Cerebral Infarction Hemorrhage Research Articles

Neurologic outcome after penetrating extracranial arterial trauma.

We undertook this study to determine factors that adversely affect outcome in patients with penetrating injury to the extracranial cerebral vasculature. Patients and methods Medical records were reviewed for all patients who had undergone surgical intervention to treat penetrating injury to the extracranial cerebral arteries between January 1989 and December 1999. Forensic autopsy findings were also reviewed for all patients who died as a result of their injury. One hundred fifty-one patients with injury to the brachiocephalic artery (n = 21), common carotid artery (n = 98), or internal carotid artery (n = 32) were identified. Overall mortality was 21.2%, and stroke rate in surviving patients was 15.1%. Twenty-five of 32 deaths (78.1%) were stroke-related. Brachiocephalic artery injury was associated with the highest mortality (38.1%), and survivor stroke rate was highest in patients with internal carotid injuries (22.7%). Hemodynamic instability at presentation led to both higher mortality (30.7%) and stroke rate (19.2%). Preoperative angiography did not influence mortality or stroke rate in hemodynamically stable patients. Procedural mortality associated with arterial ligation was 45% (9 of 20 patients), and no surviving patient experienced a change in pre-ligation neurologic state. Nine patients remained neurologically intact after ligation, and 2 patients with preoperative localized neurologic deficit were unchanged postoperatively. In 131 patients, mortality after arterial repair was 17.6%, and in 5 surviving patients (5.4%) an ischemic neurologic deficit developed. Twelve of 15 surviving patients (80%) with preoperative neurologic deficit who underwent arterial repair had improved neurologic status. Cerebral infarcts were confirmed at autopsy in 23 patients; 18 infarcts were ischemic (10, repair; 8, ligation), and 5 infarcts were hemorrhagic (all, repair). No factor was identified that was predictive of ischemic versus hemorrhagic infarction in patients undergoing repair. The presence of hypovolemic shock, internal carotid artery injury, complete vessel transection, and arterial ligation are associated with unfavorable outcome. Penetrating injury to the brachiocephalic, common carotid, or internal carotid artery should be repaired rather than ligated when technically possible. Subsequent ischemic or hemorrhagic cerebral infarction is unpredictable, but overall outcome is superior to that with ligation of the injured artery.

Perinatal Brain Damage: Underlying Mechanisms and Neuroprotective Strategies

Children who suffer from perinatal brain injury often deal with the dramatic consequences of this misfortune for the rest of their lives. Despite the severe clinical and socioeconomic significance, no effective clinical strategies have yet been developed to counteract this condition. As shown in recent studies, perinatal brain injury is usually brought about by cerebral ischemia, cerebral hemorrhage, or an ascending intrauterine infection. This review focuses on the pathophysiologic pathways activated by these insults and describes neuroprotective strategies that can be derived from these mechanisms. Fetal cerebral ischemia causes an acute breakdown of neuronal membrane potential followed by the release of excitatory amino acids such as glutamate and aspartate. Glutamate binds to postsynaptically located glutamate receptors that regulate calcium channels. The resulting calcium influx activates proteases, lipases, and endonucleases, which in turn destroy the cellular skeleton. A second wave of neuronal cell damage occurs during the reperfusion phase. This cell damage is thought to be caused by the postischemic release of oxygen radicals, synthesis of nitric oxide, inflammatory reactions, and an imbalance between the excitatory and inhibitory neurotransmitter systems. Furthermore, secondary neuronal cell damage may be brought about in part by induction of a cellular suicide program known as apoptosis. Recent studies have shown that inflammatory reactions not only aggravate secondary neuronal damage after cerebral ischemia, but may also injure the immature brain directly. This damage may be mediated by cardiovascular effects of endotoxins leading to cerebral hypoperfusion and by activation of apoptotic pathways in oligodendrocyte progenitors through the release of proinflammatory cytokines. Periventricular or intraventricular hemorrhage (PIVH) is a typical lesion of the immature brain. The inability of preterm fetuses to redistribute cardiac output in favor of the central organs and their lack of cerebral autoregulation may cause significant fluctuations in cerebral blood flow when oxygen is in short supply. Disruption of the thin-walled blood vessels in the germinal matrix with subsequent cerebral hemorrhage is often the inevitable result and is at times associated with cerebral hemorrhagic infarction. Knowledge of these pathophysiologic mechanisms has enabled scientists to develop new therapeutic strategies, which have been shown to be neuroprotective in animal experiments. The potential of such therapies is discussed here, particularly the promising effects of postischemic induction of cerebral hypothermia, the application of the calcium-antagonist flunarizine, and the administration of magnesium.

Secondary Degeneration of the Substantia Nigra and Corticospinal Tract after Hemorrhagic Middle Cerebral Artery Infarction: Diffusion-weighted MR Findings

Middle cerebral artery (MCA) infarction involving the striatum can cause secondary degeneration of the substantia nigra and corticospinal tract. We present a patient with subacute hemorrhagic MCA infarction in whom diffusion-weighted MR images showed high signal intensity in the ipsilateral substantia nigra and corticospinal tract. A corresponding apparent diffusion coefficient map revealed a uniformly decreased signal in the same area. This represents secondary degeneration and should not be mistaken for other pathological conditions, such as a new infarction.

Impact of immediate cerebral angiography for in-hospital cerebral thromboembolism after cardiovascular surgery.

Postoperative stroke remains a serious problem in cardiovascular surgery. We studied the role of cerebral angiography in postcardiotomy stroke. We retrospectively analyzed 5 in-hospital patients with stroke due to cerebral thromboembolism after cardiovascular surgery. The incidence of in-hospital cerebral thromboembolism was 0.5%, involving 5 patients among 913 adults undergoing cardiovascular operations. In-hospital cerebral thromboembolism occurred 3 to 9 days (average: 7 +/- 2 days) after surgery. Causes of cerebral thromboembolism were chronic atrial fibrillation in 1, transient atrial fibrillation in 2, artificial valve in 1, and intracranial arterial stenosis in 1. Immediate cerebral angiography, after exclusion of intracranial hemorrhage and complete cerebral infarction by computed tomography, revealed cerebral embolism in 3 and cerebral thrombosis in 2 with occlusion or stenosis of intracranial arteries. Local intraarterial administration of a thrombolytic agent was done in the 3 patients with cerebral embolism and occluded arteries were recanalized. Fibrinolysis was not done in 2 because of recanalized arteries or sufficient peripheral blood supply through collateral feeders. No patients exhibited rebleeding into the pericardial space or wound bleeding. All patients survived with moderate or full functional recovery. Immediate cerebral angiography with/without local thrombolysis may improve functional outcome and survival in patients with postcardiotomy cerebral thromboembolism.

Fatal cerebral hemorrhage associated with cyclosporin-A/FK506-related encephalopathy after allogeneic bone marrow transplantation

We report a case of cerebral hemorrhage associated with cyclosporin A (CsA)/FK506-related encephalopathy that developed in a 16-year-old woman after allogeneic bone marrow transplantation. Hematopoietic engraftment occurred on day 15, and the patient developed systemic convulsions after CsA was replaced by FK506 for the treatment of acute graft-versus-host disease (GVHD). Based on magnetic resonance imaging, laboratory findings and cerebrospinal fluid studies, she was diagnosed as having CsA/FK506-related encephalopathy with cerebral hemorrhagic infarction. Although she recovered completely after discontinuation of FK506, she developed convulsions again 15 days after re-administration of FK506. A computed tomography scan showed cerebral hemorrhage. She died of respiratory failure. Vascular damage induced by immunosuppressive drugs and enhanced by acute GVHD seemed to be the cause of the cerebral hemorrhage. Since hypertension, which was present during both of the central nervous system events, seemed to have contributed to the development of the cerebral hemorrhage, it is proposed that CsA and FK506 should be reduced or discontinued when patients who have risk factors of hypertension become hypertensive even if they have no symptoms of neurotoxicity.

Cocaine and pupillary-sparing oculomotor nerve paresis

Cocaine use has been associated with a variety of neurologic disturbances, including ischemic and hemorrhagic cerebral infarcts, subarachnoid hemorrhage, psychosis, coma, syncope, seizures, myoclonus, dystonic reactions, vertigo, headache, and paresthesias.1-4 We report on a patient who developed a pupillary-sparing oculomotor cranial nerve III (CNIII) paresis after the use of crack cocaine. Case report. A 29-year-old African-American man presented with a 2-week history of right ptosis, double vision, and headache. The patient admitted to the occasional use of cocaine. On the evening before the onset of symptoms, he inhaled cocaine by dusting the drug onto a cigarette that he then smoked. He awakened the next morning with a throbbing right retro-orbital headache, drooping of the right eyelid, and predominantly side-by-side double vision. From the time of onset to initial evaluation 2 weeks later, he had persistent right-sided ptosis, intermittent right frontal/retro-orbital throbbing headache, and double vision. He smoked cocaine once after the onset of his symptoms …

Fatal Cerebral Hemorrhage Complicating Thromboembolic Stroke in a Patient with Prosthetic Mitral Valve Thrombosis Treated with Thrombolytic Therapy

We report the case of a 66-year-old male with a history of mitral valve replacement with a Sorin tilting-disk prosthesis and a subsequent operation for severe constrictive pericarditis. After 5 years of stable anticoagulant treatment, he suffered an intracerebral hemorrhage that required temporary withdrawal of warfarin. Thrombosis of the prosthesis, presenting as acute heart failure, was then determined. Due to high-operative and hemorrhagic risk, the patient was treated with low-dose thrombolytic therapy administered as two boluses of recombinant tissue plasminogen activator (r-tPA). The patient's hemodynamics improved strikingly. However, a few hours after the second dose, a devastating cerebral hemorrhagic infarction resulted in death. Autopsy showed the primarily ischemic nature of both strokes. The schemes of thrombolytic therapy in prosthetic heart valve thrombosis and the importance of a correct interpretation of pathogenesis of stroke in anticoagulated patients are discussed. Key Words: Heart valve thrombosis— Thrombolysis—Stroke—Warfarin.

Ecgonine methyl ester, a major cocaine metabolite, causes cerebral vasodilation in neonatal sheep.

Maternal cocaine abuse has been associated with fetal and neonatal neurologic abnormalities, including hemorrhagic cerebral infarctions, but the mechanisms for cocaine's cerebral effects are unknown. We previously showed that acute cocaine injection causes cerebral vasodilation in cats and immature sheep; others have shown that cocaine causes cerebral vasoconstriction in piglets and in pressurized neonatal sheep arteries. Although methodologic and species differences may explain these conflicting results, we tested another possibility; that is, that ecgonine methyl ester (EME), a major cocaine metabolite in sheep, causes cerebral vasodilation and may account, in part, for cocaine's vascular effects. We studied the cerebral effects of a single i.v. injection of EME (2.5 mg/kg) in eight chronically catheterized, unanesthetized neonatal sheep (4 +/- 2 d old). We measured cerebral hemisphere blood flow (CBF) using radiolabeled microspheres, mean arterial pressure, heart rate, and arteriovenous oxygen content, and we calculated cerebral oxygen consumption (CMRo2) and cerebrovascular resistance at baseline and 0.5, 2, 5, and 60 min after EME injection. EME injection had no systemic effects, including no changes in mean arterial pressure, heart rate, or arterial blood gases. Within 0.5 min of injection, EME caused a 21% decrease in cerebrovascular resistance, which remained decreased for 60 min. CBF increased by 20% at 0.5, 2, and 5 min. Blood flow to brain regions other than the cerebral hemispheres paralleled changes in CBF, with cerebellar flow remaining increased at 60 min. There was no change in CMRo2. There was a small, but physiologically insignificant, decrease in arterial oxygen content. We conclude that EME causes cerebral vasodilation in neonatal sheep and may account, in part, for cocaine's cerebral vascular effects.

A Case of Adenocarinoma of the Lung Associated with Multi-oragn Infarctions

The relationship between neoplastic disease and thromboembolic disorders has been recognized since 1865, when Armand Trousseau first reported a high incidence of venous thrombosis in a series of patients with gastric carcinoma. The overall incidence of thromboembolic disease in patients with cancer has been reported to vary 1% to 15%. In a prospective study, Ambrus and associates reported that thrombosis and/or bleeding was the second most common cause of death in haspitalized cancer patients. We report a case who presented as a thromboembolic disease and subsequently confirmed to have an underlying lung malignancy. This 45 years old male patient visited our hospital with abdominal pain and distention of 3 days duration. Abdominal CT scan revealed multiple splenic and renal infarctions. On 20th haspital day, drowsy mental status was developed and hemorrhagic cerebral infarction was noted in brain CT scan. Chest CT scan revealed a 4cm sized spiculated mass on left lung apex and multiple paratracheal lymph adenopathy. With surgical biopsy of left supraclavicular lymph nodes, this patient was confirmed to have adenocarcinoma.

A case of antineutrophil cytoplasmic autoantibodies (ANCA)

An 18-year-old female was admitted to our ICU for dyspnea. She had bloody sputum, hypoxia and hypoproteinemia with proteinuria. Massive doses of methylprednisolone (750mg·day-1) were administered for 3 days. She recovered temporarily. Renal biopsy revealed crescentic glomerulonephritis and transbronchial lung biopsy revealed alveolar hemorrhage. The examination of autoantibodies was positive for perinuclear antineutrophil cytoplasmic autoantibodies (P-ANCA). Pulmonary and renal function deteriorated gradually despite the administration of prednisolone (60mg·day-1). Plasma exchange and hemodialysis were performed and massive doses of methylprednisolone (1g·day-1) were administered for 3 days. Pulmonary function recovered, but it was necessary to continue hemodialysis. Pulmonary function deteriorated again one month later. P-ANCA tested negative after plasma absorption, but pulmonary function grew worse as abnormalities in blood coagulation progressed. The patient died from hemorrhagic cerebral infarction. We believe this was a case of Wegener's vasculitis with P-ANCA. We administered of massive doses of methylprednisolone, and performed plasma exchange and plasma absorption, but these therapies proved to be ineffective. The levels of P-ANCA, white blood cells and C-reactive protein did not reflect the virulence of the disease in this patient. It is important to investigate the indices that reflect the activity of this disease and the choice of the appropriate therapy for the level of virulence.

Neurologic manifestations of pediatric systemic lupus erythematosus

Central nervous system involvement is a common but rarely reviewed feature of pediatric systemic lupus erythematosus (SLE). We retrospectively reviewed the charts of 91 patients with pediatric SLE and using a standardized data abstraction form documented 40 patients with central nervous system (CNS-SLE) involvement. The mean age of onset of SLE was 13.3 years. In 19 patients the CNS manifestation was a presenting symptom, in 12 patients CNS involvement was present within the first year of diagnosis, and in 9 patients it took up to 7 years for CNS disease to become evident. Nineteen children (48%) manifested neuropsychiatric SLE, which included depression, concentration or memory problems, and frank psychosis. Seizures were present in 8 patients (20%), 6 had cerebral ischemic events (15%), 1 had chorea (3%), 2 had papilledema (5%), and 2 patients had a peripheral neuropathy (5%). Nine patients (22%) had severe headache consistent with lupus headache. Seven children had more than one CNS manifestation. In the investigation of CNS-SLE, computed tomography and/or magnetic resonance imaging scans were helpful in patients with focal ischemic lesions and venous sinus thrombosis. Electroencephalography was abnormal only in 33% of patients with seizure disorders and rarely helpful in patients with diffuse neuropsychiatric symptoms. Single-photon emission computed tomography scans were abnormal in most patients with neuropsychiatric SLE, especially in those with frank psychosis. The lupus anticoagulant was present in the patient with chorea and was frequently present in patients with cerebral vascular events. Long-term outcome was good: only 1 child died of cerebral hemorrhagic infarction and 3 others had significant persistent CNS deficits. The majority of patients (90%) had excellent recovery from CNS-SLE.

Metoprolol for action tremor following intracerebral hemorrhage

Tremor has been rarely described as a manifestation of stroke. A 21-year-old left-handed man developed severe action tremor of his distal left upper extremity and hand following a right parieto-occipital intracerebral hemorrhage. Strength of the left upper extremity improved gradually during a 3-month period but a severe action tremor developed. The patient was treated with the cardioselective beta-blocking agent, metoprolol, initially for elevated blood pressure and tachycardia at 25mg twice daily for approximately 2 months. Metoprolol was then increased at weekly intervals by 25mg twice daily to a total of 100mg twice daily. Tremor intensity decreased clinically and graphically as monitored by a trace test by having the patient attempt to trace a horizontal and vertical axis and scoring the errors. The scores declined weekly from the first week (4,347), second week (3,786), third week (1,088), to the fourth week (484). No adverse cognitive or cardiopulmonary effects were noted. Action tremor should be considered as one of the movement disorders caused by hemorrhagic cerebral infarction. This case responded well to treatment with metoprolol.

Clinical and angiographic results of transluminal extraction coronary atherectomy in saphenous vein bypass grafts.

Transluminal extraction coronary (TEC) atherectomy is a relatively new device that has recently been approved by the Food and Drug Administration. Because of its ability to aspirate clot and atheromatous material, TEC atherectomy may be useful in patients with stenoses in saphenous vein bypass grafts. TEC atherectomy was performed on 158 saphenous vein graft lesions in 146 consecutive patients with a mean age of 65 +/- 8 years (78% men). Clinical indications for atherectomy included stable angina (37%), unstable angina (54%), and postinfarction angina after recent (< 1 month) myocardial infarction (8%). Patients with acute myocardial infarction and target vessels < 2 mm in diameter were excluded. The mean age of the bypass graft was 8.3 +/- 3.0 years, and 17% were diffusely diseased and degenerated. Complex lesion morphology included total occlusion (6%), eccentricity (64%), ulceration (18%), and thrombus (28%). The TEC atherectomy cutter was successfully advanced through 144 lesions (91%), but technical failures occurred in 14 lesions (9%), and these were subsequently managed by successful balloon angioplasty. Quantitative angiography revealed an increase in lumen diameter from 0.9 +/- 0.5 mm, to 1.5 +/- 0.7 mm after TEC atherectomy, to 2.3 +/- 0.8 mm after percutaneous transluminal coronary angioplasty (PTCA) (P < .001), which corresponded to decreases in diameter stenosis from 75 +/- 14%, to 58 +/- 20% after TEC atherectomy, to 36 +/- 22% after PTCA (P < .001). Device success was achieved in 39.2% (post-TEC atherectomy decrease in diameter stenosis > or = 20%), and procedural success was achieved in 84% (final diameter stenosis < 50% in the absence of a major complication). Angiographic complications were evident in 33 lesions (20.7%) immediately after TEC atherectomy and in 8 lesions (5%) after PTCA, including distal embolization (11.9%), no-reflow (8.8%), and abrupt closure (5.0%), but no perforations. Adjunctive PTCA (and other medical therapy) successfully managed 61% of angiographic complications. Serious clinical complications included in-hospital death in 3 patients (2.0%), emergency bypass surgery in 1 patient who died (0.7%), Q wave myocardial infarction in 3 patients (2.0%), non-Q wave myocardial infarction in 4 patients (2.7%), vascular injury requiring surgical repair and/or blood transfusion in 9 patients (6.1%), and hemorrhagic cerebral infarction in 4 patients (2.7%). Using a composite clinical end point defined as in-hospital death, emergency bypass surgery, or myocardial infarction, the strongest independent correlate (P < .001) of a severe clinical complication was the development of one or more serious angiographic complications (no-reflow, distal embolization, or abrupt closure) immediately after TEC atherectomy. Complete clinical follow-up was available in 118 (92%) of 128 eligible patients at an interval of 6.0 +/- 2.5 months after discharge. Late cardiac outcome included recurrent angina treated with medical therapy (18%), repeat percutaneous intervention on the original target lesion (26%), repeat coronary artery bypass surgery (5%), Q wave myocardial infarction (4%), and late cardiac death (7%). Angiographic follow-up in 105 (80%) of 132 eligible lesions revealed a restenosis rate of 69% (defined as a diameter stenosis > 50%), including 30 lesions (29%) with total occlusion of the original lesion. In patients with stenoses in saphenous vein bypass grafts, TEC atherectomy is limited by the frequent need for adjunctive balloon angioplasty to achieve adequate lumen enlargement and to manage TEC atherectomy-induced complications. Although the incidence of serious clinical complications is similar to that of other percutaneous interventions in vein grafts, there is a high incidence of restenosis and late vessel occlusion. Prospective randomized studies are needed to determine the best revascularization strategy for high-risk patients with old degenerated vein

Detection of hemorrhage in acute cerebral infarction evaluation with spin-echo and gradient echo MRI

We investigated the efficacy of magnetic resonance imaging (MRI) in the detection and delineation of acute hemorrhagic cerebral infarction and evaluated the role of gradient-echo imaging in these patients. This study was performed prospectively. Entry criteria were: (1) Clinical evidence of acute supratentorial infarction later confirmed by at least one imaging study, and (2) unenhanced computed tomography (CT) and MRI scans performed within 72 hours of ictus. The first 50 patients who met these criteria were included. Comparison of CT and spin-echo (SE) and gradient-echo (GE) MRI at 0.6 T for the visualization of infarction and for the detection or exclusion of hemorrhage were done. There were no cases in which CT was superior to MRI for the diagnosis of either bland or hemorrhagic infarction. All 50 infarcts were detected on long TR SE MRI and 30 50 on GE scans. Eighteen infarcts were judged to be hemorrhagic on the basis of well-established CT and MRI criteria. In all these cases, hemorrhage was most obvious on GE scans as focal areas of marked hypointensity, including 10 cases in which SE MRI and CT demonstrated subtle, equivocal, or no evidence of hemorrhage. In addition, GE MRI allowed for the exclusion of hemorrhage in five cases with equivocal findings of hemorrhage on long TR SE MRI. GE MRI is a valuable adjunct to SE sequences for the detection or exclusion of hemorrhage in acute infarcts with equivocal or mild intensity changes on SE MRI. With further improvements in fast-scanning techniques and a greater understanding of the pathophysiology and clinical implications of hemorrhagic infarction, it may be possible to replace CT with a combination of SE and GE MRI as the primary imaging modality in the evaluation of acute infarction.

Safety of anticoagulation after hemorrhagic infarction

Cerebral hemorrhagic infarction visualized on CT, secondary to embolic stroke in an anticoagulated individual, is usually associated with clinically stable or improving neurologic signs; fear of transforming the hemorrhagic infarction into a hematoma, however, usually prompts cessation of anticoagulation until the blood has cleared on CT, despite the recognized risk of recurrent embolism during this non-anticoagulated period. We now report our experience with 12 patients with hemorrhagic infarction who remained anticoagulated. Eleven men and one woman, ages 33 to 77, developed hemorrhagic infarction while on heparin, warfarin, or both, for prevention of recurrent embolism. Patients were either continued on uninterrupted anticoagulation from stroke onset (n = 6), or anticoagulation was withheld for several days and then resumed (n = 4), or it was withheld for 5 and 14 days (n = 2) after stroke onset and then continued uninterrupted despite the CT appearance of hemorrhagic infarction. Eleven patients had a definite cardioembolic source for stroke (atrial fibrillation, seven; ventricular thrombus, two; and ventricular dyskinesia, two). One patient had carotid occlusion with local intra-arterial embolism. Hemorrhagic infarcts varied in size and were located in the middle cerebral artery territory in 11 patients and posterior cerebral artery territory in one. All patients remained clinically stable or improved on anticoagulation. Serial CTs showed fading hemorrhagic areas. When the risk of recurrent embolism is high, anticoagulation may be safely used in some patients with hemorrhagic infarction.

出血性脳梗塞で発症したＴ‐ｃｅｌｌ ａｎｇｉｏｔｒｏｐｉｃ ｌｙｍｐｈｏｍａの１剖検例

We report here an autopsy case of T-cell angiotropic lymphoma with atypical clinical course. A 47-year-old male was admitted because of a speech disturbance. His brain CT revealed intracerebral hemorrhage, and an evacuation of intracranial hematoma was performed. The examination of the brain tissue resected at the operation showed hemorrhagic cerebral infarction. He was discharged on the 25th postoperative day without symptoms. Four weeks later, he was re-admitted because of high fever and dyspnea on effort. His laboratory findings showed mild hypoxemia and elevated serum LDH (6075IU). Six days after the admission, he abruptly presented tonic convulsion. His brain CT revealed hemorrhage in the left occipital lobe, and he admitted to NCU. Though steroid pulse therapy and artificial respiration were performed, respiratory failure and DIC progressed, and he died fifteen days after the admission.At autopsy, the histological examination showed a multifocal proliferation of lymphoma cells within the lumens of small blood vessels in almost all of the organs. These tumor cells had T-cell surface markers, so final pathological diagnosis was T-cell angiotropic lymphoma.Most cases of angiotropic lymphoma (neoplastic angioendotheliosis) reported in the literature are derived from B-cell lymphoma, and T-cell angiotropic lymphoma is very rare.The clinical course of our case was a rapidly progressive one, and he presented various symptoms such as hemorrhagic cerebral infarction, respiratory failure and DIC. This is the first report of intracranial hemorrhage in angiotropic lymphoma.

INTRACEREBRAL THROMBOSIS

A 29-yr-old writer presented with seizures and left hemiparesis 8 days post-partum. Studies revealed right parietal hemorrhagic infarction secondary to superior sagittal sinus thrombosis. An anticoagulant was given for clot extension associated with increasing cerebral edema and coma. Inpatient rehabilitation was undertaken for residual left hemiparesis, most severe in the leg. Left arm strength rapidly returned to normal. Significant improvement in left leg strength occurred but was delayed for many months. Intracerebral thrombosis is an uncommon but significant cause of stroke in young adults. It frequently occurs in the puerperium and may be associated with unilateral or bilateral neurologic deficits. Treatment with anticoagulants is controversial because of the risk of hemorrhagic cerebral infarction, but may be beneficial in some cases. Recovery may be delayed for several months pending recanalization of the sinus or the development of collateral circulation. The overall prognosis for neurologic and functional recovery in survivors of intracerebral thrombosis is good.

Cerebrovascular complications after orthotopic liver transplantation

We analyzed 55 autopsy cases in 1,357 patients undergoing orthotopic liver transplantation at the University of Pittsburgh and found that 13 (23.6%) patients had intracranial bleeding, and five (9%) had infarcts. Eight patients had bleeding localized to one intracranial compartment: intracerebral hemorrhage (three patients); subarachnoid hemorrhage (three patients); and subdural hematoma (two patients). Five patients had combinations of multiple sites of bleeding: three with subarachnoid hemorrhage-intracerebral hemorrhage, one with subarachnoid hemorrhage-intracerebral hemorrhage-subdural hematoma, and one with subdural hematoma-intracerebral hemorrhage. Coexistent CNS infections (fungal or bacterial) were associated with hemorrhagic infarcts and intracerebral hemorrhage in four patients. Cerebral embolism and hemorrhagic infarction from bacterial endocarditis occurred in one patient. Five patients died of intracranial bleeding. Severe coagulopathy was the major cause of intracranial bleeding and was associated with systemic bleeding in 12 patients. Significant systemic or metabolic complications were present in all patients and masked the focal signs of the intracranial process in more than one half.

Vein Patch Rupture After Carotid Endarterectomy: A Survey of the Western Vascular Society Members

To determine the prevalence, demographics and morbidity of vein patch rupture, the authors polled members of the Western Vascular Society. Forty-eight surgeons (53% of the members) reported an experience with 23,873 carotid operations. A vein patch was used in 1,760 operations (7.4%), and rupture of the patch occurred in 13 patients (0.7%), 10 women and three men. Indications for the patch were a small artery in 10 patients and restenosis in three. Saphenous vein was used for all patches and was harvested from the ankle in 12 patients and from the groin in one patient. All ruptures occurred from a split in the vein patch. Hypertension was present in seven of the 13 patients. None of the ruptures were associated with infection. Two ruptures occurred on the first postoperative day, six on the second day, three on the third day, one on the eighth day, and one on the twenty-first day. Four patients died: airway obstruction (1), hemorrhagic cerebral infarction (1), and myocardial infarction (2) were the causes. Three had a stroke and survived, one had a retinal embolus, and five underwent reoperation without complication. Vein patch of the carotid artery is used infrequently by members of the Western Vascular Society. The incidence of rupture of the patch is low (0.7%), but when it occurs, there is significant mortality (30.7%), and morbidity (30.7%). Patients with a vein patch should be observed in the hospital for three days after endarterectomy because rupture demands immediate reoperation.

Relationship of Hospitalized Stroke Rate and In-Hospital Mortality to the Decline in US Stroke Mortality

Data from the National Hospital Discharge Survey was used to estimate the admission rate and in-hospital mortality for US stroke patients from 1970 to 1987. Over this period the hospital admission rate increased from 5.0 per 1,000 population to 5.5 per 1,000, while the in-hospital mortality fell from 18.6 to 10.0% of discharges. When patients experiencing general or late effects or transient ischemic attacks were excluded, the hospital admission rate increased from 2.8 to 4.8 per 1,000 and in-hospital mortality fell from 26 to 12% of discharges. Admission rates increased from 1970 to 1987 for both hemorrhagic strokes and cerebral infarctions, but fell for ill-defined cerebrovascular events, presumably reflecting increased use of computed tomography and magnetic resonance imaging during this period. Mortality for hemorrhagic strokes decreased from 45 to 30% of discharges, mortality for infarctions decreased from 24 to 13% and mortality for ill-defined events fell from 24 to 17%. There are several limitations with the use of the National Hospital Discharge Survey data to estimate changes in hospital admission rates and in-hospital mortality. However, these data suggest a greater role for decreasing case fatality in explaining nationwide declines in stroke mortality rates than has generally been acknowledged.