Sunday, March 2, 2008

Demonic Possession or...


Since the movie The Exorcist back in the 70's, the movie public has become fascinated by devils and demons! But the question remains that no one seems to want to ask is, do demons exist? Are devils and demons just a product of the Judeo/Christian scare package to motivate converts to quickly accept their dogma?


What is a demon and demonic possession in the first place? In religion, folklore, and mythology a demon (or daemon, dæmon, daimon from Greek: δαίμων [ðaïmon]) is a supernatural being that has generally been described as a malevolent spirit, and in Christian terms it is generally understood as a Fallen angel, formerly of God. A demon is frequently depicted as a force that may be conjured and insecurely controlled. The "good" demon in recent use is largely a literary device (e.g., Maxwell's demon), though references to good demons can be found in Hesiod and Shakespeare.[1] In common language, to "demonize" a person means to characterize or portray them as evil, or as the source of evil. - Wikipedia

And demonic possession is often the term used to describe the control over a human form by the Devil himself or one of his assigned advocates. Descriptions of demonic possessions often include: erased memories or personalities, convulsions, “fits” and fainting as if one were dying.[1] Unlike in channelling or other benign forms of possession, the subject has no control over the possessing entity and so it will persist until forced to leave the victim, usually through a form of exorcism. Many cultures and religions contain some concept of demonic possession, but the details vary considerably. Some cultures, in particular the Roma people believe that demons can also possess animals, plants, deceased persons or inanimate objects.

The oldest references to demonic possession are from the Sumerians, who believed that all diseases of the body and mind were caused by "sickness demons" called gidim or gid-dim [2]. The priests who practiced exorcisms in these nations were called ashipu (sorcerer) as opposed to an asu (physician) who applied bandages and salves[3]. Many cuneiform tablets contain prayers to certain gods asking for protection from demons, while others ask the gods to expel the demons that have invaded their bodies.

Most illustrations portray these spirits as small, gruesome characters with inhuman distinctiveness. Often referenced as a witch’s “familiars” demons and other evil-spirits employed by witches are also displayed as society’s cast-offs or those beings incapable of caring for themselves thus seeking refuge with a witch. Witches would provide shelter and nourishment via the “witch’s teat” in exchange for the valuable services of the familiars in addition to spells, potions and other attempts by a witch to case evil or “maleficium” over another.[4]

Nevertheless there are no descriptions of specific punishments against possessed persons as it happened later many times in Christian societies. Shamanic cultures also believe in demon possession and shamans perform exorcisms too; in these cultures often diseases are attributed to the presence of an evil spirit or demon in the body of the patient.

Demon possession became a plague among Christians; exorcisms and executions were performed on persons allegedly possessed; many mentally ill people were accused of being demon-possessed and were killed. The Malleus Maleficarum speaks about some exorcisms that can be done in different cases. In Christianity, animals were also believed to be able of being possessed; during the Middle Ages, hundreds of cats, goats, and other animals were slain because of the idea that they were either an incarnation of a demon or possessed by one. - Wikipedia

And as stated above "many mentally ill people were accused of being demon-possessed and were killed!" Have fundamentalist gone too far and persecuted and scammed people that should be under qualified psychiatric care?

Within the DSM-IV (The Diagnostic and Statistical Manual of Mental Disorders (DSM) is an American handbook for mental health professionals that lists different categories of mental disorders and the criteria for diagnosing them, according to the publishing organization the American Psychiatric Association. It is used worldwide by clinicians and researchers as well as insurance companies, pharmaceutical companies and policy makers) provides the following definition for schizophrenia:

"

To be diagnosed with schizophrenia, a person must display:[4]

  • Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a one-month period (or less, if successfully treated)
Note: Only one of these symptoms is required if delusions are bizarre or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other.
  • Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
  • Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if successfully treated).

Additional criteria are also given that exclude the diagnosis; thus schizophrenia cannot be diagnosed if symptoms of mood disorder or pervasive developmental disorder are present, or the symptoms are the direct result of a substance (e.g., abuse of a drug/medication) or a general medical condition."

The causes can be the following:

"

While the reliability of the diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), evidence suggests that genetic and environmental factors can act in combination to result in schizophrenia.[42] Evidence suggests that the diagnosis of schizophrenia has a significant heritable component but that onset is significantly influenced by environmental factors or stressors.[43] The idea of an inherent vulnerability (or diathesis) in some people, which can be unmasked by biological, psychological or environmental stressors, is known as the stress-diathesis model.[44] The idea that biological, psychological and social factors are all important is known as the "biopsychosocial" model.

Genetic

Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin studies have suggested a high level of heritability.[45] It is likely that schizophrenia is a condition of complex inheritance, with several genes possibly interacting to generate risk for schizophrenia or the separate components that can co-occur leading to a diagnosis.[46] Recent work has suggested that genes that raise the risk for developing schizophrenia are non-specific, and may also raise the risk of developing other psychotic disorders such as bipolar disorder.[47][48]

Prenatal

It is thought that causal factors can initially come together in early neurodevelopment, including during pregnancy, to increase the risk of later developing schizophrenia. One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring, (at least in the northern hemisphere).[49] There is now evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between in utero developmental pathology and risk of developing the condition.[50]

Social

Living in an urban environment has been consistently found to be a risk factor for schizophrenia.[51][39] Social disadvantage has been found to be a risk factor, including poverty[52] and migration related to social adversity, racial discrimination, family dysfunction, unemployment or poor housing conditions.[53] Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.[54][55] Parenting is not held responsible for schizophrenia but unsupportive dysfunctional relationships may contribute to an increased risk.[56][57]

Substance use

See also: dual diagnosis

The relationship between schizophrenia and drug use is complex, meaning that a clear causal connection between drug use and schizophrenia has been difficult to tease apart. There is strong evidence that using certain drugs can trigger either the onset or relapse of schizophrenia in some people. It may also be the case, however, that people with schizophrenia use drugs to overcome negative feelings associated with both the commonly prescribed antipsychotic medication and the condition itself, where negative emotion, paranoia and anhedonia are all considered to be core features.[58] Amphetamines trigger the release of dopamine and excessive dopamine function is believed to be responsible for many symptoms of schizophrenia (known as the dopamine hypothesis of schizophrenia), amphetamines may worsen schizophrenia symptoms.[59] Schizophrenia can be triggered by heavy use of hallucinogenic or stimulant drugs.[60] One study suggests that cannabis use can contribute to psychosis, though the researchers suspected cannabis use was only a small component in a broad range of factors that can cause psychosis.[61]

Psychological

A number of psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases that have been identified in those with a diagnosis or those at risk, especially when under stress or in confusing situations, include excessive attention to potential threats, jumping to conclusions, making external attributions, impaired reasoning about social situations and mental states, difficulty distinguishing inner speech from speech from an external source, and difficulties with early visual processing and maintaining concentration.[62][63][64][65] Some cognitive features may reflect global neurocognitive deficits in memory, attention, problem-solving, executive function or social cognition, while others may be related to particular issues and experiences.[66][56] Despite a common appearance of "blunted affect", recent findings indicate that many individuals diagnosed with schizophrenia are highly emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder.[67][68][69] Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomology.[70][71][72][73] Further evidence for the role of psychological mechanisms comes from the effects of therapies on symptoms of schizophrenia.[74]

Neural

Functional magnetic resonance imaging and other brain imaging technologies allow for the study of differences in brain activity among people diagnosed with schizophrenia.
Functional magnetic resonance imaging and other brain imaging technologies allow for the study of differences in brain activity among people diagnosed with schizophrenia.

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes.[75] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[76] The role of antipsychotic medication, which nearly all those studied had taken, in causing such abnormalities is also unclear.[77]

Particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms. An influential theory, known as the Dopamine hypothesis of schizophrenia, proposed that a malfunction involving dopamine pathways was the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.[78]

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia[79] and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[80] The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia.[81] Further support of this theory has come from preliminary trials suggesting the efficacy of coagonists at the NMDA receptor complex in reducing some of the positive symptoms of schizophrenia.[82]

There have also been findings of differences in the size and structure of certain brain areas in schizophrenia, starting with the discovery of ventricular enlargement in those for whom negative symptoms were most prominent.[83] However, this has not proven particularly reliable on the level of the individual person, with considerable variation between patients. More recent studies have shown various differences in brain structure between people with and without diagnoses of schizophrenia.[84] However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia." - Wikipedia

To date, there hasn't been any scientific/medical proof of demons and/or demonic possession and Phantasmagoric World would welcome any such proof the educate our readers further!


Have a great Phantasmagoric World Day!


1 comment:

Moriah Conquering Wind said...

psych theory does what all science does when wielded by an atheist: ignores first cause. just as ignoring the existence of God in the equation of how life on earth began results in evolutionary theory so does ignoring the source or origin of certain brain phenomena produce psych theory. the only time something constitutes a delusion would be when it happens to not be real. if someone actually DOES take thoughts out of your head against your will, or insert them, or control you whether you want them to or not, or talk to you without doing you the courtesy of appearing in visible form first, all these things will be explained as psychosis by those who do not experience them. but they only regard them as unreal because they have no experience with them, and all of this essentially begs the ontological question. medicine and science happen to be excellent tools for addressing things herenow, but they cannot define ontology and in fact assume a fixed ontology in doing so which actually may not apply to every individual's experiential and existential reality.