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)