Signature Impairment of Affective Prosody Confirmed in Schizophrenia

By | SIGNATURE FINDINGS
Signature-Impairment-of-Affective-Prosody-Confirmed-in-Schizophrenia-1300x400-imgs

Signature Impairment of Affective Prosody Confirmed in Schizophrenia

Published on 4th 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
465

Joseph de Saram demonstrates how Aprosodia, a neurological condition characterized by the inability of a person to properly convey or interpret emotional Prosody. is a signature clinical finding in Schizophrenoa.

heading

text

Psycholinguistics/Prosody

Emotion is a very important part of our conveyance and understanding of language. Research has shown that our understanding and memory of sentences and speech can be altered by emotional aspects. Emotions in speech can be conveyed from the words that we...

Disturbances of affective prosody in patients with schizophrenia; a cross sectional study

The objective was to determine whether disturbances of affective prosody constitute part of the symptomatology of schizophrenia. Affective prosody is defined here as a neuropsychological function that encompasses all non-verbal aspects of language that are necessary for recognising and conveying emotions in communication. ...

IT IS EASY TO CONFIRM A COMPLETE ABSENCE OF MENTAL ILLNESS 🙂

I refer to the following article:-

Impaired Perception of Affective Prosody in Schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Affective-prosodic deficits in schizophrenia: profiles of patients with brain damage and comparison with relation to schizophrenic symptoms

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Impaired recognition and expression of emotional prosody in schizophrenia: Review and meta-analysis

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Not Pitch Perfect: Sensory Contributions to Affective Communication Impairment in Schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Altered lateralisation of emotional prosody processing in schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

The emotional paradox: Dissociation between explicit and implicit processing of emotional prosody in schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Prosody recognition and audiovisual emotion matching in schizophrenia: The contribution of cognition and psychopathology

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

Receptive and Expressive Social Communication in Schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

and refer to the following paragraphs:-

Shared clinical features

Although the disorders are distinct, they have shared clinical features.

SOCIAL WITHDRAWAL, COMMUNICATION IMPAIRMENT, and POOR EYE CONTACT

seen in ASD are similar to the negative symptoms seen in youths with schizophrenia.

11 When higher-functioning individuals with autism are stressed, they become highly anxious and at times may appear thought-disordered and paranoid, particularly when they are asked to shift set (such as being asked to change a topic of conversation or to stop an activity that they are engaged in and begin a new activity).

[DOES NOT APPLY TO ME – ASK ME ABOUT ANYTHING AND ANALYSE THE RESPONSES :)]

12 A subset of children (28%) in the ongoing NIMH study of COS have been reported to have comorbid COS and ASD.7

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

Deficits of Logical Reasoning have long been considered a Hallmark of Schizophrenia

By | SIGNATURE FINDINGS

Deficits of Logical Reasoning have long been considered a Hallmark of Schizophrenia

Published on 4th 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
486

Enter more text here

https://www.tandfonline.com/doi/abs/10.1080/hrp_8.2.73

Matters of Intelligence

"My personality is designed by me - my attitude is defined by you." - JSRDS This is an article about Intelligence and IQ, and the types of problems...

IT IS EASY TO CONFIRM A COMPLETE ABSENCE OF MENTAL ILLNESS 🙂

I refer to the following article:-

Autism and Schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

and refer to the following paragraphs:-

Shared clinical features

Although the disorders are distinct, they have shared clinical features.

SOCIAL WITHDRAWAL, COMMUNICATION IMPAIRMENT, and POOR EYE CONTACT

seen in ASD are similar to the negative symptoms seen in youths with schizophrenia.

11 When higher-functioning individuals with autism are stressed, they become highly anxious and at times may appear thought-disordered and paranoid, particularly when they are asked to shift set (such as being asked to change a topic of conversation or to stop an activity that they are engaged in and begin a new activity).

[DOES NOT APPLY TO ME – ASK ME ABOUT ANYTHING AND ANALYSE THE RESPONSES :)]

12 A subset of children (28%) in the ongoing NIMH study of COS have been reported to have comorbid COS and ASD.7

Psychiatric Disorders/Psychotic Disorders/Schizophrenia

Schizophrenia is a devastating illness that affects approximately 1% of the population. Its primary impact is on thought, and its cardinal symptom is psychotic thinking in affecting individuals. In addition, however, it can affect many aspects of...

Disturbances of Affect and Mood

Disorders of mood and affect include affective flattening,

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

which is a reduced intensity of emotional expression and responsiveness that leaves patients indifferent and apathetic. Typically, one sees unchanging facial expression, decreased spontaneous movements, poverty of expressive gestures,

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 see...

Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis

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

Transient, isolated, and mild mood disturbances are not infrequently seen in schizophrenia, with these changes tending toward elation, depression, or anxiety. A number of patients, during a partial remission of the psychotic symptoms, develop a full depressive syndrome, the so-called “post-psychotic depression” of schizophrenia.

Processing Eye Gaze is Also Affected

Eye-contact perception in schizophrenia: relationship with symptoms and socioemotional functioning.

J Abnorm Psychol. 2012 Aug;121(3):616-27. doi: 10.1037/a0026596. Epub 2012 Jan 16. Research Support, Non-U.S. Gov't...

Accurately perceiving self-referential social signals, particularly eye contact, is critical to social adaptation.

Schizophrenia is often accompanied by deficits in social cognition, but it is unclear whether this includes gaze discrimination deficits.

This study investigated whether eye-contact perception is preserved or impaired and if it is related to symptoms and broader socioemotional functioning in schizophrenia.

Twenty-six participants with schizophrenia (SCZ) and 23 healthy controls (HC) made eye-contact judgments for faces in varying gaze direction (from averted to direct in ten 10% increments), head orientation (forward, 30° averted), and emotion (neutral, fearful).

Psychophysical analyses for forward faces showed that SCZ began endorsing eye contact with

weaker eye-contact signal

and their eye-contact perception was less of a dichotomous function, as compared with HC. SCZ were more likely than HC to endorse eye contact when gaze was ambiguous, and this overperception of eye contact was modulated by head orientation and emotion. Overperception of eye contact was associated with more severe negative symptoms.

Decreased categorical gaze perception explained variance of socioemotional deficits in schizophrenia

after taking basic neurocognition into consideration, suggesting the relationship was not solely due to a general deficit problem. These results were discussed in relation to the nature of categorical gaze perception and its significance to clinical and functional presentations of schizophrenia.

and

http://www.apa.org/gradpsych/2014/04/eye-contact.aspx

Poor Eye Movement in Schizophrenia

Note the jerky movements and requirement to recorrect:-

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

I DO NOT LOOK AWAY FROM THE PERSON THAT I AM SPEAKING WITH. THIS IN ITSELF DEMONSTRATES NO SOCIAL COMMUNICATION DIFFICULTIES AND CONFIRMS AN EXTREMELY CONFIDENT PERSONA 🙂

Once again the ShitLankanTM Psychiatrists and their Sad Fraud are exposed 🙂

The case continues…

Complete Absence of Alogia Further Destroys Fraudulent Schizophrenia Diagnosis

By | SIGNATURE FINDINGS
schizophrenia-the-fraud-game-for-ages-15-25yrs-joseph-de-saram-rhodium-linkedin

Complete Absence of Alogia Further Destroys Fraudulent Schizophrenia Diagnosis (±x)

Published on 4th 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
273

Enter more text here

In psychologyalogia (Greek ἀ-, “without”, and λόγος, “speech”[1]), or poverty of speech,[2] is a general lack of additional, unprompted content seen in normal speech. As a symptom, it is commonly seen in patientssuffering from schizophrenia, and is considered a negative symptom. It can complicate psychotherapy severely because of the considerable difficulty in holding a fluent conversation.

Alogia is often considered a form of aphasia, which is a general impairment in linguistic ability. It often occurs with intellectual disability and dementia as a result of damage to the left hemisphere of the brain. People can revert to alogia as a way of reverse psychology, or avoiding questions.

Alogia is characterized by a lack of speech, often caused by a disruption in the thought process. Usually, an injury to the left hemisphere of the brain will cause alogia to appear in an individual. In conversation, alogic patients will reply very sparsely and their answers to questions will lack spontaneous content; sometimes, they will even fail to answer at all.[3] Their responses will be brief, generally only appearing as a response to a question or prompt.[4]

Apart from the lack of content in a reply, the manner in which the person delivers the reply is affected as well. Patients affected by alogia will often slur their responses, and not pronounce the consonants as clearly as usual. The few words spoken usually trail off into a whisper, or are just ended by the second syllable. Studies have shown a correlation between alogic ratings in individuals and the amount and duration of pauses in their speech when responding to a series of questions posed by the researcher.[1][5]

The inability to speak stems from a deeper mental inability that causes alogic patients to have difficulty grasping the right words mentally, as well as formulating their thoughts.

A study investigating alogiacs and their results on the category fluency task showed that people with schizophrenia who exhibit alogia display a more disorganized semantic memory than controls.

While both groups produced the same number of words, the words produced by people with schizophrenia were much more disorderly and the results of cluster analysis revealed bizarre coherence in the alogiac group.[6]

I refer to the folowing medical whitepapers:-

Alogia, attentional impairment, and inappropriate affect: Their status in the dimensions of schizophrenia

Previous factor analyses have shown that at least three factors are needed to encompass the positive and negative symptoms of schizophrenia. Despite marked similarities across studies, it remains unclear whether certain symptoms such as alogia,...

Abstract

Previous factor analyses have shown that at least three factors are needed to encompass the positive and negative symptoms of schizophrenia. Despite marked similarities across studies, it remains unclear whether certain symptoms such as alogia, attentional impairment, and inappropriate affect are more closely related to negative or positive symptoms.

[MEANING ALOGIA IS ALWAYS PRESENT BUT THE QUESTION IS WHETHER IT SHOULD BE CLASSIFIED AS A POSITIVE OR NEGATIVE SYMPTOM]

An exploratory analysis was undertaken of the separate items on the Scale for the Assessment of Positive Symptoms (SAPS) and Scale for the Assessment of Negative Symptoms (SANS) that constitute the global rating of alogia, as well as the global ratings of attentional impairment and inappropriate affect in 90 schizophrenic patients.

Findings indicate that inappropriate affect loads significantly with bizarre behavior and positive formal thought disorder on a disorganization factor, whereas attentional impairment loads significantly on psychotic, disorganization, and negative symptom factors.

The global rating of alogia appears to comprise both positive and negative symptoms, with the item poverty of content of speech loading on the disorganization factor, and other items such as poverty of speech, blocking, and increased latency loading on the negative symptom factor. It is concluded that three dimensions are needed to characterize the symptoms of schizophrenia as measured by the SAPS/SANS. The use of three dimensions may be a robust way to further explore the relationship between signs and symptoms and their underlying mechanisms in schizophrenia.

Verbal fluency in schizophrenia: relationship with executive function, semantic memory and clinical alogia | Psychological Medicine | Cambridge Core

Verbal fluency in schizophrenia: relationship with executive function, semantic memory and clinical alogia - Volume 26 Issue 1 - E. M. Joyce, S. L. Collinson, P. Crichton
Cambridge Core

To examine whether poor verbal fluency in schizophrenia represents a degraded semantic store or inefficient access to a normal semantic store, 25 normal volunteers and 50 DSM-III-R schizophrenic patients, matched for age, sex and IQ, were recruited. Although schizophrenic patients were impaired on both letter and category fluency, they showed a normal pattern of output in that category was superior to letter fluency, and an improvement in category fluency when a cueing technique was employed (Randolph et al. 1993).

These results resemble those found in disorders of frontostriatal systems (Parkinson’s and Huntington’s disease) and suggest that poor verbal fluency in schizophrenia is because of inefficient access to semantic store. A measure of improvement with cueing was directly related to performance on the Stroop executive task.

Of all symptom measures derived from SANS and Manchester Scales, only alogia was related to verbal fluency in that superior improvement correlated inversely with the degree of alogia. It is suggested that both alogia and poor verbal fluency are mediated by the same underlying cognitive abnormality that reflects frontostriatal dysfunction.

Neuropsychological correlates of alogia and affective flattening in schizophrenia ☆

We examined whether two negative symptoms, alogia and affective flattening, were more strongly associated with dysfunction of certain brain regions than with others in a sample of 27 schizophrenic subjects. Neuropsychological tests were used to...

Abstract

We examined whether two negative symptoms, alogia and affective flattening, were more strongly associated with dysfunction of certain brain regions than with others in a sample of 27 schizophrenic subjects. Neuropsychological tests were used to measure the integrity of functioning of different brain regions.

Functioning of left and right frontal regions was assessed by word fluency and design fluency, respectively, and functioning of the left temporohippocampal region was assessed by Hebb’s digit-sequences recall test. Measures of alogia and affective flattening were obtained using the Scale for the Assessment of Negative Symptoms.

The results indicated that more severe levels of these negative symptoms were associated with poorer performance on the fluency tests. These relationships were fairly specific as indicated in two ways: (1) only certain neuropsychological measures were associated with negative symptoms. In addition, affective flattening, but not alogia, appeared to be associated with lateralized dysfunction.

Category fluency performance in patients with schizophrenia and bipolar disorder: The influence of affective categories

Semantic fluency (SF) and phonological fluency (PF) were examined in large groups of schizophrenia patients, bipolar patients and controls. As well as standard SF categories (animals and food), fluency to two affective categories, happy and fear was...

Semantic fluency (SF) and phonological fluency (PF) were examined in large groups of schizophrenia patients, bipolar patients and controls. As well as standard SF categories (animals and food), fluency to two affective categories, happy and fear was measured, i.e. participants were asked to produce as many words as they could that resulted in or are associated with fear or happiness.

Schizophrenia patients showed SF and PF deficits. Bipolar patients showed PF deficits.

Thus, PF is argued to be a GOOD COGNITIVE MARKER IN BOTH DISORDERS. Severity of delusions was related to SF performance in all patients. The patient groups showed different patterns on the affective categories compared to controls: the bipolar patients were better and produced more words, especially to the happiness category, and the schizophrenia patients were impaired and produced less words. The results suggest an interesting interaction between psychotic illnesses, fluency and emotion

Evidentiary Materials

I also refer to this article:-

Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis

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

I now refer to the actual audio recordings made whilst I was in the Psychiatric Facility and subsequently, with the ShitLankanTM Psychiatrists – all 6 of them.

THESE RECORDINGS ARE IMPORTANT BECAUSE THEY CONFIRM THAT WHICH I ACTUALLY SAID OR DID NOT SAY, RATHER THAN WHAT THIRD PARTIES SUCH AS EDWARD DE SARAM MANIPULATED THEM INTO SAYING.

I WILL ADDRESS THE RESULTANT FRAUDULENT REPORTS IN ANOTHER ARTICLE.

I of course realised the underlying basis of the Psychiatric Fraud and as such my answers are contrived at times with my provision of disinformation in order for me to obtain information.

I WILL EXPLAIN WHY I HAVE SAID CERTAIN THINGS IN A SEPARATE ANALYSIS, AS A I SIMPLY TOLD THEM WHAT THEY WANTED TO HEAR 🙂

“Engage people with what they expect; it is what they are able to discern and confirms their projections. It settles them into predictable patterns of response, occupying their minds while you wait for the extraordinary moment — that which they cannot anticipate.”

― Sun TzuThe Art of War

Words Do Come Easy - Vox Populi

"Are you like a crazy person?" - ha ha, people say this to me all the time too 🙂 “All warfare is based on deception. Hence, when we are able to...

but for the moment please evaluate the Semantic Fluency (SF) as well as the Phonological Fluency (PF).

BEING ABLE TO COMMUNICATE FLUENTLY IN TERMS OF SEMANTIC AS WELL AS PHONOLOGICAL FLUENCY, AS WELL AS MY PRECISE AND COHERENT RESPONSES, MY INITIATION OF VARIOUS TOPICS AND DEMONSTRATION OF NO COGNITIVE DEFICITS WHATSOEVER UTTERLY DESTROYS THE FRAUDULENT DIAGNOSIS OF SCHIZOPHRENIA 🙂

3 HOURS 15 MINS OF WHICH I AM DOING MOST OF THE TALKING AND DIRECTING DISCUSSIONS 🙂

20151217 221934 Dr Jayananda Horadugoda

20151218 093258 Dr Dulmini Jayasundara

20151219 090034 Dr Jayananda Horadugoda

20151219 201320 Dr Assas

20151220 084746 Dr Ratnayake

20151220 202226 Dr Najira

20160102 103720 Dr Upali Peris

The Psychiatric Fraud CONVENIENTLY FACILITATED this:-

Destruction of Evidence and Perversion of the Course of Justice

20171006 UPDATE - FORENSIC EVIDENCE CONFIRMING THIRD PARTIES Notwithstanding the FACT that parties had OBVIOUSLY entered my house, and had stolen...

and it is in fact the theft of extremely valuable patents, a one-time pad and my defences and counterclaims that is the thing I am most ANGERED by…

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

Poor Eye Contact is a Core Clinical Finding in Schizophrenia and Autism

By | SIGNATURE FINDINGS
pulse/poor-eye-contact-is-a-core-clinical-finding-in-schizophrenia-and-autism-joseph-de-saram-rhodium-linkedin

Poor Eye Contact is a Core Clinical Finding in Schizophrenia and Autism (±x)

Published on 4th 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
571

Enter more text here

[I CANNOT BECOME OVERLOADED WITH MATERIAL IF MY MEMORY IS DEMONSTRABLY HYPERTHYMESTIC AS WELL AS EIDETIC 🙂

Thanks for the Memories

"We must never forget the lessons of the past in our quest for the future." - JSRDS Baby's First Words Thoughts not words in my case - one of my...

AS SUCH I ALWAYS MAINTAIN EXCELLENT EYE CONTACT, HAVE NO ISSUES IN EYE MOVEMENT THANKS TO VASTLY SUPERIOR COGNITIVE FUNCTIONS.]

Matters of Intelligence

"My personality is designed by me - my attitude is defined by you." - JSRDS This is an article about Intelligence and IQ, and the types of problems...

IT IS EASY TO CONFIRM A COMPLETE ABSENCE OF MENTAL ILLNESS 🙂

I refer to the following article:-

Autism and Schizophrenia

Emerging study results suggest that there are both clinical and biological links between autism and schizophrenia. The question regarding whether there is phenotypic overlap or comorbidity between autism and schizophrenia dates back to 1943, when Kanner1 first used the term “autism” to describe egocentricity. The distinction between the two disorders remained unclear for nearly 30 years, until DSM-II included children with autism under the diagnostic umbrella ...

and refer to the following paragraphs:-

Shared clinical features

Although the disorders are distinct, they have shared clinical features.

SOCIAL WITHDRAWAL, COMMUNICATION IMPAIRMENT, and POOR EYE CONTACT

seen in ASD are similar to the negative symptoms seen in youths with schizophrenia.

11 When higher-functioning individuals with autism are stressed, they become highly anxious and at times may appear thought-disordered and paranoid, particularly when they are asked to shift set (such as being asked to change a topic of conversation or to stop an activity that they are engaged in and begin a new activity).

[DOES NOT APPLY TO ME – ASK ME ABOUT ANYTHING AND ANALYSE THE RESPONSES :)]

12 A subset of children (28%) in the ongoing NIMH study of COS have been reported to have comorbid COS and ASD.7

Psychiatric Disorders/Psychotic Disorders/Schizophrenia

Schizophrenia is a devastating illness that affects approximately 1% of the population. Its primary impact is on thought, and its cardinal symptom is psychotic thinking in affecting individuals. In addition, however, it can affect many aspects of...

Disturbances of Affect and Mood

Disorders of mood and affect include affective flattening,

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

which is a reduced intensity of emotional expression and responsiveness that leaves patients indifferent and apathetic. Typically, one sees unchanging facial expression, decreased spontaneous movements, poverty of expressive gestures,

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 see...

Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis

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

Transient, isolated, and mild mood disturbances are not infrequently seen in schizophrenia, with these changes tending toward elation, depression, or anxiety. A number of patients, during a partial remission of the psychotic symptoms, develop a full depressive syndrome, the so-called “post-psychotic depression” of schizophrenia.

Processing Eye Gaze is Also Affected

Eye-contact perception in schizophrenia: relationship with symptoms and socioemotional functioning.

J Abnorm Psychol. 2012 Aug;121(3):616-27. doi: 10.1037/a0026596. Epub 2012 Jan 16. Research Support, Non-U.S. Gov't...

Accurately perceiving self-referential social signals, particularly eye contact, is critical to social adaptation.

Schizophrenia is often accompanied by deficits in social cognition, but it is unclear whether this includes gaze discrimination deficits.

This study investigated whether eye-contact perception is preserved or impaired and if it is related to symptoms and broader socioemotional functioning in schizophrenia.

Twenty-six participants with schizophrenia (SCZ) and 23 healthy controls (HC) made eye-contact judgments for faces in varying gaze direction (from averted to direct in ten 10% increments), head orientation (forward, 30° averted), and emotion (neutral, fearful).

Psychophysical analyses for forward faces showed that SCZ began endorsing eye contact with

weaker eye-contact signal

and their eye-contact perception was less of a dichotomous function, as compared with HC. SCZ were more likely than HC to endorse eye contact when gaze was ambiguous, and this overperception of eye contact was modulated by head orientation and emotion. Overperception of eye contact was associated with more severe negative symptoms.

Decreased categorical gaze perception explained variance of socioemotional deficits in schizophrenia

after taking basic neurocognition into consideration, suggesting the relationship was not solely due to a general deficit problem. These results were discussed in relation to the nature of categorical gaze perception and its significance to clinical and functional presentations of schizophrenia.

and

http://www.apa.org/gradpsych/2014/04/eye-contact.aspx

Poor Eye Movement in Schizophrenia

Note the jerky movements and requirement to recorrect:-

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

I DO NOT LOOK AWAY FROM THE PERSON THAT I AM SPEAKING WITH. THIS IN ITSELF DEMONSTRATES NO SOCIAL COMMUNICATION DIFFICULTIES AND CONFIRMS AN EXTREMELY CONFIDENT PERSONA 🙂

Once again the ShitLankanTM Psychiatrists and their Sad Fraud are exposed 🙂

The case continues…

Complete Absence of Anhedonia Further Destroys Fraudulent Schizophrenia Diagnosis

By | SIGNATURE FINDINGS
complete-absence-of-anhedonia-further-destroys-fraudulent-schizophrenia-diagnosis-joseph-de-saram-rhodium-linkedin

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
500

Enter more text here

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.

20151219 161428

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
RHODIUM GROUP

Stress Triggers Psychosis in Individuals Vulnerable to Schizophrenia

By | SIGNATURE FINDINGS
stress-triggers-psychosis-in-individuals-vulnerable-to-schizophrenia-joseph-de-saram-rhodium-linkedin

Stress Triggers Psychosis in Individuals Vulnerable to Schizophrenia (±x)

Published on 27th November 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
609

Enter more text here

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 anything, if I was unstable THAT would have TRIGGERED SOMETHING, but as you can see it DIDN’T… so even that DEMONSTRATES…”

and once again the ShitLankanTM Psychiatrist Dulmini Jayasundara had no response.

And actually there is another aspect of this call that CONFIRMS ABSENCE OF SCHIZOPHRENIA, – the signature Flat Affect is entirely missing as well:-

The Flat Affect in Schizophrenia

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

Medical Basis

This article explains the validity of my statement and why it is incredibly relevant to the [fraudulent] diagnosis of schizophrenia.

In a nutshell, if I actually had (a) schizophrenia or had (b) a predisposition/vulnerability to schizophrenia, the torture of 17 December 2015 and the weeks preceding would have triggered psychosis itself – it did NOT and therefore once again the

ABSENCE OF SCHIZOPHRENIA IS CONFIRMED, WHICH ALSO CONFIRMS THAT THE PSYCHIATRIC FRAUD

The Restricted Patient

One of my favourite films, and even this as a Spying / Military Theme can you believe? Ha ha] What is a Restricted Patient Restricted patients are...

FACILITATED THE DATA EXFILTRATION FRAUD CONCOMITANTLY 🙂

Destruction of Evidence and Perversion of the Course of Justice

20171006 UPDATE - FORENSIC EVIDENCE CONFIRMING THIRD PARTIES Notwithstanding the FACT that parties had OBVIOUSLY entered my house, and had stolen...

would like to present text from this medical whitepaper:-

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2774708/

interspersed with mine,

Abstract

It has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult.

Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored.

But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging.

Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.

INTRODUCTION

Decades ago there was an exploration of the role of life events and stress as etiologic factors in schizophrenia (SZ). Many studies found that patients with first-episode psychosis had a preponderance of recent life events as compared with normals. The climate then was to emphasize psychosocial factors in the development of a number of psychiatric disorders, especially SZ. This too frequently led to the blaming of families and the labeling of mothers as “schizophrenogenic.” There was an appropriate backlash to this, with the emergence of activism on the part of patients and their families to destigmatize mental illness and recognize psychiatric disorders as medical and biological disorders.

Since then, powerful technologies have been developed to examine the biological correlates of psychiatric diseases such as SZ, including structural and functional imaging, elucidation of the human genome, and modeling of pathology in animals. Evidence has accumulated in support of biological hypotheses of SZ pathophysiology, such as abnormalities in dopaminergic, glutamatergic,1 and γ-aminobutyric acid (GABA)2 function, or an integration of abnormal neurotransmission in all three.3 Also, disruption of sensory gating4 has been identified as an endophenotype in SZ and disruptions in cortical connectivity through abnormal synaptic pruning5 have been theorized to be key to the disorder.

With these advances in neuroscience, it makes sense to reevaluate stress as a potential etiologic factor in a host of disorders, including SZ, since the intricate neurobiology of the stress cascade has been elucidated by prominent researchers such as McEwen and Sapolsky. SZ is a heterogeneous illness; it is likely that stressful life events and trauma are neither necessary nor sufficient to cause it. And if stress does play a role in SZ, it is certainly not specific to the illness. But it may be that the vulnerability to SZ entails a sensitivity to the effects of trauma and stressful life events, and that the stress cascade may in some cases reveal a latent susceptibility to psychosis and perhaps also contribute to the cognitive impairments associated with SZ.

Memory Deficits in Schizophrenia

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

In this paper we will (1) describe the basic scientific work on the neurobiological effects of stress and cortisol; (2) illustrate findings that suggest similar mechanisms are at work in SZ; and (3) evaluate the neurodevelopmental and neuropathologic hypotheses of SZ etiology, with sections on gene-environment studies, magnetic resonance imaging (MRI) volumetrics, biologic plausibility, and synaptic pruning hypotheses.

THE STRESS CASCADE: ANIMAL STUDIES

An appreciation of the vulnerability of the hippocampus to stress arose from the postmortem study of vervet monkeys who had been caged in overcrowded conditions and who subsequently died. Upon autopsy, these animals were found to have extensive cell death in the hippocampus.6 In experimental conditions, Sapolsky and colleagues7,8 found similar neurotoxicity to the hippocampus as a consequence of severe stress in rodent and primate models, with both necrosis and apoptosis observed.

McEwen and colleagues9,10 expanded upon these findings, noting that across species less severe but chronic stress led to specific atrophy of apical dendrites in the CA3 region of the hippocampus. This same atrophy has been demonstrated in other regions of the hippocampus, specifically CA1 and the dentate gyrus, although to a lesser degree.11 There is some evidence that this specific mechanism may also operate in the amygdala, but the prefrontal cortex remains unexplored (B. McEwen, PhD, personal communication, 2000).

This neurotoxic process (the stress-induced atrophy of dendrites in regions of the hippocampus) was determined to be mediated through the effects of glucocorticoids, as high doses of cortisol had the same effects as chronic restraint stress.

McEwen and colleagues12 also found that pretreatment with a number of agents protected the hippocampus against these toxic effects of stress and cortisol. These agents include phenytoin, benzodiazepines, and, interestingly, tianeptine (a serotonin [5-HT] reuptake enhancer marketed in France and now available in other countries, such as Venezuela). Their known pharmacologic actions shed some light on the putative biochemical mechanisms of stress-induced changes in the hippocampus.

As phenytoin blocks glutamate release and antagonizes sodium channels, this was thought to be the mechanism for neurotoxicity, and further studies have pointed to the role of glutamate.13,14

Benzodiazepines likely work through their interactions with GABA receptors. Interestingly, tianeptine blocks toxicity but selective serotonin reuptake inhibitors do not, implicating 5-HT as an active factor in stress-induced dendritic atrophy.

[SO SOMEWHAT INCREDIBLY, THE CONTINUAL POISONING OF ME WITH ROHYPNOL

RHO-hypnol as a Data Rape Drug

Data Rape is the process by which any type of Intellectual Property is exfiltrated by the temporary or otherwise incapacitation of its Guardian...

WHICH WAS A FEATURE OF THE STAGED ROAD TRAFFIC ACCIDENT AND ITS OWN SERIES OF ISSUES,

No Ordinary Accident v2

20170512 UPDATED Video and text - please read the full article. 20161022 UPDATE Today is the First Anniversary of the Staged Accident. It was...

ACTUALLY MAY HAVE ASSISTED IN PREVENTING NEUROTOXICITY IN MY HIPPOCAMPUS WHICH THEN INCREASED RESILIENCE IN RELATION TO PARTIES TRYING TO TRIGGER COGNITIVE DEFICITS AND INDUCE PSYCHOSIS AND SCHIZOPHRENIA. HOWEVER NO INDUCTION WAS GOING TO HAPPEN REGARDLESS OF THE BENZODIAZEPINES IN ANY EVENT, BECAUSE OF SYNAPTIC PLASTICITY ETC.

Thanks for the Memories

"We must never forget the lessons of the past in our quest for the future." - JSRDS Baby's First Words Thoughts not words in my case - one of my...

Of note, although phenytoin can lower glucocorticoid levels through its activation of metabolizing hepatic enzymes, this mechanism is unlikely to explain its neuroprotective effects, as such effects persist even in the context of very high levels of cortisol. Furthermore, phenytoin likely has a specific regional protective effect in the brain, as it fails to prevent stress-induced changes in body weight and adrenal weight, as well as glucocorticoid-induced reduction of the thymus.

Much of the neurochemistry underlying the neurotoxicity of stress and glucocorticoids to the hippocampus has been elaborated. High levels of cortisol accelerate energy loss15 and inhibit glucose transport,16causing the hippocampus to be energetically limited and vulnerable to damage. Excitatory amino acids, particularly glutamate, accumulate in the synapse, where they activate glutamate receptors and pathologically mobilize free calcium in the postsynaptic neuron.

Of further interest, the neurotoxic effects of stress and cortisol on the hippocampus in rats is reflected in cognitive and behavioral changes, specifically memory deficits such as poor maze performance. Under stress, the degree of hippocampal cell loss in rats is correlated with cognitive deficits: the degree of impairment in new learning of maze escape behaviors is related to the extent of damage to the CA3 region of the hippocampus.17 These findings, along with neuroanatomic studies18,19 of patients with temporal lobe epilepsy, confirm that the hippocampus is vital to short-term memory.

Memory Loss in Trauma and Otherwise

Memory loss, also known as amnesia, is unusual forgetfulness. It may affect the ability to recall new events or to remember events in the past - or...

[AN EXCELLENT EXAMPLE OF A GENUINE MEMORY DEFICIT IN A GENUINE NON-PSYCHOSIS SCENARIO IS THIS ARTICLE:-

How the Psychiatric Truth in Singapore Exposes the Psychiatric Fraud in Sri Lanka

Dr Ang Yong Guan is a Singaporean with Balls. He is also a brilliant psychiatrist who has experience of psychiatric medicine in the military, and is...

THIS MEANS IF THERE IS ACTUALLY SOMETHING THAT STRESSES ME THEN MY MEMORY IS TEMPORARILY COMPROMISED.

THIS ALSO CONFIRMS THAT THE PSYCHIATRIC FRAUD DID NOT STRESS ME AND BECAUSE I HAD CORRECTLY IDENTIFIED IT AS A SAD MILITARY INTELLIGENCE OPERATION AND SO MY COGNITIVE FUNCTION WAS A+++ TO THE SHITLANKAN PSYCHIATRISTS’ HORROR :)]

Memory Deficits in Schizophrenia

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

THE STRESS CASCADE: TRANSLATION TO HUMAN STUDIES

Allostasis

Emphasizing translational research, McEwen20 is interested in studying the implications in humans of his work on the biologic mechanisms of the stress cascade in animals. He has coined the phrase “allostatic load” to describe how an organism changes and adapts to chronic stress. Allostasis represents a new reorganization and not simply the maintenance of a condition, which would better be described by the term “homeostasis.”

Allostasis is “maintaining stability through change” and describes adaptation rather than a return to a set point. Homeostasis describes factors such as oxygen tension and pH, whereas allostasis can describe the autonomic nervous system (variations in heart rate and blood pressure) and hormonal fluctuations in the hypothalamic-pituitary-adrenal (HPA) axis.

The brain adapts to chronic stress through the interaction of local neurotransmitters and systemic hormones to produce structural and functional changes, which include the suppression of neurogenesis in the dentate gyrus and remodeling of dendrites in the hippocampus.

[IQ IN THE 160+ RANGE AND THE ABILITY TO THINK EXTREMELY RAPIDLY IN CRISIS SITUATIONS PREVENTS DETRIMENTAL STRUCTURAL AND FUNCTIONAL CHANGES THAT EVEN ABOVE AVERAGE PEOPLE WOULD STRUGGLE WITH.]

Permanent damage to the hippocampus only occurs when stress overwhelms the organism’s resources for adaptation and stress hormones are excessive. Synaptic remodeling that results from less severe stress is in part reversible.

Adaptive strategies have a cost to the body either when they are called upon too often or when they are inefficiently managed—this is what is meant by “allostatic load.” An association between stress and illness is not unique to SZ, nor to psychiatric illnesses per se. For example, psychological stress is associated with relapse or exacerbation in a variety of medical illnesses, including ulcerative colitis, genital herpes, asthma, vaginal candidiasis, multiple sclerosis, psoriasis, and “tension-type” headaches.21 A likely model for these illnesses and SZ is that psychological stress potentiates expression of illness in individuals who are at risk for illness onset or relapse. That is, an underlying vulnerability (exposure to infectious agents, reactive airways, abnormal neural substrate, etc.) interacts with “allostatic load” to lead to disease expression.

EVIDENCE OF THE STRESS CASCADE IN HUMAN CONDITIONS

McEwen’s work has inspired a number of researchers to explore whether these elements

stress → cortisol → hippocampal toxicity → memory deficits

may play a role in a number of human conditions, including Cushing’s disease, normal human aging, and psychiatric disorders such as posttraumatic stress disorder (PTSD), depression, and SZ. In humans, functioning of the HPA axis may be evaluated in many ways, including (1) basal serum, salivary, or urinary levels of cortisol and (2) challenge tests, among the simplest being the dexamethasone suppression test (DST), which assesses the negative feedback of the HPA axis by the corticosteroid dexamethasone, which normally leads to a lowering of endogenous cortisol levels.

Cushing’s disease is a medical condition in humans that is analogous to the experimental exposure of animals to glucocorticoids, as it is marked by high levels of endogenously released cortisol. In Cushing’s disease, hippocampal volumes are inversely correlated with plasma cortisol levels.22

As in other disorders, these reductions in hippocampal volumes are also correlated with lower scores in verbal memory.

Healthy aging individuals with increasing/high cortisol levels (measured annually) were found to have impairments in explicit memory.23 In an analogous study, another group with increasing/high cortisol was found to have a 14% reduction in hippocampal volume; the annual rate of cortisol increase correlated negatively with hippocampal volume.24 Hippocampal size is also inversely related to delayed memory performance in normal human aging.25

In PTSD, combat veterans have deficits in hippocampus-dependent memory measures like the Wechsler Memory Scale and the Selective Reminding Test (these deficits correlate with reduction in right hippocampus volume).26,27 Adult survivors of childhood abuse also have similar memory deficits and decrements in hippocampal size.28

Post Traumatic Stress Disorder

Following on from my other article:- I continue the voyage into the mind and examine particular situations or disorders which prevent it...

In depression, an abnormal DST is common and has been found to be inversely correlated with hippocampal size.29 Also, in depression, baseline levels of cortisol in the urine are correlated with cognitive impairment.30 Middle-aged patients with chronic refractory depression have smaller hippocampi than do age-matched healthy controls,31 and among depressed patients the total lifetime duration of depression (but not age) correlates with smaller bilateral hippocampal volumes and lower verbal memory scores.32 Patients with depression have a statistically significant 16% smaller left hippocampus than controls.33 These volumetric studies suggest either that depressive episodes are toxic to the hippocampus (perhaps through cortisol) or that individuals with smaller hippocampi are more vulnerable to developing depression.

[I WOULD LIKE TO HAVE A MAGNETIC RESONANCE IMAGE OF MY HIPPOCAMPUS AND MARVEL AT ITS MASSIVE SIZE :)]

Of interest, psychosis is a common phenomenon in the conditions described above (except of course for normal human aging) and psychotic symptoms in these conditions have been linked to serum cortisol levels. For example, there are case reports of psychosis occurring in Cushing’s disease that remits with lowering of the endogenous hypercortisolemia by treatments such as cortisol receptor antagonists, like mifepristone,34,35 and adrenalectomy.36 In fact, psychosis is the presenting symptom in some cases of Cushing’s disease.3739 Exogeneous corticosteroid treatment for a number of disorders, such as asthma40and inflammatory bowel disease,41 may also lead to psychosis,42,43 which can likewise remit with lowering of the dose of corticosteroids.40

PTSD, a psychiatric illness defined at least in part by the occurrence of stress and trauma, has been found to have rates of psychosis as high as 40%.44 Depressive episodes are frequently accompanied by psychotic symptoms. In fact, a meta-analysis of 14 studies demonstrated that dexamethasone nonsuppresssion is significantly more common in cases of major depression with psychosis than in cases without psychosis.45 Several of the studies reviewed, such as one by Schatzberg and colleagues,46 found higher levels of cortisol in major depression with psychotic features. Newer reports confirm this finding of significant rates of dexamethasone non-suppression in major depression with psychosis.47

STRESS AND SCHIZOPHRENIA

These key elements of the stress cascade—stress, cortisol, hippocampus, and cognition—have all been found to be abnormal in SZ. Further, associations have been found among these elements in SZ. Therefore, it is plausible that the stress cascade plays a role in the expression of SZ.

Stress

An early study found that 46% of 50 patients with acute-onset SZ had been exposed to stressful life events in the preceding 3 months as compared to only 14% of 325 controls; the difference was most pronounced in the 3 weeks leading up to hospitalization.48 A meta-analysis of the literature showed significantly higher incidence of recent life events in SZ patients as compared with healthy controls in 43% of all studies reviewed; it was noted that stressors and severity of symptoms covaried over time in SZ.49

Evidence of an association between life events and SZ symptoms does not necessarily imply causation. It may be that simply by virtue of having SZ (or vulnerability to SZ) an individual is more prone to experience major life events. However, when patients are their own controls (relapse versus baseline) or when relapsing patients are compared with non-relapsing patients, an association of life events and relapse persists.5053 A preponderance of life events has been found in the weeks to months leading up to relapse.50,53 Of interest, in a prospective study Sachar54 found that cortisol levels increased by 250% immediately preceding psychotic exacerabation and then decreased to a level between that of preepisode and recovery.

Cortisol

Studies demonstrate that diurnal rhythms of cortisol are disrupted in SZ, with the common finding that cortisol remains abnormally elevated in the late evening.55 Basal cortisol levels have been found to be inversely correlated with memory and frontal tasks—both for SZ patients and controls.56 Cortisol regulation is also disrupted in a subset of patients. A meta-analysis of 46 studies yielded an overall rate of 26.4% of DST nonsuppression in SZ as compared with 5% in controls.57 In SZ, DST nonsuppression has been linked to negative and cognitive symptoms, but not to depressive symptoms.

The Hippocampus

There is abundant evidence that the hippocampus is abnormal in SZ.

A meta-analysis of 18 studies showed a bilateral reduction of volume in the hippocampus of 4%.58 A number of investigators have reported that hippocampal volumes in SZ are inversely correlated with measures of memory.5961 Magnetic resonance spectroscopy (MRS) studies suggest that neuronal integrity is compromised in the hippocampus in SZ, as low N-acetyl-aspartate (NAA) has been consistently found.62,63 Positron emission tomography studies also implicate the hippocampus as a site related to hallucinations. 64 Postmortem studies provide evidence that there is synaptic and hence circuitry abnormalities in both the hippocampus and the prefrontal cortex.65Intriguingly, cognitive and MRI volumetric assessments of twins discordant for SZ suggest that hippocampal abnormality is more prevalent in the affected twin, suggesting nongenetic influences.6668

Cognition: Hippocampus-Dependent Explicit Memory

A meta-analysis of 70 studies that examined cognition in SZ showed a consistent moderate-to-large effect size across studies for memory impairment, specifically recall. Impairment was present in hippocampus-dependent verbal and nonverbal memory, both immediate and delayed.69 Explicit memory (which is hippocampus-dependent) is selectively and more severely impaired than other cognitive domains in SZ, including in first-episode patients, who have a selective deficit in learning and memory, against a background of diffuse dysfunction.70

Stress and the Synaptic Pruning Hypothesis of Schizophrenia

In SZ there is reduced neuropil, which implicates abnormalities in axons, dendrites, and synapses46 that could occur at any stage of development, without accompanying gliosis. In fact, a leading theory of SZ pathophysiology is the theory of abnormal synaptic pruning, first articulated by Feinberg in 1982.90Support for the “developmentally reduced synaptic connectivity” hypothesis of SZ etiology comes from both computer modeling5 and neuropathologic findings.91 Stress could plausibly reduce synapses through its effects on dendrites of pyramidal cells in the hippocampus.

CONCLUSION

The prevailing hypothesis of SZ etiology is that it is primarily an early neurodevelopmental disorder. However, the heterogeneity of the illness, its long latency to expression, and its fluctuating course suggest that SZ may be a progressive neurodevelopmental disorder in which early pathologic factors, such as genetic vulnerability, prenatal insults, and obstetric complications, create an abnormal neurobiological substrate that is more vulnerable to the development of SZ symptoms.

Events that may trigger actual onset of SZ include both (1) maturational processes, such as programmed cell death and synaptic remodeling, and (2) postnatal environmental insults, such as psychosocial stress, TBI, and perhaps even substance abuse.

Substance-Induced Mental Disorders

Background As I wrote in the following article, Edward de Saram obtained and poisoned me with psychotropic medication that 'conveniently' fabricated...

A mechanism by which development unmasks latent vulnerability is plausible, and has its correlates in other brain functions, such as vision, in which later cortical development can mediate the expression of an initial insult. For example, deprivation of patterned visual input in human infants, who can only detect global contour but little detail, leads to later deficits in the adult-like expertise in processing of faces.95However, there is also evidence that postnatal environmental factors increase the risk of SZ, as has been reviewed in this paper. It is not parsimonious to assume that a brain that is vulnerable to developing SZ is a brain that is immune to environmental insults that may plausibly increase that risk. Lieberman96 argues that the neurodevelopmental theory, taken to its logical extreme, suggests both inevitability and therapeutic nihilism, which he has phrased as “doomed from the womb.”

Lieberman96 has proposed instead that SZ may result both from early neurodevelopmental events and later limited neurodegenerative processes, which may be most active in the early stages of illness and associated with the onset of psychotic symptoms. This would be consistent with the findings of progressive ventricular enlargement and ongoing reduction of brain volumes in a subset of patients with SZ. An understanding of the neuropathologic mechanisms occurring with the onset of psychosis (and concurrent cognitive symptoms) and the roles of both developmental processes and environmental factors in this process is key to developing novel treatment strategies, both pharmacologic and nonpharmacologic.

In this paper, we have presented a model whereby stress can play a role in SZ pathophysiology through its effects on synaptic organization and cortical connectivity; it should be noted, however, that other mechanisms may be at work.

For example, stress may simply lead to psychosis through the activation of dopaminergic transmission, a theory advanced by Schatzberg in the 1980s.97 In healthy individuals, cortisol has been found to increase serum levels of homovanillic acid, a key dopamine metabolite.98Walker99 has reported that cortisol increases dopamine metabolism in the nucleus accumbens and raises plasma dopamine metabolites, and hypothesizes that this may be a mechanism whereby stress precipitates psychosis.

In an animal model of SZ, rats with neonatal hippocampal excitotoxic damage show greatly increased mesolimbic release of dopamine in response to stress.100 Also, stress precipitates flashbacks to psychosis in individuals with a history of methamphetamine psychosis.101

Another mechanism by which stress may contribute to SZ pathophysiology is through excitotoxic injury to vulnerable inhibitory GABA-ergic interneurons in the hippocampus, a model advanced by Benes in 1999.102

Interestingly, it has been proposed that N-methyl-d-aspartate receptor hypofunction could lead to reduced GABA transmission and thus enhanced glutamatergic excitotoxicity that contributes to SZ.103 The effects of stress could also be mediated by excitatory inputs of the amygdala to the hippocampus.2

It may be that early neurodevelopmental events or genetic liability create a sensitivity to stress, and that this may be an important component of vulnerability to SZ. Mednick and Schulsinger104 found that environmental factors such as early parental separation and severe social disruption during pregnancy were associated with later SZ risk in offspring. Huttunen and Niskanen105 also found that maternal stress was linked to later SZ risk. Mednick and colleagues106 studied a cohort of children in Mauritius who had a high genetic risk of SZ and found that autonomic nervous system abnormalities were predictive of later serious mental illness.

Later studies have confirmed the presence of failure of habituation of autonomic nervous system activity and abnormal skin conductance in patients and individuals either genetically or clinically at risk.107,108 In another study, Mednick and colleagues found that early environmental enrichment was associated with improved psychophysiologic orienting and arousal mechanisms 6-8 years later in children, demonstrating that these variables, although being at least partly genetic in origin, could be ameliorated through early intervention.109

More prospective longitudinal studies of at-risk and prodromal individuals are currently needed. These studies require close follow-up and evaluation, especially around the time of onset of psychosis. A common perception is that psychosis onset follows a major life event or transition, This is one of many hypotheses that must be explored, as it has important implications for prevention and treatment and may help elucidate the neurobiological mechanisms underlying the important transition to psychosis.

Given the evidence in both animals and humans that environmental enrichment can have neuroprotective effects on the hippocampus and normalize deficits in arousal and focus that are also seen in SZ, it may be warranted to pilot psychosocial interventions such as stress reduction in individuals identified as at risk for SZ.

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

The Flat Affect in Schizophrenia

By | SIGNATURE FINDINGS
the-flat-affect-in-schizophrenia-joseph-de-saram-rhodium-linkedin

The Flat Affect in Schizophrenia (±x)

Published on 30th September 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
1260

Enter more text here

Flat affect, or impaired emotional functioning, is a SIGNATURE symptom of schizophrenia. It’s a term used to describe the lack of emotional expression displayed by people with schizophrenia.

It is characterized by an apathetic and unchanging facial expression and little or no modulation of the voice. This extremely limited range of emotions occurs even in situations that would normally seem very exciting or very sad.

For instance, upon hearing great news, someone with schizophrenia may not smile, laugh or have any excitement in their tone.

What Causes Flat Affect?

Flat affect, also known as blunted affect, affects millions of people. However, scientists are not entirely sure what exactly causes it but it is hypothesized to be due to differences in brain functioning.

When shown emotional stimuli, those with schizophrenia show decreased activity in the limbic system, the part of the brain responsible for your mood, instincts, and drives. Because of this, some researchers suggest that there are chemical imbalances in the brain that blunt the limbic system’s reaction to stimuli, resulting in an apathetic or emotionless response.

How Will Flat Affect Impact My Daily Life?

If you have schizophrenia and have been affected by flat affect, you may find that it negatively impacts your social functioning. People can respond negatively to a lack of emotion, assuming that you are cold or unfeeling when you really can’t help it.

It’s important to note that while you may have trouble displaying emotion, many people with schizophrenia have no difficulties recognizing emotional responses in others. This is an important factor in working with your doctor to define a treatment plan, as it gives you a foundation to build on to create appropriate social exchanges.

Can Flat Affect Be Minimized?

Flat affect can be treated to some degree. This symptom often requires comprehensive therapy, including working with a healthcare provider and taking medication. While it often cannot be completely eliminated, therapy and intervention can help you interact with others more warmly and naturally. Part of therapy usually starts with techniques to help you recognize your emotionless response and how it doesn’t match what is required in the specific situation. Your therapist may then have you practice appropriate reactions to different stimuli like grief or celebration so that you can force yourself to react as other people do. Speech therapists also can help people with schizophrenia by working on tone and modulation of voice to convey more emotion.

Source:

Gur, R., Kohler, C., Ragland, D., et al. Flat Affect in Schizophrenia: Relation to Emotional Processing and Neurocognitive Measures. Schizophrenia Bulletin, 2006, 279-287.

What Is Flat Affect and How Does It Relate to Schizophrenia?

The term flat affect's definition is a lack of emotional expression and impaired social functioning often seen in those with schizophrenia...

Reduced affect display

Reduced affect display , sometimes referred to as emotional blunting , is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings ( affect display ) either verbally or non-verbally, especially when...
Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

Memory Deficits in Schizophrenia

By | SIGNATURE FINDINGS
Memory Deficits in Schizophrenia

Memory Deficits in Schizophrenia (±x)

Published on 18th March 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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THERE ARE ALWAYS OBSERVABLE/TESTABLE MEMORY DEFICITS IN PATIENTS WHO GENUINELY SUFFER FROM SCHIZOPHRENIA.

NO MEMORY DEFICITS = NOT SCHIZOPHRENIA

AND THERE ARE OTHER REASONS FOR ANY OBSERVED SCHIZOPHRENIA-LIKE SYMPTOMS, SUCH AS POISONING, RADIATION OR

THE FRAUDS COMMITTED BY MANIPULATIVE SOUTH ASIAN PARENTS

Cognitive Deficits

Schizophrenia is a complex chronic mental illness that is characterized by positive, negative and cognitive symptoms. Cognitive deficits are most predictive of long-term outcomes, with

“ABNORMALITIES IN MEMORY BEING THE MOST ROBUST FINDING.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217593/

Episodic Memory Impairments

Episodic memory impairments represent a core deficit in schizophrenia that severely limits patients’ functional outcome. This quantitative meta-analysis of functional imaging studies of episodic encoding and retrieval tests the prediction that these deficits are most consistently associated with dysfunction in the prefrontal cortex.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885958/

Episodic Memory Dysfunction

All the studies converge to show a significant impairment of the critical feature of episodic memory: conscious recollection. Schizophrenia is also associated with a defect of autobiographical memory. The episodic memory dysfunction results from a predominant failure of strategic processing at encoding, although an impairment of strategic processing at retrieval cannot be ruled out.

Behavioural and Neurobiological Defects in Episodic Memory

Individuals with schizophrenia demonstrate behavioral and neurobiological deficits in episodic memory. However, recent work suggests that episodic memory deficits in schizophrenia may be mitigated through specific encoding strategies. The current study directly compared brain activity and memory performance associated with two different verbal encoding orientations in the same group of schizophrenia participants, in order to more fully characterize the role of strategy in memory processing in this population.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659741/

Hippocampus Volume and Episodic Memory

Previous studies of schizophrenia have suggested a linkage between neuropsychological (NP) deficits and hippocampus abnormality. The relationship between hippocampus volume and NP functioning was investigated in 24 patients with chronic schizophrenia and 24 matched healthy controls.

Overall intracranial, white and gray matter, and anterior (AH) and posterior (PH) hippocampus volumes were assessed from magnetic resonance images (MRI). NP domains of IQ, attention, and executive function were also evaluated with respect to volumetric measures.

It was hypothesized that AH and PH volumes and episodic memory scores would be positively associated in controls and that the schizophrenia group would depart from this normative pattern. NP functioning was impaired overall and AH volume was smaller in the schizophrenia group. In the controls, the hippocampus–memory relationships involved AH and PH, and correlations were significant for verbal memory measures. In the schizophrenia group, positive correlations were constrained to PH. Negative correlations emerged between AH and verbal and visual memory measures. For both groups, cortical volume negatively correlated with age, but a negative correlation between age and hippocampus volume was found only in the schizophrenia group.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878285/

Episodic Memory Deficits in Schizophrenia

Numerous studies have examined the neural correlates of episodic memory deficits in schizophrenia, yielding both consistencies and discrepancies in the reported patterns of results.

Conclusions

As can be seen above, there is ALWAYS COGNITIVE IMPAIRMENT IN PATIENTS with SCHIZOPHRENIA, which presents as an Episodic Memory Deficit

HANG ON JUST A COTTON-PICKING MINUTE !!

BUT WASN’T JOE PUT INTO A PSYCHIATRIC FACILITY BECAUSE HE HAD SCHIZOPHRENIA?

This article confirms that I have extremely powerful Episodic Memory and Autobiographical memory and there are tonnes of evidence over 45yrs that confirms this phenomenon.

What proof is there to demonstrate Joe’s A+ cognitive excellence BEFORE the 12/17 Fraud?

This is extremely easy to confirm independently:-

(a) the calls between my attorneys and myself in relation to judicial proceedings, and particularly those in which I instructed them as to the strategy to follow;

(b) affidavits and briefs that I have written;

(c) various schematics that I had produced in relation to complex accounting and taxation;

(d) the fact that there is no-one who confirms that I had a cognitive deficit except the actual perpetrators involved in the fraud.

(e) the fact that I correctly identified cellular interception and gps jamming and had evidentiary materials as well;

(f) the fact that I correctly identified the bizarre behaviour of EDS in which he extended the role of Chamaree Silva and Raymond Callingham;

(g) the fact that I correctly identified the HMRC form fraud of Raymond Callingham as well as the ‘crime scene construction’ of EDS;

(h) the fact that I correctly identified that EDS and PDS were scheming in the prior days.

What proof is there to demonstrate Joe’s A+ cognitive excellence DURING the 12/17 Fraud?

This is extremely easy to confirm independently as well:-

(i) the calls between my attorneys and myself in relation to the Psychiatric Facility fraud itself;

(j) the fact that none of parties around me noticed in any change in behaviour, and nothing necessitated psychiatric treatment and certainly not ECT;

(k) the obvious fact that I managed to lawfully get out of a psychiatric facility from within the facility, even WITHOUT the opinion of another psychiatrist in my favour;

(l) the fact that the fraudulent medical staff in the Psychiatric Facility were unable to prevent my release by producing any evidentiary materials which they would have naturally had on hand if I were actually schizophrenic;

(m) the fact that I recorded the conversations with the medical staff and many of those calls were in relation to matters of defence, cellular interception, or that I should ‘ask my mother about my release’!!

What proof is there to demonstrate Joe’s A+ cognitive excellence AFTER the 12/17 Fraud?

This is extremely easy to confirm independently as well:-

(n) the fact that I have recovered around 15% of wiped/stolen data and it is the physical evidence confirming (a), (e), (f), (g), (h).

(o) the fact that I have [just about] managed to keep it together despite the loss of evidentiary material and operational data, which is immensely stressful;

(p) the various episodic articles that I have written on LinkedIn alone, confirm a depth of knowledge and an ability to process complex matters in law, accounting and information security that a person with cognitive deficits would simply not be able to understand or demonstrate.

The REAL FACTS re Cognitive Impairment and Schizophrenia

This should now be fairly obvious by this point:-

  • JOE DID NOT / DOES NOT HAVE SCHIZOPHRENIA, AND BOGUS MEDICAL REPORTS PRODUCED BY EDS AND NEWTON RANASINGHE FOR A UK DTI MATTER IN 2001 WERE THE FOUNDATION OF THE FRAUDS IN 2015;
  • JOE HAD DISCOVERED COPIOUS AMOUNTS OF MULTI-JURISDICTIONAL FRAUDS WHICH WERE DESIGNED TO PERVERT THE COURSE OF JUSTICE IN ONGOING JUDICIAL PROCEEDINGS IN SINGAPORE AND AUSTRALIA;
  • ATTEMPTS TO WIPE JOE’S MIND AS WELL AS ALL HIS DATA BY THE PERPETRATORS HAVE FAILED MISERABLY.

THE FACT THAT THE ONLY PARTIES WHO SEEM TO THINK THERE IS A PROBLEM ARE THE CRIMINALS CONNECTED TO AND/OR PERPETRATING THE FRAUD, AND WHO HAVE HAD PHYSICAL/LOGICAL PROXIMITY TO ME AND/OR MY DRINKS/FOOD AT THE MATERIAL TIMES.

INTERESTING ISN’T IT?

So does Joe actually have Schizophrenia?

the case continues…

Joseph-S-R-de-Saram

Joseph S R de Saram (JSRDS)

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

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