I normally don’t ask for anything from tumblr, but My mom had a stroke and broke her leg in the shower. and the rehab center kicked her out and changed us for the stay when they realized our insurance would only cover 20 days. Worst part is they didn’t let us know until after it was too late.
So we are just asking for a bit of help to pay off the rehab center. We aren’t asking for a lot, just to cover the few extra days she had to spend there when we were getting everything set up for her being home.
Brain’s iconic seat of speech goes silent when we actually talk
For 150 years, the iconic Broca’s area of the brain has been recognized as the command center for human speech, including vocalization. Now, scientists at UC Berkeley and Johns Hopkins University in Maryland are challenging this long-held assumption with new evidence that Broca’s area actually switches off when we talk out
The findings, reported in the Proceedings of the National Academy of Sciences
journal, provide a more complex picture than previously thought of the
frontal brain regions involved in speech production. The discovery has
major implications for the diagnoses and treatments of stroke, epilepsy
and brain injuries that result in language impairments.
“Every year millions of people suffer from stroke, some of which can
lead to severe impairments in perceiving and producing language when
critical brain areas are damaged,” said study lead author Adeen Flinker,
a postdoctoral researcher at New York University who conducted the
study as a UC Berkeley Ph.D. student. “Our results could help us advance
language mapping during neurosurgery as well as the assessment of
Flinker said that neuroscientists traditionally organized the brain’s language center into two main regions: one for perceiving speech and
one for producing speech.
“That belief drives how we map out language during neurosurgery and
classify language impairments,” he said. “This new finding helps us move
towards a less dichotomous view where Broca’s area is not a center for
speech production, but rather a critical area for integrating and
coordinating information across other brain regions.”
In the 1860s, French physician Pierre Paul Broca pinpointed this
prefrontal brain region as the seat of speech. Broca’s area has since
ranked among the brain’s most closely examined language regions in
cognitive psychology. People with Broca’s aphasia are characterized as
having suffered damage to the brain’s frontal lobe and tend to speak in
short, stilted phrases that often omit short connecting words such as
“the” and “and.”
Specifically, Flinker and fellow researchers have found that Broca’s
area — which is located in the frontal cortex above and behind the left
eye — engages with the brain’s temporal cortex, which organizes sensory
input, and later the motor cortex, as we process language and plan which
sounds and movements of the mouth to use, and in what order. However,
the study found, it disengages when we actually start to utter word
“Broca’s area shuts down during the actual delivery of speech, but it
may remain active during conversation as part of planning future words
and full sentences,” Flinker said.
The study tracked electrical signals emitted from the brains of seven
hospitalized epilepsy patients as they repeated spoken and written
words aloud. Researchers followed that brain activity – using
event-related causality technology – from the auditory cortex, where the
patients processed the words they heard, to Broca’s area, where they
prepared to articulate the words to repeat, to the motor cortex, where
they finally spoke the words out loud.
Impaired vision is one of the most common consequences of a stroke. In rare cases, patients may even lose their ability to perceive depth. Such patients see the world around them as flat, like a two-dimensional
picture. This makes it impossible for them to judge distances accurately
– a skill they need, for instance, when reaching for a cup or when a
car is approaching them on the street. A patient with this particular
type of visual dysfunction has recently been studied in detail by the
research team at Saarland University led by Professor Georg Kerkhoff and
Anna-Katharina Schaadt in collaboration with colleagues at the Charité
university hospital in Berlin. The team has developed the first
effective treatment regime and have identified the area of the brain
that, when damaged, may cause loss of binocular depth perception. The
results of the study have been published in the respected academic
Strokes can result in a wide variety of visual impairments. ‘A
patient may, for example, be blind on one side so that he fails to
perceive obstacles or people on that side or have problems when
reading,’ explains Georg Kerkhoff, Professor of Clinical Neuropsychology
at Saarland University and head of the Neuropsychological Outpatient
Service. In some cases, however, the consequences are even more serious.
Recently, the team around Kerkhoff and Schaadt collaborated with
Professor of Neurology Dr. Stephan Brandt and his colleague Dr. Antje
Kraft, both at the Berlin Charité, in treating and supervising a patient
who had lost his stereoscopic visual perception as a result of a
stroke. Although the patient was able to perceive all the details of his
surroundings, he was not able to assess distances with any accuracy.
‘Everything for him was flat, like on a painting,’ explains
Anna-Katharina Schaadt, a doctoral research student who is supervised by
Kerkhoff and is the study’s lead author. ‘He moved as if in slow-motion
and was very uncertain about how far away a coffee cup was on a table
or how quickly a car was approaching.’ Like a blind person, he used a
long cane to find his way around.
Kerkhoff and Schaadt’s team at the Neuropsychological Outpatient
Service on the Saarbrücken campus began by looking for the cause of the
patient’s visual impairment.
‘We discovered that the patient was unable to converge the visual
impressions from each eye into a single overall image,’ says Schaadt. In
healthy individuals, this process is known technically as ‘binocular
fusion’ and is important for three-dimensional vision.
Once the diagnosis had been made, the team of neuropsychologists
provided a three-week block of therapy during which the patient
undertook daily training to improve his visual perception of depth.
Three different training methods were employed. Special visual training
equipment (prisms, vergence trainer and cheiroscope) were used to
present the patient with two images with a slight lateral offset between
them. By using what are known as convergent eye movements, the patient
attempts to fuse the two images into a single image. This involves
directing the eyes inward towards the nose while always keeping the
images in the field of view. With time, the two separate images fuse to
form a single image that exhibits stereoscopic depth, i.e. the patient
has re-established binocular single vision. ‘It was as if a switch had
been thrown; the patient was suddenly able to perceive spatial depth
again, judge distances correctly and reach out and hold objects with
confidence’, describes Schaadt. The patient has now returned to work as a
lawyer. At a follow-up examination a year later, the patient still
exhibited good stereoscopic depth perception, and can therefore be
considered to be permanently cured according to Professor Kerkhoff.
The procedure could be used in future by therapists to help treat
other stroke patients suffering from this extreme form of visual
impairment. The results of the study are also of interest to researchers
working in the field, as Professor Brandt explains: ‘The results
illustrate the very specific functional organization of our brains.
Damage to the areas known as V6 and V6A in the parietal lobe is
associated with impaired three-dimensional visual perception. This area
of the brain has been studied in primates. However, further research is
required to understand its function in humans.’
The Blind Woman Who Sees Rain, But Not Her Daughter’s Smile
Imagine a world that is completely black. You can’t see a thing — unless something happens to move. You can see the rain falling from the sky, the steam coming from your coffee cup, a car passing by on the street.This was the world that Milena Channing claimed to see, back in 2000, shortly after she was blinded by a stroke at 29 years old. But when she told her doctors about these strange apparitions, they looked at her brain scans (the stroke had destroyed basically her entire primary visual cortex, the receiving station of visual information to the brain), and told her she must be hallucinating.
“You’re blind and that’s it,” Channing remembers them saying to her.
Frustrated and convinced these visions were real, Channing made her way from doctor to doctor until she finally found one who believed her: Dr. Gordon Dutton, an ophthalmologist in Glasgow. He told her he’d once read about such a case — a soldier in World War I who, after a bullet injury to the head, could only see things in motion.
Here’s why: If this is about motion, only being able to see things in motion, she’d be able to see the stationary world, at least a little, if she herself started moving.
It helped. In the weeks and months after her visit (after employing other techniques like shaking her head), Channing began to see the world more vividly. And when she finally visited a team of neuroscientists in Canada (five years after her stroke), they filled in the picture. It turns out that one area of her brain ’s cortex — an area reserved specifically for processing motion (visual area MT, for middle temporal area) — had been preserved. So even though information wasn’t going through the primary visual cortex, somehow it was still getting out to the part of the brain that can register objects in motion.
Cue the cars. And the rain. And the coffee steam. Channing was truly seeing them.
But here’s the catch. Though this compartmentalized nature of vision may have been Channing’s blessing, it’s also proving to be a quiet curse. Just as there seems to be an area of the brain that processes motion, there is one for faces; and as much as Channing’s vision continues to improve, she still can’t recognize — even perceive — a face.
Channing says that every now and then, that hard boundary of what she can and can’t see frustrates her. “Who does she look like?” Channing wonders, as she gazes straight at her daughter’s face.
For an artist’s rendition of Milena Channing’s world, watch the video above, which also explains a bit more about the modular nature of vision.
Scientists make surprising finding in stroke research
Inflammation is activated in the brain after a stroke, but rather than aiding recovery it actually causes and worsens damage. That damage
can be devastating. In fact, stroke is responsible for 10% of deaths
worldwide and is the leading cause of disability.
understanding how inflammation is regulated in the brain is vital for
the development of drugs to limit the damage triggered by a stroke.
David Brough from the Faculty of Life Sciences, working alongside
colleagues including Professors Dame Nancy Rothwell and Stuart Allan,
has studied the role of inflammasomes in stroke. These inflammasomes are
large protein complexes essential for the production of the
inflammatory protein interleukin-1. Interleukin-1 has many roles in the
body, and contributes to cell death in the brain following a stroke.
Brough explains: “Very little is known about how inflammasomes might be
involved in brain injury. Therefore we began by studying the most well
researched inflammasome NLRP3, which is known to be activated when the
body is injured. Surprisingly we found that this was not involved in
inflammation and damage in the brain caused by stroke, even though drugs
are being developed to block this to treat Alzheimer’s disease.”
studies using experimental models of stroke demonstrated that it was
actually the NLRC4 and AIM2 inflammasomes that contribute to brain
injury, rather than NLRP3.
This discovery was unexpected, since
NLRC4, was only known to fight infections and yet Dr Brough and
colleagues found that it caused injury in the brain. This new discovery
will help the Manchester researchers discover more about how
inflammation is involved in brain injury and develop new drugs for the
treatment of stroke.
The research was funded by the Wellcome Trust and Medical Research Council and has been published in PNAS.
well as identifying new targets for potential drug treatments for
stroke Dr Brough points out how little we currently know about how the
immune system works in the brain.
He says: “We know very little
about how the immune system is regulated in the brain. However, its
important we understand this since it contributes to disease and injury.
For example, in addition to stroke, Alzheimer’s disease has an
inflammatory aspect and even depression may be driven by inflammation.”
Are bilingual stroke patients more susceptible to aphasia?
Aphasia is a condition that commonly affects stroke patients, and leads to problems with the ability to speak, read, and understand language. Patients with aphasia suffer disproportionate levels of anxiety, depression and unemployment, at just the same time as their most basic coping mechanism – talking with family and friends – is being undermined. Stroke patients want to know whether, when, and in what respects they might hope to recover lost language skills - questions that have motivated a great deal of research into the factors that predict better or worse recovery from post-stroke aphasia.
Whether bilingualism (speaking more than one language) affects the severity of aphasia compared to monolingualism (speaking just one) is unclear, but bilingualism is the norm rather than the exception in many parts of the world. Many would assume being able to speak more than one language would lessen the effects of aphasia, as there is a greater understanding of language to draw on. New research suggests however, that bilingual stroke patients are actually more susceptible to aphasia than monolingual stroke patients.
An ischemic stroke happens when a blood vessel (artery) supplying blood to an area of the brain becomes blocked by a blood clot. About 80 out of 100 strokes are ischemic strokes. A hemorrhagic stroke happens when an artery in the brain leaks or bursts (ruptures). (Source)
The majority of stroke occurs when the blood vessels that reach the brain are blocked by clots or fatty deposits which decrease the flow of blood towards its cells. It is then that an ischemic attack occurs, a pathology that leads to the degeneration of neurones, which can be fatal and not many drugs can treat.
German and Swiss scientists have discovered that the combination of two
substances help to reduce inflammation and the brain volume affected
after a cerebrovascular accident. This is glucosamine, an amino sugar
commonly used to treat arthritis and arthrosis; and certain derivatives
of fullerenes, hollow and spherical structures formed by many carbon
Before now it was known that the fullerenes capture
chemical radicals well which makes them act as neuroprotective agents,
while the glucosamine brings down the inflammation.
researchers have done is chemically bond the two compounds to produce
what is known as ‘glyconanoparticles’. These have subsequently been
administered to laboratory rats which then had a cerebrovascular
The results, published in the journal ‘Experimental Neurology’,
conclude that this combination of fullerene derivatives and glucosamine
reduces cell damage and inflammation after a stroke, according to the
MRI scans of animal brains and the improvement of their neurological
“Our study confirms that it is possible to couple
fullerenes with sugars in order to combine their protective effects and
in this way, to obtain new materials which may help to prevent and to
treat Stroke,” says Guillermo Orts-Gil, a Spanish researcher at the
Max-Planck Institute of Colloids and Interfaces (Germany) and co-author
of the research.
“Although the present study was carried out on
mice, the results indicate that these sweet buckyballs are potential new
drugs for treating Stroke also in humans. However, this must be taken
with caution, since what works in mice does not necessarily will work in
the same way in humans,” declared Orts-Gil.
This work is the continuation of another previous piece of research, published last year in the journal ‘Nano Letters’,
in which the researchers also confirmed that a protein called
E-selectin, linked to the chain of events that occur during a stroke, is
distributed throughout the brain and not only in the area where the
stroke originates, as previously thought.
A drug discovery by Adelaide and Chinese scientists could hold promise in the fight against the devastating effects of Alzheimer’s Disease.
Scientists from the University of South Australia, along with
colleagues from Third Military Medical University in Chongqing, China,
have discovered the drug Edaravone can alleviate the progressive
cognitive deficits of Alzheimer’s Disease, a major social and economic
The discovery has been published today in one of the world’s most
cited multidisciplinary scientific journals, PNAS (Proceedings of the
National Academy of Sciences of the United States of America).
Edaravone is currently available only in some Asian countries for the
treatment of ischemic stroke – the most common type of stroke which is
caused by blood clots.
Lead researcher Professor Xin-Fu Zhou, who is UniSA’s Research Chair
in Neurosciences, says Edaravone can alleviate Alzheimer’s Disease
pathologies and improve functions of learning and memory – in a mouse
model of the disease – by multiple mechanisms.
“Edaravone can bind the toxic amyloid peptide which is a major factor leading to degeneration of nerve cells,” Prof Zhou says.
Prof Zhou says lessons from failures of current clinical trials
suggest that targeting multiple key pathways of the Alzheimer’s Disease
pathogenesis is necessary to halt the disease progression.
“Edaravone can suppress the toxic functions of amyloid beta to nerve
cells – it is a free radical scavenger which suppresses oxidative stress
that is a main cause of brain degeneration,” he says.
“The drug can suppress the production of amyloid beta by inhibiting
the amyloid beta production enzyme. It also inhibits the Tau
hyperphosphorylation which can generate tangles accumulated in the brain
cells and disrupt brain functions.”
The research is a collaboration between Prof Zhou’s lab within
UniSA’s Sansom Institute for Health Research and School of Pharmacy and
Medical Sciences, and labs led by Prof Yanjiang Wang in Chongqing,
The researchers stress Edaravone should not be used for Alzheimer’s
patients before appropriate clinical trials are undertaken. Prof Zhou is
seeking investment and partnership opportunities to further the