Female reproductive cycle and obsessive-compulsive disorder

BACKGROUND: The aim of our study was to assess whether there is a relationship between reproductive cycle events and the initiation or changes in symptoms of obsessive-compulsive disorder (OCD). METHOD: Forty-six female outpatients meeting DSM-IV criteria for OCD completed a semistructured interview at our OCD unit to assess the relationship between reproductive cycle events and OCD. Dates of data collection were from January 2001 to December 2003. RESULTS: In our sample, OCD onset occurred in the same year as menarche in 22% (N = 10), at pregnancy in 2% (N = 1), at postpartum in 7% (N = 3), and at menopause in 2% (N = 1). Worsening of preexisting OCD was reported by 20% of patients (9/45) at premenstruum, 8% (1/12) at pregnancy, 50% (6/12) at postpartum, and 8% (1/12) at menopause. The number of premenstrual mood symptoms, which included anxiety, irritability, mood lability and depressed mood, was associated with both premenstrual worsening of OCD (OR = 5.1, p < .01) and onset or worsening of OCD at postpartum (OR = 2.7, p < .05). Patients with an onset or worsening of OCD at postpartum also more frequently reported pre-menstrual worsening of OCD and previous history of major depressive disorder, including postpartum depression (p < or =.05 for all). CONCLUSION: In a substantial number of patients, the onset or worsening of OCD was related to reproductive cycle events, especially at menarche and postpartum. Certain women with OCD seem to be vulnerable to worsening of OCD at different reproductive periods that imply hormonal fluctuations, and premenstruum and post-partum were the 2 reproductive events with a greater vulnerability. Those patients whose OCD symptoms appeared to be related to reproductive events also exhibited a greater history of mood symptoms (premenstrual depression and major depressive episodes).     

Seizures after a Bier block with clonidine and lidocaine

A 47-yr-old man with history of complex regional pain syndrome type 1 underwent an IV Bier block with a mixture of lidocaine and clonidine. The tourniquet was deflated after 60 min, and approximately 10 min later he presented with complex partial seizures. The possible mechanisms for this are discussed, and the effects of clonidine, lidocaine, and the mixture of both are reviewed, as are four additional published cases reporting seizures after the administration of clonidine.     

Heritability of explosive power and anaerobic capacity in humans

There is a disparity in the information about the heritability of the response of muscle anaerobic metabolism to exercise and the use of explosive power, as well as a lack of information concerning the genetic determinants of this form of work, as measured using different specific physical tests. We applied a battery of some of the commonly employed procedures (Ergojump, Wingate, maximal accumulated oxygen deficit, excess post-exercise oxygen consumption, and Δ lactate concentration) to a group of 32 Caucasian male twins, 8 monozygotic and 8 dizygotic pairs, who had similar environmental backgrounds. Results were studied using a heritability index (HI). Zygosity was determined using the identity of erythrocyte antigens, protein and enzyme polymorphism and human leucocyte antigen serologic types between co-twins. Significant HI values (P<0.05) were found in the following tests: maximal 5 s power (HI=0.74) and total power in a 30 s interval (HI=0.84) in the Wingate test, maximal lactate concentration (HI=0.82) and Δ lactate concentration (HI=0.84) in the maximal progressive test, as well as in the 2nd (HI=0.93) and in the 3rd min (HI=0.92) of recovery after the deficit test. In this study, the most relevant findings were: firstly, significant HI values for many of the variables studied; secondly, the HI values of the parameters used to evaluate explosive power were higher than those of lactic acid capacity and thirdly, the HI of certain variables from different tests measuring, in theory, similar qualities, were different. Electronic Publication     

POEMS Syndrome with central and peripheric nervous system demyelination

POEMS syndrome is characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal protein and skin changes. This polyneuropathy belongs to the chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) group. Sporadic reports have emphasized the clinical association between CIDP and central nervous system (CNS) demyelination, but as far as we know not in the context of POEMS syndrome. We report the case of a 67 years old patient who developed POEMS syndrome associated to Castleman's disease, characterized by demyelinating polyradiculoneuropathy, hepatosplenomegaly, mediastinal and supraclavicular adenopathies and monoclonal IgG lambda gammapathy. Cranial magnetic resonance imaging disclosed diffuse alteration of the cerebral white matter highly suggestive of demyelination. CNS demyelination can be another feature of POEMS syndrome. Cranial MRI should be performed in patients with POEMS syndrome in order to verify this new feature.