Chronic bronchitis and acute infections as new risk factors for ischemic stroke and the lack of protection offered by the influenza vaccination.

BACKGROUND AND PURPOSE: Acute and chronic infections may play a role in promoting complications of atherosclerotic disease. We evaluated the importance of acute infections and chronic bronchitis (CB; as a chronic inflammatory state) in several subtypes of ischemic stroke, and we investigated whether the influenza vaccination was independently associated with a reduced likelihood of stroke. METHODS: A case-control study was performed on 393 consecutive ischemic stroke patients and 393 control subjects matched for age, sex and time of year. Data were collected by a structured interview that assessed risk factors, acute infections within the preceding 2 months, CB and whether they had received the influenza vaccination. RESULTS: Infections within the 2 months before stroke onset and CB were more common among patients than control subjects [23.3 vs. 16.3% (p = 0.014) and 17.2 vs. 8.5% (p = 0.001), respectively]. After adjustment for traditional risk factors, the risk of stroke was increased in the subjects with CB (OR = 1.83, 95% CI = 1.35-2.48, p = 0.016), but not with acute infection (OR = 1.32, 95% CI = 0.98-1.78, p = 0.16). Acute infections and CB increased the risk of ischemic events in all age groups; this reached significance for patients older than 60 years. The profile of vascular risk factors was similar in patients with and without previous infections. The influenza vaccination did not prevent ischemic stroke, and it did not reduce the rate of acute previous infections in stroke patients. CONCLUSIONS: CB and infections over the previous 2 months predicted the risk of ischemic stroke. The influenza vaccination was not associated with a reduction in the incidence of stroke in our group of patients.

Estudio de los factores de riesgo en la amnesia global transitoria y su diferenciación del accidente isquémico transitorio / A study of the risk factors in transient global amnesia and its differentiation from a transient ischemic attack

Introduction. Transient global amnesia (TGA) is a clinical condition that has been described in many studies, but its pathophysiology is not fully understood. In recent years the theory of valvular insufficiency in the jugular vein has been added to the classical hypotheses that link it to migraine, to epilepsy and –the most widely accepted– to transient ischemic attacks (TIA), although the real origin of the condition has still not been determined. Patients and methods. In a retrospective study we compared 131 patients diagnosed with TGA between 1993 and 2004 with 262 patients who were diagnosed as having TIA over the same period. Results. Mean age was 65.94 years in TGA versus 71.11 years in the case of TIA. There was a higher rate of arterial hypertension among the patients with TGA and diabetes mellitus was more frequent among those with TIA (p < 0.05 in both cases). Emboligenic heart disease was scarce among patients with TGA. The number of patients with a history of ischaemic heart disease and a history and the development of cerebrovascular diseases was greater among those with TIA than in cases of TGA (p < 0.05). The TGA recurrence rate was 12%. The percentage of pathological findings in the CAT brain scan was higher in patients with TIA (p < 0.05). There are no significant differences between patients with TGA and TIAas far as treatment on hospital discharge is concerned. Conclusions. TGA does not seem to be a symptom of an arteriosclerotic pathology nor does it appear to offer a higher risk of heart or cerebrovascular disease and, therefore, antiaggregating therapy would not be indicated in such cases (AU)

Introducción. La amnesia global transitoria (AGT) es una manifestación clínica descrita en muchos estudios, pero cuya fisiopatología no está aclarada. A las hipótesis clásicas de asociación con migraña, epilepsia y la más aceptada de evento isquémico transitorio (AIT), se ha añadido en los últimos años la teoría de insuficiencia valvular yugular sin poder establecerse el origen real del cuadro. Pacientes y métodos. Estudio retrospectivo de 131 pacientes diagnosticados de AGT entre 1993 y 2004 comparados con 262 pacientes con AIT diagnosticados durante el mismo período. Resultados. Edad media de 65,94 años en AGT frente a 71,11 años en AIT. Mayor frecuencia de hipertensión arterial entre los pacientes con AGT y de diabetes mellitus en pacientes con AIT (p < 0,05 en ambos casos). Escasa cardiopatía embolígena en pacientes con AGT. Mayor frecuencia de antecedentes de cardiopatía isquémica y de antecedentes y desarrollo de enfermedad cerebrovascular en los pacientes con AIT respecto a la AGT (p < 0,05). Recurrencia de la AGT del 12%. Mayor porcentaje de hallazgos patológicos en la TC cerebral en pacientes con AIT (p < 0,05). No hay diferencias significativas en cuanto al tratamiento al alta entre los pacientes con AGT y AIT. Conclusión. La AGT no parece ser una manifestación de la patología arterioesclerótica ni presentar mayor riesgo de enfermedad cardio o cerebrovascular y, por lo tanto, no estaría indicado el tratamiento antiagregante (AU)

[A study of the risk factors in transient global amnesia and its differentiation from a transient ischemic attack]. / Estudio de los factores de riesgo en la amnesia global transitoria y su diferenciación del accidente isquémico transitorio

INTRODUCTION: Transient global amnesia (TGA) is a clinical condition that has been described in many studies, but its pathophysiology is not fully understood. In recent years the theory of valvular insufficiency in the jugular vein has been added to the classical hypotheses that link it to migraine, to epilepsy and -the most widely accepted- to transient ischemic attacks (TIA), although the real origin of the condition has still not been determined. PATIENTS AND METHODS: In a retrospective study we compared 131 patients diagnosed with TGA between 1993 and 2004 with 262 patients who were diagnosed as having TIA over the same period. RESULTS: Mean age was 65.94 years in TGA versus 71.11 years in the case of TIA. There was a higher rate of arterial hypertension among the patients with TGA and diabetes mellitus was more frequent among those with TIA (p<0.05 in both cases). Emboligenic heart disease was scarce among patients with TGA. The number of patients with a history of ischaemic heart disease and a history and the development of cerebrovascular diseases was greater among those with TIA than in cases of TGA (p<0.05). The TGA recurrence rate was 12%. The percentage of pathological findings in the CAT brain scan was higher in patients with TIA (p<0.05). There are no significant differences between patients with TGA and TIA as far as treatment on hospital discharge is concerned. CONCLUSIONS: TGA does not seem to be a symptom of an arteriosclerotic pathology nor does it appear to offer a higher risk of heart or cerebrovascular disease and, therefore, antiaggregating therapy would not be indicated in such cases.

Diagnóstico diferencial de las calcificaciones intracraneales / Differential diagnosis of intracranial calcifications

Introducción. Las calcificaciones intracraneales son un hallazgo casual frecuente en las numerosas pruebas de neuroimagen. Presentamos dos casos clínicos con calcificaciones intracraneales como característica común, pero con etiología y forma de presentación muy distinta. Casos clínicos. El primer caso, un varón de 51 años con una crisis convulsiva tonicoclónica aislada asociada a hipocalcemia secundaria a hipoparatiroidismo, que presentaba calcificaciones cerebrales extensas que afectaban a los núcleos dentados, puente, ganglios basales y periependimarios, y presentó remisión de las crisis comiciales tras normalización de cifras de Ca2+; mientras que el segundo caso corresponde a una paciente de 25 años en la que las crisis comiciales son una manifestación más del síndrome de Fahr, al que se asocia parálisis espástica, atetosis, retraso mental y en ocasiones hipoplasia del nervio óptico, y en el que las calcificaciones se localizan en los núcleos grises de cerebro y cerebelo. Conclusiones. Se necesita realizar una correcta anamnesis y exploración física y neurológica, así como un detallado estudio del metabolismo Ca2+/ P+ y hormonal; la tomografía computarizada es la técnica de neuroimagen de elección para la realización de un correcto diagnóstico diferencial y establecer un adecuado abordaje terapéutico, de acuerdo con los mecanismos fisiopatológicos que conducen a la formación de estos depósitos de calcio (AU)

Introduction. Intracranial calcifications are a frequent chance finding in many neuroimaging tests. We report two clinical cases with intracranial calcifications as a common feature, but which had very different aetiologies and presenting symptoms. Case reports. The first case involved a 51-year-old male with a single tonic-clonic convulsive seizure associated to hypocalcemia secondary to hypoparathyroidism who presented extensive brain calcifications affecting the dentate nuclei, pons, periependymal and basal ganglia, and whose convulsive attacks remitted once normal Ca2+ values were restored. The second case was a 25-year-old female patient whose convulsive seizures were yet another symptom of Fahr’s syndrome, which was associated to spastic paralysis, athetosis, mental retardation and occasionally hypoplasia of the optic nerve; the calcifications were located in the grey nuclei of the cerebrum and cerebellum. Conclusions. A correct history and physical and neurological examination must be carried out, and a detailed study of Ca2+/ P+ and hormonal metabolism is also required. A CAT scan is the preferred neuroimaging technique to achieve a proper differential diagnosis and to decide on the therapeutic approach that is best suited to the pathophysiological mechanisms that lead to the formation of these calcium deposits (AU)

[Differential diagnosis of intracranial calcifications]. / Diagnostico diferencial de las calcificaciones intracraneales.

INTRODUCTION: Intracranial calcifications are a frequent chance finding in many neuroimaging tests. We report two clinical cases with intracranial calcifications as a common feature, but which had very different aetiologies and presenting symptoms. CASE REPORTS: The first case involved a 51-year-old male with a single tonic-clonic convulsive seizure associated to hypocalcemia secondary to hypoparathyroidism who presented extensive brain calcifications affecting the dentate nuclei, pons, periependymal and basal ganglia, and whose convulsive attacks remitted once normal Ca2+ values were restored. The second case was a 25-year-old female patient whose convulsive seizures were yet another symptom of Fahr's syndrome, which was associated to spastic paralysis, athetosis, mental retardation and occasionally hypoplasia of the optic nerve; the calcifications were located in the grey nuclei of the cerebrum and cerebellum. CONCLUSIONS: A correct history and physical and neurological examination must be carried out, and a detailed study of Ca2+/ P+ and hormonal metabolism is also required. A CAT scan is the preferred neuroimaging technique to achieve a proper differential diagnosis and to decide on the therapeutic approach that is best suited to the pathophysiological mechanisms that lead to the formation of these calcium deposits.

[Amnesic stroke caused by hippocampal infarction]. / Ictus amnésico por infarto hipocámpo.

INTRODUCTION: The term amnesic stroke is used to describe a condition in which the dominant symptom is a relatively persistent acute amnesia of a vascular origin. It may appear in cases of lesions in the posterior cerebral artery (PCA), thalamic arteries and anterior choroidal artery, and clinical reports describing this condition are scarce. CASE REPORT: We describe the case of a 77-year-old male with vascular risk factors who presented sudden onset mnemonic deficit that affected basic activities of daily living, and apathy. Examination of the patient revealed an anterograde episodic amnesia with an inability to retain new information and short-term memory was also clearly affected, although access to old memories remained relatively intact. There was no other sensory-motor focus. A CAT scan showed a right-side sylvian infarction and hypodense areas in both hippocampuses. The neuropsychological evaluation revealed global amnesia: CME (in Spanish, MEC) 17/30; working memory with CME 7/27; SVF (animals): 7; the 7-minute test (visual/verbal memory: free recall 2/16, facilitated 9/16); clock test: 3/9. Later progression was good, with recovery of short-term memory and the capacity to retain concepts, and the patient was again able to perform the activities he previously carried out. CONCLUSIONS: There are three amnesic stroke syndromes with different semiological characteristics, depending on the vascular territory, that is, the PCA, thalamic arteries and anterior choroidal artery. In this case, the most striking points are the more intense disorders affecting short-term memory and retention, with relative conservation of long-term memory, and the location of the stroke in the hippocampus. Its good outcome allows it to be distinguished from vascular dementia.

Ictus amnésico por infarto hipocámpico / Amnesic stroke caused by hippocampal infarction

Introducción. El término ictus amnésico describe uncuadro de amnesia aguda relativamente persistente como síntomadominante y de origen vascular. Puede aparecer en las lesiones dela arteria cerebral posterior (ACP), las arterias talámicas y laarteria coroidea anterior. Existen pocas descripciones clínicas.Caso clínico. Varón de 77 años, con factores de riesgo vascular,que presentó déficit de memoria de instauración brusca con repercusiónen las actividades básicas de la vida diaria y apatía. En laexploración destacaba una amnesia episódica anterógrada conimposibilidad de fijar nueva información y una alteración clara dela memoria a corto plazo, con preservación relativa del acceso alos recuerdos antiguos. No existía otra focalidad sensitivomotora.En la TC se objetivó un infarto evolucionado silviano derecho yáreas hipodensas en ambos hipocampos. La evaluación neuropsicológicaobjetivó una amnesia global: MEC, 17/30; memoria detrabajo con MEC, 7/27; FVS (animales), 7; test de los siete minutosen memoria visuoverbal, recuerdo libre, 2/16, y facilitado, 9/16;test del reloj, 3/9. La evolución posterior fue favorable, con recuperaciónde la memoria y la capacidad de fijación a corto plazo eincorporación a sus actividades previas. Conclusiones. Existen tressíndromes de ictus amnésico con características semiológicas diferentesen función del territorio vascular: ACP, arterias talámicas y arteria coroidea anterior. En este caso, destaca la afectación másintensa de la memoria a corto plazo y de la fijación, con preservaciónrelativa de la memoria a largo plazo, junto a la localizaciónhipocámpica del ictus. La buena evolución permite diferenciarlo dela demencia vascular

Introduction. The term amnesic stroke is used to describe a condition in which the dominant symptom is a relativelypersistent acute amnesia of a vascular origin. It may appear in cases of lesions in the posterior cerebral artery (PCA),thalamic arteries and anterior choroidal artery, and clinical reports describing this condition are scarce. Case report. Wedescribe the case of a 77-year-old male with vascular risk factors who presented sudden onset mnemonic deficit that affectedbasic activities of daily living, and apathy. Examination of the patient revealed an anterograde episodic amnesia with aninability to retain new information and short-term memory was also clearly affected, although access to old memoriesremained relatively intact. There was no other sensory-motor focus. A CAT scan showed a right-side sylvian infarction andhypodense areas in both hippocampuses. The neuropsychological evaluation revealed global amnesia: CME (in Spanish,MEC) 17/30; working memory with CME 7/27; SVF (animals): 7; the 7-minute test (visual/verbal memory: free recall 2/16,facilitated 9/16); clock test: 3/9. Later progression was good, with recovery of short-term memory and the capacity to retainconcepts, and the patient was again able to perform the activities he previously carried out. Conclusions. There are threeamnesic stroke syndromes with different semiological characteristics, depending on the vascular territory, that is, the PCA,thalamic arteries and anterior choroidal artery. In this case, the most striking points are the more intense disorders affectingshort-term memory and retention, with relative conservation of long-term memory, and the location of the stroke in thehippocampus. Its good outcome allows it to be distinguished from vascular dementia

[Visual neglect secondary to left frontal haemorrhage]. / Negligencia visual secundaria a hemorragia frontal izquierda.

INTRODUCTION: The term visual neglect refers to a lack of attention to visual stimuli coming from the contralateral hemifield. The patient does not seek objects in the abnormal field and often only sees half of a paragraph when reading. Although the right inferior parietal lobe is the most frequently damaged region, the same symptomatology can be due to injury to the frontal lobe, the basal ganglia and the thalamus. CASE REPORT: Female aged 71 with a mitral prosthesis and atrial fibrillation in treatment with dicumarols, who presented a left frontal parenchymatous haemorrhage. The exploration revealed right visual hemineglect without ipsilateral homonymous hemianopsia, associated to a right hemiparesis. DISCUSSION: Even when visual neglect has been described in lesions affecting the parietal lobe, especially on the right hand side, the same symptomatology can be due to injury to the basal ganglia, the thalamus and the frontal lobe. In this last case, it seems that the basis for the pathogenesis lies in the damage done to the underlying white matter, which would disconnect the posterior parietal cortex from the prefrontal cortex.

Negligencia visual secundaria a hemorragia frontal izquierda / Visual neglect secondary to left frontal haemorrhage

Introducción. El término negligencia visual hace referencia a una falta de atención a los estímulos visuales procedentes del hemicampo contralateral. El paciente no busca objetos en el campo anormal, y a menudo sólo lee la mitad del párrafo. Si bien el lóbulo parietal inferior derecho es la región más frecuentemente lesionada, la misma sintomatología puede obedecer a lesiones del lóbulo frontal, ganglios de la base y tálamo. Caso clínico. Mujer de 71 años de edad portadora de prótesis mitral con fibrilación auricular y en tratamiento con dicumarínicos, que presenta una hemorragia parenquimatosa frontal izquierda. En la exploración se objetivó una heminegligencia visual derecha sin hemianopsia homónima ispilateral, asociada a una hemiparesia derecha. Discusión. Aun cuando la negligencia visual se ha descrito en lesiones que afectan al lóbulo parietal, sobre todo el derecho, la misma sintomatología puede obedecer a lesiones de los ganglios de la base, tálamo y lóbulo frontal. En este último supuesto, parece ser que la base patogénica radica en la afectación de la sustancia blanca subyacente, que desconectaría el córtex parietal posterior del córtex prefrontal (AU)

Introduction. The term visual neglect refers to a lack of attention to visual stimuli coming from the contralateral hemifield. The patient does not seek objects in the abnormal field and often only sees half of a paragraph when reading. Although the right inferior parietal lobe is the most frequently damaged region, the same symptomatology can be due to injury to the frontal lobe, the basal ganglia and the thalamus. Case report. Female aged 71 with a mitral prosthesis and atrial fibrillation in treatment with dicumarols, who presented a left frontal parenchymatous haemorrhage. The exploration revealed right visual hemineglect without ipsilateral homonymous hemianopsia, associated to a right hemiparesis. Discussion. Even when visual neglect has been described in lesions affecting the parietal lobe, especially on the right-hand side, the same symptomatology can be due to injury to the basal ganglia, the thalamus and the frontal lobe. In this last case, it seems that the basis for the pathogenesis lies in the damage done to the underlying white matter, which would disconnect the posterior parietal cortex from the prefrontal cortex (AU)

[Opercular syndrome of vascular aetiology]. / Síndrome opercular de etiología vascular.

INTRODUCTION: Facio linguo masticatory paralysis resulting from bilateral lesion of the anterior opercular region, known today as Foix Chavany Marie syndrome, appears very frequently in adult patients as a consequence of generally ischemic vascular lesions, which directly affect the Rolandic opercula or the subcortical area surrounding them. However, forms that are secondary to infections, neoplasias and even unilateral lesions have been reported. CASE REPORT: Female patient, aged 70, with unknown auricular fibrillation, which started suddenly with right faciobrachial paresis secondary to a left striated ischemic infarction. Approximately 24 hours after beginning intravenous heparinization, the patient presents anarthria, facial hypomimia without asymmetries, dysphagia above all for liquids and bilateral lingual paresis. Extraoccular movements, blinking and corneal reflex were normal. Understanding of spoken and written language was maintained and there were no apraxias or agnosias. Neurological exploration was compatible with an opercular syndrome (OS). Urgent brain CT revealed the existence of a right cortiico subcortical temporal haemorrhage, in addition to the prior contralateral ischemia. The association of both lesions, ischemic and haemorrhagic, mirrored, justified all the symptomatology. DISCUSSION: Anterior OS is characterised by a bilateral voluntary central paresis of the muscles innervated by the 5th, 7th, 9th, 10th and 12th cranial pairs with preservation of emotional or automatic mobility. Underlying mechanisms are also discussed.

Síndrome opercular de etiología vascular / Opercular syndrome of vascular aetiology

Introducción. La parálisis faciolinguomasticatoria por lesión bilateral de la región opercular anterior, conocida hoy como síndrome de Foix-Chavany-Marie, aparece en los pacientes adultos muy frecuentemente como consecuencia de lesiones vasculares generalmente isquémicas, que afectan directamente a los opérculos rolándicos o sus inmediaciones subcorticales. Se han descrito, no obstante, formas secundarias a infecciones, neoplasias e incluso lesiones unilaterales. Caso clínico. Paciente mujer, de 70 años de edad, con fibrilación auricular no conocida, que debuta bruscamente con paresia faciobraquial derecha secundaria a infarto isquémico estriado izquierdo. Aproximadamente 24 horas tras el inicio de la heparinización intravenosa, la paciente presentó anartria, hipomimia facial sin asimetrías, disfagia predominantemente para líquidos y paresia lingual bilateral. Los movimientos extraoculares, el parpadeo y el reflejo corneal eran normales. La comprensión del lenguaje oral y escrito se conservaba. No había apraxias ni agnosias. La exploración neurológica era compatible con un síndrome opercular (SO). La TAC cerebral de urgencia reveló la existencia de una hemorragia temporal corticosubcortical derecha, añadida a la previa isquémica con tralateral. La asociación de ambas lesiones, isquémica y hemorrágica, en espejo, justificaba toda la sintomatología. Discusión. El SO anterior se caracteriza por una paresia central voluntaria bilateral de los músculos inervados por los pares craneales V, VII, IX, X y XII, con preservación de la movilidad emocional o automática. Se discuten los mecanismos subyacentes (AU)

[Cerebral gliomatosis. A report of three cases and review of the literature]. / Gliomatosis cerebral. Presentación de tres casos y revisión de la literatura.

INTRODUCTION: Cerebral gliomatosis is an infiltrating, non destructive process of glial type, with a diffuse growth pattern and great clinical variation in the initial symptoms. Confirmation of the diagnosis requires histological study of the lesion showing infiltration by well differentiated mature astrocytes (atypical forms are rare). We report three cases diagnosed by our department over the past five years. CASE REPORTS: Case1. A 64 year old man presented with olfactory crises and right homonymous hemianopsia. On cerebral MR there was an extensive left occipital cortico subcortical lesion infiltrating the genum of the corpus callosum, with irregular uptake of contrast material. CASE REPORT 2: A 68 year old woman was admitted complaining of paresia of her right arm which had worsened over the past two months. On MR there was an extensive left paraventricular subcortical lesion, involving the anterior temporal and capsulo lenticular regions. Case 3. A 63 year old woman complained of staggering gait and headache. On examination she had a right facial palsy and intention tremor of her right arm. All the patients died. In all cases stereotactic biopsy confirmed the diagnosis of cerebral gliomatosis. CONCLUSIONS: Cerebral gliomatosis is an infiltrating glial disorder with a poor prognosis. The clinical diagnosis is suggested on cerebral MR studies and confirmed on histological studies.

Gliomatosis cerebral. Presentación de tres casos y revisión de la literatura / Cerebral gliomatosis. A report of three cases and review of the literature

Introducción. La gliomatosis cerebral es un proceso infiltrativo y no destructivo, de estirpe glial, con un patrón de crecimiento difuso y gran variabilidad clínica en cuanto a los síntomas de inicio. El diagnóstico de confirmación requiere el estudio histológico de la lesión y la demostración de infiltrado de astrocitos maduros bien diferenciados; son raras las atipias. Presentamos tres casos clínicos diagnosticados en nuestro servicio en los últimos cinco años. Casos clínicos. Caso 1: varón de 64 años de edad que inició con crisis olfatorias y hemoanopsia homónima derecha. En la RM cerebral se observó extensa lesión corticosubcortical occipital izquierda infiltrando el rodete del cuerpo calloso con captación irregular del contraste. Caso 2: mujer de 68 años de edad, que ingresó por paresia de extremidad superior derecha de dos meses de evolución, de carácter progresivo. La RM demostró la existencia de lesión extensa subcortical paraventricular izquierda con afectación temporal anterior y región capsulolenticular. Caso 3: mujer de 63 años de edad que inició con inestabilidad en la marcha y cefalea. En la exploración se observó paresia facial derecha y temblor de acción braquial derecho. En todos los casos la evolución fue mortal. Se realizó biopsia estereotáxica a los tres pacientes que confirmó el diagnóstico de gliomatosis cerebral. Conclusiones. La gliomatosis cerebral es un proceso infiltrativo glial con una tórpida evolución cuyo diagnóstico clínico se sugiere con la RM cerebral y se confirma con el estudio histológico (AU)

Pseudotumor cerebral: análisis de nuestra casuística y revisión de la literatura / Pseudotumor cerebri: analysis of our cases an review of the literature

Introducción. El pseudotumor cerebral (PC) es un síndrome complejo caracterizado por un aumento de la presión intracraneal (PIC) en ausencia de proceso expansivo, en general autolimitado aunque con frecuencia recidiva. El diagnóstico se basa en el registro del aumento de la PIC que será superior al límite de 250 mmH20. Su morbilidad radica básicamente en la posible pérdida visual asociada por la atrofia del nervio óptico. Cuando la etiología es desconocida esta entidad clínica se denomina hipertensión intracraneal idiopática. Pacientes y métodos. Presentamos las principales características de una serie de pacientes ingresados en nuestro servicio con el diagnóstico de PC y revisamos la literatura al respecto. Resultados. Ingresaron con el diagnóstico de PC 14 pacientes (12 mujeres y 2 varones). Doce pacientes empezaron con cefalea asociada o no a clínica visual. Los principales síntomas visuales fueron el oscurecimiento visual transitorio, escotomas, fotopsias y disminución de la agudeza visual. La cefalea fue holocraneal, continua y bien tolerada, o por el contrario uni o bilateral, pulsátil, moderada, con o sin fotofonofobia y con o sin náuseas o vómitos. En todos los pacientes se objetivó papiledema bilateral. En un caso existía además paresia facial bilateral y rigidez cervical. La campimetría fue patológica en cuatro casos (escotoma inferonasal, reducción concéntrica bilateral). La evolución fue tórpida en tan solo un caso. Conclusión. A pesar de su teórica benignidad y de las múltiples posibilidades terapéuticas, el PC puede generar una gran morbilidad visual que obliga a un precoz diagnóstico y a un estrecho seguimiento evolutivo (AU)

[Pseudotumor cerebri: analysis of our cases and review of the literature]. / Pseudotumor cerebral: análisis de nuestra casuística y revisión de la literatura.

INTRODUCTION: Pseudotumor cerebri (PC) is a complex syndrome characterized by increased intracranial pressure in the absence of any space occupying lesion, usually self limiting, but often relapsing. Diagnosis is based on a record of intracranial pressure of over a limit of 250 mmH2O. Morbidity is basically due to possible loss of vision associated with atrophy of the optic nerve. When the aetiology is unknown this clinical condition is known as idiopathic intracranial hypertension. PATIENTS AND METHODS: We describe the principal characteristics of a series of patients who were admitted to our department with the diagnosis of PC and review the relevant literature. RESULTS: Altogether 14 patients (12 women and 2 men) were admitted with the diagnosis of PC. In 12 patients the disorder presented with headache, with or without associated symptoms of disorders of vision. The main visual symptoms were transient darkening of vision, scotomas, photopsias and reduction in visual acuity. The headache was holocranial, continuous and well tolerated or alternatively uni or bilateral, pulsatile, moderate, with or without photophobia, and with or without nausea and vomiting. Bilateral papilloedema was seen in all patients. In one case there was also bilateral facial palsy and neck rigidity. In four cases visual field measurement were abnormal (inferoneasal scotoma, bilateral concentric reduction). Progress was poor in only one case. CONCLUSIONS: In spite of being theoretically benign, and there being many forms of treatment, PC may cause considerable morbidity of vision. Therefore, early diagnosis and close follow up attention is essential.

Infarto cardioembólico:características clínicas y evolutivas / Cardioembolic infarct: clinical characteristics and course

Introducción. Aproximadamente un 20 por ciento de todos los ictus isquémicos son debidos a cardioembolismo y la frecuencia es mayor en pacientes jóvenes. Nuestro objetivo es determinar las características clínicas y evolutivas de los infartos cardioembólicos (ICCE) comparándolos con aquellos infartos de otras etiologías (ICNCE). Pacientes y métodos. Se ha realizado un estudio propectivo de 354 pacientes ingresados durante un año tras excluir la isquemia transitoria y las hemorragias parenquimatosa/subaracnoidea. Establecimos dos grupos: ICCE (29,4 por ciento) e ICNCE (70,6 por ciento) y comparamos edad, sexo, factores de riesgo y evolución. Se ha realizado un estudio posterior durante dos años para valorar el índice de recurrencia. Resultados. Los pacientes con ICCE son mayores (75,89 frente a 72,58; p= 0,004), con frecuencia conocen la hora de inicio de los síntomas (p= 0,015) e ingresan preferentemente en las primeras seis horas de evolución (p= 0,01). La presencia de cardiopatía isquémica o fibrilación auricular es significativamente mayor (p= 0,0052; p= 0,005); desarrollan más complicaciones (p= 0,000); su estancia es más prolongada (13,62 frente a 11,8 días; p= 0,035); puntúan más bajo en el IB semanal (p= 0,0023) y la mortalidad es mayor (p= 0,000). Del subgrupo de 70 pacientes valorados dos años después recurrieron 11 casos sin que encontráramos diferencias significativas entre el tratamiento anticoagulante y el antiagregante. Conclusión. El ICCE acontece en pacientes más mayores, cursa con mayor déficit neurológico, se caracteriza por un peor pronóstico a corto plazo, desarrollan más complicaciones y la mortalidad es significativamente mayor (AU)

Patients with acenocoumarol treatment and migraine.

OBJECTIVE: The aim of our study was to investigate the possible effect of acenocoumarol, which is indicated for nonneurological disease, on headache. BACKGROUND: It has been suggested that anticoagulation can have beneficial effects in the control of migraine attacks. METHODS: Four hundred randomized patients on oral anticoagulant therapy were asked to complete a questionnaire regarding their headaches. RESULTS: Headache was present before or during oral anticoagulation in 166 (66 migraineurs and 100 nonmigraineurs) of 326 respondents. The major finding was that oral anticoagulation produced improvement in 63% of patients with migraine versus 38% of patients with nonmigranous headache. Improvement was related to the severity of migraine but not to age. CONCLUSIONS: Oral anticoagulant therapy can improve migraine. The way in which anticoagulant therapy acts on migraine is unknown, but potential mechanisms include its effect on platelet aggregability and pharmacological effects such as suppression of enhanced nitric oxide.

[Cardioembolic infarction: clinical course and characteristics]. / Infarto cardioembólico: características clínicas y evolutivas.

INTRODUCTION: Approximately 20% of all ischemic strokes are due to cardioembolism and occur more frequently in the younger patients. Our objective was to determine the clinical characteristics and course of cardioembolic infarcts (ICCE) comparing them with infarcts due to other aetiologies (ICNCE). PATIENTS AND METHODS: We made a prospective study of 354 patients admitted to hospital over a period of one year, after excluding transient ischaemia and parenchymatous/subarachnoid hemorrhage. Two groups were established: ICCE (29.4%) and ICNCE (70.6%), comparing age, sex, risk factors and course of the illness. Subsequently a study lasing two years was done to assess the recurrence rate. RESULTS: The ICCE patients were older (75.89 compared with 72.58, p = 0.004), often know the exact time of onset of their symptoms (p = 0.015) and usually are admitted to hospital during the first six hours of their illness (p = 0.01). There was a significantly higher incidence of ischemic cardiopathy or auricular fibrillation (p = 0.0052); p = 0.005); more complications arose (p = 0.000); stay in hospital was longer (13.62 as compared to 11.8 days; p = 0.035), there was a lower weekly BI score (p = 0.0023) and higher mortality (p = 0.000). In the subgroup of 70 patients evaluated two years later 11 cases recurred, with no difference observed between the anticoagulant and anti-aggregant groups. CONCLUSION: The ICCE occurs in older patients, they develop worse neurological defects, have a worse short-term prognosis, develop more complications and have significantly greater mortality.