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Is Schizophrenia A Degenerative Disease

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Rem Sleep Behaviour Disorder

Schizophrenia May Be an Autoimmune Condition

Predicted on theoretical grounds before it was described in man, this striking parasomnia is caused by loss of REM sleep atonia sufferers enact their dreams, which are often aggressive, placing both themselves and their bed partners at considerable risk. The diagnostic clue is that, once woken, sufferers can generally recall a dream narrative. REM sleep behaviour disorder is associated with a range of neurodegenerative disorders, particularly Parkinsons disease and multiple systems atrophy. The disorder may precede the recognisable onset of these conditions by several years. Clonazepam is often an effective treatment.

Neurological Patients Versus Functional Imaging

At their core, psychopathologies are manifest as dysfunctions in emotional, cognitive, and social functioning. Historically, studies of neurological patients have contributed immensely to fundamental discoveries in psychology related to the neural circuitry that underlies these processes. As previously noted :

Studies of neurological patients have been critical to advancing our understanding of the human brain. In some instances, fundamental insights were gained and doors opened to entire new areas of inquiry based on findings from a single patient such as Phineas Gage and the frontal lobes and Patient H.M. and the organization of memory . In other instances, findings from a small group of patients were seminal, such as epileptics treated with cerebral commissurotomy and hemispheric specialization . In addition to these spectacular advances, there has been a steady and continuing parade of findings derived from the deceptively simple strategy of identifying individuals with loss in particular brain areas of interest, determining how their abilities and functioning differ from the norm, and studying the ways that they change over time.

Disorganized Symptoms Of Schizophrenia

These are positive symptoms that show that the person canât think clearly or respond as expected. Examples include:

  • Talking in sentences that donât make sense or using nonsense words, making it difficult for the person to communicate or hold a conversation
  • Shifting quickly from one thought to the next without obvious or logical connections between them
  • Moving slowly
  • Repeating movements or gestures, like pacing or walking in circles
  • Having problems making sense of everyday sights, sounds, and feelings

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Frontotemporal Dementia Manifested As Schizophrenia With Decreased Heterochromatin On Chromosome 1

Philippos Gourzis

1Department of Psychiatry, School of Medicine and University Hospital of Patras, University of Patras, 26504 Rio, Patras, Greece

2Department of Neurology, School of Medicine and University Hospital of Patras, University of Patras, 26504 Rio, Patras, Greece

3Department of Chemistry, Laboratory of Biochemistry, University of Patras, 26504 Rio, Patras, Greece

4Department of Genetics, Alexandra Hospital, 10671 Athens, Greece

Academic Editor:


1. Introduction

Frontotemporal dementia is a mainly presenile degenerative disorder marked by progressive behavioural changes and cognitive impairment, characterized by progressive atrophy of both frontal and anterior temporal lobes . The disease has now been proved as the second most common type of presenile dementia, with a correlation ratio of about one case of FTD to four of Alzheimers disease . An autosomal dominant pattern of inheritance is found in 1027% of all FTD patients , with several genetic defects identified in some, but not all, hereditary cases of FTD .

Differentiation between FTD, primary psychiatric disorders, AD, and other dementias is crucial for case management and determining prognosis. Identification of factors relating to etiology, age of onset, and clinical presentation of FTD could help expand our understanding of the pathogenesis of the disorder, and probably enhance accurate clinical diagnosis .

2. Case Presentation

3. Discussion

Abbreviation List




What Are The Early Symptoms Of Schizophrenia


The condition usually shows its first signs in men in their late teens or early 20s. It mostly affects women in their early 20s and 30s. The period when symptoms first start and before full psychosis is called the prodromal period. It can last days, weeks, or even years. It can be hard to spot because thereâs usually no specific trigger. You might only notice subtle behavioral changes, especially in teens. This includes:

  • A change in grades
  • Difficulty sleeping

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When Do The Cognitive Impairments Emerge

There is no doubt that neurocognitive impairments are evident at the onset of illness in most patients who develop schizophrenia. However, we must also be aware that 3540% of the patients do not have a significant impairment in neurocognitive functioning i.e. they function within what must be characterized as the normal range . Nevertheless, patients functioning within the normal range may have had a reduction in neurocognitive functioning after they became ill. Also several studies of high risk groups have found that these individuals show signs of neurocognitive deficits many years prior to the onset of illness . Moreover, several prodromal studies indicate that the neurocognitive impairments evident after the psychotic breakthrough are also evident prior to the onset of illness . Probably there is a further reduction in neurocognitive functioning just prior to the first psychotic episode . A preliminary conclusion is that precursors to the cognitive deficits are evident relatively early, that these develop gradually and that they are found in corresponding form and approximately the same degree in the prodromal phase, as in remission. The psychotic experiences or symptoms exacerbate the neurocognitive deficits somewhat during the acute phase. Such a development with an early insult in the neural development that remains for the duration of life, but that does not get worse over time, may best be characterized as a static encephalopathy .

Difference Between Schizophrenia And Alzheimers

June 13, 2018 Posted by Ranidu

The key difference between Schizophrenia and Alzheimers is that the Schizophrenia is a psychiatric illness, but Alzheimers is a neurological disorder.

Schizophrenia and Alzheimers disease are chronic debilitating diseases that severely hinder the patients ability to maintain a normal life. Schizophrenia is a long-term mental disorder, involving a breakdown in the relation between thought, emotion, and behaviour leading to faulty perception, inappropriate actions, and feelings, withdrawal from reality into fantasy and delusions and a sense of mental fragmentation. Alzheimers, on the other hand, is widely regarded as the commonest cause of dementia.

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Comparison Of Psychotic Disorders

The term psychosis has been defined in various ways in the medical literature over time. The narrowest and current definition of psychosis is hallucinations and delusions, with the lack of reality testing or insight. A broader definition of psychosis would also include disorganized thought, emotions, and behaviour. This loose definition was more common in the past, and schizophrenia was often overdiagnosed as a result.

DSM-IV to DSM 5 Psychotic Disorder Criteria Changes

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Emotional And Behavioral Symptoms In Neurodegenerative Disease: A Model For Studying The Neural Bases Of Psychopathology

Charlotte Gerson on Schizophrenia

Annual Review of Clinical Psychology

Vol. 10:581-606 First published online as a Review in Advance on January 15, 2014

Robert W. Levenson,1 Virginia E. Sturm,2 and Claudia M. Haase3

1Department of Psychology and Institute of Personality and Social Research, University of California, Berkeley, Berkeley, California 94720 email:

2Memory and Aging Center, University of California, San Francisco, San Francisco 94158, California email:

3School of Education and Social Policy, Northwestern University, Evanston, Illinois 60208 email:

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Implications For Etiology Diagnosis And Treatment

Identifying neural circuits associated with core symptoms of psychopathology will surely contribute greatly to our fundamental understanding of the brain, of functional and dysfunctional behaviors, and of brain-behavior relationships. However, in public healthrelevant initiatives such as RDoC, there is a clear expectation that studying these relationships will have significant applied and practical benefits as well, leading to palpable advances in diagnosis, prevention, and treatment that will help relieve the enormous burden and suffering associated with mental illness. Envisioning how the latter might work requires a bit of extrapolation and conjecture.

In the realm of diagnosis, it is highly likely that future assessments will be expanded to include more detailed assessment of the status of key neural circuits in the brain. This may include measures of brain structure as well as measures of brain function . These kinds of assessments may be particularly helpful for diagnosing symptoms of mental illness, for identifying preclinical vulnerabilities, and for suggesting targets for early preventive interventions.

Is Schizophrenia A Degenerative Disease

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Articles On Schizophrenia Overview

Schizophrenia is a chronic, severe mental disorder that affects the way a person thinks, acts, expresses emotions, perceives reality, and relates to others. Though schizophrenia isnât as common as other major mental illnesses, it can be the most chronic and disabling.

People with schizophrenia often have problems doing well in society, at work, at school, and in relationships. They might feel frightened and withdrawn, and could appear to have lost touch with reality. This lifelong disease canât be cured but can be controlled with proper treatment.

Contrary to popular belief, schizophrenia is not a split or multiple personality. Schizophrenia involves a psychosis, a type of mental illness in which a person canât tell whatâs real from whatâs imagined. At times, people with psychotic disorders lose touch with reality. The world may seem like a jumble of confusing thoughts, images, and sounds. Their behavior may be very strange and even shocking. A sudden change in personality and behavior, which happens when people who have it lose touch with reality, is called a psychotic episode.

Understanding Cognitive Dysfunction In Schizophrenia: Animal Experiments

Face Seen From The Side. Brain Problems. Degenerative ...

Changes in synaptic plasticity in the hippocampus of patients with schizophrenia could be followed by a reduction in long-term potentiation and also long-term depression or an impaired regulation of both in terms of meta-plasticity, with implications for the functioning of the episodic memory system . However, all of these assumptions are indirect and not as tightly connected as they could be if derived from an animal model. Providing a close link between postmortem and in vivo findings in schizophrenia patients and animal models of schizophrenia, including differences in LTP and behaviour, is a challenging task. The question that immediately arises is whether a suitable animal model is able to mimic at least certain defined aspects of the clinical picture or neurobiological features or both.

Taken together, data obtained from human and animal studies provide growing evidence about the role of TCF4 not only in CNS development but foremost in higher order information processing, including cognition and sensorimotor gating. Considering that not only genetic but also environmental factors contribute to the development of schizophrenia, it is noteworthy that the cognitive performance of Tcf4tg mice can be modulated by different environmental conditions .

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Negative Symptoms Of Schizophrenia

The word “negative” here doesnât mean “bad.” It notes the absence of normal behaviors in people with schizophrenia. Negative symptoms of schizophrenia include:

  • Lack of emotion or a limited range of emotions
  • Withdrawal from family, friends, and social activities
  • Less energy
  • Loss of pleasure or interest in life
  • Poor hygiene and grooming habits

Is Schizophrenia A Neurodegenerative Disorder

It was earlier believed that the course of schizophrenia was always progressive and improvement was not possible. Kraepelin had called schizophrenia Dementia praecox, implying a progressive deterioration from which recovery was not possible. On examining the clinical course of the disorder, we see that some patients have a deteriorating rather than a static course a subgroup of patients has a chronic course with multiple exacerbations. The likelihood of deterioration correlates with the number of periods and the duration of positive symptoms.

Early treatment with antipsychotic medications may arrest this progression. A longer duration of untreated psychosis predicts a poorer outcome, suggesting that there are possible adverse neurotoxic effects of untreated psychosis. Long DUP predicted worse response to medications, higher relapse risk, and mixed association with other outcome measures. This indicates that a pathological process is occurring in the brain, against which drugs played a protective role. It is also seen that patients appear to take longer to recover and show less complete recovery over successive episodes of this illness.

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Longitudinal Studies And The Effects Of Antipsychotic Medication

Longitudinal MRI studies have now shown that brain tissue volumes decrease and CSF volumes increase over time to a greater degree in patients with schizophrenia than control subjects.,, However, there is now compelling evidence that antipsychotic medications have an important role in contributing to these progressive changes., Lieberman et al followed patients treated with either olanzapine or haloperidol for a FEP for 2 years patients treated with haloperidol but not olanzapine had worsening deficits in gray matter volumes that were already apparent after 12 weeks of treatment. It was unclear whether the relative volume reductions seen in the haloperidol-treated group reflected a disease process that was ameliorated by olanzapine but not haloperidol, a drug effect caused by haloperidol but not olanzapine, an increase in relative tissue volume related to the weight gain and metabolic effects associated with olanzapine, or a statistical artifact caused by sample attrition.

Ho et al have now demonstrated an association between antipsychotic treatment and brain volume reductions in patients ascertained with a FES who were scanned longitudinally over an average of 7.2 years. Antipsychotics were associated with decreases in gray- and white matter volumes with higher doses resulting in greater decreases.

The Time Course Of Cognitive Deficits

Subtypes of schizophrenia: different diseases within the same diagnosis

When cognitive deficits are first present and whether there is some stage of the illness during which they progress have been areas of intensive study., Cognitive deficits have been clearly demonstrated at the time of the FEP.,, Cognition has been demonstrated to remain stable or improve, rather than deteriorate following a FEP. The improvement reported in some studies may reflect practice effects rather than real improvement. Nevertheless, there is a consensus that this improvement plateaus following a FEP or FES, after which cognition does not worsen over time beyond what can be expected with normal aging.,, Whether elderly patients with schizophrenia may experience a phase of cognitive decline that is of greater slope than that observed in otherwise healthy people, remains a possibility that requires further investigation.

In accord with the above, individuals considered to be at clinical high risk for psychosis have been demonstrated to have significant cognitive deficits with those who eventually develop psychosis having greater deficits than those who do not. However, studies by Keefe et al and Becker et al were not able to demonstrate any further deterioration in cognition in those at-risk subjects who subsequently transitioned to psychosis. The potential for such studies to identify significant deterioration in cognition has been limited by their small sample sizes and their identification of at-risk subjects late in the prodromal phase.

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Neurology Psychology And Psychiatry

Neurology has an especially close relationship with psychology and psychiatry, as all three disciplines focus on the functions and disorders of a single organ, the brain. The main targets of the traditional British neurological examination may be elementary motor and sensory processes, but any adequate assessment of brain function must take account of cognition and behaviour. The notion many of us bring to neurologythat only a minority of neurological disorders has a significant psychological or psychiatric dimensionis almost certainly wrong. Cognitive and behavioural involvement is the rule, not the exception, among patients with disorders of the central nervous system . The physical and psychological symptoms of disease can therefore be related in the following ways: physical symptoms come to light by way of complex psychological processes psychological upset can manifest itself in physical symptoms physical diseases commonly cause a secondary psychological reaction one category of physical disease, affecting the brain, can give rise, more or less directly, to psychological manifestations.

We believe that all neurologists in training would benefit from spending some time with a neuropsychiatrist or with a liaison psychiatrist who is experienced in dealing with neurological patients, and should equip themselves to perform at least a basic neuropsychiatric assessment. There are several excellent textbooks which provide a background in the subject.

Schizophrenia Today: Still A Cognitive Disorder With An Unfavourable Outcome

More than a 100 years after Kraepelin popularised the term Dementia Praecox, schizophrenia still has an unfavourable prognosis. The worldwide prevalence is 1% and the first onset is usually in young adults aged between 20 and 35., Only 20% of patients are employed in the primary labour market and only 30% are able to maintain a stable relationship.

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Understanding Cognitive Dysfunction In Schizophrenia: Human Studies

As outlined above, cognitive dysfunction is one key to the unfavourable outcome in schizophrenia and may be independent of the long-term course of both positive and negative symptoms., , Recent studies suggest that cognitive disturbance in schizophrenia contributes to relapses and also has a role in the likelihood of remission. Understanding the underlying neurobiology of cognitive dysfunction is critical to improve outcome, and parallel investigations of patients and animal models form the best strategy to improve such understanding .

Figure 2

From genetic to environmental risk factors: parallels in humans and animal models. CNV, copy number variation Hi, hippocampus LTP, long-term potentiation PfCx, prefrontal cortex SZ, schizophrenia TCF4, transcription factor 4 VLMT, verbal learning and memory test.

Structural and functional alterations in specific brain networks of schizophrenia patients may be a hallmark of the underlying pathophysiology. To address this, we reviewed magnetic resonance imaging findings in schizophrenia and thereby focussed on high-quality meta-analyses based on a highly standardized literature extraction and evaluation. We focused on results from structural and functional MRI studies and did not consider the large body of evidence from positron emission tomography and spectroscopy studies for reasons of space.

The Search For Progressive Brain Changes


Researchers have sought to identify structural brain changes in schizophrenia since the time of Kraepelin. Postmortem and pneumoencephalographic studies, provided support for the presence of atrophic brain changes in some patients with chronic schizophrenia. However, the opportunity to systematically investigate brain structure emerged in the 1970s and 1980s. Computed tomography revealed that patients with schizophrenia on average had larger intracranial cerebrospinal fluid volumes, including larger lateral ventricles, and cortical sulci., Subsequent MRI studies demonstrated widespread deficits in gray matter volumes, and white matter volumes. The magnitude of these group differences was observed to be greater for more chronically ill patients. From the outset, both CT and MRI studies sought to demonstrate associations between illness duration and the magnitude of CSF and gray matter volumes, but with little success.,

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