Clinical Neuroscience

[Thrombolysis in case of ischemic stroke caused by aortic dissection]

LANTOS Judit, NAGY Albert, HEGEDŰS Zoltán, BIHARI Katalin

JANUARY 20, 2017

Clinical Neuroscience - 2017;70(01-02)

DOI: https://doi.org/10.18071/isz.70.0069

[Seldom, an acute aortic dissection can be the etiology of an acute ischemic stroke. The aortic dissection typically presents with severe chest pain, but in pain-free dissection, which ranges between 5-15% of the case, the neurological symptoms can obscure the sypmtos of the dissection. By the statistical data, there are 15-20 similar cases in Hungary in a year. In this study we present the case history of an acute ischemic stroke caused by aortic dissection, which is the first hungarian publication in this topic. A 59-year-old man was addmitted with right-gaze-deviation, acute left-sided weakness, left central facial palsy and dysarthric speech. An acute right side ischemic stroke was diagnosed by physical examination without syptoms of acute aortic dissection. Because, according to the protocol it was not contraindicated, a systemic intravenous thrombolysis was performed. The neurological sypmtoms disappeared and there were no complication or hypodensity on the brain computed tomography (CT). 36 hours after the thrombolysis, the patient become restlessness and hypoxic with back pain, without neurological abnormality. A chest CT was performed because of the suspition of the aortic dissection, and a Stanford-A type dissection was verified. After the acute aortic arch reconstruction the patient died, but there was no bleeding complication at the dissection site caused by the thrombolysis. This case report draws attention to the fact that aortic dissection can cause acute ischemic stroke. Although it is difficult to prove it retrospectively, we think the aortic dissection, without causing any symptoms or complain, had already been present before the stroke. In our opinion both the history of our patient and literature reviews confirms that in acute stroke the thrombolysis had no complication effect on the aortic dissection but ceased the neurological symptoms. If the dissection had been diagnosed before the thrombolysis, the aortic arch reconstruction would have been the first step of the treatment, without thrombolysis. ]

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Objective - To compare the intensity and the profile of psychotic symptoms and the characteristics of parental bonding of male schizophrenia patients with a history of homicide and those without a history of violent behaviour. Clinical question - We hypothesized more intense psychotic symptoms, especially positive symptoms as signs of a more severe psychopathology in the background of homicidal behaviour. We also hypothesized a more negatively perceived pattern (less Care more Overprotection) of parental bonding in the case of homicidal schizophrenia patients than in non-violent patients and non-violent healthy controls. Method and subjects - Symptom severity and symptom profiles were assessed with the Positive and Negative Syndrome Scale in a group of male schizophrenia patients (n=22) with the history of committed or attempted homicide, and another group (n=19) of male schizophrenia patients without a history of violent behaviour. Care- and Overprotection were assessed using the Parental Bonding Instrument (PBI) in a third group of non-violent healthy controls (n=20), too. Results - Positive, negative and general psychopathology symptoms in the homicidal schizophrenia group were significantly (p<0.005) more severe than in the non-violent schizophrenia group. Non-violent schizophrenia patients scored lower on Care and higher on Overprotection than violent patients and healthy controls. Homicidal schizophrenia patients showed a pattern similar to the one in the healthy control group. Conclusions - It seems imperative to register intense positive psychotic symptoms as predictive markers for later violent behaviour. In the subgroup of male homicidal schizophrenia patients negatively experienced parental bonding does not appear to be major contributing factor to later homicidal behaviour.

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Objective - Patients were assessed in terms of risk factors, hematoma size and localization, the effects of spontaneous intracerebral hemorrhage (ICH) on mortality and morbidity, and post-stroke depression. Materials and methods - The present study evaluated the demographic data, risk factors, and neurological examinations of 216 ICH patients. The diagnosis, volume, localization, and ventricular extension of the hematomas were determined using computed tomography scans. The mortality rate through the first 30 days was evaluated using ICH score and ICH grading scale. The Modified Rankin Scale (mRS) was used to determine the dependency status and functional recovery of each patient, and the Hamilton Depression Rating Scale was administered to assess the psychosocial status of each patient. Results - The mean age of the patients was 65.3±14.5 years. The most common locations of the ICH lesions were as follows: lobar (28.3%), thalamus (26.4%), basal ganglia (24.0%), cerebellum (13.9%), and brainstem (7.4%). The average hematoma volume was 15.8±23.8 cm3; a ventricular extension of the hemorrhage developed in 34.4% of the patients, a midline shift in 28.7%, and perihematomal edema, as the most frequently occurring complication, in 27.8%. Over the 6-month follow-up period, 57.9% of patients showed a poor prognosis (mRS: ≥3), while 42.1% showed a good prognosis (mRS: <3). The mortality rate over the first 30 days was significantly higher in patients with a low Glasgow Coma Scale (GCS) score at admission, a large hematoma volume, and ventricular extension of the hemorrhage (p=0.0001). In the poor prognosis group, the presence of moderate depression (39.13%) was significantly higher than in the good prognosis group (p=0.0001). Conclusion - Determination and evaluation of the factors that could influence the prognosis and mortality of patients with ICH is crucial for the achievement of more effective patient management and improved quality of life.

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