Cases reported "Encephalomalacia"

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1/47. Cranio-cerebral erosion: delayed diagnosis and treatment.

    Cranio-cerebral erosion is a well-known complication of calvarian fracture with underlying dural tear and cerebral injury in infancy and early childhood. The anatomy, pathogenesis and natural evolution of these lesions remain obscure. The common clinical symptoms are seizures, focal neurological deficits, impairment of consciousness and a soft subgaleal mass. Three patients of cranio-cerebral erosion who underwent delayed surgery in their adult lives are presented to illustrate the common and uncommon features, and their long-term outcome is discussed.
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ranking = 1
keywords = injury
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2/47. cerebrospinal fluid oligoclonal IgG bands in patients with spinal arteriovenous malformation and structural central nervous system lesions.

    OBJECTIVE: To investigate the incidence and characteristics of patients with structural central nervous system (CNS) lesions and cerebrospinal fluid oligoclonal IgG bands. DESIGN: A retrospective study. METHOD: The medical records of patients with cerebrospinal fluid oligoclonal IgG bands were evaluated for the presence of structural CNS lesions, their location and cause, and for clinical characteristics. SETTING: cerebrospinal fluid oligoclonal IgG bands were examined in the Neuroimmunology Laboratory, Hadassah University Hospital, Jerusalem, israel. patients: Two hundred seventy of 570 patients with positive cerebrospinal fluid oligoclonal IgG bands were available for analysis. Twenty patients had structural CNS lesions. RESULTS: Twenty (7.5%) of the 270 patients had structural CNS lesions: 3 patients had spinal arteriovenous malformation; 5 patients had tumors; 9 patients had compressive cervical myelopathy. Traumatic leukomalacia, arnold-chiari malformation type 1, and CNS hemosiderosis were present in 1 patient each. In 2 patients (1 patient with recurrent meningioma and 1 patient with posttraumatic encephalomalacia) the presence of a structural CNS lesion was followed by the development of multiple sclerosis. In all 3 patients with spinal arteriovenous malformation, oligoclonal IgG identification prolonged the time to diagnosis and therapy, which varied from a few weeks to 3 years. CONCLUSIONS: Structural CNS lesions, responsible for the neurological disorder, were present in 20 patients (7.5%) with cerebrospinal fluid oligoclonal IgG bands. The mechanism underlying oligoclonal IgG presence in spinal arteriovenous malformation and the coexistence of multiple sclerosis and structural CNS lesions is unknown, but may be related to recurrent tissue damage with repeated presentation of CNS antigens to the immune system.
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ranking = 0.03339988570627
keywords = trauma
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3/47. Acquisition and transfer of new verbal information in amnesia: retrieval and neuroanatomical constraints.

    Four experiments examined new associative learning in amnesia by contrasting the performance of 2 amnesic participants-1 (C.C.) with basal forebrain damage and the other (R.H.) with medial temporal lobe damage--and 3 controls. Both amnesic individuals were severely impaired on explicit memory measures but showed intact perceptual priming. On the new associations measures, only C.C., not R.H., exhibited learning by producing correct targets (HIJACKER) in the absence of perceptual cues for them (e.g., STAFF shot ???). When the perceptual cue (e.g., medicine cured _I_C_P) was provided, both C.C. and R.H. showed learning. Transfer to information containing conceptually related targets (e.g., TERRORIST or BELCH) was reliably observed only in C.C. This finding was replicated with further reduction in perceptual overlap across original (lightning torched JUNGLE) and transfer (lightning burned wilderness) sentences. Together, these findings delineate the role of experimental conditions, severity of amnesia, and different neuroanatomical structures in mediating new verbal learning in amnesia.
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ranking = 18.466044915604
keywords = brain
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4/47. arthrogryposis and multicystic encephalopathy after acute fetal distress in the end stage of gestation.

    The natural history of the rare association "multicystic encephalopathy-arthrogryposis" was traced in a fetus carefully followed after artificial insemination. The fetus exhibited normal viability and brain morphology up to the 32nd week. At 36 weeks, active movements diminished and at 37 weeks, hydramnios and signs of fetal distress led to cesarean section. The infant presented with severe arthrogryposis of the limbs and spine, but not with the other elements of a long-lasting akinesia. US showed multicystic encephalopathy. Both the clinical and the neuropathological findings established that multicystic encephalopathy was neither the cause nor the sequential consequence of the fetal akinesia, but the result of a recent diffuse, acute malacic process that also involved the anterior horn cells. Acute fetal distress, responsible for major ischemic damage to CNS but compatible with fetal survival, remains an obscure condition which allows for the development of severe arthrogryposis in a few weeks.
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ranking = 18.466044915604
keywords = brain
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5/47. Obstructive hydrocephalus caused by intraventricular collapse of malacotic brain. Case report.

    The authors present the case of a 68-year-old man who experienced acute obstructive hydrocephalus after having suffered an infarction in the occipital lobe. Histopathological and serial neuroimaging examinations revealed that portions of a large disintegrating occipital infarct had entered the lateral ventricle and obstructed the passage of cerebrospinal fluid (CSF). Ventricular drainage was performed for 2 weeks until the patient's hydrocephalus resolved. The CSF initially contained a high concentration of protein (1070 mg/dl), a high leukocyte count of 115 cells/mm3, and a rich fibrinous exudate. Findings in the present case indicate that collapse of a periventricular ischemic lesion into the ventricles may sometimes occur not only after cerebral hemorrhage but also after cerebral infarction.
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ranking = 73.864179662414
keywords = brain
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6/47. Multiple cystic and focal encephalomalacia in infancy and childhood with brain stem damage.

    Two cases are described in which damage to the brain stem was associated with extensive necrosis of the cerebral hemisphere. In the first case--a monochorionic twin--there was clear evidence that injury of an ischaemic or hypoxic type had occurred during fetal life and some evidence that an inadequate share of the placental circulation was an important aetiological factor. In the second case death occurred 4 yr after an asphyxial episode at birth. The lesions in the hemispheres and brain stem were extensive, although less than in the first example. The lesions are discussed in the context of our knowledge of the anatomy and physiology of the developing nervous system. Although they cannot as yet be fitted into the concepts of "critical periods" and "vulnerable periods" of development, this is perhaps because observations on human cases are scanty in comparison with the extensive animal studies which have been reported. The lesions are contrasted and compared with those seen in animals.
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ranking = 111.79626949362
keywords = brain, injury
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7/47. A case of pulmonary hypoplasia associated with intrauterine brainstem necrosis.

    An infant with intrauterine brain death accompanied by pulmonary hypoplasia is reported. The fetus was delivered after 36 weeks gestation, 5 weeks after fetal movements ceased. The child died 4 h after birth. Pulmonary hypoplasia and remote brainstem necrosis associated with multicystic encephalomalacia were found at autopsy. CONCLUSION: These findings suggest that damage to brainstem respiratory centres had led to pulmonary hypoplasia through the absence of fetal respiratory movement.
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ranking = 129.26231440922
keywords = brain
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8/47. Web-like malformation of the carotid artery and multicystic encephalomalacia.

    Multicystic encephalomalacia and hydranencephaly lie within a spectrum of brain lesions linked to ischemic cerebral damage. Causes include vascular malformation, thrombosis, embolism, infection, and toxins. We describe an infant with multicystic encephalomalacia associated with a peculiar web-like malformation of the right common carotid and left subclavian arteries. We postulate that this luminal bridging is a congenital malformation resulting from defective canalization of the medium-sized blood vessels but could represent organized and recanalized thrombi, the etiology of which remains unknown.
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ranking = 18.466044915604
keywords = brain
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9/47. Cystic encephalomalacia and intrauterine herpes simplex virus infection.

    Cystic encephalomalacia occurred in two preterm infants who had proven intrauterine herpes simplex virus type 2 infection. Calcification was evident in the basal ganglia. Follow-up scans indicated that the cysts had resolved over a period of two months in one infant, while in the case of the other, the cysts became progressively larger with significant ventricular dilatation developing. While cystic changes in the brain of preterm infants are usually due to periventricular leukomalacia, intrauterine infection needs to be considered as a possible cause. Antiviral treatment may be of benefit to infants with herpes simplex virus infection.
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ranking = 18.466044915604
keywords = brain
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10/47. Isolated sulphite oxidase deficiency: clinical and biochemical features in an Italian patient.

    A patient with isolated sulphite oxidase deficiency presented with seizures at 12 h of life and followed a severe course, dying at 10 months of age. There was mild facial dysmorphism and the brain showed multiple cystic fibrosis.
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ranking = 18.466044915604
keywords = brain
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