Laparoscopic adenomectomy versus Eraser laser enucleation of the prostate.

PURPOSE: To evaluate functional outcomes and morbidity rates after laparoscopic adenomectomy (LA) and Eraser laser enucleation of the prostate (ELEP). MATERIALS AND METHODS: Forty patients with lower urinary tract symptoms suggesting bladder outlet obstruction, with a prostate heavier than 70 g on transrectal ultrasound, were selected to undergo laparoscopic adenomectomy or Eraser laser enucleation of the prostate. All patients were consecutively enrolled without randomization and assessed preoperatively, 3 and 6 months postoperatively. Baseline characteristics, perioperative data, and postoperative outcomes were compared. RESULTS: The total operating time was significantly longer in the LA group (138.8 ± 11.4 vs. 78.4 ± 10.0 min, p < 0.000001). Catheter removal was performed earlier (61.2 ± 21.3 vs. 174.0 ± 13.2 h, p < 0.000001) and the hospital stay was significantly shorter (62.4 ± 21.2 vs. 187.2 ± 12.6 h, p < 0.000001) in the ELEP group. The latter group experienced significantly less perioperative hemoglobin (Hb) loss (0.71 ± 0.25 vs. 2.15 ± 1.08 g/dl, p < 0.000001), and their postoperative Hb levels (14.1 ± 1.21 vs. 11.7 ± 1.31 g/dl, p < 0.000001) were significantly higher. The resected tissue was significantly greater in the LA group (58.5 ± 23.3 vs. 87.9 ± 22.4 g, p = 0.0002). Significant improvements in Qmax, Qol, and symptom scores from baseline to each follow-up time point were noted in both groups. No statistically significant difference in symptom scores or Qmax was registered between the LA and the ELEP group throughout the follow-up period. CONCLUSION: Laparoscopic adenomectomy and ELEP were equally effective for relieving bladder outflow obstruction and lower urinary tract symptoms. The advantages of ELEP include less blood loss, shorter catheterization times, and shorter hospital stays.

[Gender-specific differences relating to depressiveness in 1st and 2nd generation migrants: results of a cross-sectional study amongst employees of a university hospital]. / Geschlechtsspezifische Unterschiede bezüglich Depressivität bei Migranten der ersten und zweiten Generation: Ergebnisse einer Querschnittsuntersuchung an Beschäftigten einer Universitätsklinik.

AIMS: This study analysed the risk of depression in men and women with a background of immigration by means of a cross-sectional study amongst employees of a German university hospital. In addition we identified gender-specific differences related to risk factors for depressiveness in the subgroups. METHODS: 7062 employees with or without a 1st (1G) or 2nd (2G) generation background of migration were questioned with regard to their socio-economic status, to single markers of acculturation, and to existing symptoms of depression assessed on the general depression scale (CES-D). Odds ratios (OR) were calculated using logistic regression. RESULTS: The response rate was 41.7% (n=2932). In comparison to non-migrants a higher risk of clinically relevant depressiveness was found for 1G male migrants (OR 2.35, 95% Cl 1.11-4.96), 1G female migrants (OR 1.94, 95% Cl 1.26-2.97) and for 2G female migrants (OR 1.82, 95% Cl 1.03-3.19). There was no significant increase in risk for 2G male migrants (OR 1.06, 95% Cl 0.31-3.62). 2G female migrants who considered themselves to retain a "close relationship to their native culture" had a significantly higher risk of depression than 2G male immigrants (OR 7.31; p = 0.032). Male 1G migrants without a "close relationship to their native culture" had a significantly higher risk of depression than those with a "close relationship to their native culture" (OR 5.79; p = 0.010). CONCLUSIONS: The results of this study point to gender-specific risk constellations for depression amongst 1st and 2nd generation migrants. It would appear that a strong orientation to the native culture increases the risk of depression for 2G female migrants, whereas for 1G male migrants this factor is associated with a lower risk of depression.

[Empirical evidence for the use of anticonvulsants in personality disorders]. / Evidenz für den Einsatz von Antikonvulsiva bei Persönlichkeitsstörungen.

OBJECTIVE: There is a common practice of polypharmacy and an increased use of mood stabilizers in personality disorders (PD). This paper reviews all randomized controlled trials (RCTs) of anticonvulsants to evaluate the evidence base supporting their use in treatment of PD. METHODS: German and English language literature cited in Medline and published between 1970 and 2008 was searched using the following terms: Borderline/personality disorder, anticonvulsant, mood stabilizer, carbamazepine, felbamate, gabapentin, lamotrigine, levetiracetam, oxcarbazepine, phenytoine, pregabalin, tiagabine, topiramate, and valproate. RESULTS: Twelve RCTs were identified which included anticonvulsants in treatment of personality disorders. The anticonvulsants valproate and topiramate appeared to have the most empirical support for having a favorable effect on symptoms of borderline personality disorder. Evidence for the use of other anticonvulsants in patients with PD is sparse. CONCLUSIONS: Valproate and topiramate, probably also lamotrigine, carbamazepine, and oxcarbazepine as well, were useful in treating symptoms of affective dysregulation and impulsive aggression in PD. However, further RCTs of anticonvulsants are greatly needed as clinical use of these agents has risen without sufficient evidence supporting their efficacy and safety in personality disorders.

[Spectrum of neuropsychiatric features associated with velocardiofacial syndrome (Deletion 22q11.2)]. / Das neuropsychiatrische Spektrum des Velokardiofazialen Syndroms (Deletion 22q11.2).

Microdeletion 22q11.2 (22q11DS) is the most frequent chromosomal deletion known in man. Velocardiofacial syndrome is one of numerous clinical syndromes that can be attributed to this micro deletion. There is an increasing recognition of associations with neuropsychiatric disorders. Particularly, schizophrenic psychosis, attention-deficit/hyperactivity disorder (ADHD), intellectual impairment and learning disabilities, seizures and motoric abnormalities have been identified in patients with 22q11DS. Recent studies supported the association of schizophrenia and 22q11DS, but the pathogenetic implications for idiopathic schizophrenia are still controversial. We report on two clinical cases in which psychotic symptoms led to the molecularcytogenetic diagnosis of microdeletion 22q11.2. Additionally, this article gives a systematic review of literature regarding psychiatric disorders, neurologic symptoms and partly corresponding morphological brain abnormalities in 22q11 deletion syndromes.

Basal ganglia calcification and psychosis in 22q11.2 deletion syndrome.

Intracerebral calcifications are a facultative symptom of hypoparathyreoidism in 22q11.2 deletion syndrome (22qDS). We describe a patient with 22qDS, basal ganglia calcification (BGC) and psychotic symptoms and discuss the etiological connection of BGC with psychiatric symptoms. Future work needs to determine the prevalence of BGC in 22qDS and psychiatric disorders.

Focal and segmental primary dystonia in north-western Germany--a clinico-genetic study.

OBJECTIVES: To determine the frequency of familial focal and segmental dystonias in a large patient cohort with primary dystonia from north-western Germany. MATERIALS AND METHODS: In this study, 130 patients with focal or segmental dystonia were examined and a family history was obtained. Whenever possible, affected relatives were examined (a total of 789 first-degree relatives). Data on disease duration, age at disease onset and age of the patients were investigated by Student's t-test and a segregation analysis was performed by Weinberg's proband method. RESULTS: Age at onset of disease was significantly later in the blepharospasm group. Only in the writer's cramp group were women outnumbered by men. A positive family history was found in 15 of the 130 index patients (11.5%). None of 102 index patients tested carried the GAG deletion in the DYT1 gene. CONCLUSIONS: In accordance with previous series our study provides evidence that primary focal dystonia may have a genetic etiology, most probably caused by an autosomal dominant trait with reduced penetrance.

Transdermal nicotine in PD: a randomized, double-blind, placebo-controlled study.

BACKGROUND: An inverse association between cigarette smoking and the risk of idiopathic PD has been found in many epidemiologic studies. The therapeutic and possible neuroprotective effects of nicotine formulations on parkinsonian symptoms are controversial. METHODS: In a 12-week, randomized, double-blind, placebo-controlled trial, the efficacy and tolerability of transdermal nicotine patches as an add-on treatment for cardinal symptoms were evaluated in 32 nonsmoking patients with PD. After a 1-week run-in phase, patients were randomized to receive nicotine patches (containing 17.5 mg nicotine in the first and 35.0 mg nicotine in the second and third weeks) or identically appearing placebo patches. After this treatment, 3 weeks without patch application followed. The same blinded examiner assessed the patients with the Columbia University Rating Scale, the Webster scale, the Schwab-England scale, a timed walking test, with an instrumental test for fine motor skills and hand tremor, and with the Hamilton Depression Scale. RESULTS: No significant drug effects between both groups were observed in any of the scores and quantitative tests. Side effects were mild and comparable in frequency between both groups. CONCLUSIONS: With the dosage and the period of treatment chosen, transdermal nicotine patches are not effective as an add-on treatment for symptoms of PD.

Exogenous levodopa is not toxic to elderly subjects with non-parkinsonian movement disorders: further clinical evidence.

We report three women between 80 and 87 years of age who had longstanding essential tremor. Due to an erroneous diagnosis of Parkinsonism they had received levodopa preparations for 13, 16 and 25 years, respectively, with cumulative levodopa equivalent doses of 18.0, 9.0, and 4.1 kg. The patients showed neither dyskinesias nor signs of Parkinsonism. These observations do not support a detrimental role of chronic levodopa exposure in elderly individuals with essential tremor.

Genetic testing for early-onset torsion dystonia (DYT1): introduction of a simple screening method, experiences from testing of a large patient cohort, and ethical aspects.

Early-onset, generalized primary torsion dystonia (PTD) is an autosomal dominantly inherited disorder, characterized by involuntary movements and abnormal postures. The majority of cases are caused by a 3-bp deletion in the DYT1 gene on chromosome 9q34 that allows for specific genetic testing. We developed a simple, reliable, and cost-effective, PCR-based screening method for this mutation. Testing results from a cohort of 550 cases, including patients with different forms of dystonia and unclassified movement disorders, revealed that 72.2% of the patients with typical early-onset generalized PTD carried the GAG deletion in the DYT1 gene. Among 300 cases with late-onset focal/segmental dystonia, only 3 patients tested positive for the GAG deletion whereas 12.8% of the patients with an unclassified movement disorder were GAG positive. Our results confirm a genotype/phenotype correlation in early-onset PTD and show that application of strict clinical criteria leads to accurate prediction of carrier status in more than two-thirds of patients with this type of dystonia. Currently, we suggest that testing be recommended in individuals with age of onset of dystonia below 30 years and/or a positive family history of early-onset PTD. Testing is not recommended in patients with onset of symptoms after 30 years or in asymptomatic individuals under the age of 18.

Search for the PARK3 founder haplotype in a large cohort of patients with Parkinson's disease from northern Germany.

A founder haplotype on chromosome 2p for autosomal dominant Parkinson's disease (PD) has been postulated for two families of Northern European descent, and a new mutation in the alpha-synuclein gene (Ala30Pro) has been found in a German PD family. We evaluated 85 German PD patients and 85 ethnically matched controls for shared markers on chromosome 2p and for the new alpha-synuclein mutation. We found no evidence for linkage disequilibrium, suggesting that the putative founder mutation on chromosome 2p is not a common cause of PD in the local population. Furthermore, no patient carried the Ala30Pro change, supporting earlier findings that mutations in the alpha-synuclein gene are extremely rare.