The following story is about a rare event where a person was diagnosed with schizophrenia but actually ended up having a brain tumor.

It is very common for people who have schizophrenia to not understand that they have schizophrenia (upwards of 50% of people who have schizophrenia don’t understand that they have schizophrenia) but occasionally the reverse it true. The lesson for all here is to make sure the psychiatrists do the proper medical diagnosis before you or someone you know is diagnosed with schizophrenia. Generally this is true – psychiatrists typically take quite a while to diagnose schizophrenia because they need to do tests to make sure the problem isn’t something else like a brain tumor. Learn as much as you can about the disease and always work to get the best possible treatment for someone who has schizophrenia.

For three hellish years I was treated for schizophrenia. But a simple blood test could have revealed the real problem. 
A True Story By LUCY LAING

WHEN Kaye Asquith was told she was suffering from schizophrenia, she was a bright young student getting top grades at school. A year later, it was revealed that a terrible mistake had been made. Kaye, now 22, who lives in Barnsley with her mother Janet, 45, a nurse, was suffering from a life threatening brain
tumour . . .

MY NIGHTMARE began when I was 14, in the summer of 1995. I’d been a happy person – I loved going to school, had lots of friends and was getting A grades at school. My ambition was to go to university.



[Paranoid-hallucinatory psychosis as primary manifestation of subactue sclerosing panencephalitis (SSPE) in a 19-year-old man].

Psychiatr Prax. 2003 May;30 Suppl 2:S70-2.
[Article in German]


Krankenhaus für Psychiatrie und Psychotherapie Schloss Werneck, Balthasar-Neumann-Platz 1, 97440 Werneck.


We report the rare case of a 19-year old man, first diagnosed with schizophrenia but finally shown to have subacute sclerosing panencephalitis (SSPE). Initial symptoms were hallucinations and negative symptoms until the onset of a seizure. Changes in the CSF, MRI, EEG and increasing neurological symptoms led to the correct diagnosis of subacute sclerosing panencephalitis. The EEG results were of particular importance as they already showed the characteristic changes, even while the patient still only presented with psychotic symptoms. This case report demonstrates the importance of ongoing neurological examinations in patients with psychiatric disorders. In the literature, there are only three case reports about children (8, 9 and 10 year old) as well as one of a 21-year old women with subacute sclerosing panencephalitis presenting with psychosis.

[PubMed – indexed for MEDLINE]

Has an angel shown the way? Etiological and therapeutic implications of the PCP/NMDA model of schizophrenia

Schizophr Bull. 2012 Sep;38(5):958-66. doi: 10.1093/schbul/sbs069.

Has an angel shown the way? Etiological and therapeutic implications of the PCP/NMDA model of schizophrenia.


Department of Psychiatry, Nathan Kline Institute for Psychiatric Research/Columbia University College of Physicians and Surgeons, Orangeburg, NY 10962, USA. javitt@nki.rfmh.org


Over the last 20 years, glutamatergic models of schizophrenia have become increasingly accepted as etiopathological models of schizophrenia, based on the observation that phencyclidine (PCP) induces a schizophrenia-like psychosis by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors. This article reviews developments in two key predictions of the model: first, that neurocognitive deficits in schizophrenia should follow the pattern of deficit predicted based on underlying NMDAR dysfunction and, second, that agents that stimulate NMDAR function should be therapeutically beneficial. As opposed to dopamine receptors, NMDAR are widely distributed throughout the brain, including subcortical as well as cortical brain regions, and sensory as well as association cortex. Studies over the past 20 years have documented severe sensory dysfunction in schizophrenia using behavioral, neurophysiological, and functional brain imaging approaches, including impaired generation of key sensory-related potentials such as mismatch negativity and visual P1 potentials. Similar deficits are observed in humans following administration of NMDAR antagonists such as ketamine in either humans or animal models. Sensory dysfunction, in turn, predicts impairments in higher order cognitive functions such as auditory or visual emotion recognition. Treatment studies have been performed with compounds acting directly at the NMDAR glycine site, such as glycine, D-serine, or D-cycloserine, and, more recently, with high-affinity glycine transport inhibitors such as RG1678 (Roche). More limited studies have been performed with compounds targeting the redox site. Overall, these compounds have been found to induce significant beneficial effects on persistent symptoms, suggesting novel approaches for treatment and prevention of schizophrenia.

[PubMed – in process]
[Available on 2013/9/1]


Patients labeled with “Schizophrenia”

Uploaded by videoberries on Jan 11, 2011

Some schizophrenia symptoms, diagnostic criteria, etc

Uploaded by QuitProfesserHiggins on Jun 21, 2011
This documentary about schizophrenia aired on HBO sometime around 1989

Uploaded by garywolfe99 on Sep 30, 2010

Portrait of a homeless man with Schizophrenia living on the streets of San Francisco. Part 1

Uploaded by garywolfe99 on Sep 30, 2010

Portrait of John Ratliff, a homeless man with schizophrenia, living on the streets of San Francisco

Published on Jun 4, 2012 by DiscoveryHealth

Jani’s friend Briana introduces us to one of her hallucinations, Seven.

Watch more videos at http://health.discovery.com#mkcpgn=yfit1

Published on Jun 4, 2012 by DiscoveryHealth

Jani experiences many accomplishments and pitfalls as a result of her condition.

Watch more videos at http://health.discovery.com/videos/embarrassing-bodies#mkcpgn=yfit1

Published on May 29, 2012 by DiscoveryHealth

Join us for the world premiere of Born Schizophrenic: Jani’s Next Chapter. In this one-hour special, we check in the with Schofield family as they raise Jani, their nine-year-old daughter who has been diagnosed with schizophrenia.

Prenatal Lead Exposure and Schizophrenia: Further Evidence and More Neurobiological Connections

Tomás R. Guilarte

In 2004, Opler et al. published a study in Environmental Health Perspectives (EHP) suggesting an association between prenatal lead (Pb2+) exposure and schizophrenia (Opler et al. 2004). In the November 2008 issue of EHP, Opler et al. (2008) further supported this association using a different cohort of subjects. In a letter published in EHP in 2004 (Guilarte 2004), I indicated that a plausible neurobiological connection between prenatal Pb2+ exposure and schizophrenia may be that Pb2+ is a potent antagonist of the N-methyl d-aspartate (NMDA) receptor (NMDAR), and NMDAR hypofunction is thought to be involved in the pathophysiology of the disease. Since then, another plausible neurobiological connection has surfaced, and this relates to hippo campal neurogenesis. Neurogenesis occurs not only during development but is also prominent in the adult brain (Laplagne et al. 2006). A well-characterized neurogenic zone in the adult brain is the subgranular zone of the dentate gyrus (DG) in the hippocampus (Zhao et al. 2008). Although the significance of newly born neurons in the adult hippocampus is currently under investigation, the overwhelming evidence supports a role in hippocampus-dependent learning (Dupret et al. 2008; Imayoshi et al. 2008).

Schizophrenia patients express cognitive deficits that may be related to hippocampal dysfunction (Gothelf et al. 2000; Sweatt 2004). So, what is the new neurobiological connection between Pb2+ exposure and schizophrenia? Recent evidence indicates that neurogenesis is decreased in schizophrenia patients, and this decrease may contribute to their cognitive dysfunction (Kempermann et al. 2008; Reif et al. 2006). In an animal model using the NMDAR antagonist phencyclidine (PCP) to induce schizophrenia-like symptoms in mice, Maeda et al. (2007) observed reduced DG neurogenesis that was reversed by the atypical anti-psychotic drug clozapine. Co-administration of d-serine and glycine also inhibited the PCP-induced decrease in neurogenesis. PCP, like Pb2+, is an NMDAR antagonist, and D-serine and glycine activate NMDAR; this suggests that chronic NMDAR hypofunction decreases neurogenesis in the hippo campus, an observation consistent with my comments in 2004 (Guilarte 2004). Models of developmental Pb2+ exposure have also shown decreased DG neurogenesis and are associated with deficits in learning (Jaako-Movits et al. 2005; Verina et al. 2007). Therefore, reduced DG neuro genesis appears to be a common factor in schizophrenia and in animal models of schizophrenia and developmental Pb2+ exposure.

Schizophrenia is a neurodevelopmental disorder that is expressed later in life. Pb2+ is a neurotoxicant that is known to cause developmental abnormalities. Animal models of developmental Pb2+ exposure express a behavioral phenotype with features that overlap with those in animal models of schizophrenia, including increased spontaneous activity, decreased social interaction, and learning deficits (Moreira et al. 2001; Nihei et al. 2000). Also, some of the behavioral effects described in adolescents with early-life Pb2+ exposure are similar to those expressed in schizophrenia patients (Opler and Susser 2005). Thus, although the environmental causes of schizophrenia have not evaluated environmental toxicants, the emerging evidence from the human studies by Opler and colleagues and animal studies suggest that prenatal Pb2+ exposure may be an environmental risk factor for schizophrenia.

Click here for full article.

Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses.

Neurotoxicology. 2012 Jun;33(3):560-74. Epub  2011 Dec 9.


Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY 10032, United States. trguilarte@columbia.edu


Schizophrenia is a devastating neuropsychiatric disorder of unknown etiology. There is general agreement in the scientific community that schizophrenia is a disorder of neurodevelopmental origin in which both genes and environmental factors come together to produce a schizophrenia phenotype later in life. The challenging questions have been which genes and what environmental factors? Although there is evidence that different chromosome loci and several genes impart susceptibility for schizophrenia; and epidemiological studies point to broad aspects of the environment, only recently there has been an interest in studying gene × environment interactions. Recent evidence of a potential association between prenatal lead (Pb(2+)) exposure and schizophrenia precipitated the search for plausible neurobiological connections. The most promising connection is that in schizophrenia and in developmental Pb(2+) exposure there is strong evidence for hypoactivity of the N-methyl-d-aspartate (NMDA) subtype of excitatory amino acid receptors as an underlying neurobiological mechanism in both conditions. A hypofunction of the NMDA receptor (NMDAR) complex during critical periods of development may alter neurobiological processes that are essential for brain growth and wiring, synaptic plasticity and cognitive and behavioral outcomes associated with schizophrenia. We also describe on-going proof of concept gene-environment interaction studies of early life Pb(2+) exposure in mice expressing the human mutant form of the disrupted in schizophrenia 1 (DISC-1) gene, a gene that is strongly associated with schizophrenia and allied mental disorders.

Copyright © 2011 Elsevier Inc. All rights reserved.

Former Washington Post Reporter Pete Earley talks about his book “Crazy: A Father’s search through America’s Mental Health Care Madness”

Uploaded by on Jan 29, 2010

Program Description:
Pete Earley will use his personal story to illustrate how difficult it is to get a loved one with a severe mental illness meaningful help. He will specifically focus on how and why persons, such as his son, often end up in our criminal justice system and why that is wrong. In addition to telling his sons story, he will describe the results of a nine month investigation that he conducted as a journalist inside the Miami Dade County jail where he followed persons with severe mental illnesses through the criminal justice system and out into the community to observe what services were available to them. The goal of his presentation is to explain why jails and prisons have become our new asylums, why this is wrong, why it wastes money, and how communities can better serve persons with mental illnesses by focusing on a variety of successful programs that help people recover rather than punish them for being ill.

Program Presenter:
In a *Washingtonian Magazine* cover story entitled, Top Journalists: Washingtons Media Elite, Pete Earley was described as one of a handful of journalists in America who have the power to introduce new ideas and give them currency. A former reporter for *The Washington Post*, he is the author of nine nonfiction books and three novels. His first book, *Family of Spies: Inside the John Walker Spy Ring*, was a New York Times bestseller and was made into a five hour miniseries shown on CBS television. For his book, The *Hot House: Life Inside Leavenworth Prison*, Earley spent a full year as a reporter inside a maximum security prison. His book, *Circumstantial Evidence* helped lead to the release of a black man from death row after he had been wrongly convicted of murdering a white teenager in Alabama. His book, *CRAZY: A Fathers Search Through Americas Mental Health Madness, *tells two stories. It describes his attempts to help is college age son, Mike, after he becomes ill with bipolar disorder and is arrested. It also describes a year that Earley spent at the Miami Dade County Jail where he followed persons with mental disorders, who had been in jail, out into the community to see what sort of services they received. His book was one of two finalists for the Pulitzer Prize in 2007 and has won awards from Mental Health America, National Alliance on Mental Illness, and the American Psychiatric Association.

Long Term Treatment with Antiviral Drugs in Psychotic Patients


Dr Segundo Mesa Castillo

Psychiatric Hospital of Havana, Cuba


Eighteen psychotic patients meeting the DSM-IIIR criteria for schizophrenia and manic-depressive psychosis were treated with antiviral drugs-aciclovir and interferon or aciclovir alone- plus the conventional treatment for more than eight months. Before treatment was begun, a biological test (BT) was performed on blood and cerebrospinal fluid, using immunoelectromicroscopic techniques, and the test was repeated eight months later. The results obtained by comparing their evolution before and after the antiviral treatment was begun show a significant favorable outcome in 89 percent of the patients treated. This is related to a modification in the BT, with a decrease in the presence of particles that reacts to the herpes simplex hominis type I virus (HSV-1) antibody or with an increase in those patients who had a relapse.


Schizophrenia. manic-depressive psychosis. herpes simplex, interferon, aciclovir, interferon, biological test.



Schizophrenia is a disease in which a viral etiology is strongly, considered because of clinical (1), epidemiological (2), laboratory (3), experimental (4), ultrastructural (5) and immunological (6) data. among others,

Favorable results following the use of Interferons in the treatment of schizophrenia (7-11) have been obtained in previous studies. In this study, we have also applied antiviral treatment in cases of manic-depressive psychosis, on obtaining BT results that could indicate a common etiology in the two diseases (12). The favorable results, obtained in these two psychiatric disorders are set forth in this paper, as is their relationship to the BT both before and after initiating the antiviral treatment, which also includes the use of aciclovir for long periods of time.


A total of 18 psychotic patients-15 schizophrenics and three manic-depressives, according to the DSM-IIIR criteria were treated with aciclovir or with aciclovir and interferon for more than eight months, with their consent or families’ consent. The patients were between 20 and 54 years old, nine were men, and nine, women. Each patient was given a questionnaire to obtain such data as name, age, date of birth, family members with psychosis, prevailing symptoms and the frequency and length of her/his crises among other things (Chart 1). Blood and cerebrospinal fluid samples were taken from each patient with their consent or families’ consent and a biological test (described in earlier papers) (13) was done, both before initiating treatment and eight (8) months later. A relationship was established between the clinical evolution and the BT results.

From the clinical point of view, a criterion of social evolution was established, which included the following points (Table 1): sexual relations, self-esteem, family relations, relations with neighbors, recreational activities, school and work. An outcome criterion was obtained from relatives, friends, attending physician, nurses and the own patient in a blind evaluation before and after treatment (Chart 1).


The higher the score, the less favorable the evolution. A questionnaire was answered both before treatment and three and eight months later, comparing each patient’s evolution with what it had been before and also keeping in mind the frequency, duration and intensity of crises. A blood study was made on each patient prior to treatment, and EEG and RMN studies were made in most cases. The treatment with neuroleptics or other treatment which each patient had was continued, adding the antiviral treatment. For 14 patients, this was aciclovir, as follows: one gram a day for one month, 800 mg. a day for three months, 600 mg. a day for three months, 400 mg. a day for three months, and then 200 mg. a day if the patient continued to evolve favorably. For four patients, aciclovir and Interferon were combined, as follows: 3 million IU of Alpha Interferon injected intramuscularly once a week for three months. changing to 3 million every 15 days if their evolution was favorable, combined with 200 mg. of aciclovir a day’ right from the start. Periodic blood studies were made later on in these cases, to observe leukocyte and blood platelet counts. Deposit fluphenazin was the neuroleptic used most frequently. Carbamazepin was used on four patients as another most frequently used drug.


Thirteen of the 14 patients

(93 percent of them) who were treated with high doses of aciclovir, following the plan described above, evolved favorably, with low scores on the scale of social evolution. The absence of relapses in 14 patients and the short duration and low intensity of the crises in two of the four who did have crises were other elements which were considered as favorable when the evolution of each patient was compared with his clinical evolution before the treatment was begun (Table 2). The two cases that did not evolve favorably maintained the same score in the social evolution scale that they had had prior to the beginning of treatment. Those two patient did not cooperate in the antiviral treatment. One of them got a lot better during the first six months of antiviral treatment; then the treatment was abandoned and the symptoms of the disease reappeared. In no patient was it necessary to suspend or decrease the treatment because of lack of tolerance or undesired effects. Both interferon and aciclovir were well tolerated, with the side effect on the day of the interferon injection controlled easily with antipyretics before the injection and two hours afterwards.

After an average of three months of treatment, the patients’ social conduct began to evolve very favorably, with some of them going to work or study. Those who did not at least allowed the relatives who take care of them to have a higher quality of life. In every case, there was a clear correspondence between the patient’s clinical evolution and the BT. In the cases which evolved favorably, there was an important decrease in the HSV-1 antigen or in the presence of viral like particles.

The presence of viral activity during crises was observed in the BTs (Figure 1) of patients who suffered relapses.


Every day, more elements favor a viral hypothesis of the etiology of schizophrenia, especially that of herpes sirnplex as the most probable candidate among the causative agents. The positive neurotropism of this virus to the temporal lobe (seat of the limbic system); its characteristic form of clinical evolution in outbreaks and remissions, as happens in the diseases that are the object of this paper, and its ability to remain latent in the central nervous system are some of the elements which support this hypothesis. An increase in antibodies against HSV-1 (3), which was observed in the patients and the presence of particles with the characteristic antigenic response and morphology, as seen under the electronmicroscope in patients, fetuses and inoculated animals (5,6), are other

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Dr. Torrey’s public statements promote the belief that all psychotic states are a result of suffering from schizophrenia, he fails to consider Best Practice Assessment of Psychosis

Posted by Maria Mangicaro


Uploaded by on Jan 11, 2011

Psychiatrist Dr. E Fuller Torrey says the man suspected in the Tucson shooting displays symptoms of Schizophrenia.

According to the British Medical Journal’s Best Practice Assessment of psychosis guidelines:

Organic causes must be considered and excluded before the psychosis is attributed to a primary psychotic disorder.

The most common cause of acute psychosis is drug toxicity from recreational, prescription, or OTC drugs.

Patients with structural brain conditions, or toxic or metabolic process presenting with psychosis, usually have other physical manifestations that are readily detectable by history, neurological examination, or routine laboratory tests.

Brain imaging is reserved for patients with specific indications, such as head trauma or focal neurological signs. The routine use of such imaging is unlikely to reveal an underlying organic cause and is not recommended.

Click here to read more.

Dr. Torrey’s public statements are misleading.

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