Antidepressants Blog

I just want to mention here how psychosomatic symptoms occur in stage three stress breakdown because of malfunction in conditioned reflexes.

A lot of the housekeeping of the body is done automatically; seeing we didn’t have to learn things like how to sneeze or coordinate stomach secretion of gastric juice with bowel movements, we can’t really forget how to co-ordinate them either. These built-in nervous system reflexes are not affected by stress breakdown.

Instead, it is those reflexes which have been learned through experience which are affected by the switching-off protective responses of the brain in stress breakdown. Thus the reflexes affected in third stage breakdown are those where we have learned, to some extent, to control body functions. These will primarily affect three areas of function.

1. Reflexes concerned with preparing for the ingestion of food.

2.   Reflexes concerned with inhibiting large bowel elimination of faeces.

3.   Reflexes concerned with the contraction of the bladder when it is filled.

When we imagine food, or visualize food before a meal, saliva is produced in anticipation of eating, and the stomach prepares to receive food by secreting gastric juice in anticipation. The preparation for receiving food into the digestive system also includes a readiness of the gall bladder to secrete bile into the small bowel, and a readiness of the pancreas to respond by excreting enzymes into the small bowel and to secrete insulin into the blood stream.

The amount of sensory input into these readiness reflexes determines the response of the system. Therefore, if the food is on the table in front of the person and the sight and smell of the food is increasing the level of input, then the law of strength of the nervous system would normally be in operation. That is, the more intense the input stimuli, the more preparation the digestive system responds with. By the time the food is in the mouth, there has already been some secretion of gastric juice and some increase in stomach movements in preparation.

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Mycoplasma pneumoniae and Chlamydia pneumoniae are rare causes of acute pharyngitis that can affect primarily young healthy adults. Their clinical characteristics are similar. Both are often associated with lower tract symptoms, such as acute bronchitis or even pneumonia, but can cause pharyngitis in the absence of lower tract symptoms. Both respond to erythromycin.

Neisseria gonorrhoeae is another rare cause of acute bacterial pharyngitis that occurs in sexually active adults as the result of oral-genital contact. If suspected, the diagnosis can be confirmed with culture on a Thayer-Martin medium. Antibiotic therapy should be initiated for gonorrhea as well as for possible coexisting genital infection with Chlamydia trachomatis. Testing for other sexually transmitted disease should be strongly considered, including human immunodeficiency virus (HIV).

Group С and group G streptococci are rare causes of acute bacterial pharyngitis that manifest similar to group A streptococcal pharyngitis. However, the symptoms and signs are often less severe with these organisms. The benefits of treatment of group С and group G streptococci are unknown, and they should be susceptible to the antibiotics used to treat group A streptococcal pharyngitis.

Diphtheria is caused by Corynebacterium diphtheriae. This disease has become rare in the United States, occurring mainly in incompletely immunized patients. Diphtheria usually manifests more gradually, with constitutional symptoms, low-grade fevers, and pharyngitis. The most distinct physical finding is a gray pseudomembrane that typically covers both tonsils and may extend throughout the oropharynx, nasopharynx, larynx, and tracheobronchial tree. If there is extensive involvement of the upper airway, airway compromise can occur. C. diphtheriae can produce a toxin that causes myocarditis and neurologic sequelae (primarily cranial neuropathies and peripheral neuritis). In addition to antibiotics, equine hyperimmune antitoxin should be administered in patients with confirmed cases of diphtheria.

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Streptococcus pneumonia

If pneumococcus is isolated, the patient should be given both vancomycin and a third-generation cephalosporin. Vancomycin has been shown in vitro to be synergistic with ceftriaxone against ceftriaxone-resistant pneumococcal strains. If the organism is found to be resistant to penicillin and to ceftriaxone, this synergistic regimen should be continued. Given the concern that steroid use can decrease the ability of vancomycin to penetrate the CSF, one should consider the addition of rifampin to promote sterilization of the CSF when using steroids. If the strain is susceptible to penicillin, this antibiotic is the ideal therapy.

Neisseria meningitides

If gram-negative diplococci are seen on Gram stain or N. meningitidis is isolated, ceftriaxone is the recommended initial therapy. Since resistant strains have been isolated in the United States, Penicillin use is not recommended until the susceptibilities are known.

Listeria monocytogenes

If Listeria is isolated, treatment with ampicillin is appropriate. Since the beta-lactams may not be bactericidal against L.monocytogenes, it is recommended that ampicillin be used in combination with gentamicin. Trimethoprim-sulfamethoxazole is an alternative bactericidal therapy against Listeria and has shown clinical success.

Group В Streptococci

For group В streptococcal meningitis, penicillin or ampicillin alone may be used. However, in children and those with severe illnesses, the addition of gentamicin should also be considered.

Gram-Negative Bacilli

The development of broad-spectrum cephalosporins has dramatically improved the mortality rate from meningitis due to gram-negative bacilli. First-line therapy for community-acquired gram-negative meningitis includes a third-generation cephalosporin, such as ceftriaxone, with the addition of gentamicin, administered either intraventricularly or intravenously. There is the possibility of the emergence of antibiotic resistance during therapy for gram-negative meningitis, and, in some cases, repeat lumbar puncture may be necessary to guide therapeutic decisions.

Staphylococci

For both S. aureus and coagulase-negative staphylococcal infections, vancomycin is appropriate initially, but an antistaphylococcal penicillin (such as nafcillin) is ideal therapy if the organism is susceptible. In CSF shunt infections, intraventricular antibiotics are often warranted and most often the shunt will need to be removed.

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Routine events for most children

Scrapes, or abrasions, are routine in many families, especially those with young children. Scrapes from falls or other accidents scratch and tear the first few layers of skin. The injury is shallow but can be very painful because millions of nerve endings are exposed. The pain usually subsides within a few days as scabbing forms. These injuries are usually very dirty and must be cleaned thoroughly to prevent infection.

What you can do

Clean the area with soap and warm water, making sure to remove all dirt and foreign particles.

Leave skin flaps in place to act as a natural bandage. Dirty skin flaps

can be cut away carefully with nail scissors. Stop cutting if it hurts.

Place an ice pack over the wound for a few minutes to alleviate most of the pain. For protection, place a washcloth between bare skin and ice. Use a pain reliever such as aspirin, acetaminophen (Tylenol) or ibuprofen if mild pain persists. NEVER give aspirin to children/ teenagers. It can cause Reye’s syndrome, a rare but often fatal condition.

Watch for signs of infection.

Large scrapes can be treated with antibiotic ointment and covered with a sterile, nonstick bandage. Put the ointment on the bandage, rather than rubbing it on the scrape.

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Then comes the third season, the season ofaging.What happens to the magnificent brain machinery as we move further through life? How golden is the “golden age”? Oddly, scientists did not endeavor to address this question until relatively recently. Hippocrates himself omitted the brain from the litany of old-age woes in his Aphorisms. About this, the leading neuroscientist of aging Naftali Raz observed:

… So overwhelming are the transformations of the aging body and so pervasive are the changes in its basic functions that it may not be particularly surprising that the most famous of the ancient servants of Aesculapius did not find the brain and higher cognitive functions sufficiently important to be included in his list of geriatric troubles.

But the brain is affected in aging, even in successful, healthy aging. It would be strange if it weren’t because, like every other organ, the brain is of the flesh. Extensive research has been conducted over the last few decades to understand such changes, and today we have a relatively comprehensive picture of what happens to the aging brain, even when the process is unencumbered by neurological illness or dementia. Much of the discussion that follows in this chapter is based on Naftali Raz’s own research and on his cogent reviews of the state of affairs in the field of brain aging research.

Some of the changes that occur as the brain ages are global. Both the weight of the brain and its volume shrink by about 2 percent every decade of adult life. The ventricles (cavities deep inside the brain containing cerebrospinal fluid) increase in size. The sulci (spaces between the walnut-like convolutions of the cortical mantle) become more prominent. All these changes suggest a modest amount of atrophy or shrinkage of brain tissue, even as part of normal aging. The connections between neurons become increasingly sparse (a process known as “debranching”), and so does the density of synapses (the sites of chemical signal transmission between neurons). Blood flow to the brain becomes less abundant, and the oxygen supply to the brain less generous.

Both gray matter and white matter are affected in aging. In the white matter, small focal lesions appear. They are sometimes called hyperintensities in the technical parlance of MRI radiology. In most cases, the aging-associated “hyperintensities” reflect vascular illness, but they may also reflect demyelination of pathways. They tend to accumulate with age. The relationship between these focal white-matter lesions and cognitive decline is not a simple linear one, but rather of a threshold nature. Up to a point, they remain benign, but once their total volume reaches a certain level, cognition begins to deteriorate. Some scientists believe that the white matter is more susceptible to the effects of aging than the gray matter.

Against the background of such global changes, certain parts of the brain fare better than others. A number of cortical and subcortical structures are affected, but to different degrees. In the neocortex, the classic neurological rule of “evolution and dissolution,” first introduced by John Hughlings Jackson, seems to operate: The phylogenetically (evolutionarily) youngest cortical subdivisions (which develop only at the later stages of “evolution”), the so-called heteromodal association cortex, are affected to the greatest extent by “dissolution” due to aging. These include inferotemporal, inferoparietal, and particularly the phyiogenetically most recent prefrontal cortex. By contrast, the phylogenetically older cortical subdivisions, which include die areas involved in receiving raw sensory information and the motor cortex, are least affected. The prefrontal cortex, a subdivision of the frontal lobe in charge of complex planning and the organization of complex behaviors in time, is affected to the greatest extent by aging.

A similar relationship exists between ontogenetic (occurring during a lifetime) development and decay: The brain structures last to develop at the organism’s growth stages are the first to succumb to decline with age. In assessing the relative vulnerability of various brain structures, the fate of the pathways projecting from and to these structures is particularly instructive. Therefore, the chronology of pathway myelination is a useful marker both of development and of decline. By this light, the longer it takes for the pathways to myelinate, the more susceptible is the corresponding structure to the effects of aging. Again, the prefrontal cortex comes out as the most vulnerable, particularly its dorsolateral subdivision. The changes in the frontal lobes involve the deterioration of both the gray matter and the white matter, as well as the depletion of major neurotransmitters (chemicals in charge of signal transmission between neurons): dopamine, norepinephrine, and serotonin. As was the case in development, the fate of the frontal lobes serves as the watershed between the second and the third seasons of the brain, the stage of maturity and the stages of aging.

Outside the neocortex, the hippocampus and the amygdala are only moderately affected by aging, not nearly as much as the frontal lobes. Hippocampus is found on the inside aspect of the temporal lobe in each hemisphere and is important in the formation of new memories. The amygdala (the word means “almond” in Greek; reflecting its shape) is found right in front of the hippocampus on the inside aspects of the temporal lobes and is important for the experience and expression of emotions.

Interestingly, the hippocampus is not affected by aging in other mammalian species, such as monkeys and rodents. This may be merely a chance difference, but it is also possible that evolutionary pressures favored the human brain with the slightly decaying hippocampus. For those among us with an unbounded faith in the adaptive nature of evolution (but prudent enough not to lapse into an outright teleological frame of mind), what could the nature of such evolutionary pressures be? Just as an idle possibility to consider, it could conceivably be related to the fact that humans depend on previously acquired cognitive templates much more than do other species. Hence, an aging human brain, unlike an aging monkey or rodent brain, may benefit from dampening the formation of excess new information, which somehow competes with these templates.

Another interesting finding is the difference in the relative vulnerability of various brain structures in normal aging and in dementia. Unlike in normal aging, in Alzheimer’s disease the hippocampus and the posterior heteromodal neocortex of the temporal and parietal lobes deteriorate more rapidly than the frontal lobe. Thus, the disparity between the deterioration of the frontal lobes and the hippocampus evident in the MRI of an aging brain may tell us whether it is undergoing the process of normal aging, or whether it exhibits early features of Alzheimer’s disease.

The fate of various subcortical structures generally follows the same Jacksonian principle of “evolution and dissolution.” The basal ganglia and the cerebellum (both important for various aspects of motor control) are moderately affected, and so is the midbrain. The pons (the brain area responsible for basic arousal) and the tectum (the first station of sensory input processing within the brain) seem to be affected very little or not at all.

How do these profound changes in brain anatomy translate into the changes in brain function, into cognitive changes? Again, numerous studies have been conducted, painstakingly documenting the adverse mental changes that attend normal aging. It appears that the overall speed of mental operations declines, as do the sensory functions (the ability to receive inputs about the physical world outside).The functions that depend on the frontal lobes appear to falter in particular. These include mental inhibition, the capacity to refrain from distractions or from habitual, knee-jerk reactions to situations. They also include “working memory,” a loosely used term employed by most scientists to refer to the ability to hold certain information in mind while engaging in some cognitive processing for which this information is germane. Another function of the frontal lobes, mental flexibility (an ability to switch rapidly from one mental process to another and from one frame of mind to another), has also been found to decline with aging.

Certain forms of attention are also impaired, particularly selective attention (the ability to pick out salient events in the environment and to concentrate on them) and divided attention (the ability to shift attention back and forth among several activities unfolding in parallel). Memory is not spared either. This particularly concerns the ability to learn new facts (semantic memory) and to form memories about specific events (episodic memory). In fact, the erosion of new learning is among the earliest manifestations of cognitive aging.

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When beginning a resistance exercise program, remember to consider your age, fitness level, and the personal goals you would like to achieve. Strength training exercises are done in a set, or a single series of multiple repetitions using the same resistance. Current research tells us that for healthy people of all ages (and for many individuals with chronic illnesses), single-set resistance programs of up to 15 repetitions per exercise, performed a minimum of two days per week, are recommended. Each workout session would include 8 to 10 different resistance exercises that involve the major muscle groups of the upper and lower extremities and the trunk. Somewhat surprisingly, single-set resistance programs have been recently recommended by the American College of Sports Medicine for the majority of the U.S. population because they produce most of the health and fitness benefits associated with much more time-consuming, traditional multiple-set programs (e.g., 3 sets of 10 repetitions of each exercise three days per week). Remember that resistance training exercises cause microscopic damage (tears) to muscle fibers, and the rebuilding process that increases the size and capacity of the muscle takes about 24 to 48 hours. Thus resistance training exercise programs should include at least one day of rest and recovery between workouts before overloading the same muscles again.

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The Beech type parent is looked upon more as a tyrant than as a loving and understanding parent in his family, and his presence evokes more awe than respect.

Even his criticism of other’s faults would not be found so oppressive, if he could ever find and appreciate some good qualities in another person.

But he always looks at the exterior with the intention of finding fault and criticize the person without ever trying to penetrate in the other’s personality and find the good qualities that he underneath, perhaps buried deep due to adverse circumstances.

Sometimes, however, when the Beech Type turns his outward look inside himself, his orderly and disciplined self tries to achieve perfection in his profession, ignoring himself the petty considerations of external outlook. Thus a very successful doctor, criticizing other co-professionals for their shoddy treatment of their patients may himself not be so punctual in his appointments, and yet be the BEECH type.

A professor, himself a very good teacher may be careless in his dress, but would criticise his coleagues for their bad teaching, although they may be very well dressed and very punctual.

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‘Agrimony’ patient does not go to a doctor when ill— he is taken to doctor by some well-wisher.

Not that ‘Agrimony’ patient is insensitive to normal human feelings. When there is a bereavement, a death, some valuable loss, he feels the pangs of pain just like any other human being. Only he does not broadcast his anguish externally. He ruthlessly suppresses his inner grief, puts on a normal look, goes about his normal routine, even smiles and laughs and cuts jokes with his friends and succeeds in concealing under a sham facade the intense mental torture which has no escape route.

With a troubled soul he cannot afford to pick up any quarrels. He shuns all arguments. Would pay anything to be saved from quarrels or arguments.

He wants society. Cannot afford to sulk and grieve in loneliness. Wants somebody to talk to, to listen to, to cut jokes, to laugh away the internal grief.

During daytime he can forget himself—the inner-self in business, in clubs, in society, but when night falls and he has to face the stark reality, the loneliness, the burning grief inside, he feels non-plussed, defeated, with ho companion, no friend to share his woe, he silently buries his head in his pillow, weeps and sobs but takes care, that no servant watches him weeping. Lies in bed but cannot sleep. Tormenting thoughts make him weeping. Goes out and keeps walking on the lawn. The faithful servant has noticed it all and when his master has taken to drinking or smoking—the voices which he had been condemning loudly before—he has also noticed it, and he can gauge the depth of his master’s internal restlessness from these actions. And when this patient is taken to a doctor for some serious ailments—here mind the words “Taken to the doctor’, because Agrimony patient would not go to the doctor himself, nor would he call a doctor when ill—this faithful servant would tell the doctor the true state of his master, the cause and the origin of his grief and the depth of his mental agony and the desparate effort he is making to conceal his mental restlessness by keeping up faces. The doctor would immediately know the Negative side of Agrimony in this patient & prescribe Agrimony as his constitutional remedy.

Even if some other medicine is prescribed on the causative factor or his present physical or mental trouble, ‘Agrimony’ would have to be prescribed in conjunction with it, and ‘Agrimony’ would be continued till the patient gets rid of the negative Agrimony state and acquires Positive Agrimony state.

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