Neurophysiological investigation of idiopathic acquired auditory-visual synesthesia.

We present a case of acquired auditory-visual synesthesia and its neurophysiological investigation in a healthy 42-year-old woman. She started experiencing persistent positive and intermittent negative visual phenomena at age 37 followed by auditory-visual synesthesia. Her neurophysiological investigation included video-EEG, fMRI, and MEG. Auditory stimuli (700 Hz, 50 ms duration, 0.5 s ISI) were presented binaurally at 60 db above the hearing threshold in a dark room. The patient had bilateral symmetrical auditory-evoked neuromagnetic responses followed by an occipital-evoked field 16.3 ms later. The activation of occipital cortex following auditory stimuli may represent recruitment of existing cross-modal sensory pathways.

Acquired auditory-visual synesthesia: A window to early cross-modal sensory interactions.

Synesthesia is experienced when sensory stimulation of one sensory modality elicits an involuntary sensation in another sensory modality. Auditory-visual synesthesia occurs when auditory stimuli elicit visual sensations. It has developmental, induced and acquired varieties. The acquired variety has been reported in association with deafferentation of the visual system as well as temporal lobe pathology with intact visual pathways. The induced variety has been reported in experimental and post-surgical blindfolding, as well as intake of hallucinogenic or psychedelics. Although in humans there is no known anatomical pathway connecting auditory areas to primary and/or early visual association areas, there is imaging and neurophysiologic evidence to the presence of early cross modal interactions between the auditory and visual sensory pathways. Synesthesia may be a window of opportunity to study these cross modal interactions. Here we review the existing literature in the acquired and induced auditory-visual synesthesias and discuss the possible neural mechanisms.

Long-term tolerability of lamotrigine: data from a 6-year continuation study.

This open-label, 6-year continuation study of several short-term clinical trials was conducted to assess the long-term tolerability and efficacy of lamotrigine when used as adjunctive therapy or monotherapy for partial seizures in adult patients (> or =16 years) with epilepsy. Study visits occurred every 24 weeks throughout the treatment period. Of the 527 patients enrolled in the long-term continuation study, 508 were exposed to lamotrigine for at least 6 months (including their exposure in the primary clinical study), and 248 were exposed to lamotrigine for at least 5 years. Of the 527 patients, 75 received initial lamotrigine exposure during this study. Investigators judged that overall clinical status at the end of the study or at time of discontinuation (whichever occurred first) was improved moderately or markedly relative to prelamotrigine clinical status for 36% of patients. The most common treatment-emergent adverse events (regardless of suspected cause) were dizziness, diplopia, and headache. The only serious treatment-emergent adverse event occurring at a frequency exceeding 2% was accidental injury (2.7% of patients). Adverse events prompted 28 patients to discontinue from the study. The most common adverse events leading to discontinuation were dizziness (1.3%), headache (0.8%), rash (0.8%), and somnolence (0.6%). All adverse events resolved without sequelae. Lamotrigine administered as monotherapy or adjunctive therapy during a 6-year open-label continuation study was associated with a low incidence of adverse events in adult patients with epilepsy.

McArdle's disease presenting as recurrent cryptogenic renal failure due to occult seizures.

Myophosphorylase deficiency (McArdle's disease) may present with episodic renal failure following exertion. We present a case of adult-onset myophosphorylase deficiency in which recurrent bouts of renal failure could not be associated with any exertional events until a tonic seizure was witnessed after the fourth episode of renal failure. In the absence of a clear exertional cause for myoglobinuria, an occult seizure disorder should be suspected.