Kwong-Kum Liao

Inherent fuzzy entropy is an objective measurement of electroencephalography (EEG) complexity, reflecting the robustness of brain systems. In this study, we present a novel application of multi-scale relative inherent fuzzy entropy using repetitive steady-state visual evoked potentials (SSVEPs) to investigate EEG complexity change between two migraine phases, i.e. interictal (baseline) and pre-ictal (before migraine attacks) phases. We used a wearable headband EEG device with O1, Oz, O2 and Fpz electrodes to collect EEG signals from 80 participants (40 migraine patients and 40 healthy controls [HCs]) under the following two conditions: during resting state and SSVEPs with five 15-Hz photic stimuli. We found a significant enhancement in occipital EEG entropy with increasing stimulus times in both HCs and patients in the inter-ictal phase but a reverse trend in patients in the preictal phase. In the 1st SSVEP, occipital EEG entropy of the HCs was significantly lower than that of patents in the preictal phase (FDR-adjusted p < 0.05). Regarding the transitional variance of EEG entropy between the 1st and 5th SSVEPs, patients in the pre-ictal phase exhibited significantly lower values than patients in the inter-ictal phase (FDR-adjusted p < 0.05). Furthermore, in the classification model, the AdaBoost ensemble learning showed an accuracy of 81±6% and AUC of 0.87 for classifying inter-ictal and pre-ictal phases. In contrast, there were no differences in EEG entropy among groups or sessions by using other competing entropy models, including approximate entropy, sample entropy and fuzzy entropy on the same dataset. In conclusion, inherent fuzzy entropy offers novel applications in visual stimulus environments and may have the potential to provide a preictal alert to migraine patients.

Background: Transcranial magnetic stimulation (TMS) is a noninvasive method to assess brain physiology and plasticity. TMS has shown that nervous system excitability may be altered in myopathy, and it presents with motor disinhibition on cortical and subcortical levels. Eight patients who had colchicine myopathy were observed to have fatigue, but they did not have significant weakness. This study investigated whether there was central reorganization to compensate for their muscle strength. Methods: TMS was applied to study the central compensative mechanism. The TMS parameters included motor evoked potentials, central conduction time, cortical silent period and intracortical inhibition of paired TMS paradigms. Results: TMS results did not show any significant differences between patient and control groups. Conclusion: Although central reorganization may occur in patients with hereditary myopathy to compensate for muscular strength, our study did not find any change in cortical excitabilities in acquired myopathy due to colchicine. Muscle fatigue may precede weakness as an early symptom of myopathy.

Fatigue may be induced by drug. Here, we reported that patients had fatigue after medication with colchicines. Eight patients (8 Males, age: 42-72 years old) had fatigue but without weakness as their chief complaints. They all described an inability to maintain a sustained effort, which was ameliorated by rest. The course of fatigue was insidious and progressive (mean 3.1 2.3 months, range 1-7 months) along with medication of colchicines (mean 20.3 5.5 months, range 11-28 months). Fatigue severity scale (patient: before drug withdrawal 5.41 0.19; 4 weeks after drug withdrawal 2.46 0.28; control 2.12 0.45) showed fatigue as their most disabling symptom, sometimes preventing them to carry on professional as well as socio-familial activities. The plasma creatine kinase elevated in these 8 patients before withdrawal of colchicines and returned to normal range in each subject 4 weeks after drug withdrawal. A probable diagnosis of drug-induced fatigue was made when symptom subsided after colchicines were discontinued. It is emphasized that side effect of drug should be considered as a differential diagnosis of fatigue in patients having colchicines. Early recognition and diagnosis will prevent serious muscle damage.

Gabapentin is well known for pain control. Here, we report that gabapentin is a good adjunct for visceral pain in a porphyria patient. A young female was admitted due to acute abdomen. On admission, she was noted to have hyponatremia, tachycardia, and hypertension. Then, she had episodes of seizure and confusion. Gabapentin was prescribed for the control of seizure and pain before the diagnosis of acute intermittent porphyria was confirmed. Seizure did not occur after gabapentin. Pain severity also significantly reduced with visual analogue scale from 10 to 4. The severity of pain rebounded after gabapentin was withdrawn. When the diagnosis was proved, the neurovisceral pain further decreased with combination of morphine and gabapentin and subsided after treatment with hematin. Our report indicates that gabapentin can be considered in porphyria patients, especially when patients had seizures or acute abdomen, when morphine is not available or contraindicated, when abdomen pain transforms as chronic pattern, and when neuropathic pain occurs in extremities.

We investigated the characteristics and correlates of high-frequency oscillations (HFOs) of somatosensory evoked potentials (SEPs). Subjects were 26 healthy volunteers. SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. HFOs were obtained by digitally filtering raw SEPs from 500 to 1000 Hz, and their amplitudes and area-under-curve, duration, and number of negative peaks were measured. We also measured amplitudes of the N20 onset-peak (N20o-p), and N20 peak-P25 peak (N20p-P25p). In normal subjects, several oscillation potentials were observed at the latency of 0 to 10 ms after the onset of N20. The mean number of negative peaks of total HFOs was 6.96 +/- 1.20 (early phase 3.36 +/- 0.62; late phase 3.60 +/- 1.14). The mean maximal amplitude of total HFOs was 0.16 +/- 0.07 microV (early phase 0.14 +/- 0.05 microV; late phase 0.15 +/- 0.07 microV). The mean duration of total HFOs was 10.19 +/- 1.98 ms (early phase 4.89 +/- 1.04 ms; late phase 5.31 +/- 1.95 ms). The mean area of total HFOs was 567.54 +/- 227.86 microV x ms (early phase 268.46 +/- 98.40 microV x ms; late phase 299.08 +/- 183.44 microV x ms). The amplitude ratio was 7.30 +/- 3.32% of HFOearly/N20o-p, 3.19 +/- 1.55% of HFOlate/N20-P25, and 3.54 +/- 1.84% of HFOtotal/N20p-P25. During the test, the amplitude of HFO was significantly reduced by drowsiness. In waking subjects, a burst of low-amplitude HFO can be extracted from the N20.

An 82-year-old woman had a transient ischemic attack and stroke of the left middle cerebral artery syndrome that turned out to be attributed to cryptococcal meningoencephalitis (CM). An initial presentation of central nervous system infection, such as fever and headache, was absent. It was masked by chronic use of corticosteroids and immunosuppressants for her rheumatoid arthritis. The diagnosis was made by the clinical setting of stroke-in-evolution and progression of hydrocephalus on the second brain imaging study. In this case, we discuss the atypical presentation of CM in an immunosuppressed patient and offer a flow chart for early diagnosis, thus improving outcome and survival rates.

A 48-year-old woman suddenly lost consciousness as a result of a right rostral pontine tegmentum haemorrhage. The patient presented with decerebrate rigidity (DR) and regained full consciousness 5 days after the initial onset. The patient was given gabapentin 1200 mg/day nasogastrically and her DR significantly improved, although other antiepileptic drugs such as phenytoin and carbamazepine were given in larger dosages to decrease muscle hypertonicity. The patients’ preserved consciousness and motor-evoked potentials to transcranial magnetic stimulation indicated a derangement of the extrapyramidal tracts with preservation of the pyramidal tracts. This case report discusses the possible mechanisms of action of gabapentin in DR.

A 30-year-old man of Guillain-Barré syndrome (GBS) had atypical descending weakness and history of exposure to expired canned meat, which caused confusion with botulism. His serum showed false-positive botulism type B by the standard mouse bioassay. The diagnosis of axonal GBS was based on clinical and electrophysiological evidence. This report highlights the fact that GBS can present descending weakness and serum false-positive botulism.