Brain Scans Reveal a New Schizophrenia Type That Almost Looks Like a 'Healthy' Brain

Not all people with schizophrenia show the same abnormal brain structure, a new study has found.

Scanning the brains of over 300 schizophrenia patients, researchers now think they've identified two neuroanatomical subtypes of this mysterious neurological disorder; one of them has never been detected before, according to the team.

Today, the neurobiology of schizophrenia is poorly understood, but historically, it's been linked to a reduction in grey matter volume, the type of brain tissue that contains the main body of neurons.

This is a typical pattern of the disease that keeps popping up in research, but while the majority of patients in this new study also showed these deficits, a large chunk had surprisingly healthy grey matter levels.

"Numerous other studies have shown that people with schizophrenia have significantly smaller volumes of brain tissue than healthy controls," explains radiologist Christos Davatzikos from the University of Pennsylvania.

"However, for at least a third of patients we looked at, this was not the case at all - their brains were almost completely normal."

The only thing that stood out was an increase in basal ganglia volume, the part of the brain primarily responsible for motor control. Although schizophrenia is a disorder of the mind that interferes with the consistent processing of reality, it can also lead to physical problems like slow movements and tics.

But these brain patterns are not exactly in line with the current consensus on schizophrenia. In fact, the idea of 'neuroanatomical heterogeneity' - where some people may show brain deficits while others don't - has only recently been considered.

"These results challenge the conventional notion that brain volume loss is a general feature of schizophrenia," the authors conclude.

Using machine learning, the team analysed the brain scans of 307 schizophrenia patients and 364 healthy controls, categorising them into neuroanatomical subtypes.

In total, nearly 40 percent of the participants with schizophrenia did not show the typical pattern of reduced grey matter. In some cases, they actually showed more brain volume in the middle of the brain, in a part called the striatum.

No clear explanation could be found for the results - not medication, age, or any other demographic factors.

"This is where we are puzzled right now," Davatzikos says.

"We don't know. What we do know is that studies that are putting all schizophrenia patients in one group, when seeking associations with response to treatment or clinical measures, might not be using the best approach."

Patients that fell into either brain subtype had experienced similar levels of symptoms and were medicated at roughly the same dose. Previous research has linked reduced cortical volumes to antipsychotic drugs, but the researchers did not detect such differences between the two subtypes.

The team notes that brain differences between the subtypes could still be influenced by the consequences of taking medication, for example, higher treatment resistance in subtype 1 compared to subtype 2, whose cortical volumes did not appear to be reduced. But other aspects - such as no difference in symptom severity - don't seem to support this explanation.


Other recent studies have also hinted at a more diverse presentation of schizophrenia in the brain; given how variable symptoms of schizophrenia can be, and how few people respond to treatment, this idea that one size does not fit all is not without merit.

But connecting these symptoms to patterns in the brain has proved extremely difficult, especially since animal models aren't useful in a disorder that is largely diagnosed through self-reporting.
"The main message is that the biological underpinnings of schizophrenia - and actually many other neuropsychiatric disorders - are quite heterogeneous," Davatzikos told ScienceAlert.

The latest classification of schizophrenia in the DSM-V categorises the condition as a spectrum based on symptoms alone, having moved away from behavioural subtypes such as paranoid and catatonic.

But Davatzikos thinks that observations of neural diversity in such disorders could ultimately take diagnostic categories much further.

"In the future, we're not going to be saying, 'This patient has schizophrenia,' We're going to be saying, 'This patient has this subtype' or 'this abnormal pattern,' rather than having a wide umbrella under which everyone is categorised."

We'll have to wait for even more research in the neuroanatomy of various disorders to see whether such a categorisation goal is attainable.

The study was published in Brain.

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Parkinson's Disease is On the Rise

Over the years, overall health has improved drastically. We have seen revolutions in pharmacology and medical technology, better nutrition, and also improvements in public healthcare. All of this promises a longer, healthier future for our global population. However, this prosperity does come at a cost. Age-related neurological conditions, such as Parkinson's disease, threaten to affect more of us than ever before. Consequently, this has set the stage for an unprecedented medical challenge. 

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A specialist om Parkinson's Disease says "By 2040, we can truly talk about a pandemic that will result in increased human suffering, as well as rocketing societal and medical costs." In his article, he highlights what we are in for in the coming decades. He predicts that current Parkinson's figures will double, if not triple over the next 20 years.
This problem is not just limited to Parkinson's disease. Dementia and Alzheimer's disease are also expected to skyrocket with our aging population. This occurs as more of us survive long enough to see our aged bodies burdened with conditions few once lived to endure. 
A big part of the problem arises due to the lack of knowledge about how many such neurological conditions develop in the first place. Parkinson's became known in the early 19th century, when an eminent British surgeon named James Parkinson outlined the characteristics of this degenerative disease in his treatise, An Essay on the Shaking Palsy. 
Today we know that the symptoms of trembling extremities, impeded mobility, rigidity, and mood changes are linked with the loss of dopamine-producing tissues deep inside one of the brain's control centers, called the basal ganglia. An estimated 6.1 million people across the planet had Parkinson's 'shaking palsy' disease, more than double 1990s figures. 

Reduced production of dopamine isn't considered to be deadly, but the overall loss of function, combined with the general senescence that comes with growing old - produces an average life expectancy of just seven to 14 years beyond diagnosis.
Records show that today, roughly around 200,000 individuals could be expected to die prematurely each year due to a result of having the condition. But, what's more worrying, is that in another twenty years, the estimated number of people who could have the condition could be as high as 12 million. 
Evidence shows that Parkinson's starts with changes in gut microbes that usually break down a diverse mix of pesticides, medications, and pollutants in our environment. But it doesn't just end there. There's another paradoxical factor at work, which is expected to drive the number up to as high as 17 million.
More than 50 years ago, researchers observed a strange link between tobacco use and Parkinson's. The relationship is especially evident today, as it is confounding. The risk of the disease drops by 40% among long-term smokers. The mechanism behind this relationship is indeed a mystery, primarily when given the broad range of health risks that are known to come with cigarettes. Of course, it is not advised that you take up smoking as a result!
As depressing as the news may seem,  researchers claim that acting now can help ensure those numbers don't get so high. After all, society has successfully confronted pandemics of polio, breast cancer, and HIV to varying degrees in the past century. 

Low iron, Vitamin B12 level may up anxiety in boys

Iron deficiency and low blood levels of Vitamin B12 in small boys may be associated with behaviour problems, such as anxiety and aggression, when they get in middle school, according to a new study.
The findings showed that iron deficiency, anemia and low plasma vitamin B12 levels in boys at around age 8 were associated with 10 per cent higher mean scores on externalising behaviours such as aggression and breaking of rules.
Iron deficiency was related to an adjusted 12 per cent higher mean on internalising problem scores like anxiety and depression.
"Some parts of the brain develop throughout childhood," said a researcher.

He explained that "structural changes in the basal ganglia, hippocampus, amygdala and prefrontal cortex of the brain may be involved in the development of behaviour problems as these brain regions respond to environmental conditions at different life stages".

For the study, appearing in a journal, the team examined 3,200 children aged 5-12.

"Interventions to curb these deficiencies must be informed by knowledge of their causes in each specific setting," he said.

Previous research on infants has shown a link between iron deficiency and lower positive affect, or a child's alertness, ability to self-sooth and self-regulation.

These problems may evolve through middle childhood and show up as behavioural concerns in adolescence and lower-self-rated mental health in adulthood.

The researchers found no associations among girls.

"We don't have a clear explanation of why there were sex differences, although we knew it was important to study boys and girls separately because they may differ in the timing of development," he said.

"Studies in rats have found that some micronutrient deficiencies affect male and female brains differently but it is not clear exactly why this may also be the case in humans," he noted.

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Dysfunction in brain structure may cause Huntington's disease

Dysfunction of a group of brain structures critical for movement and impulse control may be behind Huntington's disease, according to a new study that could lead to a therapy for the currently incurable disorder.
 
Scientists at Northwestern University in the US identified a link between Huntington's disease and dysfunction of the sub-thalamic nucleus, a component of the basal ganglia, a group of brain structures critical for movement and impulse control. Huntington's disease is characterised by the progressive loss of nerve cells in the brain and affects about one in 10,000 people. This fatal disorder is caused by a hereditary defect in a single gene.

"Although the genetic basis of the disease is well established, why the mutation leads to the expression of symptoms and loss of brain tissue remains poorly understood," said Mark Bevan, professor of physiology at Northwestern University Feinberg School of Medicine. The debilitating symptoms of Huntington's disease typically manifest in adulthood and involve loss of motor and cognitive function, depression and personality changes.

From the point of onset, symptoms develop and intensify over the following 10 to 25 years until death, typically due to complications associated with the disease.

"While research into Huntington's disease has focused on other parts of the basal ganglia, the sub-thalamic nucleus has been largely overlooked," said Bevan.

"This is surprising because patients with Huntington's disease have fewer nerve cells in the sub-thalamic nucleus. People who have suffered damage to the sub-thalamic nucleus exhibit excessive movement and impulsive behaviour, similar to patients with Huntington's disease," he said.

Using mice genetically engineered to carry the Huntington's disease gene, scientists discovered the electrical activity of the subthalamic nucleus was lost.

Impaired subthalamic activity was caused by anomalous receptor signalling, leading to defective energy metabolism and accumulation of damaging oxidants.

The researchers also found abnormalities in the sub-thalamic nucleus occur earlier than in other brain regions, and that sub-thalamic nucleus nerve cells progressively degenerate as the mice age, mirroring the human pathology of
Huntington's disease. "Our findings suggest early problems in the sub-thalamic

nucleus not only contribute to the symptoms of Huntington's disease, but are also likely to impair the processing capacity and health of other brain structures, more traditionally associated with the disease," Bevan said.

Currently, there is no cure for Huntington's disease; treatment can only alleviate some of the symptoms. A better understanding of aberrant brain receptor signalling that leads to nerve cell dysfunction could reveal a target for therapy, researchers said. 

The study was published in the journal eLife.

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