Case report: MR imaging of fat necrosis of the breast associated with lipid cyst formation following conservative treatment for breast carcinoma

A hypertensive 72-year-old male presented with a ruptured arteriovenous malformation (AVM) manifesting as hematoma indistinguishable from common putaminal hemorrhage on precontrast computed tomography scan. The AVM was located in the proximal sylvian region fed by branches of the anterior and middle cerebral arteries. The AVM was totally removed. Although bleeding from AVM in the elderly is uncommon, the cause of even common hypertensive hemorrhage should be identified by other imaging techniques such as magnetic resonance imaging and cerebral angiography to allow the optimum treatment.     

Nucleotide substitutions at the -6 position in the promoter region of the factor IX gene result in different severity of hemophilia B Leyden: consequences for genetic counseling

A case of vessel perforation by a guide wire during an interventional neuroradiological procedure is reported. The patient was a 59-year-old woman with a left frontal basal arteriovenous malformation (AVM) fed by the left anterior cerebral artery. Transarterial embolization of the AVM was attempted. During the procedure, vessel perforation by the guide wire occurred at the left A1-A2 junction and resulted in subarachnoid hemorrhage, which stopped spontaneously. The patient developed progressive obstructive hydrocephalus, and surgical treatment was performed. The AVM was totally removed after ventricular drainage, and the arterial perforation site was explored. When clot around the left A1-A2 junction was removed, hemorrhage recurred. This hemorrhage was similar to what has been observed when a small perforating artery was avulsed. The hemorrhage site was coagulated under temporary occlusion of both A1 segments. Surgical intervention was probably not necessary for this type of bleeding if it had stopped spontaneously, because the rebleeding from the small pinhole would be unlikely, and the operation was more hazardous than the usual aneurysmal surgery.     

Utility of the American Diabetes Association risk test in a community screening program

In many patients with superficial siderosis of the central nervous system (CNS) no source of bleeding can be established, despite extensive examinations. The authors report a patient with superficial siderosis and a spinal arteriovenous malformation (AVM) that was not visible on magnetic resonance (MR) imaging or myelography but was identified on angiographic studies. This 71-year-old man presented with a 2-year history of progressive gait difficulties and hearing loss. Examination showed ataxia, hearing loss, and quadriparesis. On MR imaging superficial siderosis of the brain and spinal cord as seen; however, MR imaging of the CNS, as well as cerebral angiography and myelography studies, did not reveal the source of hemorrhage. Spinal angiography revealed a small slow-flow pial AVM at the C-5 level originating from the anterior spinal artery. A C-5 corpectomy was performed and the AVM was obliterated. The patient did well and reported no further progression of his symptoms during 3 months of follow up. Spinal angiography is indicated to complete the evaluation of patients with superficial siderosis, even if results of spinal MR imaging and myelography studies are normal. Obliteration of spinal AVMs may successfully prevent the progression of superficial siderosis.     

Subarachnoid hemorrhage secondary to spinal arteriovenous malformation and aneurysm. Report of a case and review of the literature

A patient with recurrent subarachnoid hemorrhage was seen initially with intermittent signs and symptoms of intracranial and spinal cord dysfunction. Myelography and spinal angiography revealed an arteriovenous malformation (AVM) and aneurysm of the spinal cord. Extensive investigation failed to reveal any intracranial lesion. The relationship of subarachnoid hemorrhage at a spinal level to the development of remote neurological abnormalities is discussed, and previous reports of aneurysms associated with spinal AVM are reviewed.     

Subarachnoid hemorrhage and pontine hemorrhage followed by an embolization procedure of left occipital giant arteriovenous malformation: a case report

A 42-year-old woman suddenly developed headache and nausea on July 26, 1991, and the computed tomography (CT) scan showed a moderate-sized hematoma in the left occipital lobe. After one month's conservative treatment, she had recovered to a neurologically intact state. Cerebral angiography demonstrated a giant arteriovenous malformation fed by enlarged branches of the left posterior cerebral artery as well as small branches arising from the middle cerebral artery, anterior cerebral artery and the meningeal branches of the middle meningeal artery and the occipital artery. Preoperative embolization was planned on February 24, 1992. During an attempt at catheterization of the basilar artery and the left posterior cerebral artery with a balloon catheter and a Tracker-18 catheter, the patient complained of an intensification of her headache, nausea and vomiting. So the embolization procedure was stopped. The CT scan taken immediately at that time showed a severe subarachnoid hemorrhage (SAH). She became comatose about 40 minutes later. CT scan taken next day revealed also a complication of the pontine hemorrhage. Neurologically, she had gradually recovered and could communicate with some simple words 3 months after SAH. The total removal of the AVM was performed on May 26, 1992. Postoperative course was uneventful. She showed rapid and remarkable improvement in her neurological state suggesting that the blood flow in the surrounding brain area had been corrected. A blood deficit had no doubt been caused when blood had been stolen by the giant AVM.(ABSTRACT TRUNCATED AT 250 WORDS)     

Etiology of immune stromal (interstitial) keratitis

BACKGROUND: Subarachnoid hemorrhage (SAH) with a spinal origin is a rare clinical entity. The most common source of SAH is an arteriovenous malformation. Only six cases of spinal hemangioblastomas causing SAH have been reported. CASE DESCRIPTION: This 48-year-old man had experienced severe headache 12 years earlier, which was diagnosed as SAH by computed tomography (CT) scan and lumbar puncture. However, cerebral angiography could not detect either aneurysm or arteriovenous malformation. Thereafter, he spent an uneventful life until he was incidentally diagnosed with a cervical tumor on magnetic resonance imaging (MRI) study for Meniere's disease. The tumor was situated at the cervicomedullary junction, and fed by the left vertebral artery. Histologic findings of the tumor showed features typical of hemangioblastoma. CONCLUSIONS: We describe a case of cervical spinal extramedullary hemangioblastoma with a past history of SAH. In our case, the SAH of 12 years ago perhaps occurred from the cervicomedullary junction hemangioblastoma. Since the etiology of SAH could not be detected at the first angiography, not only follow-up reangiography, but also MRI of the spinal cord and spinal angiography could have played an important role.     

Subarachnoid hemorrhage as a form of onset of systemic lupus erythematosus

INTRODUCTION: The most frequent cause of spontaneous subarachnoid hemorrhage (SAH) is rupture of intracranial arterial aneurysms (> 70%). The remainder are due to many different aetiologies. Although SAH is a relatively common neuropathological finding in systemic lupus erythematosus (SLE), it is normally due to the extent of the intercerebral hemorrhage and not to its isolated presentation. CLINICAL CASE: We report the case of a 34 year old woman who presented with non-traumatic SAH at the onset of her lupus disorder. The patient was attended for SAH and at the same time a multisystemic disorder and severe thrombocytopenia were found, leading to a diagnosis of SLE. The neuroimaging techniques, selective cerebral arteriography, cerebral and spinal magnetic resonance, and magnetic resonance angiography did not show any vascular malformations. The patient was treated with immunosuppressive therapy, nimodipine, and following angiographic tests, with antiaggregants and anticoagulants. CONCLUSIONS: The greater frequency of SAH in patients with lupus, as compared to the general population, has been attributed to the presence of intracranial vasculitis. However, neuropathological studies have shown that true vasculitis is very infrequent in the central nervous system of SLE patients. In the case we describe, the first in which SAH appeared at the onset of the disease, we consider that the origin of the hemorrhage was her high arterial blood pressure and thrombopenia.     

Transluminal angioplasty and intra-arterial papaverine for the treatment of cerebral vasospasm after ruptured arteriovenous malformations

BACKGROUND: This is the first report on the use of intra-arterial papaverine and percutaneous transluminal angioplasty in two patients with severe, symptomatic cerebral vasospasm who suffered ruptured arteriovenous malformations (AVMs). CASE DESCRIPTIONS: The source of hemorrhage was a venous aneurysm in the first case and a pedicular aneurysm of the distal posterior inferior cerebellar artery in the second case. In both cases, the AVMs were located in the superior vermis and there was minimal subarachnoid hemorrhage. The first patient underwent removal of the AVM before the period of cerebral vasospasm and the second patient underwent removal of the AVM after the cerebral vasospasm had resolved. The outcome was excellent in the first patient and poor in the second patient. CONCLUSION: Arteriovenous malformation with ruptured aneurysms may be at high risk for cerebral vasospasm even when there is minimal subarachnoid hemorrhage. We recommend early treatment of AVMs with ruptured pedicular, intranidal, or venous aneurysms to avoid rebleeding and to allow for aggressive treatment of cerebral vasospasm. The management of cerebral vasospasm after AVM rupture is discussed.     

Arteriovenous malformation associated with moyamoya disease

The first case of a child with an arteriovenous malformation (AVM) associated with moyamoya disease is reported. The patient presented ischemic symptoms and underwent indirect bypass surgery on both sides when she was 5 years old. Four years later she suffered from headache, and a small AVM of the left frontal lobe associated with the moyamoya vessels was detected. Single photon emission computed tomography (SPECT) was performed at age 11 and demonstrated low local cerebral blood flow (CBF) in the left frontal lobe and right temporal lobe, although the revascularization after the bypass surgery seemed to be effective, as judged on pancerebral angiography. We feel that brain ischemia due to the moyamoya disease may have played a causative role in the development of the AVM.     

Relief of hemiballism from a basal ganglia arteriovenous malformation after radiosurgery

A patient with a 3-year history of progressive hemiballism presented with an unruptured arteriovenous malformation (AVM) in the contralateral caudate nucleus and putamen. PET demonstrated a matched reduction of cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) in the basal ganglia and adjacent frontal lobe. The patient underwent radiosurgery for the AVM. After a period of no clinical change for 6 months, the movement disorder resolved by month 7 post-treatment. The AVM was successfully obliterated 2 years after irradiation without any significant change in the regional CBF or CMRO2.     

Successful surgical removal of a large arteriovenous malformation in a patient with hemophilia: case report

OBJECTIVE AND IMPORTANCE: This is the first reported case of the successful surgical removal of a large arteriovenous malformation (AVM) in a patient with hemophilia A. CLINICAL PRESENTATION: A 19-year-old male patient was admitted to our department with intracranial hemorrhage. He had previously been diagnosed with hemophilia A and a cerebral AVM. Carotid angiography revealed a large AVM in the right temporal and parietal lobes. The neurological and neuroradiological findings, especially those of single photon emission computed tomography, identified an area of devitalization around the lesion, which was thought to reduce the risk of new deficits resulting from surgical manipulation. INTERVENTION: We resected the AVM in conjunction with supplemental infusions of Factor VIII before, during, and after the operation. A slight cerebral hemorrhage on the 7th postoperative day was observed despite control with Factor VIII, but the patient was discharged without any new deficits. CONCLUSION: We evaluated and managed all problems of a patient with multiple complications and achieved a medical cure.     

Spontaneous disappearance of arteriovenous malformation during staged treatment of multiple cerebral arteriovenous malformations--case report

A 36-year-old male presented with aphasia and right hemiparesis due to the rupture of the larger of two arteriovenous malformations (AVMs) coexisting in the left hemisphere. The two AVMs had completely separate locations and different feeding arteries and draining systems. Two months after resection of the larger AVM and evacuation of the hematoma, carotid angiography showed the residual AVM had spontaneously disappeared. He was discharged without deficits. Change of cerebral hemodynamics after removal of the larger AVM presumably caused the spontaneous regression of the smaller one. Cerebral angiograms should be carefully examined because cerebral hemodynamics may be altered after removal of an AVM.     

Motor evoked potentials in unilateral lingual paralysis after monohemispheric ischaemia

OBJECT: A retrospective analysis was conducted of 10 patients (three women and seven men) who were treated for spinal dural arteriovenous shunts (AVSs) located at the craniocervical junction. This analysis was performed to evaluate the characteristics of this unusual location in contrast with those of the more common thoracic and lumbar AVSs. METHODS: Seven patients presented with subarachnoid hemorrhage (SAH) and one with slowly progressive quadriparesis and dyspnea due to myelopathy. The other two cases were detected incidentally and included a transverse-sigmoid dural AVS and a cerebellar arteriovenous malformation. Angiographic studies revealed that the spinal dural AVSs at the C-1 and/or C-2 levels were fed by the dural branches of the radicular arteries that coursed from the vertebral artery and drained into the medullary veins. Venous drainage was caudally directed in the patient with myelopathy. In contrast, the shunt flow drained mainly into the intracranial venous system in patients with SAH. Furthermore, in four of these patients a varix was found on the draining vein. In all patients, the draining vein was interrupted surgically at the point at which this vessel entered the intradural space, using intraoperative digital subtraction angiography to monitor flow. The postoperative course was uneventful in all patients and no recurrence was confirmed on follow-up angiographic studies obtained in seven patients at 6 months after discharge. CONCLUSIONS: If computerized tomography scanning shows SAH predominantly in the posterior fossa and no abnormalities are found on intracranial four-vessel angiographic study, proximal vertebral angiography should be performed to detect dural AVS at the craniocervical junction. The results of surgical intervention for this disease are quite satisfactory.     

Assessment of intact Sarcocystis cystozoites as an ELISA antigen

Hereditary hemorrhagic telangiectasia (HHT), or Rendu-Osler-Weber disease, is an autosomal dominant disorder characterized by a triad of mucocutaneous and visceral telangiectasia, recurrent epistaxis and familial history. We reported a rare case of HHT associated with pulmonary and cerebral arteriovenous fistulae (AVF) and multiple cerebral arteriovenous malformations (AVM). The roles of multimodality therapies including artificial embolization, feeder clipping and stereotactic radiosurgery for these multiple cerebrovascular dysplasia in HHT were discussed. In particular the usefulness of radiosurgery to obliterate AVM was emphasized. It is especially useful for multiple AVM's associated with HHT. A 7-year-old boy had presented himself at another hospital 2 years previously with cyanosis of the lips and fingers on exertion. He was diagnosed as having pulmonary AVG and underwent surgery. His mother had suffered from epistaxis in her adolescence, and was then highly suspected as having HHT. She underwent surgical removal of a left fronto-parietal AVM at the age of 16 years. The family history then prompted the patient to have a brain CT done, which eventually demonstrated an abnormal enhancing mass at the left frontal region. He was transferred to our service for further evaluation. Left carotid angiograms demonstrated an AVF supplied by a dilated anterior internal frontal artery of the anterior cerebral artery (ACA), draining directly into the vein of the corpus callosum with a large aneurysmal dilatation, and then draining further into the straight sinus via the vein of Galen. In addition, right carotid angiograms revealed three small AVM's fed by the median artery of the corpus callosum, and the middle internal frontal and paracentral arteries of the right ACA, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic myelogenous leukemia received unrelated bone marrow transplantation following surgical resection of cerebral arteriovenous malformation--first case report

We report a 15-year-old boy with chronic myelogenous leukemia who received unrelated bone marrow transplantation (uBMT) after surgical resection of cerebral arteriovenous malformation (AVM). The incidence of cerebral hemorrhage caused by rupture of cerebral ABM in cases of BMT is uncertain. However, since the risk of rupture of AVM was supposed to increase due to both severe thrombocytopenia after intensive chemotherapy and increased intracranical pressure because of total body irradiation (TBI) as preconditioning therapy for BMT, we have first carried out surgical resection of the cerebral AVM, and subsequently performed uBMT. This resulted in a favorable clinical course without serious complications.     

Complete recovery from hemiplegia following excision of a giant basal ganglia arteriovenous malformation

A young female harbored a large arteriovenous malformation (AVM) in the basal ganglia associated with marked arteriovenous shunting. The complete recovery of her neurological deficit subsequent to excision of the AVM illustrates the reversibility of such severe cerebral impairment. Large lesions in the basal ganglia often have been deemed inoperable. However, modern advances in microsurgical techniques have provided the necessary illumination, magnification, and instrumentation that was needed for the exposure and gentle resection of the lesion in our patient.     

Expression of heat shock protein 27 in developing and adult human kidney

Clot removal at early surgery has been reported to be clinically effective for the prevention of cerebral vasospasm following subarachnoid hemorrhage (SAH) due to rupture of an intracranial aneurysm. We examined the most efficacious timing of mechanical clot removal on pharmacological responses in a monkey SAH model. Cynomolgus monkeys (Macaca fascicularis) were randomized into five groups: sham-operated, clot removal in which the clot was removed 48, 72, or 96 h after SAH, and clot groups. An autologous blood clot was placed around the bilateral major cerebral arteries after craniectomy to mimic the hemorrhage. Seven days after the SAH, proximal and successively distal parts of the middle cerebral arteries were cut into rings for isometric tension measurement. The contractile responses to potassium chloride, 5-hydroxytryptamine, norepinephrine, adenosine triphosphate, prostaglandin F20, and hemoglobin were greater in the proximal parts than in the distal parts in each group. Compared with the sham-operated group, the responses of the clot-removal and clot groups to the drugs were progressively attenuated. The maximum responses to 5-hydroxytryptamine in the proximal parts and to adenosine triphosphate in the distal parts started to decrease, significantly, in the clot-removal group 48 h after SAH, while most of the responses to the other agonists began to decrease in the clot-removal groups later than 72 h after SAH. These results suggest that the attenuation of cerebrovascular contractile responses 7 days after SAH is pharmacologically inevitable, even if the clot is removed as early as 48 h after the SAH. Clot removal may thus be recommended within 48h after SAH to ameliorate the severity of cerebral vasospasm following SAH.     

Referrals for obstetrical complications from Ejisu district, Ghana

Subarachnoid hemorrhage (SAH) resulting from the rupture of a cerebral aneurysm represents one major cause of stroke. SAH may be followed by a spontaneous severe contraction of major cerebral arteries, a condition referred to as cerebral vasospasm. Vasospasm may result in brain ischemia or actual tissue death. This constrictive vascular state is devastating, remains largely untreatable, and is a major cause of morbidity and mortality in SAH patients. Approximately 30,000 Americans are affected by this condition each year. The overall death rates are 25%, and significant neurological complications occur in 50% of individuals who survive the initial bleed. This report highlights some of the important aspects of this vascular disease.     

Theoretical modelling of arteriovenous malformation rupture risk: a feasibility and validation study

PURPOSE: To explore the feasibility of using a theoretical computational model to simulate the risk of spontaneous arteriovenous malformation (AVM) haemorrhage. METHODS: Data from 12 patients were collected from a prospective databank which documented the angioarchitecture and morphological characteristics of the AVM and the feeding mean arterial pressure (FMAP) measured during initial superselective angiography prior to any treatment. Using the data, a computational model of the cerebral circulation and the AVM was constructed for each patient (patient-specific model). Two model risk (Risk(model)) calculations (haemodynamic- and structural-weighted estimates) were performed by using the patient-specific models. In our previously developed method of haemodynamic-weighted estimate, Risk(model) was calculated with the simulated intranidal pressures related to its maximal and minimal values. In the method of structural-weighted estimate developed and described in this paper, the vessel mechanical properties and probability calculation were considered in more detail than in the haemodynamic-weighted estimate. Risk(model) was then compared to experimentally determined risk which was calculated using a statistical method for determining the relative risk of having initially presented with AVM haemorrhage, termed Risk(exp). RESULTS: The Risk(model) calculated by both haemodynamic- and structural-weighted estimates correlated with experimental risks with chi2 = 6.0 and 0.64, respectively. The risks of the structural-weighted estimate were more correlated to experimental risks. CONCLUSIONS: Using two different approaches to the calculation of AVM haemorrhage risk, we found a general agreement with independent statistical estimates of haemorrhagic risk based on patient data. Computational approaches are feasible; future work can focus on specific pathomechanistic questions. Detailed patient-specific computational models can also be developed as an adjunct to individual patient risk assessment for risk-stratification purposes.     

Intracranial hemorrhage due to rupture of an arteriovenous malformation in a full-term neonate

A case of neonatal intracerebral hemorrhage (ICH) secondary to rupture of an arteriovenous malformation (AVM) is reported. The baby began to vomit frequently 9 h after birth. Computed tomographic scan revealed the presence of an ICH. Intravenous digital subtraction angiography (IVDSA) demonstrated an AVM, which was successfully excised on the 2nd day after birth. It is stressed that IVDSA is safe and noninvasive in comparison with conventional angiography and is useful for diagnosis of cerebral vascular disease in neonates.