Scientists have discovered how to put an artificial image inside a mouse’s brain so that it behaves as if it actually sees it. This will be possible to do with humans in the future — potentially shaping our thoughts and behaviors.
New research could help explain why thousands of Covid-19 survivors are facing debilitating neurological symptoms months after initially getting sick. WSJ breaks down the science behind how the coronavirus affects the brain, and what this could mean for long-haul patients. Illustration: Nick Collingwood/WSJ
Stroke is far more common than you might realize, affecting more than 795,000 people in the U.S. every year. It is a leading cause of death and long-term disability. Yet until now, treatment options have been limited, despite the prevalence and severity of stroke.
Not so long ago, doctors didn’t have much more to offer stroke victims than empathy, says Kevin Sheth, MD, Division Chief of Neurocritical Care and Emergency Neurology. “There wasn’t much you could do.” But that is changing. Recent breakthroughs offer new hope to patients and families. Beating the Clock Think of stroke as a plumbing problem in the brain. It occurs when there is a disruption of blood flow, either because of a vessel blockage (ischemic stroke) or rupture (hemorrhagic stroke).
In both cases, the interruption of blood flow starves brain cells of oxygen, causing them to become damaged and die. Delivering medical interventions early after a stroke can mean the difference between a full recovery and significant disability or death. Time matters. Unfortunately, stroke care often bottlenecks in the first stage: diagnosis. Sometimes, it’s a logistical issue; to identify the type, size, and location of a stroke requires MRI imaging, and the machinery itself can be difficult to access.
MRIs use powerful magnets to create detailed images of the body, which means they must be kept in bunker-type rooms, typically located in hospital basements. As a result, there is often a delay in getting MRI scans for stroke patients. Dr. Sheth collaborated with a group of doctors and engineers to develop a portable MRI machine. Though it captures the images doctors need to properly diagnose stroke, it uses a less powerful magnet. It is lightweight and can be easily wheeled to a patient’s bedside.
“It’s a paradigm shift – from taking a sick patient to the MRI to taking an MRI to a sick patient,” says Dr. Sheth. Stopping the Damage Once a stroke has been diagnosed, the work of mitigating the damage can begin. “Brain tissue is very vulnerable during the first hours after stroke,” says vascular neurologist Nils Petersen, MD. He and his team are using advanced neuro-monitoring technology to study how to manage a patient’s blood pressure in the very acute phase after a stroke.
Dr. Petersen’s research shows that optimal stroke treatment depends on personalization of blood pressure parameters. But calculating the ideal blood pressure for the minutes and hours after a patient has a stroke can be complicated. It depends on a variety of factors—it is not a one-size-fits-all scenario. Harnessing the Immune System Launching an inflammatory reaction is how the body responds to injury anywhere in the body – including the brain, following stroke. However, in this case, the resulting inflammation can sometimes cause even more damage.
But what if that immune response could be used to the patient’s advantage? “We’re trying to understand how we can harness the immune system’s knowledge about how to repair tissues after they’ve been injured,” says Lauren Sansing, MD, Academic Chief of the Division of Stroke and Vascular Neurology. Her team is working to understand the biological signals guiding the immune response to stroke.
That knowledge can then direct the development of targeted therapeutics for the treatment of stroke that minimize early injury and enhance recovery. “We want to be able to lead research efforts that change the lives of patients around the world,” says Dr. Sansing.
Learn about these developments and more in the video above.
The number of older people, including those living with dementia, is rising, as younger age mortality declines. However, the age-specific incidence of dementia has fallen in many countries, probably because of improvements in education, nutrition, health care, and lifestyle changes.
Overall, a growing body of evidence supports the nine potentially modifiable risk factors for dementia modelled by the 2017 Lancet Commission on dementia prevention, intervention, and care: less education, hypertension, hearing impairment, smoking, obesity, depression, physical inactivity, diabetes, and low social contact.
We now add three more risk factors for dementia with newer, convincing evidence. These factors are excessive alcohol consumption, traumatic brain injury, and air pollution. We have completed new reviews and meta-analyses and incorporated these into an updated 12 risk factor life-course model of dementia prevention. Together the 12 modifiable risk factors account for around 40% of worldwide dementias, which consequently could theoretically be prevented or delayed.
The potential for prevention is high and might be higher in low-income and middle-income countries (LMIC) where more dementias occur. Our new life-course model and evidence synthesis has paramount worldwide policy implications. It is never too early and never too late in the life course for dementia prevention. Early-life (younger than 45 years) risks, such as less education, affect cognitive reserve; midlife (45–65 years), and later-life (older than 65 years) risk factors influence reserve and triggering of neuropathological developments.
Culture, poverty, and inequality are key drivers of the need for change. Individuals who are most deprived need these changes the most and will derive the highest benefit.
What you need to know
- Functional neurological disorder (FND) is associated with considerable distress and disability. The symptoms are not faked
- Diagnose FND positively on the basis of typical clinical features. It is not a diagnosis of exclusion
- FND can be diagnosed and treated in presence of comorbid, pathophysiologically defined disease
- Psychological stressors are important risk factors but are neither necessary nor sufficient for the diagnosis
Functional disorders are conditions whose origin arises primarily from a disorder of nervous system functioning rather than clearly identifiable pathophysiological disease—such as irritable bowel syndrome, fibromyalgia, and functional neurological disorder (FND)—they are the second commonest reason for new neurology consultations.1 FND is common in emergency settings,2 stroke,3 and rehabilitation services.4 It causes considerable physical disability and distress, and often places an economic burden both on patients and health services.5 Many clinicians have had little formal clinical education on the assessment and management of these disorders, and patients are often not offered potentially effective treatments.
‘Journal of Neurology, Neurosurgery & Psychiatry” (July 10, 2020):
We tested the hypothesis that apathy, but not depression, is associated with dementia in patients with SVD. We found that higher baseline apathy, as well as increasing apathy over time, were associated with an increased dementia risk. In contrast, neither baseline depression or change in depression was associated with dementia. The relationship between apathy and dementia remained after controlling for other well-established risk factors including age, education and cognition. Finally, adding apathy to models predicting dementia improved model fit. These results suggest that apathy may be a prodromal symptom of dementia in patients with SVD.
Cerebral small vessel disease (SVD) is the leading vascular cause of dementia and plays a major role in cognitive decline and mortality.1 2 SVD affects the small vessels of the brain, leading to damage in the subcortical grey and white matter.1 The resulting clinical presentation includes cognitive and neuropsychiatric symptoms.1
Apathy is a reduction in goal-directed behaviour, which is a common neuropsychiatric symptom in SVD.3 Importantly, apathy is dissociable from depression,3 4 another symptom in SVD for which low mood is a predominant manifestation.5 Although there is some symptomatic overlap between the two,6 research using diffusion imaging reported that apathy, but not depression, was associated with white matter network damage in SVD.3 Many of the white matter pathways underlying apathy overlap with those related to cognitive impairment, and accordingly apathy, rather than depression, has been associated with cognitive deficits in SVD.7 These results suggest that apathy and cognitive impairment are symptomatic of prodromal dementia in SVD.
Dr. Aimee Kao discusses key behaviors known to protect brain health. Dr. Kao looks at population trends and wonders if they tell a complete story. Watch full lecture here:
From U.S. News (July 7, 2020):
“Numerous studies have linked insufficient sleep with significant health consequences. Yet, many people ignore the signs of sleep problems or don’t allow enough time to get adequate sleep,” said lead researcher Eileen Leary. She is a senior manager of clinical research at Stanford University in Palo Alto, Calif.
“REM sleep appears to be a reliable predictor of mortality and may have other predictive health values,” Leary said. “Strategies to preserve REM may influence clinical therapies and reduce mortality risk, particularly for adults with less than 15% of REM sleep.”
REM (rapid eye movement) sleep is when dreams occur and the body repairs itself from the ravages of the day. For every 5% reduction in REM sleep, mortality rates increase 13% to 17% among older and middle-aged adults, researchers report.
For the study, Leary and her colleagues included more than 2,600 men, average age 76, who were followed for a median of 12 years. They also collected data on nearly 1,400 men and women, average age 52, who were part of another study and were followed for a median of 21 years.
Poor REM sleep was tied to early death from any cause as well as death from cardiovascular and other diseases, the researchers found.
Tension-type headaches can be either episodic or chronic. They are rarely disabling or associated with any significant autonomic phenomena, thus patients do not usually seek medical care and usually successfully self-treat. Unlike migraine, there is no significant nausea, no vomiting, and a lack of aggravation by routine physical activity.
In this podcast Mark Green, Professor of Neurology, Anesthesiology and Rehabilitation Medicine, Director of Headache and Pain Medicine, Icahn School of Medicine at Mount Sinai, New York, gives a clinical overview of the condition.
Can you imagine if each word had its own colour, or you could ‘see’ different types of music?
Synesthetes can experience the ordinary world in some pretty extraordinary ways. In this video Jamie Ward explains the variety of different ways in synesthesia can manifest itself, and what is happening in the brains of those who experience it.
Jamie Ward is Professor of Cognitive Neuroscience at the University of Sussex. He has written books a number of books about neuroscience and synesthesia.
Synesthesia is a perceptual phenomenon in which stimulation of one sensory or cognitive pathway leads to involuntary experiences in a second sensory or cognitive pathway. People who report a lifelong history of such experiences are known as synesthetes. Awareness of synesthetic perceptions varies from person to person. In one common form of synesthesia, known as grapheme–color synesthesia or color–graphemic synesthesia, letters or numbers are perceived as inherently colored. In spatial-sequence, or number form synesthesia, numbers, months of the year, or days of the week elicit precise locations in space (for example, 1980 may be “farther away” than 1990), or may appear as a three-dimensional map (clockwise or counterclockwise). Synesthetic associations can occur in any combination and any number of senses or cognitive pathways.