[Minor stroke in a patient with thrombocytopenia]. / Ictus menor en una paciente con trombocitopenia.

TITLE: Ictus menor en una paciente con trombocitopenia.

[Predictive clinical factors of response to subthalamic nucleus stimulation in Parkinson's disease]. / Factores clínicos predictivos de la respuesta a la estimulación subtalámica en la enfermedad de Parkinson.

INTRODUCTION: Subthalamic nucleus stimulation (SNE) is currently a reasonable treatment for patients with advanced Parkinson's disease (PD). Predictive factors for effective SNE have not yet been identified with precision. We have prospectively evaluated response to SNE in a series of patients with advanced PD to study the factors that influence clinical improvement after functional surgery. METHODS: We prospectively studied 20 patients with advanced PD (age: 59 +/-6.1; stage: 3.0+/-0.8) candidates for SNE. We studied these patients preoperatively and 6 months postoperatively according to Core Assessment Program for Intracerebral Transplantation (CAPIT) protocol including timed tests. CONCLUSIONS: We found a negative correlation between age and Unified Parkinson Disease Rating Scale (UPDRS) improvement; however, age did not correlate with timed tests improvement. In addition, preoperative severity (UPDRS and Hoehn-Yahr) did not correlate with UPDRS and timed tests improvement. In summary, age is a negative predictor for effective SNE.

Factores clínicos predictivos de la respuesta a la estimulación subtalámica en la enfermedad de Parkinson / Predictive clinical factors of response to subthalamic nucleus stimulation in Parkinson's disease

Introducción. Actualmente la estimulación subtalámica (EST) es una opción terapéutica razonable para pacientes con enfermedad de Parkinson (EP) avanzada. No se conocen con precisión los factores pronósticos de la respuesta a la EST. Hemos evaluado prospectivamente la respuesta a la EST en una serie de pacientes con EP avanzada para estudiar qué factores inciden en la mejoría clínica tras la cirugía funcional. Métodos. Estudiamos prospectivamente 20 pacientes con EP avanzada (edad: 59±6,1 años; estadio: 3±0,8) candidatos a cirugía funcional mediante EST. La evaluación prequirúrgica y posquirúrgica (a los 6 meses) se realizó según el protocolo Core Assessment Program for Intracerebral Transplantation (CAPIT) incluyendo pruebas cronometradas.Conclusiones. Hallamos una correlación significativa (negativa) entre la edad y la mejoría de la Unified Parkinson Disease Rating Scale (UPDRS) total tras la cirugía. Sin embargo, la mejoría en las pruebas cronometradas no se correlacionó con la edad. Por otra parte, el estado funcional prequirúrgico (UPDRS y estadio Hoehn-Yahr) tampoco se correlacionó con la respuesta a la EST. En resumen, la edad es un factor predictivo negativo en la mejoría tras la EST

Introduction. Subthalamic nucleus stimulation (SNE) is currently a reasonable treatment for patients with advanced Parkinson`s disease (PD). Predictive factors for effective SNE have not yet been identified with precision. We have prospectively evaluated resonse to SNE in a series of patients with advanced PD to study the factors that influence clinical improvement after functional surgery. Methods. We prospectively studied 20 patients with advanced PD (age: 59+-6.1; stage: 3.0+-0.8) candidates for SNE. We studied these patients preoperatively and 6 months postoperatively according to Core Assessment Program for Intracerebral Transplantation (CAPIT) protocol including timed tests. Conclusions. We found a negative correlation between age and Unified Parkinson Disease Rating Scale (UPDRS) improvement. In addition, preoperative severity (UPDRS and Hoehn-Yahr) did not correlate with UPDRS and timed tests improvement. In summary, age is a negative predictor for effective SNE

[Some reflections on the pathophysiology of abnormal movements]. / Algunas reflexiones sobre la patofisiología de los movimientos anormales.

INTRODUCTION: The field of abnormal movements is an area that is in continual expansion within Neurology and treatment is currently available for many of them, at least as far as the symptoms are concerned. Yet, the exact mechanisms of operation of the neurological structures involved in movement are not fully understood. DEVELOPMENT: It seems clear that the basal ganglia play an important role, fundamentally in pseudo-automatic movements, but because they are interconnected with many other structures it is difficult to gain a precise understanding of their individual functions. There are theories based solely on anatomical data, which are not enough to account for everything. The theory of the existence of neuronal circuits seems to explain a wider part of movement, although it still has a number of shortcomings. Another theory of movement disorders is that based on neurochemistry, according to which the imbalance of certain neurotransmitters would be the causation of the disease, but this theory does not enable us to explain all the pathologies related to movement either. A number of clinical observations and the use of animal models, however, have made it possible to draw up pathophysiological hypotheses about the generation of some abnormal movements. CONCLUSIONS: All these approaches have enabled researchers to find symptomatic treatments for certain diseases, but our knowledge of the pathophysiology involved is still far from complete and the chances of enhancing the therapeutic capacity available in such cases in the future are therefore immense.

Algunas reflexiones sobre la patofisiología de los movimientos anormales / Some reflections on the pathophysiology of abnormal movements

Introducción. El campo de los movimientos anormales esun área en continua expansión dentro de la Neurología, y existe enla actualidad tratamiento, al menos sintomático, para multitud deellos. Sin embargo, no está claro el mecanismo exacto de funcionamientode las estructuras neurológicas implicadas en el movimiento.Desarrollo. Parece cierto que los ganglios basales desempeñanun papel importante, fundamentalmente en los movimientos pseudoautomáticos,pero debido a que están interconectados con muchasotras estructuras es difícil conocer con precisión su función individual.Hay teorías basadas únicamente en datos anatómicos, que noson suficientes para explicar todo. La teoría de la existencia de circuitosneuronales parece explicar una parte más amplia del movimiento,aunque tampoco es completa. Otra teoría de los trastornosdel movimiento es aquella basada en la neuroquímica, según la cualel desequilibrio entre algunos neurotransmisores produciría laenfermedad; pero esta teoría tampoco permite explicar por completotoda la patología relacionada con el movimiento. Por otra parte,algunas observaciones clínicas y el uso de modelos animales hanpermitido elaborar hipótesis fisiopatológicas de la generación dealgunos movimientos anormales. Conclusión. Todas estas aproximacioneshan hecho posible encontrar algunos tratamientos sintomáticospara determinadas enfermedades, pero todavía el conocimientofisiopatológico está lejos de ser completo y, por tanto, lacapacidad terapéutica tiene grandes posibilidades de seguir mejorando

Introduction. The field of abnormal movements is an area that is in continual expansion within Neurology andtreatment is currently available for many of them, at least as far as the symptoms are concerned. Yet, the exact mechanisms ofoperation of the neurological structures involved in movement are not fully understood. Development. It seems clear that thebasal ganglia play an important role, fundamentally in pseudo-automatic movements, but because they are interconnected withmany other structures it is difficult to gain a precise understanding of their individual functions. There are theories based solelyon anatomical data, which are not enough to account for everything. The theory of the existence of neuronal circuits seems toexplain a wider part of movement, although it still has a number of shortcomings. Another theory of movement disorders is thatbased on neurochemistry, according to which the imbalance of certain neurotransmitters would be the causation of the disease,but this theory does not enable us to explain all the pathologies related to movement either. A number of clinical observations andthe use of animal models, however, have made it possible to draw up pathophysiological hypotheses about the generation of someabnormal movements. Conclusions. All these approaches have enabled researchers to find symptomatic treatments for certaindiseases, but our knowledge of the pathophysiology involved is still far from complete and the chances of enhancing thetherapeutic capacity available in such cases in the future are therefore immense

[New therapeutic options in Alzheimer's disease]. / Nuevas opciones terapéuticas en la enfermedad de Alzheimer.

INTRODUCTION: At present, cholinesterase inhibitors constitute the basis for therapy of Alzheimer's disease (AD); these drugs were rationally introduced given the loss of central cholinergic neurotransmission, even though there are many other systems affected in AD, including glutamatergic pathway. DEVELOPMENT: In addition to the loss of central cholinergic neurotransmission, biochemical evidence suggests glutamatergic dysfunction in AD and thus, therapeutic strategies directed at the glutamatergic system may be useful. These drugs include milacemide, cicloserine and ampakines (positive modulation) and memantine (negative modulation). Lithium seems to be a promising agent in AD, although the mechanism of action is poorly understood. Finally anti-inflammatory agents may be another therapeutic approach to AD. CONCLUSION: In addition to drugs acting on the cholinergic system, a large number of drugs with different mechanism could be used for the treatment and prevention of AD.

Nuevas opciones terapéuticas en la enfermedad de Alzheimer / New therapeutic options in Alzheimer’s disease

Introducción. En los últimos se han introducido fármacos eficaces para el tratamiento de la enfermedad de Alzheimer (EA). Los tratamientos disponibles, fundamentalmente inhibidores de la colinesterasa, se introdujeron con base racional en vista dela pérdida de neurotransmisión colinérgica en la EA. Sin embargo, la neuroquímica de la EA no se limita a un déficit colinérgico, puesto que existe disfunción de diversos sistemas de neurotransmisión, incluido el sistema glutamatérgico. Desarrollo. Además de fármacos que intervienen en el sistema colinérgico, existen posibilidades farmacológicas para modular positivamente el sistema aglutamatérgico, incluyendo la cicloserina, la milacemida y las ampakinas, y negativamente mediante la memantina. El litio es otro fármaco prometedor, aunque su mecanismo de acción sólo se conoce de forma parcial. Finalmente, cabe en lo posible que los analgésicos no esteroideos desempeñen un papel en la prevención y en etapas muy iniciales de la EA. Conclusiones. Además de los fármacos que actúan de forma directa sobre el sistema colinérgico, se están utilizando tratamientos relacionados con el sistema glutamatérgico y otros fármacos cuyo mecanismo de acción en esta patología no se conoce claramente, pero que parecen prometedores (AU)

Introduction. At present, cholinesterase inhibitors constitute the basis for therapy of Alzheimer’s disease (AD);these drugs were rationally introduced given the loss of central cholinergic neurotransmission, even though there are many other systems affected in AD, including glutamatergic pathway. Development. In addition to the loss of central cholinergic neurotransmission, biochemical evidence suggests glutamatergic dysfunction in AD and thus, therapeutic strategies directed at the glutamatergic system may be useful. These drugs include milacemide, cicloserine and ampakines (positive modulation)and memantine (negative modulation). Lithium seems to be a promising agent in AD, although the mechanism of action is poorly understood. Finally anti-inflammatory agents may be another therapeutic approach to AD. Conclusion. In addition to drugs acting on the cholinergic system, a large number of drugs with different mechanism could be used for the treatment and prevention of AD (AU)