According to recent research published in the journal Pain, "Interleukin-6 (IL-6) is an inflammatory cytokine known to modulate muscle pain. However, the mechanisms underlying this effect still remain unclear."
"Here we show that the injection of IL-6 into mice gastrocnemius muscle evoked a time-and dose-dependent mechanical hyperalgesia. This effect is in part dependent on the presence of gp130 expression in inflammatory cells in the gastrocnemius muscle as well as in DRG neurons. We also demonstrated an increased inflammatory cell recruitment and cytokines levels, namely TNF-alpha, IL-1 beta and KC. TNFR1(-/-) mice or mice pre-treated with the selective CXCR2 antagonist, SB225002, with the anti-macrophage, anti-TNF-alpha or anti-KC antibodies or with IL-1 receptor antagonist (IL-1RA) showed decreased IL-6-mediated mechanical hyperalgesia. Furthermore, systemic pre-treatment with the classically used drugs indomethacin, celecoxib, guanetidine, morphine, thalidomide or dexamethasone, also prevented IL-6-induced muscle pain. Likewise, local pre-treatment with inhibitors of phospholipase A2 (PACOCF3), phospholipase C (U73122), protein kinase C (GF109203X), protein kinase A (KT-5720) or with phosphatidylinositol 3-kinase (AS605204) also consistently diminished IL-6-induced muscle hyperalgesia. The intramuscular injection of the selective inhibitors of p38 MAPK (SB203580), ERK (PD98059) or JNK (SP60015) also prevented IL-6-mediated muscular pain. Simultaneous flow cytometry measurements revealed that ERK, p38 MAPK and JNK were phosphorylated as early as 5 min after IL-6 injection. These findings provided new evidence indicating that IL-6 exerts a relevant role in the development and maintenance of muscular hyperalgesia," wrote M.N. Manjavachi and colleagues, Federal University .
The researchers concluded: "The IL-6-mediated muscular pain response involves resident cell activation, polymorphonuclear cell infiltration, cytokine production, prostanoids and sympathomimetic amines release and the activation of intracellular pathways, especially MAPKs."
Manjavachi and colleagues published their study in Pain (Mechanisms involved in IL-6-induced muscular mechanical hyperalgesia in mice. Pain, 2010;151(2):345-355).
Most of us have already heard the loose rumor that "classical music is good for your brain", whether as brain-booster while working or as something that mothers should be doing for their developing children or even "sound as audio therapy" unto itself. For many, it may feel intuitive that listening to complex classical music pieces must somehow be better for one's brain than listening to, say, a simplistic three-chord rock anthem or a Rap track featuring a single looping drum beat with repetitive vocal (or many other genres of current pop/rock/rap music).
Or does that truly depend on the song in question, or one's world view, or one's attention to complex subtle nuances that may lie just below the surface of a seemingly trite piece of Pop?
The truth is that the potential for brain-boosting benefits from listening to music (or sound content of any type, for that matter) is a largely unstudied area, ripe for much deeper research spanning far more genres of "organized sound" (music) than certainly exist to date. The trouble is that this kind of research, like most other brain-related research, is extremely difficult to derive clear indications from... clear results and empirical data, given the massive number of variables that enter into the mix when trying to test how music truly impacts real-world human subjects.
The good news is that there already is some good research that suggests impressive, exciting news as to how music can enhance brain function, and if one takes a step back to extrapolate these research results and make an intuitive personal judgment regarding how music may help, it's a no-brainer (sic) to consider giving it a try. And why not: no side effects or contraindications with music listening, unlike supplements and medications and some foods!
The research: music with exercise? In one research study, clinical psychologist Charles Emery of Ohio State University studied the effect of music on people who listened (or did not listen) during regular physical exercise. Emery says, "I've always thought that music had many benefits for people, and increasingly people use music when they exercise, so it seemed like a logical next step in terms of a research project". So along with Evana Hsiao and Scott Hill of Ohio State, and David Frid of Pfizer, Inc., Emery put his theory to the test, with the help of 33 men and women in the final weeks of a cardiac rehabilitation program. Each of the participants were tested for mental performance after exercising without music, and exercising with music.
The results were astonishing: on average, the participants performed more than twice as well on a verbal fluency test after listening to music while exercising than they did after exercising without the music. Wow!
The music selected? Vivaldi's "The Four Seasons".
"When there was no music, there was no change," Emery says.
Emery chose Vivaldi's "The Four Seasons" for the project because prior research by other scientists with that particular piece indicated that it helped patients with lung disease perform better mentally. Emery suspects, however, that similar benefits could be gained by listening to ALL kinds of music, not just classical. It is theorized that the passionate, upbeat rhythms of "The Four Seasons" may stimulate mental performance because it is complex, thus forcing the brain to organize neural transmissions.
But other selections might work better for some people."I don't think there is anything specific to Vivaldi or even classical music that would necessarily trigger enhanced brain function," Emery says.
But he is confident that music makes a difference, whether it is jazz, hip hop, or classical. And while his research was centered on cardiac patients, because they often suffer mental decline as a result of their illness, Emery thinks it works for everybody, not just those who are sick.
Several other research studies have illustrated how listening to music is a more complex endeavor than it seems on the surface: the human brain has to sort out tones, timing, and sequencing of various sounds, in order to comprehend music. It is believed that the frontal lobe of the brain is stimulated and activated by listening to music, as it is the part of the brain that is associated with higher mental functions such as thinking abstract thoughts, or planning for the future.
Vivaldi or Mozart, but not Glass? Psychologist Frances Rauscher, now at the University of Wisconsin at Oshkosh, and her colleagues made waves with the discovery that listening to Mozart improve d people's mathematical and spatial reasoning. Even rats ran mazes faster and more accurately after hearing Mozart than after white noise or music by the minimalist composer Philip Glass. Sorry, Glass fans. Rauscher reported that, for rats at least, a Mozart piano sonata seems to stimulate activity in three genes involved in nerve-cell signalling in the brain.
But don't just listen, join in: it's one thing to listen passively to music in order to derive brain benefits. But even more brain-engaging, and even IQ-boosting, is playing or writing music, including taking music lessons.
In fact, six-year-old children who were given music lessons, as opposed to drama lessons or no extra instruction, got a 2 to 3-point boost in IQ scores compared with the others. Similarly, Rauscher found that after two years of music lessons, pre-school children scored better on spatial reasoning tests than those who took computer lessons.
Although not yet tested with adults, there is little reason why similar benefits would not also apply to adults, including the elderly, which is why we here at BrainReady (and most other cognitive health experts) routinely recommend learning to play a new instrument and learning to read and write music (visually or even intuitively through experimentation) as wonderful mental health and brain fitness steps that adults of all ages should strongly consider.
Learning a new instrument, learning to read or write music -- these activities exercise a wide range of mental skills, with their requirement for delicate and precise finger movements, listening for pitch and rhythm, learning harmony and harmonic complexity, all combined with an emotional dimension, as well as memory. And this makes sense intuitively: if you're someone who has never played an instrument or learned to read or write music, and then one day you start on the long process of learning, what do you think is happening to your brain? Would your brain be different, better, more capable, one year after consistently working at it and becoming a capable musician?
The relaxation factor: then there's the obvious other area of benefit from listening to (or playing) music...relaxation and enjoyment. When you listen to or engage in music that makes you feel happy, relaxed, deeply engaged, contemplative, you're reaping some of the same deep relaxation effects that such activities as restful sleep, a warm bath, a wonderful meal, have on your overall stress level and physiological state. Simply put, it's relaxing, and that reduces stress, and stress is one of the biggest health hazards to brain & body alike.
Now, not all music produces such a state of calm relaxation, particularly as everyone's musical tastes are somewhat unique. Some may find Speed Metal or bombastic Hip-Hop deeply calm-inducing and mentally therapeutic while becoming filled with rage at the mere thought of a Celine Dion or Barbara Streisand vocal. Others may find the inverse. But there may well be something to listening to classical orchestral music, or music that is equally complex (large number of instruments, fairly complex harmonic and lyrical structure, emphasis on notes and melodies rather than repetitive drum beats or simplistic repeating motifs as found in most Pop music). So if you're going to select your "brain health music", it may be wise to include some Mozart, Vivaldi, Bethoven, Bruckner, Stravinsky and other greats.
"A more effective and convenient alternative treatment for anisometropic amblyopia is required, especially for older children," write Jianhao Zhao, MD, from Joint Shantou International Eye Center of Shantou University and Chinese University of Hong Kong in Shantou, China, and colleagues.
"Acupuncture...has been used for treating ophthalmic disorders such as dry eye, myopia, and amblyopia. In recent years, the use of functional magnetic resonance imaging has demonstrated a correlation between vision-related acupoint stimulation and visual cortical activation, suggesting a possible basis for the use of acupuncture in treating amblyopia."
The study goal was to compare the efficacy of daily patching for 2 hours with that of acupuncture in treating anisometropic amblyopia. Participants were 88 children, aged 7 to 12 years, with an amblyopic eye, who had worn optimal eyeglasses for at least 16 weeks and had achieved a best spectacle-corrected visual acuity (BSCVA) of 0.3 to 0.8 logMAR at baseline. Children were randomly assigned to receive patching of the nonamblyopic eye for 2 hours daily or 5 sessions of acupuncture weekly. In addition, all participants received constant optical correction, 1 hour of near-vision activities daily, and follow-up at weeks 5, 10, 15, and 25. The primary study endpoint was BSCVA in the amblyopic eye at 15 weeks.
In the patching group, mean BSCVA of the amblyopic eye improved by 1.83 lines from baseline to 15 weeks compared with 2.27 lines in the acupuncture group. These improvements met the definition of equivalence (difference within 1 line) after baseline adjustment, with mean between-group difference in BSCVA of 0.049 logMAR (95% confidence interval, .005 - .092; P = .03).
Improvement in BSCVA by 2 lines or more occurred in 28 eyes (66.7%) in the patching group and in 31 eyes (75.6%) in the acupuncture group, and resolution of amblyopia occurred in 7 (16.7%) and 17 (41.5%) eyes, respectively. Tolerability and compliance were good for both treatments, with no serious adverse effects in either group.
"Acupuncture produced equivalent treatment effect for anisometropic amblyopia, compared with patching, and was statistically superior," the study authors write. "Further studies are warranted to investigate its value in the treatment of amblyopia."
Limitations of this study include the possibility that some of the observed treatment effect may have resulted from continued optical correction, and the inability to compare different durations of patching or use of different acupoints.
"Although the treatment effect of acupuncture appears promising, the mechanism underlying its success as a treatment for amblyopia remains unclear," the study authors conclude. "Acupuncture at vision-related acupoints may modulate the activity of the visual cortex. Moreover, acupuncture has been shown to be effective in increasing blood flow to the cerebral and ocular vasculatures (including the choroid), stimulating the expression of retinal nerve growth factors and leading to metabolic changes in the central nervous system."
question
I am 80 years old. Forty years ago I had a heart attack. I stopped smoking but remained very active. My blood pressure, with the help of medications, is around 125/70. I now walk 2 to 3 miles a day, work out with weights three times a week, and walk up and down 25 flights of stairs twice a week. My physician thinks I am pushing too hard and has urged me to take it easier. Is he right?
answer
I congratulate you on being so vigorous and giving your blood pressure and overall health so much attention. You are living proof that you can survive a heart attack and do extremely well for many decades. The medications and lifestyle changes you have made add up to a big reduction in your cardiovascular risk.
Your blood pressure is close to perfect, and I can only assume that your cholesterol and blood sugar are also in good shape. Obviously, stopping smoking in 1970 was a great idea.
The question of how much exercise is too much is a challenging one. Although some cardiovascular risk indicators like HDL, the so-called good cholesterol, continue to improve with extreme forms of exercise like marathon running, the risk of injury also increases. It’s safe to say that moderate exercise every day is far better for you than intense exercise followed by long periods of inactivity due to injury.
My advice is to continue what you are doing: mix it up, combining different weight-bearing activities (like walking) with weight training. Such cross-training reduces the risk of injury from repetitive stresses on specific joints and muscles. Resistance exercises like upper-extremity weight training were once thought to be bad for the heart, but experts now believe that moderate weight training is good all around — it exercises the heart and lowers blood pressure, too.
Many diet books advise people to chew slowly so they will feel full after eating less food than if they ate quickly. As we explain in the current issue eating slowly doesn’t always work, but when it does, the reason has as much to do with the brain as with the gut. Scientists have known for some time that a full stomach is only part of what causes someone to feel satisfied after a meal; the brain must also receive a series of signals from digestive hormones secreted by the gastrointestinal tract. Stretch receptors in the stomach are activated as it fills with food or water; these signal the brain directly through the vagus nerve that connects gut and brainstem. Hormonal signals are released as partially digested food enters the small intestine. One example is cholecystokinin (CCK), released by the intestines in response to food consumed during a meal. Another hormone, leptin, produced by fat cells, is an adiposity signal that communicates with the brain about long-range needs and satiety, based on the body’s energy stores. Research suggests that leptin amplifies the CCK signals, to enhance the feeling of fullness. Other research suggests that leptin also interacts with the neurotransmitter dopamine in the brain to produce a feeling of pleasure after eating. The theory is that, by eating too quickly, people may not give this intricate hormonal cross-talk system enough time to work. Of course, as anyone who has tried eating slowly in order to lose weight can attest, it’s not quite that simple. People who are obese, for example, may suffer from leptin resistance, meaning that they are less responsive to satiety or pleasure signals from this hormone. People are also sensitive to cues in the environment , such as the alluring smell of chocolate chip cookies or the sight of a juicy burger , that can trigger the desire to eat. Appetite is complex and dieting is a challenge. Even so, people who are trying to lose weight may want to start by chewing more slowly. In that way, they allow themselves enough time to experience pleasure and satiety. What are your thoughts about this theory? Has chewing slowly enabled you to feel full faster?
One of the things I like most about Thanksgiving is the laughter around the dinner table. The food is great, make no mistake. But it’s the sounds of happiness—the high peal, the good-natured guffaw, the snort-and-shaking-shoulders, and the deep belly laugh—that really make me give thanks. Laughter isn’t just a way to stay connected with family and friends. If new research pans out, it is also doing our hearts some good.
From brain scans and other tests, neuroscientists are compiling evidence that laughter triggers chemical responses in the brain that lead to feelings of pleasure and a sense of well-being. Laughter also appears to go beyond the belly and the brain—arteries respond to it in healthy ways that could improve blood flow and long-term health. (I’m talking about “mirthful” laughter here, the kind sparked by a funny story or a Billy Crystal routine. Sarcastic or other kinds of unfriendly or hostile laughter are a different story.)
At the University of Texas, Austin, researchers asked 17 healthy adults to watch a humorous 30-minute video of their choosing or a documentary, with before and after tests of blood flow. The biggest differences between the two groups were in measures of artery function (a test called flow-mediated dilation) and flexibility (the carotid artery augmentation index). These improved immediately in the volunteers who watched a comedy and stayed that way for almost 24 hours. In those who watched a documentary, though, artery function decreased a bit.
This study builds on work done by cardiologist Michael Miller and his colleagues at the University of Maryland Medical Center. They have demonstrated similar improvements in artery function after laughing at a comedy.Why this happens is all speculation. Miller and William Fry, a psychiatrist at Stanford University School of Medicine who began studying the effects of laughter on the cardiovascular system in the 1970s, hypothesize that brain chemicals called endorphins,which are released during mirthful laughter, latch onto opiate receptors in the lining of blood vessels. This interaction stimulates blood vessels to release nitric oxide, a molecule known to relax arteries. Relaxed arteries are more flexible and wider, permitting easier blood flow.
It’s a long way from laboratory measures of improved artery function to better health and longer life. That’s why you can’t rely on laughter as your only medicine. And a laughter prescription might not be as much fun as it sounds. Instead, enjoy laughter when it comes and bless it as another thread in the web of connections that help keep us happy and healthy.
Προσδίδουμε διαφορετικούς χαρακτήρες στο πόνο. Αν ένα παιδί τραυματιστεί , θα κλάψει και θα πει «έχω πληγή».Η μητέρα θα ρωτήσει: που πονάει αγάπη μου; Σκεφτείτε ότι πρόκειται για δυο διαφορετικές προσεγγίσεις στο πόνο : 1.Το συναισθηματικό στοιχείο του πόνου , που είναι φυλογενετικά πρωτόγονο και ασχολείται με το πόνο σαν κάτι δυσάρεστο , που πρέπει να αποφεύγεται και το τελευταίο πιο πρόσφατο : 2.το διακριταίο στοιχείο του πόνου , που είναι η ικανότητα να αντιλαμβάνεται ακριβώς που είναι ο πόνος και να ανταποκρίνεται κατάλληλα.
Πόνος στο φλοιό
Συνηθιζόταν να λέγεται ότι οι δομές του φλοιού μόνο επιφανειακά ασχολούνται με την αντίληψη του πόνου, αν όχι και καθόλου. Αυτό είναι λάθος , καθώς ένα πλήθος συνδέσεων , συνδέουν υψηλότερες δομές του φλοιού με κέντρα του πόνου στο θάλαμο και το εγκεφαλικό στέλεχος. Σημαντικές δομές του φλοιού είναι :
Ο πρωτεύων αισθητικός φλοιός(sensorycortex )
Oδευτερεύων αισθητικός φλοιός
Το πρόσθιο τμήμα του κεντρικού λοβού των εγκεφαλικών ημισφαιρίων ( insula)
Η προσαγωγός έλικα
Ο πρωτεύων αισθητικός φλοιός είναι υπεύθυνος για τον εντοπισμό του πόνου . Η προσαγωγός έλικα σχετίζεται με το συναισθηματικό στοιχείο του πόνου.
Ο θάλαμος
Ο θάλαμος είναι ο κεντρικός σταθμός μετάδοσης του πόνου. Αρκετοί από τους πυρήνες του ασχολούνται με το πόνο. Οι πλάγιοι πυρήνες ασχολούνται με το αισθητικό / διακριταίο στοιχείο του πόνου και οι έσω πυρήνες με το συναισθηματικό στοιχείο του πόνου.
Μεσεγκέφαλος
Υπάρχει ένα πλήθος δομών που σχετίζονται με το πόνο στο μεσεγκέφαλο .Το μεγαλύτερο μέρος αυτού του κυκλώματος σχετίζεται με το συναισθηματικό στοιχείο του πόνου , με εκτεταμένες συνδέσεις με το δικτυωτό σχηματισμό του εγκεφαλικού στελέχους. Σημαντικά στοιχεία είναι τα εξής :
Η περιϋδραγώγειος φαιά ουσία
Ο ερυθρός πυρήνας
Ο πυρήνας του Darkschewitsch
Ο διάμεσος πυρήνας του Cajal
Ο σφηνοειδής πυρήνας και ο πυρήνας του Edinger – Westphal
Toεγκεφαλικό στέλεχος
Το πιο σημαντικό κέντρο του πόνου στη γέφυρα είναι ο locuscoeruleus(υπομέλανας τόπος) .Αυτός περιέχει νοραδρεναλίνη και νευρώνες που ρυθμίζουν το πόνο μέσω οδών, που κατέρχονται προς το νωτιαίο μυελό.
Ο προμήκης μυελός
Συμμετέχει επίσης στο συναισθηματικό στοιχείο του πόνου. Σημαντικός είναι ο γιγαντοκυτταρικός πυρήνας και ο πλάγιος δικτυωτός πυρήνας.
Ο νωτιαίος μυελός
Παραδοσιακά υπήρχε η άποψη ότι οι περισσότερες ίνες του πόνου (Αδ και C ) εισέρχονται στη φαιά ουσία των οπισθίων κεράτων του νωτιαίου μυελού. Στη συνέχεια συνάπτονται διαμέσου της ανιούσας οδού με τη νωτιαίοθαλαμική οδό. Στη πραγματικότητα , οτιδήποτε πάνω από το 40% των αισθητικών ινών εισέρχεται στη κοιλιακή ρίζα.
Υπήρξε μεγάλος ενθουσιασμός όταν περιγράφηκε για πρώτη φορά η θεωρία της πύλης (gatecontrol ) .Αν και ο μηχανισμός έχει πλέον τεκμηριωθεί και έχει κλινική xρήση , είναι γνωστό ότι αποτελεί μια απλοποίηση. Η βασική ιδέα είναι ότι το εισερχόμενο ερέθισμα του πόνου μπορεί να διακοπεί από άλλα ερεθίσματα , διότι πολλά νευρικά κύτταρα επικοινωνούν μεταξύ τους στο οπίσθιο κέρας. Οι πιο σημαντικές ίνες οι οποίες εισέρχονται από τη περιφέρεια στο ραχιαίο κέρας είναι :
Αμύελες C ίνες που είναι σημαντικοί μεταφορείς του μεγάλης διάρκειας πόνου , που προκαλεί το χειρουργικό τραύμα.
Λεπτές εμμύελες Αδ ίνες που σχετίζονται με έναν πιο εντοπισμένο πόνο.
Αβ ίνες που φέρουν πληροφορίες σχετικά με την αντίληψη της θέσης από τη περιφέρεια προς το νωτιαίο μυελό
Δυσάρεστα ερεθίσματα που εισέρχονται δια των C ινών μπορούν να κατασταλούν με ταυτόχρονη διέγερση των Α-δ ινών (ερέθισμα υψηλής έντασης και χαμηλής συχνότητας , όπως για παράδειγμα με βελονισμό ) ή από ερεθίσματα που διέρχονται από τις Α-β ίνες. Για παράδειγμα TENS: διαδερμική ηλεκτρική νευρική διέγερση και η απλή τριβή του δέρματος , η οποία είναι πολύ καλά γνωστή από τις μητέρες , ότι ελαττώνει την αντίληψη του πόνου.
Ανιούσα οδός
Νωτιαίο-δίκτυο- διεγκεφαλική οδός: έχει λίγους έως καθόλου υποδοχείς οπιοειδών . Έχει ελάχιστη σχέση με την αντίληψη του πόνου , ως οδυνηρό ερέθισμα.
Κατιούσα οδός
Εξίσου σημαντικές είναι οι ίνες, που κατέρχονται από το εγκεφαλικό στέλεχος στο νωτιαίο μυελό για να τροποποιήσουν τα εισερχόμενα ερεθίσματα. Νευροδιαβιβαστές είναι η νοραδρεναλίνη ειδικά στο υπομέλανα τόπο (locuscoeruleus) και η σεροτονίνη στο raphenuclei.Οι υποδοχείς των οπιοειδών είναι ιδιαίτερα εμφανής εδώ.
Πόνος στη περιφέρεια
Οι περισσότεροι ιστοί περιέχουν ειδικούς υποδοχείς του πόνου , οι οποίοι ονομάζονται αλγοϋποδοχείς (nociceptor ).Στο παρελθόν πίστευαν ότι το επώδυνο ερέθισμα γινόταν αντιληπτό μέσω υπερδιέγερσης των υποδοχέων. Αυτό είναι λάθος. Η ποιότητα του πόνου φαίνεται να εξαρτάται από τη περιοχή διέγερσης και τη φύση των ινών που διαβιβάζουν την αίσθηση του πόνου. Ακόμη και στη περιφέρεια , υπάρχει μια διάκριση ανάμεσα στο οξύ άμεσο πόνο («ο πρώτος πόνος») διαβιβαζόμενος από τις Αδ ίνες και ο παρατεταμένος δυσάρεστος καυστικός πόνος , που διαβιβάζεται από μικρότερες αμύελες C ίνες.
Οι αλγοϋποδοχείς έχουν πολλούς διαφορετικούς υποδοχείς στην επιφάνεια τους , που διαμορφώνουν την ευαισθησία τους στη διέγερση. Αυτοί περιλαμβάνουν τους GABA , τη βραδυκινίνη , την ισταμίνη , τη σεροτονίνη , τους υποδοχείς της καψαϊκίνης , τα οπιούχα , αλλά οι ποικίλοι ρόλοι αυτών των υποδοχέων ελάχιστα αναφέρονται.
Το πιο εντυπωσιακό , όσον αφορά την αντίληψη του πόνου στη περιφέρεια , είναι ότι οι περισσότεροι αλγοϋποδοχείς παραμένουν αδρανείς. Η φλεγμονή ευαισθητοποιεί τη μεγαλύτερη πλειοψηφία των αλγοϋποδοχέων και τους οδηγεί σε μια μεγαλύτερη ευαισθησία στη διέγερση (υπεραλγησία ).Η υπεραλγησία μπορεί να είναι πρωτογενής (αισθητή στη περιοχή της διέγερσης , σχετιζόμενη με την ευαισθητοποίηση των νευρώνων αυτού του δερμοτομίου ) ή δευτερογενής (αισθητή σε μια απομακρυσμένη περιοχή απ΄το πρωταρχικό τραύμα και πιθανώς σχετίζεται με τη διαμεσολάβηση των NMDA « windup».
Νευροδιαβιβαστές
Ένα πλήθος νευροδιαβιβαστών διαμεσολαβούν τη μεταβίβαση της αίσθησης του πόνου , τόσο στον εγκέφαλο , όσο και στο νωτιαίο μυελό. Ο αριθμός των νευροδιαβιβαστών αυξάνεται καθημερινά. Μπορούμε να τους ταξινομήσουμε στις εξής κατηγορίες :
Ανασταλτικοί: Υπάρχουν πολλοί ανασταλτικοί νευροδιαβιβαστές , αλλά στο ΚΝΣ , το GABA( γ-αμινοβουτυρικό οξύ ) φαίνεται να κυριαρχεί.
Οι νευροδιαβιβαστές που εμπλέκονται στη φυγόκεντρη ρύθμιση του πόνου. Οι άλφα- 2 διεγερτικές επιδράσεις της νοραδρεναλίνης και οι δράσεις της σεροτονίνης είναι εμφανής. Τα οπιοειδή ανακουφίζουν από το πόνο , ενεργοποιώντας τους μ- και δ- υποδοχείς.
Stroke has always been a much-feared medical emergency, and rightly so. Someone in the United States has a stroke every 40 seconds, and someone dies of a stroke every four minutes, amounting to 795,000 strokes and 137,000 deaths annually. Stroke is the third leading cause of death in the United States, behind heart disease and cancer.
Not all strokes are preventable, so it is very important to recognize the early signs of stroke and get treatment as rapidly as possible. Stroke damages brain tissue, but that loss can be minimized by getting quickly to an emergency room that can connect to a rapid-response stroke center.
Everyone should learn the following warning signs of stroke. If you experience any of these symptoms, immediately dial 911 or go to an emergency room:
weakness in an arm, hand, or leg
numbness on one side of the body
sudden dimness or loss of vision, particularly in one eye
sudden difficulty speaking
inability to understand what someone is saying
dizziness or loss of balance
sudden, lasting, excruciating headache.
It is difficult to overemphasize the importance of identifying and treating a stroke as soon as possible. Warning signs can begin anywhere from a few minutes to days before a stroke (see “Stroke warning signs and symptoms,” above). In a Gallup survey, 97% of people over age 50 did not recognize the warning signs of a stroke. Everyone, especially those who are at increased risk for stroke, should learn these warning signs and know what to do if they occur. The National Stroke Association has devised the FAST checklist (see “Act FAST”) to help determine whether a person is having a stroke.
ACT FAST
If the answer to any of the questions below is yes, there’s a high probability that the person is having a stroke.
Face
Ask the person to smile. Does one side of the face droop?
Arms
Ask the person to raise both arms. Does one arm drift downward?
Speech
Ask the person to repeat a simple sentence. Are the words slurred? Does he or she fail to repeat the sentence correctly?
Time
If the answer to any of these questions is yes, time is important. Call 911 or get to the hospital fast. Brain cells are dying.
When stroke symptoms occur, quick action is vital. If you think you or someone with you is having a stroke or transient ischemic attack (TIA), call 911. You should be taken to a hospital emergency room, preferably one that specializes in treating stroke as it occurs (called acute stroke). If you know you are at risk for stroke, find out ahead of time the name and location of the nearest hospital that specializes in treating acute stroke.
Since the 1980s, researchers have developed rapid, safe, and effective diagnostic techniques that accurately identify the extent and location of a stroke and the nature of the blood vessel (vascular) problem causing it. The goal of treatment is to restore blood circulation before brain tissue dies. The time frame for reaching this goal is frighteningly slim. To prevent brain cell death that is significant enough to cause disability, treatment is most effective if it starts within 60 minutes of the onset of symptoms.
One of the main clot-dissolving drugs, recombinant tissue-plasminogen activator (tPA), must be given within three hours of the start of stroke symptoms, but earlier is better. An important goal of research is to find treatments that can buy time by protecting the patient’s brain until blood circulation is restored, thus improving the odds of survival and decreasing disability.
Lung cancer is usually discovered late when it’s difficult to treat and has often spread outside the lung. A reliable screening test to find it at an earlier, more treatable stage would be a legitimate breakthrough—and could potentially save thousands of lives. About 160,000 Americans die each year from lung cancer, which is more than who die from breast, prostate and colon cancer combined. Chest x-rays do a good job of finding small lung cancers that can be removed surgically. Why not use them to screen for lung cancer? Because at least a half-dozen studies have been done and for reasons that aren’t entirely clear, early detection with chest x-rays hasn’t translated into prevention of fewer deaths from lung cancer. And in screening, early detection is a means to an end. The real goal is preventing deaths from the disease that is being screened for (and deaths in general).
So it was big news today when the National Cancer Institute announced today that a large study sponsored by the instituteshowed that screening current and former heavy smokers with computed tomography (CT) scans did, in fact, reduce the risk of dying from lung cancer by 20% compared with screening them with chest x-rays. Moreover, those who were screened with CT scans were 7% less likely to die from any cause during the study’s five-year follow-up period.
Good news, and a long time coming for those who have watched disappointing findings from the chest x-ray studies pile up.
But if today was first time that most of us heard about the National Lung Screening Trial, it probably wouldn’t be the last. It’s almost certainly going to stir up more than its fair share of controversy.
Here are a few of the hot buttons:
The NCI says there are more than 94 million current and former smokers in the United States (mind you, not all of them are heavy smokers, so the population to be screened may be smaller). It will be very expensive to screen them all with CT scans. How much a screening CT of the lung will cost is hard to say, especially if they become routine, but the NCI says the current Medicare reimbursement rate for a diagnostic CT scan of the lung is $300.
Some may argue that smokers shouldn’t be entitled to such an expensive test—or should have to shoulder a large share of the cost. The counterargument is why single out smokers when other bad health habits result in expensive tests and treatments.
The NCI itself showed that there’s concern that some people may see an effective screening test as a reason to tune out the dire health warnings about tobacco and cigarettes. In a Q&A about the study posted on its Web site today (which is well worth reading if you want more detail about the study), the third question is, “Is it OK to keep smoking because there is a screening test that has benefit?” The answer begins with an emphatic, “No.” It’s hard to imagine that people would actually ask such question, but the NCI apparently was worried enough to pose it.
Radiation exposure and the cancer risk from medical imaging (and CT scans in particular) has become a major issue. Will the radiation from CT screening for lung cancers add to the problem? The NCI position: the radiation from a screening CT is far less than the dose from a diagnostic one and that benefit of finding and treating early lung cancer will likely outweigh the risk from a low dose of radiation from CT scanning.
In the Q&A about the study, the NCI says that between 20% and 60% of screening CT scans of current and former smokers show some kind of abnormality and that most are not lung cancer. CT scanning for lung cancer could generate a large number of false positives: results that indicate the possibility of cancer but turn out not to be. False positives result in worry and additional tests, which in the case of lung cancer would include invasive biopsies.
Of course many of our current screening tests for cancer have shortcomings, cost plenty, and are controversial. The debates about the value of mammography never seem to end. Yet we get behind screening tests for a whole variety of reasons, not the least of which is that cancer caught late is so lethal and, these days, astronomically expensive to treat.
