• Bronchial asthma neuropharmacological treatment.
    Dr. Lechinīs research team has found that symptomatic asthma patients show increased plasma serotonin levels and that these serotonin values correlate positively with clinical severity and negatively with pulmonary function. They found that drugs which reduce plasma serotonin levels were greatly effective therapeutic agents. These drugs provoke sudden and dramatic improvement.

  • Sleep Disorder, neuropharmacological treatment.
    Neuroscientists have demonstrated that waking state depends on activity of the pedunculus pontine nucleus. Serotonin released at this level by axons of dorsal raphe neurons inhibit this nucleus. Dr. Lechinīs research team demonstrated that drugs which enhances uptake by presynaptic serotonergic axons are potent anti-narcoleptic agents in patients resistant to methylphenidate (see figures) .

    At the present, our institute posseses a sleep laboratory in order to investigate plasma neurotransmitters during every sleep stage.

  • Myasthenia gravis neuropharmacological treatment.
    Affected by myasthenia gravis in October, 1996, Dr. Fuad Lechin became his own study case when he rejected the advise of U.S. experts to undergo immunosuppressive therapy. He was submitted to neuroendocrine plus immunological investigation, concluding he was severely stressed (his profile was that registered in subjects maladapted to stress). An antistress treatment to reduce both adreno-medullary secretion and plasma serotonin levels and to rise central noradrenergic activity provoked disappearance of symptoms within two weeks of starting treatment on February 15, 1997. Up to the present, we have successfully treated 53 severe Myastenia Gravis patients with no failures or relapses.

  • Crohnīs disease neuropharmacological treatment.
    Sixteen severe cases over the past nine years have been treated successfully, employing neuropharmacological agents to provoke progressive immunosuppression. Serotonin releasing agent, serotonin precursors, dopaminergic blocking agents, and central noradrenergic activity suppressors are the tools Dr. Lechinīs team used as effective neuroimmunomodulators (see figures) .

  • Ulcerative colitis (UC) neuropharmacological treatment.
    Dr. Lechinīs research team was the first to demonstrate the antidiarrheic effect of clonidine, dihydroergotamine, and other alpha adrenergic antagonists, as well as dopaminergic blocking agents. All them suppress rectal motility and rise sigmoidal tone (leading to constipation). Although these drugs significantly improved symptoms in UC patients, effective doses also provoked undesirable side effects. In order to avoid UC exacerbation Dr. Lechinīs team introduced several neuropharmacological immunosuppressant drugs which resulted very effective therapeutic agents (see figures).

  • Pancreatitis neuropharmacological treatment.
    Both acute and chronic pancreatitis are successfully and dramatically improved by alpha-2 agonist drugs. Normalization of amylase plasma levels as well as clinical symptoms occur within the first 24-48 hours of treatment. Dr. Lechinīs team has treated more than 15 patients.

  • Irritable bowel syndrome neuropharmacological treatment.
    Opposing pathophysiologic conditions make up the irritable bowel syndrome: some patients show high distal colon motility plus rectal hypoactivity, whereas other patients show low distal colon motility plus rectal hyperactivity. The former, spastic colon, presents constipation, abdominal pain and distention; it should be treated with serotonin releasing drugs. The second, nervous diarrhea, is not accompanied by pain and should be treated with alpha adrenergic blocking agents.

  • Trigeminal neuralgia neuropharmacological treatment.
    The neuroendocrine profile shown by trigeminal neuralgia sufferers during attacks is that observed in maladapted to stress subjects. Pain shows great improvement with drugs to increase central serotonergic activity. Dopaminergic blocking agents are also dramatically effective in treating trigeminal neuralgia. However, the use of these drugs may provoke akathisia.

  • Headache syndrome neuropharmacological treatment.
    Tension headache patients show the typical neuroendocrine profile of major depression, calling for treatment to reduce central noradrenergic activity as well as augment central serotonergic activity.

    Cluster headache patients show during exacerbation periods (migraine) the maladapted stress profile: low central noradrenergic, serotonergic and dopaminergic activity. Neuropharmacological therapy is required to reverse these imbalances. It is also most important to reduce plasma free serotonin levels provoked by raised platelet aggregation registered in these patients during attacks.

  • Hypoglycemia (postprandial or reactive) neuropharmacological treatment.
    According to oral glucose tolerance tests, hypoglycemia patients fall into two groups: those presenting typical maladapted to stress profile (excessive adrenomedullary secretion), and those showing excess noradrenaline plasma levels during this test. The former are greatly improved with antistress treatment: potentiation of central noradrenergic activity plus reduction of the increased free serotonin plasma levels found in these patients. The second group is improved with drugs reducing central noradrenergic activity plus drugs boosting central serotonergic activity. This group presents the typical neuroendocrine profile of endogenous depression.

  • Infertility (non-organic) neuropharmacological treatment.
    Infertility in women showing no organic causes has been suppressed by neuropharmacological therapy to increase central dopaminergic activity. Dr. Lechinīs research team has successfully treated more than 50 patients.

  • Somatoform disorders neuropharmacological treatment.
    This syndrome usually disappears with low dosis of dopaminergic blocking agents (D2-antagonists). Dosification of plasma neurotransmitters in these patients reveals raised dopamine levels (much higher than adrenaline levels).

  • Cancer neuropharmacological treatment.
    Our research group has treated some 2300 cancer patients during the last 15 years, reporting significant improvement in all cases. Experimental results have been partially published in journals and scientific congresses. Dr. Lechin has visited cancer hospitals in USA (MD Anderson Cancer Center at Houston, Arthur James Cancer Center at Ohio State University, University of South Florida at Tampa, National Institute of Cancer at Bethesda, Buenos Aires University Hospital, and many others) presenting our cancer investigations.

    Total disappearance of tumors and/or metastases have been observed in most non advanced cancer patients following neuropharmacological therapy. This type of therapy has proven to be 100% effective when started immediately after adequate surgery. Those who have received chemotherapy or radiotherapy responded less effectively, although patients with lynphoma responded better when previously treated with chemotherapy. Most effectivity was registered in cancer of stomach, kidney, ovary, prostate gland and breast. One case of rabdomyosarcoma (small intestine) was completely clear of cancer within 8 months of treatment. Colon and lung cancer patients, as well as melanoma patients, register great improvement but usually show tumor exacerbation after two to five years. Poor response is observed in pancreatic and esophageal cancer patients.
    (See figures).

    The neuropharmacological approach to cancer aims to normalize the neuroendocrine plus immunological profile associated with maladapted stress which these patients unfailingly present during exacerbation periods. Thus it is necessary to control plasma neurotransmitters (noradrenaline, adrenaline, dopamine, platelet serotonin, plasma free serotonin and tryptophane); plasma hormones (cortisol, growth hormone, prolactin); lymphocyte subsets, NK cell activity, etc.

    The establishment of normal sleep profile is highly important as immunoactivation is produced during delta sleep period. All drugs provoking immunosuppresion must be avoided (benzodiazepines, opioids, prostaglandin inhibitors, hormones, dopaminergic blocking agents, serotonin releasing drugs, etc.).

    Benzodiazepines and other hypnotics induce phases 1 and 2 of slow wave sleep but interfere with phases 3 and 4 (delta sleep) and REM sleep.

    Dopaminergic blocking agents have been found to provoke immunosuppression and accelerate tumor growth and provoke the onset of metastasis.

  • Post-traumatic stress disorder neuropharmacological treatment.
    Dr. Lechinīs team found these patients show total exhaustion of central noradrenergic, dopaminergic and serotonergic activity. They respond to any small stress challenge with uncontrolled release of adreno-medullary secretion. Neuropharmacology treatment to restore noradrenergic and serotonergic activity should be undertaken slowly and progressively. Large doses of neuro-active drug should be avoided as these patients have supersensitive post-synaptic receptors.

  • Osteoporosis neuropharmacological treatment.
    Osteoporosis, even advanced cases, may be normalized through appropriate neuropharmacological plus neuroendocrine manipulations to increase GHRH and GH. Dr. Lechinīs team obtained positive results in all cases they treated. They do not use other hormones like estrogens and progestogens.

  • Akathisia neuropharmacological treatment.
    This involuntary movement disorder, when found to be unresponsive to biperiden administration, should be treated with drug which interfere with the release of serotonin at synaptic level.

  • Fibrocystic mastitis (mammary dysplasia) neuropharmacological treatment.
    This disorder (with or without hyperprolactinemia) is associated with a neurotransmitter profile compatible with low central dopaminergic (DA) activity. Low doses of DA precursors and/or low doses of psychoactive drugs which increase sensitivity of DA receptors are effective in most cases. Dr. Lechinīs team has treated more than 50 cases.

  • Hyperkinetic children (attention deficit disorder) neuropharmacological treatment.
    Dr. Lechinīs team has found two types of neurochemical disorders underlying this syndrome. One presents excessive free serotonin in the plasma while the other shows excessive dopaminergic activity plus noradrenergic overactivity. The former is improved with drugs favoring serotonin uptake at the synaptic level. The second group is improved with serotonin precursors. These treatments can be carried out in combination with methylphenidate. Dr. Lechinīs team has treated more than 50 patients.

  • Gilles de la Tourette disease neuropharmacological treatment.
    Hyperdopaminergic activity underlies the physiological disorder of this disease. However, low levels of serotonergic activity should be consider as cofactor. This finding suggests that low level of serotonin exists at the synaptic cleft. Results showing that these patients are improved with dopaminergic antagonists plus serotonin precursors plus serotonin potentiating drugs. Dr. Lechinīs team has treated 12 cases.

  • Vertigo neuropharmacological treatment.
    Most patients affected by this syndrome are wrongly diagnosed as labyrinthitis. Dr. Lechinīs team has found that they have raised levels of free serotonin in plasma. They improved dramatically upon increasing serotonin uptake through neuropharmacological manipulation.