Comparison of the use of nalbuphine and fentanyl during third molar surgery

In a double-blind, randomized plan of drug administration, nalbuphine, fentanyl, and a placebo were compared for efficacy in sedation and analgesia during third molar removal. Fifty-eight patients participated in this study. Using accepted intravenous sedation and surgical techniques, fentanyl and nalbuphine were found to be better than placebo for anxiety and pain control in third molar surgery. Fentanyl had a longer duration of pain relief postoperatively than did nalbuphine. The study confirmed the need for a narcotic supplement to sedation techniques for third molar surgery.     

Organization of amygdaloid projections to the mediodorsal thalamus and prefrontal cortex: a fluorescence retrograde transport study in the rat

Previous studies have shown that the amygdala projects to both the mediodorsal thalamic nucleus (MD) and its cortical projection area, the prefrontal cortex (PFC). In this investigation rats received injections of different fluorescent retrograde tracers (true blue and diamidino yellow) into MD and either the lateral, polar, or medial PFC in order to examine the relationship of amygdaloid neurons with cortical and/or thalamic projections. PFC injections labeled neurons in the basolateral (BL), basomedial (BM), ventral endopiriform (EnV), and rostral lateral nuclei as well as the periamygdaloid cortex (PAC) and the medial part of the amygdalohippocampal area (AHA). In BL, which contained the great majority of neurons projecting to PFC, most labeled cells were concentrated in particular parts of the nucleus and were topographically organized. The overwhelming majority of labeled neurons in BL were large pyramidal or piriform cells that correspond to class I neurons described in Golgi studies. Occasional small neurons with thin dendrites were also observed; these cells may be class II neurons. MD injections labeled numerous cells in the anterior division of the cortical nucleus, medial nucleus, and caudomedial part of the central nucleus. Moderate numbers of labeled cells were found in caudal portions of BM and PAC, whereas scattered cells were observed throughout the rest of the amygdala with the exception of the lateral nucleus. In BL and AHA many MD-projecting neurons were observed along nuclear boundaries and in the adjacent white matter. Neurons in BL, BM, and AHA usually had large elongated or irregular somata and two to four primary dendrites that branched sparingly. Other cells had smaller ovoid somata. The morphology and distribution of MD-projection cells in the basolateral amygdala indicate that they are primarily large class II neurons. Double-labeled amygdaloid neurons, labeled by both cortical and thalamic injections, were observed only in a small number of animals. Control experiments suggest that most of the double-labeled cells in these cases were artifacts caused by spread of the thalamic injectate into the third ventricle with subsequent uptake by fibers in the anterior commissure. Thus the findings of this study suggest that different neuronal populations in the amygdala project to the two poles of the MD-PFC system. In the basolateral amygdala class I neurons are the predominant cell type involved in PFC projections, whereas a subpopulation of class II neurons, hitherto thought to be primarily local-circuit neurons, project to MD.     

Neurotransmitters and neuropeptides in Alzheimer's disease.

The neurotransmitter and neuropeptide changes in Alzheimer's disease are outlined in Table 1. Many of the changes, such as decreases in CSF ACh and SRIF, are well documented and correlate with the severity of the dementia; however, they are relatively nonspecific. The changes in neurotransmitter availability have offered new insight into both the pathophysiology and possible treatment strategies in Alzheimer's disease. It is evident that the disease is characterized by pathologic involvement of multiple neurotransmitter systems, including those that utilize ACh, SRIF, CRF, and, most probably, monoamines and excitatory amino acids. The role each system has in the signs and symptoms of Alzheimer's disease remains obscure.     

Complications of endodrainage retinotomies created during vitreous surgery for complicated retinal detachment

The authors report nine cases of endodrainage retinotomy site complications that occurred after vitreous surgery for complicated retinal detachments (RDs). Postoperative subretinal neovascularization developed in four eyes at the retinotomy drainage site. In two eyes, postoperative proliferation at a posteriorly placed endodrainage site created traction macular detachments. Redetachment due to retinotomy opening caused by postoperative drainage site proliferation developed in three eyes. The retinas of all nine eyes were eventually reattached, and vision improved from the preoperative level. These complications are related to retinal pigment epithelium and/or Bruch's membrane damage during internal subretinal fluid drainage and retinotomy endolaser photocoagulation. Careful evaluation of extrusion instruments, drainage techniques, retinotomy placement, and subsequent endolaser treatment is necessary to minimize these complications.     

A reassessment of the risk of multiple sclerosis developing in patients with optic neuritis after extended follow-up.

One hundred and one of 146 patients presenting with isolated idiopathic optic neuritis, previously reviewed in 1978, were reassessed clinically, and retyped for HLA antigens and Factor B alleles, after a mean follow-up of 11.6 years. Fifty eight patients (57%) had developed multiple sclerosis at the time of reassessment in the present study, of whom 51 (88%) had clinically definite disease. This compared with 40% of the original group, in 1978, of whom 62% then had clinically definite multiple sclerosis. When the life-table method of analysis was used, the probability of developing multiple sclerosis was 75%, 15 years after the initial episode of optic neuritis. The frequencies of HLA-DR2 and the recently defined D-region antigen, DQw1, were significantly increased in patients with isolated optic neuritis and those who subsequently developed multiple sclerosis compared with normal controls, but neither allele appears to influence progression from optic neuritis to multiple sclerosis. Patients with optic neuritis who were HLA-DR3 positive had an increased risk for the development of multiple sclerosis (RR = 2.8) and this risk was further enhanced when DR3 occurred in combination with DR2 (RR = 6.7). The overall increased risk of developing multiple sclerosis for patients with this combination was 26 times that for the normal population. When the patients' original tissue-typing was considered BT 101 no longer influenced conversion of optic neuritis to multiple sclerosis. This may partly be explained by improved methods of tissue-typing, since not all BT 101 patients were subsequently found to be positive for HLA-DR2 or HLA-DQw1 and vice versa and by extended follow-up as multiple sclerosis conversion in HLA-DR2 negative individuals increased with time. All 101 patients were typed for Factor B alleles. No significant differences in frequencies were found between individuals with isolated optic neuritis or those who progressed to multiple sclerosis compared with the control population. Recurrent episodes of optic neuritis were associated with an increased risk for the development of multiple sclerosis in this study.     

Substance P-immunoreactive sensory axons in the rat respiratory tract: a quantitative study of their distribution and role in neurogenic inflammation.

Substance P is one of the peptides released from sensory nerves that mediate "neurogenic inflammation." Although substance P-immunoreactive (SP-IR) axons are known to be present within the mucosa of the respiratory tract, the relative extent of the innervation of various components of the mucosa is not known. Therefore, we determined the distribution and number of SP-IR axons in the rat trachea and bronchi, by using immunohistochemistry on tissue whole mounts. Specifically, we sought to learn whether these axons directly innervate the postcapillary venules involved in neurogenic plasma extravasation, the arterioles involved in neurogenic vasodilatation, and the airway smooth muscle involved in bronchoconstriction in pathogen-free, adult male F344 rats. We found that 90% of the SP-IR axons were single axons, usually having varicosities. Eighty-five percent of these were in the epithelium, 6% innervated arterioles, and the remainder elsewhere in the lamina propria. Only 10% of the mediator-sensitive postcapillary venules (i.e., venules labeled with Monastral blue pigment after challenge with capsaicin or substance P) were within 10 microns of SP-IR axons. SP-IR axons were more than 10 times as frequent in the smooth muscle of the distal bronchi as in the trachea. Capsaicin pretreatment (168 mg/kg over 7 days) reduced the number of SP-IR axons in the trachea by 96%, which is consistent with their being sensory. Unilateral vagotomy reduced the number of SP-IR axons bilaterally in the trachea and ipsilaterally in the main stem bronchus. Using an antibody to Protein Gene Product 9.5 as a nonspecific marker for all nerves in the trachea, we determined that SP-IR axons constituted 90% of the axons in the epithelium, 32% of the axons on arterioles, and only 4% of the axons in the smooth muscle. We conclude that most SP-IR nerves in the trachea are sensory axons and most of these axons end in the epithelium. SP-IR axons innervate mucosal arterioles, but few innervate postcapillary venules. Therefore, the mechanism by which sensory axons evoke plasma extravasation from these venules is likely to involve the diffusion of the peptide or a secondary mediator from the epithelium or from the arterioles upstream.     

Anticytoplasmic autoantibodies in the diagnosis and follow-up of Wegener's granulomatosis

Sixty-five patients with biopsy-proven Wegener's granulomatosis (WG), 54 with systemic vasculitis, 22 with relapsing polychondritis, 20 with sarcoidosis, 20 with malignant pulmonary lesions, and 15 with other conditions underwent determination of anticytoplasmic autoantibodies (ACPA) by the indirect immunofluorescence technique on neutrophil cytospin preparations to assess the specificity of ACPA for WG, their sensitivity in relationship to the extent and activity of the disease, and their value for follow-up of WG. Of these 65 patients with WG, 38 were ACPA positive. Two patients in the vasculitis group, best categorized as having microscopic polyarteritis, were ACPA positive. We obtained 125 serum samples from the 65 patients with WG and assigned them to one of two categories (limited or generalized), based on the extent of disease. Each of these categories was then subdivided into "active" or "in remission." Median ACPA titers were significantly different between active disease and remission in each category, as well as between active limited and active generalized disease. All patients whose disease changed from active to in remission had reductions in ACPA titer levels; those who experienced flares had titer increases. Patients with intercurrent illnesses or complications of treatment, mimicking WG flares, did not have titer increases. We conclude that ACPA determined by the indirect immunofluorescence technique is highly specific for WG. The sensitivity is dependent on the extent and activity of WG, and serial titer determinations are valuable in monitoring disease activity.