TEMPOROMANDIBULAR JOINT PAIN-DYSFUNCTION SYNDROME: A RARE CAUSE OF HEADACHES IN ADOLESCENTS

The temporomandibular joint pain-dysfunction syndrome has received little attention in the literature on pediatric neurology. Five adolescents with this syndrome are reported, all of whom complained initially of headaches. In all cases the headaches were either continuous or daily and all patients had tenderness of the muscles of mastication and restricted or deviant jaw-opening. The literature is reviewed, and etiology, diagnosis and treatment are discussed. It is concluded that this is a rare but distinct syndrome which can cause headaches in adolescents, appears to have multiple etiologies and should be treated conservatively.     

IN VIVO ESTIMATION OF CHANGES IN DISTAL TUBULE FLOW AND THEIR ROLE IN DEXAMETHASONE-INDUCED KALIURESIS IN CONTROL AND POTASSIUM-ADAPTED RATS

The aim of this study was to determine whether the kaliuresis associated with glucocorticoids is due to a direct tubular action or is secondary to effects of glucocorticoids on distal tubule flow. A whole kidney technique was used to avoid the problem, inherent in microperfusion and micropuncture studies, of deciding whether (all) the appropriate nephron segment(s) are being studied. The method used was to determine the best whole kidney measure of distal tubule flow (the independent variable) by correlating this with the dependent variable (potassium excretion, corrected for differences in plasma potassium, UkV/PIK+) in conscious intact and adrenalectomized control and potassium-adapted rats. After an intragastric potassium chloride load, the correlation of UkV/PIK+ with UkV + UNaV was better than with either UNaV or UV, as measures of distal tubule flow. From the relationship a measure of potassium excretion independent of distal tubule flow can thus be calculated as UkV/PIK+ divided by (UkV + UNaV), defined as UK#. Measurement of UK# clearly demonstrates decreases in potassium excretion with adrenalectomy and increases in potassium excretion with aldosterone and in the potassium-adapted rat, consistent with described changes in potassium secretion. In contrast, with dexamethasone treatment, whilst there was an increase in UkV and UkV/PIK+, there was no change in UK# either in the control of potassium-adapted rats. These results suggest that the kaliuretic effect of dexamethasone cannot be attributed to direct tubular effects of glucocorticoids but rather can be explained by its effect on distal tubule flow.     

Effect of filming on tooth brushing performance in uninstructed adults in north-east England

Video recordings were obtained of 90 adults aged 18-22 yr brushing their teeth. Thirty subjects were unaware they were being filmed and 60 subjects had been informed that they would be filmed while they brushed their teeth. From repeated viewing of the tapes the areas of the mouth that were brushed, the total brushing time and the proportion of time spent brushing each of 16 areas of the mouth were obtained for each subject. Subjects who knew they were being filmed brushed significantly more mandibular occlusal surfaces, and lingual areas in both arches than subjects who were unaware they were being filmed. There was no significant difference in the mean toothbrushing time between the two groups. The informed group spent proportionally less time brushing posterior buccal areas and more time on occlusal and lingual areas than the group who were unaware they were being filmed, the difference being statistically significant for the mandibular arch areas. It was concluded that knowledge of filming alters toothbrushing behaviour to a small extent so that care should be taken when interpreting behavioural changes in future intervention studies.     

Airway Protection Following Simulated Gastro-Oesophageal Reflux In Sedated And Sleeping Neonatal Piglets During Active Sleep

1. In infants, promethazine has been implicated in the pathogenesis of sleep apnoea, apparent life threatening events (ALTE) and the Sudden Infant Death syndrome (SIDS). The aim of the present study was to investigate, in a neonatal animal, the effects of a commonly used promethazine-containing medication on airway protective mechanisms and cardiorespiratory reflexes following simulated gastro-oesophageal reflux (GER) to different levels in the oesophagus and pharynx. 2. Physiological and radiographic recordings were made in 21 naturally sleeping (controls) and 21 sedated (1.5 mg/kg, p.o., promethazine) piglets. On 3 consecutive days physiological recordings were made in all piglets during active sleep. Gastro-oesophageal reflux was simulated by the injection of boluses of 0.5 mL HCl, pH 2 or 3, or NaCl (0.9%) at 37 degrees C into the pharynx, upper or lower oesophagus. 3. In healthy neonatal piglets, minimal sedation with promethazine, which did not affect behaviour during wakefulness, revealed previously unreported findings during active sleep. 4. The most significant effects were observed following simulated GER to the pharynx, with no effect observed in the lower oesophagus. In sedated piglets, compared with naturally sleeping piglets, there was a significant reduction in swallowing (P < 0.01), delayed radiological clearance of fluid (P < 0.05), a reduction in breathing rate, oxygen saturation and heart rate and an increase in apnoea. 5. These findings are consistent with a low dose of promethazine producing a significant attenuation of airway protective mechanisms and, thus, stimulation of the laryngeal chemoreflex. The results suggest a mechanism for the association observed between promethazine use and the occurrence of ALTE and SIDS. The results support continued caution and suggest the need for greater regulation of promethazine-containing medications in infants.     

The haemotoxicity of azathioprine in repeat dose studies in the female CD-1 mouse

Azathioprine (AZA) is a cytotoxic immunosuppressive drug used in the prevention of rejection in organ transplants and the treatment of auto-immune diseases. However, AZA is haemotoxic causing significant bone marrow depression. The present studies were to characterize the haemotoxicity of AZA in the female CD-1 mouse. In Experiment 1, a dose-ranging study, with AZA gavaged daily for 10 days, clinical evidence of toxicity was evident at 125 mg/kg and above. Experiment 2 was a dose–response study with AZA gavaged daily for 10 days at 40–120 mg/kg. At day 1 after the final dose, AZA induced a dose-related pancytopaenia, reduced femoral marrow cellularity, increases in serum levels of the cytokine fms-like tyrosine kinase 3 ligand, reduction in granulocyte-monocyte colony-forming units and erythroid colonies, and increased bone marrow apoptosis. Histology demonstrated hepatocyte hypertrophy, thymic atrophy, reduced splenic extramedullary haemopoiesis, and reduced cellularity of sternal bone marrow. In Experiment 3, AZA was dosed for 10 days at 100 mg/kg with autopsies at 1, 3, 9, 22, 29, 43 and 57 days postdosing. At 1, 3 and 9 days, haematological parameters reflected changes in Experiment 2. At 22/29 days, many blood parameters were returning towards normal; at 43/57 days, most parameters compared with controls. However, there was some evidence of a persistent (i.e. residual/late-stage) mild reduction in RBC and erythroid progenitor cell counts at day 43/57. We conclude that the CD-1 mouse provides an acceptable model for the haemotoxicity of AZA in man.