La influencia de la gestión organizativa en el tiempo puerta-aguja del tratamiento fibrinolítico / The influence of organisational management on door-to-needle times for fibrinolytic treatment

Introducción: El tiempo puerta-aguja (TPA) es el principal indicador del proceso del código ictus (CI). Según la guía de 2018 de la American Heart Association/American Stroke Associa-tion, el objetivo TPA debe ser inferior a 45 minutos. Para conseguirlo son necesarios protocolos eficaces y revisados de actuación extrahospitalaria e intrahospitalaria. Método: Analizamos la influencia de cambios organizativos entre 2011 y 2019 en el TPA y en la evolución clínica de los pacientes tratados con fibrinólisis. Utilizamos los datos de nuestro centro monitorizados y custodiados por el Pla Director en l’àmbit de la Malaltia Vascular Cerebral dela Generalitat de Catalunya. Entre otras medidas se han analizado las diferencias entre los a ̃nos y las derivadas de la implantación del modelo Helsinki. Resultados: Se estudiaron 447 pacientes, existiendo diferencias estadísticamente significativas en el TPA entre los diferentes a ̃nos. La activación del CI de forma extrahospitalaria en 315(70,5%) pacientes redujo el TPA una mediana de 14 minutos. Sin embargo, el modelo de regresión lineal sólo evidenció una relación inversamente proporcional entre la adopción del modelo deCI Helsinki (MH) y el TPA (coeficiente beta −0,42; p < 0,001). La eliminación de la figura delneurólogo vascular tras la adopción del MH empeoró el TPA y la mortalidad a los 90 días.Conclusión: El modelo organizativo influye en el TPA, siendo en nuestra muestra la aplicacióndel MH, la existencia de la figura del neurólogo vascular referente y la prenotificación del CIfactores claves para la reducción del TPA y la mejora clínica del paciente.(AU)

Introduction: Door-to-needle time (DNT) has been established as the main indicator in codestroke protocols. According to the 2018 guidelines of the American Heart Association/AmericanStroke Association, DNT should be less than 45 minutes; therefore, effective and revised pre-admission and in-hospital protocols are required. Method: We analysed organisational changes made between 2011 and 2019 and their influenceon DNT and the clinical progression of patients treated with fibrinolysis. We collected datafrom our centre, stored and monitored under the Master Plan for Cerebrovascular Disease ofthe regional government of Catalonia. Among other measures, we analysed the differencesbetween years and differences derived from the implementation of the Helsinki model.Results: The study included 447 patients, and we observed significant differences in DNTbetween different years. Pre-hospital code stroke activation, recorded in 315 cases (70.5%),reduced DNT by a median of 14 minutes. However, the linear regression model only showed aninversely proportional relationship between the adoption of the Helsinki code stroke model andDNT (beta coefficient, —0.42; P < .001). The removal of vascular neurologists after the adoptionof the Helsinki model increased DNT and the 90-day mortality rate. Conclusion: DNT is influenced by the organisational model. In our sample, the application ofthe Helsinki model, the role of the lead vascular neurologist, and notification of code strokeby pre-hospital emergency services are key factors for the reduction of DNT and the clinicalimprovement of the patient.(AU)

The influence of organisational management on door-to-needle times for fibrinolytic treatment.

INTRODUCTION: Door-to-needle time (DNT) has been established as the main indicator in code stroke protocols. According to the 2018 guidelines of the American Heart Association/American Stroke Association, DNT should be less than 45minuts; therefore, effective and revised pre-admission and in-hospital protocols are required. METHOD: We analysed organisational changes made between 2011 and 2019 and their influence on DNT and the clinical progression of patients treated with fibrinolysis. We collected data from our centre, stored and monitored under the Master Plan for Cerebrovascular Disease of the regional government of Catalonia. Among other measures, we analysed the differences between years and differences derived from the implementation of the Helsinki model. RESULTS: The study included 447 patients, and we observed significant differences in DNT between different years. Pre-hospital code stroke activation, recorded in 315 cases (70.5%), reduced DNT by a median of 14minutes. However, the linear regression model only showed an inversely proportional relationship between the adoption of the Helsinki code stroke model and DNT (beta coefficient, -0.42; P<.001). The removal of vascular neurologists after the adoption of the Helsinki model increased DNT and the 90-day mortality rate. CONCLUSION: DNT is influenced by the organisational model. In our sample, the application of the Helsinki model, the role of the lead vascular neurologist, and notification of code stroke by pre-hospital emergency services are key factors for the reduction of DNT and the clinical improvement of the patient.

The influence of organisational management on door-to-needle times for fibrinolytic treatment. / La influencia de la gestión organizativa en el tiempo puerta-aguja del tratamiento fibrinolítico.

INTRODUCTION: Door-to-needle time (DNT) has been established as the main indicator in code stroke protocols. According to the 2018 guidelines of the American Heart Association/American Stroke Association, DNT should be less than 45minutes; therefore, effective and revised pre-admission and in-hospital protocols are required. METHOD: We analysed organisational changes made between 2011 and 2019 and their influence on DNT and the clinical progression of patients treated with fibrinolysis. We collected data from our centre, stored and monitored under the Master Plan for Cerebrovascular Disease of the regional government of Catalonia. Among other measures, we analysed the differences between years and differences derived from the implementation of the Helsinki model. RESULTS: The study included 447 patients, and we observed significant differences in DNT between different years. Pre-hospital code stroke activation, recorded in 315 cases (70.5%), reduced DNT by a median of 14minutes. However, the linear regression model only showed an inversely proportional relationship between the adoption of the Helsinki code stroke model and DNT (beta coefficient, -0.42; P<.001). The removal of vascular neurologists after the adoption of the Helsinki model increased DNT and the 90-day mortality rate. CONCLUSION: DNT is influenced by the organisational model. In our sample, the application of the Helsinki model, the role of the lead vascular neurologist, and notification of code stroke by pre-hospital emergency services are key factors for the reduction of DNT and the clinical improvement of the patient.

Incidental findings on brain MRI in a cohort of diabetic patients.

OBJECTIVE: To study the frequency and management of incidental findings in nonenhanced brain MRI of a middle-aged population of type 2 diabetic patients. METHODS: We retrospectively analyzed the results of 289 brain MRI obtained from subjects between 40-75 years recruited from a previous study. Incidental findings were classified into three categories: (1) Vascular findings; (2) neoplastic findings; and (3) others. On the other side, we made a classification of referral findings. To compare our results, we reviewed the prevalence and evidence about management of both incidental and referral findings in other series. RESULTS: We found an overall prevalence of incidental findings of 10.4% (30/289). Incidental findings raised according to age. The most common incidental findings were: 7 vascular (2.4%), 6 calcifications (2.1%), 6 cystic (2.1%) and 5 neoplastic (1.7%) lesions. A percentage of 1.7% (5/289) were referral findings which required further clinical work-up. CONCLUSION: Incidental findings are relatively common in patients with type 2 diabetes. The most frequent are vascular findings, accordance with previous studies. Referral findings are uncommon. Clinical evidence about how to best manage the majority of incidental findings is lacking.

The determination of copeptin levels helps management decisions among transient ischaemic attack patients.

BACKGROUND: Most approaches to transient ischaemic attack (TIA) triage use clinical scores and vascular imaging; however, some biomarkers have been suggested to improve the prognosis of TIA patients. METHODS: Serum levels of copeptin, adiponectin, neopterin, neuron-specific enolase, high-sensitivity C-reactive protein, IL-6, N-terminal pro-B-type natriuretic peptide, S100ß, tumour necrosis factor-alpha and IL-1α as well as clinical characteristics were assessed on consecutive TIA patients during the first 24 h of the onset of symptoms. RESULTS: Among 237 consecutive TIA patients, 12 patients (5%) had a stroke within 7 days and 15 (6%) within 90 days. Among all candidate biomarkers analysed, only copeptin was significantly increased in patients with stroke recurrence (SR) within 7 days (P = 0.026) but not within 90 days. A cut-off point of 13.8 pmol/l was established with a great predictive negative value (97.4%). Large artery atherosclerosis (LAA) [hazard ratio (HR) 12.7, 95% CI 3.2-50.1, P < 0.001] and copeptin levels ≥13.8 pmol/l (HR 3.9, 95% CI 1.01-14.4, P = 0.039) were independent predictors of SR at the 7-day follow-up. LAA was the only predictor of 90-day SR (HR 7.4, 95% CI 2.5-21.6, P < 0.001). ABCD3I was associated with 7- and 90-day SRs (P = 0.025 and P = 0.034, respectively). The association between copeptin levels and LAA had a diagnostic accuracy of 90.3%. CONCLUSIONS: Serum copeptin could be an important prognostic biomarker to guide management decisions among TIA patients. Therefore, TIA patients with copeptin levels below 13.8 pmol/l and without LAA have an insignificant risk of 7-day SR and could be managed on an outpatient basis.

Prediction of myocardial infarction in patients with transient ischaemic attack.

BACKGROUND: Determinants of risk of myocardial infarction (MI) after transient ischaemic attack (TIA) are not well defined. The aim of our study was to determine the risk and risk factors for MI after TIA. METHODS: We prospectively recruited patients within 24 h of transient ischaemic cerebrovascular events between October 2006 and January 2013. A total of 628 TIA patients were followed for six months or more. MI and stroke recurrence (SR) were recorded. The duration and typology of clinical symptoms, vascular risk factors and aetiological work-ups were prospectively recorded and established prognostic scores (ABCD2, ABCD2I, ABCD3I, Essen Stroke Risk Score, California Risk Score and Stroke Prognosis Instrument) were calculated. RESULTS: Twenty-eight (4.5%) MI and 68 (11.0%) recurrent strokes occurred during a median follow-up period of 31.2 months (16.1-44.9). In Cox proportional hazards multivariate analyses, we identify previous coronary heart disease (CHD) (hazard ratio [HR] 5.65, 95% confidence interval [CI] 2.45-13.04, P < 0.001) and sex male (HR 2.72, 95% CI 1.02-7.30, P = 0.046) as independent predictors of MI. Discrimination for the prognostic scores only ranged from 0.60 to 0.71. The incidence of MI did not vary among the different aetiological subtypes. Positive diffusion weighted imaging (DWI) (7.5% vs 2.5%, P = 0.007), and ECG abnormalities (Q wave or ST-T wave changes) (13.6% vs 3.6%, P = 0.001) were associated to MI. CONCLUSION: According to our results, discrimination was poor for all previous risk prediction models evaluated. Variables such as previous CHD, male sex, DWI and ECG abnormalities should be considered in new prediction models.

N-terminal pro-brain natriuretic peptide level determined at different times identifies transient ischaemic attack patients with atrial fibrillation.

BACKGROUND AND PURPOSE: The etiological classification of patients with transient ischaemic attack (TIA) is a difficult endeavor and the use of serum biomarkers could improve the diagnostic accuracy. The aim of this study was to correlate atrial fibrillation, the main cardioembolic etiology (CE), with different serum biomarkers measured in consecutive TIA patients. METHODS: The concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha, neuron-specific enolase, high-sensitivity C-reactive protein, IL-1-α and the N-terminal pro-B type natriuretic peptide (NT-proBNP) were quantified in the serum of 140 patients with TIA and 44 non-stroke subjects. Measurements were performed at different times throughout evolution: within 24 h of symptoms onset and at days 7 and 90. RESULTS: With the exception of IL-6, all biomarkers were higher in TIA patients than in controls. NT-proBNP was significantly related to the presence or new diagnosis of AF at all time points analyzed. Furthermore, the baseline NT-proBNP level was significantly higher than values at the 7-day and 90-day follow-up. For this reason, different cut-off values were obtained at different times: 313 pg/ml at baseline [odds ratio (OR) = 18.99, P < 0.001], 181 pg/ml at 7 days (OR = 11.4, P = 0.001) and 174 pg/ml (OR = 8.46, P < 0.001) at 90 days. CONCLUSION: High levels of NT-proBNP determined during the first 3 months after a TIA were associated with AF. Consequently, this biomarker may be useful to reclassify undetermined TIA patients as having disease of CE.

IMRT: preliminary results in a series of advanced head-and-neck cancer patients

PURPOSE: To determine retrospectively 2-3 year local and regional control (LRC), free-of-disease survival (FDS) and overall survival (OS), as well as summarized toxicities in a group of 31 advanced head-and-neck cancer patients, treated at our institution between 2004 and 2011 with definitive IMRT low-dose concomitant boost, the majority of them with concurrent chemotherapy based on cisplatin. The results are also shown in the sub-group of nasopharyngeal cancer patients (NPC: 15 cases). PATIENTS AND METHODS: Radiological basal and contrasted CT series, MR-CT or PET/CT fused images in the setup position with immobilization mask were registered in simulation therapy patients. Planed doses were: 70 Gy in primary tumor and positive nodes >1 cm; 63 Gy in high-risk areas of microscopic diseases +10 mm safety margin; and 56 Gy in low risk of diseases regional lymph nodes. Treatment was delivered using a Varian 2100 Clinac with sliding windows IMRT. Spinal cord doses were limited to a strict maximum of 45 Gy, and optimization aimed for mean doses in parotid glands below 26 Gy, especially in the contralateral parotid gland. Online DRR-portal X-ray comparison images were taken every day with a deviation module tolerance ≤3 mm. RESULTS: The mean follow-up since IMRT was 34 months (interval: 8-89; median 31 months). Median follow-up in living patients was 22 months. The 2-year rate for global LRC was 64 %, for FDS 61 % and OS 77 %. For the NPC group after 2 years, LRC was 73 %, FDS 73 % and OS 93 %. The 3-year rates were similar. Seven patients died as a consequence of local and/or regional progression (mean time 10 months). Relapses were observed in eight patients (26 %), but only seven could be confirmed by biopsy (22.6 %; mean time to relapse: 8.6 months). Global acute mucositis was 61 % and chronic mucositis was shown in six cases which developed xerostomia (19 %) in the first control after IMRT, but 1 year later it was reduced to only four patients, two Grade 2 and two Grade 1. CONCLUSIONS: No excessive, unwarranted toxicities were observed using concomitant low doses boost in IMRT. High rates of compliance to concurrent chemotherapy were achieved. Late xerostomia associated with this regime decreased 1 year after conclusion of treatment. The implementation of IMRT requires advances in imaging for better tumor delineation; otherwise the physician loses the advantage of dose modulation or faces a risk of geographical miss (AU)

Patterns of diffusion-weighted magnetic resonance imaging associated with etiology improve the accuracy of prognosis after transient ischaemic attack.

OBJECTIVE: diffusion-weighted magnetic resonance imaging (DWI) is a sensitive diagnostic tool for detecting acute ischaemic lesions in patients with transient ischaemic attacks (TIAs). The additional predictive value of DWI lesion patterns is not well known. METHODS: two hundred and fifty-four consecutive patients with TIA underwent DWI within 7 days of symptom onset. The presence and pattern of acute ischaemic lesions were related to clinical features, etiology, and stroke recurrence at seven- and 90-day follow-up. RESULTS: diffusion-weighted images abnormalities were identified in 117 (46.1%) patients. The distribution of DWI lesions was cortical, 31; subcortical, 32; scattered lesions in one arterial territory (SPOT) 42; and in multiple areas, 12. SPOT were significantly associated with motor weakness, large-artery atherosclerosis (LAA), and the cardioembolic subtype of TIA. Single cortical lesions were also associated with cardioembolism, whereas subcortical acute lesions were associated with recurrent episodes, dysarthria, and motor weakness. During follow-up, seven patients had a stroke within 7 days (2.8%, 95% CI 2.9-6.4%), and 12 had a stroke within 3 months (4.7%%, 95% CI 2.9-6.4%). In the Cox logistic regression model, the combination of LAA and positive DWI remained as independent predictors of stroke recurrence at 90-day follow-up (HR 5.78, 95 CI 1.74-19.21, P = 0.004). CONCLUSION: according to our results, MRI, including DWI, should be considered a preferred diagnostic test when investigating patients with potential TIAs. The combination of neuroimaging and vascular information could improve prognostic accuracy in patients with TIA.

Predictive value of ankle brachial index in patients with acute ischaemic stroke.

BACKGROUND: The ankle brachial index (ABI) is a known measure of lower-limb peripheral artery disease (PAD), as well as a marker for other cardiovascular disease events. OBJECTIVE: Our goal was to compare the prevalence of abnormal ABI scores (ABI or=3 (33.8% vs. 7.1%, P = 0.001) and large-artery atherosclerosis (LAA) (43.5% vs. 19.4%, P = 0.015). Multivariate analyses (logistic regression) only identified VRF > 3 as independently associated with low ABI (OR: 6.46; 1.81-23.02; P = 0.004). Abnormal ABI was associated with stroke recurrence (32.1% vs. 13.6%, P = 0.027) and the appearance of any major vascular event (50.0% vs. 17.0%, P < 0.001). In the logistic regression analysis, adjusted for VRF, age, and LAA, ABI remained as an independent predictor of vascular events (HR 3.99; 1.90-8.41 P < 0.001). CONCLUSION: Abnormal ABI was associated with classical risk factors, especially hypertension. The measurement of ABI amongst patients with IS appeared to be useful to identify high-risk patients and plan adequate prevention therapies.

Primary Sjögren Syndrome with tumefactive central nervous system involvement.

Brain MR imaging abnormalities in primary Sjögren syndrome (pSS) are generally discrete white matter lesions. We describe a 50-year-old woman with recurrent neurologic deficits. MR imaging revealed a large brain lesion. A diagnosis of pSS was made on the basis of clinical features, positive anti-Ro and anti-La antibodies, abnormal Schirmer test findings, and salivary gland scintigraphy. The patient was treated with oral prednisone with good response. Large tumefactive brain lesions are a complication of pSS.

[Detection of silent peripheral arterial disease in stroke patients with a low ankle-arm index]. / Detección mediante el índice tobillo-brazo de enfermedad arterial periférica silente en pacientes con ictus isquémico.

INTRODUCTION: A low ankle-arm index (AAI) is a strong predictor of vascular events and stroke. Nevertheless few studies have prospectively determined AAI in stroke patients. We aimed to investigated the prevalence of low AAI in stroke patients and which variables are associated with abnormal AAI. METHODS: Clinical data and ultrasonographic findings were collected in 79 consecutive stroke patients (20 transient ischemic attacks and 59 cerebral < ischemic infarction). During admission, AAI was measured in all subjects with the Doppler. An AAI cutoff of 0.90 was used to categorize individuals (< or =0.90: abnormal). RESULTS: A low AAI was calculated in 16 (20.3%) patients. AAI < or = 0.90 was associated with hypertension, smoking, hypercholesterolemia, coronary disease, previous peripheral arterial disease, male gender, internal carotid stenosis>50% (p<0.10). The presence of peripheral artery disease varied between subtypes. The incidence was higher for large artery atherosclerosis, 25.0 % and small vessel disease (31.5%). Multivariate analyses (logistic regression) only identify the association of>3 risk factors as independent predictor of low AAI (odds ratio: 4.41; confidence interval 95%: 1.39-4.01; p=0.012). CONCLUSION: Stroke patients had higher incidence of low AAI. Abnormal AAI was associated with classical risk factors. Existence of silent peripheral arterial disease in these patients may be an indicator of cerebral atherosclerosis extension. The measurement of AAI may be useful in order to plan adequate prevention therapies.

Detección mediante el índice tobillo-brazo de enfermedad arterial periférica silente en pacientes con ictus isquémico / Detection of silent peripheral arterial disease in stroke patients with a low ankle-arm index

Introducción. Un índice tobillo-brazo bajo (ITB) es un predictor de episodios vasculares, entre ellos los isquémicos cerebrales. Pese a ello casi no existen estudios sobre la incidencia de ITB anormales en pacientes con ictus isquémico. El objetivo del estudio es determinar la prevalencia y las variables clínicas asociadas a ITB bajo. Métodos. Estudiamos de forma consecutiva a 79 pacientes con un ictus isquémico (20 ataques isquémicos transitorios y 59 infartos cerebrales). Se recogieron datos clínicos y ultrasonográficos. Durante el ingreso se determinó mediante doppler el ITB. Se consideró como patológico un ITB <= 0,9. Resultados. Se observó un ITB<=0,9 en 16 (20,3 %) casos. El ITB patológico se asoció a antecedentes de hipertensión arterial, tabaquismo, dislipemia, cardiopatía isquémica, enfermedad arterial periférica, sexo varón y estenosis carotídea >50% (p < 0,10). El ITB bajo fue más frecuente en pacientes con ictus lacunar (31,5 %) o ateromatoso (25,0 %). En el análisis multivariante (regresión logística) la acumulación de más de tres factores de riesgo vascular se comportó como único predictor independiente de ITB <= 0,9 (odds ratio: 4,41; intervalo de confianza del 95 %: 1,39-14,01; p = 0,012). Conclusión. Existe un alto porcentaje de ITB bajo en pacientes con ictus isquémico. El ITB patológico se asocia a la presencia de factores de riesgo vascular clásicos. La existencia de enfermedad arterial periférica silente en estos pacientes podría traducir una extensión del proceso aterosclerótico cerebral. La determinación del ITB podría condicionar la elección del tratamiento de prevención secundaria más adecuado

Introduction. A low ankle-arm index (AAI) is a strong predictor of vascular events and stroke. Nevertheless few studies have prospectively determined AAI in stroke patients. We aimed to investigated the prevalence of low AAI in stroke patients and which variables are associated with abnormal AAI. Methods. Clinical data and ultrasonographic findings were collected in 79 consecutive stroke patients (20 transient ischemic attacks and 59 cerebral < ischemic infarction). During admission, AAI was measured in all subjects with the Doppler. An AAI cutoff of 0.90 was used to categorize individuals (<=0.90: abnormal). Results. A low AAI was calculated in 16 (20.3%) patients. AAI <= 0.90 was associated with hypertension, smoking, hypercholesterolemia, coronary disease, previous peripheral arterial disease, male gender, internal carotid stenosis>50% (p<0.10). The presence of peripheral artery disease varied between subtypes. The incidence was higher for large artery atherosclerosis, 25.0 % and small vessel disease (31.5%). Multivariate analyses (logistic regression) only identify the association of>3 risk factors as independent predictor of low AAI (odds ratio: 4.41; confidence interval 95%: 1.39-4.01; p=0.012). Conclusion. Stroke patients had higher incidence of low AAI. Abnormal AAI was associated with classical risk factors. Existence of silent peripheral arterial disease in these patients may be an indicator of cerebral atherosclerosis extension. The measurement of AAI may be useful in order to plan adequate prevention therapies

Monitorización de la respuesta a aciclovir en la encefalitis herpética / No disponible

No disponible

[Carotid thrombus and cerebral infarction as the initial clinical manifestation of polycythemia vera]. / Trombo carotídeo e infarto cerebral como manifestación clínical inicial de policitemia vera.

Polycythemia vera (PV) can produce cerebral infarction. The mechanisms proposed by most authors are hyperviscosity-related diminished cerebral blood flow and platelet function abnormalities. We present a 36-year-old woman whose initial clinical manifestation of PV consisted of cerebral ischemia due to a carotid thrombus, as well as occlusion of the middle cerebral artery and cortical branches of the anterior cerebral artery demonstrated by angiography. To our knowledge, this is the first published case of cerebral infarction in PV caused by a thrombus of an extracranial artery. Therefore, PV can produce ischemic stroke due to thrombosis not only in small distal arteries or arterioles but also in the carotid artery or main branches. Treatment of intraluminal thrombus in non-arteriosclerotic carotid artery is discussed. Myeloproliferative disorders, including PV, must be suspected in all stroke patients with an elevated platelet count, even in those who have potential causes of reactive thrombocytosis.

Trombo carotídeo e infarto cerebral como manifestación clínica inicial de policitemia vera / Carotid thrombus and cerebral infarction as the initial clinical manifestation of polycythemia vera

La policitemia vera (PV) puede producir infarto cerebral como complicación neurológica. Los mecanismos más aceptados son la disminución del flujo cerebral por hiperviscosidad, así como alteraciones de la función plaquetaria. Presentamos una mujer de 36 años cuya manifestación clínica inicial de PV consistió en un infarto cerebral debido a un trombo carotídeo asociado a oclusión de la arteria cerebral media y de ramas corticales de la arteria cerebral anterior, demostrado por angiografía cerebral. Este caso demuestra, pues, que la PV puede producir un ictus isquémico no sólo por fenómenos trombóticos de vaso pequeño, sino también por trombosis de la arteria carótida interna o arterias cerebrales proximales. Asimismo, revisamos el tratamiento de los trombos intraluminales en arterias sin aterosclerosis ni otra patología arterial previa. Como conclusión, los síndromes mieloproliferativos, incluida la PV, deben sospecharse en todo paciente con ictus isquémico con aumento del número de plaquetas, incluso en aquellos con causas potenciales de trombocitosis reactiva

Polycythernia vera (PV) can produce cerebral infarction. The rnechanisrns proposed by most authors are hyperviscosity-related diminished cerebral blood flow and platelet function abnormalities. We present a 36-year-old woman whose initial clinical rnanifestation of PV consisted of cerebral ischernia due to a carotid thrornbus, as well as occlusion of the rniddle cerebral artery and cortical branches of the anterior cerebral artery demonstrated by angiography. To our knowledge, this is the first published case of cerebral infarction in PV caused by a thrornbus of an extracranial artery. Therefore, PV can produce ischernic stroke due to thrornbosis not only in srnall distal arteries or arterioles but also in the carotid artery or main branches. Treatment of intraluminal thrombus in non-arteriosclerotic carotid artery is discussed. Myeloproliferative disorders, including PV, must be suspected in all stroke patients with an elevated platelet count, even in those who have potential causes of reactive thrornbocytosis

Infección por citomegalovirus simulando una pseudomigraña con pleocitosis / Cytomegalovirus infection mimicking a pseudomigraine with pleocytosis

No disponible