the HORRIBLE TRUTH about the 2004 SE Asia Tsunami REVEALED first time, 1 year later

[MattMarriott]

the HORRIBLE TRUTH about the 2004 SE Asia Tsunami REVEALED worldwide first time one year later
by Matt Marriott
26 December 2004 - the illuminati were about to place the last piece - the decision of Ukraine's Supreme Court, that they controlled, to rejects all complaints against the election fraud - required to immediately after order the full scale nuclear strike against Russia.
Just before the planned holocaust, the SE Asia tsunami wiped out the largest concentration of strategic bombers ever assembled outside the US.
They were sitting at the southeastern (most exposed) corner of the largest atoll structure in the world (the reason why the Somalian/Kenyan coast wasn't completely wiped out).
They were supposed to play the key roles, using the Pakistan/Afghanistan, Iraq/Turkey/Ukraine and Iran corridors, to approach the heart of land based russian nuclear capabilities.
God gave one (last?) grace time to the sheeple in Illuminatiland.
There is no secret about the rest - at least for those reading the russian state news agency - see news from today here:
http://www.godlikeproductions.com/bb...ssageid=163381

[MattMarriott]

The KEY to the HORRIBLE TRUTH that would be completely exposed one year later was revealed two days before .... or exactly 90 years after ....
Last survivor of ´Christmas truce´ tells of his sorrow truth666


One year later, after the last survivor is no more - see last post, #19, in first link

[edjerider^]

.........................

[MattMarriott]

Christmas 1942 - the Key Map for World War 2

Christmas 2004 - Nuclear War - Key Map for Ground Operations is ... one of the most isolated oceanic islands in the world....
See map in first post

[MattMarriott]

One day before Wake hit by eyewall of hurricane Ioke
US Strategic Bases - Destruction - 2004 Diego Garcia, 2006 Wake Island?
http://www.goldismoney.info/forums/t...ke-island.html

[P-99er]

My goodness, a poster and a board (at the link) that makes the membership here seem rational. I never thought I would live to see that.

[Wyldwil]

I can't even decipher who is being blamed for doing what?? WTF???:confused: :confused:

[P-99er]

It has to be the zionists being blamed. They cause everything from boowevils that weaken our crops, to tsunami's that killed hundreds of thousands.

[runcible]

Poor HT. He's been dethroned. :(

[bjgnome]

Love your stuff Matt... keep it coming.

[Carl]

I see that Matt's parents are letting him play on the computer unsupervised again.


.

[des00s]

If you got all of the GIM crown into one room they would not be able to agree on one the true version of one single event in the history of the world. Nor would they be able to (as a conscensus) name one great American that ever existed that wasnt part of a conspiracy of some sort.

[Jasper]

Originally Posted by des00s

If you got all of the GIM crown into one room they would not be able to agree on one the true version of one single event in the history of the world.

Yes. It's called RADICAL INDIVIDUALISM.

Instead of thanking a poster for his efforts to bring something new and interesting before us, we have been conditioned to react negatively and to take more pleasure in disagreeing than in agreeing.

Then of course there is the clique of professional trolls looking to score brownie points by scoffing at and sneering at and ridiculing almost everything.

I call them 'scoffmeisters.'

Ah well.

[Carl]

If you would bother to read his links you would discover that the story was discredited even before he linked it here. The guy is nothing more than a spammer. It's not called "RADICAL INDIVIDUALISM", it's called being dismissive of a spammer and yes, I take joy it pointing that out.


.

[des00s]

I was just joshing around Jasper. But just for kicks, can you name one honest and great famous American from our history?

[Wyldwil]

Originally Posted by des00s

I was just joshing around Jasper. But just for kicks, can you name one honest and great famous American from our history?

Previously posted and stolen by me from an un-named GIM-member.....
(I couldn't resist )

[des00s]

Thats the funniest thing I've ever seen and I dont know why.

[omegaman]

In regards to the original post. Huh?

[Blair Munroe]

Matt seems a bit crazy to me

[MattMarriott]

1. Hiding the US Carriers, the most important strategic weapon at that time, played a key role in the Pearl Harbor cover-up, planned as the begin of World War II for the US - see
Pearl Harbor, Reichstag Fire I (OKC bombings) and World War III explained. Reichstag Fire II (9/11) announced to be imminent. From WebArchive
http://web.archive.org/web/200108201...r_may2001.html
Archived Aug 20, 2001

BTW, the story of Peal Harbor was completed just months after that article:
http://www.goldismoney.info/forums/t...o-minutes.html

2. In World War III, carriers are totally worthless sitting ducks, except for the first "battles", i.e. air bombing countries that did not want to or could not respond, i.e. Serbia and Iraq (Afghanistan was a fake war).

Showing the US Carriers, which includes psy-op work repeating "news" about "another carrier group heading to the Persian Gulf", plays a key role in the "US atttack to Iran" hoax, part of the cover-up of the next planned attack, which happens to be also the last attack of World War III.

BTW, the next attack is nothing but take 2 from what End Times Prophet predicted two days before and REVEALED completely first time, 1 year later:
the HORRIBLE TRUTH about the 2004 SE Asia Tsunami

This time the cover-up is extended with the Eastern Europe ABM hoax. Search for it here:
http://www.goldismoney.info/forums/t...hiroshima.html

From
US Carriers in begin of World War II and end of WWIII - another End Times Paradox

[MattMarriott]

Last survivor... Peace on Earth... take 2
http://www.google.com/search?hl=en&q...+last+survivor

[____hoot____]

Matt, do you grow your own stuff? Otherwise I would find a new supplier. if I were you.

[Kahlil Gibran]

................

[Antonio]

Haloperidol
Brand name: Haldol


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Drug monograph
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Contents
Pharmacology
Indications
Contraindications
Warnings
Precautions
Adverse Effects
Overdose
Dosage
Supplied
Research

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Pharmacology
Antipsychotic

Haloperidol is a butyropherone derivative with antipsychotic properties that has been considered particularly effective in the management of hyperactivity, agitation, and mania. Haloperidol is an effective neuroleptic and also possesses antiemetic properties; it has a marked tendency to provoke extrapyramidal effects and has relatively weak alpha-adrenolytic properties. It may also exhibit hypothermic and anorexiant effects and potentiate the action of barbiturates, general anesthetics, and other CNS depressant drugs.

The mechanism of action of haloperidol has not been entirely elucidated, but has been attributed to the inhibition of the transport mechanism of cerebral monoamines, particularly by blocking the impulse transmission in dopaminergic neurons.

Peak plasma levels of haloperidol occur within 2 to 6 hours of oral dosing and about 20 minutes after i.m. administration. The mean plasma (terminal elimination) half-life has been determined as 20.7+/-4.6 (SD) hours, and although excretion begins rapidly, only 24 to 60% of ingested radioactive drug is excreted (mainly as metabolites in urine, some in feces) by the end of the first week, and very small but detectable levels of radioactivity persist in the blood and are excreted for several weeks after dosing. About 1% of the ingested dose is recovered unchanged in the urine.

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Indications
Haloperidol is indicated in the management of manifestations of acute and chronic psychosis, including schizophrenia and manic states. It may also be of value in the management of aggressive and agitated behavior in patients with chronic brain syndrome and mental retardation and in the symptomatic control of Gilles de la Tourette's syndrome.

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Contraindications
Comatose states and CNS depression due to alcohol or other depressant drugs; severe depressive states; previous spastic diseases; lesions of the basal ganglia; Parkinson's syndrome, except in the case of dyskinesias due to levodopa treatment; sensitivity to haloperidol; senile patients with pre-existing Parkinson-like symptoms.

Children:
Safety and effectiveness in young children have not been established; therefore, haloperidol is contraindicated in this age group.

Pregnancy and Lactation:
Safety for use in pregnancy and lactation has not been established; do not administer to women of childbearing potential or nursing mothers unless, in the opinion of the physician, the expected benefits of the drug outweigh the potential hazard to the fetus or child. Haloperidol is excreted in breast milk.

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Warnings
Tardive Dyskinesia:
Tardive dyskinesia is known to occur in patients treated with neuroleptics with antipsychotic properties and other drugs with substantial neuroleptic activity. Although the dyskinetic syndrome may remit partially or completely if the medication is withdrawn, it is irreversible in some patients. At the present time there is uncertainty as to whether neuroleptic drugs differ in their potential to cause tardive dyskinesia.

Since there is a significant prevalence in this syndrome associated with the use of neuroleptic drugs, and since there is no known effective treatment, chronic use of these drugs should generally be restricted to patients for whom neuroleptics are known to be effective and for whom there is no alternative therapy available with better risk acceptability. If manifestations of tardive dyskinesia are detected during the use of a neuroleptic, the drug should be discontinued.

The risk of a patient developing tardive dyskinesia and of the syndrome becoming irreversible appear to increase with the duration of treatment and the total amount of drugs administered, although, in some instances, tardive dyskinesia may develop after relatively short periods of treatment at low doses. The risk of developing tardive dyskinesia may, therefore, be minimized by reducing the dose of the neuroleptic drug used and its duration of administration, consistent with the effective management of the patient's condition. Continued use of neuroleptics should be periodically reassessed.

Withdrawal Emergent Neurological Signs:
Generally, patients receiving short-term therapy experience no problems with abrupt discontinuation of antipsychotic drugs. However, some patients on maintenance treatment experience transient dyskinetic signs after abrupt withdrawal. In certain of these cases the dyskinetic movements are indistinguishable from the syndrome described under Tardive Dyskinesia except for duration. It is not known whether gradual withdrawal of antipsychotic drugs will reduce the rate of occurrence of withdrawal emergent neurological signs but until further evidence becomes available it seems reasonable to gradually withdraw use of antipsychotic drugs.

An encephalopathic syndrome (characterized by weakness, lethargy, fever, tremulousness and confusion, extrapyramidal symptoms, leukocytosis, elevated serum enzymes, BUN and FBS, followed by irreversible brain damage) has occurred in a few patients treated with lithium plus haloperidol. A causal relationship between these events and the concomitant administration of lithium and haloperidol has not been established; however, patients receiving such combined therapy should be monitored closely for early evidence of neurological toxicity and treatment discontinued promptly if such signs appear.

Elderly or debilitated patients receiving the drug should be carefully observed for lethargy and a decreased sensation of thirst due to central inhibition which might lead to dehydration and reduced pulmonary ventilation and could result in complications, such as terminal bronchopneumonia.

Occupational Hazards:
Although haloperidol is a relatively nonsedating neuroleptic, sedation may occur in some patients. Therefore, physicians should be aware of this possibility and caution patients about the danger of participating in activities requiring complete mental alertness, judgement and physical coordination, such as driving and operating dangerous machinery.

Haloperidol may prolong the hypnotic action of barbiturates and may potentiate the effects of alcohol and other CNS depressant drugs such as anesthetics and narcotics; caution should therefore be exercised when it is used with agents of this type and adjustments in their dosage may be required.

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Precautions
Administration to patients with severe cardiac involvement should be guarded, despite the fact that haloperidol is well tolerated by patients with cardiac insufficiency and that it has been used with favorable results to maintain the cardiovascular function of patients with excitive crises. In very rare instances, it has been felt that haloperidol was contributory to the precipitation of attacks in angina prone patients. Moderate hypotension may occur with parenteral administration or excessive oral doses of haloperidol; however, vertigo and syncope occur only rarely.

Haloperidol may lower the convulsive threshold and has been reported to trigger seizures in previously controlled known epileptics. When instituting haloperidol therapy in these patients, adequate anticonvulsant medication should be maintained concomitantly.

As with other antipsychotic agents, haloperidol should be administered cautiously to patients with severe impairment of liver or kidney function, and to patients with known allergies or history of allergies to other neuroleptic drugs. Caution is also advised in patients with pheochromocytoma and conditions predisposing to epilepsy, such as alcohol withdrawal and brain damage.

Haloperidol has lowered cholesterol concentrations in the serum and liver of monkeys. An accumulation of desmosterol has been observed in the serum of rats given repeated high doses (10 mg/kg) of haloperidol. In man, mild transient decreases in serum cholesterol were reported in preliminary studies. However, in a study involving a group of schizophrenic patients on extended medication, significant lowering of serum cholesterol was not observed with haloperidol, and there was no accumulation of desmosterol or 7-dehydrocholesterol. A significant lowering of cholesterol together with accumulation of another sterol (possibly 7-dehydrocholesterol) has been reported in patients receiving a chemically related drug (trifluperidol), and skin and eye changes (ichthyosis and cataracts) have occurred clinically with another butyrophenone derivative. Skin and eye changes have not been observed in patients receiving haloperidol. However, all patients receiving haloperidol for a prolonged period of time should be carefully observed for any changes in the skin and eyes. If such changes are seen, discontinue the drug promptly.

Drug Interactions:
Haloperidol has been reported to interfere with the anticoagulant properties of phenindione in an isolated case, and the possibility should be kept in mind of a similar effect occurring when haloperidol is used with other anticoagulants.

Haloperidol may antagonize the action of epinephrine and other sympathomimetic agents and reverse the blood pressure-lowering effects of adrenergic-blocking agents, such as guanethidine.

Enhanced CNS effects may occur when haloperidol is used in combination with methyldopa.

Haloperidol inhibits the metabolization of tricyclic antidepressants, thereby increasing plasma levels of these drugs. This may result in increased tricyclic antidepressant toxicity (anticholinergic effects, cardiovascular toxicity, lowering of seizure threshold).

When prolonged carbamazepine treatment is added to haloperidol therapy, this results in a significant reduction of haloperidol plasma levels. Therefore, during combination treatment, the haloperidol dose should be adjusted, when necessary. After stopping carbamazepine, it will be necessary to reduce the dosage of haloperidol.

Haloperidol may impair the antiparkinson effects of levodopa.

If an antiparkinson agent is used concomitantly with haloperidol, both drugs should not be discontinued simultaneously, since extrapyramidal symptoms may occur due to the slower excretion rate of haloperidol.

The physician should keep in mind the possibility of an increase in intraocular pressure when anticholinergic drugs, including antiparkinson agents, are administered concomitantly with haloperidol.

When haloperidol is used to control mania in cyclic disorders, there may be a rapid mood swing to depression.

The antiemetic action of haloperidol may obscure signs of toxicity due to overdosage of other drugs or mask the symptoms of some organic diseases, such as brain tumor or intestinal obstructions.

Severe neurotoxicity (rigidity, inability to walk or talk) may occur in patients with thyrotoxicosis who are also receiving antipsychotic medication, including haloperidol.

Carcinogenicity studies in mice (18 months) and rats (24 months) showed a significant increase in mammary gland neoplasia and total tumor incidence in female mice at 1.25 and 5 mg/kg/day and in pituitary gland neoplasia in female mice at 5 mg/kg. A significant dose related increase in pituitary gland hyperplasia was observed in female rats at 1.25 and 5 mg/kg/day. The potential significance of these findings to man is not known.

Neuroleptic drugs elevate prolactin levels; the elevation persists during chronic administration. Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro, a factor of potential importance if the prescription of these drugs is contemplated in a patient with a previously detected breast cancer. Although disturbances such as galactorrhea, amenorrhea, gynecomastia, and impotence have been reported, which are presumed to be linked to elevated prolactin levels, the clinical significance of elevated serum prolactin levels is unknown for most patients. An increase in mammary neoplasms has been found in rodents after chronic administration of neuroleptic drugs. Neither clinical studies nor epidemiologic studies conducted to date, however, have shown an association between chronic administration of these drugs and mammary tumorigenesis. The available evidence is considered too limited to be conclusive at this time.

FD and C Yellow No. 5 (tartrazine) may cause allergic-type reactions (including bronchial asthma) in certain susceptible individuals. Although the overall incidence of tartrazine sensitivity in the general population is low, it is frequently seen in patients who also have ASA hypersensitivity. Tartrazine is contained in the 1, 5 and 10 mg haloperidol tablets.

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Adverse Effects
Neurological:
Neuromuscular (extrapyramidal) effects such as Parkinson-like symptoms, akathisia, dyskinesia, dystonia, hyperreflexia, rigidity, opisthotonos, and, occasionally, oculogyric crisis are the most frequently reported side effects associated with the administration of haloperidol. Headache, vertigo and cerebral seizures have also been reported. The extrapyramidal reactions are usually dose related in occurrence and severity and, as a rule, tend to subside when the dose is reduced or the drug is temporarily discontinued.

However, considerable interpatient variability exists, and, although some individuals may tolerate higher than average doses of haloperidol, severe extrapyramidal reactions, necessitating discontinuation of the drug, may occur at relatively low doses. Administration of an antiparkinson agent is usually, but not always, effective in preventing or reversing neuromuscular reactions associated with haloperidol.

Tardive dyskinesias:
As with all antipsychotic agents, tardive dyskinesia may appear in some patients on long-term therapy or may appear after drug therapy has been discontinued. The risk appears to be greater in elderly patients on high dose therapy, especially females. The symptoms are persistent and in some patients appear to be irreversible. The syndrome is characterized by rhythmical, involuntary movements of the tongue, face, mouth or jaw (e.g. protrusion of tongue, puffing of cheeks, puckering of mouth, chewing movements). Sometimes these may be accompanied by involuntary movements of extremities.

There is no known effective treatment for tardive dyskinesia; antiparkinsonism agents usually do not alleviate the symptoms of this syndrome. It is suggested that all antipsychotic agents be discontinued if these symptoms appear. Should it be necessary to reinstitute treatment, or increase the dosage of the agent, or switch to a different antipsychotic agent, the syndrome may be masked. The physician may be able to reduce the risk of this syndrome by minimizing the unnecessary use of neuroleptic drugs and reducing the dose or discontinuing the drug, if possible, when manifestations of this syndrome are recognized, particularly in patients over the age of 50. It has been reported that fine vermicular movements of the tongue may be an early sign of the syndrome and if the medication is stopped at that time the syndrome may not develop.

Tardive dystonia, not associated with the above syndrome, has also been reported. Tardive dystonia is characterized by delayed onset of choreic or dystonic movements, is often persistent, and has the potential of becoming irreversible.

Behavioral:
Insomnia, depressive reactions, and toxic confusional states are the more common effects encountered. Drowsiness, lethargy, stupor and catalepsy, confusion, restlessness, agitation, anxiety, euphoria, and exacerbation of psychotic symptoms, including hallucinations, have also been reported.

Cardiovascular:
Tachycardia, hypertension and ECG changes including prolongation of the QT interval and ECG pattern changes compatible with the polymorphous configurations of torsades de pointes have been reported. Hypotension has occurred, but severe orthostatic hypotension has not been reported. However, should it occur, supportive measures, including i.v. vasopressors such as norepinephrine, may be required. Epinephrine should not be used, since haloperidol may block the vasoconstrictor effects of this drug.

Autonomic:
Dry mouth, blurred vision, urinary retention, incontinence, diaphoresis and priapism have been reported.

Allergic and Toxic:
The overall incidence of significant hematologic changes in patients on haloperidol has been low. Occasionally there have been reports of mild and usually transient leukopenia and leukocytosis, decreases in blood cell counts, anemia, and a tendency toward lymphomonocytosis. Agranulocytosis has rarely been reported with the use of haloperidol, and then only in association with other medication. Impairment of liver function (jaundice or hepatitis) has been reported rarely. One case of photosensitization is known and isolated cases of idiosyncratic cutaneous involvement have been observed.

Endocrine:
Lactation, breast engorgement, mastalgia, menstrual irregularities, gynecomastia, impotence, increased libido and changes in blood sugar concentrations have been reported.

Gastrointestinal:
Heartburn, nausea, vomiting, anorexia, weight loss, constipation, diarrhea and hypersalivation have been reported.

Miscellaneous:
Other untoward effects encountered include peripheral edema, hypocholesterolemia, alopecia, laryngospasm, bronchospasm and increased depth of respiration and stasis pneumonia. Hyperammonemia has been reported in a 5 1/2 year old child with citrullinemia, an inherited disorder of ammonia excretion, following treatment with haloperidol.

Cases of sudden and unexpected death have been reported in association with the administration of haloperidol. The nature of the evidence makes it impossible to determine definitively what role, if any, haloperidol played in the outcome of the reported cases. The possibility that haloperidol caused death cannot, of course, be excluded, but it is to be kept in mind that sudden and unexpected death may occur in psychotic patients when they go untreated or when they are treated with other neuroleptic drugs.

Neuroleptic Malignant Syndrome:
As with other neuroleptic drugs, a symptom complex sometimes referred to as neuroleptic malignant syndrome (NMS) has been reported. Cardinal features of NMS are hyperpyrexia, muscle rigidity, altered mental status (including catatonic signs), and evidence of autonomic instability (irregular pulse or blood pressure). Additional signs may include elevated CPK, myoglobinuria (rhabdomyolysis), and acute renal failure. NMS is potentially fatal, requires intensive symptomatic treatment and immediate discontinuation of neuroleptic treatment.

Hyperpyrexia and heat stroke, not associated with the above symptom complex, have also been reported.

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Overdose
Symptoms:
In general, the symptoms of overdosage would be an exaggeration of known pharmacologic effects and adverse reactions, the most prominent of which would be: (1) severe extrapyramidal reactions, (2) hypotension, or (3) sedation. The patient would appear comatose with respiratory depression and hypotension which could be severe enough to produce a shock-like state. The extrapyramidal reaction would be manifested by muscular weakness or rigidity and a generalized or localized tremor as demonstrated by the akinetic or agitans types respectively. The risk of ECG changes associated with torsades de pointes should be considered (see Adverse Effects).

Treatment:
Gastric lavage or induction of emesis should be carried out immediately followed by administration of the universal antidote. Since there is no specific antidote, treatment is primarily supportive. Establish a patent airway by use of an oropharyngeal airway or endotracheal tube or, in prolonged cases of coma, by tracheostomy. Respiratory depression may be counteracted by artificial respiration and mechanical respirators. Hypotension and circulatory collapse may be counteracted by use of i.v. fluids, plasma, or concentrated albumin, and vasopressor agents such as norepinephrine. Epinephrine should not be used. In case of severe extrapyramidal reactions, antiparkinsonian medication should be administered. ECG and vital signs should be monitored especially for signs of QT prolongation or dysrhythmias and monitoring should continue until the ECG is normal. Severe arrhythmias should be treated with appropriate antiarrhythmic measures.

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Dosage
Initial dosage should be individualized through consideration of severity of symptoms, age, weight, health, previous response to neuroleptic drugs and concomitant disease states. It is important initially to increase dosage adequately until symptoms are controlled or side effects requiring lowering the dosage or discontinuing the drug are encountered. When a satisfactory therapeutic response is achieved, reduce dosage gradually to the lowest effective maintenance level.

Patients with previous adverse responses to other neuroleptic drugs, children and the elderly or debilitated may require less haloperidol. The optimal response in such patients is best obtained if therapy is initiated at a lower dosage level and titration is more gradual.

Oral:
1 to 2 mg 2 or 3 times daily, initially, followed by upward adjustment as tolerated until the desired effect is achieved or limiting side effects appear. Clinical experience has shown that it is seldom necessary to employ dosages greater than 4 to 6 mg 3 times daily. However, 30 to 40 mg daily may be required in severely disturbed patients who remain inadequately controlled by lower doses. Up to 100 mg daily has been used occasionally in particularly resistant patients. Nevertheless, the safety of prolonged administration of the higher doses has not been established. After a therapeutic response has been achieved, dosages should be gradually adjusted downwards until a schedule providing adequate maintenance is reached. Maintenance dosages are commonly in the range of 1 to 2 mg 3 or 4 times daily.

Children, debilitated and geriatric patients:
Lower doses are recommended in these patients since they may be more sensitive to the drug.

Initial daily doses ranging from 0.5 to 1.5 mg (0.25 to 0.5 mg, 2 or 3 times a day) should be employed. Upward adjustment of these doses should be made gradually; maximum and maintenance doses should be individualized and are generally lower in this type of patient.

Parenteral:
When symptoms are severe or rapid control is desired, administer haloperidol by i.m. route. Dosages in the range of 2.5 to 5 mg are recommended, and should be employed on a prn basis until the desired effect is achieved. Administration every 4 to 6 hours is sufficient in most cases, although for resistant patients the dosage may be repeated as often as every hour if required. Parenteral administration of high doses may be accompanied by rapid appearance of extrapyramidal effects as control of symptomatology is achieved.

Children:
The safety and effectiveness of i.m. administration in children have not been established.

The oral dosage form should supplant the injectable as soon as practical. For an initial approximation of the total daily dose required, the parenteral dose administered in the preceding 24 hours may be used. Since this dose is only an initial estimate, it is recommended that careful monitoring of clinical signs and symptoms, including clinical efficacy, sedation, and adverse effects be carried out periodically for the first several days following the initiation of switchover. In this way, dosage adjustments, either upward or downward, can be quickly accomplished. Depending on the patient's clinical status, the first oral dose should be given within 12 to 24 hours following the last parenteral dose.

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Supplied
Ampuls:
Each mL of clear colorless solution contains: Haloperidol 5 mg, methylparaben 1.8 mg, propylparaben 0.2 mg in water and lactic acid sufficient to adjust the pH within the range of 3.2 to 3.6. Do not dilute with sterile saline. Ampuls of 1 mL, units of 10 and 100.

Solution:
Each mL of clear, colorless, odorless, tasteless solution contains: Haloperidol 2 mg. Also contains methylparaben USP 2 mg/mL. Sodium-free. Dropper bottles of 100 mL (droppers calibrated 1 mg in 0.5 mL) and bottles of 500 mL.

Tablets:
Each round, scored, uncoated tablet, biconcave with beveled edges, embossed McNEIL on one side, contains: Haloperidol 500 mcg (white, marked 1/2 on the reverse side), 1 mg (yellow, marked 1 on the reverse side), 2 mg (pink, marked 2 on the reverse side), 5 mg (green, marked 5 on the reverse side), 10 mg (aqua, marked 10 on the reverse side) or 20 mg (salmon, marked 20 on the reverse side). Energy: 500 mcg: 0.459 kJ (0.109 kcal); 1 mg: 0.448 kJ (0.106 kcal); 2 mg: 0.432 kJ (0.103 kcal); 5 mg: 0.447 kJ (0.106 kcal); 10 mg: 0.845 kJ (0.202 kcal); 20 mg: 0.490 kJ (0.117 kcal). Sodium-free (500 mcg). Sodium: <1 mmol (<1 mg)/1, 2, 5, 10 and 20 mg tablets. Also contains tartrazine (1, 5 and 10 mg). Bottles of 100 (500 mcg, 1, 2, 5, 10 and 20 mg); bottles of 1000 (500 mcg, 1, 2 and 5 mg).

All tablets are gluten-free, lactose-free and metabisulfite-free.

Dispense tablets and oral solution in a tight light-resistant container.

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Research
The research information is available separately on Internet Mental Health.


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Note: This information is from a Canadian monograph. There can be differences in indications, dosage forms and warnings for this drug in other countries.

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Internet Mental Health (www.mentalhealth.com) copyright © 1995-2005 by Phillip W. Long, M.D.

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