RESUMO
Non-convulsive seizures and non-convulsive status epilepticus (NCSE) are believed common in comatose patients and are suggested to worsen outcome. The purpose of this study was to prospectively evaluate outcome in patients in critical care units in whom NCSE was suspected to determine how often evidence of seizure activity existed based on an isolated standard 20 minute electroencephalogram (EEG) and to determine what clinical factors predicted outcome. We prospectively reviewed EEGs and clinical charts of patients admitted to a critical care unit at a tertiary care center who were suspected to have non-convulsive seizures. Outcomes were correlated with EEG findings, clinical factors, and acute therapies using univariate and multivariate logistic analyses. Of 189 patients, complete information was available in 169. Eighty-one (47.9%) patients died, 67 (39.6%) were discharged home, and 21 (12.4%) were discharged to long-term care. Four patients had electroencephalographic seizures, two of whom had no clinical manifestations (i.e. non-convulsive). On univariate analysis, increased age, an admitting diagnosis of cardiac arrest, a Glasgow Coma Scale (GCS) score8, and burst suppression were correlated significantly with poor outcome. A past history of seizures and unequivocal tonic-clonic convulsions were correlated significantly with a better outcome. On multivariate analysis, increased age, cardiac arrest, and a GCS score8 were associated with increased mortality (p<0.05). Clinical factors, including age, underlying etiology and GCS score are the most important predicators of outcome in coma. A standard 20 minute EEG did not correlate with a high detection rate of seizure activity. Furthermore, EEG patterns and treatment with anticonvulsant medications did not correlate with outcome.
Assuntos
Coma/mortalidade , Eletroencefalografia/métodos , Convulsões/diagnóstico , Convulsões/mortalidade , Estado Epiléptico/diagnóstico , Estado Epiléptico/mortalidade , Adolescente , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Coma/fisiopatologia , Comorbidade , Morte Súbita Cardíaca/epidemiologia , Eletroencefalografia/estatística & dados numéricos , Epilepsia Tônico-Clônica/diagnóstico , Epilepsia Tônico-Clônica/epidemiologia , Feminino , Escala de Coma de Glasgow , Humanos , Masculino , Pessoa de Meia-Idade , Avaliação de Resultados em Cuidados de Saúde/métodos , Valor Preditivo dos Testes , Estudos Prospectivos , Fatores de Risco , Convulsões/fisiopatologia , Sensibilidade e Especificidade , Índice de Gravidade de Doença , Estado Epiléptico/fisiopatologia , Fatores de Tempo , Adulto JovemRESUMO
BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) identifies acute cerebral ischemia and DWI lesions are thought to indicate irreversibly damaged areas. However, new evidence suggests that DWI lesions may be reversible, especially with reperfusion. We present a patient who showed substantial reversal of her acute DWI lesion following partial aortic occlusion with Neuroflo™, a novel dual balloon catheter (Neuroflo™, CoAxia, MN). METHODS: Case report/literature review. RESULTS: A 48-year-old woman presented with left-sided weakness and demonstrated an acute DWI lesion in the right middle cerebral artery territory, with diffusion-perfusion mismatch. She was enrolled into an experimental study in which a dual balloon catheter was inflated in the lower aorta. The patient improved and her postprocedure magnetic resonance image showed a significant reduction in lesion volume on diffusion and perfusion-weighted imaging. At 1 month, a repeat computed tomography scan showed a small infarction in the right insula, lentiform nucleus, and frontal cortex. The patient had recovered with no significant disability at her 3-month follow-up. CONCLUSION: Reperfusion can improve DWI lesions. Partial aortic obstruction with a novel dual balloon catheter may be useful to promote reperfusion.
Assuntos
Aorta/cirurgia , Oclusão com Balão/métodos , Imageamento por Ressonância Magnética/métodos , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/cirurgia , Feminino , Humanos , Pessoa de Meia-Idade , Resultado do TratamentoAssuntos
Terapia Trombolítica , Insuficiência Vertebrobasilar/patologia , Insuficiência Vertebrobasilar/terapia , Adulto , Artéria Basilar/patologia , Isquemia Encefálica/patologia , Coma/etiologia , Fibrinolíticos/uso terapêutico , Escala de Coma de Glasgow , Humanos , Imageamento por Ressonância Magnética , Masculino , Ativador de Plasminogênio Tecidual/uso terapêutico , Insuficiência Vertebrobasilar/complicaçõesRESUMO
OBJECTIVE: Establishing time of onset is important in acute stroke management. Current imaging modalities do not allow determination of stroke onset time. Although correlations between sodium magnetic resonance imaging signal intensity within ischemic lesions and time of onset have been shown in animal models, the relation to onset time has not been established in human stroke. Utilizing high-quality sodium images, we tested the hypothesis that sodium signal intensity increases with time from symptom onset in human ischemic stroke. METHODS: Twenty-one stroke patients (63 +/- 15 years old) were scanned 4 to 104 hours after symptom onset. Follow-up images were obtained in 10 patients at 23 to 161 hours after onset, yielding a total of 32 time points. A standard stroke imaging protocol was acquired at 1.5 Tesla, followed by sodium magnetic resonance imaging at 4.7 Tesla. Relative sodium signal intensity within each lesion was measured with respect to the contralateral side. RESULTS: The sodium image quality was sufficient to visualize each acute lesion (lesion volume range, 1.7-217cm(3)). Relative sodium signal intensity increased nonlinearly over time after stroke onset. Sodium images acquired within 7 hours (n = 5) demonstrated a relative increase in lesion intensity of 10% or less, whereas the majority beyond 9 hours demonstrated increases of 23% or more, with an eventual leveling at 69 +/- 18%. INTERPRETATION: Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55-62.
Assuntos
Isquemia Encefálica/diagnóstico , Imagem de Difusão por Ressonância Magnética/métodos , Isótopos de Sódio , Acidente Vascular Cerebral/diagnóstico , Adulto , Idoso , Idoso de 80 Anos ou mais , Isquemia Encefálica/complicações , Mapeamento Encefálico , Intervalos de Confiança , Feminino , Seguimentos , Humanos , Processamento de Imagem Assistida por Computador/métodos , Masculino , Pessoa de Meia-Idade , Acidente Vascular Cerebral/etiologia , Fatores de TempoRESUMO
BACKGROUND AND PURPOSE: The objective was to evaluate the relationship between circulating endothelial progenitor cells (EPC) and age-related white matter changes (ARWMC). Endothelial dysfunction plays a role in the development of ARWMC. EPC incorporate into sites endothelial damage and are thought to be involved in the repair of vascular risk factor induced endothelial injury. ARWMC can be evaluated using CT or MRI. METHODS: In 172 individuals, circulating EPC were defined by the surface markers CD31 and von Willebrand factor. ARWMC were rated on CT scan using the ARWMC scale and divided into 3 groups based on ARWMC scale score (ARWMC score 0 [none], score 1-10 [mild-to-moderate], score >10 [severe]). Severity of ARWMC was correlated with levels of EPC and vascular risk factors. RESULTS: On univariate analysis, EPC were found to be significantly lower in patients with severe ARWMC (P=0.01). ARWMC were also associated with hypertension (P<0.001), age (P<0.001), creatinine clearance (P=0.031), C-reactive protein (P<0.001), and use of angiotensin-converting enzyme or angiotensin receptor blocker (P=0.004). Multiple logistic regression analysis identified EPC level, age, hypertension, and hypertriglyceridemia as significant independent predictors of severe ARWMC. CONCLUSIONS: Levels of circulating EPC were significantly lower in patients with severe ARWMC. Other variables significantly associated with severe ARWMC were age, hypertension, and hypertriglyceridemia. Further study is required to delineate the pathophysiological relationship between EPC, vascular risk factors, and ARWMC.
Assuntos
Envelhecimento/patologia , Encéfalo/patologia , Demência/patologia , Células Endoteliais/citologia , Fibras Nervosas Mielinizadas/patologia , Células-Tronco/citologia , Distribuição por Idade , Idoso , Envelhecimento/metabolismo , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Encéfalo/irrigação sanguínea , Encéfalo/fisiopatologia , Proteína C-Reativa/análise , Proteína C-Reativa/metabolismo , Contagem de Células , Artérias Cerebrais/metabolismo , Artérias Cerebrais/fisiopatologia , Creatina/metabolismo , Demência/diagnóstico por imagem , Demência/fisiopatologia , Progressão da Doença , Células Endoteliais/fisiologia , Feminino , Humanos , Hipertensão/complicações , Hipertrigliceridemia/complicações , Masculino , Pessoa de Meia-Idade , Neovascularização Fisiológica/fisiologia , Molécula-1 de Adesão Celular Endotelial a Plaquetas/análise , Molécula-1 de Adesão Celular Endotelial a Plaquetas/metabolismo , Regeneração/fisiologia , Células-Tronco/fisiologia , Tomografia Computadorizada por Raios X , Fator de von Willebrand/análise , Fator de von Willebrand/imunologia , Fator de von Willebrand/metabolismoRESUMO
PURPOSE: Guillain-Barré syndrome (GBS) is an acute immunologic attack of the peripheral nerves causing rapidly ascending weakness and areflexia. Occasionally, weakness is severe enough to leave patients paralyzed and without adequate respiratory function. In such patients, intensive care unit (ICU) admission is required. Infrequently, GBS occurs in patients already admitted to the ICU. When this occurs, it can be difficult to distinguish GBS from critical illness neuropathy (CIN). However, it is important to consider GBS in these cases, since treatment options are available, and early treatment is associated with significantly improved outcome. CLINICAL FEATURES: A 28-yr-old man involved in a motor vehicle collision sustained multiple injuries, including T6-T7 thoracic vertebrae fracture. Magnetic resonance imaging identified spinal cord compression at T6-T7, without brain or cervical cord injury. Shortly after admission, the patient developed marked autonomic instability with fluctuating temperatures and severe hypotension. Lower extremity weakness rapidly worsened to paraplegia and new weakness developed affecting bilateral upper extremities and face. Electrodiagnostic studies showed severe axonal polyneuropathy, with denervation in all extremities. The cerebrospinal fluid protein concentration was 5.03 g.L(-1). The patient was treated empirically for the possibility of GBS. Six months later, the patient recovered significant strength in his face and extremities, including his legs. CONCLUSIONS: Guillain-Barré syndrome in trauma patients is rare and is limited to case reports following head trauma. This case also highlights the similarities and the subtle differences between GBS and CIN. Ultimately, definitive diagnosis of GBS may not be possible; however, an empiric course of intravenous immunoglobulins or plasma-exchange may be warranted, if GBS is a reasonable possibility.
Assuntos
Síndrome de Guillain-Barré/etiologia , Debilidade Muscular/etiologia , Polineuropatias/diagnóstico , Traumatismos da Medula Espinal/complicações , Adulto , Síndrome de Guillain-Barré/terapia , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Masculino , Debilidade Muscular/terapia , Troca Plasmática , Polineuropatias/imunologia , Polineuropatias/terapia , Traumatismos da Medula Espinal/terapia , Vértebras Torácicas , Resultado do TratamentoAssuntos
Artéria Braquial/patologia , Mãos/fisiopatologia , Infarto da Artéria Cerebral Média/etiologia , Infarto da Artéria Cerebral Média/patologia , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/patologia , Anticoagulantes/uso terapêutico , Antifibrinolíticos/uso terapêutico , Aortografia , Artéria Braquial/diagnóstico por imagem , Tronco Braquiocefálico/diagnóstico por imagem , Tronco Braquiocefálico/patologia , Embolia/tratamento farmacológico , Embolia/etiologia , Embolia/prevenção & controle , Feminino , Mãos/irrigação sanguínea , Humanos , Hipotermia/etiologia , Hipotermia/fisiopatologia , Infarto da Artéria Cerebral Média/diagnóstico por imagem , Pessoa de Meia-Idade , Fluxo Sanguíneo Regional/fisiologia , Temperatura Cutânea/fisiologia , Acidente Vascular Cerebral/diagnóstico por imagem , Trombose/diagnóstico por imagem , Trombose/tratamento farmacológico , Trombose/patologia , Ativador de Plasminogênio Tecidual/administração & dosagem , Tomografia Computadorizada por Raios X , Resultado do TratamentoAssuntos
Doenças dos Gânglios da Base/microbiologia , Doenças dos Gânglios da Base/patologia , Gânglios da Base/microbiologia , Gânglios da Base/patologia , Meningite Criptocócica/patologia , Antifúngicos/uso terapêutico , Gânglios da Base/fisiopatologia , Doenças dos Gânglios da Base/fisiopatologia , Derivações do Líquido Cefalorraquidiano , Transtornos da Consciência/microbiologia , Transtornos da Consciência/patologia , Cryptococcus neoformans/isolamento & purificação , Quimioterapia Combinada , Humanos , Hipocinesia/microbiologia , Hipocinesia/patologia , Hipocinesia/fisiopatologia , Imunocompetência/imunologia , Hipertensão Intracraniana/etiologia , Hipertensão Intracraniana/cirurgia , Imageamento por Ressonância Magnética , Masculino , Meningite Criptocócica/líquido cefalorraquidiano , Meningite Criptocócica/fisiopatologia , Pessoa de Meia-Idade , Resultado do TratamentoAssuntos
Infarto Encefálico/etiologia , Surtos de Doenças , Cefaleia/etiologia , Neurossífilis/epidemiologia , Infarto Encefálico/patologia , Humanos , Aneurisma Intracraniano/etiologia , Aneurisma Intracraniano/patologia , Masculino , Pessoa de Meia-Idade , Neurossífilis/complicações , Neurossífilis/patologiaAssuntos
Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Meníngeas/diagnóstico por imagem , Meningioma/diagnóstico por imagem , Idoso de 80 Anos ou mais , Neoplasias Encefálicas/complicações , Eletroencefalografia , Epilepsia do Lobo Temporal/diagnóstico , Epilepsia do Lobo Temporal/etiologia , Feminino , Humanos , Meningioma/complicações , Lobo Temporal/diagnóstico por imagem , Tomografia Computadorizada por Raios XRESUMO
There are a number of causes of raised intracranial pressure (ICP) following aneurysm rupture. These include primary and diffuse hypoxic brain injury, intracranial hematomas, cerebral ischemia or infarction, and obstructive hydrocephalus. More localized brain swelling can also occur: the result of vasogenic and cytotoxic edema resulting from overlying bleeding in the subarachnoid spaces. In the case of rupture of an anterior communicating artery (ACommA) aneurysm and interhemispheric subarachnoid hemorrhage (SAH), this swelling can occur in both frontal lobes and when extensive, and the resulting intracranial hypertension can be difficult to manage with ventricular drainage and medical treatment. We describe two patients in whom decompressive bifrontal craniectomy was associated with successful ICP management and good clinical outcomes.