La información en esta monografía tiene la intención de servir para fines informativos únicamente, y está diseñada para ayudar a los usuarios a aclarar sus inquietudes de salud. La información está basada en la revisión de datos de investigación científica, patrones históricos de práctica y experiencia clínica. Esta información no se debe interpretar como un consejo médico especifico. Los usuarios deben consultar con un proveedor médico calificado para preguntas específicas respecto a terapias, diagnósticos y/o enfermedades, antes de tomar decisiones acerca de una terapia.
The primary focus on serotonin deficiency as the main cause of depression has created treatment failure in many depressed and addicted patients. Other happy (excitatory) neurotransmitters are often ignored and some patients become more depressed when treated with medication. The classic depressive disorder patient who presents to Florida Detox ® is Susan, a 42-year-old professional female who seeks medical attention for depression from her local physician. Dr. Jones immediately assumes that she would benefit from a serotonin enhancer such as Paxil, Prozac, or Lexapro. If indeed this patient suffers from low serotonin levels, her depression should respond within 2-4 weeks of treatment with the serotonin enhancer. Typically, prescribed a medication like Paxil (20 mg per day), she returns one month later insisting her depression is worse. Dr. Jones raises the Paxil to 40 mg per day. Frequently these patients are prescribed extremely high doses (60 mg to 80 mg per day) in the physician’s effort to conquer the problem. Unfortunately Dr. Jones disregards the continuous report from the patient that they are not feeling any better and may actually feel more depressed. What is the problem? If serotonin is unilaterally elevated above normal levels with the mediation, the brain will down regulate production of dopamine. This makes the patient with dopamine deficiency even more dopamine deficient. These patients will typically begin to self medicate with dopaminergic drugs like Percocet, Vicodin, or OxyContin to counteract the decreased production. All of these drugs produce increased dopamine activity in the brain’s pleasure center (nucleus accumbens). When these patients are accurately diagnosed with their genetic dopamine/glutamate deficiency and treated with appropriate dopamine/glutamate enhancing medication, they quickly experience cessation of their depression and lose the craving (psychological and biochemical) for drugs and alcohol. Treatment results in better relapse statistics with the application of this scientific approach to addiction and depression. Unilateral elevation of serotonin without dopamine level protection will result in markedly elevated prolactin levels. Prolactin will increase appetite and decrease sex drive. When dopamine levels are enhanced to normal levels, sex drive will return as will better appetite control.
EPs are recordings of the nervous system’s electrical response to the stimulation of specific sensory pathways (., visual, auditory, general sensory). In tests of evoked potentials, a person’s recorded responses are displayed on an oscilloscope and analyzed on a computer that allows comparison with normal response times. Demyelination results in a slowing of response time. EPs can demonstrate lesions along specific nerve pathways whether or not the lesions are producing symptoms, thus making this test useful in confirming the diagnosis of MS. Visual evoked potentials are considered the most useful in MS.