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In cochlear implant simulation with vocoders, narrow-band carriers deliver the envelopes from each analysis band to the cochlear positions of the simulated electrodes. However, this approach does not faithfully represent the continuous nature of the spiral ganglion. The proposed "SPIRAL" vocoder simulates current spread by mixing all envelopes across many tonal carriers. SPIRAL demonstrated that the classic finding of reduced speech-intelligibility benefit with additional electrodes could be due to current spread. SPIRAL produced lower speech reception thresholds than an equivalent noise vocoder. These thresholds are stable for between 20 and 160 carriers.

S. L. Harris, BSc, PhD, K. Mansfield, BSc, D. A. Marston, BSc, N. Johnson, BSc, PhD, K. Pajamo, BSc, N. O’Brien, BSc, MSc, C. Black, L. M. McElhinney, BSc, MSc, PhD, A. R. Fooks, BSc, MBA, PhD, CBiol, FiBiol, Rabies and Wildlife Zoonoses Group, WHO Collaborating Centre for the Characterisation of Rabies and Rabiesrelated Viruses, Veterinary Laboratories Agency – Weybridge, New Haw, Addlestone, Surrey KT15 3NB

Antibodies to factor XII (FXII) have previously been identified in some patients who were lupus anti-coagulant-positive. The relationship between these antibodies and FXII levels appeared to be variable. The aim of the present study was to confirm the presence of antibodies to FXII in patients with well characterized antiphospholipid syndrome (APS) and to establish their potential effect on levels of FXII. Forty-two patients with APS were studied; 21 patients were found to have either immunoglobulin (Ig)G or IgM antibodies to FXII by enzyme-linked immunosorbent assay (ELISA) using a highly purified preparation of FXII (99% pure). Levels of FXII were statistically significantly lower (P = 0.02) in patients with antibodies to FXII when compared with patients without antibodies to FXII (median = 91 micro/dl, s.d. = 39.1, median = 122 micro/dl, s.d. = 41.1 respectively). Four of the 21 patients with antibodies to FXII were found to have FXII levels below the laboratory normal range. Antibodies to FXII are present in significant numbers of patients with APS and may lead to acquired FXII deficiency.

We report on the transient, patterned expression of p75 in the ventrobasal (VB) thalamus, the major thalamic relay for somatosensation. We immunostained the brains of developing rats ranging in age from embryonic day (E) 14.5 to postnatal day (PD) 15 with an antibody against p75. To compare p75 expression with the developing synaptic organization within VB, we also immunolocalized the synaptic-vesicle-associated protein, synaptophysin (SYN), on alternate sections. p75-immunoreactivity (IR) was dense and uniform in the ventroposterior medial nucleus (VPM) in the late embryonic and early postnatal periods (E 16.5 to PD 3). In contrast, from PD 4-10, p75-IR in the VPM was patterned, reminiscent of cytochrome-oxidase-stained barreloids, a characteristic feature of the VB in rodents. By PD 14, p75-IR in the VPM was no longer detectable. The ventroposterior lateral nucleus (VPL), in contrast, exhibited no p75-IR. No p75-IR was detected in the ventroposterior lateral nucleus (VPL) at any developmental stage in which VPM could be distinguished from VPL. Light, but clearly patterned SYN-IR, first detectable on PD 2-3, increased in intensity in both VPL and VPM through PD 15. Sectioning the infraorbital nerve on PD 0 resulted in blurred patterns of p75- and SYN-IR within VPM in PD 7-9 rat pups. Removing large portions of the somatosensory cortex on PD 0 resulted in subsequent greatly reduced p75- and SYN-IR within VB. To specify the source of the p75-IR terminals, we stereotaxically injected into the VPM of PD 4-5 rats a monoclonal antibody to p75. One to 2 days later, IR of retrogradely transported p75 antibodies could be traced within axons and cell bodies of neurons associated with the trigeminothalamic pathway through the caudal diencephalon and mesencephalon; labelling was confined to the contralateral trigeminal principal sensory nucleus. The observed, transiently patterned p75-IR in VPM the early postpartum period suggests a role for p75 in synaptogenesis and pattern formation.

The predictive power of age and IQ at time of admission to an intensive treatment program using applied behavior analysis were examined in a 4- to 6-year follow-up of educational placement. Twenty-seven children with autistic disorder who were between the ages of 31 and 65 months and had IQs on the Stanford Binet between 35 and 109 at time of admission to the Douglass Developmental Disabilities Center were followed up 4 to 6 years after they left the preschool. The results showed that having a higher IQ at intake (M = 78) and being of younger age (M = 42 months) were both predictive of being in a regular education class after discharge, whereas having a lower IQ (M = 46) and being older at intake (M = 54 months) were closely related to placement in a special education classroom. The results are interpreted as pointing to the need for very early intervention for children with Autistic Disorder. It is also emphasized that older children and those with lower IQs in the present study showed measurable gains in IQ from treatment. The data should not be taken to suggest that children older than 4 years of age do not merit high quality treatment.

The family physician is often the primary source of continuing guidance for the parents of autistic, schizophrenic, or brain-damaged children. It is essential to anticipate problems in such areas as use of medication, early education, reactions of siblings, and stresses within the lives of the parents. The family physician can help parents find the resources to cope with the multitude of problems confronting them and their children.