Adolescent immunization: rationale, recommendations, and implementation strategies.
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Biomedical subjects
Publications and source records attributed to E Brink.
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On March 11-12, 1996, a workshop on how to implement new adolescent immunization (AI) recommendations was held in Atlanta, Ga. Sponsored by the Centers for Disease Control and Prevention, it was a collaborative effort of the National Immunization Program, the Division of Adolescent and School Health/National Center for Chronic Disease Prevention and Health Promotion, and the Hepatitis Branch/National Center for Infectious Diseases. The workshop brought together organizations and individuals interested in adolescent health and immunizations so they could address how new AI recommendations can be implemented most effectively. This article offers an overview of their discussions and suggestions, including issues of cooperation, education, legislation, and AI program development among health provider organizations, health department, schools, community groups and various other agencies relating to adolescent health services.
This article reports the results of a survey undertaken to determine the current level of collaboration between Women, Infants and Children (WIC) programs and immunization services. While the results of this study are encouraging, WIC needs to continue to place emphasis on using written or computerized immunization records for client screening, utilize available computer hardware and software to assist assessments, and expand the use of food voucher incentives as a strategy to improve coverage.
The technique of percutaneous microneurography was used to record from 60 mechanosensitive cutaneous afferents in patients (n = 5) who were recovering from acute Guillain-Barré syndrome (GBS) and who displayed residual sensory deficits in the hands. Recordings were obtained from median and ulnar nerves, between 1 and 31 months following plasma exchange therapy. The behaviour of all four types of cutaneous afferents known to innervate the glabrous skin of the normal hand (rapidly adapting types RA and PC and slowly adapting types SAI and SAII) was studied in response to mechanical skin stimulation. Some of the units could not be fully classified. Additionally, intradermal electrical stimulation was used to study conduction velocity and absolute refractory period. Abnormal response behaviour was encountered in RA, PC and slowly adapting afferents. The abnormalities consisted of a generation of only a single action potential to above threshold stimuli (RA), inability to follow high frequency vibration (PC) and, in slowly adapting afferents, reduced discharge rates during sustained skin indentations or cessation of discharge during indentation. Abnormally responding units were more frequently found in patients with marked, than in those with mild, clinical sensory symptoms. In the former, half of all units in each patient responded abnormally (12 out of 23 in total). In patients with mild symptoms, most units (33 out of 37) were normal in response behaviour as well as in other measures made: threshold to mechanical stimuli, static discharge rate, receptive field size, conduction velocity, absolute refractory period. Spontaneous activity of unknown origin was also encountered in some patients. The activity consisted of highly regular discharge bursts or relatively regular unitary discharges. The data indicate that the encoding capabilities of all types of cutaneous afferents (RA, PC, SAI and SAII) may be affected in GBS, contributing to the sensory deficits of the disease. The abnormal encoding most likely reflects a limited ability of the axons to conduct trains of action potentials.
The aim of the study was to investigate whether common or independent neuronal pathways are used to evoke primary afferent depolarization (PAD) from selectively activated group Ia and Ib afferents of different muscles. To this end, the spatial facilitation of effects of various afferents, indicating convergence on the same interneurons, was used as a test. Its occurrence was assessed on dorsal root potentials (DRPs) evoked in unspecified fibers or using intra-axonal recording from identified group Ia muscle spindle afferents or group Ib tendon organ afferents. Spatial facilitation has been found in PAD pathways a) from various Ia-afferents, whether of flexors or extensors; b) from various Ib-afferents, whether of flexors or extensors; and c) from flexor Ib-afferents and flexor or extensor Ia-afferents. In contrast, no indications have been found for common pathways from extensor Ib- and any Ia-afferents under conditions that proved effective in other combinations. Latencies of those components of PAD that appeared as a result of the spatial facilitation ranged from 2 to more than 7 ms, indicating that the convergence occurred in the shortest (trisynaptic) as well as longer pathways. The same patterns of convergence have been found in PAD pathways to extensor and flexor Ia-afferents (in experiments with intraaxonal recording from these afferents). The possibility might thus be considered that some neuronal pathways are used to modulate transmission via Ia-afferents independently of their muscle origin. The same might hold true for extensor and flexor Ib-afferents. Generally, it is concluded that the minimal number of distinct neuronal populations subserving PAD of group I afferents may be two to six. Additionally, actions of cutaneous, joint, and interosseous afferents on DRPs from Ia-afferents were reexamined to further the comparison between neurons mediating PAD and those mediating postsynaptic excitation or inhibition of motoneurons. Only depression of Ia DRPs followed stimulation of these afferents at intensities of 1.5-2.0 times threshold and higher; lower threshold afferents were apparently ineffective. On the basis of lack of convergence of extensor Ib and Ia muscle afferents and of low-threshold cutaneous afferents, interneurons mediating PAD may thus be distinguished from the interneurons subserving Ib and Ia-like-Ib postsynaptic actions in motoneurons. The latter are coexcited by these three groups of afferents.
The technique of recording post-synaptic potentials from a population of motoneurones, by recording from ventral roots perfused with isotonic sucrose, has been applied to investigate the action of single last-order interneurones; the target motoneurones were in either caudal L7 or S1 segments. Using spike-triggered averaging, the inhibitory action of 70% of previously identified last-order interneurones (Renshaw cells and lamina VII Ia inhibitory interneurones) has been detected. Previous observations had suggested that interneurones mediating disynaptic non-reciprocal inhibition from group I muscle afferents should be characterized by (i) location in laminae V-VI, (ii) monosynaptic group I input and (iii) ascending collateral axonal projection to upper lumbar segments. 65% of interneurones with these characteristics were found to inhibit motoneurones. In addition, spike-triggered averaging from this group of laminae V-VI interneurones sometimes revealed a depolarizing potential which preceded the inhibitory potential evoked by the interneurone. The depolarizing potential is interpreted as being due to the action of some presynaptic fibres which branch to innervate both the investigated interneurones and motoneurones.
A hypothesis has been verified that laminae V-VI interneurones which mediate non-reciprocal inhibition of motoneurones from group I muscle afferents have collateral actions on other laminae V-VI interneurones. Stimulation within the areas of projection of these inhibitory interneurones in motor nuclei and in Clarke's column would be expected to give rise to monosynaptic i.p.s.p.s in interneurones with disynaptic i.p.s.p.s from group I afferents if the hypothesis were correct. Intracellular records were made from eighty-five laminae V-VI interneurones with input from group Ia muscle spindle and/or group Ib tendon organ afferents. Weak intraspinal stimuli applied in motor nuclei in L7 and S1 segments, or in the lateral funiculus just caudal to Clarke's column in L4, were found to evoke monosynaptic i.p.s.p.s in seventy-two interneurones. These i.p.s.p.s were systematically correlated with disynaptic inhibition from group Ia or Ib afferents but not from other fibres. Such monosynaptic i.p.s.p.s evoked by intraspinal stimuli were seen in forty-two interneurones which themselves projected to the level of Clarke's column and therefore (on the basis of previous evidence) should mediate inhibition of motoneurones. For seven of these interneurones it was also shown directly that they projected to motor nuclei. The inhibition of such interneurones demonstrates mutual interactions between those interneurones which are interposed in inhibitory pathways from group I afferents. Only indirect indications have been obtained for inhibition of interneurones in the excitatory pathways.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.