Retardo En La Llegada De Pacientes Con Ictus Isquémico A Un Hospital Terciario De Ecuador / Delay In The Arrival Of Ischemic Stroke Patients At A Tertiary Hospital In Ecuador

Resumen Introducción: El tratamiento del ictus isquémico con trombolisis farmacológica en el entorno de una unidad de ictus se asocia a una mejor recuperación. El objetivo de este estudio es identificar variables que pudieran relacionarse con un retardo en la llegada al hospital. Métodos: Se realizó un estudio prospectivo, longitudinal, en los pacientes con diagnóstico de ictus isquémico que ingresaron en la Unidad de Ictus del Hospital de especialidades Eugenio Espejo de la ciudad de Quito, Ecuador, en el periodo comprendido entre noviembre de 2016 a julio de 2017. Se compararon los pacientes que fueron tratados con r-Tpa con los que llegaron después de las 4,5 horas. Resultados: Se estudiaron un total de 61 pacientes: 51 de ellos arribaron al hospital después de las 4,5 horas, y 10 (16,4 %) fueron sometidos a trombolisis en periodo de ventana terapéutica. Ninguna de las variables sociodemográficas y clínicas excepto el antecedente de fibrilación auricular se relacionó con el arribo precoz. En el grupo que recibió r-Tpa el porcentaje de pacientes que buscó atención médica en el hospital como primera opción fue significativamente mayor respecto a los que llegaron después del periodo de ventana (90 vs 49 %, p 0,0170). El mayor impacto de la remisión precoz y la trombolisis fue sobre la diferencia de puntaje entre la evaluación inicial y al alta en la escala del NIHSS. Conclusiones: Los resultados apuntan a que existe desconocimiento acerca del ictus y qué conducta asumir. El tratamiento con r-Tpa demuestra beneficios en nuestro medio.

Abstract Introduction: In an Stroke unit, the ischemic stroke treatment with a pharmacological thrombolysis is associated with a better recovery. The aim of this study is to identify the variables having a significant impact in the delay of the arrival of patients at a tertiary hospital. Methods: A prospective and longitudinal study was undertaken in patients with an ischemic stroke diagnosis, who were admitted to the Stroke Unit of Eugenio Espejo Hospital of Quito city in Ecuador in the time period from November 2016 to July 2017. Patients treated with r-Tpa were compared to those who arrived 4,5 hours later. Results: A total of 61 patients were analyzed: of those, 51 arrived 4,5 hours after first symptoms at the hospital, and 10 (16,4%) were thrombolysed in the period of therapeutic window. None of the social, demographic and clinical variables were related to the early arrival, except the history of an atrial fibrillation. In the group of patients who received r-Tpa, a significantly higher percent sought for medical care as a first option compared with those arriving after the 4,5 hours (90 vs 49%, p 0,0170). The greatest impact of the early referral and the thrombolysis concerned the difference of score between the initial medical evaluation and the hospital discharge in the NIHSS scale. Conclusions: The results of this study point out to the unawareness of the stroke and the behavior to follow. The r-Tpa treatment shows clear benefits to the patients in our environment.

Estatus epiléptico. Factores asociados a una evolución desfavorable en un centro terciario / Status Epilepticus. Prognostic Variables for an Unfavorable Outcome in a tertiary center of care

Resumen Introducción: El Estatus Epiléptico (EE) es una causa frecuente de emergencia neurológica. Escasos son los estudios realizados en Suramérica para evaluar los factores pronósticos de mortalidad y discapacidad en pacientes con EE. Objetivo: Determinar las variables asociadas a una evolución desfavorable (ED) al alta hospitalaria en pacientes con EE. Método: Se realizó un estudio retrospectivo durante el periodo enero 2016-junio 2017. Un total de 26 pacientes fueron diagnosticados con EE en sus diferentes variantes. Se evaluó el efecto de las variables clínicas, radiológicas y electroencefalográficas sobre la evolución hospitalaria final acorde la escala de Rankin. Resultados: 12 (46,2%) de los pacientes tuvieron una ED al alta hospitalaria, con una mortalidad que alcanzó el 23%. Existió un predominio del sexo masculino (76,9%). Las variables asociadas de forma independiente con una ED fueron el número de comorbilidades (p=0.01, OR: 4.27-95%CI1.33-13.6), lesiones en la imagen por Resonancia Magnética (IRM) (p=0.04, OR: 3.92-95%CI1.05-14.61) y el EE refractario (p=0.01, OR: 12.52-95%CI1.85-84.44), y la edad (p=0.07 OR: 1.03-95%CI0.99-1.07). Mientras que, un buen estado clínico inicial acorde la escala de Glasgow fue un factor protector (p=0.00 OR: 0.49-IC95%0.29-0.84) de tener una ED. Conclusiones: Tener una ED se asocia a la edad, el estado clínico inicial del paciente acorde la escala de Glasgow, así como lesiones en la IRM. EE refractario y más de 4 comorbilidades también fueron predictores de una ED al alta hospitalaria.

Abstract Introduction: Status Epilepticus (SE) is a frequent neurologic emergency. Little research has been done in South America to evaluate the prognostic variables of mortality and disability in patients with SE. Objective: To determine the variables associated to an unfavorable outcome at hospital discharge in the patients who were treated for SE. Methods: A retrospective study was performed during the period of January 2016-June 2017. A total of 26 patients were diagnosed of SE and its different variants. The effects of clinical, radiological, and electroencephalographic features on hospital outcome according Rankin scale were evaluated. Results: Twelve (46.2%) patients had an unfavorable outcome at hospital discharge, while the mortality rate reached 23.1%. There was a predominance of males with a 76.9% of all the patients. The independent variables associated with an unfavorable outcome were the number of comorbidities (p=0.01, OR: 4.27-95%CI1.33-13.6), structural lesions on the Magnetic Resonance Image (MRI) (p=0.04, OR: 3.92-95%CI1.05-14.61) and refractory SE (p=0.01, OR: 12.52-95%CI1.85-84.44). There was also a trend for age (p=0.07 OR: 1.03-95%CI0.99-1.07). While an initial good clinical condition, according to the Glasgow Scale represent a protective factor (p=0.00 OR: 0.49-IC95% 0.29-0.84) of an unfavorable outcome. Conclusions: The unfavorable outcome was marginally associated with patient age, clinical status at the onset of SE according to the Glasgow Coma Scale, as well as brain lesions on brain MRI. Refractory SE and more than 4 comorbidities are predictors of an unfavorable outcome at hospital discharge.

Foramen oval permeable, un diagnóstico posible en manos del neurólogo. Descripción de caso / Patent Foramen Ovale, A Possible Diagnosis From The Neurologist. Case Report

Resumen Introducción: En pacientes con ictus isquémico criptogénico se ha descrito una alta prevalencia de alteraciones del septum auricular relacionadas con un riesgo aumentado de presentar recurrencia. Objetivo: Presentar la historia clínica de un paciente joven con antecedente de diabetes mellitus e ictus isquémico en el que no se demuestran alteraciones arteriales. A partir de la realización de un estudio de Doppler trasncraneal con test de burbujas se diagnostica un foramen oval permeable. Conclusión: En el paciente que describimos, la realización de un estudio de DTC como parte de la evaluación inicial ayudó a precisar la etiología. La demostración de un foramen ovale permeable tiene implicaciones en la prevención secundaria del ictus.

Abstract Introduction: A high prevalence of atrial septal defects is reported in patients with cryptogenic ischemic stroke, also related to an increase of the risk of recurrence. Objective: To report case of a young patient with a history of diabetes mellitus and ischemic stroke without arterial changes proven. A transcraneal Doppler study with a bubble test helped to diagnose a patent foramen ovale. Conclusion: As part of the initial evaluation of this patient, a TCD study has helped to clarify the stroke etiology. The demonstration of a patent foramen ovale has implications for the secondary prevention of stroke.

TCD diastolic velocity decay and pulsatility index increment in PVS cases.

BACKGROUND: Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS. METHODS: We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm. RESULTS: Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients. CONCLUSIONS: We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.

Eficacia del Doppler transcraneal para la detección del vasoespasmo en las arterias cerebrales anteriores / Effectiveness of transcranial Doppler ultrasonography for the detection of vasospasm in the anterior

Introducción. Las arterias cerebrales anteriores son ven afectadas con frecuencia por el vasoespasmo secundario a hemorragia subaracnoidea. La eficacia del ultrasonido Doppler transcraneal para detectar esta complicación no se ha determinado con exactitud. Objetivo. Comprobar la utilidad del ultrasonido Doppler transcraneal para diagnosticar el vasoespasmo de las arterias cerebrales anteriores en pacientes con hemorragia subaracnoidea. Pacientes y métodos. Estudiamos 56 pacientes entre los días 4 y 14 de la hemorragia subaracnoidea, a los cuales se realizó un estudio neurovascular contrastado y monitorización diaria con Doppler transcraneal. Todos los pacientes se encontraban con grado clínico de la escala de la Federación Mundial de Cirujanos Neurológicos entre 1 y 3; 46 tenían aneurismas y en 20 el sangramiento fue intenso (grado 3-4 en la escala de Fisher). Resultados. La frecuencia de vasoespasmo angiográfico fue del 41% en las arterias cerebrales anteriores. Las velocidadesmedias del flujo en los enfermos con vasoespasmo fueron de 84,5 cm/s. Los picos máximos de velocidad de flujo media se obtuvieron en el décimo día. La sensibilidad fue del 57,9% para velocidades de flujo iguales o superiores a 87,5 cm/s, y el valor predictivo positivo fue del 66,6%. No se encontró relación significativa entre el resultado del Doppler transcraneal, el grado clínico y la intensidad del sangramiento en la tomografía axial computarizada. Conclusión. La precisión global de la prueba fue buena, la especificidad y el valor predictivo negativo fueron excelentes; sin embargo, la sensibilidad fue baja (AU)

Introduction. The anterior cerebral arteries are often affected by vasospasm secondary to subarachnoid haemorrhage. The effectiveness of transcranial Doppler ultrasonography to detect this complication has still not been accurately determined. Aim. To assess the usefulness of transcranial Doppler ultrasonography for diagnosing vasospasm of the anterior cerebral arteries in patients with subarachnoid haemorrhage. Patients and methods. We studied 56 patients between the 4th and 14th days of their subarachnoid haemorrhage; all of them were submitted to a contrast-enhanced neurovascular study and daily monitoring with transcranial Doppler ultrasonography. All the patients had a clinical degree of between 1 and 3 on the World Federation of Neurological Surgeons scale, 46 of them had aneurysms, and bleeding was intense in 20 cases (degree 3-4 on the Fisher scale). Results. The frequency of angiographic vasospasm was 41% in the anterior cerebral arteries. The mean flow velocities in patients with vasospasm were 84.5 cm/s. The maximum peaks of mean blood flow rate were obtained on the tenth day. Sensitivity was 57.9% for flow rates equal to or above 87.5 cm/s, and the predictive positive value was 66.6%. No significant relation was found between the findings of the transcranial Doppler ultrasonography scan, the degree of clinical symptoms and the intensity of bleeding in the computerised axial tomography scan. Conclusions. The overall precision of the test was good, the specificity and predictive negative value were excellent, but sensitivity was low (AU)

Criterios diagnósticos de la muerte encefálica según la resolución 90 del Ministerio de Salud Pública / Diagnostic criteria of encephalic death according to Resolution 90 from Health Public Ministry

Se presentan los criterios diagnósticos de la muerte con base legal en nuestro país, según la Resolución 90 del Ministerio de Salud Pública. Se consideraron tres posibles escenarios para diagnosticar la muerte: 1) Fuera de los cuidados intensivos (sin soporte vital). Los médicos aplican los criterios cardiocirculatorios y respiratorios clßsicos; 2) En situaciones forenses. Se aplican los llamados signos cadavéricos; 3) En condiciones de cuidados intensivos (con apoyo vital). Es cuando se aplican los criterios para determinar pérdida irreversible de las funciones encefálicas, o sea, se lleva a cabo el diagnóstico de la muerte encefálica. No obstante, eso no quiere decir que existen distintos tipos de muerte, pues la Comisión Nacional para la determinación y certificación de la muerte concluyó que existe solo una muerte en el ser humano, y es cuando ocurre una pérdida irreversible de las funciones encefálicas. Una parada cardiorrespiratoria solamente conlleva a la muerte cuando la anoxia y la isquemia son lo suficientemente prolongadas para destruir las estructuras intracraneales, teniéndose en cuenta además la posibilidad de que el sujeto esté bajo el efecto o no de neuroprotectores, como es en los casos de hipotermia accidental. En esa Resolución se decidió mostrar al médico los métodos para diagnosticar la muerte agrupados en los llamados signos ciertos de la muerte, como se han considerado en los textos clásicos de medicina forense, resumidos en 9 signos. El signo cierto número 9 se refiere a la pérdida irreversible de las funciones integradas en el encéfalo, o sea el diagnóstico de la muerte encefálica, que se describe en este trabajo(AU)

Authors showed the death diagnostic criteria legally based in our country, according the Resolution 90 of the Public Health Ministry. Three possible scenarios were considered to diagnose the death: out of intensive care (without vital support). Physicians apply the classic cardio-circulatory and respiratory criteria; in forensic situations the so-called cadaveric signs are applied; in intensive care conditions (with vital support) it is when the criteria to determine the irreversible loss of brain functions are applied, i.e. a diagnosis of brain death is made. However, that no means that there are different types of death, since the National Commission for death assessment and certification concluded that there is only a death in the human being, and it is when happen a irreversible loss of brain functions. A cardio-respiratory arrest only leads to death when anoxia and ischemia are enough prolonged to destroy the intracranial structures, considering also the possibility that subject be or not under the neuroprotection effect, like in the cases of accidental hypothermia. In such Resolution the physicians may to see the methods to diagnose the death grouped in the so called true signs of death considered in the classic texts of forensic medicine, summarized in 9 signs. The true sign nomber 9 is to refer to the irreversible loss the brain functions, i.e. brain death diagnosis, described in this paper(AU)

Mecanismos fisiopatógicos en la muerte encefálica / Physiopathologic mechanisms in encephalic death

La muerte encefálica se basa en un diagnóstico clínico, y se acepta como sinónimo de muerte del individuo. Se llega a este estado cuando una lesión catastrófica provoca un coma irreversible, con ausencia de reflejos de tronco encefálico y apnea. La muerte encefálica se define como la pérdida irreversible de las funciones de todo el encéfalo, incluyendo los hemisferios cerebrales y el tronco encefálico. Las causas que llevan a la pérdida irreversible de las funciones del encéfalo son las mismas descritas que provocan un coma, las cuales se han agrupado en: estructurales y multifocales-metabólicas-difusas. Las causas estructurales se subdividen en compresivas y destructivas. Las lesiones compresivas causan conflictos de espacio en la cavidad intracraneana dando lugar a un aumento de la presión intracraneana y herniaciones. Las causas destructivas que llevan a la muerte encefálica afectan el diencéfalo, tronco encefálico y hemisferios cerebrales. Las etiologías multifocales-metabólicas-difusas constituyen un grupo muy variado de causas que provocan la pérdida irreversible de las funciones del encéfalo a través de diversos mecanismos bioquímicos y fisiopatológicos. No obstante, las etiologías descritas provocan la ausencia irreversible del flujo sanguíneo cerebral, que es la causa final que da lugar a la destrucción de las estructuras intracraneales. Aunque la muerte encefálica se basa en un diagnóstico clínico, el conocimiento de la fisiopatología de este estado permite estudiar los posibles mecanismos que llevan a que un enfermo evolucione hacia una muerte encefálica, lo que da la certeza acerca de la irreversibilidad de este diagnóstico(AU)

Encephalic death is bases on a clinical diagnosis and it is accepted like a synonym of subject death. The person arrives to this stage when a catastrophic lesion provokes an irreversible coma with a lack of reflexes from the encephalic trunk and apnea. The encephalic death is defined like an irreversible loss of all encephalon including the brain hemispheres and the encephalic trunk. The different causes of irreversible loss of encephalon functions are the same described provoking a coma, which are grouped in: structural and diffuse-metabolic multifocal. The structural causes are subdivided in compressive and destructives. The compressive ones cause space problems in intracranial cavity leading to an increase of intracranial pressure and herniations. The destructive ones leading to encephalic death affect the diencephalon, the encephalic trunk and brain hemispheres. Diffuse-metabolic multifocal etiologies are a very varied group of causes provoking the irreversible loss of encephalon functions through diverse biochemical and physiopathologic mechanisms. However, the etiologies described provoke the irreversible lack of brain blood flux the final cause leading to destruction of intracranial structures. Although the encephalic death is based on a clinical diagnosis, knowledge of physiopathology of this status allows to study the potential mechanisms leading to a patient evolve to an encephalic death and be certain that there is a irreversibility of this diagnosis(AU)

Mecanismos fisiopatógicos en la muerte encefálica / Physiopathologic mechanisms in encephalic death

La muerte encefálica se basa en un diagnóstico clínico, y se acepta como sinónimo de muerte del individuo. Se llega a este estado cuando una lesión catastrófica provoca un coma irreversible, con ausencia de reflejos de tronco encefálico y apnea. La muerte encefálica se define como la pérdida irreversible de las funciones de todo el encéfalo, incluyendo los hemisferios cerebrales y el tronco encefálico. Las causas que llevan a la pérdida irreversible de las funciones del encéfalo son las mismas descritas que provocan un coma, las cuales se han agrupado en: estructurales y multifocales-metabólicas-difusas. Las causas estructurales se subdividen en compresivas y destructivas. Las lesiones compresivas causan conflictos de espacio en la cavidad intracraneana dando lugar a un aumento de la presión intracraneana y herniaciones. Las causas destructivas que llevan a la muerte encefálica afectan el diencéfalo, tronco encefálico y hemisferios cerebrales. Las etiologías multifocales-metabólicas-difusas constituyen un grupo muy variado de causas que provocan la pérdida irreversible de las funciones del encéfalo a través de diversos mecanismos bioquímicos y fisiopatológicos. No obstante, las etiologías descritas provocan la ausencia irreversible del flujo sanguíneo cerebral, que es la causa final que da lugar a la destrucción de las estructuras intracraneales. Aunque la muerte encefálica se basa en un diagnóstico clínico, el conocimiento de la fisiopatología de este estado permite estudiar los posibles mecanismos que llevan a que un enfermo evolucione hacia una muerte encefálica, lo que da la certeza acerca de la irreversibilidad de este diagnóstico.

Encephalic death is bases on a clinical diagnosis and it is accepted like a synonym of subject death. The person arrives to this stage when a catastrophic lesion provokes an irreversible coma with a lack of reflexes from the encephalic trunk and apnea. The encephalic death is defined like an irreversible loss of all encephalon including the brain hemispheres and the encephalic trunk. The different causes of irreversible loss of encephalon functions are the same described provoking a coma, which are grouped in: structural and diffuse-metabolic multifocal. The structural causes are subdivided in compressive and destructives. The compressive ones cause space problems in intracranial cavity leading to an increase of intracranial pressure and herniations. The destructive ones leading to encephalic death affect the diencephalon, the encephalic trunk and brain hemispheres. Diffuse-metabolic multifocal etiologies are a very varied group of causes provoking the irreversible loss of encephalon functions through diverse biochemical and physiopathologic mechanisms. However, the etiologies described provoke the irreversible lack of brain blood flux the final cause leading to destruction of intracranial structures. Although the encephalic death is based on a clinical diagnosis, knowledge of physiopathology of this status allows to study the potential mechanisms leading to a patient evolve to an encephalic death and be certain that there is a irreversibility of this diagnosis.

Criterios diagnósticos de la muerte encefálica según la resolución 90 del Ministerio de Salud Pública / Diagnostic criteria of encephalic death according to Resolution 90 from Health Public Ministry

Se presentan los criterios diagnósticos de la muerte con base legal en nuestro país, según la Resolución 90 del Ministerio de Salud Pública. Se consideraron tres posibles escenarios para diagnosticar la muerte: 1) Fuera de los cuidados intensivos (sin soporte vital). Los médicos aplican los criterios cardiocirculatorios y respiratorios clßsicos; 2) En situaciones forenses. Se aplican los llamados signos cadavéricos; 3) En condiciones de cuidados intensivos (con apoyo vital). Es cuando se aplican los criterios para determinar pérdida irreversible de las funciones encefálicas, o sea, se lleva a cabo el diagnóstico de la muerte encefálica. No obstante, eso no quiere decir que existen distintos tipos de muerte, pues la Comisión Nacional para la determinación y certificación de la muerte concluyó que existe solo una muerte en el ser humano, y es cuando ocurre una pérdida irreversible de las funciones encefálicas. Una parada cardiorrespiratoria solamente conlleva a la muerte cuando la anoxia y la isquemia son lo suficientemente prolongadas para destruir las estructuras intracraneales, teniéndose en cuenta además la posibilidad de que el sujeto esté bajo el efecto o no de neuroprotectores, como es en los casos de hipotermia accidental. En esa Resolución se decidió mostrar al médico los métodos para diagnosticar la muerte agrupados en los llamados signos ciertos de la muerte, como se han considerado en los textos clásicos de medicina forense, resumidos en 9 signos. El signo cierto número 9 se refiere a la pérdida irreversible de las funciones integradas en el encéfalo, o sea el diagnóstico de la muerte encefálica, que se describe en este trabajo.

Authors showed the death diagnostic criteria legally based in our country, according the Resolution 90 of the Public Health Ministry. Three possible scenarios were considered to diagnose the death: out of intensive care (without vital support). Physicians apply the classic cardio-circulatory and respiratory criteria; in forensic situations the so-called cadaveric signs are applied; in intensive care conditions (with vital support) it is when the criteria to determine the irreversible loss of brain functions are applied, i.e. a diagnosis of brain death is made. However, that no means that there are different types of death, since the National Commission for death assessment and certification concluded that there is only a death in the human being, and it is when happen a irreversible loss of brain functions. A cardio-respiratory arrest only leads to death when anoxia and ischemia are enough prolonged to destroy the intracranial structures, considering also the possibility that subject be or not under the neuroprotection effect, like in the cases of accidental hypothermia. In such Resolution the physicians may to see the methods to diagnose the death grouped in the so called true signs of death considered in the classic texts of forensic medicine, summarized in 9 signs. The true sign nomber 9 is to refer to the irreversible loss the brain functions, i.e. brain death diagnosis, described in this paper.

TCD systolic spikes in a malignant MCA infarct.

INTRODUCTION: Malignant MCA infarction results in significant space occupying effect and intracranial pressure (ICP) increment. Due to the high mortality rate in such patients, the term malignant MCA infarction was coined. METHODS: We studied a patient who developed a sudden onset of slurred speech, right hemiplegia, and decreased level of arousal. Two days later CT scan showed a massive cerebral infarct, involving the left MCA territory. RESULTS: A transcranial Doppler exam showed a normal flow pattern in the right hemisphere, but in the left hemisphere systolic spikes without diastolic flow were observed in internal carotid artery, anterior cerebral artery, as well as in the MCA. CONCLUSIONS: The pathophysiologic mechanisms leading to BD might asymmetrically begin in cerebral hemispheres in malignant MCA infarcts.

Brain death diagnosis and apnea test safety.

The apnea test is a mandatory examination for determining brain death (BD), because it provides an essential sign of definitive loss of brainstem function. However, several authors have expressed their concern about the safety of this procedure as there are potential complications such as severe hypotension, pneumothorax, excessive hypercarbia, hypoxia, acidosis, and cardiac arrhythmia or asystole. These complications may constrain the examiner to abort the test, thereby compromising BD diagnosis. Nevertheless, when an appropriate oxygen-diffusion procedure is used, this technique is safe. We review here the prerequisites to begin the test, its procedure, potential complications, and the use of alternative ancillary tests. We recommend that the apnea test be retained as a mandatory procedure for the diagnosis of BD. In those situations when the apnea test is terminated by the examiner for some reason or when it is impossible to carry it out in a patient due to the presence of some pathologic condition, alternative ancillary tests should be used to confirm BD.

Subsequent bilateral thalamic haemorrhage.

Simultaneous or subsequent bilateral thalamic haemorrhage is rare, and most reported cases are from Asian countries. An 80-year-old white Cuban man, with a history of arterial hypertension, suffered sudden onset of right hemiparesis. Computed tomography (CT) scan showed a left posteromedial thalamic haemorrhage. Two days later his condition suddenly deteriorated: blood pressure was 220/105 mm Hg, he was stuporous and tetraplegic, respiration was ataxic, and his gaze was fixed and deviated downward and inward. CT scan showed haemorrhages in both thalami, extending to the ventricles. 32 h later the patient died. There are few previous publications of simultaneous or subsequent bilateral thalamic haemorrhages and this is the first report involving a Hispanic patient. Prognosis in patients with bilateral thalamic haemorrhage is poor, and the mechanism underlying the development of subsequent and symmetrical bleeding is not clear.

Duplicated middle cerebral artery.

Duplicated middle cerebral artery (DMCA) is an anomalous vessel arising from the internal carotid artery. The incidence DMCA is relatively law, and an association between this anomaly and cerebral aneurysms has been documented. There is a controversy whether DMCA may have perforating arteries. This is an important fact to consider in aneurysm surgery. We report the case of a 34-year-old black woman who suffered a subarachnoid hemorrhage and the angiography a left DMCA, and an aneurysm in an inferior branch of the main MCA. The DMCA and the MCA had perforating arteries. The aneurysm was clipped without complications. The observation of perforating arteries in our patient confirms that the DMCA may have perforating arteries. This is very important to be considered in cerebral aneurysms surgery. Moreover, the DMCA may potentially serve as a collateral blood supply to the MCA territory in cases of MCA occlusion.

Coexistence of vasospasm and microembolism detected by transcranial Doppler ultrasonography in a patient with subarachnoid haemorrhage.

Delayed cerebral ischaemia as a clinical expression of vasospasm is one of the main complications of subarachnoid haemorrhage. In some cases, ischaemic manifestations can be related to cerebral emboli, but the relationship between vasospasm, damaged endothelial lining, and embolism, remains to be proven. The case is presented of a 56-year-old female patient who, 5 days after the clipping of an aneurysm in the left middle cerebral artery (MCA), suffered transient ischaemic attacks (TIAs) of this arterial territory. Transcranial Doppler ultrasonography showed an increment of the left MCA mean flow velocity, and 12 microembolic signals were detected in 30 mins. The coexistence of microemboli signals with severe vasospasm in the same arterial segment might suggest a causal relationship between cerebral embolism, severity of vasospasm, and TIAs.