Epileptic Seizures


Marker


Findings/significance


Analysis


Prolactin


Elevated; does not differentiate between epilepsy and syncope


• Serum, 80% vs. 60% (Lusic et al., 1999)


• Serum, 80% (Tumani et al., 1999)


 


Lowered during treatment with anticonvulsants


Serum (Wong et al., 2002)


Creatine kinase


Postictal CK increase, maximum after about 40 h, slow normalization within about 4 days


• Serum (Chesson et al., 1983)


• Serum (Wyllie et al., 1985)


Telencephalin (ICAM-5)


Indicator of temporal lobe dysfunction


Serum (Rieckmann et al., 1998)


NSE (indicator of neuronal damage)


• Increased in CSF and/or serum:


– Status epilepticus


– Epileptic seizure


– Nonconvulsive status epilepticus


• Correlates with seizure duration and outcome


• Serum (Rabinowicz et al., 1995)


• CSF (Correale et al., 1998)


• Serum (Büttner et al., 1999)


• Serum (Tumani et al., 1999)


• Animal model, CSF (Hasegawa et al., 2002)


 


• Unchanged:


– Absence status, febrile seizure (focal > generalized), epileptic seizure


– Epilepsy in children (symptomatic > idiopathic)


• CSF, serum (Shirasaka, 2002)


• CSF, serum (Tanabe et al., 2001)


• CSF (Palmio et al., 2001)


• CSF (Wong et al., 2002)


Hormones (cortisol, ACTH, T3, T4, TSH, LH, FSH, GH)


Postictal increases persist for about 2 h


Motta et al., 2000


 

















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Jun 4, 2016 | Posted by in NEUROLOGY | Comments Off on Epileptic Seizures

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Table 15.2 CSF analysis following the first epileptic seizure: possible causes of the disease and CSF findings

Disease


Typical findings in CSF and/or serum


Meningoencephalitis


Acute inflammatory changes (pleocytosis, barrier dysfunction, synthesis of pathogen-specific antibodies)


Autoimmune encephalitis


Changes suggestive of chronic inflammation (possibly mild pleocytosis, oligoclonal IgG bands)