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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six children with neonatal cerebral infarction of the middle cerebral artery are reported. Seizures or respiratory distress were the initial symptoms. In some cases abnormal findings appeared earlier on EEG than on ultrasound. The EEG changes were concordant with the localization of the lesion. Ultrasound examinations revealed an echodense structure within the vascular territory, after a phase of appearing to be normal, highly suggestive of cerebral infarction. The diagnosis was confirmed by CT scan. Findings on EEG, cranial ultrasound and CT suggested that the stroke represented a late intra-uterine event. At long-term follow-up, six children had failed to develop normally for age and had become obviously hemiplegic as gross motor development proceeded. Four of the patients had developed epilepsy. These data indicate that the outcome of neonatal stroke may not be as positive as previously reported.
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PMID:Neonatal stroke involving the middle cerebral artery in term infants: clinical presentation, EEG and imaging studies, and outcome. 789 Jan 25

This hypothesis notes the similarities in the respiratory distress syndrome (RDS) of premature neonates, sudden infant death syndrome (SIDS) of postneonates, and the seizure-shock syndrome of acute magnesium (Mg) deficiency in stressed weanling animals, and suggests a common pathogenic link between the three. In each of these syndromes the lung is the major target organ, with haemorrhage, oedema, and microvascular congestion. It is suggested that platelet aggregation, leading to the transient release of mediators of shock, causes an acute, self-limited arachidonic acid cascade. The result of the shock is early death or spontaneous recovery with a propensity for recurrence; premature neonates who have had RDS are at particularly high risk for SIDS. Cases linking RDS and SIDS are cited.
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PMID:Hypothesis: possible links between the respiratory distress syndrome of the premature neonate, the sudden infant death syndrome, and magnesium deficiency shock. 836 97

The clinical and laboratory features of severe falciparum malaria in 180 Gambian children were studied between 1985 and 1989. Of the 180 children, 118 (66%) presented with seizures, 77 (43%) had cerebral malaria, 35 (20%) had witnessed seizures after admission, 29 (16%) were hypoglycemic, and 27 (15%) died. Respiratory distress was a common harbinger of a fatal outcome. The differences in admission parasite counts in the blood, hematocrit, and opening cerebrospinal pressures for patients who died and survivors were not significant. A multiple logistic regression model identified neurological status (coma, particularly if associated with extensor posturing), stage of parasite development on the peripheral blood film, pulse rate of > 150 or respiratory rate of > 50, hypoglycemia, and hyperlactatemia (plasma lactate level, > 5 mmol/L) as independent indicators of a fatal outcome. Biochemical evidence of hepatic and renal dysfunction was an additional marker of a poor prognosis, but, in contrast to severe malaria in adults, none of these children with severe malaria had acute renal failure.
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PMID:Clinical features and outcome of severe malaria in Gambian children. 852 47

1. The possible contribution of endogenous endothelin (ET) to the pathogenesis of seizure-associated pulmonary oedema was examined in mechanically ventilated rats after intravenous bolus injection of the gamma-aminobutyric acid (GABA) antagonist, bicuculline (1.2 mg kg-1). 2. Recurrent seizure activity elicited by bicuculline injection led to rapidly developing pulmonary oedema. Within 4 min after bicuculline application (1.2 mg kg-1), arterial O2 partial pressure (PaO2) significantly dropped from 17.49 +/- 1.20 kPa to 7.51 +/- 2.21 kPa (P < 0.01) and arterial CO2 partial pressure (PaCO2) significantly increased from 4.64 +/- 0.56 kPa to 8.15 +/- 0.99 kPa (P < 0.01). Gradually a progressive acidosis developed. Moreover, mean arterial blood pressure (MABP) and end-inspiratory airway pressure (Paw) rapidly increased. 3. Concomitantly there was a time-dependent increase of big ET-1 and ET-1 levels in bronchoalveolar lavage (BAL) as determined by combined reverse phase high performance liquid chromatography (h.p.l.c.) and radioimmunoassay. BAL levels of both peptides increased up to 8 min after bicuculline injection and slowly decreased subsequently. In contrast, BAL from animals injected with vehicle did not contain detectable amounts of ET. 4. Pretreatment with the endothelin-converting enzyme inhibitor, phosphoramidon (5.4 mg kg-1, i.v.) for 5 min significantly (P < 0.001) reduced peak ET-1 levels in BAL fluid by 65.4 +/- 9.9% at 8 min after bicuculline injection. Simultaneously it afforded protection from hypoxia. PaCO2 did not increase and PaO2 decreased only slightly from 14.63 +/- 1.00 kPa to 12.97 +/- 0.61 kPa (P > 0.05) after phosphoramidon pretreatment. In contrast, vehicle-treated animals that received bicuculline showed both significant hypercapnia as well as profound hypoxia. Phosphoramidon significantly diminished the maximum increase in Paw by 76.7 +/- 12.4% (P <0.005), but only slightly affected the MABP. Phosphoramidon pretreatment had no effect on the acidosis.5. Pretreatment with the ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.), for 5 min did not affect the levels of ET-1 in the BAL fluid at 8 min after bicuculline injection but did ameliorate the development of hypoxia. No hypercapnia developed and Pa02 decreased only moderately from 16.65 +/-0.25 kPa to 14.19 +/-2.15 kPa (P>0.05) in BQ-123-treated animals. In contrast, vehicle-treated animals that received bicuculline exhibited significant hypercapnia as well as profound hypoxia. BQ-123 significantly reduced the increase in Paw by 51.3 +/- 12.8% (P < 0.01). It affected MABP only slightly and had no effect on the acidosis.6. These results suggest that ET peptides play a significant role in this model of neurogenic pulmonary oedema and may act as mediators of respiratory distress. The deleterious effects of endogenous ET in this model are primarily mediated via the ETA receptor, for they were inhibited by the ETA receptor antagonist, BQ-123. ETA receptor antagonists may therefore be of potential therapeutic value in respiratory distress.
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PMID:A role for endothelin in bicuculline-induced neurogenic pulmonary oedema in rats. 854 73

A retrospective analysis was undertaken in a consecutive series of 33 full-term infants (birth weight > 2500 g and a minimum of 37 weeks gestational age) with symptomatic intracranial hemorrhage (ICH) admitted to a regional neonatal intensive care unit from January 1986 to December 1992. Eleven infants were born in our institution; 17 were male. The estimated local incidence of symptomatic ICH for the inborn population was 4.9/10000 live births, with a regional incidence of 2.7/10000 live births. Twenty-four (72.3%) infants presented with seizures, apnea, or respiratory distress. Five (15.1%) children developed ICH associated with extracorporeal membrane oxygenation, ventriculoperitoneal shunting, and cardiac surgery. There were two deaths (6.1%) associated with a grade IV periventricular hemorrhage (PVH) and cardiac surgery. Nine infants (27.3%) showed PVH, while an additional nine children developed multifocal cortical hemorrhages. Eight infants (24.2%) showed extra-axial ICH, four children (12.1%) sustained lobar hemorrhages, and three children (9.1%) showed ICH associated with prenatal CNS abnormalities. Excluding five children with iatrogenic ICH, coagulopathies occurred in 9 of 28 infants (32.1%) and constituted a major determinant of the development of ICH. Neurosurgical intervention was limited to one infant with massive ICH and one child with hydrocephalus as a late sequela of ICH. Developmental follow-up was complete in 32 children with a mean and median duration of 3.4 years. Full-term infants with ICH associated with risk factors for hypoxic-ischemic injury showed a significantly greater risk of developmental delay compared to infants with uncomplicated ICH.
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PMID:Symptomatic intracranial hemorrhage in full-term infants. 875 Sep 52

A case of acute microangiopathic hemolytic anemia in a 29-year-old primiparous patient is presented. Following an unsuspicuous pregnancy and uncomplicated delivery, the patient developed upper abdominal symptoms and transient psychopathologic abnormalities 2 days after delivery. Because of a series of generalized tonic-clonic seizures and respiratory distress she was admitted to the Neuro ICU. Focal neurological symptoms were absent, and CSF analysis was normal. Laboratory findings indicated hemolytic anemia with fragmented erythrocytes in smear specimens, thrombocytopenia, reticulocytosis, marked elevation of liver and pancreatic enzymes, and microhematuria. T2-weighted MR scans of the brain discluded multiple ischemic lesions of the cerebral white and gray matter, caudate nucleus and pons, displaying a hemodynamic pattern. Specific treatment included administration of corticosteroids, repeated plasmapheresis with substitution by fresh frozen plasma and antithrombin III. A control MR performed on the 3rd day of treatment demonstrated the absence of nearly all abnormal findings previously obtained. During a 3-week clinical course the patient showed full recovery, including normalization of hematologic and neuroradiologic findings. This case demonstrates ischemic cerebral lesions in acute microangiopathic hemolytic anemia to be potentially reversible if specific treatment is provided.
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PMID:[Reversible cerebral MRI findings in acute microangiopathic hemolytic anemia]. 876 6

A female infant presented with cyanosis, respiratory distress and unique to-and-fro murmur which she had since the age of 1-month-old. Absent pulmonary valve syndrome was diagnosed by echocardiography. She developed seizure disorders with hypocalcemia and pneumonia at the age of 2-month-old. The patient died from sepsis, intractable respiratory and heart failure. The postmortem study confirmed the diagnosis of congenital absent pulmonary valve associated with DiGeorge syndrome.
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PMID:Absent pulmonary valve syndrome associated with DiGeorge syndrome: report of one case. 894 31

A 21-year-old man presented with fever, rash, seizure, stiff neck and rapidly progressive bilateral pulmonary infiltrates. Cerebrospinal fluid (CSF) study revealed pleocytosis with predominant polymorphonuclear cells, and hypo-glycorrhachia. Status epilepticus occurred, followed by acute respiratory distress syndrome with respiratory failure. Blood and CSF cultures for bacteria were negative, but an indirect immunofluorescence assay revealed a fourfold rise in antibody to Rickettsia tsutsugamushi in paired serum and a 1:2560 (+) IgM antibody titer. Severe scrub typhus with meningoencephalitis and extensive pneumonitis was diagnosed. The patient survived after intravenous minocycline therapy and intensive care, including aggressive seizure control, supportive mechanical ventilation and avoidance of fluid overloading. He had a nearly complete recovery. Practicing physicians in Taiwan should be aware of this reportable disease and its potentially serious complications if not promptly diagnosed and treated.
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PMID:Life-threatening scrub typhus with meningoencephalitis and acute respiratory distress syndrome. 908 Jul 62

The efficacy and safety of the angiotensin converting enzyme inhibitor enalapril in dogs with naturally acquired class III or class IV heart failure was evaluated in this study. Eighteen small-breed dogs with insufficiency of their mitral valves, but without other diseases were included in this study over a period of six months. When necessary due to massive pulmonary edema or high serum potassium concentrations, furosemide was added to the therapy with enalapril. No other drugs, including digitalis, were used in this study. The treatment was followed by anamnesis, clinical examinations, electrocardiography, radiography, echocardiography and laboratory diagnosis. Examinations were performed before treatment and after one week, after six weeks and after six months of treatment. 72% of the dogs improved in NYHA classification until the end of the study (p < 0.05). The incidence of seizures due to syncopes or severe respiratory distress decreased during this study (p < 0.01). For 28% of the dogs this treatment was not successful. In the electrocardiographic, radiographic and laboratory examinations statistically significant changes could not be recorded. The decrease in heart rate did not reach statistical significance. The echocardiographic investigation evaluated a significant decrease in fractional shortening and in the diastolic diameter of the left ventricular wall (p < 0.05 respectively p < 0.01), but no significant change in the diastolic or systolic diameter of the interventricular septum. The average oral dose of enalapril was 0.38 mg/kg body weight b.i.d., the average dose of furosemide was 0.37 mg/kg body weight b.i.d. in the first week of the study and was raised to 0.74 mg/kg body weight b.i.d. until the end of the study. Side effects like diarrhea, vomiting or reduced appetite did not increase during the course of the study. However one dog was excluded from the study because of repeated vomiting after six weeks of treatment. This study shows the beneficial clinical and hemodynamic effects and the security of the therapy with enalapril for dogs with heart failure due to mitral insufficiency.
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PMID:[Treatment of mitral valve insufficiency in dogs with the ACE inhibitor enalapril. A clinical progress study]. 953 70

A dysmorphic infant is described who presented with laryngeal collapse leading to intubation and respiratory problems that were assigned clinically to the Sussman syndrome. The baby had repeated episodes of respiratory distress necessitating assisted ventilation. At 6 months old, uvulopharyngopalatotomy was done to enlarge the supraglottic airway without any benefit. Surgical reduction of the tongue and cricoid splitting did not ameliorate the respiratory distress; repeated extubation attempts failed with the baby developing stridor, respiratory distress, and episodes of cardiac arrest. At 10 months old he developed seizures and computed tomography showed diffuse cerebral atrophy consisted with hypoxic-ischaemic damage. He died at 17 months old. Western blots using antibodies against collagen alpha 1 (II) showed an absence of collagen type II in laryngeal tissue, which may explain the laryngeal collapse and impaired respiratory functions.
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PMID:Deficiency of laryngeal collagen type II in an infant with respiratory problems. 971 15


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