Sodium oxybate for cluster headache. Possible mechanisms of action are as follows
GautamGanguly, Physician, Neurology Consultants Medical Group[email protected]
Submitted August 23, 2011
The paper by Khatami et al. [1] suggested that the possible mechanism of action of sodium oxybate in reduction of cluster headaches is by increasing slow wave sleep (SWS). However, suppression of REM sleep may also be important in preventing cluster headache attacks. Medications with both these properties—like lithium and sodium oxybate—are effective for cluster headache prevention.
Cluster headaches are generated by secondary activation of the trigeminovascular system with secondary recruitment with a marked activation of the grey matter of the hypothalamus. Hypothalamus (the ventrolateral preoptic nucleus) and Pons (the pedunculopontine nucleus) are the main generators of non-REM and REM sleep respectively. Increase in SWS is a result of prolonged VLPO activation which secretes GABA thereby suppressing wake promoting and REM sleep nuclei in the forebrain and pons. This prolonged inhibitory influence from GABA in the hypothalamus may be suppressing the cluster headache generating areas of the hypothalamus and the trigeminal nucleus in the Pons—suppressing the trigeminovascular system—and thereby preventing cluster headache attacks.
References
1. R. Khatami, MD, Tartarotti. S, MD et al. Long term efficacy of sodium oxybate in 4 patients with chronic cluster headache. Neurology 2011;77:67-70.
2.Chervin RD, Zallek SN, Lin X, Hall JM, Sharma N, Hedger KM. Sleep disordered breathing in patients with cluster headache. Neurology 2000;54:2302-2306.
3. Graff-Radford SB, Newman A. Obstructive Sleep Apnea and Cluster Headache. Headache 2004;44:607-610.
The paper by Khatami et al. [1] suggested that the possible mechanism of action of sodium oxybate in reduction of cluster headaches is by increasing slow wave sleep (SWS). However, suppression of REM sleep may also be important in preventing cluster headache attacks. Medications with both these properties—like lithium and sodium oxybate—are effective for cluster headache prevention.
Cluster headaches are generated by secondary activation of the trigeminovascular system with secondary recruitment with a marked activation of the grey matter of the hypothalamus. Hypothalamus (the ventrolateral preoptic nucleus) and Pons (the pedunculopontine nucleus) are the main generators of non-REM and REM sleep respectively. Increase in SWS is a result of prolonged VLPO activation which secretes GABA thereby suppressing wake promoting and REM sleep nuclei in the forebrain and pons. This prolonged inhibitory influence from GABA in the hypothalamus may be suppressing the cluster headache generating areas of the hypothalamus and the trigeminal nucleus in the Pons—suppressing the trigeminovascular system—and thereby preventing cluster headache attacks.
References
1. R. Khatami, MD, Tartarotti. S, MD et al. Long term efficacy of sodium oxybate in 4 patients with chronic cluster headache. Neurology 2011;77:67-70.
2.Chervin RD, Zallek SN, Lin X, Hall JM, Sharma N, Hedger KM. Sleep disordered breathing in patients with cluster headache. Neurology 2000;54:2302-2306.
3. Graff-Radford SB, Newman A. Obstructive Sleep Apnea and Cluster Headache. Headache 2004;44:607-610.