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Biomedical subjects

M V Squier

Publications and source records attributed to M V Squier.

At least 37 records · Page 2Linked to original sources
PubMed1995

Model to identify potentially preventable cerebral palsy of intrapartum origin.

A six stage model was applied to a geographically defined population of 210 singleton children born at term who had a diagnosis of cerebral palsy at 5 years of age. Thirty five children were identified as those most likely to have cerebral palsy of intrapartum origin; in 26 of these there was evidence of suboptimal care. It is suggested that this simple model should be tested on populations of children with cerebral palsy and the underlying principles used when considering the likely cause of cerebral palsy in individual children.

Birth Injuries↗
PubMed1994

Increased apoptosis in the cingulate sulcus of newborn piglets following transient hypoxia-ischaemia is related to the degree of high energy phosphate depletion during the insult.

An increase in the number of cells undergoing apoptosis was observed in the cingulate sulcus of newborn piglets 48 h after a global hypoxic-ischaemic insult. Apoptotic death was identified morphologically (by light and electron microscopy) and by DNA fragmentation, detected by in situ end labelling. The number of apoptotic cells was directly related to the degree of high-energy phosphate depletion during hypoxia-ischaemia, measured using continuous 31P magnetic resonance spectroscopy. These results may have implications for the understanding and treatment of perinatal hypoxic-ischaemic brain injury.

Animals↗
PubMed1994

Clinical associations of prenatal ischaemic white matter injury.

Neuropathological examinations were carried out at necropsy on 274 cases of intrauterine death or neonatal death at or before three days after birth. Fifty six (20.4%) subjects had evidence of prenatal ischaemic brain damage. On review of the maternal case notes to ascertain antenatal clinical associations there was an increased incidence of intrauterine growth retardation, either based on birth weight for gestational age (odds ratio (OR) 2.0; 95% confidence interval (CI) 1.1 to 3.7) or diagnosed antenatally (OR 2.7; 95% CI 1.3 to 5.6). Oligohydramnios was also more common (OR 2.9; 95% CI 1.2 to 7.0). The association of intrauterine growth retardation and white matter damage remained after excluding fetuses with a major congenital anomaly (OR 2.4; 95% CI 1.1 to 5.1). The findings suggest that chronic intrauterine hypoxia may be associated with damage to cerebral white matter among fetuses and infants who die. The relation between ischaemic white matter damage and cerebral palsy among survivors remains speculative.

Brain↗
PubMed1994

Post-traumatic syringomyelia.

Post-traumatic syringomyelia was previously thought to be an infrequent but serious sequel to spinal cord injury. Clinical and CT studies have shown an incidence of between 1% and 5%, but more recently MRI has suggested an incidence of up to 22%. Twenty spinal cords have been examined after death from two days to 43 years after injury. Four had syrinxes, 20% of the series, approaching the incidence found by MRI. The acute and chronic pathological changes after trauma are described. Post-traumatic syringomyelia seems to develop from cores of necrotic tissue (myelomalacic cores) rather than lysis of haematoma. The mechanism of extension of syrinxes remains unexplained.

Adolescent↗
PubMed1993

Fetal type II lissencephaly: a case report.

Type II lissencephaly is a rare cortical malformation associated with a number of clinical syndromes, including Walker-Warburg syndrome and some forms of congenital muscular dystrophy. The neuropathology of a 20-week fetus is described showing the pathogenesis of the malformation, which appears to result from abnormal migration of neurons through the pial-glial barrier into the leptomeninges.

Brain Stem↗
PubMed1993

Development of the cortical dysplasia of type II lissencephaly.

A detailed neuropathological study of five immature brains with type II lissencephaly is reported. The cases described include two pairs of siblings. One infant survived for 2 months after birth, the others died at 18, 20, 20 and 32 weeks of gestation. This series of cases demonstrates the sequence in which the malformation develops from mid-gestation to post-natal life and shows that type II lissencephaly is not an intracortical malformation but is the result of massive glial and neuronal ectopia in the leptomeninges. This results from a failure of arrest of neuronal migration due to defects in the integrity of the pial/glial barrier.

Brain↗
PubMed1992

Case report: neuropathology of methyl bromide intoxication.

The neuropathological findings in a man and his dog both of whom died after acute exposure to methyl bromide are presented. The dog had cerebral oedema, most marked in the depths of cortical sulci. The man survived 30 days after the initial illness and his brain contained well-defined symmetrical lesions in the mammillary bodies and inferior colliculi. He also had a peripheral neuropathy and lymphocytic thyroiditis. The pathology in the central nervous system has features resembling Wernicke's encephalopathology; the mechanism by which methyl bromide may produce such lesions is discussed.

Adult↗
PubMed1992

Lethal olivopontoneocerebellar hypoplasia with dysmorphic features in sibs.

This report describes the clinical and neuropathological features in male and female sibs who died shortly after birth as a result of frequent convulsions and lack of spontaneous respiratory effect. Both sibs had a prominent occiput with mild contractures and the female also had overlapping fingers and rockerbottom feet. The genetic and neuropathological findings were consistent with a diagnosis of an autosomal recessive form of olivopontoneocerebellar hypoplasia/atrophy.

Abnormalities, Multiple↗
PubMed1988

Sensory perineuritis.

A case of sensory perineuritis is described, affecting individual cutaneous nerves in the extremities and with a chronic inflammatory exudate confined to the perineurium in a sural nerve biopsy. No cause was found. The condition slowly resolved on steroid treatment.

Axons↗
PubMed1987

An unusual metabolic myopathy: a malate-aspartate shuttle defect.

Studies on a 27-year-old man with a 3-year history of exercise-induced muscle pain, passage of red urine and elevated serum creatine kinase are described. Histological examination of a biopsy from quadriceps revealed non-specific myopathic changes with occasional clusters of subsarcolemmal mitochondria. The phosphorylase stain was normal. Phosphorous nuclear magnetic resonance (NMR) spectroscopy studies of gastrocnemius and flexor digitorum superficialis muscles showed no abnormalities at rest. During aerobic exercise there was an abnormally rapid decrease in phosphocreatine concentration but the pH remained within the normal range. There was a build-up of phosphomonoester (probably glucose 6-phosphate), usually indicative of a block in glycolysis. However, a primary defect in the glycolytic pathway seemed unlikely because muscle acidified normally during ischaemic exercise. Recovery from exercise was unusual in that phosphocreatine resynthesis and inorganic phosphate disappearance followed similar prolonged time courses (in control subjects the rate of inorganic phosphate disappearance was about twice as fast as the rate of phosphocreatine resynthesis). The transport of inorganic phosphate into the mitochondria appeared to be delayed. These slow recovery data suggested that oxidative metabolism was impaired. However, with all substrates tested, isolated muscle mitochondria had rates of oxygen uptake that were similar to control values, thereby ruling out a primary defect in mitochondrial respiration. A system involving several mitochondrial transport systems, the malate-aspartate shuttle, was measured. The activity in the patient's isolated mitochondria was less than 20% of the activity present in samples from control subjects. This patient is the only one so far reported with a defect involving the malate-aspartate shuttle system.

Adult↗
PubMed1982

A biochemical and immunohistological study of collagen synthesis in Ewing's tumour.

The synthesis and localization of collagen have been studied on material from a total of 16 primary Ewing's tumours. The predominant collagen extracted from the tissues and synthesized in short-term cultures was type I. The proportion of type III collagen was relatively small and variable (0-8%) in the direct tumour extracts, but a higher proportion (29-38% of the total collagens) was synthesized in culture. Immunofluorescence studies showed that positive staining for all types of collagen tested (types I, III, IV and V) was restricted to stroma; there was no evidence of collagen either within the tumour cells or in their pericellular matrix, a finding endorsed by negative staining for reticulin in the same areas. The absence of any evidence for type IV or V collagen synthesis by Ewing's cells argues against an endothelial origin for the tumour, and indicates that collagen analysis is unlikely to be of value in the diagnosis of this particular sarcoma.

Bone Neoplasms↗