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Cyclic vomiting and elevation of creatine kinase associated with bitemporal hypoperfusion and EEG abnormalities: a
J Oki1, A Miyamoto, S Takahashi
1Department of Pediatrics, Asahikawa Medical College, Japan.
Insights
This study presents a case of a 13-year-old boy with recurrent vomiting attacks, diagnosed as migraine equivalent. Phenytoin successfully suppressed these episodes, suggesting a link to temporal lobe vascular abnormalities.
Area of Science:
- Neurology
- Pediatrics
Background:
- A 13-year-old boy with intellectual disability experienced recurrent, prolonged vomiting episodes since infancy.
- These attacks were triggered by infections, exercise, or stress and were associated with behavioral changes and elevated creatine kinase (CK), ACTH, and cortisol levels.
Observation:
- During episodes, the patient exhibited irritability, agitation, and amnesia, without headaches or seizures.
- Electroencephalograms (EEGs) showed frontotemporal delta activity during attacks, and Interictal single-photon emission computed tomography (SPECT) revealed temporal hypoperfusion.
Findings:
- Elevated serum CK levels were attributed to muscle hypertonicity.
- The clinical presentation and neuroimaging findings suggested a paroxysmal vascular abnormality in the temporal regions, mimicking migraine equivalent.
- The condition differed from periodic ACTH-ADH discharge syndrome, lacking hypertension and depression.
Implications:
- The findings highlight the importance of considering migraine equivalent in cases of recurrent vomiting and behavioral changes, especially when distinguishing from focal epilepsy.
- Early consideration of migraine equivalent can guide appropriate treatment, such as phenytoin, to manage these episodes effectively.
Abstract:
A 13-year-old mentally retarded boy suffered from repeated vomiting attacks since infancy. Each episode lasted 2 to 10 days, and was precipitated by respiratory infection, exercise or stress. During an attack he became irritated, agitated and amnesic, but did not have headaches or seizures. Associated findings were transient elevation of serum creatine kinase (CK) (331-3381 IU/l), and of plasma ACTH and cortisol. The raised CK level was the result of muscle hypertonicity. Ictal EEGs showed delta activity in the front-temporal areas, and inter-ictal IMP-SPECT revealed hypoperfusion in both temporal regions. Unlike the periodic ACTH-ADH discharge syndrome, neither hypertension nor depression developed. These attacks were diagnosed as a migraine equivalent and were suppressed with phenytoin. From the EEG and SPECT findings, we concluded that the vomiting and behavioural changes were related to the paroxysmal vascular abnormality in the temporal regions, but it was not easy to make the distinction between migraine and focal epilepsy. Before a diagnosis of the periodic ACTH-ADH discharge syndrome is made, the possibility of migraine equivalent should be considered.