Information

What sections of the brain can be removed without causing instant death?

What sections of the brain can be removed without causing instant death?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Years ago I've read about a young man you had lost a large section of his brain (frontal lobe) in an accident but surprisingly he survived it and continued his normal life. You may have read about that.

Now let's break down the question into 3 steps. Which parts of the brain can we remove without:

  1. Affecting the normal life. This means, still being able to see, talk, understand, and more. Just like a normal person.
  2. Losing conscious. This includes just being able to maintain conscious, being able to think and understand.
  3. Dying. Which means only having the crucial organs such as heart and lungs running.

UPDATE

I'm neither looking for a list of every part of brain's million sections, nor it's possible to cover them all in a single answer. I'm merely looking for a list of widely-known largely-scaled sectioned, such as the below image.

Image credits goes to Mid Brain Power.


Many areas of the cerebral cortex aren't essential to life/consciousness, damaging/removing them will only destroy the function associated with that area, e.g. visual cortex in the occipital lobe, auditory cortex in the temporal lobe etc. The Corpus Callosum can sometimes be bissected without any major detrimental effects to the "patient/victim".

Edit: The point here is that what appears to be a major link between the hemispheres of the cerebral cortex can be destroyed without necessarily killing the patient. Whether it falls under the same surgical category as a frontal lobotomy or not, I don't know.

Generally the "lower" portions of the brain, midbrain and brainstem are more important as regulatory centres. However these are each made up of multiple smaller regions, each involved in multiple functions, e.g. the Pons, medulla, thalamus. Removing any of these could have wide-ranging consequences, e.g. the thalamus is important for integrating multisensory information.

So, broadly speaking, cortex damage is OK, midbrain/brainstem, probably not unless you only removed very small regions (e.g. removing the cochlear nuclei from the Pons would probably only affect hearing).

If you use the added image, you can predict what removing each brain area would affect, removing the brainstem would remove respiratory centres, certain death. Removing visual areas would lead to blindness, but probably not death.

Fully answering your question would probably require an entire book to list all of the known brain regions and the implications of removing them.


Study sheds light on treatment options for devastating childhood brain cancer

Medulloblastoma is a rare but devastating childhood brain cancer. This cancer can spread through the spinal fluid and be deposited elsewhere in the brain or spine. Radiation therapy to the whole brain and spine followed by an extra radiation dose to the back of the brain prevents this spread and has been the standard of care. However, the radiation used to treat such tumors takes a toll on the brain, damaging cognitive function, especially in younger patients whose brains are just beginning to develop.

A national study led by Washington University School of Medicine in St. Louis and St. Jude Children's Research Hospital suggests that children with what is called "average risk medulloblastoma" can receive a radiation "boost" to a smaller volume of the brain at the end of a six-week course of radiation treatment and still maintain the same disease control as those receiving radiation to a larger area. But the researchers also found that the dose of the preventive radiation treatments given to the whole brain and spine over the six-week regimen cannot be reduced without reducing survival. Further, the researchers showed that patients' cancers responded differently to therapy depending on the biology of the tumors, setting the stage for future clinical trials of more targeted treatments.

Children with average risk medulloblastoma have five-year survival rates of 75% to 90%. In contrast, children with what's called "high risk medulloblastoma" have five-year survival rates of 50% to 75%. Other factors -- such as a child's age and whether the tumor has spread -- help determine the risk category. For this study, the researchers focused on patients with average risk medulloblastoma.

The findings appears online June 10 in the Journal of Clinical Oncology.

"Medulloblastoma is a devastating disease," said first and corresponding author Jeff M. Michalski, MD, the Carlos A. Perez Distinguished Professor of Radiation Oncology at Washington University. "It is a malignant brain tumor that develops in the cerebellum, the back lower part of the brain that is important for coordinating movement, speech and balance. The radiation treatment for this tumor also can be challenging, especially in younger children whose brains are actively developing in these areas. There's a balance between effectively treating the tumor without damaging children's abilities to move, think and learn."

Children with average risk medulloblastoma typically undergo surgery to remove as much of the tumor as possible. They also receive chemotherapy and radiation therapy to prevent the spread of the tumor to other parts of the brain and spine through the cerebrospinal fluid.

"We wanted to investigate whether we could safely reduce the amount of radiation these patients receive -- sparing normal parts of the brain and lessening the side effects for children with this type of brain cancer -- while also maintaining effective treatment," said Michalski, also vice chair and director of clinical programs in the Department of Radiation Oncology. "We found that reducing the dose of radiation received over the six-week course of treatment had a negative impact on survival. But we also found that we could safely reduce the size of the volume of the brain that receives a radiation boost at the end of the treatment regimen. We hope such measures can help reduce the side effects of this treatment, especially in younger patients."

Collaborating with children's hospitals across the U.S. and internationally, the researchers evaluated 464 patients treated for average risk medulloblastoma that was diagnosed between ages 3 and 21. Younger patients, ages 3 to 7 -- a key time for brain development -- were randomly assigned to receive either standard dose (23.4 gray) or low dose (18 gray) radiation to the head and spine region in each of 30 treatments given over six weeks. Older patients all received the standard dose, since their brain development is less vulnerable to radiation. In addition, all patients were randomly assigned to receive two different sizes of a radiation "boost" at the end of the six weeks of therapy. For the boost, all patients received a cumulative radiation dose of 54 gray to either the entire region of the brain called the posterior fossa, which includes the cerebellum, or to a smaller region of the brain that includes the original outline of the tumor plus an additional margin of up to about two centimeters beyond the original tumor boundary.

"The patients who received the smaller boost did just as well as those who received the whole posterior fossa boost," said Michalski, who treats patients at Siteman Kids at Washington University School of Medicine and St. Louis Children's Hospital. "Many doctors have already adopted this smaller boost volume, but now we have high-quality evidence that this is indeed safe and effective."

For patients receiving the smaller boost volume, 82.5% survived five years with no worsening of the cancer. And for those receiving the larger boost volume to the entire posterior fossa, 80.5% survived five years with no worsening of the disease. These numbers were not statistically different. In a subset of tumors with mutations in a gene called SHH, patients actually showed improved survival with the smaller boost volume.

But for the younger children, the lower dose of radiation over six weeks did not result in similar survival numbers. Of those receiving the standard dose of craniospinal radiation, about 83% survived five years with no worsening of the cancer. Of those receiving the lower dose, about 71% survived five years with no worsening of the cancer. That difference in survival was statistically significant.

"We saw higher rates of recurrence and tumor spreading in the younger patients receiving the lower dose of craniospinal radiation," Michalski said. "In general, it's not safe to lower the dose of radiation in children with medulloblastoma even if we know the lower dose might spare their cognitive function. However, a specific subgroup of patients -- those with mutations in a gene called WNT -- did well on the lower dose, so we're now doing studies just with these specific patients to see if we can safely lower the radiation dose for them."

The tumors were categorized into four molecular subgroups based on their gene expression and predicted biology. The first group's tumors have mutations in WNT signaling pathways the second have mutations in the SHH gene and the third and fourth groups' tumors each have different and more complex patterns of gene mutations. The researchers found differences in tumors' responses to treatment based on tumor biology that can guide the design of future clinical trials.

"We've made great strides over the last 15 years in appreciating the molecular diversity of medulloblastoma," said senior author Paul Northcott, PhD, of St. Jude Children's Research Hospital. "We performed whole-exome sequencing and DNA methylation profiling to assign patients to molecular subgroups. This was a critical step in contextualizing this trial based on the latest biology and showed us some important differences in how children respond to therapy that would otherwise not have been clear. Results from this study will play a vital role in designing the next generation of clinical trials for children with medulloblastoma."

This work was supported by the National Cancer Institute (NCI) of the National Institutes of Health (NIH), including a National Clinical Trials Network Operations Center Grant, number U10CA180886 a Children's Oncology Group (COG) Chairs Grant, number U10CA098543 a National Clinical Trials Network Statistics & Data Center Grant, number U10CA098413 and other NCI grants, including U10CA180899, QARC U10CA29511, IROC U24CA180803 and COG Biospecimen Bank Grant U24CA196173. Funding was also provided by St. Baldrick's Foundation, The Brain Tumor Charity, American Lebanese Syrian Associated Charities and St. Jude Children's Research Hospital.


Nobody Declared Brain Dead Ever Wakes Up Feeling Pretty Good

A day rarely goes by that I don't read a few sensational headlines: "Man Declared Dead Feels 'Pretty Good'" or "Husband Celebrates Miracle as 'Brain Dead' Wife Wakes Up in Hospital." I recently read an article that seemed to describe a man on death row in Huntsville, Texas. It attempted to shock its readers with the claim that a college student had been declared brain dead and "just hours before he was slated to be killed and his organs given to another patient," he miraculously recovered. That's right, they said "killed."

As a neurologist who specializes in brain injury, I have cared for many brain-injured patients and there were times when they did better than I anticipated, but sensational articles like these only confuse the public. During the health care legislation debates, the mere mention of insurance coverage for consultation on end-of-life decisions brought forth hysterical cries of "death panels" from people like Sarah Palin who exhorted that "my parents or my baby with Down's Syndrome will have to stand in front of Obama's 'death panel'. " But if the headlines are fiction, what is the truth?

HOW OUR BRAIN ACTUALLY WORKS

Brains are far more complex machines than even the most sophisticated computer. We turn on our computer with a simple switch. The screen entertains us as it boots up and we start to check our email, linger on Facebook to catch up with friends, or read the latest headlines. Have you ever wondered what your brain is doing in the early morning as you awaken to your automatic coffeemaker brewing that first cup of joe?

The main part of our brain, the cerebrum, sits inside our skull and is attached to our spinal cord by the small, but critical, brain stem. Inside the brain stem is a small, but critical, group of nerve cells known as the Reticular Activating System (RAS) that send messages up into the brain, not only to wake us up, but also to keep us alert. We call this process arousal -- no, not that tingling that you get when you kiss the man or woman of your dreams, but stimulation that keeps you awake. But just being awake isn't enough.

We need an intact upper brain to be aware of ourselves and our surrounding environment. Awareness is a higher-level function that requires areas of the cerebrum to process the information we see and hear. A patient may have their eyes open and look like they're awake, but if the brain is severely damaged they may have no awareness of their surroundings. We call this a vegetative state.

On the other hand, people who are in a coma are not awake and have no awareness of themselves or their environment. You can talk to them, pinch them, show them pictures of their family -- they will not respond. However, these patients are not brain dead. This is the source of the confusion that leads to the sensational headlines and stories.

In 1976, Karen Ann Quinlan was in a vegetative state, but lived for nine more years after her ventilator was discontinued. Theresa Schiavo had been in a vegetative state for 15 years. After a protracted legal battle her husband was granted permission to withdraw her nutritional support and she died. Both young women, like the people in the headlines, were not brain dead. People in a vegetative state usually have extensive brain damage, but may blink their eyes and look around, breathe on their own, yawn, chew, and even withdraw their arms or legs to painful stimulation. They are not brain dead, and no one is going to take their organs.

WHAT, EXACTLY, IS BRAIN DEATH?

What is the difference between someone in a coma, who may or may not improve, and someone who is truly brain dead and may be a candidate to donate their organs? Brain death is the irreversible cessation of all functions of the entire brain, including the all-important brain stem that houses the RAS and the mechanism that controls our breathing. Dead is dead. Brain death isn't a different type of death, and patients who meet the criteria of brain death are legally dead.

There are strict criteria for brain death and these criteria (PDF) are carefully followed before a patient becomes an organ donor or their ventilator is unplugged. They must be in a coma with no brain stem or pupillary reflexes. They do not breathe on their own when taken off their ventilator, and an electroencephalogram (EEG) records a complete absence of brain activity. Although most states only require the diagnosis of one physician, the patient's family can always ask for a second opinion.

The sensational headlines hinder our efforts as physicians to educate the public about organ donation and cause unnecessary anxiety for families who are considering donating their loved one's organs. No one who has met the criteria for brain death has ever survived -- no one. It can be difficult to predict a person's outcome after a severe brain injury, but it can be said with certainty that a brain dead individual is dead, the same as if their heart was not beating.

In most hopeless situations, our society's current default is to continue all medical measures unless otherwise clearly stated. At the same time, there is a move afoot in state capitols to pass legislation that would make the withdrawal of nutrition and hydration impossible unless it is specifically stated prior to injury. As of 2007, only 41 percent of people had a living will and both living wills and advanced directives tend to be very general. Now is the time to sit down with your family and discuss what you want done if you were in a hopeless situation or brain dead. There is still a critical shortage of organs available for donation. If the concept of brain death is keeping you from becoming a donor, you can check that off your list and sign up now.


After you die, your brain knows you’re dead, terrifying study reveals

You’ve probably heard about how those who have died and come back to life say they saw light at the end of a tunnel.

Or that they floated above their bodies, watching as doctors frantically worked to keep them alive.

But until now, it was not known if the mind kept working after the body died.

Just like the remake of the 󈨞s cult horror “Flatliners,” starring Ellen Page, scientists have discovered that a person’s consciousness continues to work after they have died.

In the film, a group of young doctors conducts a dangerous experiment to see what happens in the afterlife by taking turns stopping their hearts.

Dr. Sam Parnia and her team from New York University Langone School of Medicine had the same question.

They set out to find the answer in a much less dangerous fashion, looking at studies in Europe and the US on people who have suffered cardiac arrest and “come back to life.”

“They’ll describe watching doctors and nurses working and they’ll describe having awareness of full conversations, of visual things that were going on, that would otherwise not be known to them,” Parnia told Live Science.

Their recollections were also verified by medical staff who reported their patients could remember the details.

Death, in a medical sense, is when the heart stops beating and cuts off blood to the brain.

This means the brain’s functions also stop and can no longer keep the body alive.

Parnia explained that the brain’s cerebral cortex — the so-called “thinking part” of the brain — also slows down instantly, and flatlines, meaning that no brainwaves are visible on an electric monitor, within 2 to 20 seconds.

This eventually results in the death of the brain.

Parnia and his colleagues are also observing how the brain reacts during a cardiac arrest to determine how much of these experiences relate to brain activity.

“At the same time, we also study the human mind and consciousness in the context of death, to understand whether consciousness becomes annihilated or whether it continues after you’ve died for some period of time — and how that relates to what’s happening inside the brain in real time,” he said.

It is not the first time brain activity after death has been recorded.

In March, doctors at a Canadian intensive care unit discovered that one person had persistent brain activity for up to 10 minutes after they turned off their life support machine, but three others did not.

For more than 10 minutes after the medics declared the person clinically dead, brain waves, like those we experience in our sleep, continued to occur.

The researchers also found the experience of death can be very different for individual patients.

Each patient recorded different electroencephalographic results — the electrical activity in the brain — both before and after death.


Biology

Cysticercosis is the disease associated with the development of the larval form (cysticercus) of the pork tapeworm, Taenia solium, within an intermediate host. Swine are the usual intermediate host for T. solium but humans, the usual definitive host, can serve as accidental intermediate hosts following ingestion of infectious eggs. Note that cysticercosis is only acquired from the fecal-oral route (ingestion of eggs), not via the ingestion of cysticerci in undercooked pork, which is associated with intestinal taeniasis.

Life Cycle

Cysticercosis is an infection of both humans and pigs with the larval stages of the parasitic cestode, Taenia solium. This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier . These eggs are immediately infectious and do not require a developmental period outside the host. Pigs and humans become infected by ingesting eggs or gravid proglottids , . Humans are usually exposed to eggs by ingestion of food/water contaminated with feces containing these eggs or proglottids or by person-to-person spread. Tapeworm carriers can also infect themselves through fecal-oral transmission (e.g. caused by poor hand hygiene). Once eggs or proglottids are ingested, oncospheres hatch in the intestine , invade the intestinal wall, enter the bloodstream, and migrate to multiple tissues and organs where they mature into cysticerci over 60&ndash70 days , . Some cysticerci will migrate to the central nervous system, causing serious sequellae (neurocysticercosis).

This differs from taeniasis, which is an intestinal infection with the adult tapeworm. Humans acquire intestinal infections with T. solium after eating undercooked pork containing cysticerci . Cysts evaginate and attach to the small intestine by their scolices. Adult tapeworms develop to maturity and may reside in the small intestine for years .

Hosts

Humans are normal definitive host for T. solium cysticercosis results from humans acting as accidental intermediate hosts for the parasite (this role is normally fulfilled by swine).

Geographic Distribution

Taenia solium is found nearly worldwide. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Poor sanitation leading to environmental fecal contamination is a major factor in transmission. Cysticercosis mainly affects low- and middle-income countries in Africa, Asia (e.g., India, China, and Nepal) and Latin America (e.g., Guatemala, Nicaragua, El Salvador).

It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human T. solium tapeworm carrier (e.g. on contaminated food items), and thus can still occur in populations that neither eat pork nor share environments with pigs, as long as the human carrier is present.

Clinical Presentation

The symptoms of cysticercosis vary depending upon the location and number of cysticerci. Cysticerci may develop in skeletal and heart muscle, skin, subcutaneous tissues, the lungs, liver, and other tissues, including the oral mucosa. In most locations, cysticerci cause few symptoms and spontaneously degenerate.


How Brain Death Works

The examination for brain death is based on response to external stimuli. Since the brain is the organ that feels outside pain, when the brain is dead the patient feels nothing. Before the examination is performed, the physician will have a toxicology test performed to make sure the patient does not have any muscle relaxants in his system, and will check that the patient's body temperature is not extremely abnormal, either of which may reduce neurological reflexes.

The positive examination for brain death includes the following:

  1. The patient has no response to command, verbal, visual or otherwise.
  2. The patient is flaccid, with areflexic extremities. The patient has no movements -- the arms and legs are raised and allowed to fall to see if there are adjacent movements, restraint or hesitation in the fall.
  3. The pupils are unreactive (fixed). The patient's eyes are opened and a very bright light is shined into the pupil. The light will activate the optic nerve and send a message to the brain. In the normal brain, the brain will send an impulse back to the eye to constrict the pupil. In the non-viable brain, no impulse will be generated. This is performed in both eyes.
  4. The patient has no oculocephalic reflex. The patient's eyes are opened and the head turned from side to side. The active brain will allow a roving motion of the eyes the non-functional brain will not. The eyes remain fixed.
  5. The patient has no corneal reflexes. A cotton swab is dragged across the cornea while the eye is held open. The intact brain will want the eye to blink. The dead brain will not. This is performed in both eyes.
  6. The patient has no response -- either purposeful or posturing -- to supra-orbital stimulation. The patient's eyebrow ridge is compressed with the thumb. The resulting stimulation pressure will cause motion of the extremities, either purposeful or primitive posturing, in the living-brain patient, but none in the brain-dead patient.
  7. The patient has no oculovestibular reflex. The patient's ear canal is inspected to ensure an intact tympanic membrane and that the ear is free of wax. While holding the eyes open, ice water is injected into the ear canal. The drastic change in ear temperature will cause a violent eye twitching by the intact brain but no reaction in the brain-dead patient. This is performed in both ears.
  8. The patient has no gag reflex. The movement of the breathing tube (in and out) or the insertion of a smaller tube down the breathing tube will cause a gag reflex in a comatose patient, but will not elicit a reflex in the brain-dead patient.
  9. The patient has no spontaneous respiration. The patient is temporarily removed from life support (the ventilator). With the cessation of breathing by the machine, the body will immediately start to build up metabolic waste of carton dioxide (CO2) in the blood. When the CO2 level reaches a level of 55 mm Hg, the active brain will cause the patient to breathe spontaneously. The dead brain gives no response.

If, after this extensive clinical examination, the patient shows no sign of neurological function and the cause of the injury is known, the patient can be pronounced "brain dead." In some states, more than one physician is required to make this pronouncement in order for brain death to become legal death.

Although the patient has a dead brain and dead brain stem, there may be spinal cord reflexes that can be elicited (a knee jerk, for example). In some brain dead patients, when the hand or foot is touched in a particular manner, the touch will elicit a short reflex movement.

Many physicians will order a confirmatory test for brain death when the clinical examination demonstrates no neurological function.


Do gut bacteria make a second home in our brains?

SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating.

“This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.”

The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain.

Talking hoarsely above the din of the exhibit hall on Tuesday evening, neuroanatomist Rosalinda Roberts of The University of Alabama in Birmingham (UAB), told attendees about a tentative finding that, if true, suggests an unexpectedly intimate relationship between microbes and the brain.

Her lab looks for differences between healthy people and those with schizophrenia by examining slices of brain tissue preserved in the hours after death. About 5 years ago, neuroscientist Courtney Walker, then an undergraduate in Roberts’s lab, became fascinated by unidentified rod-shaped objects that showed up in finely detailed images of these slices, captured with an electron microscope. Roberts had seen the shapes before. “But I just dismissed them, because I was looking for something else,” she says. “I would say ‘Oh, here are those things again.’”

But Walker was persistent, and Roberts started to consult colleagues at UAB. This year, a bacteriologist gave her unexpected news: They were bacteria. Her team has now found bacteria somewhere in every brain they’ve checked—34 in all—about half of them healthy, and half from people with schizophrenia.

Roberts wondered whether bacteria from the gut could have leaked from blood vessels into the brain in the hours between a person’s death and the brain’s removal. So she looked at healthy mouse brains, which were preserved immediately after the mice were killed. More bacteria. Then she looked at the brains of germ-free mice, which are carefully raised to be devoid of microbial life. They were uniformly clean.

RNA sequencing revealed that most of the bacteria were from three phyla common to the gut: Firmicutes, Proteobacteria, and Bacteroidetes. Roberts doesn’t know how these bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose. And she can’t say much about whether they’re helpful or harmful. She saw no signs of inflammation to suggest they were causing harm, but hasn’t yet quantified them or systematically compared the schizophrenic and healthy brains. If it turns out that there are major differences, future research could examine how this proposed “brain microbiome” could maintain or threaten the health of the brain.

In the initial survey of the electron micrographs, Roberts’s team observed that resident bacteria had puzzling preferences. They seemed to inhabit star-shaped cells called astrocytes, which interact with and support neurons. In particular, the microbes clustered in and around the ends of astrocytes that encircle blood vessels at the blood-brain barrier. They also appeared to be more abundant around the long projections of neurons that are sheathed in the fatty substance called myelin. Roberts can’t explain those preferences but wonders whether the bacteria are attracted to fat and sugar in these brain cells.

Why haven’t more researchers seen bacteria in the brain? One reason could be that few researchers subject postmortem brains to electron microscopy, Roberts says. “Pairing up a neuroanatomist with a brain collection just doesn’t happen very often.” And neuroscientists may—as she did until recently—disregard or fail to recognize bacteria in their samples.

Roberts acknowledges that her team still needs to rule out contamination. For example, could microbes from the air or from surgical instruments make it into the tissue during brain extraction? She plans to hunt for such evidence. She also wants to rule out that the solutions that preserve mouse brains introduce or nourish bacteria. Among visitors to the poster, “There were a few skeptics,” Roberts notes. “I have that part of me, too.” But even if the bacteria were never really thriving in living brains, the patterns of their postmortem invasion are intriguing, she says.

If we really have the brain microbiome Roberts proposes, “There is much to investigate,” says Teodor Postolache, a psychiatrist at the University of Maryland in Baltimore. He has studied the protozoan parasite Toxoplasma gondii, which invades the brain but doesn’t always cause obvious disease. “I’m not very surprised that other things can live in the brain, but of course, it’s revolutionary if it’s so,” he says. If these common gut bacteria are a routine, benign presence in and around brain cells, he says, they might play a key role in regulating the brain’s immune activity. “It’s a long road to actually prove that,” he says, but “it’s an exciting path.”


Cortical Strokes vs Subcortical Strokes

Before we dive into the different areas of the brain affected by stroke, you should know the difference between cortical vs subcortical strokes.

The cerebral cortex/cerebrum is a large part of the brain that includes 4 lobes: the frontal lobe, parietal lobe, occipital lobe, and temporal lobe. Strokes in these regions are known as a cortical strokes.

Aside from the cerebrum, there are subcortical structures that lie deep within the brain. Strokes in these areas of the brain are also known as subcortical strokes.

The arteries that supply the subcortical areas of the brain are smaller and more delicate. Subcortical strokes are often hemorrhagic strokes due to the fragile arteries bursting, often from high blood pressure.

There are many differences between cortical and subcortical strokes. For example, cortical strokes often impact higher level functioning and it’s uncommon for subcortical strokes to result in language difficulties.

We will discuss other patterns next!


The Two Hemispheres

The surface of the brain, known as the cerebral cortex, is very uneven, characterized by a distinctive pattern of folds or bumps, known as gyri (singular: gyrus), and grooves, known as sulci (singular: sulcus), shown in Figure 1. These gyri and sulci form important landmarks that allow us to separate the brain into functional centers. The most prominent sulcus, known as the longitudinal fissure, is the deep groove that separates the brain into two halves or hemispheres: the left hemisphere and the right hemisphere.

Figure 1. The surface of the brain is covered with gyri and sulci. A deep sulcus is called a fissure, such as the longitudinal fissure that divides the brain into left and right hemispheres. (credit: modification of work by Bruce Blaus)

There is evidence of some specialization of function—referred to as lateralization—in each hemisphere, mainly regarding differences in language ability. Beyond that, however, the differences that have been found have been minor (this means that it is a myth that a person is either left-brained dominant or right-brained dominant). [1] What we do know is that the left hemisphere controls the right half of the body, and the right hemisphere controls the left half of the body.

The two hemispheres are connected by a thick band of neural fibers known as the corpus callosum, consisting of about 200 million axons. The corpus callosum allows the two hemispheres to communicate with each other and allows for information being processed on one side of the brain to be shared with the other side.

Normally, we are not aware of the different roles that our two hemispheres play in day-to-day functions, but there are people who come to know the capabilities and functions of their two hemispheres quite well. In some cases of severe epilepsy, doctors elect to sever the corpus callosum as a means of controlling the spread of seizures (Figure 2). While this is an effective treatment option, it results in individuals who have split brains. After surgery, these split-brain patients show a variety of interesting behaviors. For instance, a split-brain patient is unable to name a picture that is shown in the patient’s left visual field because the information is only available in the largely nonverbal right hemisphere. However, they are able to recreate the picture with their left hand, which is also controlled by the right hemisphere. When the more verbal left hemisphere sees the picture that the hand drew, the patient is able to name it (assuming the left hemisphere can interpret what was drawn by the left hand).

Figure 2. (a, b) The corpus callosum connects the left and right hemispheres of the brain. (c) A scientist spreads this dissected sheep brain apart to show the corpus callosum between the hemispheres. (credit c: modification of work by Aaron Bornstein)

Much of what we know about the functions of different areas of the brain comes from studying changes in the behavior and ability of individuals who have suffered damage to the brain. For example, researchers study the behavioral changes caused by strokes to learn about the functions of specific brain areas. A stroke, caused by an interruption of blood flow to a region in the brain, causes a loss of brain function in the affected region. The damage can be in a small area, and, if it is, this gives researchers the opportunity to link any resulting behavioral changes to a specific area. The types of deficits displayed after a stroke will be largely dependent on where in the brain the damage occurred.

Consider Theona, an intelligent, self-sufficient woman, who is 62 years old. Recently, she suffered a stroke in the front portion of her right hemisphere. As a result, she has great difficulty moving her left leg. (As you learned earlier, the right hemisphere controls the left side of the body also, the brain’s main motor centers are located at the front of the head, in the frontal lobe.) Theona has also experienced behavioral changes. For example, while in the produce section of the grocery store, she sometimes eats grapes, strawberries, and apples directly from their bins before paying for them. This behavior—which would have been very embarrassing to her before the stroke—is consistent with damage in another region in the frontal lobe—the prefrontal cortex, which is associated with judgment, reasoning, and impulse control.

Link to Learning

Watch this video to see an incredible example of the challenges facing a split-brain patient shortly following the surgery to sever her corpus callosum.


Watch this second video about another patient who underwent a dramatic surgery to prevent her seizures. You’ll learn more about the brain’s ability to change, adapt, and reorganize itself, also known as brain plasticity.


Try It


Mind & Body Articles & More

When dawn rouse watches the home video of her daughter’s third birthday, she sees the familiar details of a child’s party: family, friends, cake. But something is painfully wrong with the picture. Dawn appears detached and vacant onscreen, and ultimately she wanders off while the party goes on without her.

That’s because for years after her daughter Emily’s birth, Dawn struggled with a debilitating depression that kept her from enjoying even the presence of her own little girl. Sometimes she felt sad and distant at other times she was haunted by anxieties she couldn’t control. On one occasion, she remembers pushing Emily’s stroller and suddenly thinking, “I could drop her to the bottom of the lake and it would be at least four hours before anyone would know. Then at least I could get four or five hours of solid sleep.”

Dawn Rouse struggled with depression in the years after he daughter's birth. She's now pursuing a Ph.D. in child development and has become committed to raising public awareness on postpartum illness. © Claudio Calligaris

Surveys show that many mothers—even those not diagnosed as depressed—experience similarly disturbing thoughts, images, and fantasies. Research has found that 85 percent of new mothers experience the “baby blues,” a passing period of sadness or irritability. A mother likely has postpartum depression, a serious condition that affects about 15 percent of new mothers, when her depressed mood persists, intrusive thoughts become increasingly distressing or frequent, and other symptoms of major depression arise. Many of these mothers imagine horrifying scenarios involving their newborns and, sometimes, suffer from tremendous guilt and fear as a result.

Like Dawn, the vast majority would never act on these frightening impulses. Only exceedingly rare cases, termed postpartum psychosis, lead to actual violence against infants.

Yet despite the prevalence of these thoughts among new parents, mothers rarely feel comfortable enough to discuss them. Instead, afraid or ashamed, they suffer in silence, confused by what’s going on in their minds and terrified that it means they’re unfit mothers.

New research findings may offer some consolation to these mothers. For the first time ever, scientists are using specialized techniques to examine the postpartum brain. Their findings are honing in on physiological and evolutionary explanations for why so many mothers are prone to intrusive thoughts, and why this normal level of postpartum anxiety might, for mothers like Dawn, escalate into a serious illness. In the process, this and other research could serve as a catalyst for more open discussion and, eventually, a better understanding of postpartum depression.

Scanning the postpartum brain

At Yale University, researchers recently completed a groundbreaking study of new moms and dads. They used functional magnetic resonance imaging (fMRI)—a technique that tracks blood flow and related patterns of activity in the brain—to see which neural circuits became active when healthy parents saw and heard their babies. Prior studies had examined parents’ brains as they looked at photos of their babies, finding activity in brain areas associated with pleasure and positive mood. But when parents in the Yale study heard their babies cry, the researchers observed activity in neural networks closely associated with obsessive-compulsive disorder (OCD), as well as in brain areas associated with social emotions such as empathy.

Strikingly, it seemed that listening to their babies cry triggered a deeply anxious neural response even in parents who hadn’t been diagnosed with a psychological problem.

OCD is a psychiatric condition characterized by highly distressing thoughts (obsessions) and ritualistic behaviors (compulsions). OCD patients experience a heightened sense of anxiety and a corresponding need to compensate for those distressing thoughts with compulsive behavior, which could include incessant hand washing, praying—or constantly checking on a newborn child.

The researchers offer an evolutionary hypothesis for the neural signs of anxiety they saw in these parents. They believe that, after the birth of a child, a period of high alert may have helped parents protect their babies from environmental harm in times when this was a treacherous and all-consuming task. “Those mothers who were more careful with the baby were more likely to have a baby live,” and thus pass on this obsessive-compulsive tendency, suggests James Swain, a psychiatrist and neuroscientist who worked on the project.

James Leckman, another investigator on the project and the research director of the Yale Child Study Center, says he’s found that a certain level of elevated anxiety and distress is normal in parents. In fact, in an earlier study, he and other researchers found that 30 percent of healthy parents reported having thoughts that they themselves would harm their newborns. In the weeks before delivery, 95 percent of mothers and 80 percent of fathers reported OCD-type thoughts. In this healthy population, obsessive thoughts are fleeting and only mildly distressing. The Yale researchers hypothesize that the healthy maternal brain is hardwired for a period of “transient OCD.”

But, says Swain, once mothers are endowed with this kind of neural “machinery,” there’s a danger they “could connect up OCD behaviors with irrational things not for survival.” In a paper on their research, the Yale scientists write, “Perhaps evolution is not a perfect editor.” In other words, sometimes certain behaviors persist beyond the point that they’re useful.

Their evolutionary hypothesis suggests it is critical for mothers to respond emotionally to their newborns but, the researchers write, “Too much or too little primary parental preoccupation may be problematic.” Some mothers with postpartum depression feel emotionally numb and cannot care for or interact with the newborn. These mothers report a disorienting sense of detachment and apathy. On the other hand, mothers with a more anxious depression feel emotionally charged and cannot inhibit thoughts and impulses concerning the baby’s care. And for many mothers, the symptoms of depression and anxiety overlap. The researchers suggest that while very mild OCD might be adaptive in healthy mothers, a lack or an excess of this obsessive emotional vigilance could play a role in postpartum depression and anxiety.

Ruta Nonacs, a psychiatrist at the Women’s Mental Health Clinic at Massachusetts General Hospital, says the Yale study’s findings resonate with her clinical experience. “Both depressed and nondepressed mothers have a heightened sense of vigilance, the tendency to obsess, but then you have this proportion of women who go way beyond,” she says. “There’s no squelch mechanism. Those impulses just go on and on.” Katherine Stone, who was diagnosed with postpartum OCD after giving birth to her son, was one of those mothers who didn’t have that squelch mechanism. “I was supercharged—hypervigilant,” she says. “I kept having thoughts about dropping him down the stairs, drowning him. You get to this point where you don’t trust yourself because the self you knew would never have that thought. It’s a vicious cycle.”

Leckman and Swain’s findings add to a substantial body of research that has uncovered specific biological mechanisms associated with parental care and postpartum depression. Leckman says that postpartum depression likely has a genetic basis In fact, research has already identified 10 distinct genes associated with parental behavior. In “gene knockout” studies of rodents, he says, researchers have removed entire genes associated with maternal care in some studies, those rodents responded by ignoring their pups or losing the aggressiveness needed to defend them. In humans, Leckman explains, the issue is not a complete absence of certain genes, but may instead involve genetic variations that influence maternal behavior.

Nonacs also suggests that some cases of postpartum depression may be linked to changes in women’s hormone levels after they give birth, particularly in mothers who are already vulnerable to depression. These women might have prolonged hormonal imbalances after childbirth, causing them to respond with excessive emotion to stressful events. For instance, following a distressing incident, they might experience a rapidly beating heart or intense concentration, but then lack the hormonal responses to crank these physiological changes back down to normal levels. As a result, they find themselves in a perpetual state of high arousal.

Social factors probably exacerbate these biological underpinnings of postpartum illness. Prolonged sleep deprivation, for example, is a known risk factor for psychiatric illness and may help explain why, for many mothers, the onset of postpartum depression is gradual rather than sudden. Sandra Poulin, a mother in Dallas, Texas, says she was overjoyed after the birth of her daughter. But as months passed without sleep, she found herself becoming more and more depressed. “I couldn’t move—I was just lead. I was exhausted to the core.”

New studies on the biology of postpartum illness may help remove some of the stigma and silence surrounding depression after childbirth. Combined with the statistics on the prevalence
of postpartum depression, the Yale study’s results indicate that a considerable number of new mothers experience some sadness or anxiety in addition to the often-reported elation or fulfillment of having a child. Indeed, Leckman and Swain’s research suggests there may be a very fine line between natural, even healthy changes in new mothers’ brains and changes that can become disruptive and dysfunctional. This finding could help bolster advocates’ efforts to open up public discussion about the complexities and difficulties associated with early parenting.

These advocates claim that contemporary public discourse emphasizes the joys of motherhood while downplaying the natural anxieties that come with it. Jane Honikmann, the founder and former president of Postpartum Support International, an organization that promotes research, advocacy, and support groups for postpartum depression, calls this “the myth of motherhood and the fantasy of fatherhood.” The skewed representation of what it’s like to be a new parent leaves some women feeling that they are bad mothers. “Nobody talks about it,” says Sandra Poulin, “they’re frightened to death.”

Katherine Stone says she lived in fear that her son would be taken from her if she disclosed what was going through her mind. “I didn’t tell a soul,” she says.
Stone believes silence takes its toll on mothers like her, who feel they have no choice but to remain quiet. Social norms dictate that mothers be “supreme and wonderful, and sacrifice,” she says. If they suffer from negative thoughts about their child, she adds, they fear how they’ll be perceived by others. “You’re like a defective woman. You don’t work properly.”

The scientists at Yale say it might help new parents to know that having disturbing thoughts does not mean they are bad parents. By showing the complexities of postpartum illness—that even the healthy maternal brain is wired for a certain level of anxiety—the Yale research might help remove some of the stigma around those willing to speak up about what they’ve been through, and encourage others to seek help.

For women who do seek help, common methods of treatment include psychotherapy and postpartum support groups, as well as anti- depressant medication. Some mothers benefit from the aid of “postpartum doulas”—helpers who come into the home to assist with both the new mother and child’s health and well-being. Mothers also say that the support of family and friends and the chance to catch up on sleep help alleviate the exhaustion and sense of isolation that can worsen the illness.

But advocates also say that the medical system needs to do a better job appealing to mothers and training health professionals to recognize signs of depression. Sandra Poulin of Texas says that current efforts to reach mothers have the timing all wrong. Some hospitals give out packets on postpartum depression, but in the excitement and disorientation of new motherhood, she says, that information usually ends up in the trash. It is after several months of sleep deprivation that such information would be more useful, according to Poulin. She says she would like to see the routine “well-baby” visits reconceptualized and renamed “well-baby, well-mommy visits.”

Poulin also wishes that all pediatric offices had the Postpartum Support International’s poster hanging directly above the infant scale. The poster reads, “Depression is the #1 Complication of Childbirth.” That poster—with information on how to get help—could save lives, she says.

Indeed, some anthropological studies have found that in cultures that provide extensive postpartum support, there are lower rates of depression among new mothers.

New Jersey set a national precedent in 2006 by approving a law that makes screening for postpartum depression mandatory. The driving force behind the law was New Jersey’s then-first lady, Mary Jo Codey, who had suffered from postpartum depression herself. She decided to come forward with her experience in the hopes of effecting positive change for others. Legislators and advocates in a number of states are now pushing for similar reforms aimed at education, screening, and prevention.

Swain says the Yale study may serve as a first step toward understanding the differences between healthy mothers and those with an illness—and eventually improving treatments for those mothers who need it. He and Leckman caution, though, that it is too soon to say for certain what OCD circuits will look like in mothers with a postpartum illness. The next phase of Swain’s research will involve scanning the brains of depressed mothers immediately after childbirth, then again after they receive different forms of treatment. Together, the studies of healthy mothers and of mothers with an illness will help researchers construct a more precise neurological picture of the postpartum brain.

Swain hopes that one day brain imaging on mothers will help them get preemptive treatment. “A lot of this is about prevention,” he says, “about knowing who gets better. Then we can hopefully start to sort this out and say, ‘Chances are, you’ll benefit from this kind of therapy.’ It would be great if we could do such a brain scan and tell someone that they are at risk long before they’ve even noticed [symptoms of depression].”

Better treatment of mothers has direct implications for infants and children, as well. Research has consistently shown that children of chronically depressed mothers have greater emotional and cognitive difficulties as they grow up. But the outlook for these children isn’t bleak at all if their mothers receive treatment. A recent Columbia University study found that the children of depressed mothers showed significant improvements in mental health when their mothers were treated with antidepressants.

“Mothers getting treatment helps kids go on to live healthy, happy lives,” says Ruta Nonacs of Massachusetts General Hospital. She adds that treatment for mothers is only one part of what children and families need. “There are many things that make kids resilient, like having other care providers who are not depressed—a husband, extended family.”

Perhaps some of the greatest advocates and resources for these families are those mothers who have recovered and gone on to tell their stories. After years of suffering, Dawn Rouse saw a therapist who described some of the biochemical mechanisms involved in postpartum depression. As she listened, Dawn suddenly realized, “Oh my God, I am not an evil, horrible mother.” She started taking medication but then learned therapeutic strategies so that she was eventually able to cope without it. Her relationship with now-nine-year-old Emily has been transformed. Finally, she says, “I am finding joy in my daughter.”


Brain oxygen levels can sometimes suddenly drop, such that your nonessential body processes shut down, allowing the vital functions of the brain to continue. Fainting is the result. Symptoms such as light-headedness, nausea and a feeling of warmth may precede fainting, according to the Mayo Clinic. If you faint regularly, see your doctor to determine if there is a serious underlying cause.

  • Brain oxygen levels can sometimes suddenly drop, such that your nonessential body processes shut down, allowing the vital functions of the brain to continue.
  • If you faint regularly, see your doctor to determine if there is a serious underlying cause.



Comments:

  1. Hart

    Instead of criticism write the variants.

  2. Kantit

    Charming idea

  3. Yale

    We will have everything we just want! The main thing is not to be afraid!

  4. Tharen

    Perhaps I will refuse))

  5. Elne

    In my opinion, you are wrong. I propose to discuss it.



Write a message