Biomedical subjects
Publications and source records attributed to A Spallone.
Seven members from a large family who showed signs of incontinentia pigmenti were examined. A clear X-linked dominant transmission was demonstrated, lethal in males. Study of this family shows that vascular abnormalities of the retina and disorders of the retinal pigment epithelium are the most important ocular lesions in the Bloch-Sulzberger syndrome.
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This study concerns 64 patients with angiographically negative subarachnoid haemorrhage (SAH) hospitalized in the period 1970-1982. Requisites for inclusion in the study were adequate angiographic demonstration of the carotid and vertebrobasilar systems and no clinical signs of spinal SAH or spontaneous intracerebral haematoma. The clinical data on the 64 cases confirm the close similarity, except for the prognostic factors, between angiographically negative SAH and SAH secondary to rupture of an intracranial saccular aneurysm. The study underlines the benign character of the clinical course and of the medium and long-term prognosis of the condition under study. In view of this, the hypothesis advanced sometime ago relating angiographically negative SAH to the rupture of microaneurysms (phi less than 2 mm) of the large cerebral arteries with subsequent complete repair of the artery wall, or to the spontaneous thrombosis of intracranial saccular aneurysms, with the possibility of subsequent recanalization and risk of fresh rupture, would appear to be a reasonable one.
An 11-year-old girl was admitted with a 3-year history of decreasing hearing, and headache, occasional vomiting and poor school performance of 8 months duration. Neurologically she showed signs of a cerebellopontine angle mass. This was confirmed by CT scan, which showed an enhancing lesion in the right cerebellopontine angle. The lesion was totally removed, with excellent results. Histologically the tumor appeared to be a choroid plexus papilloma. Choroid plexus papillomas of the cerebellopontine angle are extremely rare in children.
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Two patients with retinitis pigmentosa of the dominant type and a Coats'-like syndrome were studied. The aetiology of the Coats'-like syndrome in retinitis pigmentosa is obscure. The principal theories will be reported in this paper. The association between retinitis pigmentosa and Coats'-like disease has been reported many times in a sporadic way (Zamorani, 1956; Morgan and Crawford, 1968). As far as we know this association in more than one member of the same pedigree has been published only in two papers (Schmidt and Faulborn, 1972; Lanier, McCrary and Justice, 1976). Below we describe the case of two brothers suffering from retinitis pigmentosa of the dominant type and Coats'-like syndrome. To our knowledge this is the first report in English of the occurrence in a family of association of retinitis pigmentosa of the dominant type and Coats'-like syndrome which occurred in two brothers of non consanguineous parents.
Cerebral vasospasm is one of the most dreaded consequences of a ruptured intracranial aneurysm. Although exceptions may be found, the relationship between angiographic narrowing of cerebral arteries and deterioration of clinical status is supported by many authors. The cause of cerebral vasospasm still remains obscure. Several substances such as serotonin, prostaglandins, catecholamines appear to have a vasoconstrictive effect on the cerebral vessels. Recent evidence indicates that erythrocyte lysis within the subarachnoid spaces may play a major role in the genesis of delayed clinically relevant cerebral vasoconstriction following aneurysmal subarachnoid hemorrhage (SAH). The pathophysiology of brain ischemia following aneurysmal rupture, and the correlation between angiographic vasospasm, neurological condition, intracranial pressure (ICP) value, cerebral blood flow and CT findings are briefly discussed. It is concluded that, at present, blood volume expansion and/or induced hypertension, and pharmacological control of increased ICP provide the best basis for clinical management of the cerebral ischemic complications of SAH. Preoperative antifibrinolytic therapy and delayed surgical obliteration of the bleeding aneurysm, i.e. the policy at present most frequently adopted, are currently undergoing critical review in the light of the fact that antifibrinolytic therapy seems to be accompanied by a higher rate of ischemic SAH complications and vasospasm, whilst there are very recent suggestions that the results of early intracranial aneurysm surgery may be better than those of delayed surgery, if account is taken of the patients lost because of recurrent SAH or ischemia during the waiting period.
An experimental model of microsurgical carotid endarterectomy in rats developed recently in our laboratory was used in the present study. Our adult Sprague-Dawley rats were killed by in vivo perfusion-fixation at 5 minutes, 15 minutes, 30 minutes, 3 hours, 1 day, and 3 days after the completion of carotid endarterectomy, and vessels were studied by scanning electron microscopy, light microscopy, and transmission electron microscopy for evaluation of thrombotic changes at the level of arterial injury. Although no postoperative carotid occlusion was observed, thrombus formation was noted as early as 15 minutes after recirculation. Thrombus formation reached its peak at 3 hours and was no longer detected 3 days after the procedure. Microsurgical carotid endarterectomy in rats may be a useful experimental model for the evaluation of antithrombotic drugs.
The pharmacological prevention of thrombosis after surgical arterial injury is still an open question. In the present study, a recently developed model of carotid endarterectomy in rats was used to assess the effectiveness of heparin, prostacyclin (PGI2), and OKY-1581, a selective thromboxane A2 (TXA2) synthetase inhibitor, in preventing thrombus formation. Thirty-six male Sprague-Dawley rats were divided into six groups: A--controls (no treatment), B--tris (hydroxymethyl) aminomethane (Tris)-HCl buffer (vehicle of PGI2), C--heparin (100 IU/kg), D--OKY-1581 (100 microns/kg/minute), E--low dose PGI2 (10 ng/kg/minute), F--high dose PGI2 (50 ng/kg/minute). The animals were killed by in vivo perfusion-fixation 15 minutes after recirculation. The endarterectomized vessels were submitted to scanning electron microscopy examination and were evaluated blindly according to the following scale: 1, (almost) normal appearance of the endarterectomized surface; 2, moderately abnormal appearance; and 3, definitely abnormal appearance. The results in terms of thrombus prevention were as follows: controls congruent to Tris-HCl buffer less than OKY-1581 congruent to low dose PGI2 less than high dose PGI2 less than heparin. When combined, the two control groups did significantly worse than all four treated groups (P greater than 0.05). Fisher's exact test showed a statistically significant difference between controls and the heparin group (P = 0.01) and between controls and high dose PGI2-treated rats (P less than 0.05), but not between controls and low dose PGI2-(P less than 0.16) or OKY-1581-treated animals (P less than 0.16). In conclusion, the present study confirms that anticoagulation with heparin is effective in reducing thrombus formation after carotid endarterectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to develop an inexpensive experimental model of carotid endarterectomy. Unilateral common carotid endarterectomies 3 mm in length were performed on 25 rats using microsurgical techniques. The pattern of endothelial regrowth after endarterectomy, the pinocytosis of regenerated endothelial cells, and the effects of heparin and thromboxane A2 synthetase inhibitor on thrombus formation were examined 7 days after the resumption of flow. Pinocytotic vesicular transport in endothelial cells was evaluated using horseradish peroxidase. All endarterectomized vessels in both control and drug-treated groups were patent 7 days after operation without apparent mural thrombus formation. Regenerated endothelial cells had spindle-shaped nuclei and cell bodies with long axes oriented parallel to the direction of blood flow. There were several instances where the leading edge of the endothelium at the distal end was reflected back in the distal direction. The extent of the endothelial ingrowth was often greater from the proximal end of the endarterectomy than from the distal end. These observations suggest that hemodynamic force affects endothelial regeneration. Pinocytotic activity was less in the regenerated endothelium than in either the endothelium remaining at the periphery of the endarterectomy or the endothelium of the control animals.
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The author reports on a case of MCA aneurysm for which the decision to operate was based above all on the CT examination. In this regard the practical importance of the CT in diagnosis and treatment of subarachnoid hemorrhage (SAH) is again emphasized.
A middle-aged man who had undergone two previous operations on a cerebellar haemangioblastoma was found at CT follow-up thirteen years later to have a double supra-and infra-tentorial haemangioblastoma. The tumors were confirmed by vertebral angiography and removed by two-stage surgery. The importance of careful CT follow-up to detect the recurrence of multifocal haemangioblastoma is clear.
Two patients with recently ruptured intracranial aneurysms underwent surgical repair of these vascular lesions. Postoperatively, they showed clinical and laboratory evidence of disseminated intravascular coagulation (DIC). In both patients severe cerebral ischemic complications occurred. In one case the ischemic complications and the hematological changes were successfully reversed. This syndrome is a potential complication of aneurysmal subarachnoid hemorrhage (SAH), which requires prompt diagnosis and appropriate management. The relationship between hematological changes suggesting DIC and the ischemic complications of SAH should be extensively investigated.
An aneurysm-induced hydrocephalus was observed in two series of patients who were treated antifibrinolytically in different ways: A = 3 g/day of AMCA + 3 - 400,000 KIU/day of aprotinins, B = 6 g/day of AMCA. Group A showed significantly less formation of hydrocephalus and ischaemic complications. In the survey, various factors (neurological condition, number of haemorrhages, localisation of the aneurysm) play a part in the formation of the hydrocephalus following subarachnoid haemorrhage (SAH). The same is true of the high correlation with preceding severe ischaemic complications after SAH (p less than 0.005). The administration of antihypertensives leads to a significantly higher rate of ischaemic complications but does not exert an influence on the formation of hydrocephalus. It is assumed that the close relationship is the essential cause of cerebral ischaemia and development of hydrocephalus after SAH, that is, erythrocyte decomposition products which explain the observed relations between the two. The results obtained do not support the thesis of periventricular ischaemia as the cause of the development of a clinically significant hydrocephalus after SAH.
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The results of two different antifibrinolytic therapeutic modalities (A = AMCA 3 gm daily + Aprotinin, 3-400000 K.I.U. daily, B = AMCA, 6 gm daily) were compared retrospectively in a series of 137 patients harbouring recently ruptured intracranial aneurysms. The rates for rebleeding and thromboembolic complications were similar in both differently treated groups of patients, whilst that for ischaemic complications was significantly (p less than 0.025) lower in cases managed with modality A. In these also the incidence of hydrocephalus was decreased, although not significantly (0.20 greater than p greater than 0.19). According to these data, low-dose AMCA + Aprotinin seems to be a rational therapeutic combination for cases of ruptured intracranial aneurysms, in which antifibrinolytics are indicated.
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