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Åùå ðàç óòî÷íÿþ. ÀÐÏ - îñòàíîâêà äûõàíèÿ íà âûäîõå ïîñëå ãëóáîêîãî âäîõà âî âðåìÿ ïëà÷à.
Òîãäà ÀÐÏ - ñîñòîÿíèå , êîòîðîå ìîæíî íàáëþäàòü ïðàêòè÷åñêè ó âñåõ äåòåé . |
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Ïî ïîâîäó îñòàíîâîê äûõàíèÿ è òåðìèíîëîãèè.  1986 ãîäó National Institutes of Health Consensus Panel on Infantile Apnea and Home Monitoring äàë îïðåäåëåíèå ïàòîëîãè÷åñêèõ àïíîý (âêëþ÷åííûõ â ñòðóêòóðó â ò.÷. ÀÐÏ) - ýòî îñòàíîâêà äûõàíèÿ áîëåå 20 ñåêóíä. Îçíàêîìüòåñü ñ [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] Åùå ðàç ñóììèðóþ. Íåò äîêàçàòåëüñòâ, ÷òî ëå÷åíèå àíòèýïèëåïòè÷åñêèìè ïðåïàðàòàìè äàåò ïàöèåíòó êàêèå-ëèáî âûãîäû â ñðàâíåíèè ñ îòñóòñòâèåì ëå÷åíèÿ. Ðåêîìåíäàöèÿ ê ïðèìåíåíèþ íåäîñòàòî÷íî îáîñíîâàííîãî ìåòîäà ìîæåò ïðèíåñòè âðåä. |
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Âîò ãëàâà èç ðóêîâîäñòâà Child neurology J.Menkes (6 èçäàíèå)
BREATH-HOLDING SPELLS It is common for a small child to hold his or her breath when crying. These episodes, termed breath-holding spells, are readily recognized and follow a distinct clinical pattern. In a typical attack, the child who has been frightened or frustrated begins to cry and ceases breathing. Usually the breath is held in expiration, and after a few seconds the infant becomes cyanotic to varying degrees. Consciousness is lost, the infant becomes limp and can experience a few clonic convulsions of the extremities. Lombroso and Lerman found breath-holding spells in 4.6% of infants, with the majority of spells (76%) beginning in infants between 6 and 18 months of age (802). In a large number, the first attack was observed during the neonatal period. The frequency of attacks varies considerably. Approximately 10% of patients experience two or more attacks a day, and another 20% experience an average of one spell a day. A family history of breath-holding spells can be elicited in a significant number of first-degree relatives. In the series of DiMario and Sarfarazi, 27% of parents and 21% of siblings had current or prior breath-holding spells. These authors suggest that the condition is transmitted as an autosomal dominant with reduced penetrance (803). With increasing age, spells become less common; in almost all instances they finally disappear by age 5 to 6 years. Lombroso and Lerman believe that infants with breath-holding spells can be divided into two well-defined groups of approximately equal size: one group in which spells are conspicuously cyanotic and another in which they are characterized by pallor (802). The latter group is particularly sensitive to vagal stimulation as elicited by ocular compression, which induces a prolonged asystole and an occasional seizure. Gauk and coworkers demonstrated a rapid decrease in arterial oxygen saturation as measured by ear oximetry, probably the result of oxygen use (804). As indicated previously, a breath-holding spell accompanied by a seizure can be differentiated from an epileptic convulsion (apneic seizure) in that an obvious precipitating factor, which has induced the child to cry, can always be elicited in the breath-holding spell. Cyanosis generally follows the onset of convulsions in an epileptic attack, but it precedes breath-holding spells (805). Finally, the interictal EEG is invariably normal in patients with breath-holding spells. Apneic seizures, which represent true epileptic attacks probably arising from the limbic system, can occur during both the waking and sleeping state. They are generally seen in neurologically damaged infants and are accompanied by EEG abnormalities. Treatment with anticonvulsants can be effective in apneic seizures. In the experience of Daoud and colleagues iron therapy significantly reduced the frequency of breath-holding spells, even though not all children who responded were iron deficient and not all iron-deficient children responded (806). Drug therapy for breath-holding spells is neither indicated nor effective, although atropine is said to be helpful in the pallid type of breath-holding spell. Donma, however, has found piracetam, a cyclic derivative of GABA, to be extremely effective in the control of breath-holding spells (807). These observations have not been confirmed. Basically, breath-holding spells are triggered by a disciplinary conflict between parent and child, with the child using the attacks or the threat of an attack to assert him- or herself and to express anger. Proper family counseling and assurance to parents that the attacks do not represent any danger to the child are often effective in stopping them (805). Although breath-holding spells disappear spontaneously in every case, many patients become prone to syncope and develop behavior disturbances, particularly temper tantrums. The incidence of true epilepsy in children with breath-holding spells, however, is no greater than is found in the general population. One of the most difficult problems confronting the clinician is the patient with paroxysmal episodes of aggressive and explosive behavior, a condition commonly termed episodic dyscontrol. In a significant proportion of cases, the first attack follows a head injury; in other instances, a history of temper tantrums, learning disabilities, and isolated seizures are seen. The neurologic aspects of this entity are reviewed more extensively by Rickler (808). |
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Êñòàòè, âîò ÷òî åùå èíòåðåñíî: ÍÑÏÂÏ (àñïèðèí, íàïð.) ýôôåêòèâíû ïðè ìèãðåíè è íåâðàëãèÿõ, à âîò ïðè àñòìå èìè ïàöèåíòà çàïðîñòî ìîæíî óáèòü, õîòÿ ñïåöèôè÷åñêèõ ðàçëè÷èé íà óðîâíå ìåäèàòîðîâ ïðîöåññîâ âîñïàëåíèÿ ïðè ýòèõ çàáîëåâàíèÿõ ïîêà íå íàéäåíî. Íî íåêîòîðûå ÍÑÏÂÏ ìîãóò òàêæå ñïîñîáñòâîâàòü âîçíèêíîâåíèþ ýïèëåïòè÷åñêèõ ïðèïàäêîâ. Ëþáîïûòíî âñå-òàêè... Öèòàòà:
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À ñ îïðåäåëåííîé è íåî÷åâèäíîé íà ïåðâûé âçãëÿä ñõîæåñòüþ ìåõàíèçìîâ è êëèíè÷åñêîé êàðòèíû ÀÐÏ è àñòìû äåëî îáñòîèò òàê: Ñîãëàñíî ñîâðåìåííûì ïðåäñòàâëåíèÿì, áðîíõèàëüíàÿ àñòìà ÿâëÿåòñÿ õðîíè÷åñêèì âîñïàëèòåëüíûì çàáîëåâàíèåì [1] ñ ïàðîêñèçìàëüíîé êëèíè÷åñêîé êàðòèíîé [2], è íåéðîãåííûå ôàêòîðû îêàçûâàþò áîëüøîå âëèÿíèå íà âîçíèêíîâåíèå è òå÷åíèå àñòìû [1, 3]. Ïîâûøåííûé òîíóñ áëóæäàþùåãî íåðâà ïðè àñòìå ÿâëÿåòñÿ ôàêòîðîì, ïðîâîöèðóþùèì áðîíõîñïàçì [1]. Òàêæå èçâåñòíî, ÷òî âûäîõ âî âðåìÿ ïðèñòóïà àñòìû ãîðàçäî áîëåå çàòðóäíåí, ÷åì âäîõ [4], ÷òî, ê ñîæàëåíèþ, íå ÿâëÿåòñÿ ïðåäìåòîì ñåðüåçíîãî àíàëèçà áîëüøèíñòâà ó÷åíûõ è êëèíèöèñòîâ, õîòÿ ïîõîæèå ñîñòîÿíèÿ ìîãóò áûòü ïîëó÷åíû ýëåêòðîñòèìóëÿöèåé ðàçëè÷íûõ îòäåëîâ ÖÍÑ [8, 9]. Àôôåêòèâíî-ðåñïèðàòîðíûå ïàðîêñèçìû (ÀÐÏ) ïðåäñòàâëÿþò ñîáîé ïàðîêñèçìàëüíûå ïðèñòóïû ýêñïèðàòîðíîãî àïíîý ïðè ïëà÷å ó äåòåé ðàííåãî âîçðàñòà. Ó äåòåé ñ ÀÐÏ, êàê è ïðè àñòìå, âî âðåìÿ ïðèñòóïà ïîâûøåí òîíóñ áëóæäàþùåãî íåðâà è çàòðóäíåí âûäîõ. ×àñòîòà ÀÐÏ ó äåòåé - 4 – 5% [5]. Òàêèì îáðàçîì, ïîâûøåííûé òîíóñ áëóæäàþùåãî íåðâà, ïàðîêñèçìàëüíàÿ êëèíè÷åñêàÿ êàðòèíà è çàòðóäíåííûé âûäîõ ÿâëÿþòñÿ õàðàêòåðíûìè êàê äëÿ àñòìû, òàêè äëÿ ÀÐÏ. Íà÷àëî ÀÐÏ â áîëüøèíñòâå ñëó÷àåâ ïðèõîäèòñÿ íà ïåðâûé ãîä æèçíè [5]. Àñòìà îáû÷íî íà÷èíàåòñÿ â áîëåå ïîçäíåì âîçðàñòå [6]. Èñõîäÿ èç ýòîãî, âîçìîæíî, ÷òî ÀÐÏ ìîãóò ïðåäøåñòâîâàòü ðàçâèòèþ àñòìû ó äåòåé. Äëÿ ïðîâåðêè íàøåãî ïðåäïîëîæåíèÿ ìû ðåøèëè èçó÷èòü ÷àñòîòó ÀÐÏ â àíàìíåçå äåòåé ñ áðîíõèàëüíîé àñòìîé, è ñðàâíèòü ïîëó÷åííûå äàííûå ñ ÷àñòîòîé ÀÐÏ â àíàìíåçå çäîðîâûõ äåòåé. È äàëåå: Ïîâûøåííûé òîíóñ áëóæäàþùåãî íåðâà òèïè÷íû äëÿ äåòåé êàê ñ àñòìîé, òàê è ñ ÀÐÏ. Èçâåñòíî, ÷òî ïîâûøåííûé òîíóñ áëóæäàþùåãî íåðâà ïðîâîöèðóåò ðàçâèòèå íåéðîãåííîãî âîñïàëåíèÿ â äûõàòåëüíûõ ïóòÿõ [7], ÷òî ÿâëÿåòñÿ õàðàêòåðíûì ïðè àñòìå [3]. Èìåííî ýòî è ìîæåò ëåæàòü â îñíîâå ýïèäåìèîëîãè÷åñêîé êîððåëÿöèè àñòìû è ÀÐÏ ó äåòåé: ïîâûøåííûé òîíóñ áëóæäàþùåãî íåðâà ó äåòåé ñ ÀÐÏ ìîæåò â äàëüíåéøåì ñïîñîáñòâîâàòü âîçíèêíîâåíèþ íåéðîãåííîãî âîñïàëåíèÿ äûõàòåëüíûõ ïóòåé, ÷òî è ìîæåò ïðèâåñòè ê âîçíèêíîâåíèþ àñòìû. 1. Global Initiative for Asthma. Global strategy for asthma management and prevention. National Institutes of Health, NHLBI/WHO workshop report, update 2004. 2. Canadian asthma consensus report. CMAJ 1999; 161 (11Suppl): S1-S5. 3. Groneberg DA, Quarcoo D, Frossard N, Fischer A. Neurogenic mechanisms in bronchial inflammatory diseases. Allergy, 2004; 59(11): 1139-1152. 4. Mathow E. New classification of bronchial asthma. Allergol Immunopath.1981; 9(3):241-256. 5. Ðàòíåð À.Þ. Ðîäîâûå ïîâðåæäåíèÿ íåðâíîé ñèñòåìû. Èçä. Êàçàíñêîãî Óíèâåðñèòåòà, 1985. 6. Mutius E von, Martinez FD. Epidemiology of Childhood Asthma. In: Pediatric asthma. Kelly HW, Murphy S, eds. Marcel Deccer, NY, Basel, 1999. 7. Morikawa M. Sekizawa K. Sasaki H. Inhibitory actions of cyclic AMP on neurogenic plasma extravasation in rat airways. Eur J Pharmacol 1993; 241(1): 83-87. 8. Æàóãàøåâà Ñ.Ê. Î âëèÿíèè ãàëèäîðà íà ýêñïåðèìåíòàëüíûé áðîíõîñïàçì. Ôàðìàêîëîãèÿ è òîêñèêîëîãèÿ, 1976, ¹ 1, ñ. 50-53. 9. Ïåêêåð È.Ë., Æàóãàøåâà Ñ.Ê., Áàëõàíîâà Ñ.À. Âëèÿíèå íåêîòîðûõ ëåêàðñòâåííûõ ïðåïàðàòîâ íà áðîíõèàëüíóþ ïðîõîäèìîñòü â ýêñïåðèìåíòå è êëèíèêå.  êí.: Ïàòîëîãèÿ îðãàíîâ äûõàíèÿ. Ë., 1975, ñ. 41-44. Öèòàòà:
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Íàñ÷åò ïèðàöåòàìà – ïî-ìîåìó, óæå îäîáðåí, õîòÿ ÿ íå óâåðåí â ýòîì. Íàñ÷åò óâàæàåìûõ ðóêîâîäñòâ – íå çíàþ, íî ñàì âèäåë, ÷òî â ãîñóäàðñòâåííîé êëèíèêå Christian Doppler Landesnervenklinic, Salzburg, Austria, â 1999 ãîäó ïèðàöåòàì â/â â êà÷åñòâå national guideline ïðèìåíÿëè â îñòðîì ïåðèîäå èøåìè÷åñêîãî èíñóëüòà. P.S. Ïðîøó ïðîùåíèÿ ó êîëëåã çà òî, ÷òî íà÷àë âðà÷åáíóþ äèñêóññèþ â ôîðóìå, ïðåäíàçíà÷åííîì äëÿ èíôîðìèðîâàíèÿ ïàöèåíòà. Sorry… |
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Peptidergic Nerves Peptidergic nerves in the lung are predominantly sensory. Sensory nerve endings contain neuropeptides including substance P and neurokinin A, which, when stimulated by specific action at irritant receptors, result in release of these peptides in the airway microenvironment. At the same time, action potentials are conducted toward the central nervous system to convey the presence of this irritant stimulus. However, as these action potentials cross the terminal ramifications of the airway nerves, antidromic conduction causes the release of the sensory peptides throughout the territory innervated by the specific axon dendrite. This action results in an effective local axon reflex in which sensory nerves serve a motor function. It is well established that both substance P and, to an even greater degree, neurokinin A can constrict airway smooth muscle, thus contributing to the asthmatic diathesis. In addition, these peptides can mediate bronchovascular leak, which may contribute to the pathobiology we recognize as asthma. In this setting it is important to understand an endogenous down-regulatory mechanism that keeps the physiological effects of these peptides in check. The membrane-bound enzyme neutral metalloendopeptidase (NEP, E.C. 3.4.24.11) is present in the microenvironment where the peptides are released from nerves. It has been shown in both animals and humans that the ability of this enzyme to cleave and inactivate the neuropeptides competes with the ability of neuropeptides to stimulate their specific receptors. It is thought, therefore, that the action of NEP is similar to the action of acetylcholinesterase on acetylcholine; i.e., it is a physiologically important enzyme limiting the expression of the biological actions of neuropeptides. It is of interest to note that conditions such as viral infections and exposure to certain pollutants are associated with decreased NEP activity, which would allow peptides cleaved by NEP not to be cleaved and their “proasthmatic” actions to be amplified. Ïàòîãåíåç àñòìû îòíþäü íå èñ÷åðïûâàåòñÿ. ß áû íå ñòàë äåëàòü èç èññëåäîâàíèÿ íà êðûñàõ, êîòîðûì ýëåêòðè÷åñêèì òîêîì ñòèìóëèðîâàëè âàãóñ êàêèõ-òî äàëåêî èäóùèõ âûâîäîâ Öèòàòà:
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Ó ÷åëîâåêà è îñüìèíîãà òîæå ìíîãî îáùåãî - ó ÷åëîâåêà âî ðòó åñòü ñëèçèñòûé îòðîñòîê, ó îñüìèíîãà èõ äàæå âîñåìü. È ÷åëîâåê è îñüìèíîã ìîãóò êîãî-òî çàäóøèòü. Îíè îáà óìåþò ïëàâàòü. Öèòàòà:
À ÷òî åùå ìîæåò ïðåäøåñòâîâàòü ðàçâèòèþ àñòìû ó äåòåé? Äàæå âûáîðû íîâîãî ïðåçèäåíòà Óðóãâàÿ ìîãóò ïðåäøåñòâîâàòü ðàçâèòèþ àñòìû ó äåòåé. Ñíà÷àëà èçáðàëè, à ïîòîì - àñòìà. Ïðè÷åì ó ìíîæåñòâà äåòåé Öèòàòà:
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À ïðîâåäåíèå àíàëîãè÷íîãî èññëåäîâàíèÿ ñ öåëüþ ïîäòâåðäèòü èëè îïðîâåðãíóòü ðåçóëüòàòû – îáùåïðèíÿòàÿ ïðàêòèêà. Êîòîðàÿ, óâû, óæå îòõîäèò â ïðîøëîå. Öèòàòà:
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È ïî÷åìó èìåííî 20 ñåêóíä? Ïî÷åìó íå 16,5 èëè íå 22? È êàê áûòü ñ õàðàêòåðîëîãè÷åñêèìè îòêëîíåíèÿìè, ïðèâåäåííûìè â ãëàâå, êîòîðóþ Âû ïðîöèòèðîâàëè? Îíè çàâèñÿò îò äëèòåëüíîñòè àïíîý? Êòî-íèáóäü ýòî äîêàçàë? Ïîéìèòå, ÿ âîâñå íå ãîâîðþ, ÷òî ëå÷åíèå àíòèêîíâóëüñàíòàìè - ñàìîå õîðîøåå. Âîçìîæíî, ëå÷åíèå àòðîïèíîì – ëó÷øå, ó ìåíÿ íåò ñîîòâåòñòâóþùåãî êëèíè÷åñêîãî îïûòà. Íî íåóâÿçîê è ðàçíî÷òåíèé â ïðèâåäåííûõ òóò öèòàòàõ ñòàòåé – õâàòàåò. Çíà÷èò, â äàííîì ñëó÷àå íåëüçÿ áûòü êàòåãîðè÷íûì: íå íàäî ëå÷èòü, è âñå òóò. ß íå íàñòàèâàþ, ÷òî ëå÷èòü íàäî ëèøü àíòèêîíâóëüñàíòàìè. ß ãîâîðþ î ëè÷íîì êëèíè÷åñêîì îïûòå è îïûòå òûñÿ÷ ìîèõ êîëëåã. À ïîäòâåðæäåííûõ ñâåäåíèé î íåýôôåêòèâíîñòè àíòèêîíâóëüñàíòîâ è î íåíóæíîñòè ëå÷åíèÿ ìåòîäàìè EBM – íåò. Âïðî÷åì, êàê è îáðàòíûõ ïîäòâåðæäåíèé. À íà íåò – è ñóäà íåò. Îñòàåòñÿ ëèøü êëèíè÷åñêèé îïûò âðà÷à. Öèòàòà:
À äîñòîâåðíûõ äîêàçàòåëüñòâ ñîãëàñíî EBM - íåò, Âû ïðàâû. |
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Letter to the Editor Carbamazepine in asthma: First do no harm! Î÷åíü ñïðàâåäëèâîå óòâåðæäåíèå,èìõî Êñòàòè â ýòîì æå íîìåðå èíòåðåñíàÿ ñòàòüÿ î ýâîëþöèè âçãëÿäîâ íà àñòìó. Óçíàëà, ÷òî åùå â 19 âåêå ñôîðìèðîâàëàñü âîñïàëèòåëüíàÿ êîíöåïöèÿ àñòìû, íî è "íåðâíàÿ òåîðèÿ" àñòìû èìååò äëèòåëüíóþ èñòîðèþ.  öåëîì ñîâðåìåííûå áðîíõîëèòèêè, òîæå êàê-áû äåéñòâóþò íà íåðâíûå îêîí÷àíèÿ (è âàãóñ â òîì ÷èñëå), íî àñòìó íå êîíòðîëèðóþò. Ïðè÷åì, íåñìîòðÿ íà âûñîêóþ ñåëåêòèâíîñòü è èíãàëÿöèîííûå ôîðìû. âñå ðàâíî èìåþò ïîáî÷íûå ýôôåêòû. |
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