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Results for “ENCEPHALOMALACIA”

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PubMed2004

Hypoxic-ischemic encephalopathy: correlation of serial MRI and outcome.

Twenty-four patients with hypoxic-ischemic encephalopathy were examined with serial magnetic resonance imaging up to 4 years of age. Magnetic resonance imaging studies were performed in the neonatal period, at the fourth month and the fourth year of age, and the findings were compared with the patients' neurodevelopmental outcome at the fourth year of age. Periventricular signal alterations and deep gray matter involvement were usually evident in the initial magnetic resonance imaging studies, and encephalomalacia, periventricular leukomalacia, and atrophy were the common findings on follow-up magnetic resonance imaging studies. In the patients with hypoxic-ischemic encephalopathy, some correlation between magnetic resonance imaging findings and neurodevelopmental outcome was recognized. The patients with deep gray matter involvement on the initial magnetic resonance imaging had a poor prognosis, and the ones with normal magnetic resonance imaging findings had a favorable neurodevelopmental outcome. On the follow-up magnetic resonance imaging findings, encephalomalacia and periventricular leukomalacia were associated with poor neurodevelopmental outcome. In predicting the neurologic outcome at 4 years of age, magnetic resonance imaging findings of the neonatal period had the highest negative predictive value, whereas magnetic resonance imaging findings at 4 months of age and 4 years of age had the highest positive predictive value.

Brain↗

PubMed1999

Posttraumatic smell loss: relationship of psychophysical tests and volumes of the olfactory bulbs and tracts and the temporal lobes.

RATIONALE AND OBJECTIVES: The purpose of this study was to define the primary sites of injury in patients with posttraumatic anosmia and hyposmia with magnetic resonance (MR) imaging and to determine if these sites correlated with the results of psychophysical olfactory tests. MATERIALS AND METHODS: Thirty-six patients with subjective loss in olfaction after head trauma underwent volumetric MR studies of the olfactory bulbs and tracts and temporal lobes. Pearson correlations were computed between olfactory bulb and tract and temporal lobe volumes and the patients' scores on tests of odor identification (including the University of Pennsylvania Smell Identification Test [UPSIT]), detection, and memory. Analysis of variance was used to compare volumes of the control subjects and the posttraumatic patients. RESULTS: The olfactory bulbs and tracts (32 [89%] of 36 patients), the subfrontal lobes (22 [61%] of 36 patients), and the temporal lobes (11 [31%] of 36 patients) showed the highest incidence of posttraumatic encephalomalacia. Left olfactory bulb and tract volumes showed a statistically significant correlation with left and total UPSIT scores. A statistically significant difference (P < .001) was found in the right and left olfactory bulb and tract volumes between anosmic and hyposmic patients and between posttraumatic patients and control subjects. CONCLUSION: Olfactory bulb and tract damage may correlate with deficits in odor identification. Olfactory bulb and tract and frontal lobe encephalomalacia coexist in many patients.

Adolescent↗

PubMed1999

Encephalopathy in suckling mice infected with Kasba (Chuzan) virus.

Kasba (Chuzan) virus (an orbivirus), strain K-47, produced encephalopathy with severe necrosis in suckling mice inoculated intracerebrally. On day 3 after inoculation with 10(3)TCID50, the mice showed severe focal encephalomalacia and meningitis. On day 4, necrosis had spread to the midbrain, cerebellum and spinal cord. From one day after inoculation, virus was recovered from the brain and the titre rose over the next 3 days. Immunohistochemical examination demonstrated viral antigens in the cytoplasm of both degenerate and intact neurons, and ependymal cells in or around necrotic lesions. The study indicated that the virus has an affinity for immature nerve cells in the brains of suckling mice and causes primary encephalomalacia. Since the lesions resembled those of the hydranencephaly-cerebellar hypoplasia syndrome in calves (Chuzan disease), the system described should prove useful in studies on pathogenesis.

Animals↗

PubMed1992

Risk factors for brain abscess in patients with congenital cyanotic heart disease.

Brain abscess is a serious complication of congenital cyanotic heart disease. We retrospectively evaluated the risk factors for brain abscess in 21 such patients treated between 1975 and 1990 in comparison with a control group. The mean arterial oxygen saturation, arterial partial pressure of O2, arterial blood oxygen content, and base excess in patients with brain abscess were significantly lower than in the control patients. The mean arterial partial pressure of CO2, pH, hematocrit, hemoglobin, and red blood cell content in patients with brain abscess were not significantly different. Patients with congenital cyanotic heart disease may develop minute encephalomalacia due to severe hypoxemia and increased blood viscosity resulting from compensatory polycythemia. The increased blood viscosity and reduced blood flow in the microcirculation may induce cerebral thrombosis or exaggerate minute encephalomalacia during dehydration or cardiac dysfunction, and shunted blood containing infectious organisms at such sites may be followed by focal cerebritis.

Brain Abscess↗

PubMed2005

Serial diffusion-weighted magnetic resonance imaging in cases of glioma: distinguishing tumor recurrence from postresection injury.

OBJECT: Diffusion-weighted magnetic resonance (MR) imaging is an invaluable tool in the diagnosis of acute stroke and other types of brain injury. Abnormalities in and around the resection cavity on diffusion-weighted imaging have been observed following surgery for infiltrating glioma. The purpose of this study was to investigate prospectively the incidence, time course, and ultimate outcome of these abnormalities. METHODS: Forty-four consecutive patients with newly diagnosed gliomas were prospectively observed using serial MR imaging including diffusion-weighted sequences. Clinical and surgical data were also collected. Immediately postoperatively neuroimaging identified 28 patients (64%) in whom areas of reduced diffusion appeared in or around the resection cavity (mean volume 8.2 +/- 1.5 cm3). Complete resolution of this reduced diffusion was demonstrated within 90 days in 24 patients (86%). On subsequent neuroimages these areas demonstrated Gd enhancement as early as postoperative Day 15 and as late as Day 198 and ultimately took on the appearance of encephalomalacia in 26 (93%) of 28 cases. Postoperative reduced diffusion was not predicted by the clinical or surgical parameters that were assessed. No clinical deficits were attributable to the reduced diffusion. CONCLUSIONS: An abnormality related to diffusion-weighted sequences on postoperative MR imaging can occur after resection of newly diagnosed gliomas. In this study the abnormality typically resolved and was replaced by contrast enhancement on follow-up imaging, ultimately demonstrating encephalomalacia on long-term follow up. Findings on neuroimaging during the period of enhancement could be confused with recurrent tumor and interpreted as early treatment failure. Based on the findings of this study the authors strongly suggest that the inclusion of diffusion-weighted sequences in postoperative MR imaging is essential, as is MR imaging immediately before radiation therapy to monitor disease progression. A new enhancement observed after glioma surgery should be interpreted in the context of the diffusion-weighted image obtained immediately postoperatively.

Adult↗

PubMedDate not supplied

Clinical spectrum of meningococcal infection in infants younger than six months of age.

BACKGROUND: Neisseria meningitidis is one of the most significant bacterial infections in children and adolescents. As transplacental antibodies in the circulation gradually decline, the prevalence of meningococcal disease among young infants is high, and often presents an invasive clinical manifestation. The purpose of the study was to investigate the clinical spectrum of meningococcal infection in young infants. METHODS: We retrospectively reviewed of the medical charts and analyzed the clinical characteristics and outcomes of 10 infants younger than 6 months old with meningococcal disease at the Chang Gung Children's Hospital from 1994 through 2004. RESULTS: A total of 10 male infants with a mean onset age of 2.9 +/- 1.79 months old were enrolled. All patients presented initial symptoms of fever and decreased activity. Seizure attack was noted in six cases, and only three patients had purpuric or petechial rash. Laboratory findings reflected pyogenic infection including elevated C-reactive protein (159.1 +/- 108.8 mg/L), pleocytosis (791.11 +/- 660.83/microL), high protein levels (190.43 +/- 157.91 g/dl) and hypoglycorrhachia (28 +/- 20.89 mg/dl) in the cerebrospinal fluid. Seven cases presented meningitis; among those, N. meningitidis was isolated from blood in two cases. Three of the remaining patients had meningococcemia. Penicillin was the most common drug of choice; cephalosporin was the alternative. Prolonged antimicrobial therapy (range, 14 to 42 days) was prescribed in six patients complicated with subdural empyema. No deaths were documented. During long-term follow up, two patients developed mental retardation, and one of those two also had epilepsy. Both of them had lower birth body weight, altered initial conscious level, leukocytopenia and subdural empyema with encephalomalacia on brain images. One had insufficient therapy and another one was infected by a penicillin resistant strain. CONCLUSIONS: Clinicians should be aware of meningococcal infection in young infants because the initial presentations may be difficult to distinguish from viral syndrome, and may rapidly progress to clinical deterioration. Patients with subdural empyema required prolonged courses of antimicrobial therapy. Brain images confirmed the presence of encephalomalacia which increased the risk of permanent neurologic deficit.

Follow-Up Studies↗

PubMed1990

Hydrops fetalis associated with red cell pyruvate kinase deficiency.

A hydrops fetalis and multicystic encephalomalacia were diagnosed in a neonate who was one of twins. The co-twin had died 5 weeks prior to delivery. The most likely explantation for both hydrops and multicystic encephalomalacia was fetal anemia caused by a red cell pyruvate kinase deficiency, and aggravated by an intrauterine disseminated intravascular coagulation.

Erythrocytes↗

PubMed1989

Central nervous system pathology in pediatric AIDS: an autopsy study.

The neuropathologic findings of brains and spinal cords removed at autopsy from 26 infants and children with AIDS is described; in two cases, only the spinal cords were available. The most common finding in the brains was dystrophic calcification of blood vessels of all calibers in the basal ganglia and deep cerebral white matter (21 og 24 cases). The next most frequent finding was subacute encephalitis (SE) (15 of 24 cases) with microglial nodules and multinulceated giant cells. Immunocytochemical and in situ hybridization studies showed HIV antigen or genetic sequences only in the brains of cases with SE. Multinucleated giants cells (MGC) were the most frequent cells with reaction products. MGC were labeled with ricinus lectin (RCA), but not with leukocyte common antigen (LCA) or glial fibrillary acidic protein. Many cells in microglial nodules were labeled with RCA, but not LCA; cells in the perivascular compartment were labeled with LCA, but not RCA. Corticospinal tract degeneration was noted in 15 of 20 spinal cords. In six cases tract degeneration was consistent with delayed myelination, and the remaining cases had axonal injury consistent with Wallerian degeneration. Opportunistic infections were rare (three cases). Central nervous system lymphoma occurred in three children and was the most common mass lesion. In two cases lymphoma occurred in the setting of a systemic polyclonal immunoproliferation possibly related to Epstein-Barr virus infection. Cerebrovascular accidents were noted in seven cases. Two cases had hemorrhage associated with immune thrombocytopenia; one hemorrhage was catastrophic. Two children had large vessel arteriopathy with multiple encephalomalacias. Two children had a necrotizing encephalopathy with encephalomalacia and vascular changes suggestive of a mitochondrial cytopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed1986

[Hypertonic central nervous system complications from the viewpoint of the pathologist].

Based on 2130 autopsies with a hypertension it is reported on the hypertensive CNS-lesions. The frequency of encephalomalacia was 12%. By 9.7% was founded brain haemorrhages. The relapse rate of haemorrhages was about 5%. The encephalomalacia existed by way of secondary finding in 24.7%, and the haemorrhage in 2.2%. The investigations showed an important arteriosclerosis by 39.8% in haemorrhages and by 51.6% in brain infarct. It was remarkable by the hypertensive brain haemorrhages a dominant right hemisphere.

Adolescent↗

PubMed1994

[Neurodegenerative disorders of the central nervous system in horses].

The most important neurodegenerative diseases of the horse are reviewed. In addition to the literature, neurodegenerative diseases occurring in patients (horses, Mongolian Przewalski-horses, and two zebras) referred to the Utrecht Veterinary Faculty are mentioned. Neurodegenerative diseases described are: I. ataxia associated with: A/ static stenosis, B/ dynamic stenosis, C/ lesions at various locations in the central nervous system, D/ equine herpesvirus infections, E/ equine degenerative myelo-encephalopathy, or F/ cerebellar abiotrophy; II. equine motor neuron disease; III. grass sickness or equine dysautonomia; IV. postanaesthetic myelomalacia; and V. equine leuko-encephalomalacia. The patient descriptions show, that mixed forms of some of the differentiated diseases can be diagnosed. Little is known with certainty about the aetiology of the neurodegenerative lesions found. In some patients vitamin E may play a role, possibly in combination with other factors. A mycotoxin known to interfere with myelin metabolism is involved in leuko-encephalomalacia.

Animals↗

PubMed1998

Etiology, timing of insult, and neuropathology of cerebral palsy evaluated with magnetic resonance imaging.

To define the patterns of pathologic changes in cerebral palsy (CP) and to assess the etiology and time of brain damage, we reviewed the magnetic resonance images and clinical records of 86 pediatric CP patients seen over 8 years. Patients were divided into two groups, based on the gestational age at birth. The majority of CP patients (69) had spasticity. In the premature group (< 37 wk gestational age) n = 27), spastic diplegia (12 patients) and quadriplegia (8) were the major subtypes. In the term group (> or = 37 wk gestational age) ( n = 59), spastic hemiplegia (23) and quadriplegia (12) were most common. The other main clinical manifestations in the two groups were seizures (36) and mental retardation (15). Magnetic resonance (MR) imaging provided significant findings in 82 patients (95%). In the 27 patients born prematurely, MR imaging revealed periventricular leukomalacia (17), multicystic encephalomalacia (3), cortical and subcortical atrophy (4), migration disorders (2), and basal ganglia injury (1). Among the patients born at term, the MR imaging findings were more heterogeneous; they included cortical and subcortical atrophy (17), brain malformations (17), periventricular leukomalacia (6), multicystic encephalomalacia (5), porencephaly (4), hemiatrophy (3), delayed myelination (3), and none (4). MR imaging alone could define the time of brain insults in 73 of our 86 CP patients. Combined with clinical histories, MR imaging could help assess the time of insult in 93% of patients. The brain insults occurred prenatally in 34 of our patients, perinatally in 37, and postnatally in eight. The time of insult could not be determined in six patients. In the premature patients, the insult occurred most frequently perinatally (74%), whereas in the term group it occurred most frequently prenatally (54%). MR imaging was found to be very helpful in the evaluation of the various neuropathologic changes in CP, in the depiction of the etiology, and in the determination of the time of brain injury.

Adolescent↗

PubMed2000

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.

Adult↗

PubMed1996

The sequential in utero death of heterokaryotic monozygotic twins. A case report and literature review.

A case of monozygotic twins in a 19-year-old primigravida is presented. Ultrasound examination at 15 weeks' gestation showed one twin to have a cystic hygroma and hydrops fetalis. The other twin appeared normal. The twins appeared to occupy the same amniotic cavity. Fluid was taken from the cystic hygroma under ultrasound guidance for karyotyping and this showed 45,XO chromosomes. Conservative management was adopted. Serial ultrasound examination showed deteriorating hydrops and at 26 weeks the first twin died. Intensive monitoring of the remaining twin was undertaken with weekly ultrasound, cardiotocography (CTG), and clotting screens. At 29 weeks' gestation the CTG and clotting were normal, but ultrasound revealed that multicystic encephalomalacia had developed in the second twin. A very thin dividing membrane was seen for the first time between the twins. The parents decided to terminate the pregnancy. Prior to an intracardiac potassium chloride injection, a fetal blood sample was taken which revealed 46,XX chromosomes and a normal clotting screen including natural anticoagulant levels. Labour was then induced. Delivery took place 5 h later and the woman made an uneventful recovery. The mechanism for genetic differences between monozygotic twins is discussed and the literature reviewed. A non-disjunction event around the time of splitting of the twins is proposed as the cause. The prognosis for the remaining twin is also discussed, as is the pathogenesis of the cerebral damage.

Adult↗

PubMed1992

Posttraumatic segmental axial dystonia.

Isolated dystonia of trunk and neck muscles without involvement elsewhere has been termed segmental axial dystonia--a rare disorder. We report a 31-year-old man who developed marked dystonia of paraspinal muscles and progressive scoliosis 6 months after a closed head injury. Computed tomography (CT) disclosed three small areas of encephalomalacia, one involving the head of the caudate nucleus. Treatment with trihexyphenidyl resulted in significant improvement of the dystonia and scoliosis.

Accidental Falls↗

PubMed1998

Repin-induced neurotoxicity in rodents.

Russian knapweed is a perennial weed found in many parts of the world, including southern California. Chronic ingestion of this plant by horses has been reported to cause equine nigropallidal encephalomalacia (ENE), which is associated with a movement disorder simulating Parkinson's disease (PD). Repin, a principal ingredient purified from Russian knapweed, is a sesquiterpene lactone containing an alpha-methylenebutyrolactone moiety and epoxides and is a highly reactive electrophile that can readily undergo conjugation with various biological nucleophiles, such as proteins, DNA, and glutathione (GSH). We show in this study that repin is highly toxic to C57BL/6J mice and Sprague-Dawley rats and acutely induces uncoordinated locomotion associated with postural tremors, hypothermia, and inability to respond to sonic and tactile stimuli. We also show that repin intoxication reduces striatal and hippocampal GSH and increases total striatal dopamine (DA) levels in mice. Striatal microdialysis in rats, however, has demonstrated a significant reduction of extracellular DA levels. These findings, coupled with the absence of any demonstrable change in striatal DOPAC levels, suggest that repin acts by inhibiting DA release, a hypothesis that is further supported by our demonstration that, in cultured PC12 cells, repin inhibits the release of DA without affecting its uptake. We believe, therefore, that inhibition of DA release represents one of the earliest pathogenetic events in ENE, leading eventually to striatal extracellular DA denervation, oxidative stress, and degeneration of nigrostriatal pathways. Since the neurotoxic effects of repin appear to be mediated via oxidative stress, and since repin is a natural product isolated from a plant in our environment that can cause a movement disorder associated with degeneration of nigrostriatal pathways, clarification of the mechanism of repin neurotoxicity may provide new insights into our understanding of the pathogenesis of PD.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1983

Destructive lesions of the brain.

The congenital destructive lesions of the brain include focal lesions (porencephaly) and diffuse lesions (micrencephaly, hydranencephaly). According to the time the injury occurred and following the assumption of Yakovlev and Wadworth (1946), they are classified as agenetic porencephalies, either - bilateral (schizencephaly) or unilateral, when the injury occurs early enough in gestation (before 6 months) to disturb the growth of the cerebral mantle: abnormal sulcal pattern and heterotopic gray matter are then observed. They are classified as encephaloclastic when the destruction affects an otherwise normal cerebrum (last trimester). The porencephalies should be differenciated from post natal lesions (multicystic encephalomalacia, focal cavitations). By showing the fluid cavity and the cortical distortion, neuroradiology permits precise diagnosis of the defect itself and the associated cortical disorder, as well as an evaluation when they occurred.

Abnormalities, Multiple↗

PubMed1996

MRI of encephalitis in children: comparison of CT and MRI in the acute stage with long-term follow-up.

We examined 14 children aged 28 days to 12.7 years with encephalitis by CT or MRI. Of the patients examined by CT 58% had a normal first scan, whereas all MRI investigations demonstrated abnormalities. The clinical features correlated with several MRI investigations. On MRI herpes (HSV) encephalitis started in the medial temporal lobe and encephalomalacia developed within a few weeks. All patients had a follow-up examination 0.5 to 6.5 years after the acute phase. MRI revealed abnormalities in 13 of the 14 children; one boy, with lesions in only the white matter, had a normal follow-up MRI. Even with immediate, optimal therapy the children demonstrated severe parenchymal abnormalities. Signal abnormalities seen in the acute phase of the disease were likely to persist. In children with HSV encephalitis atypical lesions in different areas were seen.

Acute Disease↗

PubMed1996

CT and MRI characteristics of intracranial hemorrhage complicating breech and vacuum delivery.

The CT/MRI brain findings and sequelae of intracranial hemorrhage resulting from traumatic breech and vacuum delivery of 16 term newborn infants are presented. Eleven infants were vacuum extracted, while the remaining five infants were delivered breech. Except for three breech-delivered infants who had intraventricular hemorrhage, the location and nature of hemorrhage were similar in both groups. Nine of the 11 vacuum-extracted babies showed complete resolution of hemorrhage on follow-up examination. None of the breech cases had a normal outcome. All five of the latter group had hydrocephalus, and one case each demonstrated porencephaly and encephalomalacia.

Birth Injuries↗