Fetal Neurological Damage

Existing research about the passing of a maternal coagulation disorder to a fetus has focused primarily on such disorders' role in the onset of neurologic damage, especially encephalopathy and cerebral palsy. Encephalopathy, which is a generalized (as opposed to localized) brain dysfunction leading to speech, cognition, and orientation impairment, affects a large number of children born every year. The effects of encephalopathy range from mild instances that may only be identified through neurological testing to severe instances in which the patient may be almost entirely unresponsive.

Cerebral palsy clinically may be defined as a condition involving motor impairment that is secondary to anomalies or lesions of the brain. Although these anomalies or lesions arise in the early stages of the brain's development, it is currently not possible to properly diagnose cerebral palsy in the neonatal period because its symptoms are rarely exhibited by newborns. Because of this, all infants and children – especially those with risk conditions for cerebral palsy (eg intrapartum asphyxia or maternal infection) – are evaluated for delays in attaining developmental milestones to provide early clues to recognizing cerebral palsy. The onset of such developmental delays can give health care professionals clues that a child may suffer from cerebral palsy.

Cerebral palsy occurs in between two and two and a half per every 1000 live births. However, no single cause can be established in a significant portion of these cases. Certain research suggests that between 6% and 8% of cerebral palsy cases are the result of birth asphyxia, while 10% may be attributed to postnatal problems. Prenatal events are currently thought to cause the onset of approximately 75% of all cases of cerebral palsy, although it is often impossible to identify the nature and timing of such events. Those looking for the cause of the onset of cerebral palsy or other neurological defect caused by a prenatal event should look not only at the traditional sources of blame, but also at alternative factors.

New Areas for Investigation

Historically, there has been limited research into the potential neonatal causes of encephalopathy and cerebral palsy because of the incorrect assumption that the majority of such cases resulted primarily from intrapartum asphyxia or other traditionally accepted culprits. Research into the causes of these conditions therefore focused on these occurrences as the primary reason for long-term neurologic defects to the exclusion of others. However, it is becoming clear that perinatal asphyxia or postnatal problems are rarely the sole causes of neonatal encephalopathy or cerebral palsy. Instead, perinatal asphyxia and other traditional causes may be just one step in a longer series of causation events, sometimes along more than one causal pathway, leading to the onset of neonatal encephalopathy or cerebral palsy.

For instance, research suggests that the presence of maternal coagulation disorders (eg, the factor V Leiden mutation, antithrombin-III deficiency, and abnormalities of protein C or protein S) could contribute to the origin of cerebral palsy. These maternal coagulation abnormalities may transmit from a mother to her fetus through the placenta or, in the alternative, the fetus itself may be predisposed to such coagulation disorders.

Such assertions are supported by several studies summarized in a report published by the American College of Obstetricians and Gynecologists' Task Force on Neonatal Encephalopathy and Cerebral Palsy. One such study found that 20 of 31 examined children with cerebral palsy of an unknown cause had at least one coagulation abnormality. Grether, Nelson, Drambosia, Phillips: Interferons and Cerebral Palsy. J Pediatrics 1999, 134:324-332. That study's authors theorized that coagulation disorders, along with intrauterine infection, constitute risk factors for spastic cerebral palsy in children born at or near term. A separate study, conducted in 1994, concluded that certain types of brain injury may occur entirely separately from the childbirth process. Grafe: The Correlation of Prenatal Brain Damage with Placental Pathology. J Neuro Exper Neurol 1994; 53:407-415.

Other research has shown that fetuses carrying the factor V Leiden mutation suffer a propensity to death and placental infarction. A case study of eight children carrying the factor V Leiden mutation who were later diagnosed with cerebral palsy revealed the following conditions in varying combination: fetal distress, intrauterine growth restriction, low birth weight, neonatal seizures, respiratory problems, and a diagnosis of birth asphyxia. Lynch, Nelson, Curry, Grether: Cerebrovascular Disorders in Children With the Facor V Leiden Mutation. J Child Neurol 2001; 16:735-744.

The presence of the factor V Leiden mutation in all eight children cannot be dismissed when evaluating the cause of the onset in these, and other, cases. The study's authors noted that the V Leiden mutation should be considered in the evaluation of children with a stroke or its sequelae, including infants with perinatal stroke. The quantity and quality of research suggesting that the presence of a maternal coagulation disorder may cause the onset of neurologic damage in children should compel anyone examining such a case to evaluate whether such a disorder may have caused the onset in the case being evaluated.

V Leiden mutation disorders are present in a fairly large number of mothers. For example, the factor V Leiden mutation is the most common hereditary blood coagulation disorder in the United States, present in between 4% and 6% of the population. The mutation produces an abnormal factor V that cannot be destroyed in the bloodstream, leading to excess clotting that ultimately may contribute to the onset of neurologic defects or cerebral palsy in the fetuses of mothers carrying the mutation. While the factor V Leiden mutation likely contributes to many cases of neurologic defects or cerebral palsy it is entirely possible for an individual with the mutation to live a healthy life. A simple blood test, available since 1993, can test for the factor V Leiden mutation.

These studies provide strong evidence that maternal coagulation disorders play a role in causing the onset of neurological disorders and cerebral palsy. Attorneys evaluating the onset of neurologic disorders may take several routes to determine whether a maternal coagulation disorder contributed to such an onset. For one, the attorney may request that the factor V Leiden mutation blood test be performed on the mother and her child to identify whether the maternal anticoagulant disorder is present. There are also specific blood tests that may identify a mother's antithrombin-III deficiency or abnormalities of protein C or protein S that may have been passed to the child. If one of these disorders is identified in a plaintiff then the defense attorney may offer these studies at trial to prove the possibility of an alternative causation.

Of course, an attorney seeking to introduce these studies will be required to do so through the testimony of a hematologist, an obstetrician-gynecologist with a subspecialty in these issues, or a similar expert witness. This expert witness testimony must first establish that the plaintiff herself suffered from one of these maternal coagulation disorders. The expert then must educate the judge and jury, perhaps in a Daubert-type hearing if necessary, as to the scientific literature indicating the role such disorders commonly play in causing cerebral palsy and other neurologic injuries.

Conclusion

The research suggesting that the majority of cerebral palsy cases likely are caused by antepartum factors rather than isolated intrapartum events or trouble arising during the labor or delivery process adds an important component to the evaluation of cases and potential cases involving the onset of neurologic damage and cerebral palsy. The presence of the factor V Leiden mutation and the other maternal coagulation disorders we've discussed are sufficiently common to warrant investigation into whether one of these mutations is at least a contributing cause of the onset of neurologic defects or cerebral palsy.

Attorneys preparing a defense in which alleged negligence during the labor or delivery process potentially caused such neurologic defects or cerebral palsy should investigate whether the mother and/or fetus themselves, rather than physician negligence, actually precipitated such neurologic damage or cerebral palsy. Correspondingly, plaintiffs' attorneys bringing claims against physicians also should be prepared to address whether the client herself contributed to the neurologic damage or, alternatively, whether she was predisposed to the onset of such conditions.

These alternative theories of causation can establish a powerful argument that the defendant's alleged negligence had nothing to do with the outcome. It certainly is worth the time and energy to investigate this developing medical issue fully to see if it has any applicability to your client's case.

Recent research suggests that attorneys evaluating claims involving newborn neurologic damage and cerebral palsy should also be looking at a new potential cause of such conditions. Some research suggests that physiological problems in certain mothers – and perhaps fetuses themselves — actually contribute to neonatal encephalopathy or cerebral palsy that previously would have been assumed to be the result of intrapartum asphyxia, infections, metabolic defects, developmental malformations, or some other cause.

While perinatal asphyxic events and other traditional causes certainly can cause cerebral palsy and other newborn neurologic damage, attorneys handling cases involving such conditions should be aware that new research shows these injuries are often the result of the mother's passing maternal coagulation disorders to the fetus.

Neurologic Damage and Cerebral Palsy

Existing research about the passing of a maternal coagulation disorder to a fetus has focused primarily on such disorders' role in the onset of neurologic damage, especially encephalopathy and cerebral palsy. Encephalopathy, which is a generalized (as opposed to localized) brain dysfunction leading to speech, cognition, and orientation impairment, affects a large number of children born every year. The effects of encephalopathy range from mild instances that may only be identified through neurological testing to severe instances in which the patient may be almost entirely unresponsive.

Cerebral palsy clinically may be defined as a condition involving motor impairment that is secondary to anomalies or lesions of the brain. Although these anomalies or lesions arise in the early stages of the brain's development, it is currently not possible to properly diagnose cerebral palsy in the neonatal period because its symptoms are rarely exhibited by newborns. Because of this, all infants and children – especially those with risk conditions for cerebral palsy (eg intrapartum asphyxia or maternal infection) – are evaluated for delays in attaining developmental milestones to provide early clues to recognizing cerebral palsy. The onset of such developmental delays can give health care professionals clues that a child may suffer from cerebral palsy.

Cerebral palsy occurs in between two and two and a half per every 1000 live births. However, no single cause can be established in a significant portion of these cases. Certain research suggests that between 6% and 8% of cerebral palsy cases are the result of birth asphyxia, while 10% may be attributed to postnatal problems. Prenatal events are currently thought to cause the onset of approximately 75% of all cases of cerebral palsy, although it is often impossible to identify the nature and timing of such events. Those looking for the cause of the onset of cerebral palsy or other neurological defect caused by a prenatal event should look not only at the traditional sources of blame, but also at alternative factors.

New Areas for Investigation

Historically, there has been limited research into the potential neonatal causes of encephalopathy and cerebral palsy because of the incorrect assumption that the majority of such cases resulted primarily from intrapartum asphyxia or other traditionally accepted culprits. Research into the causes of these conditions therefore focused on these occurrences as the primary reason for long-term neurologic defects to the exclusion of others. However, it is becoming clear that perinatal asphyxia or postnatal problems are rarely the sole causes of neonatal encephalopathy or cerebral palsy. Instead, perinatal asphyxia and other traditional causes may be just one step in a longer series of causation events, sometimes along more than one causal pathway, leading to the onset of neonatal encephalopathy or cerebral palsy.

For instance, research suggests that the presence of maternal coagulation disorders (eg, the factor V Leiden mutation, antithrombin-III deficiency, and abnormalities of protein C or protein S) could contribute to the origin of cerebral palsy. These maternal coagulation abnormalities may transmit from a mother to her fetus through the placenta or, in the alternative, the fetus itself may be predisposed to such coagulation disorders.

Such assertions are supported by several studies summarized in a report published by the American College of Obstetricians and Gynecologists' Task Force on Neonatal Encephalopathy and Cerebral Palsy. One such study found that 20 of 31 examined children with cerebral palsy of an unknown cause had at least one coagulation abnormality. Grether, Nelson, Drambosia, Phillips: Interferons and Cerebral Palsy. J Pediatrics 1999, 134:324-332. That study's authors theorized that coagulation disorders, along with intrauterine infection, constitute risk factors for spastic cerebral palsy in children born at or near term. A separate study, conducted in 1994, concluded that certain types of brain injury may occur entirely separately from the childbirth process. Grafe: The Correlation of Prenatal Brain Damage with Placental Pathology. J Neuro Exper Neurol 1994; 53:407-415.

Other research has shown that fetuses carrying the factor V Leiden mutation suffer a propensity to death and placental infarction. A case study of eight children carrying the factor V Leiden mutation who were later diagnosed with cerebral palsy revealed the following conditions in varying combination: fetal distress, intrauterine growth restriction, low birth weight, neonatal seizures, respiratory problems, and a diagnosis of birth asphyxia. Lynch, Nelson, Curry, Grether: Cerebrovascular Disorders in Children With the Facor V Leiden Mutation. J Child Neurol 2001; 16:735-744.

The presence of the factor V Leiden mutation in all eight children cannot be dismissed when evaluating the cause of the onset in these, and other, cases. The study's authors noted that the V Leiden mutation should be considered in the evaluation of children with a stroke or its sequelae, including infants with perinatal stroke. The quantity and quality of research suggesting that the presence of a maternal coagulation disorder may cause the onset of neurologic damage in children should compel anyone examining such a case to evaluate whether such a disorder may have caused the onset in the case being evaluated.

V Leiden mutation disorders are present in a fairly large number of mothers. For example, the factor V Leiden mutation is the most common hereditary blood coagulation disorder in the United States, present in between 4% and 6% of the population. The mutation produces an abnormal factor V that cannot be destroyed in the bloodstream, leading to excess clotting that ultimately may contribute to the onset of neurologic defects or cerebral palsy in the fetuses of mothers carrying the mutation. While the factor V Leiden mutation likely contributes to many cases of neurologic defects or cerebral palsy it is entirely possible for an individual with the mutation to live a healthy life. A simple blood test, available since 1993, can test for the factor V Leiden mutation.

These studies provide strong evidence that maternal coagulation disorders play a role in causing the onset of neurological disorders and cerebral palsy. Attorneys evaluating the onset of neurologic disorders may take several routes to determine whether a maternal coagulation disorder contributed to such an onset. For one, the attorney may request that the factor V Leiden mutation blood test be performed on the mother and her child to identify whether the maternal anticoagulant disorder is present. There are also specific blood tests that may identify a mother's antithrombin-III deficiency or abnormalities of protein C or protein S that may have been passed to the child. If one of these disorders is identified in a plaintiff then the defense attorney may offer these studies at trial to prove the possibility of an alternative causation.

Of course, an attorney seeking to introduce these studies will be required to do so through the testimony of a hematologist, an obstetrician-gynecologist with a subspecialty in these issues, or a similar expert witness. This expert witness testimony must first establish that the plaintiff herself suffered from one of these maternal coagulation disorders. The expert then must educate the judge and jury, perhaps in a Daubert-type hearing if necessary, as to the scientific literature indicating the role such disorders commonly play in causing cerebral palsy and other neurologic injuries.

Conclusion

The research suggesting that the majority of cerebral palsy cases likely are caused by antepartum factors rather than isolated intrapartum events or trouble arising during the labor or delivery process adds an important component to the evaluation of cases and potential cases involving the onset of neurologic damage and cerebral palsy. The presence of the factor V Leiden mutation and the other maternal coagulation disorders we've discussed are sufficiently common to warrant investigation into whether one of these mutations is at least a contributing cause of the onset of neurologic defects or cerebral palsy.

Attorneys preparing a defense in which alleged negligence during the labor or delivery process potentially caused such neurologic defects or cerebral palsy should investigate whether the mother and/or fetus themselves, rather than physician negligence, actually precipitated such neurologic damage or cerebral palsy. Correspondingly, plaintiffs' attorneys bringing claims against physicians also should be prepared to address whether the client herself contributed to the neurologic damage or, alternatively, whether she was predisposed to the onset of such conditions.

These alternative theories of causation can establish a powerful argument that the defendant's alleged negligence had nothing to do with the outcome. It certainly is worth the time and energy to investigate this developing medical issue fully to see if it has any applicability to your client's case.