Postictal Serum Creatine Kinase in the Diagnosis of Seizure Disorders

Lueders, Hans; Pippenger, C. E.; VanLente, Frederick

doi:10.1001/archneur.1985.04060020033010

Cited by 76 publications

(50 citation statements)

References 21 publications

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“…91 Other serum measures. Other serum measure studies to differentiate GTC ES from PNES have included the use of elevations in peripheral white blood count, 92 cortisol, 93 creatine kinase, 94 and neuron-specific enolase 95 ; however, there was limited discriminative power of these serological tests in differentiating epilepsy from PNES. 96 Capillary oxygen saturation on pulse oximetry is lower for epilepsy than for PNES.…”

Section: Pnesmentioning

confidence: 99%

Functional Neuroanatomy and Neurophysiology of Functional Neurological Disorders (Conversion Disorder)

Voon¹,

Cavanna²,

Coburn³

et al. 2016

JNP

131

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Much is known regarding the physical characteristics, comorbid symptoms, psychological makeup, and neuropsychological performance of patients with functional neurological disorders (FNDs)/conversion disorders. Gross neurostructural deficits do not account for the patients' deficits or symptoms. This review describes the literature focusing on potential neurobiological (i.e. functional neuroanatomic/neurophysiological) findings among individuals with FND, examining neuroimaging and neurophysiological studies of patients with the various forms of motor and sensory FND. In summary, neural networks and neurophysiologic mechanisms may mediate "functional" symptoms, reflecting neurobiological and intrapsychic processes. J Neuropsychiatry Clin Neurosci 2016; 28:168-190; doi: 10.1176/appi.neuropsych.14090217 Functional neurological disorders (FNDs; or psychogenic neurological symptoms), also known as conversion disorder, are a classic neuropsychiatric disorder, existing in the border between neurology and psychiatry. Unexplained neurological symptoms are common, occurring in up to one-third of patients in neurological outpatient clinics.1 Relative to disorders such as Parkinson's disease, FND is associated with similar levels of disability and physical quality of life with poorer mental health quality of life. 2 The prognosis is poor, with a recent reviewshowing that up to 40% of patients with FND report similar or worse outcomes at 7-year follow-up. 3 Given the frequency, consequences, prognosis, and burden, FND has been called a "crisis for neurology." 4 Despite this, FND is poorly understood. In the last decade, an increasing number of studies have focused on underlying neurobiological mechanisms. FND is defined in DSM-5 as the presence of one or more symptoms of altered voluntary or sensory function, with clinical findings providing evidence of incompatibility between the symptom and recognized neurological or medical conditions.5 The DSM-5 diagnosis differs from that of the DSM-IV diagnosis of conversion disorder by adding the criterion of incorporating physical diagnostic features and by relegating to the accompanying text the criteria requiring (a) an association with psychological stressors and (b) the exclusion of malingering or factitious disorder to make the diagnosis. DSM-5 FND diagnosis criteria now allow for potential greater interrater reliability, making them appropriate for research studies and greater compatibility with specialtyspecific diagnoses including psychogenic movement disorder (PMD) and psychogenic nonepileptic seizures (PNES). 6The putative biopsychosocial mechanisms underlying FND are complex and have been extensively reviewed.7 Our review focuses on the physiological mechanisms that may underlie FND and does not specifically focus on the extensive literature on the antecedents of early childhood experiences and temperament (Figure 1). At the outset, regarding the proposed model, we acknowledge that predisposing factors for functional neurological symptoms are not limited to genetics, te...

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Section: Pnesmentioning

confidence: 99%

Functional Neuroanatomy and Neurophysiology of Functional Neurological Disorders (Conversion Disorder)

Voon¹,

Cavanna²,

Coburn³

et al. 2016

JNP

131

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“…The (3)(4)(5)(6). A correlation between decreased pH and base excess with seizures has been reported in neonates (7).…”

Section: Ammonia Generated In the Gut From Protein Digestion And Deammentioning

confidence: 99%

Hyperammonemia is Associated with Generalized Convulsion

2008

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“…Temporal elevation of serum CPK level is demonstrated in epileptic and nonepileptic seizure patients. It is reported that convulsions produce changes in muscle tissue membranes that persist for three to eight days and result in CPK leakage into plasma and extracellular fluid (13). On the other hand, it is known that activation of inflammation may occur after epileptic seizures without any evidence of systemic or central nervous system infection (14).…”

Section: Discussionmentioning

confidence: 99%