Time-frequency analysis methods to quantify the time-varying microstructure of sleep EEG spindles: possibility for dementia biomarkers?

The time-varying microstructure of sleep EEG spindles may have clinical significance in dementia studies and can be quantified with a number of techniques. In this paper, real and simulated sleep spindles were regarded as AM/FM signals modeled by six parameters that define the instantaneous envelope (IE) and instantaneous frequency (IF) waveforms for a sleep spindle. These parameters were estimated using four different methods, namely the Hilbert transform (HT), complex demodulation (CD), matching pursuit (MP) and wavelet transform (WT). The average error in estimating these parameters was lowest for HT, higher but still less than 10% for CD and MP, and highest (greater than 10%) for WT. The signal distortion induced by the use of a given method was greatest in the case of HT and MP. These two techniques would necessitate the removal of about 0.4s from the spindle data, which is an important limitation for the case of spindles with duration less than 1s. Although the CD method may lead to a higher error than HT and MP, it requires a removal of only about 0.23s of data. An application of this sleep spindle parameterization via the CD method is proposed, in search of efficient EEG-based biomarkers in dementia. Preliminary results indicate that the proposed parameterization may be promising, since it can quantify specific differences in IE and IF characteristics between sleep spindles from dementia subjects and those from aged controls.

A case of refractory secondary paroxysmal kinesigenic dyskinesia with high sensitivity to phenytoin monotherapy.

We report on a 42-year-old man with paroxysmal kinesigenic dyskinesia who was referred as a refractory case to any drug used in the past as monotherapy or in combination. Our decision to discontinue his current combined medication and to administer only high-dose phenytoin led to significant improvement. It is of interest to note that the previous use of phenytoin in combination with other antiepileptic and neuroleptic drugs had no effect. In addition, the co-administration of gabapentin led to a dramatic recurrence of the episodes.

Stimulus-induced bilateral central periodic discharges, cortical myoclonus and arousal responses in mild reversible coma.

OBJECTIVE: To study the association between stimulus-induced periodic epileptiform discharges (PEDs), arousal EEG responses and limb jerking in a comatose patient with reversible viral encephalitis. METHODS: We recorded video EEG in Intensive Care Unit (ICU) for strictly clinical purposes. Back averaging was performed off-line using Neuroscan 4.3. RESULTS: We recorded spontaneous and stimulus-induced bilateral central PEDs (bi-central PEDs) that were followed by phasic vertex potentials, customarily considered as EEG arousal responses. Bi-central PEDs were associated with myoclonus when provoked by strong and protracted stimuli, but remained subclinical when elicited by auditory or mild tactile stimuli. Spontaneous and stimulus-induced bi-central PEDs disappeared after full neurological recovery. CONCLUSION: These findings link stimulus-induced PEDs to epileptic cortical myoclonus, and further suggest that in certain comatose patients they may represent reflex epileptic activity, even when clinically silent. The term "reflex seizures of the critically ill" may be appropriate in such patients. Our findings may also provide a model of the reciprocal relationship between arousals and epileptiform activity. SIGNIFICANCE: Consideration of the possibility that stimulus-induced PEDs are reflexive epileptic phenomena in some comatose ICU patients may rationalise further their acute management, including antiepileptic treatment.

An unusual case of insomnia associated with Whipple encephalopathy: first case reported from Greece.

Whipple disease is a relapsing systemic illness caused by Tropheryma whippelii. Central nervous system involvement occurs in 5%-40% of all patients. Hypothalamic manifestations occur in 31% of Whipple encephalopathy, including polydipsia, hyperphagia, change in libido and insomnia. We report a case of a 48-year-old man with severe insomnia, depression, dementia, dysarthria, myoclonic movements of the limbs and ophthalmoplegia. The diagnosis of Whipple encephalopathy was confirmed by PCR analysis of blood and faeces. He received a full dose of antibiotic treatment. Despite clinical improvement, resolution of the lesions detected in MRI scan of the brain and negative results of the PCR in blood, faeces and cerebrospinal fluid six months later, insomnia persisted and finally subsided after the administration of carbamazepine (600 mg/day). Our case supports the finding that carbamazepine might be useful in the treatment of insomnia associated with Whipple encephalopathy.