Emergency orthodontic treatment after the traumatic intrusive luxation of maxillary incisors.

Treatment of traumatically intruded teeth is based largely on empirical clinical experience rather than on scientific data. The aim of this qualitative meta-analysis was to provide an evidence base to evaluate the orthodontic repositioning approach. In a MEDLINE search of the literature in English, 14 reported patients involving 22 teeth were found to have been treated by this modality. Additionally, 3 new patients, involving 9 intruded teeth and presented herein, were combined to form a total study sample of 17 subjects (7 girls, 10 boys, aged 8.9 +/- 1.2 years). Orthodontic extrusive forces were applied in the immediate posttrauma period (up to 3 months), with a variety of orthodontic appliances. Repositioning was achieved for 90.3% of the affected teeth but failed in 9.7% because of inflammatory resorption (2 teeth) or a misdiagnosis of root fracture (1 tooth). Early complications included loss of pulp vitality and external root resorption. All intruded teeth with closed root apices lost their vitality regardless of the degree of intrusion, whereas among those with incomplete apices, 45.5% that had been moderately intruded remained vital. External resorption was encountered in 54.8% of the teeth. Loss of marginal bone support was rarely encountered. Late complications included inflammatory root resorption in teeth with closed apices, in which endodontic treatment was not initially performed, and obliteration of the pulp tissue in teeth that remained vital. The results show that this method is superior to other treatment alternatives.     

Detecting pediatric autoimmune neuropsychiatric disorders associated with streptococcus in children with obsessive-compulsive disorder and tics.

BACKGROUND: A subgroup of children with obsessive-compulsive and tic disorders are proposed to have an infectious trigger. The purpose of this study was to investigate the relationship between group A streptococcal titers and symptom fluctuations in children with a clinical course resembling that described for pediatric autoimmune neuropsychiatric disorders associated with streptococcus. METHODS: Twenty-five children with obsessive-compulsive disorder and/or tic disorder were evaluated for neuropsychiatric severity and group A streptococcal antibody titers (streptolysin O, deoxyribonuclease B, and carbohydrate A) at 6-week intervals for > or = six consecutive evaluations (total visits=277). RESULTS: Children with large symptom fluctuations (n=15) were compared with children without dramatic fluctuations (n=10). Co-movements of obsessive-compulsive/tic severity and group A streptococcal antibodies were assessed. In subjects with large symptom changes, positive correlations were found between streptococcal titers and obsessive-compulsive severity rating changes (p=.0130). These subjects were also more likely to have elevated group A streptococcal titers during the majority of observations (p=.001). Tic symptom exacerbations occurred more often in the fall/winter months than spring/summer months (p=.03). CONCLUSIONS: Patients with marked obsessive-compulsive/tic symptom changes may be characterized by streptococcal titer elevations and exhibit evidence of seasonal tic exacerbations.     

Optimal use of electroconvulsive therapy: choosing a treatment schedule.

Choice of treatment schedule is an important component of the ongoing efforts to optimize electroconvulsive therapy (ECT) administration and thereby maximize therapeutic benefit while reducing cognitive adverse effects. Frequency of ECT administration (that is, the spacing between treatments) and the total number of treatments in a series are the two factors that define the ECT schedule. Available evidence supports the view that a schedule of twice weekly ECT with a total of six to eight treatments is an effective therapeutic regiment that potentially reduces cognitive morbidity associated with more frequent administration and a larger number of treatments. More frequent administration, however, may accelerate antidepressant response and may be indicated in cases in which rapidity of therapeutic effect is a significant clinical consideration. This consideration may be at the cost of greater cognitive impairment, which could be reduced by limiting the number of treatments administered. Aside from their clinical relevance, these issues have important implications for understanding the mechanisms of action of ECT.     

Adjunct endarterectomy of the left anterior descending coronary artery

During a three-year period, complete revascularization of diffusely diseased left anterior descending (LAD) coronary arteries was accomplished by extensive endarterectomy in conjunction with bypass grafting in 37 patients in whom conventional bypass was not feasible. This group constituted 7.0% of all patients undergoing nonemergency coronary revascularization during this period. The left internal mammary artery was used to bypass the endarterectomized LAD artery in 22 patients. There was 1 (2.7%) operative death and 1 perioperative myocardial infarction. At follow-up, which was 100% with a mean of 41.4 months, all endarterectomy patients were in New York Heart Association Functional Class I or II. Twenty-four endarterectomy patients underwent first-pass radionuclide angiographic stress testing 20 months after operation. Twenty patients (83%) had excellent postoperative exercise tolerance, achieving 5 to 7 mets on treadmill testing. Left ventricular functional reserve was preserved, as evidenced by an increase of global ejection fraction from 48 +/- 15% at rest to 59 +/- 18% (p less than 0.005) with exercise. A similar increase was measured in the proximal and distal anterior wall segmental ejection fractions. No difference in response to exercise was found between the internal mammary artery and the vein graft groups. Thus, complete revascularization of the diffusely diseased LAD artery can be accomplished by adjunct endarterectomy without added morbidity or mortality and with excellent functional results.     

Changes in the rate of formation and resistance to reabsorption of cerebrospinal fluid during deliberate hypotension induced with adenosine or hemorrhage.

Adenosine is recommended for induction of deliberate hypotension. Although its effects on brain vasculature and metabolism and intracranial pressure have been reported, its effects on cerebrospinal fluid dynamics have not. In this study the rate of cerebrospinal fluid formation (Vf), resistance to reabsorption of cerebrospinal fluid (Ra), and electroencephalogram (EEG) activity were determined in rabbits before and during decrease of cerebral perfusion pressure (CPP) with intravenous (iv) adenosine or hemorrhage. In the adenosine group (n = 6), Vf and Ra were determined at control CPP, at CPP of 50, 35, and 28 mmHg achieved with iv adenosine, and at CPP greater than 60 mmHg achieved with iv adenosine combined with iv phenylephrine. In the hemorrhage group (n = 6), Vf and Ra were determined at the first four experimental conditions only. Control values for Vf (9 +/- 3 and 9 +/- 4 microliter.min-1, mean +/- SD) and Ra (428 +/- 567 and 412 +/- 144 cmH2O.ml-1.min) did not differ between groups. In the adenosine group, Vf did not change significantly when CPP was decreased. However, in the hemorrhage group, Vf decreased significantly at CPP of 50 and 35 mmHg and became unmeasurable at CPP of 28 mmHg. Ra did not change significantly in either group. An increase of low-frequency (0.5-3.0 Hz) EEG activity and/or decrease of higher-frequency (3.5-30 Hz) EEG activity occurred at CPP of 28 mmHg in the adenosine group and at CPP of 35 mmHg in the hemorrhage group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dexamethasone and indomethacin do not affect brain edema following head injury in rats

Head trauma was induced in rats by a weight-drop device, falling over the exposed skull over the left hemisphere. The neurological state of the rats was evaluated by a neurological severity score at 1 h and 18 h post head trauma. At 18 h post head trauma, rats were decapitated and tissue from the vicinity of the injury and from a corresponding area in the contralateral hemisphere was taken for specific gravity (SG) determination using linear gradient columns. Slices were taken from the same sites for incubation in Krebs-Ringer solution, and the concentrations of prostaglandin (PG)E2, 6-keto-PGF1 alpha, and thromboxane B2 accumulated in the medium during 1 h were measured by radioimmunoassay. In one experimental group, rats were pretreated with intraperitoneal dexamethasone sodium phosphate (4 mg/kg) 18 and 2 h before head trauma, and a third dose was given 8 h post head trauma. Another group was treated with intraperitoneal indomethacin (10 mg/kg) 1 h before and 7 h after head trauma. Other groups were treated immediately and 8 h after head trauma with 4, 8, 15, or 30 mg/kg of dexamethasone sodium phosphate. Another group of rats was treated with free dexamethasone (10 mg/kg) right after head trauma and 8 h later. Head trauma induced edema, as expressed by decreased SG, in the left hemisphere of all traumatized rats. Neither treatment protocol affected the neurological severity score of the injured rats or the SG of the contused hemisphere. PG synthesis, on the other hand, was significantly reduced following indomethacin or free dexamethasone, both in sham and traumatized rats, but not in dexamethasone sodium phosphate-treated rats. We conclude that pretreatment with indomethacin, dexamethasone sodium phosphate, or dexamethasone, used in the present protocols, does not affect posttraumatic cerebral edema. Thus, the role of PGs as mediators of edema formation remains unclear.     

Methylprednisolone does not decrease eicosanoid concentrations or edema in brain tissue or improve neurologic outcome after head trauma in rats.

Methylprednisolone was recently reported to significantly improve motor and sensory function after acute spinal cord injury in patients. Our study was designed to determine whether methylprednisolone exerts a beneficial effect after head injury. Diethyl ether-anesthetized rats were assigned to receive surgery with no cranial impact and no methylprednisolone (group A, n = 13); surgery with no cranial impact and intraperitoneal methylprednisolone (greater than or equal to 60 mg/kg) (group B, n = 8); surgery with cranial impact and no methylprednisolone (group C, n = 8, and group E, n = 8); or surgery with cranial impact and methylprednisolone (greater than or equal to 60 mg/kg) (group D, n = 15, and group F, n = 13). Neurologic severity score was determined at 1, 2, 4, and 24 h (when appropriate) after injury, and brain tissue eicosanoid levels and cerebral edema were determined when the animals were killed (4 h after injury in groups C and D and 24 h after injury in groups E and F). Treatment with methylprednisolone did not improve neurologic severity score or edema formation and did not alter brain tissue levels of prostaglandin E2, thromboxane B2, or 6-keto-prostaglandin F1 alpha at any time period. The authors conclude that methylprednisolone does not exert a beneficial effect on brain tissue edema or functional activity after cranial impact in rats.     

Laser-assisted fibrinogen bonding of vascular tissue

Characterization of the stress-strain profiles of welded tissue would provide an additional means of analyzing this new technology and comparing it with alternative anastomosing techniques. Rabbit longitudinal aortotomies were repaired with either 7-O polypropylene sutures or an 808-nm diode laser (power density, 4.8 watts/cm2) after topical application of fibrinogen mixed with indocyanine green dye (peak absorption, 805 nm). The rabbits were sacrificed between 0 and 28 days, and the fresh aortic specimens were strained axially in diluted plasma solution until ultimate breakage occurred in order to produce a stress-strain profile graph. No significant differences were noted between sutured and bonded aorta at any time interval. Nonincised aortic tissue (378 lb/in2) withstood significantly higher stress (P less than 0.05) than both sutured (257 lb/in2) and bonded (210 lb/in2) groups at the time of creation. By 7 days after operation, however, no significant differences were noted among any of the three groups. At 28 days after operation, the laser-bonded aorta was significantly stronger than the control aorta (P less than 0.05). The only significant difference in modulus (stretchability) identified the sutured aorta (373 lb/in2) to be more rigid than the control aorta (231 lb/in2) (P less than 0.05). Both sutured and laser-bonded anastomoses are weaker than control aorta initially; however, after an early critical period, both treatments achieve the strength of control aorta. By 1 month postoperatively, sutured anastomoses have the disadvantage of being less distensible.     

Primary Localized Cutaneous Lichen Amyloidosus of the vulva

A woman, age 72, gravida 5, para 5, was hospitalized for a vulvar biopsy. Her past history revealed a generally healthy woman, menopausal from the age of 53, who had a vaginal hysterectomy and repair at the age of 68 because of genital prolapse. One year before her present admission, the woman started complaining of pruritus vulvae, which progressively worsened. On admission, general physical examination revealed no outstanding pathologic findings; gynecologic examination revealed advanced atrophy of the external genitalia and the vaginal wall. The clitoris and the small labia were atrophic, scarred, and only slightly elevated off the surface (Fig. 1). The vulvar skin was shiny with scattered white patches that were not elevated and had no shiny borders. The rectal examination was normal, and inguinal lymph nodes were not palpable. Laboratory tests revealed the following: sedimentation rate 15/26, hemoglobin 15 gidl, WBC 6400/mm³ (with normal differential count), thrombocytes 150,000/mm-³, serum alkaline phosphatase 100 mu/ml (normal 30–85), uric acid 7 mg/dl (upper normal value 6.4). Serum electrolytes, blood urea nitrogen, glucose, cholesterol, creatinine, total proteins, albumin, glutamic ox-aloacetic transaminase, lactic dehydrogenase, creatine phosphokinase, diastase, urine analysis, chest x-ray, and electrocardiogram were normal. Vulvar biopsy was per-formed under general anesthesia. Histologic examination of vulvar skin was as follows: the epidermis was hyperkeratotic with granulosis and acanthosis (Fig. 2). There were enlarged blood vessels in the dermis with thickened and hyalinized walls and foci of infiltration of round cells. The papillaris and reticularis revealed amorphic areas that stained positively with Congo red (Fig. 3). The histologic diagnosis was amy-loidosis of the vulvar skin. After the histologic report was received, further investiga-tions were done, as follows: urine Bence Jones protein was negative, serum protein electrophoresis and immunoelec-trophoresis were normal, and no free light chains were found in the plasma. Serum antinuclear factor and tubercu-lin skin test were negative. The patient refused to undergo rectal biopsy. She was initially treated with local application of testosterone ointment. After 2 months of treatment, the itching worsened and we started with applications of iso-conazole nitrate and diflucortolone valerate. This treatment was followed by prompt relief of symptoms, although the gross appearance of the lesions had not changed. One year later, the patient feels well and refuses repeat biopsy.