Retraso mental como factor de riesgo para el desarrollo de un trastorno psicótico / Mental retardation as a risk factor to develop a psychotic disease

Introducción. En las últimas tres décadas uno de los principales objetivos de la investigación en esquizofrenia ha sido la identificación de los síntomas y signos precursores de la enfermedad antes de su aparición. Objetivo. Buscamos en nuestro estudio los antecedentes que se otorgan previamente a pacientes antes de ser filiados como esquizofrenia. Método. Se trata de un estudio caso-control sobre el que utilizamos un registro de datos que incluye los campos del Conjunto Mínimo Básico de Datos y el período de tiempo considerado fue entre 1999-2005. Resultados. Encontramos una frecuencia de 3,6% de retraso mental y un 2,1% de antecedentes de trastornos del comportamiento y de las emociones de comienzo habitual en la infancia y adolescencia, ambos como diagnóstico previo. La odds ratio de que un paciente con retraso mental sufra psicosis en la edad adulta es de 4,6 (IC 95% [3,43-6,26]), esquizofrenia de 5,8 [IC 95% (4,20-7,88)], esquizofrenia paranoide de 4,8 (IC 95% [3,39 –6,93]), esquizofrenia residual de 7,0 (IC 95% [4,81 -10,09]), trastorno por ideas delirantes de 2,7 (IC 95% [1,57 -4,73]). Conclusiones. De nuestro estudio se puede concluir que existe una frecuencia incrementada del diagnóstico de retraso mental entre los antecedentes patológicos de sujetos que posteriormente serán diagnosticados de esquizofrenia paranoide y esquizofrenia residual. Este hecho, supone un apoyo a la hipótesis etiológica de la esquizofrenia que involucra alteraciones en el neurodesarrollo (AU)

Introduction. One of the main aims of research on schizophrenia has been to pinpoint the early symptoms and signals of the disease before its appearance. Objectives. We have examined the diagnoses previously given to patients before they were diagnosed of schizophrenia. Method. This is a case-control study in which we used a data register including the fields of minimum basic data set (MBDS) whose time period included 1999 to 2005. Results. In our study, there was a 3.6% frequency of mental retardation and 2.1% one of behavioral and emotional disorders with onset usually occurring in childhood and adolescence, both diagnosed previously. The estimated odds ratio for a mentally retarded patient to suffer adult onset psychosis is 4.6 (95%CI [3.43-6.26]), schizophrenia 5.8 (95% CI [4.20-7.88]), paranoid schizophrenia 4.8 (95% CI [3.39 –6.93]), residual schizophrenia 7.0 (95% CI [4.81 -10.09]) and persistent delusional disorder 2.7 (95% CI [1.57 -4.73]). Conclusions. It can be concluded from our study that there is an increased frequency of mental retardation among the pathological records of subjects who will be diagnosed with paranoid schizophrenia and residual schizophrenia in the future. This fact supports the etiological thesis of schizophrenia (AU)

[Stiff-person syndrome: a case report]. / Síndrome de la persona rígida: a propósito de un caso.

INTRODUCTION: Stiff-person (stiff-man) syndrome is characterised by symptoms of muscular rigidity and spasms, which are generally of an axial nature. Involuntary contractions of the agonist and antagonist muscles caused by activity of the motor units during rest are the main clinical and electrophysiological marker of the disease. The nature of the syndrome is considered to be autoimmune, with positive glutamic acid decarboxylase (anti-GAD) antibodies in most patients. These antibodies exert an influence over GABAergic transmission. CASE REPORT: A 29-year-old female who was admitted to hospital with a diagnosis of psychogenic mutism. While in hospital the patient developed a clinical picture consisting in generalised stiffness that was predominantly axial and proximal with hyperreflexia in the four limbs and strong contraction of the muscles of the abdomen. The most striking lab finding was the presence of anti-GAD, anti-parietal cells, anti-microsomal/TPO and antithyroglobulin antibodies, together with oligoclonal immunoglobulin G bands in the cerebrospinal fluid. Treatment was established with benzodiazepines, antispastic agents and corticosteroids, and the clinical symptoms progressively improved until they had partially remitted at two months. The lab findings and clinical features are compatible with stiff-person syndrome in a patient with associated psychiatric comorbidity. CONCLUSIONS: Anti-GAD antibodies are not exclusive to stiff-person syndrome and can also be found in a number of other autoimmune disorders. Other mechanisms which can also produce a dysfunction of the GABAergic system have also been suggested. The syndrome can be difficult to diagnose from the clinical point of view and it must therefore be borne in mind in patients who begin with unexplainable stiffness and spasms because it is a potentially treatable pathology.

Síndrome de la persona rígida: a propósito de un caso / Stiff-person syndrome: A case report

Introducción. El síndrome de la persona rígida (stiff-man) se caracteriza por un cuadro de rigidez muscular y espasmos, generalmente de carácter axial. Las contracciones involuntarias de los músculos agonistas y antagonistas causadas por la actividad de las unidades motoras durante el reposo son el principal marcador clínico y electrofisiológico de la enfermedad. La naturaleza del síndrome se considera autoinmune, con anticuerpos antidecarboxilasa glutámica ácida (anti-GAD)positivos en la mayoría de los pacientes. Estos anticuerpos influyen en la transmisión gabérgica. Caso clínico. Mujer de 29 años que ingresó con el diagnóstico de mutismo psicógeno. Durante su ingreso desarrolló un cuadro que consistía en una rigidez generalizada de predominio axial y proximal con hiperreflexia en las cuatro extremidades y una importante contracción de la musculatura abdominal. En los estudios analíticos destacó la presencia de anticuerpos anti-GAD, anticélulas parietales, antimicrosomales TPO y antitiroglobulina, junto con la presencia de bandas oligoclonales de inmunoglobulina G en el líquido cefalorraquídeo. Se instauró un tratamiento con benzodiacepinas, antiespásticos y corticosteroides, con una mejoría progresiva del cuadro, hasta remitir parcialmente a los dos meses. Los hallazgos de laboratorio y el cuadro clínico son compatibles con un síndrome de la persona rígida en una paciente con comorbilidad psiquiátrica asociada. Conclusiones. Los anticuerpos anti-GAD no son exclusivos del síndrome de la persona rígida y también se pueden encontrar en numerosos trastornos autoinmunes. También se han postulado otros mecanismos por los cuales se produce una disfunción del sistema gabérgico.El síndrome puede ser de difícil diagnóstico desde el punto de vista clínico, por lo que debemos tenerlo presente en pacientes que comiencen con rigidez y espasmos inexplicables, dado que se trata de una patología potencialmente tratable

Introduction. Stiff-person (stiff-man) syndrome is characterised by symptoms of muscular rigidity and spasms, which are generally of an axial nature. Involuntary contractions of the agonist and antagonist muscles caused by activity of the motor units during rest are the main clinical and electrophysiological marker of the disease. The nature of the syndrome isconsidered to be autoimmune, with positive glutamic acid decarboxylase (anti-GAD) antibodies in most patients. These antibodies exert an influence over GABAergic transmission. Case report. A 29-year-old female who was admitted to hospital with a diagnosis of psychogenic mutism. While in hospital the patient developed a clinical picture consisting in generalised stiffness that was predominantly axial and proximal with hyperreflexia in the four limbs and strong contraction of the musclesof the abdomen. The most striking lab finding was the presence of anti-GAD, anti-parietal cells, anti-microsomal/TPO and antithyroglobulin antibodies, together with oligoclonal immunoglobulin G bands in the cerebrospinal fluid. Treatment was established with benzodiazepines, antispastic agents and corticosteroids, and the clinical symptoms progressively improveduntil they had partially remitted at two months. The lab findings and clinical features are compatible with stiff-person syndrome in a patient with associated psychiatric comorbidity. Conclusions. Anti-GAD antibodies are not exclusive to stiffperson syndrome and can also be found in a number of other autoimmune disorders. Other mechanisms which can also produce a dysfunction of the GABAergic system have also been suggested. The syndrome can be difficult to diagnose from the clinical point of view and it must therefore be borne in mind in patients who begin with unexplainable stiffness and spasms because it is a potentially treatable pathology

Errores de diagnóstico y estabilidad temporal en el trastorno bipolar / Diagnostic errors and temporal stability in bipolar disorder

Introducción. El diagnóstico de trastorno bipolar se modifica con frecuencia a lo largo de la evolución de la enfermedad. Material y métodos. Se describen los cambios de diagnóstico y error asociado de 1.153 pacientes mayores de 18 años diagnosticados de trastorno bipolar y con un seguimiento mínimo de 10 visitas en base a un registro clínico de atención ambulatoria especializada en psiquiatría y hospitalizaciones psiquiátricas de 25.152 pacientes representativos de un área urbana de 240.000 habitantes. Se usó como criterio de estabilidad diagnóstica mantener el diagnóstico de trastorno bipolar en al menos el 75% de las visitas. Resultados. De los 342 pacientes diagnosticados de trastorno bipolar en la primera consulta, el 46,1% mantuvieron el diagnóstico estable. Se cometió un error inicial de infradiagnóstico con 108 pacientes estables no diagnosticados en la primera visita. Ciento ochenta y cuatro de los 342 pacientes diagnosticados en la primera visita obtuvieron posteriormente al menos un 25% de diagnósticos diferentes de bipolar y podrían ser considerados como sobre diagnóstico inicial. Doscientos nueve de 443 pacientes diagnosticados como bipolares en la última visita no mantuvieron criterios de estabilidad en su evolución y podrían, por tanto, considerarse como sobre diagnóstico final. Treinta y dos pacientes estables no diagnosticados en la última visita constituirían el error final de infradiagnóstico. Diagnósticos del espectro de la esquizofrenia (F2) aparecen casi en una de cada cuatro visitas al psiquiatra de los pacientes del estudio. Otras tres categorías presentan solapamiento: los trastornos de ansiedad (F4), los trastornos de personalidad (F6) y los trastornos por consumo de sustancias. Conclusión. El trastorno bipolar es un trastorno de difícil diagnóstico en su evolución inicial (AU)

Introduction. The diagnosis of bipolar disorder is frequently modified during the course of the illness. Material and methods. Diagnostic changes and associated errors are described for 1,153 patients diagnosed as bipolar disorder, aged over 18 years and with at least ten follow-up visits. Data was extracted from a clinical registry of out-patient care specialized in Psychiatry and psychiatric hospitalizations of 25,152 patients representative of an urban area of 240,000 in habitants. Limit for diagnostic stability was established as the maintenance of the bipolar disorder diagnosis in at least 75% of the visits. Results. A total of 158 (46.1 %) out of 342 patients diagnosed as having a bipolar disorders in the first visit kept this diagnostic constant in subsequent evaluations. Infradiagnostic initial error was committed with 108 stable patients who were not diagnosed in the first visit. 184 patients diagnosed in the first visit with bipolar disorder had less than 75 % concordant diagnosis along the follow-up and could be considered as initial over diagnosis. Two hundred and nine out of the 443 patients who were diagnosed as bipolar disorder in their last visit did not keep stability criteria in their follow-up and could be considered therefore as final over diagnosis. Thirty two stable patients not diagnosed in their last visit could be considered as infradiagnosis final error. Diagnosis from schizophrenia spectrum (F2) appears in one of every four psychiatric visits of the patients included in this study. Overlap was seen in three other categories: anxiety disorders (F4), personality disorders (F6) and substance abuse disorders. Conclusion. Initial course of bipolar disorder causes difficulties in the diagnosis (AU)