Probe tine diameter and probing depth

The aim of this study was to assess the effect of difference in tine diameter on probing pocket depth measurement. 2 sets of tines with Williams markings at 1, 2, 3, 5, 7, 8, 9 and 10 mm, and with a "round" tip, diameter 0.5 mm, were compared. One set was described as parallel-sided, the other as tapered. The parallel-sided tine was almost parallel from the 10 mm marking to the tip (tip diameter mean = 0.46 mm, 95% C.I. 0.456-0.464), while the corresponding diameter for the tapered tine varied (tip diameter mean = 0.48 mm, 95% C.I. 0.473-0.489). Calibration markings appeared highly consistent with the expected value to within 0.01 mm. The tines were mounted in Brodontic handles at 0.25 N. Examiner probing repeatability yielded kappa 0.86 for "parallel-sided" and 0.81 for "tapered" tines in vivo. 412 approximal pockets were assessed in 53 patients with routine chronic adult periodontitis, mean age 42.1 years. Each site had a probing depth of greater than or equal to 5 mm, PlI less than or equal to 1, GI less than or equal to 1, PBI less than or equal to 1. Each site was probed 2x with a 15-min interval. At the first 251 sites, the parallel-sided tine was used initially, and the tapered at the remaining 161 sites. Results indicated a highly significant tendency for the parallel-sided tine to yield a deeper reading when a difference occurred. These findings indicate that with adequate training providing high examiner repeatability, one source of error in probing data can be minimised.     

Transient trochlear nerve palsy as the presenting neurological sign of panarteritis nodosa

INTRODUCTION: Panarteritis nodosa (PAN) is a systemic vasculitis affecting small and medium-sized arteries. Neuro-ophthalmological complications of PAN are rare but numerous, and may affect the eye, the visual and the oculomotor pathways. Such complications occur mainly in patients previously diagnosed with PAN. OBSERVATION: A 51-year-old woman presented with an isolated right trochlear (IV) palsy, in the setting of headaches and fluctuating fever of unknown etiology. Erythrocyte sedimentation rate was 13 mm and full blood cell count was normal. Previous chest X-ray and blood studies were negative for an infection or inflammation. Orbital and cerebral CT scan was normal. Spontaneous recovery of diplopia ensued over four days. Two days later, paresthesia and sensory paresis of the dorsal portion of the left foot were present. Lumbar puncture revealed 14 leucocytes (76 percent lymphocytes) with elevated proteins, but blood studies and serologies were negative. A diagnosis of undetermined meningo-myelo-radiculoneuritis was made. Because of a possible tick bite six weeks previously the patient was empirically treated with 2 g intravenous ceftriaxone for 3 weeks. Fever rapidly dropped. Six weeks after the onset of diplopia, acute onset of blindness in her right eye, diffuse arthralgias and fever motivated a new hospitalization. There was a central retinal artery occlusion of the right eye. Blood studies now revealed signs of systemic inflammation (ESR 30 mm, CRP 12 mg/L, ANA 1/80, pANCA 1/40, leucocytosis 12.4 G/L, Hb 111 g/L, Ht 33 percent). Biopsy of the left sural nerve revealed arterial fibrinoid necrosis. A diagnosis of PAN was made. CONCLUSIONS: Transient diplopia can be the heralding symptom of a systemic vasculitis such as PAN, giant cell arteritis and Wegener granulomatosis. In this patient the presence of accompanying systemic symptoms raised a suspicion of systemic inflammation, but the absence of serologic and imaging abnormalities precluded a specific diagnosis initially. A few weeks later, the presence of a second ischemic event (retinal) and positive blood studies led to a further diagnostic procedure. Oculomotor and abducens palsies have rarely been reported in association with PAN. We report the first case of trochlear nerve paresis as the inaugural neurological sign of PAN. This case highlights the importance of considering inflammatory systemic disorders in patients with acute diplopia particularly when they are young, lack vascular risk factors or cause, and complain of associated systemic symptoms.     

Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders

In response to the increase of resistant depressive disorders and in spite of improved treatments, numerous studies were conducted in the last thirty Years aiming at assessing the pre-morbid thyroid state of depressed patients resistant to well conducted tricyclic treatments. "Minimal" thyroid abnormalities were evidenced as well as central thyroid disorders which may not be detected by peripheral-i.e plasmatic- dosages. Regarding the premorbid thyroid status, the hypothesis of subclinical hypothyroidism was considered by many Authors.It is marked by four grades including T3 and T4 decreased levels, basal TSH concentration abnormalities as well as increased TSH response to TRH stimulation, and the presence of antimicrosomal and antithyroglobulin antibodies. Although, there are different views on the existence or not of these abnormalities, we'll focus our attention on a metaanalysis including six studies.It shows in a population with a resistant depression, 52% of patients with subclinical hypothyroidism, against 8 to 17% in patients with simple depression and 5% in the overall population.Similarly, antithyroid antibody levels (group IV hypothyroidism) were significantly higher in depressed patients (9% to 20% against 7,5% in the overall population). For many Years, a central hypothyroidism was hypothesized on the basis of an exhausted T3-T4 transference mechanism and a lowered TRH hypothalamic biodisponibility.In the last Years, new data emerged on the role of transthyretin, a cerebral carrier T4 protein, whose concentration in the CSF was found significantly lower in depressed patients than in a control group, the lowest levels being observed in the most severely depressed.This decreased level of transthyretin would result in a lower central T4 biodisponibility-hence, in view of a T4-T3 desiodation insufficiency, a T3 deficit is observed. A low transthyretin level associated or not to subclinical hypothyroidism could be a factor of depressive vulnerability on one hand, of resistance to tricyclic treatment on the other one. Conversely, subclinical hypothyroidism could be a predictive factor of a good response to a potentializing strategy. The pharmacological mechanisms involved in this potentializing phenomenon are now well known: they consist in an interaction between depression, adrenergic receptors and thyroid hormones biodisponibility. The decreased norepinephrine level observed in depressive patients is associated, in case of increased thyroid hormones biodisponibility, with a higher sensitivity of adre-nergic receptors, mostly betaadrenergic. This seems to underly the recovery process. According to some Authors, the serotoninergic system might be involved in the potentialization of tricyclics by thyroid hormones. We know that in animals with hypothyroidism, the serotonin synthesis is decreased and that the administration of T3 increases the brain levels of serotonin and its 5HIA catabolite. In addition, T3 could correct the down-regulation induced by serotoninergics on beta-adrenergic receptors. On the basis of numerous studies carried out on the potentializing of tricyclics, we suggest practical modalities of treatment - which until today did not materialize in every day practice in the absence of a clear consensus based on statistically reliable data: after four to six weeks of inefficient tricyclic or serotoninergic treatment on a correct dosage testified by plasmatic dosages, it is recommended to initiate a T3 treatment on a effective posology (25 to 50 micrograms per day), which must be reached in 2 or 3 days, except in case of rare and transitory side effects (sweating, shaking, tachycardia, nervousness, anxiety). If the treatment is not rapidly efficient, it must be discontinued in case there is no improvement after 3 weeks. Until today, there is no consensus about the duration of a T3 treatment. It is important to take into account the predictive criteria of good or bad response to a T3 potentialization, since they have direct consequences on the management of depressed patients. For example, a high degree of chronic evolution with resistance to numerous treatments, associated disorders according to the DSM IV axis I and a comorbidity of addiction, point to a bad prognosis of a potentialization treatment. In addition, we'll examine the few recent studies on the potentializing of serotoninergic antidepressant drugs by thyroid hormones.     

Fluoxetine: an update of its use in major depressive disorder in adults

The selective serotonin reuptake inhibitors (SSRIs) have emerged as a major therapeutic advance in psychiatry. They have emphasized the pathophysiological role of serotonin (5-HT) in affective disorders. Indeed, SSRIs were developed for inhibition of the neuronal uptake for serotonin (5-HT), a property shared with the TCAs (tricyclic anti-depressants), but without affecting the other various central neuroreceptors (ie, histamine, acetylcholine and adrenergic receptors) that are responsible for many of the safety and tolerability problems with TCAs. In this way, fluoxetine and other SSRIs represent a major advance over tricyclics, because of their lower toxicity. While the position of fluoxetine relative to other selective serotoninergic antidepressants requires further investigation, fluoxetine has a more favorable tolerability profile for a similar efficacy in comparison to tricyclic antidepressants. The pharmacokinetic and pharmacodynamic properties of fluoxetine are well described. After oral administration, fluoxetine is almost completely absorbed. Due to hepatic first-pass metabolism, the oral bioavailability is < 90%. Fluoxetine has a half-life of 2-7 days, whereas the half-life of norfluoxetine ranges between 4 and 15 days. This long half-life of fluoxetine may be advantageous when the patient omits a dose since drug concentrations decrease slightly. On the other hand, in the case of fluoxetine non-response, long washout periods are necessary before switching the patient to a TCA or a MAO inhibitor to avoid drug interactions or the development of a 5-HT syndrome. As a class, SSRIs are considerably more selective in comparison to TCAs in terms of their central nervous system mechanisms, but differ in other clinically relevant aspects. This action affects several specific 5-HT receptors, which, in turn, effects a multitude of neural systems and signalization pathways. However, despite the facilitating serotoninergic neurotransmission, the direct mechanism by which a SSRI exerts its anti-depressant activity remains uncertain. The therapeutic response in major depression for SSRIs (ie 15-20 days) maybe due to a progressive desensitization of somatodendritic 5-HT autoreceptors in the midbrain raphe nucleus. On the other hand, it has also been postulated that 5-HT is a modulator of several neurophysiological pathways, including dopamine, noradrenaline, but also neurotrophic factors, intra-cytoplasmic phosphorylations and nuclear genes expression. Therapeutic activity of SSRIs may finally results in a complex modulation and homeostasis between monoaminergic neurotransmisson and neuronal plasticity. In term of health-care, the introduction of fluoxetine and other SSRIs in the 1980s has radically changed the treatment of depressive disorder worldwide and they have emerged as the first line of treatment for depressive disorders. The efficacy of fluoxetine is now well established in the treatment of major depressive disorder. Indeed, this efficacy has been assessed in numerous clinical controlled trials involving patients with major depressive disorders. Meta-analysis were carried out and confirmed that fluoxetine was as effective as the tricyclic antidepressants, and appeared more effective than placebo in improving the symptoms of depression. However, there is no scientific evidence to suggest that any one SSRI is more effective than another, but not all patients respond to the same agent. Looking to the future, we need further comparative studies of the SSRIs with the next generation of antidepressants such as 5-HT noradrenaline reuptake inhibitors (SNRIs, Venlafaxine). Actually, it is interesting to note that, whereas the emphasis with the SSRIs has been on their selectivity, recent developments have tended to move towards less selective agents, and now to other neurobiological pathways (ie neurotrophic factors). Finally, fluoxetine, in common with other SSRIs, remains today a first-line treatment option for major depressive disorder.