The Other 1%
Letter to CDC's Yeargin-Alsopp "Why isn't SEED looking at vaccines and toxins in autism?"

Risperdal and S100B: Prolactin, Tumors and Tardive Dyskinesia


By Teresa Conrick

With Autism numbers climbing, there are those who look to the profit margin of knowing thousands of children, teens and young adults may need medications to "target behavior."   It is unfortunate and incorrect that Autism is still being looked at as a behavioral and developmental disability for many instead of a neuroimmune disease that manifests in repetitive behaviors, anxiety and verbal/social regression. For many, like my daughter, that regression came about after vaccinations.  These children tend to be very vulnerable canaries to toxins, thus medications can prove to be problematic for many.  It is important to know the mechanism of action in treating symptoms short term, but especially long term as some of these drugs have severe side effects that increase with dosage as well as duration.

Recently, I wrote about a new study showing that over a third of children with an autism diagnosis had high levels of S100B in their blood, a calcium-binding protein that is produced primarily by astrocytes and is indicative of active brain injury.  While reading about S100B, I started to realize that some abstracts and research about Risperdal and other anti-psychotic medications were appearing that seemed to show a pattern. 

(Note: below is a public video from a parent unrelated to AofA showing her son's Risperdal-related side effect. Her message attached to the video reads, This is my son Nathan he is 13yrs old and started with the neck twitching about 3 months ago. He has been on Risperdal (risperdone) for about 8 years now. I have seen his doctors on a regular basis to discuss the side effects and to see what we can do about weening him off. However he did not say this was Tardive Dyskinasia, he gave me another medication to help with this side effect, but I am not going to keep giving my son medication to solve the problem of a drug side effect. I am trying to get answers, he is scheduled for a Neurologist appt in July and in the mean time we are currently at .05 mg risperdone, he was taking 3 mg before then dropped down to 2, then 1 and now 0.5. I am so confused everything I have looked up on Tardive Dyskinasia shows me that this is what my son has. Nathan is autistic and his doctor recently prescribed us Congentin to help with the neck twitching, but what I have read on Congentin says this is not for patients with Tardive Dyskinesia, its so confusing. All i know is that his twitching gets really bad to where he is so sore from his neck and his doctor also reccomended us taking Benadryl has anyone ever heard of that..???)


Some Facts About the S100B
Autism Study   

- High S100B levels offer an indicator of cell damage when standard diagnostic procedures are still silent.

- Increased serum S100B protein levels reflect neurological damage.

- Elevated S100B protein may be indicative of active cell injury and can reflect an axonal and glial pathology.

- Serum and cerebrospinal fluid (CSF) levels of S100B protein levels are raised in some autoimmune neuropsychiatric disorders, reflecting the presence of glial cell pathology and continuing neurological damage.

- S100B protein levels were elevated in autistic children, and they were significantly correlated with the degree of the severity of autism

- patients with associated allergic, inflammatory or autoimmune disorders; and patients who were receiving any medications  -- were excluded.

I thought it would be helpful to set this up with an "abstract" that is based on studies connecting these dots. Their is a longer version also for any who want to read the corresponding studies:


Elevated S100B is a sign of active cell injury to the brain.  S100B protein is chiefly found in glial cells and Schwann cells in the central nervous system (CNS) [1].   The content of S100B in various brain areas is regulated by serotonin. [1a]

Risperdal and other anti-psychotics seem to target the astroglial cells. It is known that S100B is secreted but there is uncertainty on levels of possible injury. [2a] Interestingly, many information sites on Risperdal report that its mechanism in treating psychosis is unknown [2b] or that it is possibly due to helping fix neurotransmitters in the brain.[2c]

Astrocytes (etymology: astron gk. star, cyte gk. cell), also known collectively as astroglia, are characteristic star-shaped glial cells in the brain and spinal cord. They are the most abundant cell of the human brain. They perform many functions, including biochemical support of endothelial cells that form the blood-brain-barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries. [3]

Risperdal especially, induced a statistically significant increment of about 80% in S100B secretion from astroglia. [4]

Other studies have shown secreted glial S100B exerts trophic ["nutritious"] or toxic ["poisonous"] effects depending on its concentration. [5a]

Structural damage to glial cells causes leakage of S100B protein into the extracellular compartment and cerebrospinal fluid; it also causes it to enter the bloodstream. [5b]

Some research has shown increased S-100B plasma levels in some patients suffering from schizophrenia. These findings suggest that serum S100B levels in chronic schizophrenia under antipsychotic medication may be increased [6] Other research showed no difference in medicated and non-medicated patients, [6a] while others showed significant increases in medicated patients. [6b]

Several studies show that calcium-binding protein S100B is increased in schizophrenia and may be involved in the pathogenesis of tardive dyskinesia. [7] 

Risperdal especially has produced tardive dyskinesia in users. [8]  [8a] [8b] [8c] [8d]

Risperdal  and similar medications can raise the blood levels of a hormone known as prolactin, causing a condition known as hyperprolactinemia.  [9]

There have been higher-than-expected postmarketing reports of pituitary tumors associated with Risperidone,  Risperidone had the highest adjusted reporting ratios for hyperprolactinemia, galactorrhea, and pituitary tumor among the seven antipsychotics, and one of the highest scores for all drugs in the AERS database.  [10]

Increasing S100B concentrations indicate tumor progression. [11]   There is evidence that S100 protein in pituitary cells can stimulate prolactin releases [11a]

SInce 2006, reports showed Schizophrenia drugs may up tumor risk.  Seventy percent of these reports were in patients taking Risperdal. [12]


There seems to be a pattern here that has either not been connected or has been denied.  That pattern could be this:

 ---- Risperdal targets glial cells >>> Glial cells can be injured by leaking S100B >>> S100B can cause tardive dyskinesia >>>S100B can cause pituitary tumors >>> Risperdal can cause both tardive dyskinesia and pituitary tumors. ----

Instead, the pattern has been this:

----"When you put all the data together, you get a strong biochemical plausibility that this is a Risperdal effect," Doraiswamy tells WebMD.>>>"But we cannot rule out the possibility it is a spurious association. >>> No one should stop Risperdal because of this. Even if Risperdal is linked to pituitary tumors, it may turn out to be fairly rare." >>> Johnson & Johnson is a WebMD sponsor."----


[1]-  A lack of association between elevated serum levels of S100B protein and autoimmunity in autistic children 
"S100B protein is chiefly found in glial cells and Schwann cells in the central nervous system (CNS) [4]. The clinical significance of S100B protein has substantially increased throughout several areas of clinical neuroscience as it can be used as a reliable and early predictor of poor physiological and cognitive neurological outcomes [5]. Serum and cerebrospinal fluid (CSF) levels of S100B protein levels are raised in some autoimmune neuropsychiatric disorders, reflecting the presence of glial cell pathology and continuing neurological damage [6-8]."

[1a]- S100B in Brain Damage and Neurodegeneration 
"This was shown by several different approaches:......Also, an increase of serotonin levels by fluoxetine [PROZAC] administration increased S100B concentrations (Haring et al., 1993; Manev and Manev, 2001).

[2a]- In this context, we have investigated the effect of risperidone on astroglial cells, evaluating morphology, membrane integrity, viability, secretion of S100B, a neurotrophic astrocyte-derived protein and glutamate metabolism (glutamate uptake, glutamine synthetase activity and glutathione synthesis). We demonstrate for the first time that risperidone was able to modulate cell morphology and glial adhesion (Quincozes-Santos et al., 2008), contributing to the proposal that glial cells also are targets of antipsychotics. In addition, risperidone also increased S100B secretion by astroglial cells. S100B is a calcium-binding protein involved in the regulation of cytoskeleton and the proliferation of astrocytes. Beyond its intracellular role, S100B,depending on its concentration, works as a cytokine for neighboring cells (astrocytes, neurons, and microglia) and is able to protect hippocampal neurons against glutamate toxicity. "

[2b] Stanford School of Medicine-Psychiatric Medications 
"Risperdal is the brand name for Risperidone, an antipsychotic agent used to treat certain types of psychotic thinking. It has been found to improve both positive and negative symptoms of schizophrenia. The exact mechanism of action of risperidone is unknown."

"The exact mechanism of action of risperidone is not known, but, like other anti-psychotics, it is believed that risperidone affects the way the brain works by interfering with communication among the brain's nerves. Nerves communicate with each other by making and releasing chemicals called neurotransmitters. The neurotransmitters travel to other nearby nerves where they attach to receptors on the nerves. The attachment of the neurotransmitters either stimulates or inhibits the function of the nearby nerves. Risperidone blocks several of the receptors on nerves including dopamine type 2, serotonin type 2, and alpha 2 adrenergic receptors. It is believed that many psychotic illnesses are caused by abnormal communication among nerves in the brain and that by altering communication through neurotransmitters, risperidone can alter the psychotic state.

[3]- Astrocyte -Wikipedia
"They are the most abundant cell of the human brain. They perform many functions, including biochemical support of endothelial cells that form the blood-brain-barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries." 

[4]-Effect of the atypical neuroleptic risperidone on morphology and S100B secretion in C6 astroglial lineage cells.
"We investigated the effect of the atypical neuroleptic risperidone on morphology and S100B secretion in C6 glioma cells, considering the putative involvement of astroglial cells in neuropsychiatric disorders. In the presence of high experimental doses of risperidone, C6 cells become stellate, with process-bearing cells and partial retraction of the cell body followed by detachment from the adhesion surface with practically no cell death. These results indicate that risperidone is able to interfere with C6 cell adhesion without toxic effects. RhoA activator LPA prevented the effects of risperidone on cell morphology. From 6 h risperidone induced a statistically significant increment of about 80% in S100B secretion. These data contribute to the proposal that glial cells are targets of risperidone, which could be involved in the therapeutic response of risperidone to improve autism symptoms."

[5a]- S100B in Brain Damage and Neurodegeneration 
"Secreted glial S100B exerts trophic or toxic effects depending on its concentration. At nanomolar concentrations, S100B stimulates neurite outgrowth and enhances survival of neurons during development. In contrast, micromolar levels of extracellular S100B in vitro stimulate the expression of proinflammatory cytokines and induce apoptosis. In animal studies, changes in the cerebral concentration of S100B cause behavioral  disturbances and cognitive deficits. In humans, increased S100B has been detected with various clinical conditions. Brain trauma and ischemia is associated with increased S100B concentrations, probably due to the destruction of astrocytes. In neurodegenerative, inflammatory and psychiatric diseases, increased S100B levels may be caused by secreted S100B or release from damaged astrocytes. "

[5b]-  The S100B protein in biological fluids: more than a lifelong biomarker of brain distress
the S100B protein was detected for the first time in extracellular biological fluids (CSF) of MS patients in concomitance with the acute phase of exacerbation, being essentially undetectable during remission. At that time the appearance of the protein in biological fluids was regarded as a consequence of leakage from damaged cells. Today, the growing recognition that S100B may be regarded as a released neuroinflammatory protein makes it possible to reinterpret the original data as indicating the active participation of S100B in the exacerbation phase of MS. A subsequent longitudinal study that monitored the CSF of MS patients revealed a peak followed by a decrease."

[6]- Increased serum S100B levels in chronic schizophrenic patients on long-term clozapine or typical antipsychotics       
 "These findings suggest that serum S100B levels in chronic schizophrenia under antipsychotic medication may be increased, suggesting that a dysfunction of astrocytes and/or oligodendrocytes may play a role in the pathogenesis of schizophrenia. Long term treatment with both typical and atypical antipsychotics may produce similar effects on the S100B serum levels, which however remains to be characterized in a large sample of first-episode, medication-naïve patients with schizophrenia using a longitudinal design."            

[6a]- Increased serum S100B in never-medicated and medicated schizophrenic patients. 
"Our results showed significantly increased serum S100B levels in both never-medicated and medicated patients compared to normal controls "       

[6b]- Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia.
"Previous studies reported controversial results concerning alterations of astrocytes in schizophrenia. Because S100B may be regarded as a marker for astrocytes, the objective of this study was to examine S100B serum concentrations in 30 patients with schizophrenia with a monoclonal two-site immunoluminometric assay that specifically detects S100B. An ANOVA revealed medication (p<0.005) and deficit vs. nondeficit syndrome (p<0.05) as factors that influenced S100B significantly. S100B was higher in schizophrenic patients treated with antipsychotic drugs for approximately 3 weeks (241.1+/-152.5 ng/l) in comparison with unmedicated patients (111.4+/-31.8 ng/l, p<0.005), and healthy age-matched controls (112.8+/-53.4 ng/l, p<0.001; Bonferroni corrected two-tailed Student's t-test). There was no difference of S100B between unmedicated patients and controls (p>0.05)."  

[7]- Increased S100B serum levels in schizophrenic patients with tardive dyskinesia: Association with dyskinetic movements
"Several studies show that calcium-binding protein S100B is increased in schizophrenia and may be involved in the pathogenesis of tardive dyskinesia (TD). We therefore compared serum S100B levels in normal controls (n=60), schizophrenic patients with (n=32) and without TD (n=50). Assessments included the abnormal involuntary movement scale (AIMS) and the positive and negative syndrome scale (PANSS). Serum S100B levels were measured by enzyme-linked immunosorbent assay (ELISA). The results indicated that patients with TD had higher serum S100B levels than normals and those without TD. Serum S100B levels were positively correlated with AIMS scores in patients with TD. These data suggest that increased S100B levels may be related to neuro-degeneration, associated with TD pathophysiology. "        

[8]- Tardive Dyskinesia With Risperidone and Anticholinergics   
"To the Editor: The following are reports on three Japanese women who developed early-onset tardive dyskinesia during short-term risperidone treatment while taking an anticholinergic agent. "

[8a]- Risperidone-Induced Tardive Dyskinesia
"Here we report a case of tardive dyskinesia that developed while a patient was on a regimen of risperidone"

[8b]- Tardive dyskinesia following risperidone treatment in Tourette's syndrome
We discuss the case of a 24-year-old male who first exhibited repetitive head and neck twisting movements that started at 15 years of age....Oral risperidone was started as well as maintained at 1mg with dinner and fluoxetine was increased to 40mg with breakfast. Although his tics were minimal at this dose (YGTSS = mild), he developed severe TD of the lower jaw (oro-mandibular dyskinetic movements) after four months of treatment [Abnormal Involuntary Movement Scale (AIMS) rating = severe]. This movement was entirely different from the initial symptoms both anatomically and phenomenologically... We wish to highlight the need for awareness among clinicians and patients about the potential risk of getting new movement disorders during the course of treatment with risperidone for tic disorders."

[8c]- Risperidone and Tardive Dyskinesia: A Case of Blepharospasm 
We present the case of a young male diagnosed with schizophrenia who developed a blepharospasm form of tardive dyskinesia in association with risperidone."

[8d]- Risperidone-induced tardive movements in young adult patients
"Here, we report a series of four cases with risperidone-induced tardive dyskinesia and dystonia and discuss their management."

and similar medications can raise the blood levels of a hormone known as prolactin, causing a condition known as hyperprolactinemia. Blood levels of prolactin remain elevated with continued use. Some side effects seen with these medications include the absence of a menstrual period; breasts producing milk; the development of breasts by males; and the inability to achieve an erection. The connection between prolactin levels and side effects is unknown."

[10]- Atypical antipsychotics and pituitary tumors: a pharmacovigilance study.
"Risperidone had the highest adjusted reporting ratios for hyperprolactinemia (EBGM 34.9, 90% confidence interval [CI] 32.8-37.1]), galactorrhea (EBGM 19.9, 90% CI 18.6-21.4), and pituitary tumor (EBGM 18.7, 90% CI 14.9-23.3) among the seven antipsychotics, and one of the highest scores for all drugs in the AERS database. Some tumors were associated with visual field defects, hemorrhage, convulsions, surgery, and severe (>10-fold) prolactin elevations. The EBGM values for risperidone for these adverse events were higher in women, but high EBGM values for these events were also seen in men and children. Moreover, the rank order of the EBGM values for pituitary tumors corresponded to the affinities of these seven drugs for D2 receptors."

[11]- S100 proteins as cancer biomarkers with focus on S100B in malignant melanoma.
"S100B concentrations reflect tumor mass. Serum S100B levels predict efficacy of treatment. Decreasing S100B concentrations reflect response to therapy while increasing S100B concentrations indicate tumor progression."

[11a]- Regulation Of Pituitary Hyperlasia and Neoplasia
"The development of prolactin cell hyperplasia and the transformation to neoplastic prolactin producing pituitary tumors will be investigated in rats using morphological, immunohistochemical and biochemical methods. Morphological and immunohistochemical studies at the light and electron microscopic levels will be used to characterize various subtypes of prolactin cells and mammosomatotropic cells (which produced both prolactin and growth hormone) in hyperplastic and neoplastic MtT/W15 and MtT/F4 tissues. The functions of the pituitary folliculostellate cells in normal, hyperplastic and neoplastic pituitaries will be investigated by immunohistochemical and ultrastructural studies. The role of S100 protein in regulating prolactin secretion will be investigated. Preliminary findings indicate that S100 protein which is present in pituitary folliculo-stellate cells can stimulate prolactin releases in vitro suggesting that these cells may exert a paracrine type regulation of prolactin release.

[12]- Schizophrenia Drugs May Up Tumor Risk
"A statistical "signal" links Risperdal and other schizophrenia drugs to pituitary tumors, FDA researchers report....Seventy percent of these reports were in patients taking Risperdal. "When you put all the data together, you get a strong biochemical plausibility that this is a Risperdal effect," Doraiswamy tells WebMD.



I am so sorry Marie;
Good luck your law suit.

The best way for them to tell you how sorry they are is to pay a lot.


I have just been diagnosed with a pituitary lesion (1.8mm) and this is from resperidone, i will be filing a lawsuit, i was not informed of any side effects, or pre cautions of this medication. The doctors failed at what they were supposed to be doing, and on top of that it was a mis diagnosis and i never needed the medication at all.

Tasha Rae

Oh ya i have been doing my own research all day and that is how i found out that the pituitary tumor can be caused by the medication respiridol/risperidone sincerely tasha rae

Tasha Rae

I have been perscribed risperidone a couple years ago no one told me about any side effects and now after 2 or more years of taking these meds i have been diagnosed with a pituitary tumor and i am scared i still havnt even seen the specialist yet i just found out a few weeks ago and i am turning to lawyers in my area i have to suffer and even miss work and wait and wait so if anyone out there is on this medication (resperidone) / (repiridal ) and you are experiening bad headaches and or any milky discharge from your breasts and or vission worstening and or no periods for a long time even if you used to be on depoprevera and also problems having an oragasm make sure that you demand an MRI right away oh ya a pituitary tumor is a tumor on the pituitary gland and wich is located in the brain the pituitary is a part of the sexual organ but can cause blindness i am going through this right now and dont wish it upon anyone it is scary sincerely tasha rae :)

Veronica Nellis

Just an update my son did see the neurologist and was diagnosed with tardive dyskinesia. We are going to be seeing a movement specialist and hopefully in Az at the mayo clinic. It all depends if the dr will see him if not we will have to travel to see a dr who sees children..


Thanks Senoaid;
That was very helpful, and it made sense! And now I know what tardive means.


Hi Benedetta

I think 'Tardive'means drug-induced symtpoms, whereas Tourette's is a condition in its own right. But as I understand, ASD, ADHD, Tourette's, OCD are all in the same ballpark so to speak. I think all children with regressive autism could have more than one of these conditions - or at least susceptibilites. I had wondered if different symptoms depended on which part of the brain was damaged / affected? Seemingly Tourette's very often disappears in time - though I don't know why! I have tried to find a link between TS and seizure activity - those over firing neurons? - and did find references in a couple of neurology books. With over 80% of ASDs having some sort seizure activity going on, I thought it quite possible. But you're right. They just don't know!


My son pulled out his hair when they upped his dose of ridalin but it went away when we stopped it.

He does have tourettes; he snorts through his nose like he just has allergies, and he blinks his eyes a lot.

What is the difference in tardive and tourettes?

Is this one of those psy things again?

If so then I guess we are going to get down to really minute details of each behavior.
Medically - let me guess - they have not a clue!

I bet it is all in the same area of the brain, all the same thing.


Hi Vicki

I'm just a mum but would agree that the neck movements displayed by this young man could be Tourette's and it can be a drug side effect. [Tardive Tourettism] My son showed exactly this type of movement when antipsychotic drug doses were high enough. He also had what he called 'bad thoughts' which a Tourette's helpline told me were a form of tic and very common in TS. Unfortunately when doses were raised my son started verbalising those bad thoughtss - coprolalia. The psychiatrist told me it was Tardive Tourettism. Symptoms disaappeared when doses were lowered. In our experience these antipsychotic drugs can cause underlying susceptibilities to appear. Depending on the individual, it might be OCD, TS, self harming, psychosis, agression, ADHD, subclinical or low grade seizure activity which manifests. My son does not have epilepsy, but did at one point have a drug-induced seizure.
Thank you Teresa for this most informative article. With so many people with ASDs now reaching adulthood, there is a great danger of them being caught in the same trap as my son.

Vicki Hill

I'm not a medical professional. I was president of the local chapter of the Tourette Syndrome Association for 3 years, so I have some familiarity with movement disorders. And I have personally known several people with tardive dyskenesia.

The movements in the video, to me, look more like tics than tardive dyskenesia. TD most commonly affects the tongue (a snake-like thrusting), the fingers or the toes (a motion as if you were rolling a pill between the thumb and forefinger). The movements of TD are generally continuous. In contrast, this young man has movements with varying number of seconds in-between. And he is 13 years old, the peak "season", if you will, for tics.

Could this be a medication side effect? Yes, it could. Cogentin is frequently used to counteract a medication side effect and has been for years. So suggesting cogentin while titrating the dose down was a responsible suggestion from the doctor. (It is usually not recommended to stop meds like this 'cold turkey', as that approach can produce even more side effects.)


Thanks you Teresa, it is always amazing to me how you can put this all together yet the medical/scientific community remains "puzzled."

Aimee Doyle I totally understand where you are ocming from - - it seems we do/try everything and the behaviors still come raging back. My son is 17 and high doses of Inositol really helped him (6-9 grams per day). He also still requires somewhat intensive behavioral intervention, his entire day is structured and his behavior support plan is aggressively managed - - if his behaviors are up and the strategies aren't working, the plan is adjusted by the BCBA until we see the data coming down. Yes this is expensive but I don't see how my son will ever work or live somewhat independently without high quality behavioral support. With my son, you can't just "intervene" when behaviors flare up, it requires constant maintenance to allow him to have any semblence of basic quality of life. This is what is most disappointing to me about adult services and the myth that behavioral therapy is only effective for young children. I use the analogy of Braille for a blind person; denying behavioral support to my son is like denying a blind person access to Braille. It is literally the mode through which he communicates, yet our social services system and insurance providers hardly even recognize it for adults.


Thanks for helping me out. But of course - any brain injury would cause the production of S100B.

Good Gosh!
I wonder if they have tested other drugs for this too?


I brought the abstracts on S100 and severity of autism to my son's neurologist last week. He said that if it doesn't come down to him from the NIH as being "best practice" he won't run the test since he won't treat it. I just wanted the test because if my son came up positive I would take him to the Cleveland Clinic. Son has been on pulse steroids for seizures for almost two years and is non-functional off them - he cannot stay on these forever and we need answers. I wish we had a neurologist on our team who is willing to dig to find answers. Would he be this dismissive if it were his child?

Teresa Conrick

Hi Benedetta,

Thanks for your thoughts.
Well in answer to your question -- and I am a reporter of that study -- my question then -- it seems that S100B is implicated in brain injury - ongoing -- so if a third of the kids are actively having this in their blood as a marker of astroglial injury - why is no one looking more deeply into why that is AND what can be done? It is not only autism and the connections to symptoms give a lot of hints and bold clues that things like vaccines (ingredients-amounts-doses) and environmental toxins (mercury, certain prescription drugs) are injuring the brain. Seems pretty important to me.

Teresa Conrick

Hi Aimee,

Thanks for posting.

I can't tell you what may be happening with your son but will tell you some tests that have explained why my daughter and many others have had aggression over the years-These all effect the gut and brain.

Bacteria- Strep- per blood testing/throat swab; Lyme--- A BIG one for many and hard to nail down always via testing- start with Western Blot and if some bands positive but inconclusive, use Igenex testing (google); Mycoplasma- blood test; and here is a good excerpt regarding the MANY bacterial and viral connections in autism symptoms, behaviors--pain: All are medical reasons why a child can become very ill. Autism is an immune system disease.

This list is good and compiled from the TACA website-

Other infections that are linked to neurological issues include: Rabies, Lyme, HIV, Herpes, Polio, Coxackie, Rubella, Borna, Epstein’s Barr (EPV), Eterovirus, Influenza, Measles, Westnile – Borrelia, Shingles, Anthrax, Meningococcus, Mycobacterium, Syphilis, Malaria, Chlamydia, Ricketts, and Candidiasis.

Infections that are in implicated in the medical literature as causing or triggering cases of autism include: Herpes, Rubella, Mycoplasma Pneumoniae, Shingella, Borna, Malaria, Blastocystics, Varicella, Cytomegalo Virus (CMV), Syphilis, Toxplasmosis, Neurocysticercosis, and Clostridium.
In reference to Clostridium, an interesting study was conducted by Dr. McFabe that showed injecting rats with propionic acid caused the onset of autism symptoms. A main source of proprionic acid is Clostridia, a bacterial infection common in autism.

Another test to rule out is an ANA test for autoimmunity-

Also need to add 24 hr EEG to rule out seizures. Many children have inflammation and ibuprofen has shown to be extremely helpful for reducing pain (and microglial activation). Also, homeopathic remedies have been helpful. Detox obviously is the big issues as metals( mercury/aluminum) , viruses (measles, etc) and bacterial, fungal infections are ground zero.

Not sure what you have done but I see so many of the kids having these connections. Add in hormones and it can become fuel on the fire. We must all keep vigilant on the good and bad of treatment options as these children are so very ill.


Thanks for the article, I just wanted to tell you that my son was prescribed risperdal at a quarter of a teaspoon and it triggered a seizure in him. We never went down the road of antipsychotic drugs again, doctors have tried but we will not have any of it.


Daniel Haszard;
Seroquel is taken at this house too. That is one more powerful drug!

My daughter is on Seroquel - she takes it when she is backed againest the wall either with a mania high or a very low depreesion and crying. It knocks her out cold and and then when she is half way awake she comes stumbling down to get anything sweet in the house. Which is few and far between - sugar free jello and whipped cream is about it.

And then there is the seizure medications. And on the paper that comes with them - they always say first - they are not sure how they work.

Epilepsy is having their conference in Chicago this year, I would love to go.

Just got this in the email today, it is suppose to explain how some of these epileptic medicines work. I have not looked at it yet, but will tonight. I thought I would pass it along.

We do have to be careful. We do have to do our research. We cannot depend up on the doctor because he is getting his information from the drug companies and they are out to sale, and not for our health!

Depokote would be one of those that my son missed by a hair and only because it probably cost us one of our family members lives - my mother-in-law - so I refused it for my son.

Aimee Doyle

I absolutely agree with the problems of Risperdal. My 22 year old son has been on it twice.

The first time, in adolescence, he was hitting himself and hitting others and yelling for hours (usually in the middle of the night). We had been doing biomedical intervention since age 4, and nothing old (or new) that we tried stopped the behaviors. Desperate, we turned to drugs -- half a dozen trials of different drugs. Nothing worked on his self-injurious and aggressive behaviors except Risperdal.

When he improved we started to slowly wean him off the drug and he was drug-free for almost two years. Then we saw the behaviors creeping back. We returned to Risperdal. Second time the side effects were worse -- tremors and breast growth. Once again we weaned him off.

Now, in the last couple of weeks, we're seeing the behaviors again -- hitting himself, hitting others, spitting at others full in the faced. We aren't planning to put him back on Risperdal, but what do we do? Biomed hasn't dealt with these behaviors, and neither has behavioral intervention. For that matter, none of the other drugs we have tried have worked. Studies on effective treatment for adolescents and adults on the spectrum are sparse. In fact, about the only intervention studied is drugs.

I hate having only bad choices. We can't live with the drug and we can't live with the behaviors.

Theodore M. Van Oosbree

Astrocytes, glial cells, S100B - all this scientific stuff! Why don't you just take a medical approach and forget the whole thing - just take 'em home and love 'em!

A ford

I took haldol a related drug and during that short time I had trouble thinking and had insomnia. the part about astrocyts and Schwann cells disturbs me because I have a confirmed case of neurofibromatosis and people with this disease get Schwann cell tumors. I also took risperidone for a while back also and had twitches thank god they went away. Why did I take it? behavior problems from asperger and ADHD.


Help me out here Tereasa.
So Risperdal causes increase in S100B in the brian.
Autism is caused - perhaps by the increase of S100B or at least that is what is showing up in blood test of kids with autism.
But Risperdal is increasing S100B in certain areas of the brain that is perhaps were the behavior is coming from????

Risperdal interferrs with the signalling in those parts of the brain.

And if it interferrs too much it could cause Tardive D.

But we do know that Risperdal does cause pituary tumors.

Human knowledge has expanded in the areas of machines, and computers but we still must live in the dark ages when it come to medicine and drugs. Ever sheet that I read on seizure medications - there is always that clause that says we really are not sure why it works or how it works but we think -----------

Devil and the Deep Blue Sea!

Daniel Haszard

Thank you for reporting this,the atypical antipsychotic drug promoters of Risperdal,Zyprexa,Seroquel are 'reaping the whirlwind' of side effects.My case was with Eli Lilly Zyprexa same saga.Four years of off-label Zyprexa use gave me life-long diabetes.

Google *Risperdal reproached*-I am Daniel Haszard victim advocate for patients harmed by the atypical antipsychotic racket —

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