Articles: subarachnoid-hemorrhage.
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Despite intensive investigation into the cause of cerebral vasospasm (focal ischemic deficit) after subarachnoid hemorrhage, the morbidity and mortality associated with this condition remain high. Various studies have shown levels of catecholamine in plasma and cerebrospinal fluid (CSF) to be increased in subarachnoid hemorrhage, and it is possible that these vasoactive substances play an important role in the subsequent vasospasm. In an attempt to elucidate this possibility, the study presented here was undertaken to investigate the relationship between catecholamine levels in plasma and CSF and focal ischemic deficit (FID); the rupture of aneurysms on blood vessels supplying the hypothalamus as compared with the rupture of aneurysms on blood vessels supplying other areas of the brain; and the clinical outcome of the patients. ⋯ Further detailed analysis of the interrelationships showed that, within the group of patients with FID, those with rupture of aneurysms on blood vessels supplying the hypothalamus had significantly higher catecholamine levels in plasma than did those with rupture of aneurysms on other cerebral vessels. Furthermore, in the group of patients with rupture of aneurysms on blood vessels supplying the hypothalamus, those with a bad clinical outcome had significantly higher catecholamine levels in plasma than did those with a good clinical outcome. These findings lend support to the possibility that damage to the hypothalamus and subsequent elevations in catecholamine levels may be associated with FID and poor clinical outcome.
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We performed a retrospective analysis of 398 patients with subarachnoidal hemorrhage (SAH) confirmed by CT. On the first CT examination the temporal horns were enlarged in 84%, the frontal horns in 32%, and the third ventricle in 21% of the patients. The amount of blood in the basal cisterns was highly correlated to dilatation of the temporal horns. ⋯ The frontal and temporal horns were dilated only when moderate or large amounts of blood were present in the cisterns. In 24 patients no blood was seen in the basal cisterns on CT performed within 5 days of the hemorrhage; none of the 3 patients with aneurysms showed normal temporal horns while 18 without demonstrable aneurysms had normal, and 3 had moderately dilated, temporal horns. Because the temporal horns cannot usually be seen at CT of healthy individuals, dilatation could be a useful sign in the diagnosis of SAH.
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A 35-year-old man was hospitalized after a sudden onset of transient syncopal attack without accompanying complaints of headache or nausea. He was slightly disorientated but neurologically normal. He had a blood pressure of 150/90mmHg and a pulse rate of 40/min. ⋯ As bradyarrhythmia in patients with SAH is an uncommon finding, its mechanism has not yet been defined. Transient sinus bradycardia with advanced AV block in this patient might have been caused not by elevated intracranial pressure (Cushing phenomenon) but by drastic discharge of the parasympathetic nerve. This case serves to illustrate the vigilance required in determining whether abnormalities of cardiac rhythm are instrumental in causing neurological symptoms and signs or a disorder of cerebral function.
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We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. ⋯ So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.
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To evaluate the effect of factors existing before aneurysmal subarachnoid haemorrhage on outcome of haemorrhage. ⋯ Heavy drinking impairs outcome mainly through severe rebleeding and delayed ischaemia and to a lesser extent through a poor initial condition and presence of intracerebral haematoma.