Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis

By 3 December 2017SIGNATURE FINDINGS
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Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis (±x)

Published on 3rd December 2017
Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

Information Security Architect / Intelligence Analyst / Computer Scientist / Human Rights Activist / COMSEC / SIGINT / TSCM
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Medical Definition of Anhedonia

Anhedonia: Loss of the capacity to experience pleasure. The inability to gain pleasure from normally pleasurable experiences.

Anhedonia is a CORE CLINICAL FEATURE of depression, schizophrenia and some other mental illnesses.

Anhedonia is the inability to experience pleasure from activities usually found enjoyable or the impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always associated with conscious awareness. The term was first introduced by Théodule – Armand Ribot. It’s easier to understand this with examples. For instance, a mother will find no joy in playing with her child or a passionate dancer will be uneager to dance. An other, alternative, theory, suggests that anhedonia derives from the incapability to sustain good feelings over time3. In this case, pleasure might be experienced fully, but briefly, not long enough to maintain an interest or involvement in the action.

Types of Anhedonia

There are five (5) types of anhedonia; consummatory, motivational, social, sexual and specific musical. Consummatory, exists when the person gains no satisfaction from activities, previously or not, considered enjoyable. There’s no anticipation for a reward. Motivational, describes a person who shows no interest in taking part in pleasurable activities, because not even a reward is enough of a motivation to them. Social, is about a person who withdraws from all social gatherings and contacts. They’ve no interest to interact or make friends, they want to be alone all the time and have a hard time adjusting socially, contrasting to introversion.

Sexual or ejaculatory, is most common in men and qualifies the state of not feeling fulfillment or enjoyment from the sexual action.

This form of anhedonia might be caused by low testosterone levels, fatigue, or physical illness. The fifth type is the specific musical anhedonia. In this case, the individual has no problem processing musical sounds or beats, but receives no pleasure from listening to music. This state, however, shouldn’t be confused with “melophobia” the fear of music.

Symptoms, Causes & Treatment

The symptoms of anhedonia are many, some of them being an incredibly flat mood with no variations and the suffering individual being unable to react properly or feel anything. It is associated with many schizophrenia – spectrum disorders, depression and social anxiety.

Anhedonia may result from the breakdown in the brain’s reward system. Every time we feel pleasure, the neurotransmitter chemical called dopamine, fills the part of our brains called striatum. The disease may be linked with a lower activity in a part of our brain’s called prefrontal cortex, also used with its abbreviation, PFC. Anhedonia causes its effects through this cortex, which controls the dopamine releases.

Though it is related to depression and anxiety disorder, anhedonia isn’t the only reason for these disorders. Risk factors of it are a history of major depression disorder (MDD) or schizophrenia, a recent traumatic or stressful event, a history of abuse or neglect, a major illness, an eating disorder or it might be due to a recreational drug use.

The disease can only be diagnosed through counseling. You should tell your therapist about your symptoms, including the loss of experiencing pleasure. Your doctor may want to run a blood test to check for a vitamin deficiency or a thyroid problem. Unfortunately, there’s no validated treatment, especially for social anhedonia. There’s no medication developed specifically aiming at anhedonia.

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The folowing audio recording is from 19 December 2015 and is between my attorney Rienzie Arseculeratne PC and I.

As can be heard I am LAUGHING HEARTILY despite the trauma of Aggravated Kidnapping and Unlawful Imprisonment. It was not really that traumatic for me because I had correctly identified the POLITICAL PSYCHIATRY involved in a COMPLETELY BOTCHED Military Intelligence / EXTRAORDINARY RENDITION. However I did have serious physical injuries and was in severe pain and the stress I was experiencing was obviously more than nominal levels.

MY ABILITY TO DERIVE PLEASURE FROM MERELY A SOCIAL INTERACTION OVER THE PHONE CONFIRMS THE TRUE POSITION IN RELATION TO MY MENTAL HEALTH OR OTHERWISE 🙂

Stress Triggers Psychosis in Individuals Vulnerable to Schizophrenia

The below audio recording was made on 18 December 2015 when I unlawfully imprisoned in the Psychiatric Facility:- A key statement I made is "If...

BEING ABLE TO DERIVE PLEASURE FROM THE SOCIAL INTERACTION, AS WELL AS MOTIVATING MYSELF (AND ANTICIPATING MY FORTHCOMING PLEASURE FROM THE ‘JAILBREAK’ THAT I WAS PLANNING) UTTERLY DESTROYS THE FRAUDULENT DIAGNOSIS OF SCHIZOPHRENIA 🙂

I refer to the following medical whitepaper:-

Negative symptoms of schizophrenia: Clinical characteristics, pathophysiological substrates, experimental models and prospects for improved treatment

Schizophrenia is a complex and multifactorial disorder generally diagnosed in young adults at the time of the first psychotic episode of delusions and hallucinations. These positive symptoms can be controlled in most patients by currently-available...

Abstract

Schizophrenia is a complex and multi-factorial disorder generally diagnosed in young adults even the ages range is wrong for me:-

Schizophrenia - The Fraud Game for Ages 15-25yrs

Video Analysis Referring to the video above, the gorgeous blonde babe states (in relation to 'arm pain') "Common sense tells me that as bad as arm...

Auditory and Visual Hallucinations - Definitely Schizophrenia

* * OBVIOUSLY IT IS NOT A HALLUCINATION IF THERE IS VOLUMINOUS FORENSIC EVIDENCE RELATING TO THE 12/17 FRAUD, WHICH CAN BE ANALYSED 650 DAYS...

These positive symptoms can be controlled in most patients by currently-available antipsychotics. Conversely, they are poorly effective against concomitant neurocognitive dysfunction

Memory Deficits in Schizophrenia

THERE ARE ALWAYS OBSERVABLE/TESTABLE MEMORY DEFICITS IN PATIENTS WHO GENUINELY SUFFER FROM SCHIZOPHRENIA. NO MEMORY DEFICITS = NOT SCHIZOPHRENIA AND...

deficits in social cognition and negative symptoms (NS), which strongly contribute to poor functional out

The Flat Affect in Schizophrenia

Flat affect, or impaired emotional functioning, is a SIGNATURE symptom of schizophrenia. It's a term used to describe the lack of emotional expression

and “avolition”, which embraces amotivation, asociality and “anhedonia” (inability to anticipate pleasure). Recent studies implicate a dysfunction of frontocortico-temporal networks in the aetiology of NS, together with a disruption of cortico-striatal circuits, though other structures are also involved, like the insular and parietal cortices, amygdala and thalamus.

At the cellular level, a disruption of GABAergic–glutamatergic balance, dopaminergic signalling and, possibly, oxytocinergic and cannibinoidergic transmission may be involved. Several agents are currently under clinical investigation for the potentially improved control of NS, including oxytocin itself, N-Methyl-d-Aspartate receptor modulators and minocycline.

Further, magnetic-electrical “stimulation” strategies to recruit cortical circuits and “cognitive–behavioural–psychosocial” therapies likewise hold promise. To acquire novel insights into the causes and treatment of NS, experimental study is crucial, and opportunities are emerging for improved genetic, pharmacological and developmental modelling, together with more refined readouts related to deficits in reward, sociality and “expression”.

The present article comprises an integrative overview of the above issues as a platform for this Special Issue of European Neuropsychopharmacology in which five clinical and five preclinical articles treat individual themes in greater detail. This Volume provides, then, a framework for progress in the understanding – and ultimately control – of the debilitating NS of schizophrenia.

Anhedonia in Schizophrenia: A Deficit in Translating Reward Information into Motivated Behavior

Anhedonia has long been considered a core clinical feature of schizophrenia, which is thought to be an important predictor of functional outcome and disease liability. However, recent developments in

Abstract

Anhedonia has long been considered a core clinical feature of schizophrenia, which is thought to be an important predictor of functional outcome and disease liability.

However, recent developments in the affective neuroscience of schizophrenia suggest that the traditional understanding of anhedonia as a diminished capacity for pleasure may not correctly characterize the affective abnormalities that occur in this patient population.

In the current chapter, literature is reviewed to suggest that anhedonia in schizophrenia primarily reflects a deficit in initiating activities aimed at receiving rewards, rather than a reduced capacity to experience pleasure when patients are exposed to rewards.

Multiple psychological and neural mechanisms appear to impair the translation of intact hedonic responses into goal directed behavior in schizophrenia. Several of these mechanisms are reviewed here, including: (1) dopamine-mediated basal ganglia systems that support reinforcement learning and the ability to predict cues that lead to rewarding outcomes; (2) orbitofrontal cortex-driven deficits in generating, updating, and maintaining value representations; (3) aberrant effort-value computations, which may be mediated by disrupted anterior cingulate cortex and midbrain dopamine functioning; (4) altered activation of the prefrontal cortex, which is important for generating exploratory behaviors in environments where reward outcomes are uncertain.

Overall, findings suggest that aberrant cortical-striatal interactions are involved with the reduced frequency of pleasurable activities that CHARACTERIZES SCHIZOPHRENIA.

Suggestions are provided for the development of novel behavioral intervention strategies that make use of external cues and reinforcers designed to facilitate goal-directed behavior in light of these various reward-processing deficits. Future directions for examining anhedonia in relation to modern affective neuroscience perspectives are also discussed.

The case continues…

Complete Absence of Alogia Further Destroys Fraudulent Schizophrenia Diagnosis

In psychology, alogia (Greek ἀ-, “without”, and λόγος, “speech”[1]), or poverty of speech,[2] is a general lack of additional, unprompted content seen...
Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

Information Security Architect / Intelligence Analyst / Computer Scientist / Human Rights Activist / COMSEC / SIGINT / TSCM
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