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What Causes Schizophrenia In The Brain

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Neuroleptics And Progressive Brain Change

What is schizophrenia? – Anees Bahji

Lieberman and colleagues recently published a paper in the Archives in General. Psychiatry from a study comparing olanzapine with haloperidol in first-episode patients and comparing any brain changes to control changes over time. They claim that, over a 2-year period, whole gray matter volume decreases significantly more in patients administered haloperidol than in controls or patients on olanzapine. However, the time of the follow-up MRI scans was short there were many dropout subjects in this study and disproportionately among the groups and some time periods were missing in one group entirely, thus hampering interpretation of these results.

There have now been several other studies attempting to examine the question of neuroleptic effects on brain structure. While it, appears consistently in most, but, not all, studies that the caudate enlarges with typical neuroleptics, the changes seen with respect, to other cortical regions and ventricular enlargement have yet to be shown to be due to medication .

Methylation B12 Folic Acid And B6

Methylation is a critical process in the brain that helps maintain the right chemical balance. An indicator of faulty methylation is having a high level of a toxic amino acid in the blood called homocysteine. The body makes homocysteine from dietary protein and, provided you are getting enough of certain vitamins1, especially folic acid, B12 and B6, homocysteine levels decrease. Many people with schizophrenia, especially young males, tend to have a high level of homocysteine, despite no obvious dietary lack of these vitamins. High levels of homocysteine and low blood levels of folic acid have been reported by many research groups. These unusually high levels dont appear to relate to diet or lifestyle factors, such as smoking. People diagnosed with schizophrenia are more likely to have inherited a genetic variation of a key homocysteine lowering enzyme, which may make them need more of these and other nutrients.

Research at Kings College Hospital psychiatry department in London has found high doses of folic acid to be highly effective in schizophrenic patients. They used 15mg a day, which is 75 times the RDA! Folic acid is not toxic at this level. We recommend starting with 1mg a day, increasing the dose only under supervision of your health care provider.

Wheres the evidence? Search our evidence database and enter folate or folic acid and schizophrenia into the search field for a summary of studies that demonstrate the effect of folic acid on schizophrenia.

What Is Schizophrenia Or Paranoid Schizophrenia

Schizophrenia is a challenging brain disorder that often makes it difficult to distinguish between what is real and unreal, to think clearly, manage emotions, relate to others, and function normally. It affects the way a person behaves, thinks, and sees the world.

The most common form is paranoid schizophrenia, or schizophrenia with paranoia as its often called. People with paranoid schizophrenia have an altered perception of reality. They may see or hear things that dont exist, speak in confusing ways, believe that others are trying to harm them, or feel like theyre being constantly watched. This can cause relationship problems, disrupt normal daily activities like bathing, eating, or running errands, and lead to alcohol and drug abuse in an attempt to self-medicate.

Many people with schizophrenia withdraw from the outside world, act out in confusion and fear, and are at an increased risk of attempting suicide, especially during psychotic episodes, periods of depression, and in the first six months after starting treatment.

Take any suicidal thoughts or talk very seriously

If you or someone you care about is suicidal, call the National Suicide Prevention Lifeline in the U.S. at 1-800-273-TALK, visit IASP or Suicide.org to find a helpline in your country, or read Suicide Prevention.

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What Risks And Complications Can Schizophrenia Cause

Physical health

Research suggests that people with serious mental illness , such as schizophrenia, have a shorter life expectancy. People with mental illness may die 15 to 20 years earlier than the general population. This may because people who live with SMI are at higher risk of having a range of health issues. Such as being overweight, having heart disease, smoking and diabetes.

Because of these issues, NICE recommends that when you start taking antipsychotic medication, your doctor should do a full range of physical health checks. This should include weight, blood pressure and other blood tests. These checks should be repeated regularly.

Mental health professionals are responsible for doing these checks for the first year of treatment. Responsibility may then pass to your GP. Your doctor or mental health team should offer you a programme which combines healthy eating and physical health checks. You should be supported by a healthcare professional to help stop smoking.

Suicide

The risk of suicide is increased for people with schizophrenia. Research indicates that around 513% of people who live with with schizophrenia die by suicide.

Research has found that the increased risk is not usually because of positive symptoms. The risk of suicide is associated more to affective symptoms, such as low mood.

Key risk factors for suicide include:

  • previous suicide attempts,

What Are Glial Cells

Schizophrenia: Summing it Up

The brains glial cells are neurons that make up the supportive tissue in the brain. Their main role is to facilitate the communication between other neurons located not only in the central nervous system, but also in the peripheral one.

Glial cells are of two main types: astrocytes and oligodendrocytes. The former surround the synapses and facilitate interneuronal communication and make sure that any waste between the cells is eliminated, while the latter are responsible for producing myelin that is, the fatty tissue that forms a protective sheath around the axons of the neurons.

During the fetal development of the brain, glial cells form from glial progenitor cells, which are a type of pluripotent stem cell namely, an embryonic cell that can turn into any other kind of cell.

Scientists believe that genetic faults in these glial progenitor cells may lead to dysfunctional cell activity, thus causing schizophrenia.

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Does Inflammation Affect Specific Circuits And Neuromodulatory Systems

Although there is no doubt that the immune system plays a critical role in shaping brain development and contributes to disease states when dysregulated, there is a need to understand which specific circuits and neuromodulatory systems in particular are most impacted by abnormal immune signaling. It is clear that complement proteins facilitate the removal of synapses and that the upregulation of complement proteins contributes to circuit miswiring . However, SCZ is also characterized by alterations in inhibitory circuits , neuromodulatory systems such as dopamine and glutamate , and changes in the connectivity between brain regions such as the hippocampus and PFC . Do inflammatory responses alter specific neurotransmitter systems and networks differentially?

Figure 4. Neuroinflammation-induced dysfunctions that alter glutamatergic transmission in SCZ. Changes in glutamatergic transmission are known to occur in SCZ. Neuroinflammation impacts excitatory circuitry in SCZ through complement-mediated engulfment of excitatory synapses, the production of autoantibodies against NMDARs, changes in glutamate homeostasis potentially mediated by alterations in astrocytes and changes in the gut-brain axis, a known regulator of glutamate synthesis that is able to impact CNS functions such as stress responses. These changes in excitatory transmission can alter brain circuitry, for example, by altering synaptic plasticity and long-range excitation.

The Brain In Schizophrenia

Physical changes in the brain have been identified in some people with schizophrenia. The analysis of brain tissue after death has revealed a number of structural abnormalities, and new brain-imaging techniques have revealed changes in both the structure and function of the brain during life. Techniques such as magnetic resonance imaging reveal changes in the size of different parts of the brain, especially in the temporal lobes. The fluid-filled spaces in the interior of the temporal lobes are often enlarged and the temporal lobe tissue diminished. The greater the observed changes the greater the severity of the persons thought disorder and his or her auditory hallucinations.

Some imaging techniques, such as positron emission tomography , measure the actual functioning of the brain and provide a similar picture of abnormality. PET scanning reveals hyperactivity in the temporal lobes, particularly in the hippocampus, a part of the temporal lobe concerned with orientation and very short-term memory. Another type of functional imaging, electrophysiological brain recording using EEG tracings, shows that most people with schizophrenia seem to be excessively responsive to repeated environmental stimuli and more limited in their ability to blot out irrelevant information. In line with this finding, those parts of the brain that are supposed to screen out irrelevant stimuli, such as the frontal lobe, show decreased activity on PET scan.

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Role Of Amygdala And Entorhinal

Amygdala

Entorhinal-hippocampal system

Bilateral hippocampal size reduction in SZ, has been described as early as the first psychotic episode . Morphometric neuroimaging, magnetic resonance spectroscopy, and functional neuroimaging, have provided evidence for abnormal hippocampal structure and functionality in SZ. Hippocampal volume reduction is now one of the most consistent structural abnormalities found in SZ it can be found at onset of the illness and to a lesser degree in first-degree relatives of SZ patients. Decreased levels of N-acetyl-aspartate imply a cellular or axonal basis for the volume changes. Functional neuroimaging studies have demonstrated enhanced levels of hippocampal activity at rest, during the experience of auditory verbal hallucinations , and during the performance of memory retrieval tasks. These neuroimaging study results complete the evidence of post-mortem and behavioural studies, which have found specific regional hippocampal abnormalities and of memory function in SZ .

Patients with SZ undergoing fMRI during visual tasks showed reduced habituation of the hippocampus and visual cortex, and a lack of neural discrimination between old and new images in the hippocampus. Hippocampal discrimination correlated with memory performance, suggesting reduced habituation may contribute to the memory deficits commonly observed in SZ patients .

Modelling Psychosis: The Use Of Animal Models

Schizophrenia gene linked to early brain development

Potentially, the most useful avenue for animal models to assist in schizophrenia research will be identifying convergent aetiological pathways. Understanding which neurotransmitter systems and brain regions are most involved may help to identify the core neurobiological features of schizophrenia. For example, changes in dopaminergic systems are observed in animal models after manipulation of factors based on schizophrenia epidemiology, , genetics, pharmacology and related hypotheses. These include changes in early dopamine specification factors, , sensitivities to psychostimulants,,, and alterations in dopamine neurochemistry,,, . Evidence of subcortical dopaminergic hyperactivity or sensitivity in animal models is proposed to represent the face validity for psychosis in patients. The most commonly used behavioural assessments of positive symptoms in animal models include enhanced amphetamine-induced locomotion and deficits in prepulse inhibition . These tests are widely used because they are relatively simple to perform. However, we propose that given current knowledge of the neurobiology in schizophrenia, they have outlived their usefulness as measures of positive symptoms.

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Early Warning Signs Of Schizophrenia

In some people, schizophrenia appears suddenly and without warning. But for most, it comes on slowly, with subtle warning signs and a gradual decline in functioning, long before the first severe episode. Often, friends or family members will know early on that something is wrong, without knowing exactly what.

In this early phase of schizophrenia, you may seem eccentric, unmotivated, emotionless, and reclusive to others. You may start to isolate yourself, begin neglecting your appearance, say peculiar things, and show a general indifference to life. You may abandon hobbies and activities, and your performance at work or school can deteriorate.

Challenges In Diagnosing Schizophrenia

Psychiatric symptoms exist on continua from normal to pathological, meaning the threshold for diagnosis of schizophrenia in clinical practice can be challenging. The clinical diagnosis of schizophrenia relies heavily on the positive symptoms associated with a prolonged psychotic episode. However, a relatively high percentage of the general population report delusional experiences or hallucinations in their lifetime,,, but for most people these are transient. Psychotic symptoms are also not specific to a particular mental disorder. The clinical efficacy of antipsychotic drugs is heavily correlated with their ability to block subcortical dopamine D2 receptors, , suggesting dopamine signalling is important. In spite of this, no consistent relationship between D2 receptors and the pathophysiology of schizophrenia has emerged, . In contrast, the clinical evidence points towards presynaptic dopamine dysfunction as a mediator of psychosis in schizophrenia.

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What Are Psychotic Disorders

Simply defined, a psychotic disorder is a condition that distorts someones reality, making it difficult for them to distinguish what is real from what is not. Increased dopamine levels in the brain cause an individual to have a different sensory experience than those around them. These brain health conditions can come in the form of bipolar disorder, a primary mood disorder that can lead to psychosis, and schizophrenia, a primary psychotic disorder.

Schizophrenia is characterized by negative and positive symptoms. Negative symptoms are harder to identify and usually occur during prodrome the stage that occurs right before a psychosis episode.

What If I Am Not Happy With My Treatment

What places in the human brain does schizophrenia affect ...

If you are not happy with your treatment you can:

  • talk to your doctor about your treatment options,
  • ask for a second opinion,
  • get an advocate to help you speak to your doctor,
  • contact Patient Advice and Liaison Service and see whether they can help, or
  • make a complaint.

There is more information about these options below.

Treatment options

You should first speak to your doctor about your treatment. Explain why you are not happy with it. You could ask what other treatments you could try.

Tell your doctor if there is a type of treatment that you would like to try. Doctors should listen to your preference. If you are not given this treatment, ask your doctor to explain why it is not suitable for you.

Second opinion

A second opinion means that you would like a different doctor to give their opinion about what treatment you should have. You can also ask for a second opinion if you disagree with your diagnosis.

You dont have a right to a second opinion. But your doctor should listen to your reason for wanting a second opinion.

Advocacy

An advocate is independent from the mental health service. They are free to use. They can be useful if you find it difficult to get your views heard.

There are different types of advocates available. Community advocates can support you to get a health professional to listen to your concerns. And help you to get the treatment that you would like.

The Patient Advice and Liaison Service

Complaints

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What Are The Symptoms Of Schizophrenia And How Is It Diagnosed

How is schizophrenia diagnosed?

Only a psychiatrist can diagnose you with schizophrenia after a full psychiatric assessment. You may have to see the psychiatrist a few times before they diagnose you. This is because they need to see how often you are experiencing symptoms.

There are currently no blood tests or scans that can prove if you have schizophrenia. So, psychiatrists use manuals to diagnose schizophrenia and other mental illnesses.

The 2 main manuals used by medical professionals are the:

  • International Classification of Diseases which is produced by the World Health Organisation , or
  • Diagnostic and Statistical Manual which is produced by the American Psychiatric Association .

NHS doctors use the ICD-10.

The manuals explain which symptoms should be present, and for how long for you to receive a diagnosis. For example, according to the NHS you need to be hearing voices for at least 1 month before you can be diagnosed. Mental health professionals may say you have psychosis before they diagnose you with schizophrenia.

What is the future of diagnosis in schizophrenia?There are many research studies being conducted across the world on how to better diagnose schizophrenia. For example, a recent study found through looking at images of the brain, there may be different sub-types of schizophrenia.

What are the symptoms of schizophrenia?

The symptoms of schizophrenia are commonly described as positive symptoms or negative symptoms. This doesnt mean that they are good or bad.

Family Education And Support

Educational programs for family members, significant others and friends offer instruction about schizophrenia symptoms and treatments, and strategies for assisting the person with the illness. Increasing key supportersâ understanding of psychotic symptoms, treatment options and the course of recovery can lessen their distress, bolster coping and empowerment, and strengthen their capacity to offer effective assistance.

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Treatment For Psychotic Disorders

The stigma surrounding psychotic disorders has changed greatly over the years. Patients went from no treatment available, to rather questionable treatment methods, to old-school medications with notable side effects.

Weve come a long way in terms of research, therapy and medication. Psychiatrists now use a combination of both science-based methods and emotional approaches . Having a sense of understanding and respect for those living with these conditions has also made recovery a real possibility for them.

You cant prevent a psychotic disorder, especially if its genetic, but you can avoid possible triggers.

Just like any physical condition, working out, eating well and limiting your substance use can play a positive role in improving your mental health.

If you or a loved ones brain does experience psychosis, you should treat it like any other part of the body and get help. With the right medication, therapy and support from your Valleywise Health community, you or your friends and family members can feel confident in getting back to a more normal life.

Is Scz An Inflammatory Disease

What Causes Schizophrenia?

There is growing evidence from both human and animal studies that many of the risk factors for SCZ converge on their ability to promote neuroinflammation, and that these effects are mediated in part by microglia. However, is there a pro-inflammatory phenotype in SCZ? Post-mortem and clinical studies show an increase in pro-inflammatory markers in people with SCZ compared to controls . Moreover, there is evidence for elevated levels of cytokines in blood samples from people with SCZ, whether they are medication-naive or receiving antipsychotic treatment, during episodes of psychosis . Thus, such studies suggest that inflammation might contribute to the development of SCZ and also drive its progression and cyclic nature.

Indeed, there are multiple disease-associated microglial subtypes such as those seen in neurodegenerative disorders and dark microglia which were recently observed in SCZ post-mortem brain samples . More work is needed to fully understand microglial subtypes that are more prevalent in disease states and how they contribute together to pathology, however data suggest they partially contribute to disease by enhancing synaptic pruning . Future studies should also aim to develop more translational animal models so that in vivo studies can be performed to gain greater understanding into how microglia functionally impact synaptic development and circuit function in pathological states.

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