Comparative study of two types of exercise treatment for paroxysmal positioning vertigo.
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Biomedical subjects
Publications and source records attributed to A Beckers.
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Hormone production was studied in situ by immunocytochemical methods in 20 pituitary adenomas. Special attention was given to 13 adenomas removed from acromegalic patients. Out of them, 6 had mild to moderate hyperprolactinemia. Immunohistochemistry revealed PRL-containing cells without any close relationship with high PRL serum level in 6 patients. Double immunogold staining revealed mammosomatotrope cells characterized by simultaneous presence of GH and PRL in the same granules in 2 patients. Since mammosomatotropes have never been demonstrated in the normal pituitary, our results probably signify gene dysregulation in pituitary cells of those acromegalic patients.
The use of exercises can be an excellent method for treating benign paroxysmal positional vertigo (BPPV). We compared the results obtained by a progressive training method, vestibular habituation training (VHT), with a brisk exercise method. While VHT can be applied in all kinds of "provoked" (positional) vertigo of peripheral origin, the brisk method can be used only in typical BPPV, provided the vertigo is unilaterally provoked. A series of patients with such typical "unilateral" cases were treated by the brisk method and were compared with a second series of identical cases treated by the VHT technique. The results after 1 week seemed to be different: with the brisk method 52% of the patients were free of vertigo, while only 32% with VHT were vertigo free. This difference is not statistically significant. However, those cases treated by VHT and still having vertigo after 1 week had a striking reduction in the severity of their vertigo, as estimated by the score-system used. In contrast, the scores were unchanged for those cases not responding to the brisk method. Continuation of treatment of these latter cases using VHT exercises showed that the final result after 6 weeks was equal for both groups.
Vestibular Habituation Training (VHT) is the treatment of choice for paroxysmal positional vertigo (ppv). The origin of the disturbance is peripheral and the data observed in the cases treated confirm that it is not located in horizontal canal function. However, canal dysfunction can be present together with ppv. Usually a separate course is observed for the phenomena attributed to horizontal dysfunction and those to the ppv lesion. The specificity of the Dix-Hallpike manoeuvres linked to the typical ppv is also confirmed by the data obtained by testing for VHT (VHT-test-battery). Ppv can have a repercussion upon the vestibulospinal reflex. That the same ppv disturbance can coincide with normal as well as with abnormal posturographic data, pleads for the intervention of central adaptive mechanisms. The effect of VHT is due to stimulation of these central adaptive mechanisms and not to any impact upon the peripheral lesion.
Balance dysfunction may be a cause of falling in the elderly. Disturbance of the vestibular system may have a repercussion upon balance performance, causing instability. Unilateral vestibular hypofunction (UVH) and its disturbing influence upon the vestibulospinal reflex (VSR), measured by the postural sway, has been studied. This influence is dependent on the interfering action of central adaptive and compensatory mechanisms. This central compensation may be different for vestibulo-ocular reflex (VOR) and the VSR. This comparative study shows that the elaboration of compensation in elderly people is less efficacious at the VSR level than at the VOR level. The influence of visual fixation is also stressed by comparing the posturographic recordings made with eyes open and eyes closed.
Two vestibular syndromes comprising attacks of spontaneous vertigo were studied and disturbance of the vestibulospinal reflex was evaluated. Patients with Menière's disease were examined between attacks and patients with a sudden unilateral vestibular loss syndrome at least 3-4 weeks after the initial attack. Posturography, (recording and analysing the postural sway) was used to evaluate the influence of these disorders upon the vestibulospinal reflex. In 50% of the patients, the postural sway was disturbed compared with the performance of a normal control group. Menière's disease had a more pronounced effect on the posturographic results, whereas for the unilateral vestibular loss syndrome the rotation tests showed more asymmetry. It is obvious that the effect upon the vestibulospinal reflex cannot be deduced from the rotational test results. Indeed in a large number of patients discordance between rotational test results and posturography was seen. The presence or absence of attacks during the previous year in patients with Menière's disease had no influence on the presence of abnormal posturographic results. If other complaints of dizziness were mentioned by the patient, posturography was nearly always abnormal. It is evident that a complete evaluation of such patients must include information obtained by posturography.
A number of cases with typical positioning vertigo (BPPV) show a unilateral vestibular hypofunction (UVH) by caloric testing. However, treatment by habituation exercises (VHT) improves vertigo independently of the presence of UVH. Moreover, VHT has no influence upon the results of caloric and rotation tests. These findings prove the independence of the pathogenetic mechanisms of the peripheral vestibular disturbances UVH and BPPV.
Posturographic recording with the patient's head in retroflexion has been proposed as a reliable test for diagnosing cervical vertigo. The clinical experience suggests that a positive result in this test-condition could be accepted as suggestive for cervical involvement, when other data corroborate it, but that it is not per se pathognomonic. In fact, this test is negative in most cases with other cervical indications, whereas it has been found positive, in cases with no cervical indications. A positive test, however, is significantly more frequent in "cervical" cases. On the other hand, otolithic influence upon the test-performance has also to be taken into account.
Peripheral vestibular pathology disturbs the vestibulospinal reflex in a number of cases. The recording of postural sway furnishes an evaluation of this vestibulospinal influence. Two common peripheral vestibular syndromes were studied: Ménière's disease and peripheral unilateral vestibular hypofunction. It is evident that, by posturography, vestibulospinal disturbance is shown in these peripheral syndromes, whereas its occurrence cannot be predicted by other tests, e.g. caloric and rotation tests. Normalization of the vestibulospinal reflex depends on central adapting mechanisms, which were evidently still incomplete in a number of the cases examined. Whereas abnormal postural results were equally observed in both groups, rotation tests showed better vestibulo-ocular compensation in Ménière's disease, compared to the cases with unilateral vestibular hypofunction. It mattered not whether the Ménière patient was in an active or a stabilized phase. A striking difference was noted for those Ménière patients with atypical vertigo complaints, who showed a high frequency of posturographic disturbances.
Presentation of a 48-y old woman who developed a neuroendocrine tumor of the nasal cavities. This lesion progressed rapidly despite an extensive resection and repeated chemotherapy. The patient refused radiotherapy. Before her death, 28 months later, she exhibited a paraneoplastic Cushing-like syndrome. At autopsy, restricted to the brain, there was a 5 cm diameter tumor invading the frontal area without alteration of the hypothalamus or the pituitary gland. Routine histology and electron microscopy confirmed the neuroendocrine nature of the tumor. Immunohistochemistry revealed the tumor to be positive only for neurone specific enolase, negative for S-100 protein, neurofilament and ACTH. The pituitary gland was positive for most usual hormones (GH, PRL, TSH, LH, FSH) but only few cells were slightly positive for ACTH. Many Crooke cells were observed. These findings suggest that the tumor secreted an ACTH-like substance (not detected actually by immunochemistry) that stimulated the activity of the adrenal cortex but inhibited normal production of ACTH at the pituitary gland level.
In eight hyperprolactinemic amenorrheic women who had a microprolactinoma, LH secretion was examined by measuring its concentration in blood samples collected every 15 min for 6 h before and 8 days after successful selective adenomectomy. Computer analysis was used for LH peak evaluation. In both circumstances, serum PRL and basal estradiol (E2) levels were also determined. Before operation, the number of LH peaks ranged from zero to one per 6 h in seven patients and was two per 6 h in the eighth patient. In all patients, serum PRL was normal on the eighth postoperative day, while E2 levels remained low, similar to the values usually found in the early follicular phase of the cycle in normal women. Postoperatively, mean LH levels were similar to preoperative levels, but there was a dramatic increase in the number of LH peaks (three to five per 6 h) in five of the eight patients. These observations confirm the impairment of LH pulsatility in hyperprolactinemia and demonstrate that normalization of PRL levels by surgery can restore LH pulsatile secretion in certain women as early as the eighth day after operation in the absence of a significant change in serum E2 levels. Thus, the preoperative impaired pulsatility of LH secretion was probably a central effect of hyperprolactinemia.
This retrospective study concerns 40 patients with an apparently nonsecretory pituitary adenoma who were operated on during an 11-yr period from 1971 to 1981. Among them, 6 men had elevated serum FSH levels. LH levels were normal in 5 and slightly elevated in 1. Testosterone levels were low in 2 patients and within normal limits in 2 others. Sexual impotency had developed from 6 months to 1 yr before surgery in all patients. Primary hypogonadism could be eliminated on clinical grounds (recent onset of hypogonadism, previous fertility of 5 of the 6, and postoperative improvement). After transsphenoidal adenomectomy, FSH levels returned to normal values in all, and clinical recovery occurred in most patients. Tumor tissue obtained at operation stained positively for the gonadotropins, but was negative for other pituitary hormones in all patients. The most probable explanation for these findings was that the tumors were responsible for the elevated FSH secretion. This explanation is supported by the immunocytochemical identification of gonadotropin-containing cells in the tumors. We conclude that these 6 men from a series of 40 patients who presented with pituitary tumor but no GH, PRL, or ACTH hypersecretion had primary gonadotropinomas.
Human pituitary adenomas were fixed in glutaraldehyde and embedded in epon. Ultrathin sections were incubated either with anti-hGH, anti-hPRL or anti-hLH. They were incubated with second step goat anti-rabbit immunoglobulins linked to gold particles. Two PRL secreting adenomas, one GH and PRL secreting adenoma, one ACTH secreting adenoma and two non secreting adenomas were studied. The specificity and the limits of the method were discussed in relation with the results obtained in light microscopy with the PAP method.
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Albino rats and white mice were infected with populations of Trypanosoma brucei gambiense isolated from patients in four different areas in Central Africa. Differences in virulence as shown by the level of parasitaemia, number of relapses, and length of survival time, were observed amongst the stocks according to their geographical origin and secondarily to the degree of adaptation to the rodents. All the stocks are pathogenic for the laboratory rodents, and the presence of extravascular trypanosomes in the brain was confirmed in all infected animals. Spleen, liver, and kidneys were less constantly found to be positive. The morphology of the extravascular parasites was highly variable, ranging from long slender trypomastigotes to spheromastigotes and even amastigotes.
Histopathological findings on brain, heart, liver, and spleen of albino rats and white mice, infected with different stocks of Trypanosoma brucei gambiense of human origin are presented. Classical brain lesions, including chronic inflammation of the choroid plexuses, were observed in all infected animals, the severity of which increased with the chronicity of the disease. Parasite stocks which gave rise to a less acute course of the disease more often induced myocarditis, while brain lesions were less pronounced, suggesting that virulence of the parasites is more closely related to the advent of myocarditis than to the appearance of brain lesions. Liver lesions were not obvious. In spleens, a variable and often very pronounced degree of lymphoid hyperplasia was observed.
Two recently isolated stocks of Trypanosoma brucei gambiense of human origin gave rise to a moderate to severe proliferative or membranoproliferative glomerulonephritis in 40 or 44 NMRI and C57BL/6J mice infected for 7-22 weeks. Extensive granular deposits of C3, IgG1 and IgG3 were found in the mesangium, together with smaller quantities of IgG2a, IgG2b, and IgM. No trypanosomal antigen could be detected in the deposits though specific anti-trypanosoma antibodies were found in kidney eluates. By electron microscopy, a conspicuous proliferation of mesangial and endothelial cells was observed and electron-dense deposits were seen in a mesangial and subepithelial localization. With one of these trypanosome stocks, four of seven Wistar rats infected for 9-15 weeks developed morphologically similar glomerular lesions. Four other trypanosome stocks did not evoke renal alterations in 17 other rats infected for 13-56 weeks. Experimental infection in mice or rats appears to be a suitable model for the study of renal disease in chronic African sleeping sickness.