Seckel syndrome is a very rare autosomal recessive disorder also known as bird headed dwarfism”. It is characterised by proportional short stature, low birth weight, dysmorphic facial appearance, and mental retardation. In addition to its dysmorphic features, skeletal, endocrine, gastrointestinal, haematologic, genitourinary, and nervous system has been involved. Cardiovascular features very rarely associate with Seckel syndrome. We report two patients with Seckel syndrome, one with dilated cardiomyopathy and the other with multiple ventricular septal defects. Dilated cardiomyopathy and isolated ventricular septal defect have not been previously reported in Seckel syndrome. Cardiovascular evaluation should be performed in all patients with Seckel syndrome. Early diagnosis of congenital and acquired heart diseases will reduce morbidity and mortality in these patients.

Primary microcephaly (MCPH) is an autosomal recessive sporadic neurodevelopmental ailment with a trivial head size characteristic that is below 3–4 standard deviations. MCPH is the smaller upshot of an architecturally normal brain; a significant decrease in size is seen in the cerebral cortex. At birth MCPH presents with non-progressive mental retardation, while secondary microcephaly (onset after birth) presents with and without other syndromic features. MCPH is a neurogenic mitotic syndrome nevertheless pretentious patients demonstrate normal neuronal migration, neuronal apoptosis and neural function. Eighteen MCPH loci (MCPH1–MCPH18) have been mapped to date from various populations around the world and contain the following genes: Microcephalin, WDR62, CDK5RAP2, CASC5, ASPM, CENPJ, STIL, CEP135, CEP152, ZNF335, PHC1, CDK6, CENPE, SASS6, MFSD2A, ANKLE2, CIT and WDFY3, clarifying our understanding about the molecular basis of microcephaly genetic disorder. It has previously been reported that phenotype disease is caused by MCB gene mutations and the causes of this phenotype are disarrangement of positions and organization of chromosomes during the cell cycle as a result of mutated DNA, centriole duplication, neurogenesis, neuronal migration, microtubule dynamics, transcriptional control and the cell cycle checkpoint having some invisible centrosomal process that can manage the number of neurons that are produced by neuronal precursor cells. Furthermore, researchers inform us about the clinical management of families that are suffering from MCPH. Establishment of both molecular understanding and genetic advocating may help to decrease the rate of this ailment. This current review study examines newly identified genes along with previously identified genes involved in autosomal recessive MCPH.

Zika virus has captivated the world with its quick spread throughout the Western Hemisphere. Increased emphasis has been placed on the infection of pregnant women and subsequent adverse and severe effects in the developing fetus and newborn. This article supplements a previous article and provides updated information on new and evolving evidence that strengthens the association between Zika virus and unique congenital and neurologic diseases, updates what is known about the epidemiology of the disease, and provides new and updated material for primary care providers as they counsel patients who may be exposed or infected. With the extent of disease spread, it is expected that Zika virus will become endemic to the Western Hemisphere and will change the public health parameters and approach in this area of the world. (Disaster Med Public Health Preparedness. 2017;11:163–167)

Selective feticide by fetoscopic air embolism was carried out in six twin pregnancies complicated by discordance for a severe abnormality. In three, a previous diagnostic fetoscopy had been performed. The procedure was effective and uncomplicated in all cases. One patient is undelivered and five have delivered healthy babies, three at term and two preterm. One of the latter, delivered at 28 weeks, died of complications in the neonatal period.