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Reboxetine is an antidepressant that functions as a NorAdrenaline Reuptake Inhibitor (NARI).
1. Reboxetine
role in antidepressant therapy
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Tianeptine |
Moclobemide | Deprenyl | Picamilon | Milnacipran
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an article by Richard Brown MD However,
picamilon is more versatile than this. It can be useful in patients post-stroke.
I also commonly see patients with Parkinson's disease, depression, and evidence
of cerebral vascular disease from a history of strokes or abnormal findings on
magnetic resonance imaging. Picamilon can be extremely helpful in giving
these patients a decrease in anxiety and depression, without sedation and with a
mild pleasant stimulation. It may be used in a variety of other organic
brain syndromes. For example, one patient in his mid-fifties had developed
a treatment resistant depression during the course of which he also suffered
several strokes and cognitive impairment. This was ultimately found to be due to
an antiphospholipid antibody syndrome. Although his depression was at least
partially responsive to Effexor®, his cognitive functioning and energy were
poor. His daily activity was quite limited, particularly because of apathy and
fatigue. In this case the patient was greatly helped by the addition of acetyl-L-carnitine, picamilon, and SAM-e. For all three medications the
doses had to be given aggressively. If any one medication were decreased
he would basically become non-functional. Racetams:
The European Alternatives Another
group of medications which are relatively unfamiliar to most American physicians
are the pyrolidones or racetams. I most commonly use aniracetam or piracetam
from this class. These
medications have a positive effect on nerve cell energy metabolism and seem to
boost the function of cholinergic and NMDA-glutamate receptor systems.
Pyrollidones facilitate the transfer of information between the cerebral
hemispheres across the corpus callosum. They improve the function of the
verbal areas of the left cerebral cortex. They can be used to lessen the
cognitive side effects of anticonvulsants, as well boost the anticonvulsant
efficacy of these medications. Even less well known is that there are
several studies showing that the racetams can boost the efficacy of
antidepressants. Yet they are extremely benign in terms of side effects,
rarely causing stimulation and over activation. For
example, a 55-year-old lawyer who had been extremely highly functioning came to
see me several years ago, after approximately a ten-year course of deterioration
following the development of an ovarian hyperstimulation syndrome, secondary to
taking fertility medication. She developed physical symptoms of this disorder,
as well as depression and cognitive problems that became so pronounced that she
became unable to work. Her deficits were documented on neuropsychological tests
which were consistent with blood flow abnormalities, seen on SPECT (Single
Proton Emission Computed Tomography) scans of her brain. Her depression
responded well to a combination of Zoloft® and SAM-e. However, her cognitive
functioning remained poor. She was also extremely hypersensitive to light,
sound, and touch. (It should be noted that ovarian hyperstimulation syndrome
causes marked changes in the vasculature of animals, as well as overproduction
of stress hormones through the stress response system). The patient had
great difficulty tolerating conventional psychotropic medications and
experienced extremely severe side effects. Fortunately, her brain function
improved dramatically when she was given pramiracetam 600 mg twice a day.
For the first time in ten years, the patient felt that her brain had been
returned to her. She was able to read and do other mental work without
collapsing in a short time. Another less dramatic example is a 23-year-old patient who was tested in childhood and found to possess a genius level IQ. He went to a prestigious college. At about that time he developed an idiopathic autoimmune disease which caused diabetes mellitus requiring insulin and an idiopathic alopecia. He developed severe cognitive problems which were well documented, not only on neuropsychological testing but also on brain scans. Conventional treatments by neurologists and psychiatrists were to no avail. The patient had some response to donepezil, a cholinesterase inhibitor, over a nine-month period. However, the response was not satisfactory and I began to treat him with galantamine up to 24 mg a day with a partial positive response. Picamilon 50 mg a day further improved his cognitive functioning and energy. Adding aniracetam 600 mg per day has enabled him to recover his previous cognitive function level as documented by repeat neuropsychological testing. If he takes more of any of these medications he is over stimulated and has trouble sleeping. However, if any of the medications are lowered, his ability to function comes to a screeching halt.
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