February 8, 2020

While you were sleeping, your brain was working overtime

bean bag sleep



By Padraic Monaghan

Professor, Lancaster University


Sleep has profound importance in our lives, such that we spend a considerable proportion of our time engaging in it. Sleep enables the body—including the brain—to recover metabolically, but contemporary research has been moving to focus on the active rather than recuperative role that sleep has on our brain and behavior.

Sleep is composed of several distinct stages. Two of these, slow-wave (or deep) and REM sleep, reflect very different patterns of brain activity, and have been related to different cognitive processes.

Slow-wave sleep is characterized by synchronized activity of neurons in the neo-cortex firing at a slow rate, between 0.5 and three times per second. The neo-cortex comprises the majority of the cerebral cortex in the brain which plays a role in memory, thought, language, and consciousness. In contrast during REM sleep, when most of our dreaming happens, neuronal firing is rapid and synchronized at much higher frequencies, between 30 to 80 times per second.

Such patterns of brain activity during REM sleep are reminiscent of those observed during wakefulness, and for this reason REM sleep is often referred to as “paradoxical” sleep.

Cognitive functions

There is growing evidence that slow-wave sleep is related to the consolidation of memory and is involved in transferring information from the hippocampus, which encodes recent experiences, and forging long-term connections within the neo-cortex. REM sleep has been linked to processes involving abstraction and generalization of experiences, resulting in creative discovery and improved problem solving.

Though there are substantial similarities between wakefulness and REM sleep, numerous studies have explored differences in the activity of brain regions between these states, with the cingulate cortex, hippocampus and amygdala more active during REM sleep than wakefulness. These regions are particularly interesting to cognitive neuroscientists because they are key areas involved in emotional regulation and emotional memory.

However, which sub-regions are active within these broader cortical and limbic areas—the pathways in the brain that produce these patterns of activation—and the precise function of the activity in these regions during REM sleep is currently under-described.

Cortical activity in rats

A new study published in Science Advances studied the physiology and functionality of REM sleep in a group of rats and provides insight into the cortical activity and the sub-cortical pathways that result in this activity. The level of detail of this study provides a major step forward for our understanding of the effect that REM sleep has on our brain and cognitive behavior.

The authors studied groups of rats who were allowed to sleep, but prevented from entering REM sleep for three days. Six hours before assessment, half of the rats were allowed to sleep normally, and half continued to be deprived of REM sleep. The rats that were permitted to sleep normally then demonstrated raised levels of REM sleep within those six hours. This enabled a comparison of the effect of recent REM sleep between groups. An additional control group of rats were allowed to sleep normally throughout the study.

Gene expression analysis involves tracking the presence of particular mRNA or proteins that can be identified as the consequences of certain genes operating. The rats who underwent substantial REM sleep before testing were found to demonstrate greater expression of several genes that are associated with syntaptic plasticity (how quickly their synapses can adapt to changes in a local environment) and which affects the efficiency of neural transmission in the hippocampus.

In the neo-cortex, the gene expressions related to how well our synapses adapt also increased following REM sleep, but those related to neural transmission were reduced compared with the group that was prevented from REM sleep. So, the function of REM sleep appears to be due to changes in the way that neurons communicate. This is consistent with the view that REM sleep allows the brain’s memory processing systems to re-balance, which enables effective responses to experiences the next day.

Where in the brain?

In a further study, the same group determined the precise location of where these changes actually occur in the brain. In the neo-cortex, there was a general increase in plasticity throughout several areas, including sensorimotor regions that bring together sensory and motor functions. In the hippocampus, it was generally confined to the dentate gyrus, which is thought to contribute to forming new episodic memories among other things. REM sleep was also associated with reduced neuro-transmission throughout many regions of the neo-cortex, indicating that REM sleep likely results in a general weakening of the connections between synapses, which may enable brain networks to better learn from multiple experiences rather than be affected only by single instances.

The final studies the group conducted determined the source of the cortical changes in plasticity and neuro-transmission during REM sleep. By tracking signal transmission between different brain areas together with chemical lesioning (in which brain areas are temporarily inactivated), they identified two further areas called the claustrum and the supramammillary nucleus as having key roles during REM sleep.

These two areas have been identified as involved in integrating emotion and memory. The claustrum is a very thin layer of neurons that are found underneath the inner neo-cortex. It is known to link to and from very many regions of this part of the brain. As such, the claustrum has been implicated in integrating stimuli from several senses and is involved in linking areas involved in emotional processing and attention.

The supramammillary nucleus, within the hippocampus, is also known to interconnect to multiple areas of the brain, several of which are associated with emotional processing.

The implications of this work provide converging evidence that REM sleep modulates activation and synaptic processing in areas of the brain that contribute to the processing of emotion. This is also consistent with previously untested accounts that suggest REM sleep is important for encoding memories (but without their emotional content). While the role of dreaming during REM sleep is still yet to be linked to observed effects from neuro-chemicals in the brain, understanding what is happening in our brains when we dream could yet prove to be key to processing of emotion and memory.

January 12, 2020

Parkinson’s Myths

There are many myths about Parkinson's. Here are the five we hear about most. Share this film to help bust them!

There are many myths about Parkinson's. Here are the five we hear about most. Share this film to help bust them!

Home Rehab Therapists are here to help. Parkinson’s Disease can be debilitating and public awareness can be very limited. Following research on the internet we present myths that are leading at common misconceptions about Parkinson’s disease.
It’s important to sort through certain persistent misconceptions about the condition because they may keep patients with Parkinson’s from being treated properly and taking care of themselves. The experts at the Johns Hopkins Parkinson’s Disease and Movement Disorders Center uncover seven myths and the facts you need to know :
Myth 1: Parkinson’s is “only” a motor condition.
Fact: While it’s true that Parkinson’s disease symptoms include shaking and tremor, rigid muscles, slowness of movement, and a frozen or “flat” expression, it’s a lot more than that.
Non-motor symptoms deserve — and are getting — more attention from doctors and researchers. These symptoms include cognitive impairment or dementia (usually in later stages), anxiety and depression, fatigue, sleep problems and more.
For some patients, non-motor symptoms are more disabling than motor symptoms, which are the focus of treatment. Be sure to talk to your doctor about other issues so you can get all of your symptoms addressed.
Myth 2: Parkinson’s medications cause symptoms.
Fact: Even though the myth that Parkinson’s disease medicines are toxic and make the condition progress faster was completely debunked, it persists. Levodopa is the main drug therapy for Parkinson’s disease. It’s a potent drug that helps patients with motor symptoms. But many people got the idea that over time, it makes the disease progress faster. The myth was that levodopa is somehow toxic and is somehow making the Parkinson’s progression faster, hurting patients.
It’s true that levodopa isn’t a cure — as yet, there is no cure for Parkinson’s disease — but it’s not toxic.
Myth 3: Everyone with Parkinson’s disease has tremors.
Fact: It’s easy to connect tremor to Parkinson’s disease because it’s a prominent and recognisable symptom. But some people with Parkinson’s never have a tremor, and even those who do may not have it at the start of the condition.
Myth 4: Aside from medication, there isn’t much you can do.
Fact: This “it is what it is; there’s nothing I can do to help myself” myth is counterproductive. There is a lot you can do — chiefly, keeping as active as you can. A recent study found that patients with Parkinson’s who took part in weekly, hourlong exercise sessions were able to do more in their daily lives than those who did not.
Myth 5: Parkinson’s disease is fatal.
Fact: Although a diagnosis of Parkinson’s is devastating, it is not — as some people may still believe — a death sentence. Parkinson’s disease is not a direct killer, like stroke or heart attack. That said, much depends on the quality of your care, both from your medical team and yourself.
As the disease progresses, you may become more vulnerable to falls, which can be dangerous. That’s why exercise and physical therapy are so important.
Infection is another problem. In later stages of Parkinson’s, people often miss those signals and may not notice something’s up until it’s too late. That can be, literally, a killer — so be sure to stay up to date with check-ups.
Myth 6: Deep brain stimulation is “experimental” therapy.
Fact: Deep brain stimulation, or DBS, is a procedure in which doctors place electrodes in the brain at the point when medications are less effective in masking motor symptoms, such as tremor, stiffness and slowness of movement.
While it may sound frightening and futuristic, it’s been around and successfully used for decades. DBS works very similarly to a pacemaker, except the wire is in the brain, not in the heart. It’s been a standard procedure for the past two decades.
Myth 7: Parkinson’s research is stalled.
Fact: It may feel as though there’s nothing dramatic going on in the Parkinson’s disease field, but there are several recent and very exciting breakthroughs regarding our understanding of the underlying pathology and disease mechanism. This will translate into actual clinical results in the next few years.

January 2, 2020

What is Ataxia?

Ataxia is a rare neurological disease.
It is progressive – affecting a person’s ability to walk, talk, and use fine motor skills.
What is Ataxia?
Ataxia is a degenerative disease of the nervous system. Many symptoms of Ataxia mimic those of being drunk, such as slurred speech, stumbling, falling, and incoordination. These symptoms are caused by damage to the cerebellum, the part of the brain that is responsible for coordinating movement. Ataxia treatment involves a combination of medication to treat symptoms and therapy to improve quality of life.

People affected by Ataxia may experience problems with using their fingers and hands, arms, legs, walking, speaking or moving their eyes. Ataxia affects people of all ages. Age of symptom-onset can vary widely, from childhood to late-adulthood. Complications from the disease are serious and oftentimes debilitating. Some types of Ataxia can lead to an early death.

Ataxia symptoms vary by person and type of Ataxia. Rate of progression varies as well. Symptoms may worsen slowly, over decades – or quickly, over mere months. Common symptoms of Ataxia are:

Lack of coordination
Slurred speech
Trouble eating and swallowing
Deterioration of fine motor skills
Difficulty walking
Gait abnormalities
Eye movement abnormalities
Heart problems
Individuals with Ataxia often require the use of wheelchairs, walkers, and/or scooters to aid in their mobility.


Falls Prevention - Easy steps to remain active, fit and achieve better quality of living

Here are six simple exercises used by physiotherapists to keep muscles strong and keep us mobile and independent as we age. Try out heel raises, toe raises, heel toe stand, one leg stand, heel toe walking, and sit to stand exercises.

What is FND?
A Functional Neurological Disorder (FND) can encompass a diverse range of symptoms including limb weakness, paralysis, seizures, walking difficulties, spasms, twitching and more.

Whilst the symptoms may appear similar to those seen in neurological diseases such as Multiple Sclerosis, Parkinson’s and Epilepsy, and can be just as debilitating, they are not caused by structural disease of the nervous system. Instead, they are caused by a problem with the “functioning” of the nervous system.

The structure of the body is fine, but there is a problem with how the nervous system is functioning, and how the brain fails to send and receive messages correctly. This impacts on how the body responds to different tasks such as movement control.

Functional Neurological Disorders are often explained to patients as a psychological reaction due to past experiences, or as symptoms due to stress. These explanations usually fail and result in patients feeling alienated, stigmatised and not-believed. The main reason for the failure of such explanations is that they take a potential risk factor and turn it into the cause of the problem.

A diagnosis can, and should be, made from positive neurological signs and tests that are specific to Functional Neurological Disorders. The Hoovers Sign, for example, is a specific test in relation to limb weakness. Whilst traditional MRIs cannot detect symptoms, research studies are beginning to provide evidence of grey matter abnormalities in the brain.

Functional neurological symptoms are commonly seen in Neurology and Epilepsy clinics, and in paediatric care. Disappointingly there are currently no national statistics to support this, so is based on limited regional reporting and patient feedback. These symptoms should not be classified under Medically Unexplained Symptoms (MUS).

Treatment for symptoms can overlap both Neurology and Psychology, and because of this it has led to many people ‘falling down a gap’ and left to fend by themselves, or has led to inadequate and inappropriate care. As understanding of Functional Neurological Disorders has advanced, so too has the debate among medical professionals regarding the diagnostic criteria and terminology.

Current understanding is that biological, psychological and social factors may contribute towards a person’s vulnerability to developing a Functional Neurological Disorder. Further research is needed to ascertain a clearer picture of the causes and mechanisms.

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