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Continuous cerebral electrical impedance monitoring in sick preterm infants.

Cerebral electrical impedance (dZ) and intra-arterial blood pressure were measured continuously during the first 48 h after birth in 26 sick ventilated preterm infants with a birth weight less than 1500 g. The aim was to establish whether any patterns of dZp or the variability of either blood pressure or dZp would allow identification of those infants who developed intraventricular haemorrhage (IVH), periventricular leucomalacia (PVL) or a poor neurological outcome. IVH and PVL were diagnosed by ultrasound image obtained every 6 h. Cerebral electrical impedance recordings were unsuitable for analysis in three patients and a further three died within 14 h of birth. In the remaining 20 patients, no step changes that may have been related to the onset of IVH or PVL were evident and whilst three patterns of dZp were identified, they were not useful in distinguishing between normal infants or those who developed IVH, PVL or had a poor neurological outcome. Using multiple linear regression, the coefficient of variation of dZp was significantly associated with both IVH and outcome, as was the coefficient of variation of blood pressure. Continuous measurement of cerebral electrical impedance, whilst technically feasible in sick preterm infants, was not found useful as a method of identifying those who developed IVH, PVL or had a poor neurological outcome.

Blood Pressure Determination↗

Reliability of sonography in non-hemorrhagic periventricular leucomalacia.

Sonographic pictures of the brain of 19 newborn infants who died at a mean age of 4.2 days after birth (range 1-23 days) were examined independently by five experienced sonographers. In all infants information on postmortem brain pathology was available. Diagnoses made by the sonographers based on the sonographic pictures were compared with the gross postmortem findings. The results of the study show that except for one infant with a subarachnoid hemorrhage all cerebral hemorrhages were diagnosed accurately by all sonographers. Non-hemorrhagic periventricular leucomalacia (PVL), however, was missed on sonography in 2 of the 3 cases. Surprisingly, PVL was diagnosed on sonography in 1 (8%) to 6 (50%) of 12 infants in which postmortem examination of the brain revealed no PVL. It is concluded that non-hemorrhagic PVL cannot be diagnosed accurately using sonography in the first days of life, if a 5 MHz transducer is used.

Diagnostic Errors↗

Early echographic findings in non-hemorrhagic periventricular leukomalacia of the premature infant.

The ultrasonic detection of periventricular leukomalacia is described in two neonatal patients. Confirmation of this condition by CT and post mortem was obtained in one case. CT scan and further echography was positive in the other. Neither patient had evidence of an intracranial hemorrhage. It is suggested that echography is of value in the early diagnosis of this lesion which may be similar to intraparenchymal hemorrhage in its mechanism and prognosis.

Brain Diseases↗

Lipid oxidation products and chick nutritional encephalopathy.

Safflower oil and its distilled methyl esters were thermally oxidized and fed to young chicks in a vitamin E deficient diet. At a dietary level of 10%, the oxidized lipids caused more severe nutritional encephalopathy (NE) than the unoxidized methyl esters, indicating that factors other than dietary linoleic acid and vitamin E affect the development of NE. A polar lipid extract from oxidized methyl esters accelerated the induction of NE, as did the synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids. Dicumarol exerted a protective action against NE. The possibility is discussed that conjugated keto-polyenoic fatty acids, provided by oxidized oils or formed endogenously in vitamin E deficiency, may play a role in causing NE.

Aging↗

The same chemicals induce different neurotoxicity when administered in high doses for short term or low doses for long term to rats and dogs.

Dose- and term-dependent differences in the location and nature of brain lesions induced in rats and dogs by 2,5-hexanedione (2,5-HD), misonidazole, clioquinol, and acrylamide are reported. Subchronic neuropathies ("distal axonopathy") were induced by low-dose administration of these neurotoxicants and at high doses, lesions caused by acute or subacute neurotoxicity were found in the central nervous system (CNS). In rats, 2,5-HD induced extracellular edema, nerve cell degeneration, and axonal degeneration in the cerebellar and vestibular nuclei. Similar lesions were observed in misonidazole-treated dogs and clioquinol induced nerve cell degeneration in the hippocampus and malacia in the piriform lobes of these animals. In rats, acrylamide induced degeneration of Purkinje cells. Although the mechanism(s) underlying the differential neurotoxicity of high and low doses of these neurotoxicants remains unclear, we suggest certain biochemical mechanisms, cytotoxic edema and excitotoxicity, as factors in the production of such lesions after high-dose treatment.

Acrylamide↗

Diffusion-weighted MR imaging of Carmofur-induced leukoencephalopathy.

Carmofur (1-hexylcarbamyl-5-fluorouracil), a derivative of 5-fluorouracil (5-FU), has been widely used in Japan as a postoperative adjuvant chemotherapy agent for colorectal and breast cancer. Periventricular hyperintensity on T2-weighted MR images in carmofur-induced leukoencephalopathy confront the physician with a broad range of differential diagnoses. We describe two cases of carmofur-induced leukoencephalopathy in which diffusion-weighted MR imaging revealed periventricular hyperintensity. We compared their findings with those of age-related periventricular hyperintensity in five patients and found discrepancies in signal intensity of periventricular areas. Our results suggest that diffusion-weighted MR imaging may be useful to differentiate carmofur-induced leukoencephalopathy from age-related periventricular hyperintensity.

Adult↗

Growing skull fracture: a posttraumatic neosuture.

CONTEXT: A case of a growing skull fracture presenting in adulthood is reported. Pertinent literature was reviewed with an emphasis on pathogenesis. EVIDENCE ACQUISITION: A search through MEDLINE from 1994 through 2004 was used and supplemented by searches of secondary sources retrieved from referenced articles. EVIDENCE SYNTHESIS: Current hypotheses for the pathogenesis of growing skull fractures were critically analyzed. A new hypothesis based in more recent data is proposed in an attempt to better understand this process. CONCLUSIONS: The proposed hypothesis seems to explain better the timing in which the clinical features in growing skull fracture develop.

Adult↗

Neurocognitive assessment before and after cranioplasty.

OBJECTIVE: This paper addresses the possible value of neurocognitive tests on the evaluation of patients before and after cranioplasty for large cranial defects. METHODS: In a single patient with a large corrected cranial defect a detailed neurocognitive analysis was performed utilizing the EXIT interview and Cognistat before and after surgery. Planning and development of the surgical prosthesis were based on the pre-operative reconstruction of the head CT and on pre-operative pictures of the patient. Xenon-CT anatomical and quantitative cerebral blood flow (CBF) analysis was performed before and periodically after cranioplasty. FINDINGS: A significant improvement in major cognitive functions was observed after surgery. INTERPRETATION: Cognistat is a detailed neuropsychological battery that permits a better assessment of patients in diverse neurological conditions. The EXIT interview gives a better rapid assessment of cognition not provided by other methods, such as the mini-mental status examination (MMSE). The utilization of these techniques permits a better understanding of long-term outcomes for patients with diverse neurological conditions, including post-cranioplasty patients.

Adult↗

The natural history of late diagnosed or untreated growing skull fractures: report on two cases.

Growing skull fractures (GSF) are rare complications of head trauma. Cases after childhood are extremely rare and demonstrate complicated pathological conditions which necessitate extensive treatment. We report on two rare cases of intracranial cysts related to growing skull fractures which are secondary to trauma sustained during childhood, and have been discovered in adolescence.

Adolescent↗

The association of fetal and newborn metabolic acidosis with severe periventricular leukomalacia in the preterm newborn.

One hundred twenty preterm newborns less than 34 weeks' gestational age have been studied prospectively to determine the frequency of fetal and newborn metabolic acidosis and to examine the relationship of metabolic acidosis to periventricular leukomalacia as demonstrated by serial newborn ultrasonographic examinations. Fetal metabolic acidosis, based on an umbilical artery buffer base less than 34 mmol/L at delivery, occurred in three cases (2%), one of which had evidence of periventricular leukomalacia. Newborn metabolic acidosis that is based on a buffer base less than 34 mmol/L during the 4 days after delivery occurred in 12 cases (10%), five of which had evidence of periventricular leukomalacia. There is a significant relationship between the degree and duration of newborn metabolic acidosis and the occurrence of periventricular leukomalacia. This study indicates that systemic metabolic acidosis is an important pathophysiologic marker of periventricular leukomalacia. Intrapartum fetal asphyxia with metabolic acidosis, although an infrequent occurrence in the preterm newborn, may account for a few cases of periventricular leukomalacia, while the more common newborn metabolic acidosis, when of sufficient degree and duration, carries a high risk of periventricular leukomalacia.

Acidosis↗