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PubMed2002

Effect of posterior temporal-parietal hematoma on orbital frontal chemistry in relation to a cognitive and anxiety state: a combined 1H-MRS and neuropsychological study of an unusual case as compared with 16 healthy subjects.

The authors report the unusual case of a 58-year-old woman (MJP) suffering from left temporal throbbing headache, associated with confusion. Magnetic resonance imaging showed a 5 x 3 x 2 cm hematoma at the left posterior temporal--parietal junction (PTPJ). Repeated MRI of MJP's brain performed during a 4-month follow-up period showed decrease in hematoma size (2.3 x 1.5 x 1) with evidence for development of encephalomalacia and resorption of blood products involving the area of hemorrhage. MJP had mild transcortical sensory aphasia characterized by difficulty with reading and processing, with semantic paraphasic errors while speaking and some difficulty with repetition. MJP had remained normotensive and seizure free, on Vasotec therapy and Dilantin prophylaxis. An in vivo proton magnetic resonance spectroscopy (1H-MRS) performed during an 8-month follow-up period showed reduced concentration for N-acetyl aspartate (NAA) by 19.3% (F=4.09, P<0.04), and myo-inositol by 32.0% (F=5.16, P<0.02) in the left orbital frontal cortex (OFC) as compared with 16 healthy subjects (age- and sex-matched). Cognitive tests (the Wechsler abbreviated scale of intelligence (WASI) and the Stroop color--word interference) showed a significant impairment suggesting involvement of higher-order cognitive functioning (memory, learning, and general intelligence) and attentional system. The Spielberger state-trait anxiety inventory (STAI) showed increased anxiety at the moment of the current examination and decreased tendency to be anxious over a long period of time. The Beck Anxiety and Depression Inventory revealed minimal anxiety and mild to moderate levels of depression. It is hypothesized that the PTPJ hematoma triggered long-distance pathways linking PTPJ area and frontal lobe, including OFC, which resulted in abnormal chemical changes in the left OFC and in cognitive tests impairment, and in long-term anxiety state changes.

Anxiety↗

PubMedDate not supplied

Usefulness of T1-weighted image with fast inversion recovery technique in intracranial lesions: comparison with T1-weighted spin echo image.

To evaluate the usefulness of T1-weighted images using the fast inversion recovery (T1FIR) technique as compared with routine T1-weighted spin echo (T1SE) images in various intracranial lesions. Routine spin echo and T1FIR images were performed in 15 consecutive patients with 18 lesions, cerebral infarction in five, astrocytoma in four, vascular lesion in three, encephalomalacia and hemorrhage in each two, arachnoid cyst and meningioma in each one. T1FIR images were performed with 1.5-T Signa [repetition time (TR)/echo time (TE)/inversion time (TI) was 2000/34/800 in 14, 4000/34/1200 in four lesions] and qualitatively compared with the T1SE images in signal intensity, lesion detectability, determination of lesion extent and conspicuity, contrast between lesion and background. Additionally, gray-to-white matter and cerebrospinal fluid (CSF)-to-white matter contrast were evaluated. The signal intensity of the lesions was similar on both T1FIR and T1SE images in all cases. The lesion detectability was similar on both sequences in 15 lesions, and the determination of the lesion extent was definitely higher in 16 lesions on the T1FIR images. Lesion conspicuity was superior in 11, similar in 5, and inferior in 2 patients on the T1FIR images. And also, contrast of lesion-to-background, gray-to-white matter, and CSF-to-white matter was superior on the T1FIR images. The T1FIR technique improved the determination of lesion extent and lesion conspicuity and was qualitatively superior for image contrast as compared with T1SE, but it takes more time than T1SE. The clinical application of T1FIR images depends on whether the superior aspect of the T1FIR images outweighs the disadvantage of the longer time required for this technique.

Brain↗

PubMed2003

[Growing skull fracture in childhood. Presentation of 12 cases].

Growing skull fractures (GSF) are rare complications of head injury (HI) in childhood. This entity consists of a skull fracture with an underlying dural tear that courses with a progressive enlargement of the fracture to produce a cranial defect. The pathophysiology and some aspects of its management are still controversial. In this review we present 12 patients diagnosedd and treated for a GSF at our institution between 1980 and 2002. 11 patients were under the age of 3 years and one patient was 5 years old at the moment of HI. The most common cause of injury was a fall from height. In the initial plain x-rayfilms, 11 patients showed a diastatic skull fracture and one patient only had a linear fracture. At this time, CT scan showed cortical contussion underlying the fracture in every case. The mean time between injury and presentation of GSF was 11.6 weeks. Diagnosis was made by palpation of the cranial defect and confirmed with skull x-rayfilms. The most frecuent location of GSF was in the parietal region. Associated lesions like hydrocephalus, encephalomalacia, lepto-menigeal cysts, brain tissue herniation and ipsilateral ventricular dilatation, were found in the preoperative CT or MRI. All patients underwent a dural repair with pericranium or fascia lata. The cranial defect was covered with local calvarial bone fragments in every case. Only one patient needed a cranioplasty with titanium mesh. Every child with a skull fracture must be followed until the fracture heals. Patients under the age of 3 years with a diastatic fracture and a dural tear, demostrated by TC or MRI, are more prone to develop GSF. In these cases, early repair must be adviced in order to prevent progressive brain damage.

Child, Preschool↗

PubMed1984

Intrauterine fetal demise in multiple gestation.

Fifteen cases were reviewed over a five-year period at a perinatal centre with intrauterine demise of one member of a multiple gestation. Nine cases were monozygotic twin pairs, two were dizygotic, and two were triples . Gestational age ranged from 27 to 39 weeks. The management protocol consisted of delivery in all cases after confirmation of the diagnosis. In 4 cases delivery was immediate because of spontaneous labor. In the other cases elective delivery was performed if the gestational age was 37 weeks or greater or there was evidence of preeclampsia or if amniocentesis revealed a mature lecithinsphingomyelin (L/S) ratio. Steroids were given if the L/S was immature or the attempt at amniocentesis was unsuccessful and delivery was performed 48 hours after initiation of steroid therapy. Cesarean section was the mode of delivery in 14 of the 15 cases. All of the cotwins and cotriplets survived. One survivor of a monozygous twin pair has multicystic encephalomalacia possibly implicating perinatal arterial occlusion or in utero disseminated intravascular coagulation (DIC). The intrauterine deaths are categorized into possibly avoidable deaths (2/15), unavoidable due to congenital anomalies (3/15), and unknown or unavoidable deaths (8/15).

Cesarean Section↗

PubMed2003

Polymicrogyria in monozygous twins and an elder sibling.

Monozygous twin births have been associated with brain lesions such as hydranencephaly, multicystic encephalomalacia, and porencephaly. Prenatal circulatory injury has been considered to be the cause. Polymicrogyria is rare but has been reported in autopsied cases. The sibship in this case report, comprising monozygotic male twins and their elder sister from the same non-consanguineous parents, all had global developmental delay. Brain MRI showed polymicrogyria. We suggest that, apart from circulatory compromise, genetic etiology must be implicated as the cause of polymicrogyria.

Brain↗

PubMed1994

Unusual evolution and computerized tomographic appearance of a gliosarcoma.

A patient with a remote infarct, seizures, mild hemiparesis, and dysphasia became obtunded over four months and died. Computerized tomography (CT) over 5 years showed a consistent, large, wedge-shaped left hemisphere hypodensity with a central calcification, but without signs of mass effect. This was interpreted as an infarct of the left middle cerebral artery territory. Post-mortem examination of the brain revealed the entire area appearing as infarct on CT was a gliosarcoma. We suspect that the unusual CT appearance of the lesion was likely caused by multiple pathologies: a low grade glioma transforming into a gliosarcoma that was able to spread throughout the area of infarct encephalomalacia without revealing a typical CT appearance of mass effect. The patient's brief period of deterioration probably coincided with transformation of the tumor into a gliosarcoma. The variable CT characteristics of gliosarcomas are reviewed.

Brain Neoplasms↗

PubMed2004

Inactivation of the cytotoxic activity of repin, a sesquiterpene lactone from Centaurea repens.

Prolonged ingestion of Yellow Starthistle (Centaurea solstitialis) and Russian Knapweed (Centaurea repens) by horses has been shown to result in a fatal neurodegenerative disorder called equine nigropallidal encephalomalacia (ENE). Bioassay-guided fractionation of extracts from Centaurea species using the PC12 cell line have led to the identification of one of several putative agents, which may contribute to ENE, namely, the sesquiterpene lactone (SQL) repin (1), previously linked to ENE due to its abundance in C. repens. To characterize the molecular basis of repin-induced neurotoxicity, the present study was designed to identify reactive functional groups that may contribute overall to its toxicity. The reaction of repin (1) with glutathione (GSH) led to the exclusive addition of GSH to the alpha-methylenebutyrolactone affording a GSH conjugate (3b) that lacked toxicity in the PC12 cell assay, while selective reduction of the alpha-methylenebutyrolactone double bond of 1 also resulted in an analogue (2) that was devoid of toxicity relative to the parent compound. Unlike repin, analogue 2 failed to decrease cellular dopamine levels in PC12 cells, further substantiating the requirement of the alpha-methylenebutyrolactone group. Results from this study are suggestive that GSH depletion by the SQL repin may be a primary event in the etiology of ENE, increasing the susceptibility to oxidative damage.

Animals↗

PubMed2001

Fatal neonatal echovirus 6 infection: autopsy case report and review of the literature.

A full-term, healthy male neonate was delivered by caesarian section to a 26-year-old primigravida woman who had a history of fever and upper respiratory tract infection. On the fourth day of life, the neonate developed a sepsis-like syndrome, acute respiratory and renal failure, and disseminated intravascular coagulopathy. He died 13 days after birth. Postmortem examination revealed jaundice, anasarca, massive hepatic necrosis, adrenal hemorrhagic necrosis, renal medullary hemorrhage, hemorrhagic noninflammatory pneumonia, and severe encephalomalacia. Echovirus type 6 was isolated from blood, liver, and lungs. Although uncommon, echovirus type 6 infection may produce a spectrum of pathologic findings similar to those seen with the more commonly virulent echovirus type 11.

Adrenal Glands↗

PubMed2000

Experimental Elaphostrongylus cervi infection in sheep and goats.

The pathogenesis and migratory life cycle of Elaphostrongylus cervi were studied in four sheep and six goats killed and examined 6 days to 5 months after inoculation with infective third-stage larvae (L3). Detailed histological studies demonstrated that the L3 followed a porto-hepatic, and probably also a secondary lymphatic, migratory route from the abomasum and small intestine to the lungs, with subsequent spread via the general circulation to the central nervous system (CNS) and other tissues. In addition, the results suggested that haematogenously spread L3, arrested in arterial vessels outside the spinal cord, migrated into the cord along the spinal nerves. During migration, the L3 caused focal inflammation and necrosis in the organs and along the spinal nerve roots, and infarcts occurred in the myocardium, kidneys and CNS. Nematode development took place in the CNS. During development, there was a gradual die-off of nematodes and patent infections were not observed. However, in one animal many mature nematodes were demonstrated in the CNS. In the nervous system, the nematodes caused encephalomyelitis, focal traumatic encephalomalacia, gliosis, meningitis, choroiditis, radiculitis and perineuritis. Two goats and one sheep displayed long-lasting paraparesis starting 6 weeks after inoculation. The signs apparently resulted from nematode-induced spinal nerve root lesions. From 19 weeks after inoculation the sheep also showed signs of severe brain disturbances due to traumatic and inflammatory lesions caused by adult E. cervi in the cerebral parenchyma. We conclude that E. cervi represents a potential cause of neurological disease in small ruminants grazing areas inhabited by red deer. This is the first report confirming the infectivity of E. cervi for domestic ruminants.

Animals↗

PubMed2002

Post-traumatic intradiploic leptomeningeal fistula and cyst.

A 59 year old female patient presented with ataxia and difficulty in walking. The neurological examination revealed right homonymous hemianopia and ataxia. Radiographic evaluation revealed a large occipital intradiploic cyst mainly in the left suboccipital area. There was also moderate hydrocephalus and encephalomalacia of the left occipital pole. Bone window studies also demonstrated a growing fracture extending from the upper pole of the cyst to the vertex. Both pathologies were attributed to child abuse the patient suffered when she was a child. At first surgery, decompression of the cerebellum was followed by duroplasty and acrylic cranioplasty to the posterior cranial fossa. A month later, a shunt had to be inserted for hydrocephalus. At 7 months postoperatively, the patient is well and free of any symptoms or recurrence.

Arachnoid Cysts↗

PubMedDate not supplied

[Intrauterine herpes simplex virus infection].

BACKGROUND: Early fetal herpes simplex virus (HSV) infection is rarely documented. Only the minority of affected fetuses survive this condition. PATIENT AND METHODS: At 19 weeks of gestation the first episode of a genital HSV-infection of a pregnant woman was treated with local interferon beta. At 34 weeks of gestation hydrocephalus with secondary microcephaly and microphthalmia of both eyes was detected by ultrasonography. In the amniotic fluid HSV type 2 (HSV-2) was isolated and HSV-2-DNA was detected by PCR. The serum of the mother proved positive for HSV-2 (glycoprotein G2)-specific IgG-antibodies. No other infectious causes were apparent on further testing. At 35 + 4 weeks gestation a small-for-gestational-age neonate (2130 g) with microcephaly (29 cm head circumference) was born by spontaneous vaginal delivery. Scarce ulcerative skin lesions and vesicles, hepatosplenomegaly and microphthalmia were diagnosed. Furthermore, encephalomalacia with parenchymal destruction, cataract of both eyes and aplasia of the maculae and papillae were found. HSV-2-PCR was tested positive in chorionic cells and an umbilical segment of the placenta as well as in swabs from both eyes, throat, and a herpetic skin lesion collected during the first 5 days of life. HSV-IgM-antibodies were found in the umbilical cord blood. Local and intravenous treatment with aciclovir was started. The infant exhibited signs of a severely malfunctioning central nervous system. At the age of 4 months the boy suffered from generalised cerebral seizures. He died at the age of 9 months as a consequence of respiratory insufficiency with consecutive circulation failure. RESULTS: The case of an intrauterine HSV-2-infection is presented. The time of onset of fetal infection was most probably at the time of the maternal disease (19 weeks of gestation). Inspite of the very early infection the fetus did not die in utero. CONCLUSIONS: Especially, if a primary genital HSV-2-infection of a pregnant woman is suspected, which can be proven by serological means only several weeks after infection, systemic therapy of the mother with aciclovir should be considered since materno-fetal transmission may occur due to the risk of maternal viraemia.

Abnormalities, Multiple↗

PubMedDate not supplied

[Neonatal ultrasonographic cerebral findings: association with risk factor for cerebral palsy].

BACKGROUND: Is it possible to identify patients with cerebral palsy (CP) with postnatal ultrasound scan? Which risk factors are associated with an increased risk of CP?. PATIENTS AND METHODS: The data of 37 children with CP, who were sonographically investigated during the first 24 hours of life were analyzed retrospectively. The data of 21 preterm infants with gestational age </= 32 wk were compared with the data of 59 without CP. RESULTS: A tetraparesis was found in 15/21 of preterm babies </= 32 wk, a hemiparesis in 4/8 of premature infants >/= 33 wk and in 5/8 of the mature babies. The mature babies had prenatal brain atrophy or hypoxic-ischaemic cerebral lesions. Cytomegaly and encephalitis were detected in two babies. Immature babies >/= 33 wk showed prenatal porencephaly or encephalomalacia after asphyxia. Premature babies </= 32 wk had cystic periventricular leucomalacia (n=12) or cerebral haemorrhage (n=3); 3 babies had meningitis. Only two prematures </= 32 wk with mild CP had inconspicuous ultrasound scans. Factors associated with cerebral palsy were: cystic periventricular leucomalacia (OR 24,89; 95 % CI: 5,85 - 105,87), cerebral atrophy (OR 4,84; 95 % CI: 1,61 - 14,51), fetal hypoxia (CTG) - (OR 4,78; 95 % CI: 1,31 - 17,45), abruptio placentae (OR 4,32; 95 % CI: 1,16 - 16,13), anemia after birth (OR 18,13; 95 % CI: 1,97 - 166,43), abnormal neurological behavior at term (OR 14,00; 95 % CI: 3,29 - 59,55). CONCLUSION: Cerebral ultrasound scan after birth is a useful method detect for cerebral lesions in patients with CP-risks.

Abruptio Placentae↗

PubMed2003

Intrauterine herpes simplex infection.

Neonatal herpes simplex virus (HSV) infection is usually acquired at birth. We present an infant with intrauterine HSV infection acquired after rupture of membranes. The infant was born prematurely to a woman with a first episode of genital herpetic infection in early pregnancy and rupture of membranes 11 days prior to delivery. The infant, at delivery had extensive brain damage, hemorrhage, and cystic encephalomalacia due to herpes infection. On 2nd day of life, Magnetic Resonance Imaging, suggested that the hemorrhage had occurred 7 to 14 days before the scan and the placental pathology was supportive of an ascending infection. The case of an ascending herpetic intrauterine infection after rupture of the membranes raises the question of prevention and suppressive antiviral therapy.

Abnormalities, Multiple↗

PubMedDate not supplied

[Differential diagnosis of periventricular pseudocysts in the neonatal period].

Periventricular pseudocysts are important sequelae of different noxious insults in the developing brain. Accurate diagnosis of those pathologic entities during early life has therefore become of direct concern to the clinician. When present at birth, they suggest an intrauterine pathology. It has only been with the advent of real-time cranial ultrasonography that subependymal cystic lesions can be detected antemortem. 25 infants were postnatal diagnosed in ultrasound as having periventricular cystic lesions. They belonged to different pathological entities: focal paraventricular pseudocysts (5 cases), periventricular leukomalasia (6 cases), polycystic encephalomalacia (1 case), subependymal pseudocyst (9 cases), connatal viral infection (3 cases), and chromosomal abnormality (1 case). Sequelae of noxious insults in fetal life appear clearly different to those after perinatal injury. Ultrasound findings should be interpreted in combination with obstetric history. Some obstetric complications during 2. trimester can cause paraventrikular cystic formation in fetus. Neurotrophic viral infection and chromosomal abnormalities have also been implicated to produce cystic lesions in this region. This work implies that a wide variety of intracranial pathology is found in newborns with periventricular cystic lesion. Those lesions are not a terminal event in infant, but may be a condition of major clinical importance for further neurologic development.

Cerebral Hemorrhage↗

PubMed1987

[Vitamin E requirement of chicks and young hens].

In 4 experiments young chickens of the species White Leghorn received semisynthetic rations with a vitamin E content less than 1 mg/kg basal ration. Sunflower oil heated with FeCl3 supplement was used as a factor increasing requirement. Feed intake, live weight gain and feed expenditure with semisynthetic rations without oil supplements did not depend on vitamin E supplements. After the feeding of rations without vitamin E animal losses were higher. The losses were normalized by 1 mg vitamin E supplement per kg feed. Rations containing sunflower oil without vitamin E supplementation resulted in encephalomalacia of the young chickens. Vitamin deficiency increased triiodine thyronine content in the blood plasma. Antibody formation after the application of human gamma globulin did not depend on the vitamin E supply studied. A vitamin E requirement of young chickens and young hens of the laying species of less than 1 mg/kg mixed feed is derived from the results.

Animal Feed↗

PubMed1980

Cause of death in the extreme aged--a pathologic survey of 5106 elderly persons 80 years old and over.

The most important disease and the most contributory cause of death were pathologically surveyed among 5106 subjects aged 80 years old and over. Bronchopneumonia, encephalomalacia, myocardial infarction, gastric cancer, generalized arteriosclerosis and myocardial hypertrophy were the most prevalent diseases in order of frequency. With advancing age, bronchopneumonia and cerebral and cardiac arterisclerotic diseases increased, while cancer decreased. This death pattern of the extreme aged has developed during the last 25 years in Japan, and is very similar to the present situation in some European countries.

Aged↗

PubMed2001

Critique of the requirement for vitamin E.

The Food and Nutrition Board of the Institute of Medicine recently published a comprehensive evaluation of antioxidants in human diets that includes dietary reference intakes for vitamin E. The new dietary reference intake is 15 mg (35 mol)/d for adults, which is 50% greater than the generous allowance in the 10th edition of Recommended Dietary Allowances published in 1989. Much of the data interpreted in these publications came from studies sponsored by the Committee of Nutritional Studies at Elgin State Hospital (Elgin, IL) of an earlier Food and Nutrition BOARD: The 50% increase in the recommended dietary allowances for vitamin E is not supported by any new data. It is possible that the publication of the Institute of Medicine did not take into consideration the effects of the oxidized lipids in the diets used to promote the development of vitamin E deficiency. If lipids, oxidized to remove tocopherols, had not been a part of the experimental diets, the minimum requirement for vitamin E would have been too small for possible evaluation. Studies on the different effects of saturated and oxidized lipids in the production of encephalomalacia in chicks and muscular dystrophy in rats are reviewed. The tolerable upper intake level of vitamin E supplementation is reported to be 1000 mg/d. It is possible that the universal consumption of aspirin may not have been taken into consideration when this level was determined. Vitamin E plus aspirin may increase the tendency to hemorrhage, which makes a lower upper intake level worth consideration.

Animals↗

PubMed1979

Micronema deletrix meningoencephalitis in an adult man.

This is apparently the second report of a case of human meningoencephalitis caused by the nematode Micronema deletrix. The patient had severe granulomatous meningoencephalitis with numerous foci of hemorrhage and encephalomalacia. Numerous adult female and larval M. deletrix were in the brain. The organisms probably inhabit decaying organic material, but occasionally parasitize the kidney, nose, or central nervous system of the horse. In its parasitic form the nematode replicates parthenogenetically.

Brain↗