Cases reported "Subarachnoid Hemorrhage"

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1/48. Acute left ventricular dysfunction and subarachnoid hemorrhage.

    OBJECTIVE: Severe left ventricular (LV) dysfunction associated with acute subarachnoid hemorrhage (SAH) due to cerebral aneurysm rupture. SETTING: An adult 12-bed surgical intensive care unit of a university hospital. PATIENT: A female patient presenting with SAH (Hunt & Hess grade III) and severe left ventricular dysfunction. INTERVENTIONS: central venous pressure, arterial blood pressure, extravascular lung water catheter, transesophageal echocardiography, blood gas analysis, electrocardiograms, and chest x-ray for clinical management. MEASUREMENTS AND MAIN RESULTS: On admission to the district hospital, an electrocardiogram (ECG) revealed a sinus rhythm with transient ST elevations. A transesophageal echocardiography showed a left ventricular ejection fraction (LV-EF) of approximately 10%. Severe LV dysfunction required inotropic and vasopressor support to maintain mean arterial pressure above 60 mmHg, while the first measurement of an extravascular lung water catheter revealed a cardiac index of 2.0 L/min/m2 and moderate hypovolemia. Despite stepwise volume loading that increased intrathoracic blood volume--an indicator of cardiac preload--from 719 mL/m2 to 927 mL/m2, cardiac index remained poor. enoximone lead to a marked increase of cardiac index up to 3.9 L/min/m2 and LV-EF to about 30%, but had to be stopped due to thrombopenia. Surgical clipping of an intracranial aneurysm was postponed because of the impaired cardiac function and was performed on day 18 after admission. Interestingly, neurologic outcome was not as poor as might be expected from the literature. CONCLUSION: Severe left ventricular dysfunction may occur in acute SAH and may necessitate delay of aneurysm surgery.
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keywords = ventricular dysfunction, left ventricular dysfunction, dysfunction
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2/48. Making sense out of jargon: a neurolinguistic and computational account of jargon aphasia.

    OBJECTIVE: To identify the cognitive and neuroanatomic bases of neologistic jargon aphasia with spared comprehension and production of written words. methods: Detailed analysis of performance across experiments of naming, reading, writing, repetition, and word/picture matching by a 68-year-old woman (J.B.N.) served to identify which cognitive mechanisms underlying naming and word comprehension were impaired. J.B.N.'s impairments were then simulated by selectively "lesioning" a computer model of word production that has semantic, word form, and subword phonologic levels of representation (described by Dell in 1986). RESULTS: In comprehension experiments, J.B.N. made far more errors with spoken word input than with written word or picture input (chi-square = 40-59; df = 1; p < 0.0001) despite intact auditory discrimination. In naming experiments (with picture, definition, or tactile input), J.B.N. made far more errors in spoken output relative to written output (chi-square = 14-56; df = 1; p < 0.0001). These selective impairments of spoken word processing were simulated by reducing connection strength between word-level and subword-level phonologic units but maintaining full connection strength between word-level and semantic units in Dell's model. The simulation yielded a distribution of error types that was nearly identical to that of J.B.N., and her CT and MRI scans showed a small subarachnoid hemorrhage in the left sylvian fissure without infarct. Cerebral angiogram showed focal vasospasm in sylvian branches of the left middle cerebral artery. CONCLUSION: Focal left perisylvian dysfunction can result in a highly selective "disconnection" between word-level and subword-level phonologic representations manifest as neologistic jargon aphasia with intact understanding and production of written words.
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3/48. Reversible left ventricular dysfunction associated with raised troponin i after subarachnoid haemorrhage does not preclude successful heart transplantation.

    Transient abnormalities in ECGs, echocardiograms, and cardiac enzymes have been described in the acute setting of subarachnoid haemorrhage. In addition, left ventricular dysfunction has been reported at the time of brain death. A patient with an acute subarachnoid haemorrhage who presented with raised troponin i (TnI) concentrations and diffuse left ventricular dysfunction is described. After declaration of brain death 32 hours later, the heart was felt initially not suitable for transplantation. A normal cardiac catheterisation, however, lead to successful transplantation of the donor heart. Raised catecholamine concentrations and metabolic perturbations have been proposed as the mechanisms leading to the cardiac dysfunction seen with brain death. This may be a biphasic process, allowing time for myocardial recovery and reversal of the left ventricular dysfunction. awareness of this phenomenon in the acutely ill neurologic population needs to be raised in order to prevent the unnecessary rejection of donor hearts.
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ranking = 1.1653325807525
keywords = ventricular dysfunction, left ventricular dysfunction, dysfunction
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4/48. Intraspinal haematoma following lumbar epidural anaesthesia in a neonate.

    A neonate with chromosomal 9 abnormality and omphalocele received a lumbar epidural catheter after laparotomy. Several attempts were needed to establish this catheter. Bleeding occurred from the operative wound after surgery. Using an epidural infusion with ropivacaine 0.1% for 48 h postoperative pain relief was sufficient. Four days after epidural catheter removal, dysfunction of the sacral parasympathetic nerves was noted. Motor and sensor function of the lower limbs were unaffected. magnetic resonance imaging showed a localized intraspinal haematoma in the lower lumbar region.
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5/48. Severe subarachnoid hemorrhage with pulmonary edema successfully treated by intra-aneurysmal embolization using Guglielmi detachable coils--Two case reports.

    A 48-year-old male and a 39-year-old female presented with subarachnoid hemorrhage (SAH) due to ruptured anterior communicating artery aneurysms. Both patients were comatose on admission. Chest radiography disclosed pulmonary edema. They were conservatively treated under controlled ventilation, but cardiopulmonary dysfunction persisted over 2 days. The patients were then treated by intra-aneurysmal embolization with Guglielmi detachable coils (GDCs) 2 days after the onset. The postoperative courses were uneventful, and the patients showed full recovery from pulmonary edema and were discharged without neurological deficits. Neurogenic pulmonary edema is one of the serious complications of SAH, and is a leading cause of poor clinical outcome. The favorable outcomes of the present cases suggest that intra-aneurysmal embolization with GDCs is an excellent choice for the patients with severe aneurysmal SAH complicated with pulmonary edema, in whom conventional surgical treatment under general anesthesia is difficult to perform in the acute stage.
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6/48. Functional methods for evaluation the occurrence of delayed ischemic deficit in patients with subarachnoid hemorrhage.

    Detection of early circulatory and electrophysiologic changes due to vasospasm (VS) after subarachnoid hemorrhage (SAH) is a necessity for in-time and adequate therapeutic management. The aim of the present case report is to describe and demonstrate the results of transcranial Doppler (TCD) monitoring and brainstem auditory evoked potentials (BAEPs) examination, which indicate the development of combined circulatory insufficiency in two vascular systems. On the 14th day after SAH, TCD showed accelerated velocities in the territory of middle cerebral artery (MCA) and basilar artery (BA). BAEPs, after ipsilateral stimulation, performed on the same day verified changes of potentials on the left side with abnormal I/V amplitude ratio. These results were suggestive of brainstem dysfunction. The CT examination of the next day revealed infarction in the posterior parietal borderline zone of the left hemisphere. The patient had clinical signs of sensory aphasia, which resolved completely after one-week treatment with nimodipine.
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7/48. A spectrum of exertional headaches.

    Headaches that have an explosive onset with exercise, including sexual activity, generally are benign in origin. A subarachnoid hemorrhage, a mass lesion in the brain, or an anomaly of the posterior fossa must be considered, however. The mechanisms that produce sexually induced or cough headaches of abrupt onset are unknown. It is known, however, that a rapid increase in intrathoracic pressure suddenly reduces right atrial pressure and presumably decreases venous sinus drainage from the brain. This situation results in a transient increase in intracranial pressure. jaw pain that occurs with chewing often is considered to be TMJ dysfunction when arthritic in quality and if subluxations of the jaw can be shown on the physical examination. giant cell arteritis and common or external carotid artery occlusive disease should be considered when the pain is ischemic in quality. An anginal equivalent is another possibility. Headaches that worsen with vigorous exercise are commonly migrainous. When their onset is apoplectic with exertion (particularly exertion against a closed glottis), the most likely diagnoses are increased intracranial pressure, a posterior fossa abnormality, or benign exertional headaches. Most cardiac induced headaches, but not all, are of a more gradual onset. If there are significant risk factors for coronary artery disease, an exercise stress test is appropriate. A therapeutic trial of nitroglycerin may help to establish a diagnosis if it improves the headache. Using antimigraine drugs as a diagnostic test is inappropriate because triptans and ergots are contraindicated in the presence of coronary artery disease, and a positive response is not diagnostic of migraine.
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8/48. Hypodipsic hypernatremia and diabetes insipidus following anterior communicating artery aneurysm clipping: diagnostic and therapeutic challenges in the amnestic rehabilitation patient.

    Hypodipsic hypernatremia (HH) represents a pathological increase in serum sodium due to a lack of thirst and defect in hypothalamic osmoreceptors. While 15% of patients with HH have a vascular aetiology, few cases have been described. Moreover, the presence of such abnormalities in the amnestic patient can have particularly threatening implications, as HH tends to recur unless the patient complies with a regimen of water intake. This study reports the case of a 46-year-old male admitted for rehabilitation of functional deficits following subarachnoid haemorrhage (SAH), with clipping of an anterior communicating artery (ACoA) aneurysm. Clinical examination was remarkable for profound short-term memory loss and inability to retain new information. Blood chemistry on admission showed a serum sodium level of 160 mEq/L, increasing to 167 mEq/L the following day. The patient denied thirst, and showed no clinical signs of dehydration. Neuroendocrine evaluation revealed diabetes insipidus (DI) and HH. Treatment initially included DDAVP and intravenous hydration, later supplemented with chlorpropramide. Stabilization of serum sodium and osmolality did not ensue until the treatment regimen included hydrochlorothiazide and supervision of enforced fluid intake. Endocrine abnormalities may be encountered among patients with vascular lesions adjacent to the hypothalamus. rehabilitation interventions include establishing a structured medication regimen with fluid administration in the amnestic patient with hypothalamic dysfunction.
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9/48. Early development and rupture of de novo aneurysm--case report.

    A 38-year-old non-smoker man presented with a ruptured aneurysm one month after clipping of a previous aneurysm. He was first admitted because of sudden onset of severe headache. Brain computed tomography showed subarachnoid hemorrhage. angiography showed an aneurysm of the left anterior choroidal artery which was surgically clipped. Two weeks later, he was discharged without neurological deficits. One month after the initial hemorrhage, he was readmitted to the emergency room with stuporous mentality. Repeat angiography showed two aneurysms of the A2 portion of the left anterior cerebral artery which were not demonstrated by the initial angiography. The diagnosis was de novo aneurysms. The larger aneurysm was clipped and the other was coated. De novo aneurysm should be suspected if a patient with a previously clipped aneurysm complains of typical headache or any suggestive symptoms or signs of cranial nerve dysfunction, especially if known risk factors are present.
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10/48. neuroimaging analysis of a case with left homonymous hemianopia and left hemispatial neglect.

    PURPOSE: To correlate the neuro-ophthalmological observations with the magnetic resonance images (MRI) and positron emission tomographic (PET) findings in a case with left homonymous hemianopia and left hemispatial neglect. CASE: A 57-year-old woman underwent surgery for a ruptured anterior communicating artery aneurysm. After she recovered consciousness, it was found that she had left homonymous hemianopia and left hemispatial neglect. Although the hemispatial neglect slowly improved, the homonymous hemianopia persisted. MRI and measurements of cerebral glucose metabolism by 2-fluoro-2-deoxy-D-glucose(FDG)-PET were performed 1 year later. RESULTS: MRI revealed infarctions on the medial surface of the frontal lobe, on the right medial surface of the occipital lobe, and global atrophy of the right cortical hemisphere. FDG-PET disclosed severe glucose hypometabolism in the entire right hemisphere. glucose metabolism in the right occipital cortex was 61.1% of that in the homologous region on the left side, 62.8% in the right anterior cingulate gyrus, and 93.8% in the temporal-parietal-occipital junction. CONCLUSIONS: The low glucose metabolism in the right visual cortex explains the persistent left hemianopia, and that in the right anterior cingulate gyrus and the right temporal-parietal-occipital junction may be responsible for the left hemispatial neglect. The relatively mild damage in the right temporal-parietal-occipital junction explained the recovery of the neglect symptom. Measurements of regional cerebral glucose metabolism by PET are useful for determining the cause of cerebral visual dysfunction and its prognosis after a cerebral lesion.
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