Academic literature on the topic 'Infant neurological morbidity'

Neonatal encephalopathy has been defined as “a clinically defined syndrome of disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal level of consciousness and often seizures”. It occurs in about 2–3 per 1000 births in developed countries. In developing countries, neonatal encephalopathy accounts for the largest number of deaths in infancy and childhood – approximately 1 million per year worldwide. Neonatal encephalopathy is associated with significant morbidity and mortality and is an important predictor of long term neurodevelopmental disability in near- and full-term newborn infants. Fifteen to 20 percent of infants with neonatal encephalopathy die in the neonatal period, and a further 25 percent have permanent neurologic deficits.

Infant mortality is a major problem in developing countries and, unfortunately, this is the case of our country as well, given that Romania ranks first in the European Union in this respect, with an infant mortality rate of 9 ‰, compared to an average of roughly 4 ‰. Worldwide, over 15 million babies are born prematurely each year and, out of these, more than a million die due to prematurity and infections, which are the main risk factors for neonatal mortality. The risk of infection is several times higher in preterm newborns than in full-term newborns – about 80% of neonatal infections occur in premature infants. A significant proportion of the survivors of prematurity will have important neurological sequelae because of neonatal infections as well as of intracerebral bleeding or hypoxia at birth. Continuing medical education in both the general population and the medical sector is crucial in preventing premature births and neonatal infections and, consequently, in decreasing infant morbidity and mortality rates in our country.

AbstractIntrauterine death of one fetus in a multiple gestation is associated with significant morbidity and mortality in the surviving infant. This study is a retrospective review of 38 twin and 3 triplet gestations involving the intrauterine death of at least one fetus. The obstetrical history, placental pathology, autopsy findings, and neonatal history of the surviving infant are reviewed. Three cases involved the recent stillbirth of both twins, the remaining cases involved a surviving infant. In one case, neonatal death of a surviving twin occurred on day 19. In two sets of triplets, two stillbirths occurred, in the third case two infants were liveborn. The incidence of preterm delivery was 34%, which decreased to 18% if fetal cotwin death had occurred before 20 weeks gestation. Cesarean section was the method of delivery in 16 cases. There was an excess of velamentous cord insertions, which was most pronounced in the stillborn twin. Monochorionic placentation was found in 72%, also an excess.Neurological damage was known to have occurred in 19 of the 39 surviving infants. Fifteen of these 19 (79%) were associated with monochorionic placentation. The neurologically damaged twin infants, when compared to the normal infants, had the cotwin die later in gestation (31 vs 16.5 weeks), had a shorter duration between the death of the cotwin and delivery (2.5 vs 21 weeks), and delivered earlier in gestation (36.5 vs 39.5 weeks). The probable cause of neurological damage, in our opinion, was either exsanguination into the dead twin fetus, or disseminated intravascular coagulation which occurred in at least 13 cases. The incidence of antepartum death in a multiple gestation, and the potential for neurological damage is probably higher than previously thought. A review of the literature is presented and the clinical implications of this phenomenon are discussed.

Encephalitis is a complex neurological disease that is associated with significant morbidity and mortality, and the etiology of the disease is often not identified. Human metapneumovirus (hMPV) is a common cause of upper and lower respiratory tract infections in children. Few reports are available showing possible involvement of hMPV in development of neurologic complications. Here, we describe an infant, the youngest case in literature, with refractory status epilepticus and severe encephalitis in whom hMPV was detected in respiratory samples and review diagnostic workup of patient with encephalitis.

Preterm birth is associated with a high risk of morbidity and mortality including brain damage and cerebral palsy. The development of brain injury in the preterm infant may be influenced by many factors including perinatal asphyxia, infection/inflammation, chronic hypoxia and exposure to treatments such as mechanical ventilation and corticosteroids. There are currently very limited treatment options available. In clinical trials, magnesium sulfate has been associated with a small, significant reduction in the risk of cerebral palsy and gross motor dysfunction in early childhood but no effect on the combined outcome of death or disability, and longer-term follow up to date has not shown improved neurological outcomes in school-age children. Recombinant erythropoietin has shown neuroprotective potential in preclinical studies but two large randomized trials, in extremely preterm infants, of treatment started within 24 or 48 h of birth showed no effect on the risk of severe neurodevelopmental impairment or death at 2 years of age. Preclinical studies have highlighted a number of promising neuroprotective treatments, such as therapeutic hypothermia, melatonin, human amnion epithelial cells, umbilical cord blood and vitamin D supplementation, which may be useful at reducing brain damage in preterm infants. Moreover, refinements of clinical care of preterm infants have the potential to influence later neurological outcomes, including the administration of antenatal and postnatal corticosteroids and more accurate identification and targeted treatment of seizures.

Background: Birth asphyxia is an important cause of static development and neurological handicap in both term and preterm infants. Birth asphyxia is found to be responsible for 28.7% deaths in hospital settings and 20% deaths in rural/tribal areas. Approximately the same number develops serious sequelae which cripples these children both physically and mentally. Children who have suffered moderate encephalopathy had varying rates of infant death and morbidity. Precise determination of the prognosis in the term new born, who sustains a hypoxic ischemic insult is hindered by difficulty in determining the severity of insult.Methods: This was a prospective longitudinal, observational study was conducted in the Department of Paediatrics, CMC Bhilai with close association with the Department of Obstetrics and Gynecology, Department of Radio diagnosis and Department of Neurology. All deliveries taking place in the Department of Obstetrics and Gynecology of CMC Bhilai were enrolled for the study. Each enrolled infant underwent a detailed neurologic examination within the first 12 hours after birth. During the period of data collection 180 babies with birth asphyxia were admitted to NICU. Out of which 126 babies had fulfilled the inclusion criteria and completed one year follow up, hence as cases. Babies who lost follow up were not included in study. The neurological examination was performed 14 days after discharge, then at 1 month, 3-month, 6-month, 9 month and 12 months. Long term outcome in this study is defined as outcome at one year of age in terms of morbidity and mortality.Results: The female and male ratio is 0.4:1. Most of the asphyxiated newborn, 81 (64%) were in 2500-3000gm. Among the study population, maximum number of cases 76 (60%) were suffering from HIE-I. Majority of study population, 87 (69%) were born by LSCS. Normal CUS in 93 babies and abnormal in 33 babies; with normal CUS, there were no death in study population and out of 33 abnormal CUS, 12 deaths occurred. Out of the different complications enlisted in the table convulsions (66.7%) is most common followed by Apnea (65.08%). Recurrent infections (45.24%) is the most common complication followed by seizure disorders (22.63%) and failure to thrive (20.63%).Conclusions: Hypoxic ischemic encephalopathy is one of the major consequences of perinatal asphyxia. Despite of best care, some babies are likely to develop it.

ABSTRACT The cases of 13 infants (median age, 3 months) who sustained nonaccidental trauma were reviewed. All presented with profound neurological impairment, seizures, retinal hemorrhages, and intracranial subarachnoid and/or subdural hemorrhages. Of 8 infants who died, autopsy was performed on 6. No patient had a skull fracture, and only one had an extracalvarial contusion. Five of the 6 patients on whom autopsy was performed had injuries at the cervicomedullary junction consisting of sub- or epidural hematomas of the cervical spinal cord with proximal spinal cord contusions. The authors conclude that direct cranial trauma is not an essential element of the injury mechanism in young patients who sustain severe whiplash-shake injuries. In addition to the classic injuries reported to occur with the shaken-baby syndrome, hemorrhages and contusions of the high cervical spinal cord may contribute to morbidity and mortality.

ObjectivesIt is unclear how newer methods of respiratory support for infants born extremely preterm (EP; 22–27 weeks gestation) have affected in-hospital sequelae. We aimed to determine changes in respiratory support, survival and morbidity in EP infants since the early 1990s.DesignProspective longitudinal cohort study.SettingThe State of Victoria, Australia.ParticipantsAll EP births offered intensive care in four discrete eras (1991–1992 (24 months): n=332, 1997 (12 months): n=190, 2005 (12 months): n=229, and April 2016–March 2017 (12 months): n=250).Outcome measuresConsumption of respiratory support, survival and morbidity to discharge home. Cost-effectiveness ratios describing the average additional days of respiratory support associated per additional survivor were calculated.ResultsMedian duration of any respiratory support increased from 22 days (1991–1992) to 66 days (2016–2017). The increase occurred in non-invasive respiratory support (2 days (1991–1992) to 51 days (2016–2017)), with high-flow nasal cannulae, unavailable in earlier cohorts, comprising almost one-half of the duration in 2016–2017. Survival to discharge home increased (68% (1991–1992) to 87% (2016–2017)). Cystic periventricular leukomalacia decreased (6.3% (1991–1992) to 1.2% (2016–2017)), whereas retinopathy of prematurity requiring treatment increased (4.0% (1991–1992) to 10.0% (2016–2017)). The average additional costs associated with one additional infant surviving in 2016–2017 were 200 (95% CI 150 to 297) days, 326 (183 to 1127) days and 130 (70 to 267) days compared with 1991–1992, 1997 and 2005, respectively.ConclusionsConsumption of resources for respiratory support has escalated with improved survival over time. Cystic periventricular leukomalacia reduced in incidence but retinopathy of prematurity requiring treatment increased. How these changes translate into long-term respiratory or neurological function remains to be determined.

Background: The burden of postpartum depression is significant because it remains unrecognized and it not only affects the mother adversely but also has a negative consequence on the family life and the development of the infant. This research aims to aid the early diagnosis of postnatal depression using Edinburgh postnatal depression scale (EPDS) and the psychosocial and reproductive risk factors of postnatal depression among women delivering in a tertiary hospital in Kerala state, India.Methods: 500 women were subjected to a standard questionnaire for assessing psychosocial and reproductive characteristics. The diagnosis of postnatal depression was made using a pretested and validated Malayalam version of EPDS with a score cut off of 13 or more.Results: The proportion of postnatal depression six weeks after delivery at TD Medical College, Alappuzha was found to be 8.6%. Marital harmony (p value=0.002) was significantly associated with postnatal depression. Diabetes (p value=0.037), hypertensive disorders (p value=0.013), antepartum hemorrhage (p value=0.036), neurological disorders (p value <0.001), type of delivery (p value=0.042), postpartum complications (p value=0.003), mode of infant feeding (p value=0.001), infant illness (p value=0.001), symptoms of maternity blues (p value <0.0001), premenstrual syndromes (p value=0.008) and infertility treatment (p value=0.03) were significantly associated with postnatal depression.Conclusions: Early screening of the women and counselling of women and their family will reduce the maternal morbidity and adverse child outcomes.

Substances abuse and HIV infection are major health issues globally, with a significant increase in morbidity and mortality. But what are the consequences of the association between the two, especially in a pregnant woman? Substance abuse in a pregnant HIV positive woman, regardless of the substance used (tobacco, alcohol, marijuana, cocaine, opioids etc.) is at greater risk of HIV maternal-fetal transmission, as well as obstetric, neonatologic and pediatric complications, such as miscarriage, abruptio placentae, premature birth, eclampsia, fetal alcohol syndrome, stillbirth, sudden infant death syndrome and neurological deficits. For these reasons cessation of substance abuse is mandatory before planning a pregnancy, especially for HIV infected women. This can be achieved through counselling, guidance towards rehab facilities and prenatal screening programs, often with optimistic results, as pregnancy is the time with the highest success rate regarding substance abuse cessation than any other time in a woman’s life.

Background Due to small iron stores and rapid growth during the first months of life, infants with low birth weight (LBW) are at risk of iron deficiency (ID). ID in infancy is associated with irreversible impaired neurodevelopment. Preventive iron supplementation may reduce the risk of ID and benefit neurodevelopment, but there is also a possible risk of adverse effects. More than 50% of all LBW infants are born with marginally LBW (MLBW, 2000-2500g), and it is not known if they benefit from iron supplementation. Methods We randomized 285 healthy, Swedish, MLBW infants to receive 3 different doses of oral iron supplements; 0 (Placebo), 1, and 2 mg/kg/day from six weeks to six months of age. Iron status, during and after the intervention was assessed and so was the prevalence of ID and ID anemia (IDA), growth, morbidity and the interplay with iron and the erythropoetic hormones hepcidin and erythropoietin (EPO). As a proxy for conduction speed in the developing brain, auditory brainstem response (ABR) was analyzed at six months. In a follow up at 3.5 years of age, the children were assessed with a cognitive test (WPPSI-III) and a validated parental checklist of behavioral problems (CBCL), and compared to a matched reference group of 95 children born with normal birth weight. Results At six months of age, the prevalence of ID and IDA was significantly higher in the placebo group compared to the iron supplemented infants. 36% had ID in the placebo group, compared to 8% and 4 % in the 1 and 2mg/kg/day-groups, respectively. The prevalence of IDA was 10%, 3% and 0%, respectively. ABR-latencies did not correlate with the iron intake and was not increased in infants with ID or IDA. ABR wave V latencies were similar in all three groups. Hepcidin correlated to ferritin and increased in supplemented infants while EPO, which was negatively correlated to iron status indicators, decreased. At follow up there were no differences in cognitive scores between the groups but the prevalence of behavioral problems was significantly higher in the placebo group compared to those supplemented and to controls. The relative risk increase of CBCL-scores above a validated cutoff was 4.5 (1.4 – 14.2) in the placebo-group compared to supplemented children. There was no detected difference in growth or morbidity at any age. Conclusion MLBW infants are at risk of ID in infancy and behavioral problems at 3 years of age. Iron supplementation at a dose of 1-2 mg/kg/day from six weeks to six months of age reduces the risks with no adverse effects, suggesting both short and long term benefit. MLBW infants should be included in general iron supplementation programs during their first six months of life.

Ciljevi: Cilj ove studije je da ispita bezbednost rane karotidne endarterektomije (CEA) u odnosu na odložene CEA nakon akutnog ishemijskog neurološkog deficita (TIA/CVI). Drugi cilj je da istražimo da li postoji razlika u brzini neurološkog oporavka između navedenih grupa. Metode: Ukupno 157 ispitanika u prospektivnoj studiji je praćeno 30 dana postoperativno. Grupa I ili rana CEA, je imala 50 ispitanika operisanih od 3. do 14. dana po TIA/CVI događaju. Grupa II ili odložena CEA, je imala 107 ispitanika operisanih od 15. do 180. dana nakon TIA/CVI. Praćen je proceduralni opšti i specifični morbiditet i mortalitet u 30-dnevnom postoperativnom periodu. Rankin skor (mRS) smo koristili za procenu neurološkog invaliditeta. U odnosu na vrednost mRS skora smo formirali dve podgrupe mRS<3 i mRS3. U statističkoj analizi koristili smo Pirsonov hi test, Studentov test, ANOVU analizu varijanse, Boniferonijev test i multiplu analizu varijanse za ponovljena merenja (GLM- general line model), kao i parametarsku i neparametarsku korelaciju i regresiju. Nivo značajnosti je bio 0,05. Rezultati: Prosečna starost ispitanika je bila 66,72 godine uz 66,2% osoba muškog pola. U grupi I je prosečno vreme do intervencije bilo 9,5 dana, a u grupi II 72,22 dana. Grupe su homogene u odnosu na faktore rizika i komorbiditet. Grupa I je imala 54% nestabilnih aterosklerotskih plakova u poređenju sa grupom II gde ih je bilo 31,8% (χ2 = 7.084; p < 0.01). U grupi I TIA je imalo 50% ispitanika, a u grupi II CVI nalaza je bilo 68,2% (χ2 =4.825; p <0.05). CVI do 1 cm veličine je statistički značajno više zastupljen u grupi I , a CVI do 2 cm u grupi II (χ2 = 6.913; p <0.05). Stopa CVI je u grupi I bila 2.0% a u grupi II je 2.8% (F = 0.083; p > 0.05). Stopa postoperativnog infarkta miokarda (IM) je u grupi I je 2.0% a u grupi II je 1.9%. Stopa specifičnog hirurškog morbiditeta je u grupi I 4.0% a u grupi II 3.7%. U grupi I ukupni morbiditet bio 6.0% a u grupi II 7.5%, razlika nije bila statistički značajna (F =0.921; p > 0.05). Mortaliteta u obe grupe nije bilo. CVI/IM/smrt stopa je u grupi I bio 4.0% a u grupi II je bio 4.7% (F = 0.122; p >0.05). Hiperlipidemija je signifikantan faktor rizika za CVI/IM/smrt (χ2 = 4.083; p < 0.05). Poboljšanje mRS je u grupi I imalo 52%, a u grupi II 31,8% pacijenata (χ2 = 5.903; p <0.01). Relativni rizik je 2,4 odnosno toliko puta je veća šansa da kod bolesnika dođe do promene mRS ako je bolesnik u grupi I. Pad mRS koji nastupa između trećeg i desetog dana nakon CEA je statistički visoko značajno izraženiji u grupi ranih CEA ( F 3,701 df 1 p=0,029). Kod bolesnika sa TIA u preko 60% slučajeva došlo je do pada mRS, a kod onih koji su imali CVI u oko 25.5% (χ2 = 18.050; p < 0.01). Kod Rankin skora podgrupe mRS<3 i mRS3 je pad bio značajan i po vremenu (F 18,774; df 6; p=0,000) i po podgrupi ali je daleko brži pad zapažen u podgrupi mRS<3(F 6,010; df 1; p=0,003). Zaključak: Rana CEA je jednako bezbedna kao i odložena CEA u pogledu incidence perioperativnog morbiditeta i mortaliteta. Ranom CEA se postiže znatno brži neurološki oporavak pacijenata, naročito onih sa TIA i mRS<3 skorom.
Objectives: The aim of this study was to investigate the safety of early carotid endarterectomy (CEA) in relation to the delayed CEA after acute ischemic neurological events (TIA / CVI). The second objective was to investigate whether there is a difference in speed of neurological recovery between these groups. Methods: A total of 157 patients in the prospective study followed 30 days postoperatively. Group I or early CEA, had 50 patients operated from 3 to 14 days after TIA / CVI event. Group II or delayed CEA, had 107 patients operated from 15 to 180 days after the TIA / CVI. Accompanied by the general and specific procedural morbidity and mortality in 30-day postoperative folow up. Rankin score (mRS) were used for evaluation of neurologic disability. In relation to the value of mRS score we formed two subgroups mRS <3 i mRS3. In the statistical analysis we used the Pearson chi test, Student's test, ANOVA analysis of variance, Boniferony test and multiple analysis of variance for repeated measures (GLM- general line model), as well parametric and nonparametric correlation and regression. The significance level was 0.05. Results: The mean age was 66.72 years with 66.2% of males. In Group I is the average time to intervention was 9.5 days, and in group II 72.22 days. The groups were homogeneous in relation to risk factors and comorbidities. Group I had 54% of unstable atherosclerotic plaques compared with group II, where it was 31.8% (χ2 = 7.084; p <0.01). In the group I TIA had 50% of respondents, while in group II CVI was 68.2% (χ2 = 4.825; p <0.05). CVI to 1 cm in size were significantly more frequent in the group I, a CVI to 2 cm in group II (χ2 = 6.913; p <0.05). CVI rate in the group I was 2.0%, and in group II was 2.8% (F = 0.083, p> 0.05). Postoperative myocardial infarction (MI) in the group I is 2.0%, and in group II was 1.9%. Specific surgical morbidity rate in the group I and 4.0% in the group II 3.7%. In group I total morbidity was 6.0% in group II 7.5%, the difference was not statistically significant (F = 0.921; p> 0.05). Mortality in both groups was not. CVI/IM/death rate in group I was 4.0% in group II was 4.7% (F = 0.122; p> 0.05). Hyperlipidemia is a significant risk factor for CVI/IM/death (χ2 = 4.083; p<0.05). Improving mRS in the group I had 52% and in group II 31.8% of patients (χ2 = 5.903; p <0.01). The relative risk was 2.4 times as much and is more likely to occur in patients mRS changes if the patient in group I. Improving mRS that occurs between the third and tenth days after CEA was highly statistically significantly greater in the group of early CEA (F 3,701 df 1 p = 0.029). In patients with TIA in 60% of cases there was a decline mRS, and those had CVI in about 25.5% (χ2 = 18.050; p <0.01). In Rankin score subgroups mRS <3 i mRS 3 the decline was significant and time (F 18,774; df 6; p =0.000) and in the subgroup but it is far more rapid decline observed in the subgroup mRS <3 (F 6.010; df 1; p = 0.003). Conclusions: Early CEA is as safe as the delayed CEA in respect incidence of perioperative morbidity and mortality. Early CEA is achieved significantly faster recovery of neurological patients, especially those with TIA and mRS <3 compared with delayed CEA.

Myelomeningocele (MMC) is a spinal birth defect associated with significant morbidity directly related to the exposure of meninges and neural structures. Further neurological dysfunction may occur secondary to Chiari II malformation and hydrocephalus. MMC repair is typically performed postnatally within the first 24 to 48 hours of life due to the concern for infection. Prenatal MMC correction is performed in select cases after studies showed improved neurological outcomes. Anesthesia for MMC repairs can be challenging, and appropriate screening should be performed preoperatively. During postnatal repair, care must be taken when positioning the infant to avoid any pressure on the MMC sac. Anesthesia can be maintained with a combination of inhalational agents and intravenous opioids. Prenatal MMC repairs must consider both fetal and maternal safety outcomes. They can be performed through both open and fetoscopic routes, with anesthesia focused on maintaining maternal blood pressure, optimizing uterine relaxation, and adequate pain control.

Glutaric aciduria type I is a rare organic aciduria caused by inherited deficiency of glutaryl-CoA dehydrogenase, a mitochondrial enzyme involved in the final common catabolic pathways of L-lysine, L-hydroxylysine, and L-trytophan. The majority of untreated patients develop striatal injury and secondary dystonia during infancy and childhood, whereas identification by newborn screening and immediate start of metabolic treatment (low-lysine diet, carnitine supplementation, metabolic emergency treatment) helps to prevent severe neurological complications in the majority of patients. The morbidity and mortality of dystonic patients is high, whereas asymptomatic patients have normal life expectancy. Effective antidystonic treatment requires a multidisciplinary approach. In a subgroup of patients, first clinical symptoms (headaches, vertigo, gait disturbance, hand tremor) may not manifest before adulthood. Cranial MRI studies in these patients reveal T2 hyperintensities of supratentorial white matter. A few women with glutaric aciduria type I have had unremarkable pregnancies, deliveries, and postpartal periods.

Until very recently, the discussion about infections in pregnancy was focused on specific microorganisms, how the pregnant mother acquired the organism and transmitted it to the fetus, the effects of the infection on fetal survival, fetal loss, fetal growth, and development, and on the long-term sequelae. The narrative applied to the ‘TORCHES’ group of infections namely toxoplasmosis, rubella, cytomegalovirus, herpes, and syphilis, dominated the scene before the emergence of newer perinatal infections such as parvovirus B19 and HIV in the later years of the twentieth century. Numerically, the TORCHES group of infections accounts for fewer perinatal complications and morbidity than the more common but less specific ascending subclinical infections encountered clinically as chorioamnionitis and its precursors such as bacterial vaginosis, intermediate vaginal flora, aerobic vaginitis, group B streptococci, and other variants of abnormal lower genital tract flora. The contribution of ascending subclinical infections to the incidence of preterm delivery, long-term neurological and respiratory morbidity, and exacerbation of intrapartum hypoxic ischaemic injury is grossly understated worldwide while disproportionate amounts of resources continue to be expended globally on screening for and the management of the TORCHES group and related infections. In this chapter, the authors aim to cover the common and important perinatal infections and attempt to redress the imbalance in emphasis by drawing attention to the role of ascending subclinical infections in the aetiology of major adverse perinatal outcomes such as brain injury in both the term and the preterm infant.

Hypoglycaemia is defined as a blood glucose level less than 2.6 mmol/l. This is based on the consistent impairment of central nervous system function observed in subjects when blood glucose levels are below this (1). Glucose homeostatic mechanisms should maintain blood glucose level to preserve cognitive function. Hypoglycaemia triggers protective glucose homeostatic mechanisms and persistent hypoglycaemia is the result of a failure of homeostasis. This is a medical emergency with serious short- and long-term consequences, which result from a reduced supply of glucose to the brain. Recurrent and persistent hypoglycaemia does cause significant morbidity and death due to brain damage. In an adult, after recovery of glucose levels, neurological impairment usually recovers over minutes to hours. In children, the duration of hypoglycaemia leading to permanent damage is not known, but is presumed to depend on the age of the child, the frequency of hypoglycaemia, the degree and the rapidity of the fall in glucose, concurrent circumstances such as infection, trauma and hypoxia, the degree of resilience of the brain tissue at the current stage of development. and the energy demands of the particular parts of the brain. The reasons for the increased sensitivity in children appear to relate to the higher energy requirements and immaturity of the homeostatic mechanisms of the brain. In congenital hyperinsulinism of infancy (CHI) the rates of severe neurological impairment remain high at 20–50%, permanent neurological impairment with damage occurring mainly in the cerebral cortex, hippocampus, and caudate putamen. Appropriate long term management of hypoglycaemia requires the correct diagnosis, and this depends on obtaining ‘critical blood and urine samples’ during a hypoglycaemic episode. In the first 48 h of life 20% of normal full–term infants have a blood glucose level <2.6 mmol/l (2), after this it is relatively uncommon in infancy and childhood with the incidence of various underlying diagnoses varying with age. The causes of hypoglycaemia can be classified into five groups: ◆ excess insulin (or insulin-like factors) for the given circumstances ◆ lack of one or more of the counter regulatory hormones (cortisol, growth hormone) ◆ disturbance of intermediate metabolism causing impairment of gluconeogenesis and/or glycogenolysis ◆ disturbance of fat breakdown or ketone body formation or utilization ◆ lack of nutrient sufficient for current energy demands

With an annual incidence of more than 600,000 cases, thromboembolic stroke is the third leading cause of death in the United States after heart disease and cancer (Kochanek et al., 2004). The number of stroke survivors has increased to 4.5 million adults nationally as the management of acute stroke continues to improve (AHA, 2002). Psychiatric syndromes are common complications of stroke and are associated with psychologic distress, increased impairment, poor rehabilitation outcomes, and excess morbidity. The purpose of this chapter is to describe clinically important poststroke psychiatric disorders and suggest appropriate treatment. Cognitive deficits are the most common psychiatric complication of stroke and affect nearly all stroke survivors. The type of cognitive disturbance depends on the location of the brain injury. Left hemisphere strokes frequently cause aphasia. Right hemisphere strokes cause substantial (but often underrecognized) cognitive impairments such as diminished insight, decreased attention, impaired spatial reasoning, and neglect syndromes. Furthermore, depending on the location of a stroke, other functions such as motivation, memory, judgment, and impulse control may also be affected. A large stroke or a series of small strokes affecting both hemispheres may lead to the global cognitive impairment of dementia. When a series of strokes is involved, the cognitive decline develops in a stepwise manner. This vascular dementia or multi-infarct dementia may be difficult to distinguish from Alzheimer’s disease. Autopsy studies of patients diagnosed with vascular dementia have often demonstrated the presence of Alzheimer’s disease pathology. As many as 25% of all dementia cases are attributable to a combined neuropathology of Alzheimer’s disease and multiple infarcts (Massoud et al., 1999). In addition to strategies such as speech and language therapy, physical and occupational therapy, and cognitive rehabilitation, pharmacologic treatment may improve cognitive deficits in some stroke patients. The parallels between vascular dementia and Alzheimer’s disease, as well as the evidence that reduced cholinergic function may play a role in both (Gottfries et al., 1994) have encouraged the use of acetylcholinesterase inhibitors (eg, donepezil) in vascular dementia. These drugs have shown modest benefits in such patients (Roman et al., 2005), and their use is described in Chapter 20.