a different brain function map than non-aggressive participants, researchers said.

Interestingly, while watching scenes from violent movies, the aggressive group had less brain activity than the non-aggressive group in the orbitofrontal cortex, a brain region associated by past studies with emotion-related decision making and self-control. The aggressive subjects described feeling more inspired and determined and less upset or nervous than non-aggressive participants when watching violent (day 1) versus just emotional (day 2) media. In line with these responses, while watching the violent media, aggressive participants' blood pressure went down progressively with time while the non-aggressive participants experienced a rise in blood pressure.

"How an individual responds to their environment depends on the brain of the beholder," said Dr. Alia-Klein. "Aggression is a trait that develops together with the nervous system over time starting from childhood; patterns of behavior become solidified and the nervous system prepares to continue the behavior patterns into adulthood when they become increasingly coached in personality. This could be at the root of the differences in people who are aggressive and not aggressive, and how media motivates them to do certain things. Hopefully these results will give educators an opportunity to identify children with aggressive traits and teach them to be more aware of how aggressive material activates them specifically."

Can Neuropathic Pain Prematurely Age the Brain

Another interesting article from conquerchiari.org (see link below) talks about the long term effect of chronic pain on the brain. Logical really but not something which we normally think of first when considering neuropathy side effects. The fact that long-term HIV-patients are often confronted with brain-aging, related diseases, is a little disconcerting when you realise that consistent neuropathic pain may just be enabling that process a little more. Yet another thing to discuss with your HIV-specialist, especially if you are beginning to notice changes in your own brain behaviour.

Chronic Pain Is Hard On The Brain...
--Rick Labuda

Chronic pain prematurely ages the brain. That was the most significant - and disturbing - finding of a group of researchers from Northwestern University. Scientists have known for some time that chronic pain alters neurons in the spine, but Dr. Apkarian, a neuroscience researcher, and his colleagues wanted to know if and how chronic pain effected the structure of the brain.

In order to study this, Dr. Apkarian and his team used MRI's to measure the volume and density of the brains of 26 people with chronic back pain (CBP) and compared them to the brains of 26 healthy volunteers. They published their results in the November 17, 2004 issue of the Journal of Neuroscience.

Each of the 26 members of the pain group had experienced unrelenting pain for more than a year in their lower back. In some, the pain radiated down into the legs, in others it didn't. In addition to the brain MRI's the CBP subjects reported their pain intensity and how long they had been in pain. To aid in the analysis, members of the pain group were also classified as having neuropathic pain - due to nerve damage - or non-neuropathic pain. The 26 volunteers that composed the control group were recruited to match the age and gender makeup of the CBP group as closely as possible.

The researchers used two different techniques to measure the volume of the neocortical gray matter (the part of the brain responsible for most higher order functions) from the MRI's. They found that overall, the subjects in the pain group had 5%-11% less gray matter volume than the control subjects, a statistically significant finding. People normally lose about 0.5% of their gray matter each year as they age, so this result translates to the pain patients experiencing 10-20 years of aging compared to the control group.

In looking at neuropathic versus non-neuropathic pain, the team found that in the neuropathic pain group, the volume loss was related to pain duration. In fact, in the neuropathic group, each year of pain equated to a 0.2% loss in gray matter (1.3cm3). In the non-neuropathic group, pain duration was not related to volume loss.

The neuropathic pain group also fared worse when the team measured the density of the gray matter in specific regions of the brain. In the prefrontal cortex - responsible for high level functions - they found that people in neuropathic pain had gray matter that was 27% less dense than the control group, and people with non-neuropathic pain had gray matter that was 14% less dense. They also found that the thalamus - a region of the brain which relays pain and other sensations - was significantly less dense in the pain group as compared to the control group.

Although this study can not prove it conclusively, the authors believe the results mean that the chronic back pain is causing brain tissue to atrophy in certain areas. If proven to be true, this would mean that chronic pain not only alters the neurons of the spine, but has a structural effect all the way to the brain as well. While it is a significant finding, it is also important to keep in mind that this study looked at chronic back pain specifically and the results may be different for other types of chronic pain.

Still, with millions of people in the US alone suffering from chronic pain, and with neuropathic pain an all too common problem for CM/SM patients, this area of research is definitely worth paying attention to..

--Rick Labuda

http://www.conquerchiari.org/subs%20only/Volume%203/Issue%203(1)/Chronic%20Pain%20Brain%203(1).asp

TOXIN SECRETING STEM CELLS TREAT BRAIN TUMORS IN MICE

Harvard Stem Cell Institute scientists at Massachusetts General Hospital have devised a new way to use stem cells in the fight against brain cancer. A team led by neuroscientist Khalid Shah, MS, PhD, who recently demonstrated the value of stem cells loaded with cancer-killing herpes viruses, now has a way to genetically engineer stem cells so that they can produce and secrete tumor-killing toxins.

In the AlphaMed Press journal Stem Cells, Shah's team shows how the toxin-secreting stem cells can be used to eradicate cancer cells remaining in mouse brains after their main tumor has been removed. The stem cells are placed at the site encapsulated in a biodegradable gel. This method solves the delivery issue that probably led to the failure of recent clinical trials aimed at delivering purified cancer-killing toxins into patients' brains. Shah and his team are currently pursuing FDA approval to bring this and other stem cell approaches developed by them to clinical trials.

"Cancer-killing toxins have been used with great success in a variety of blood cancers, but they don't work as well in solid tumors because the cancers aren't as accessible and the toxins have a short half-life," said Shah, who directs the Molecular Neurotherapy and Imaging Lab at Massachusetts General Hospital and Harvard Medical School.

"A few years ago we recognized that stem cells could be used to continuously deliver these therapeutic toxins to tumors in the brain, but first we needed to genetically engineer stem cells that could resist being killed themselves by the toxins," he said. "Now, we have toxin-resistant stem cells that can make and release cancer-killing drugs."

Cytotoxins are deadly to all cells, but since the late 1990s, researchers have been able to tag toxins in such a way that they only enter cancer cells with specific surface molecules; making it possible to get a toxin into a cancer cell without posing a risk to normal cells. Once inside of a cell, the toxin disrupts the cell's ability to make proteins and, within days, the cell starts to die.

Shah's stem cells escape this fate because they are made with a mutation that doesn't allow the toxin to act inside the cell. The toxin-resistant stem cells also have an extra bit of genetic code that allows them to make and secrete the toxins. Any cancer cells that these toxins encounter do not have this natural defense and therefore die. Shah and his team induced toxin resistance in human neural stem cells and subsequently engineered them to produce targeted toxins.

"We tested these stem cells in a clinically relevant mouse model of brain cancer, where you resect the tumors and then implant the stem cells encapsulated in a gel into the resection cavity," Shah said. "After doing all of the molecular analysis and imaging to track the inhibition of protein synthesis within brain tumors, we do see the toxins kill the cancer cells and eventually prolonging the survival in animal models of resected brain tumors."

Shah next plans to rationally combine the toxin-secreting stem cells with a number of different therapeutic stem cells developed by his team to further enhance their positive results in mouse models of glioblastoma, the most common brain tumor in human adults. Shah predicts that he will bring these therapies into clinical trials within the next five years.

HOMOEOPATHIC REMEDIES FOR BRAIN FAG

Brain fag is a condition characterized by excessive mental tiredness. While most people have experienced symptoms of mental fatigue from time to time, true mental fatigue can potentially lead to serious problems, including reduced productivity, poor job performance and impaired physical functioning. Learning to recognize the symptoms of mental fatigue can help prevent unnecessary complications.

Brain fag may manifest in different ways for each person. Difficulty concentrating and solving problems, anxiety, irritability with co-workers and loss of passion for work are potential symptoms of mental fatigue. Other symptoms include sleeplessness and confusion or frustration triggered by problem-solving tasks like simple math.

While there is no set time frame for mental fatigue, symptoms may persist indefinitely if not addressed early on. Generally, mental fatigue is associated with symptoms that get worse over time, though it may be transient in some cases. External factors such as career stress and academic pressure can greatly influence the duration of mental fatigue.

HOMOEOPATHIC REMEDIES

AESCULUS HIP. 3X- Loss of memory. Sadness. Confused and bewildered

ALLIUM CEPA 30—After wine

ALUMINA 30- Confusion of intelligence. Unable  to affect a decision. Judgement disturbed. The things that he knows or has known to be real seem to him to be unreal and he is in doubt whether they are so or not

AMRA GRISEA 30- Nervous and mental weakness due to shock of loss in business, death of a loved one, failures, etc. Dwells  upon disagreeable  happenings  unnecessarily

ANACARDIUM ORI. 30- Brain fag with marked loss of memory  or due to over study

ARGENTUM NITRICUM 30-Brain fag and general debility. Impulses to jump  out of windows. Trembling. Vertigo. Fear of death. Headache with coldness. Feeling of strangulation in throat

BELLADONNA 30- Brain fag after delirium

CALCAREA CARB. 30- Brain fag on account of fear of failure, tension, depression, or wounded pride

COCA 30-Wearing out under mental and physical strain

HYDROCYANIC ACID 30- Feels as if cloud going over brain

IGNATIA AMARA 30-Changeable mood. Silient brooding. Mental and physical depression . Sad  and tearful. Sighing and sobbing

KALI BROM . 30- In melancholia, caused by overwork, sensation as if about to lose senses

KALI PHOS 6x, 200x- One of the best remedies for prostration of brain, mental and physical depression. For sleeplessness use 200x , otherwise use 6x potency

LACHESIS 200- Brain fag in diphtheria

NATRUM MUR. 30- Sleeplessness due to dwelling over unpleasant events of the past and thus tires his brain

NUX VOMICA 30- Fatgue caused by mental work or by worries

PICRIC ACID 30- Mental fatigue due to headache . Mental fatigue in teachers who have to teach lengthy hours against their will. Mental fatigue of literary persons and writers who work for long hours

SILICEA 30- Brain fag in students, lawyers, clergymen, due to prolonged efforts and sleepless nights in completing their task

SULPHUR 200-Brain appears tired on waking up in the morning

ZINCUM PHOS 30- Brain fag due to business worries. Weak memory. Attacks of vertigo which is better on rest and lying down

Brain and its disorders

Brain and its disorders

NERVOUS SYSTEM – Brain and its disorders

Man is the most intelligent of all animals. The human brain seems to have more IQ (intelligent quotient) than any other living creature. All animals use their brain only for continued existence, i.e., to get food, to escape from danger, to get protected, etc. But human beings think rationally and invent new things for leading life more comfortably. Human brain seems to be a mystery and seems to be extraordinarily complex.

Brain is very much essential for our living, survival and communication comfort with environments. It is the main switch of the wired network of our body. With electrical impulses, they communicate, interact, interpret, coordinate and function efficiently, in a very fast manner in a fraction of a second through the cranial nerves (12 pairs) and spinal nerves (31 pairs). Billions and billions of nerve cells are engaged in the maintenance work of our body under the supervision of the brain. This super computer (brain) has uniqueness of mind and memory also. They can conduct messages at the rate more than 20 km per minute. This speed makes its functions invaluable.

All our body’s virtual functions are carried out, controlled, correlated and regulated by the brain. Due to its importance, nature has placed it in a high position and in a safe vault (skull). Really, one needs to bow one’s head before Nature’s mystery.

Human brain – weighing less than 1.5 kg, is the boss of the body. It weighs approximately 2 per cent of the total body weight. This is the highest proportion among all living creatures comparing

brain and body weight. The richness of connection accounts for human intellect and talent. IQ and ability of brain varies from person to person and also from male to female. Here experiences and interest of the person also count. At a young age, it is highly adaptable and good in learning things easily. For moulding it perfectly to lead a good future, education in early life is thus very important.

Brain consists of an inner white and outer grey matter. Human brain has many folds with bulges and grooves for having more extended surface for recording. But, of course, all the theories say that human beings do not use more than 50 per cent of their brain’s capacity. The bulges are called gyri and grooves are called sulci. Brain has rich blood supply from carotid and vertebral arteries. In addition, it has been nourished through cerebrospinal fluid which circulates from ventricles of the brain to the entire spinal column.

Brain can be divided into three divisions:

• Fore brain – consists of cerebrum, thalamus, hypothalamus and glands (pineal and pituitary)
• Mid brain – Reticular formation, i.e., connecting area of forebrain and brain stem
• Hind brain – consists of cerebellum and brain stem (medulla oblongata and pons)

Fore brain and its functions Cerebrum – covers 80 per cent of the brain’s weight and volume. Cerebrum has two symmetrical hemispheres separated by a deep fissure. Even though they can mimic attributes, their functions seem to be entirely different. Each area has specific responsibility and function. Two hemispheres are interrelated with connecting fibres called corpus callosum.

Crossing over of nervefibres occurs in brain stem, so that the right side of the body is controlled by the left cerebral hemisphere and the left side of the body is controlled by the right side brain (cerebral hemisphere). The reason for crossing over is less understood. For human beings, commonly (for right handed persons – most common), the left hemisphere of the brain seems to be dominant and has the speech area (Broca’s area). Due to the left hemisphere’s dominance, every day- to-day activities will be taken care of with the right hand and leg in a more powerful manner than the left.

Cerebrum is an authority for development of personality, behaviour, intelligence, memory, emotions, etc. It also controls the voluntary muscles engaged in speech, breathing and swallowing. Cerebrum is covered by cerebral cortex and meninges (insulation layer). Cerebral cortex is the registry for memories, plans, ambition, etc. Unless otherwise this area is kept perfect, one cannot remember anything even about himself. In gist,

• Left cerebral hemisphere is responsible for thoughts, speech, words, etc.
• Right cerebral hemisphere is responsible for cognitive processing, rational thinking, fine skills, creativity, etc.

Further, cerebrum can be divided into four lobes and named after their covering bones

• Frontal lobe – responsible for planning, rational thinking and memories
• Parietal lobe – responsible for vision and understanding
• Temporal lobe – responsible for auditory
• Occipital lobe – responsible for vision

Thalamus – it is the base of the fore brain and the roof of the mid brain. It works more with sensory organs, i.e., eyes, ears, nose, tongue, fingers, etc.

Hypothalamus – controls emotions, body temperature, thirst, sleep, appetite, pulse, etc.

Pituitary and pineal glands with thalamus and hypothalamus work for growth and controlling body hormones for maintaining good body functions.

Mid brain and its functions – It is a very small connecting area of fore brain and brain stem. It is called as reticular formation. It controls and coordinates all the actions of brain. It filters impulses and gives importance and value according to urgency and interest, for example – one who sleeps in

the midst of TV sound wakes up for a calling bell. Here all the TV sounds have been filtered by this reticular formation and calling bell has been given importance and allowed to wake up the brain.

Hind brain and its functions
Cerebellum is a Latin word which means little brain (cerebellum itself resembles brain). It is placed in the back end of the head (occipital region) and it is also divided into two hemispheres like the cerebrum. It is the authority for coordination and balancing during movement and while changing body posture, for example during drawing, playing, running, etc.

Brain stem consists of medulla oblongata and pons. It is the collection of nerve fibres that ascend from the body and descends from the brain. It coordinates all the body impulses and brain’s messages. It also controls automatic functions, like breathing, heart beat / rate, blood pressure, swallowing, digestion, blinking, etc.

Brain problems – There are innumerous complaints that can arise from brain – starting from simple tiredness to coma, i.e., dizziness, drowsiness, sleeplessness, sleepiness, lack of concentration, loss of memory, headache, migraine, fits / seizure / epilepsy, paresis, paralysis, cerebrovascular disorders ( stroke ), brain tumours, meningitis, encephalitis, Parkinson’s disease, Alzheimer’s disease, brain atrophy, etc.

Prevention of brain problems – brain cannot be replaced, so prevention is most important. Also prevention is simple, i.e. need to care for head against any injury or disease. If any disease is not treated properly, it can end life ultimately by spreading to / attacking brain. For example – coma arises due to uncontrolled diabetes , hypertension, liver disorders, kidney disorders, heart disorders, etc.

Do’s

• Physical as well as mental exercises (reading, thinking, solving puzzles / problems)
• Wear helmet while riding bike or working in mines or industry to avoid head injury
• Keep diabetes, hypertension and cholesterol level under control
• Proceed to treatment as early as possible in all complaints

Avoid

• Narcotics, sedatives, smoking, alcohol and unnecessary drugs
• Unnecessary anxiety, fear, tension and worries

Diagnostic techniques – Brain functions and diseases are usually analysed with weakness, coordination of movement(s), reflexes, spasticity, alteration in sensations and functions, etc., to plan for treatment. The common tests required to detect brain disorders are

• Routine blood tests and urine tests
• X-ray skull (in AP view and lateral view)
• CT / MRI scan
• Electroencephalography (EEG)
• Analysing cerebrospinal fluid with spinal puncture

for new hope

Dr. S. Chidambaranathan, BHMS, MD (Homeo)

Laxmi Homeo Clinic

24 E. New Mahalipatti Road

Madurai, TN 625 001

India

Tel:  +91-452-233-8833 | +91-984-319-1011 (Mob)

Fax: +91-452-233-0196

E-mail:  drcheena@yahoo.com

www.drcheena.com  / www.drcheena.in

(Disclaimer - The contents of this column are for informational purpose only. The content is not intended to be a substitute for professional healthcare advice, diagnosis, or treatment. Always seek the advice of healthcare professional for any health problem or medical condition.)

WHY YOUR BRAIN MAKES YOU REACH FOR JUNK FOOD

Will that be a pizza for you or will you go for a salad? Choosing what you eat is not simply a matter of taste, conclude scientists in a new study at the Montreal Neurological Institute and Hospital of McGill University and the McGill University Health Centre. As you glance over a menu or peruse the shelves in a supermarket, your brain is making decisions based more on a food's caloric content.

The study, published in Psychological Science, is based on brain scans of healthy participants who were asked to examine pictures of various foods. Participants rated which foods they would like to consume and were asked to estimate the calorie content of each food. Surprisingly, they were poor at accurately judging the number of calories in the various foods, but their choices and their willingness to pay still centered on those foods with higher caloric content.

"Earlier studies found that children and adults tend to choose high-calorie food" says Dr. Alain Dagher, neurologist at the Montreal Neurological Institute and Hospital and lead author of the study. "The easy availability and low cost of high-calorie food has been blamed for the rise in obesity. Their consumption is largely governed by the anticipated effects of these foods, which are likely learned through experience. Our study sought to determine how people's awareness of caloric content influenced the brain areas known to be implicated in evaluating food options. We found that brain activity tracked the true caloric content of foods."

Decisions about food consumption and caloric density are linked to a part of the brain called the ventromedial prefrontal cortex, an area that encodes the value of stimuli and predicts immediate consumption.

Understanding the reasons for people's food choices could help to control the factors that lead to obesity, a condition affecting 1 in 4 Canadian adults and 1 in 10 children. Obesity is linked to many health problems including high blood pressure, heart disease and type 2 diabetes. Treating Canadians who have these problems costs billions of tax health dollars.

This work was funded by the Canadian Institutes of Health Research.

IMMUNE PROTEINS MOONLIGHT TO REGULATE BRAIN CELL CONNECTIONS

When it comes to the brain, "more is better" seems like an obvious assumption. But in the case of synapses, which are the connections between brain cells, too many or too few can both disrupt brain function.

Researchers from Princeton University and the University of California-San Diego (UCSD) recently found that an immune-system protein called MHCI, or major histocompatibility complex class I, moonlights in the nervous system to help regulate the number of synapses, which transmit chemical and electrical signals between neurons. The researchers report in the Journal of Neuroscience that in the brain MHCI could play an unexpected role in conditions such as Alzheimer's disease, type II diabetes and autism.

MHCI proteins are known for their role in the immune system where they present protein fragments from pathogens and cancerous cells to T cells, which are white blood cells with a central role in the body's response to infection. This presentation allows T cells to recognize and kill infected and cancerous cells.

In the brain, however, the researchers found that MHCI immune molecules are one of the only known factors that limit the density of synapses, ensuring that synapses form in the appropriate numbers necessary to support healthy brain function. MHCI limits synapse density by inhibiting insulin receptors, which regulate the body's sugar metabolism and, in the brain, promote synapse formation.

Senior author Lisa Boulanger, an assistant professor in the Department of Molecular Biology and the Princeton Neuroscience Institute (PNI), said that MHCI's role in ensuring appropriate insulin signaling and synapse density raises the possibility that changes in the protein's activity could contribute to conditions such Alzheimer's disease, type II diabetes and autism. These conditions have all been associated with a complex combination of disrupted insulin-signaling pathways, changes in synapse density, and inflammation, which activates immune-system molecules such as MHCI.

Patients with type II diabetes develop "insulin resistance" in which insulin receptors become incapable of responding to insulin, the reason for which is unknown, Boulanger said. Similarly, patients with Alzheimer's disease develop insulin resistance in the brain that is so pronounced some have dubbed the disease "type III diabetes," Boulanger said.

"Our results suggest that changes in MHCI immune proteins could contribute to disorders of insulin resistance," Boulanger said. "For example, chronic inflammation is associated with type II diabetes, but the reason for this link has remained a mystery. Our results suggest that inflammation-induced changes in MHCI could have consequences for insulin signaling in neurons and maybe elsewhere."

MHCI levels also are "dramatically altered" in the brains of people with Alzheimer's disease, Boulanger said. Normal memory depends on appropriate levels of MHCI. Boulanger was senior author on a 2013 paper in the journal Learning and Memory that found that mice bred to produce less functional MHCI proteins exhibited striking changes in the function of the hippocampus, a part of the brain where some memories are formed, and had severe memory impairments.

"MHCI levels are altered in the Alzheimer's brain, and altering MHCI levels in mice disrupts memory, reduces synapse number and causes neuronal insulin resistance, all of which are core features of Alzheimer's disease," Boulanger said.

Links between MHCI and autism also are emerging, Boulanger said. People with autism have more synapses than usual in specific brain regions. In addition, several autism-associated genes regulate synapse number, often via a signaling protein known as mTOR (mammalian target of rapamycin). In their study, Boulanger and her co-authors found that mice with reduced levels of MHCI had increased insulin-receptor signaling via the mTOR pathway, and, consequently, more synapses. When elevated mTOR signaling was reduced in MHCI-deficient mice, normal synapse density was restored.

Thus, Boulanger said, MHCI and autism-associated genes appear to converge on the mTOR-synapse regulation pathway. This is intriguing given that inflammation during pregnancy, which alters MHCI levels in the fetal brain, may slightly increase the risk of autism in genetically predisposed individuals, she said.

"Up-regulating MHCI is essential for the maternal immune response, but changing MHCI activity in the fetal brain when synaptic connections are being formed could potentially affect synapse density," Boulanger said.

Ben Barres, a professor of neurobiology, developmental biology and neurology at the Stanford University School of Medicine, said that while it is known that both insulin-receptor signaling increases synapse density, and MHCI signaling decreases it, the researchers are the first to show that MHCI actually affects insulin receptors to control synapse density.

"The idea that there could be a direct interaction between these two signaling systems comes as a great surprise," said Barres, who was not involved in the research. "This discovery not only will lead to new insight into how brain circuitry develops but to new insight into declining brain function that occurs with aging."

Particularly, the research suggests a possible functional connection between type II diabetes and Alzheimer's disease, Barres said.

"Type II diabetes has recently emerged as a risk factor for Alzheimer's disease but it has not been clear what the connection is to the synapse loss experienced with Alzheimer's disease," he said. "Given that type II diabetes is accompanied by decreased insulin responsiveness, it may be that the MHCI signaling becomes able to overcome normal insulin signaling and contribute to synapse decline in this disease."

Research during the past 15 years has shown that MHCI lives a prolific double-life in the brain, Boulanger said. The brain is "immune privileged," meaning the immune system doesn't respond as rapidly or effectively to perceived threats in the brain. Dozens of studies have shown, however, that MHCI is not only present throughout the healthy brain, but is essential for normal brain development and function, Boulanger said. A 2013 paper from her lab published in the journal Molecular and Cellular Neuroscience showed that MHCI is even present in the fetal-mouse brain, at a stage when the immune system is not yet mature.

"Many people thought that immune molecules like MHCI must be missing from the brain," Boulanger said. "It turns out that MHCI immune proteins do operate in the brain -- they just do something completely different. The dual roles of these proteins in the immune system and nervous system may allow them to mediate both harmful and beneficial interactions between the two systems."