[Iodinated contrast-induced encephalopathy: a pathology that must be borne in mind when carrying out endovascular examinations]. / Encefalopatia por contraste iodado: una patologia que se debe tener en cuenta en el desarrollo de las exploraciones endovasculares.

INTRODUCTION: In recent years there has been an increase in the number of endovascular examinations in the study of both cardiovascular and cerebrovascular diseases. One very infrequent complication is neurotoxicity due to contrast, and it must be suspected within the context of a neurological deficit following such examinations in order to be able to diagnose it. CASE REPORT: A 61-year-old male who presented an epileptic attack and later deficit in the left hemisphere following diagnostic arteriography. After ruling out the possibility of an urgent vascular pathology, he was submitted to a magnetic resonance brain scan with the suspicion of this condition. The clinical signs and symptoms were limited to 72 hours with cortisone therapy. CONCLUSIONS: Contrast-induced encephalopathy covers a wide range of clinical features which, in the vast majority of cases, are self-limiting to 24-72 hours, and within the context of neuronal damage following contrast infusion. Its prognosis is excellent, and diagnostic suspicion is crucial in its treatment.

TITLE: Encefalopatia por contraste iodado: una patologia que se debe tener en cuenta en el desarrollo de las exploraciones endovasculares.Introduccion. En los ultimos años ha aumentado el numero de exploraciones endovasculares en el estudio de la patologia tanto cardiovascular como cerebrovascular. Una de las complicaciones poco frecuentes es la neurotoxicidad por contraste y su sospecha resulta imprescindible en el contexto de un deficit neurologico tras dichas exploraciones para llegar a su diagnostico. Caso clinico. Varon de 61 años que tras una arteriografia diagnostica en el estudio de una hemorragia subaracnoidea presento una crisis epileptica y posteriormente deficit hemisferico izquierdo. Tras descartar una patologia vascular urgente, se realizo una resonancia magnetica cerebral con sospecha de encefalopatia poscontraste. La clinica se limito en 72 horas con corticoterapia. Conclusiones. La encefalopatia por contraste abarca un amplio espectro clinico, en la inmensa mayoria de los casos autolimitado en 24-72 horas, y en el contexto del daño neuronal tras la infusion de contraste. Su pronostico es excelente y la sospecha diagnostica es vital en el tratamiento.

Exploración neurológica y atención primaria. Bloque II: motilidad voluntaria, funciones corticales superiores y movimientos anómalos / Neurological examination and primary care. Block II: voluntary motility. Higher cortical functions. Abnormal movements

La exploración neurológica es, junto con la anamnesis, la base del diagnóstico de la patología del sistema nervioso. El médico de Atención Primaria, con un acceso limitado a pruebas de alta resolución, debe de conocer los aspectos más importantes de dicha exploración, siendo importante que esta se realice de manera sistemática.En un primer bloque se abordó la exploración de los pares craneales, la sensibilidad, los signos meníngeos, el cerebelo y la coordinación, y en esta segunda parte se analizan la función motora, las funciones corticales superiores y los movimientos anómalos (AU)

The neurological examination is, along with the anamnesis, the basis of the diagnosis of nervous system disease. The Primary Care doctor, with limited access to high resolution tests, must know the most important aspects of this examination; the most important being that this is carried out systematically. In the first Block, the examination of the cranial pairs, sensitivity, meningeal signs, cerebellum and coordination were looked at. In this second Block, motor function, higher cortical functions and abnormal movements are analysed (AU)

Exploración neurológica y atención primaria. Bloque I: pares craneales, sensibilidad, signos meníngeos. Cerebelo y coordinación / Neurological examination and primary care. Part 1: cranial pairs, sensitivity, meningeal signs, cerebellum and coordination

La exploración neurológica es, junto con la anamnesis, la base del diagnóstico de la patología del sistema nervioso. El médico de atención primaria, con un acceso limitado a pruebas de alta resolución, debe de conocer los aspectos más importantes de dicha exploración, siendo importante que ésta se realice de manera sistemática. Para una mejor compresión se ha dividido los diferentes apartados de la exploración neurológica en dos bloques: un primer bloque en el que se abordan la exploración de los pares craneales, la sensibilidad, signos meníngeos, cerebelo y coordinación, y un segundo bloque en que se analizan la función motora, las funciones corticales superiores y los movimientos anómalos (AU)

The neurological examination is, along with the anamnesis, the diagnostic basis of diseases of the nervous system. The Primary Care physician, with limited access to high resolution tests, must know the most important aspects of this examination. It is important that this examination is performed systematically. For a better understanding, the different sections of the neurological examination has been divided into two parts: the first one looks at the examination of the cranial pairs, sensitivity, meningeal signs, cerebellum and coordination, and the second will analyse motor function, higher cortical functions, and abnormal movements (AU)

[Recurrent aseptic meningitis secondary to taking ibuprofen and ketorolac]. / Meningitis recurrente aséptica secundaria a toma de ibuprofeno y ketorolaco.

INTRODUCTION: Aseptic meningitis is a process that is characterised by an inflammatory reaction of the meninges that is not due to any infectious agent. Its aetiology is varied and is most frequently caused by rheumatologic and/or autoimmune processes, chemical or medication-induced meningitis, the most notable drugs involved being antibiotics and non-steroidal anti-inflammatory drugs (NSAI). CASE REPORT: We report the case of a 70-year-old male, with no relevant history, who was admitted to hospital five times over a period of 16 months because of acute meningitis with polymorphonuclear pleocytosis, high protein levels in cerebrospinal fluid and normal glucose in cerebrospinal fluid. No evidence of an infectious causation, chemical meningitis, carcinomatosis or autoimmune disease was found and the patient was diagnosed with recurrent aseptic meningitis. It was found that the patient had taken ibuprofen or ketorolac on several occasions, a few hours before the appearance of symptoms. These episodes were quickly resolved after withdrawal of this medication. CONCLUSIONS: A number of NSAI have been reported as inducers of aseptic meningitis, one of the most notable being ibuprofen. We report the case of a patient who, as a consequence of taking ibuprofen and ketorolac, presented episodes of recurrent aseptic meningitis. To our knowledge this side effect of ketorolac has not been reported before. Its clinical features are impossible to differentiate from those of infectious meningitis. Diagnosis is reached by exclusion and a careful pharmacological study, including over-the-counter drugs like some of the NSAI, must be performed in patients with this condition, since it is a problem that can easily be solved by withdrawing the drug that causes it.

Meningitis recurrente aséptica secundaria a toma de ibuprofeno y ketorolaco / Recurrent aseptic meningitis secondary to taking ibuprofen and ketorolac

Introducción. La meningitis aséptica es un proceso que se caracteriza por una reacción inflamatoria meníngea no causada por ningún agente infeccioso. Su etiología es variada, y la más frecuente es la secundaria a procesos reumatológicos y/o autoinmunes, meningitis química e inducida por fármacos, entre los que destacan los antibióticos y los antiinflamatorios no esteroideos (AINE). Caso clínico. Varón de 70 años de edad, sin antecedentes relevantes, que en el período de 16 meses ingresó en cinco ocasiones por meningitis aguda con pleocitosis polimorfonuclear, hiperproteinorraquia y glucosa normal en el líquido cefalorraquídeo, en las que se descartó una etiología infecciosa, meningitis química, carcinomatosis o enfermedad autoinmune y se le diagnosticó meningitis aséptica recurrente. Se comprobó la toma de ibuprofeno o ketorolaco en distintas ocasiones, unas pocas horas antes de la aparición de la clínica. Estos episodios se resolvieron rápidamente tras la retirada de dicha medicación. Conclusiones. Se han implicado varios AINE como inductores de meningitis aséptica, entre los que destaca el ibuprofeno. Presentamos un paciente que, como consecuencia de la toma de ibuprofeno y ketorolaco, sufrió episodios de meningitis recurrente aséptica. En nuestro conocimiento no se ha comunicado previamente este efecto secundario con el ketorolaco. Su clínica es indistinguible de la meningitis infecciosa; el diagnóstico se efectúa por exclusión, y debe realizarse una cuidadosa historia farmacológica, que incluya fármacos de libre dispensación como algunos AINE, en pacientes con esta patología, puesto que se trata de un problema fácilmente solucionable con la retirada de la medicación que lo causa (AU)

Introduction. Aseptic meningitis is a process that is characterised by an inflammatory reaction of the meninges that is not due to any infectious agent. Its aetiology is varied and is most frequently caused by rheumatologic and/or autoimmune processes, chemical or medication-induced meningitis, the most notable drugs involved being antibiotics and non-steroidal anti-inflammatory drugs (NSAI). Case report. We report the case of a 70-year-old male, with no relevant history, who was admitted to hospital five times over a period of 16 months because of acute meningitis with polymorphonuclear pleocytosis, high protein levels in cerebrospinal fluid and normal glucose in cerebrospinal fluid. No evidence of an infectious causation, chemical meningitis, carcinomatosis or autoimmune disease was found and the patient was diagnosed with recurrent aseptic meningitis. It was found that the patient had taken ibuprofen or ketorolac on several occasions, a few hours before the appearance of symptoms. These episodes were quickly resolved after withdrawal of this medication. Conclusions. A number of NSAI have been reported as inducers of aseptic meningitis, one of the most notable being ibuprofen. We report the case of a patient who, as a consequence of taking ibuprofen and ketorolac, presented episodes of recurrent aseptic meningitis. To our knowledge this side effect of ketorolac has not been reported before. Its clinical features are impossible to differentiate from those of infectious meningitis. Diagnosis is reached by exclusion and a careful pharmacological study, including over-thecounter drugs like some of the NSAI, must be performed in patients with this condition, since it is a problem that can easily be solved by withdrawing the drug that causes it (AU)

[Aphasia and parietal syndrome as the presenting symptoms of a demyelinating disease with pseudotumoral lesions]. / Afasia y síndrome parietal como forma de presentación de una enfermedad desmielinizante con lesión pseudotumoral.

INTRODUCTION: Multiple sclerosis (MS) often presents with sensory symptoms, which are usually due to spinothalamic or spinal cord disorders; parietal syndrome is, however, very rare as the initial symptom. Likewise, aphasia is also an infrequent symptom of MS; in the few cases that have been reported, it is usually linked to the existence of important pseudotumoral lesions. CASE REPORT: We describe the case of a 31-year-old female with a 48-hour history of a progressive clinical picture consisting in nominal aphasia and a sensory parietal syndrome. Magnetic resonance imaging showed a lesion 3.6 cm in diameter that was hyperintense in T2 with perilesional edema and minimal gadolinium uptake, along with other images that revealed increased signal intensity in the periventricular subcortical white matter on the right-hand side and in the left-hand frontal subcortical region. A spectroscopic analysis of the largest lesion revealed that this lesion showed evidence of inflammation, with cell destruction and replacement, although it was not possible to distinguish between a demyelinating disease and a high grade glioma. Hence, a brain biopsy was required in order to reach the final diagnosis of demyelinating pseudotumoral lesion. CONCLUSIONS: Giant pseudotumoral plaques are a rare form of presenting symptom in MS; use of the clinical features, simple images and spectroscopy is not a very reliable means of reaching a differential diagnosis with a tumour and this often makes it necessary to conduct a biopsy study of the lesion.

Afasia y síndrome parietal como forma de presentación de una enfermedad desmielinizante con lesión pseudotumoral / Aphasia and parietal syndrome as the presenting symptoms of a demyelinating disease with pseudotumoral lesions

Introducción. Las manifestaciones sensitivas son frecuentes como síntomas iniciales de la esclerosis múltiple (EM), generalmente por alteración espinotalámica o medular; pero es excepcional un síndrome parietal como forma de inicio. Igualmente, la afasia es una manifestación infrecuente en la EM; en los pocos casos descritos suele asociarse a la existencia de grandes lesiones pseudotumorales. Caso clínico. Mujer de 31 años con un cuadro progresivo de 48 horas de evolución, consistente en afasia nominal y un síndrome sensitivo parietal. En la resonancia magnética se observó una lesión de 3,6 cm de diámetro hiperintensa en T2 con edema perilesional y con mínima captación de gadolinio, además de otras imágenes de aumento de intensidad de señal en sustancia blanca subcortical periventricular derecha y en zona subcortical frontal izquierda. El análisis espectroscópico de la lesión de mayor tamaño reveló que dicha lesión presentaba datos de inflamación, con destrucción y recambio celular, sin poder distinguir entre enfermedad desmielinizante o glioma de alto grado; se precisó para ello la realización de una biopsia cerebral para alcanzar el diagnóstico final de lesión pseudotumoral desmielinizante. Conclusiones. Las placas gigantes pseudotumorales constituyen una forma infrecuente de inicio de la EM; su diagnóstico diferencial con un tumor por la clínica, la imagen simple y la espectroscopia son poco fiables, por lo que, con frecuencia, es preciso recurrir a la biopsia de la lesión

Introduction. Multiple sclerosis (MS) often presents with sensory symptoms, which are usually due to spinothalamic or spinal cord disorders; parietal syndrome is, however, very rare as the initial symptom. Likewise, aphasia is also an infrequent symptom of MS; in the few cases that have been reported, it is usually linked to the existence of important pseudotumoral lesions. Case report. We describe the case of a 31-year-old female with a 48-hour history of a progressive clinical picture consisting in nominal aphasia and a sensory parietal syndrome. Magnetic resonance imaging showed a lesion 3.6 cm in diameter that was hyperintense in T2 with perilesional edema and minimal gadolinium uptake, along with other images that revealed increased signal intensity in the periventricular subcortical white matter on the right-hand side and in the left-hand frontal subcortical region. A spectroscopic analysis of the largest lesion revealed that this lesion showed evidence of inflammation, with cell destruction and replacement, although it was not possible to distinguish between a demyelinating disease and a high grade glioma. Hence, a brain biopsy was required in order to reach the final diagnosis of demyelinating pseudotumoral lesion. Conclusions. Giant pseudotumoral plaques are a rare form of presenting symptom in MS; use of the clinical features, simple images and spectroscopy is not a very reliable means of reaching a differential diagnosis with a tumour and this often makes it necessary to conduct a biopsy study of the lesion

Epilepsia como forma de presentación de esclerosis múltiple con lesión pseudotumoral / Epilepsy as the form of onset of multiple sclerosis with a pseudotumoral lesion

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