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Biomedical subjects

N Dahmen

Publications and source records attributed to N Dahmen.

At least 19 recordsLinked to original sources
PubMed2006

[Involuntary patient admission and treatment against patient's will by emergency physicians].

INTRODUCTION: The treatment of acutely ill patients who presumably lack the insight or judgement to determine their need for medical treatment, is a difficult challenge for emergency physicians. We have carried out a study to assess the frequency and relevance of involuntary treatment and procedures in medical emergency services. METHODS: Retrospective chart analysis for a 1-year period was performed for all treatment protocols of a medical emergency service unit and for all court-ordered treatments of a guardianship court. Cases of involuntary treatment by emergency physicians were identified and analysed. RESULTS: In 10.4% of all emergency calls analysed a relevant and acute psychiatric condition was found. In 0.3% of the cases or 4.8% of the psychiatric cases, involuntary inpatient commitment was chosen by the emergency physician. DISCUSSION: Involuntary inpatient commitment by emergency physicians was only necessary in relatively few cases. Nevertheless, in order to be able to correctly consider treatment and management options, emergency physicians should be aware of the basic conditions for treatment without a patient's consent.

Adolescent↗
PubMed2005

GRIN1 locus may modify the susceptibility to seizures during alcohol withdrawal.

N-Methyl-D-aspartate (NMDA) receptors, members of the glutamate receptor channel superfamily, are generally inhibited by alcohol. The expression and alternative splicing of the obligatory NR1 subunit is altered by alcohol exposure, emphasizing the involvement of the NR1 subunit, which is coded by the GRIN1 gene, in alcohol-mediated effects. We performed an association study in patients with alcohol dependence with the GRIN1 locus. Two independent case control samples consisting of a total of 442 alcohol-dependent patients and 442 unrelated controls were included. There was no overall difference in allele or genotype frequency between patients and controls. However, the 2108A allele and A-containing genotypes were over-represented in the patients with a history of withdrawal-induced seizures when compared to healthy volunteers (allele: chi(2) = 5.412, df = 1, P = 0.020) or an independent sample of patients without a history of seizures (allele: chi(2) = 4.185, df = 1, P = 0.041). Age at onset, years of alcohol dependence, and a history of delirium tremens did not differ between genotype or allele groups. These findings support the hypothesis that the GRIN1 locus may modify the susceptibility to seizures during alcohol withdrawal. This novel finding warrants replication.

Adult↗
PubMed2005

The catechol-O-methyltransferase Val108/158Met polymorphism affects short-term treatment response to mirtazapine, but not to paroxetine in major depression.

The catechol-O-methyltransferase (COMT) is a major degrading enzyme in the metabolic pathways of catecholaminergic neurotransmitters such as dopamine and norepinephrine. This study investigated whether the functionally relevant Val(108/158)Met gene variant is associated with differential antidepressant response to mirtazapine and/or paroxetine in 102 patients with major depression (DSM-IV criteria) participating in a randomized clinical trial with both drugs. In patients treated with mirtazapine, but not paroxetine, allelic variations in the COMT gene were associated with differential response. COMT(VAL/VAL) and COMT(VAL/MET) genotype carriers showed a better response than COMT(MET/MET)-bearing patients in the mirtazapine group. Moreover, carriers of the COMT(VAL/VAL) or COMT(VAL/MET) genotype had significantly greater HAMD-17 (Hamilton Rating Scale for Depression 17 item version) score reductions than COMT(MET/MET) homozygotes from week 2 to 6, respectively, in the mirtazapine group. Time course of response and antidepressant efficacy of mirtazapine, but not paroxetine, seem to be influenced in a clinically relevant manner by this allelic variation within the COMT gene.

Adult↗
PubMed2004

A rare form of narcolepsy (HLA-DR2-) shows possible association with (functionally relevant) alpha-interferon gene polymorphisms.

Narcolepsy is a neuropsychiatric disease caused by complex disturbance of sleep regulation. The main symptoms comprise daytime sleepiness and cataplexy. Although the aetiology remains unclear so far, narcolepsy is genetically characterized by strong linkage to the human leukocyte antigen complex as more than 90% of the patients are typed HLA-DR2+. Recently, it has become apparent that the orexin (hypocretin) neurotransmitter system plays a key role in the pathogenesis of the disease. Canine narcolepsy is caused by mutations in the orexin receptor 2 gene, and narcoleptic patients show specifically decreased cerebrospinal fluid orexin levels. Decreased promotor activity of the prepro-orexin gene is caused by binding of alpha-interferon in vitro. To investigate the possible role of IFNA gene polymorphisms in the pathogenesis of narcolepsy, we have genotyped two single nucleotide polymorphisms in IFNA genes as well as a neighbouring microsatellite. No association was evident in the prevalent DR2+ group. Yet, the IFNA10 single nucleotide polymorphisms and the IFNA microsatellite are associated with the DR2- patient group. Thus, the pathogenetic role of interferons needs to be defined in DR2- narcolepsy.

Carrier Proteins↗
PubMed2003

Association of a MAOA gene variant with generalized anxiety disorder, but not with panic disorder or major depression.

This study was conducted to detect a possible association of a T941G single nucleotide polymorphism (SNP) in the monoamine oxidase A (MAOA) gene with generalized anxiety disorder (GAD), panic disorder (PD), or major depression (MD). Fifty GAD patients (34 females and 16 males), 38 PD patients (21 females and 17 males), and 108 MD patients (80 females and 28 males) were included. The comparison group consisted of 276 (132 females and 144 males) unrelated healthy individuals. The 941T allele was over-represented in patients suffering from GAD (chi(2) = 6.757; df = 1; P < 0.01, not corrected for multiple testing) when compared to healthy volunteers. No association was observed in MD or PD. This is the first study specifically analyzing the MAOA G941T polymorphism in GAD and thus needs to be replicated in an independent sample. However, the results are in line with previous data suggesting an association between the MAOA locus and regulation of complex human behavior.

Adult↗
PubMed2003

TNFA promoter polymorphisms and narcolepsy.

Narcolepsy is a debilitating sleep disorder that affects up to 0.05% of individuals in Caucasian populations. It is highly associated with the HLA-DR2 group antigen or the HLA-DRB1*1501-DQB1*0602 haplotype, respectively. However, the HLA association by itself cannot sufficiently explain the increased risk to family members, as HLA-DR2 is quite common in the general population and most people harboring the respective genotype do not develop any symptoms of narcolepsy. Situated in the HLA class II region, the TNFA gene is translated into the pro-inflammatory cytokine TNF-alpha. TNFA promoter polymorphisms have been linked to several inflammatory and autoimmune diseases. We analyzed three SNP of the TNFA promoter and one adjacent microsatellite in 103 patients and 96 controls. The T-allele of the C-857T polymorphism was strongly associated with narcolepsy in the subgroup of DRB1*15/16 (HLA-DR2 type) negative patients, but not in DRB1*15/16 positive patients. These results point towards an etiological influence of TNFA alleles in narcolepsy and support previous findings suggesting genetic heterogeneity and differences in pathophysiological characteristics of HLA-DR2 positive and negative narcolepsy.

Alleles↗
PubMed2003

Increased frequency of migraine in narcoleptic patients: a confirmatory study.

Previously we have reported an increased prevalence of migraine in narcoleptic patients. Because of the theoretical and clinical implications of this finding we recruited an independent new study sample of 100 patients with proven narcolepsy and conducted a structured 26-item interview based on the international diagnostic criteria for headache disorders, the Kiel Headache Questionnaire. Narcolepsy symptoms were measured by means of the Stanford Centre for Narcolepsy Sleep Inventory. Migraine prevalence was twofold to fourfold increased in the narcoleptic patients and amounted to 44.4% in women and 28.3% in men. The onset of narcolepsy symptoms was 12.3 +/- 11.4 years before the onset of migraine symptoms. The results might be regarded as indicative of a common pathophysiological pathway relevant to both of the two disorders.

Adult↗
PubMed2002

Narcoleptic and schizophrenic hallucinations. Implications for differential diagnosis and pathophysiology.

The differential diagnosis of narcolepsy versus schizophrenia is sometimes complicated by similar phenomenology, particularly when hallucinations predominate. REM sleep disturbances seem fundamental in the pathophysiology of narcolepsy, and REM sleep intrusions during periods of wakefulness are often associated with hallucinations also in healthy controls and in patients with other brain disorders including schizophrenia. This study used a semistructured interview to investigate different aspects of hallucinations (frequency, modality, content, and dependence on body posture) in 148 patients with narcolepsy, 21 patients with acute exacerbation of a schizophrenic disorder, and 128 healthy subjects. About 80% of patients with narcolepsy, 81% of schizophrenics, and 37% of healthy subjects reported lifetime occurrence of hallucinations (at least once). Auditory hallucinations were reported by 81% of schizophrenic patients (narcoleptics 45%, healthy controls 9%), whereas 83% of narcoleptic patients reported visual hallucinations (schizophrenics 29%, healthy controls 19%). Kinetic hallucinations were experienced by 71% of patients with narcolepsy and 53% of healthy controls in contrast to only 5% of schizophrenics. Accordingly, the content of hallucinations differed substantially between the groups. Most hallucinations in narcoleptics but not in schizophrenics, were sleep-related and dependent on body posture. Taken together, the qualitative aspects of hallucinations in narcolepsy and schizophrenia were so different that a common underlying mechanism of hallucinations in the two conditions is unlikely. Although the clinical separation of patients with narcolepsy and schizophrenia with predominant hallucinations is sometimes difficult, clinical features including the patient's illness history, and careful psychopathological assessments can help to avoid misdiagnoses and treatment failures.

Journal Article↗
PubMed2002

Depression, emotional blunting, and akinesia in schizophrenia. Overlap and differentiation.

Depression, negative symptoms, and extrapyramidal signs (EPS) frequently occur together in schizophrenia. Their overlap is due partly to the lack of specificity of assessment instruments. However, to disentangle the three syndromes is clinically important as treatment of schizophrenia requires a differentiated approach. This study investigated the overlap between depression, emotional blunting as a core part of the negative syndrome, and akinesia as manifestation of EPS, using the Calgary Depression Rating Scale (CDSS), the Rating Scale for Emotional Blunting (SEB), and the akinesia score of the Simpson-Angus Scale (SAS) as the most specific assessment instruments presently available. We investigated 57 medicated schizophrenic patients before discharge from hospitalization. Mutual relationships were assessed with linear and partial correlations. Substantial linear associations emerged between SEB and SAS scores. The correlation between CDSS and SAS scores was significantly lower, but also different from zero. When SEB scores were statistically controlled, the association between CDSS and SAS scores dropped to nonsignificance; the correlation between SEB and SAS scores remained nearly unchanged when controlling for depression. The correlation between CDSS and SEB scores decreased to nonsignificance when controlling for SAS scores. Neither gender, age, illness duration, nor type of medication had an influence on the findings. High levels of akinesia were related to emotional blunting but not independently to depressive symptoms in medicated schizophrenic patients. Although the results cannot be assumed to be specific for schizophrenia, they corroborate the partial independence of depression and affective blunting in schizophrenia and the relationship of negative symptoms to EPS.

Journal Article↗
PubMed2001

ApoE polymorphisms in narcolepsy.

BACKGROUND: Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The ApoE4 allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well. METHODS: To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the ApoE gene in 103 patients with narcolepsy and 101 healthy controls. RESULTS: The frequency of the E4 allele of the ApoE gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4+ and ApoE4- patient groups. CONCLUSION: Our results exclude the ApoE4 allele as a major risk factor for narcolepsy.

Journal Article↗
PubMed2001

A prepro-orexin gene polymorphism is associated with narcolepsy.

The orexin (hypocretin) neurotransmitter system was recently shown to be directly involved in the pathogenesis of narcolepsy in two animal models. Furthermore, decreased levels of orexin A in the CSF were shown in narcoleptic patients. To define any genetic contribution of orexin to the etiology of narcolepsy, the authors screened the entire prepro-orexin gene for mutations or polymorphisms in 133 patients suffering from narcolepsy. They report an association of a rare polymorphism in the prepro-orexin gene with narcolepsy in a cohort of 178 patients.

DNA Primers↗
PubMed2001

Increased prevalence of obesity in narcoleptic patients and relatives.

Increased Body Mass Indices (BMIs), increased prevalences of non insulin-dependent diabetes and sleep apnoe syndrome have been reported to be associated with narcolepsy. Our objective was to explore and possibly confirm the association of narcolepsy and increased BMI. In addition, we addressed the question whether increased BMIs also occur in relatives of narcoleptic patients. Together with narcolepsy-related clinical parameters we measured body weight and height of 132 narcoleptic patients who agreed to participate in our narcolepsy research program. In addition, 52 first degree relatives of 22 index patients, mostly from multiplex families, were included in the study. Data were compared to published general population surveys, recently conducted in Germany and Switzerland as well as to collective of 104 psychiatric inpatients. Narcoleptic patients had significantly increased BMIs in comparison to general populations or psychiatric controls. BMIs of first degree relatives were lower than those of index patients but significantly higher than those found in the general population. BMIs were not related to symptom severity or to medication status. Thus, the elevated BMIs appeared not to be secondary to behavioral consequences of narcolepsy but may reflect a trait at least partially common to index patients and relatives.

Adult↗
PubMed2001

Serotonergic polymorphisms in patients suffering from alcoholism, anxiety disorders and narcolepsy.

1. Alterations in the serotonergic neurotransmission have been frequently described for patients suffering from alcoholism, anxiety disorders and narcolepsy. 2. The authors tested for association of the 5-HT2A receptor polymorphism (T102C) and the intron 7 tryptophan hydroxylase (TPH) polymorphism (A218C) among 176 alcohol dependent patients, 35 patients with panic disorder, 50 patients with generalized anxiety disorder, 55 patients with narcolepsy and 87 healthy controls. 3. Allele and genotype frequencies of the 5-HT2A receptor polymorphism (T102C), the intron 7 TPH polymorphism (A218C) were almost similar between the patients suffering from alcohol dependence, panic disorder, generalized anxiety disorder and narcolepsy. 4. There was no association between the 5-HT2A receptor polymorphism (T102C), the intron 7 TPH (A218C) polymorphisms and alcohol dependence, panic disorder, generalized anxiety disorder and narcolepsy in our subsets of German patients.

Adult↗
PubMed2001

No association between the dopamine d2 receptor taqi a1 allele and earlier age of onset of alcohol dependence according to different specified criteria.

BACKGROUND: The presence of the A1 allele of the dopamine D2 receptor TaqI restriction fragment length polymorphism has been reported to be associated with an earlier age of onset of alcohol dependence as a marker for severity. METHODS: We tested this hypothesis with special regard to the definition of the age of onset of alcoholism in 243 patients with alcohol dependence, according to DSM-IV criteria assessed by the standardized interview Münchner Composite International Diagnostic Interview (M-CIDI), consecutively admitted for detoxification. Additionally, the Addiction Severity Index (ASI) was performed. The TaqIA polymorphism was amplified by polymerase chain reaction (PCR), and the PCR product was digested by the restriction enzyme TaqI. Patients were subsequently divided into an A1 (presence of at least one A1 allele, n = 88) and an A2 group (absence of an A1 allele, n = 155). The following criteria for different definitions of age of onset were used: (1) age of onset of the first occurring symptom necessary for the diagnosis of alcohol dependence according to M-CIDI; (2) age of onset of the last symptom of alcohol dependence according to M-CIDI; (3) age of onset of more than 3 drinking days per week on a regular basis according to ASI; (4) age of onset of more than 3 drinking days-of more than five drinks per drinking day-or at least one binge drinking episode per week on a regular basis according to ASI. RESULTS: The frequency of the A1 allele in our patient sample was 0.208. No statistically significant association between the A1 allele and the age of onset of alcoholism was found. The mean age of onset according to criterion 1 was 30.4 +/- 10.8 years for the A1 group and 30.2 +/- 10.2 years for the A2 group (p = 0.89); for criterion 2, it was 33.3 +/- 10.0 years for the A1 group and 33.9 +/- 10.2 years for the A2 group (p = 0.77); for criterion 3, it was 18.0 +/- 7.5 years for the A1 group and 18.1 +/- 6.1 years for the A2 group (p = 0.92); and for criterion 4, it was 22.3 +/- 9.7 years for the A1 group and 21.8 +/- 8.5 years for the A2 group (p = 0.76). CONCLUSIONS: No association was found between the A1 polymorphism and age at onset of alcohol dependence according to different specified criteria.

Adolescent↗