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Samuel R. Dominguez - One of the best experts on this subject based on the ideXlab platform.

  • EXPEDITED PUBLICATION PEDIATRICS MRI Findings in Children with Acute Flaccid Paralysis and Cranial Nerve Dysfunction Occurring during the 2014
    2016
    Co-Authors: Enterovirus Doutbreak, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, J. A. Maloney, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in AugustandSeptember2014.During this time, severalpatientspresentedtoour institutionwithacuteflaccidparalysis andcranial nervedysfunction.The purpose of this report is to describe the unique imaging findings of this neurologic syndromeoccurring during an enterovirusD68outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and GrayMatter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis

  • cluster of acute flaccid paralysis and cranial nerve dysfunction in children temporally associated with an enterovirus d68 outbreak in colorado p5 048
    Neurology, 2015
    Co-Authors: Teri Schreiner, Kevin Messacar, John Maloney, Adam Wallace, Jan Ludke, Samuel R. Dominguez
    Abstract:

    OBJECTIVE: To describe a cohort of patients with acute flaccid paralysis and cranial nerve dysfunction. BACKGROUND: Clusters of acute flaccid paralysis (AFP) with cranial nerve dysfunction are uncommon. In August 2014, we identified a cluster of children with AFP and cranial nerve dysfunction temporally associated with an enterovirus D68 (EV-D68) respiratory outbreak. DESIGN/METHODS: A case was defined as any child admitted to Children’s Hospital Colorado after August 1, 2014 with AFP, and/or cranial nerve dysfunction with spinal cord Gray Matter, and/or brainstem lesions on MRI. RESULTS: Thirteen children met the case definition (median age = 10 years; range, 1-18 years; nine male). All had a prodromal febrile illness preceding neurologic symptoms by a median of 7 (range, 3-16) days. Neurologic deficits included flaccid limb weakness (n=9; 6 asymmetric), bulbar weakness (n=7), cranial nerve 6 dysfunction (n=3), and cranial nerve 7 dysfunction (n=2). Eleven had confluent, longitudinally extensive spinal cord lesions of the Central Gray Matter with predominant anterior horn involvement, and ten had brainstem lesions. Eleven children had cerebrospinal fluid pleocytosis. Nasopharyngeal specimens from nine of twelve children tested on admission were positive for rhinovirus/enterovirus by polymerase chain reaction (PCR), of which five were subsequently typed as EV-D68. EV PCR of cerebrospinal fluid, blood, and rectal swabs were negative. Electrophysiologic studies were done on six children. Findings were consistent with motor neuronopathy/motor neuropathy. All 6 children had normal sensory nerve conduction studies. Twelve children have residual deficits to date. CONCLUSIONS: Recovery to date has been poor for this cohort of patients despite treatment with a variety of therapies. Though causality must be proven, this first geographically and temporally defined cluster of AFP and cranial nerve dysfunction in children associated with an outbreak of EV-D68 respiratory illness suggests the possibility of a link between EV-D68 and severe neurologic damage in children. Disclosure: Dr. Schreiner stands to receive personal compensation for activities with Teva Neuroscience. Dr. Messacar has nothing to disclose. Dr. Maloney has nothing to disclose. Dr. Wallace has nothing to disclose. Dr. Ludke has nothing to disclose. Dr. Dominguez has nothing to disclose.

  • mri findings in children with acute flaccid paralysis and cranial nerve dysfunction occurring during the 2014 enterovirus d68 outbreak
    American Journal of Neuroradiology, 2015
    Co-Authors: John Maloney, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in August and September 2014. During this time, several patients presented to our institution with acute flaccid paralysis and cranial nerve dysfunction. The purpose of this report is to describe the unique imaging findings of this neurologic syndrome occurring during an enterovirus D68 outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and Gray Matter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis.

Teri Schreiner - One of the best experts on this subject based on the ideXlab platform.

  • EXPEDITED PUBLICATION PEDIATRICS MRI Findings in Children with Acute Flaccid Paralysis and Cranial Nerve Dysfunction Occurring during the 2014
    2016
    Co-Authors: Enterovirus Doutbreak, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, J. A. Maloney, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in AugustandSeptember2014.During this time, severalpatientspresentedtoour institutionwithacuteflaccidparalysis andcranial nervedysfunction.The purpose of this report is to describe the unique imaging findings of this neurologic syndromeoccurring during an enterovirusD68outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and GrayMatter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis

  • cluster of acute flaccid paralysis and cranial nerve dysfunction in children temporally associated with an enterovirus d68 outbreak in colorado p5 048
    Neurology, 2015
    Co-Authors: Teri Schreiner, Kevin Messacar, John Maloney, Adam Wallace, Jan Ludke, Samuel R. Dominguez
    Abstract:

    OBJECTIVE: To describe a cohort of patients with acute flaccid paralysis and cranial nerve dysfunction. BACKGROUND: Clusters of acute flaccid paralysis (AFP) with cranial nerve dysfunction are uncommon. In August 2014, we identified a cluster of children with AFP and cranial nerve dysfunction temporally associated with an enterovirus D68 (EV-D68) respiratory outbreak. DESIGN/METHODS: A case was defined as any child admitted to Children’s Hospital Colorado after August 1, 2014 with AFP, and/or cranial nerve dysfunction with spinal cord Gray Matter, and/or brainstem lesions on MRI. RESULTS: Thirteen children met the case definition (median age = 10 years; range, 1-18 years; nine male). All had a prodromal febrile illness preceding neurologic symptoms by a median of 7 (range, 3-16) days. Neurologic deficits included flaccid limb weakness (n=9; 6 asymmetric), bulbar weakness (n=7), cranial nerve 6 dysfunction (n=3), and cranial nerve 7 dysfunction (n=2). Eleven had confluent, longitudinally extensive spinal cord lesions of the Central Gray Matter with predominant anterior horn involvement, and ten had brainstem lesions. Eleven children had cerebrospinal fluid pleocytosis. Nasopharyngeal specimens from nine of twelve children tested on admission were positive for rhinovirus/enterovirus by polymerase chain reaction (PCR), of which five were subsequently typed as EV-D68. EV PCR of cerebrospinal fluid, blood, and rectal swabs were negative. Electrophysiologic studies were done on six children. Findings were consistent with motor neuronopathy/motor neuropathy. All 6 children had normal sensory nerve conduction studies. Twelve children have residual deficits to date. CONCLUSIONS: Recovery to date has been poor for this cohort of patients despite treatment with a variety of therapies. Though causality must be proven, this first geographically and temporally defined cluster of AFP and cranial nerve dysfunction in children associated with an outbreak of EV-D68 respiratory illness suggests the possibility of a link between EV-D68 and severe neurologic damage in children. Disclosure: Dr. Schreiner stands to receive personal compensation for activities with Teva Neuroscience. Dr. Messacar has nothing to disclose. Dr. Maloney has nothing to disclose. Dr. Wallace has nothing to disclose. Dr. Ludke has nothing to disclose. Dr. Dominguez has nothing to disclose.

  • mri findings in children with acute flaccid paralysis and cranial nerve dysfunction occurring during the 2014 enterovirus d68 outbreak
    American Journal of Neuroradiology, 2015
    Co-Authors: John Maloney, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in August and September 2014. During this time, several patients presented to our institution with acute flaccid paralysis and cranial nerve dysfunction. The purpose of this report is to describe the unique imaging findings of this neurologic syndrome occurring during an enterovirus D68 outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and Gray Matter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis.

John Maloney - One of the best experts on this subject based on the ideXlab platform.

  • cluster of acute flaccid paralysis and cranial nerve dysfunction in children temporally associated with an enterovirus d68 outbreak in colorado p5 048
    Neurology, 2015
    Co-Authors: Teri Schreiner, Kevin Messacar, John Maloney, Adam Wallace, Jan Ludke, Samuel R. Dominguez
    Abstract:

    OBJECTIVE: To describe a cohort of patients with acute flaccid paralysis and cranial nerve dysfunction. BACKGROUND: Clusters of acute flaccid paralysis (AFP) with cranial nerve dysfunction are uncommon. In August 2014, we identified a cluster of children with AFP and cranial nerve dysfunction temporally associated with an enterovirus D68 (EV-D68) respiratory outbreak. DESIGN/METHODS: A case was defined as any child admitted to Children’s Hospital Colorado after August 1, 2014 with AFP, and/or cranial nerve dysfunction with spinal cord Gray Matter, and/or brainstem lesions on MRI. RESULTS: Thirteen children met the case definition (median age = 10 years; range, 1-18 years; nine male). All had a prodromal febrile illness preceding neurologic symptoms by a median of 7 (range, 3-16) days. Neurologic deficits included flaccid limb weakness (n=9; 6 asymmetric), bulbar weakness (n=7), cranial nerve 6 dysfunction (n=3), and cranial nerve 7 dysfunction (n=2). Eleven had confluent, longitudinally extensive spinal cord lesions of the Central Gray Matter with predominant anterior horn involvement, and ten had brainstem lesions. Eleven children had cerebrospinal fluid pleocytosis. Nasopharyngeal specimens from nine of twelve children tested on admission were positive for rhinovirus/enterovirus by polymerase chain reaction (PCR), of which five were subsequently typed as EV-D68. EV PCR of cerebrospinal fluid, blood, and rectal swabs were negative. Electrophysiologic studies were done on six children. Findings were consistent with motor neuronopathy/motor neuropathy. All 6 children had normal sensory nerve conduction studies. Twelve children have residual deficits to date. CONCLUSIONS: Recovery to date has been poor for this cohort of patients despite treatment with a variety of therapies. Though causality must be proven, this first geographically and temporally defined cluster of AFP and cranial nerve dysfunction in children associated with an outbreak of EV-D68 respiratory illness suggests the possibility of a link between EV-D68 and severe neurologic damage in children. Disclosure: Dr. Schreiner stands to receive personal compensation for activities with Teva Neuroscience. Dr. Messacar has nothing to disclose. Dr. Maloney has nothing to disclose. Dr. Wallace has nothing to disclose. Dr. Ludke has nothing to disclose. Dr. Dominguez has nothing to disclose.

  • mri findings in children with acute flaccid paralysis and cranial nerve dysfunction occurring during the 2014 enterovirus d68 outbreak
    American Journal of Neuroradiology, 2015
    Co-Authors: John Maloney, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in August and September 2014. During this time, several patients presented to our institution with acute flaccid paralysis and cranial nerve dysfunction. The purpose of this report is to describe the unique imaging findings of this neurologic syndrome occurring during an enterovirus D68 outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and Gray Matter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis.

Nicholas V Stence - One of the best experts on this subject based on the ideXlab platform.

  • EXPEDITED PUBLICATION PEDIATRICS MRI Findings in Children with Acute Flaccid Paralysis and Cranial Nerve Dysfunction Occurring during the 2014
    2016
    Co-Authors: Enterovirus Doutbreak, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, J. A. Maloney, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in AugustandSeptember2014.During this time, severalpatientspresentedtoour institutionwithacuteflaccidparalysis andcranial nervedysfunction.The purpose of this report is to describe the unique imaging findings of this neurologic syndromeoccurring during an enterovirusD68outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and GrayMatter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis

  • mri findings in children with acute flaccid paralysis and cranial nerve dysfunction occurring during the 2014 enterovirus d68 outbreak
    American Journal of Neuroradiology, 2015
    Co-Authors: John Maloney, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in August and September 2014. During this time, several patients presented to our institution with acute flaccid paralysis and cranial nerve dysfunction. The purpose of this report is to describe the unique imaging findings of this neurologic syndrome occurring during an enterovirus D68 outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and Gray Matter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis.

Kevin Messacar - One of the best experts on this subject based on the ideXlab platform.

  • EXPEDITED PUBLICATION PEDIATRICS MRI Findings in Children with Acute Flaccid Paralysis and Cranial Nerve Dysfunction Occurring during the 2014
    2016
    Co-Authors: Enterovirus Doutbreak, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, J. A. Maloney, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in AugustandSeptember2014.During this time, severalpatientspresentedtoour institutionwithacuteflaccidparalysis andcranial nervedysfunction.The purpose of this report is to describe the unique imaging findings of this neurologic syndromeoccurring during an enterovirusD68outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and GrayMatter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis

  • cluster of acute flaccid paralysis and cranial nerve dysfunction in children temporally associated with an enterovirus d68 outbreak in colorado p5 048
    Neurology, 2015
    Co-Authors: Teri Schreiner, Kevin Messacar, John Maloney, Adam Wallace, Jan Ludke, Samuel R. Dominguez
    Abstract:

    OBJECTIVE: To describe a cohort of patients with acute flaccid paralysis and cranial nerve dysfunction. BACKGROUND: Clusters of acute flaccid paralysis (AFP) with cranial nerve dysfunction are uncommon. In August 2014, we identified a cluster of children with AFP and cranial nerve dysfunction temporally associated with an enterovirus D68 (EV-D68) respiratory outbreak. DESIGN/METHODS: A case was defined as any child admitted to Children’s Hospital Colorado after August 1, 2014 with AFP, and/or cranial nerve dysfunction with spinal cord Gray Matter, and/or brainstem lesions on MRI. RESULTS: Thirteen children met the case definition (median age = 10 years; range, 1-18 years; nine male). All had a prodromal febrile illness preceding neurologic symptoms by a median of 7 (range, 3-16) days. Neurologic deficits included flaccid limb weakness (n=9; 6 asymmetric), bulbar weakness (n=7), cranial nerve 6 dysfunction (n=3), and cranial nerve 7 dysfunction (n=2). Eleven had confluent, longitudinally extensive spinal cord lesions of the Central Gray Matter with predominant anterior horn involvement, and ten had brainstem lesions. Eleven children had cerebrospinal fluid pleocytosis. Nasopharyngeal specimens from nine of twelve children tested on admission were positive for rhinovirus/enterovirus by polymerase chain reaction (PCR), of which five were subsequently typed as EV-D68. EV PCR of cerebrospinal fluid, blood, and rectal swabs were negative. Electrophysiologic studies were done on six children. Findings were consistent with motor neuronopathy/motor neuropathy. All 6 children had normal sensory nerve conduction studies. Twelve children have residual deficits to date. CONCLUSIONS: Recovery to date has been poor for this cohort of patients despite treatment with a variety of therapies. Though causality must be proven, this first geographically and temporally defined cluster of AFP and cranial nerve dysfunction in children associated with an outbreak of EV-D68 respiratory illness suggests the possibility of a link between EV-D68 and severe neurologic damage in children. Disclosure: Dr. Schreiner stands to receive personal compensation for activities with Teva Neuroscience. Dr. Messacar has nothing to disclose. Dr. Maloney has nothing to disclose. Dr. Wallace has nothing to disclose. Dr. Ludke has nothing to disclose. Dr. Dominguez has nothing to disclose.

  • mri findings in children with acute flaccid paralysis and cranial nerve dysfunction occurring during the 2014 enterovirus d68 outbreak
    American Journal of Neuroradiology, 2015
    Co-Authors: John Maloney, Kevin Messacar, Samuel R. Dominguez, David M Mirsky, Teri Schreiner, Nicholas V Stence
    Abstract:

    BACKGROUND AND PURPOSE: Enterovirus D68 was responsible for widespread outbreaks of respiratory illness throughout the United States in August and September 2014. During this time, several patients presented to our institution with acute flaccid paralysis and cranial nerve dysfunction. The purpose of this report is to describe the unique imaging findings of this neurologic syndrome occurring during an enterovirus D68 outbreak. MATERIALS AND METHODS: Patients meeting a specific case definition of acute flaccid paralysis and/or cranial nerve dysfunction and presenting to our institution during the study period were included. All patients underwent routine MR imaging of the brain and/or spinal cord, including multiplanar T1, T2, and contrast-enhanced T1-weighted imaging. RESULTS: Eleven patients met the inclusion criteria and underwent MR imaging of the brain and/or spinal cord. Nine patients presented with brain stem lesions, most commonly involving the pontine tegmentum, with bilateral facial nerve enhancement in 1 patient. Ten patients had longitudinally extensive spinal cord lesions; those imaged acutely demonstrated involvement of the entire Central Gray Matter, and those imaged subacutely showed lesions restricted to the anterior horn cells. Ventral cauda equina nerve roots enhanced in 4 patients, and ventral cervical nerve roots enhanced in 3, both only in the subacute setting. CONCLUSIONS: Patients presenting with acute flaccid paralysis and/or cranial nerve dysfunction during the recent enterovirus D68 outbreak demonstrate unique imaging findings characterized by brain stem and Gray Matter spinal cord lesions, similar to the neuroimaging findings described in previous outbreaks of viral myelitis such as enterovirus 71 and poliomyelitis.