If the mother is infected with rubella during the ninth week, a crucial week for internal ear development, destruction of the organ of Corti can occur, causing deafness. In the heart, the ductus arteriosus can remain after birth, leading to hypertension. Rubella can also lead to atrial and ventricular septal defects in the heart. If exposed to rubella in the second trimester, the fetus can develop central nervous system malformations. However, because infections of rubella may remain undetected, misdiagnosed, or unrecognized in the mother, and/or some abnormalities are not evident until later in the childs life, precise incidence of birth defects due to rubella are not entirely known. The timing of the mothers infection during fetal development determines the risk and type of birth defect. As the embryo develops, the risk of abnormalities decreases. If exposed to the rubella virus during the first four weeks, the risk of malformations is 47%. Exposure during weeks five through eight creates a 22% chance, while weeks 9–12, a 7% chance exists, followed by 6% if the exposure is during the 13th-16th weeks. Exposure during the first eight weeks of development can also lead to premature birth and fetal death. These numbers are calculated from immediate inspection of the infant after birth. Therefore, mental defects are not accounted for in the percentages because they are not evident until later in the childs life. If they were to be included, these numbers would be much higher.Other infectious agents include cytomegalovirus, the herpes simplex virus, hyperthermia, toxoplasmosis, and syphilis.
Bladder sphincter dyssynergia (also known as detrusor sphincter dyssynergia (DSD) (the ICS standard terminology agreed 1998)  and neurogenic detrusor overactivity (NDO)) is a consequence of a neurological pathology such as spinal injury  or multiple sclerosis which disrupts central nervous system regulation of the micturition (urination) reflex resulting in dyscoordination of the detrusor muscles of the bladder and the male or female external urethral sphincter muscles. In normal lower urinary tract function, these two separate muscle structures act in synergistic coordination. But in this neurogenic disorder, the urethral sphincter muscle, instead of relaxing completely during voiding, dyssynergically contracts causing the flow to be interrupted and the bladder pressure to rise. Presentation
People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition. Pseudodyssynergia has different causes but presents similarly. Pathology
The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. Treatment
Botulinum A toxin is a valuable alternative for patients who do not want surgical methods. References
Further reading


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