RESUMEN
Lithium is potentially toxic to the central nervous system. Clinical lithium neurotoxicity may appear at any time during therapy and may go unrecognized. Failure to appreciate this fact leads to delays in diagnosis and treatment, placing the patient at risk of permanent neurological damage or death. In spite of a largely clinical diagnosis of lithium intoxication, the EEG provides an objective criterion of intoxication. We report a case of lithium intoxication with neurotoxic symptoms associated with marked EEG changes despite moderate lithium serum levels. In contrast to the interindividually varying EEG changes under uncomplicated lithium therapy, pathological EEG findings are the rule in the case of intoxication. Several reports evince a closer relationship between neurotoxic symptoms with EEG changes than with serum levels of lithium. This is of clinical interest with respect to intoxication under therapeutic lithium serum levels, since the EEG is the only examination indicating an intoxication. In patients with intoxication, the phenomenon of long-lasting EEG changes after discontinuation of lithium is discussed with respect to neuronal storing of lithium and persisting neurological disturbances.
Asunto(s)
Electroencefalografía/efectos de los fármacos , Litio/efectos adversos , Anciano , Antidepresivos Tricíclicos/uso terapéutico , Trastorno Depresivo/complicaciones , Trastorno Depresivo/genética , Trastorno Depresivo/psicología , Humanos , Imagen por Resonancia Magnética , Masculino , Mianserina/análogos & derivados , Mianserina/uso terapéutico , MirtazapinaRESUMEN
Recent reports have suggested that genetic polymorphisms in the alpha-2 macroglobulin (A2M) gene are associated with an increased risk for Alzheimer's disease. In the present study we tested two polymorphisms in the alpha-2 macroglobulin gene, a 5 bp deletion at the 5' splice site of exon 18 and a G/A point mutation (V1000I) in exon 24, in a sample of 118 healthy, non demented controls and 238 consecutively recruited gerontopsychiatric patients, diagnosed as: Alzheimer's disease (N=88), mild cognitive impairment (N=32), subjective cognitive complaints (N=54) and depression/other psychiatric disorders (N=64). The aim of this study was to test whether the investigated polymorphisms has a high enough selectivity and specificity to distinguish between the different gerontopsychiatric disorders or to differentiate genetically AD from other forms of dementia, respectively. Also a possible relation to the APOE varepsilon4 polymorphism was examined. Our study failed to show an association between the two investigated polymorphisms in the alpha-2 macroglobulin gene and any of the four different psychogeriatric patient subgroups, either alone or in combination with the APOE varepsilon4 genotype.
Asunto(s)
Enfermedad de Alzheimer/genética , Trastornos del Conocimiento/genética , Depresión/genética , Polimorfismo Genético , alfa-Macroglobulinas/genética , Anciano , Alelos , Enfermedad de Alzheimer/diagnóstico , Apolipoproteína E4 , Apolipoproteínas E/genética , Estudios de Casos y Controles , Trastornos del Conocimiento/diagnóstico , Depresión/diagnóstico , Diagnóstico Diferencial , Femenino , Frecuencia de los Genes , Pruebas Genéticas , Genotipo , Alemania , Humanos , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , Sensibilidad y Especificidad , Población Blanca/genéticaRESUMEN
Interferon-alpha (IFN-alpha) is the only effective treatment for chronic hepatitis B and C. Over 2/3 of methadone-substituted patients suffer from chronic hepatitis C but a history of psychiatric disorders or drug addiction is still seen as a contraindication for IFN-alpha because of a possible increased risk of severe psychiatric side effects such as depression, suicide attempts or psychotic episodes. We report on the case of a 33-year-old patient with chronic hepatitis C and a positive psychiatric history (drug abuse, borderline personality and four suicide attempts). After 4 months of therapy with IFN-alpha he developed a psychosis with persecution mania, complex thought disorder, disturbance of sexual identity, sleeplessness, anxiety, depression and increased irritability with suicidal thoughts. Symptoms did not disappear after discontinuation of interferon treatment. To our knowledge, there are no other reports of persistent psychosis with a possible association to interferon treatment. Development of psychosis and other psychiatric side-effects may be an indication of possible neuromodulatory effects of IFN-alpha with long-term treatment. On the other hand, the treatment for hepatitis C was successful. Ideas for safer treatment in methadone patients with psychiatric co-morbidity and chronic hepatitis C are needed.
Asunto(s)
Antivirales/efectos adversos , Hepatitis C Crónica/tratamiento farmacológico , Interferón-alfa/efectos adversos , Psicosis Inducidas por Sustancias/etiología , Adulto , Contraindicaciones , Humanos , Masculino , Metadona/uso terapéutico , Narcóticos/uso terapéuticoRESUMEN
Several studies have attempted to confirm an association between a deletion/insertion polymorphism within the promoter region of the serotonin transporter gene (5-HTT) and Alzheimer's disease independent from the apolipoprotein E (APOE) varepsilon4 status. We examined this deletion/insertion polymorphism of the serotonin transporter gene in a sample of 222 consecutively recruited gerontopsychiatric patients which was divided into four different diagnostic groups: Alzheimer's disease (N=84), mild cognitive impairment (N=29), subjective cognitive complaints (N=49), depression/other psychiatric disorders (N=56) and 118 healthy, non-demented controls. The aim of this approach was to test whether the investigated polymorphism has a high enough selectivity and specificity to distinguish between the different gerontopsychiatric disorders or to differentiate genetically AD from other forms of dementia, respectively. We could not detect any significant differences in the allelic distribution of the deletion/insertion polymorphism of the 5-HTT gene between the four patient subgroups and the control group. This finding indicates that the serotonin transporter does not appear to be a major susceptibility factor in the pathophysiology of Alzheimer's disease and other psychogeriatric disorders.