In re: ‘Experimental Music’

John Cage is universally associated with the phrase experimental music. But what did that phrase mean, for Cage and for Cage’s predecessors? I begin with Cage and Lejaren Hiller, both writing important texts on ‘experimental music’ in 1959. From there, I trace the phrase backwards, eventually reaching Emile Zola, Gertrude Stein, and William James. A final section traces the phrase forward to Cage and Hiller’s collaboration on HPSCHD (1969)

Understanding indeterminate music through performance: Cage’s Solo for piano

This article demonstrates how performance may further understanding of – and offer new perspectives on – indeterminate music, and in particular the ways in which performers realize the indeterminate aspects of the scores. Cage’s Solo for Piano (1957–8), one of the most celebrated indeterminate scores, is used as the model for such an approach. The close involvement that performers have with the score and the music over what is often a prolonged period of time leads to a particular kind of understanding, different from that of nonperformers, which, when articulated, can offer valuable insights. After a brief outline of the score, the article begins by discussing the performances of other pianists, notably David Tudor. It then examines in detail the author’s own approach to making a realization, discussing the implications of such an approach from both practical and aesthetic perspectives

Migraine: Calcium Channels and Glia

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the α1A subunit of the P/Q-type voltage-gated calcium channel