and popliteal arteries and similar areas in the left superficial femoral and both profunda femoris arteries. Flow to the lower legs was reduced. Treatment, including right lumbar sympathetic blockade and catheter dilatation of the right superficial femoral and popliteal arteries, restored peripheral pulses and perfusion in three days. Clinical and electromyographic evidence of right common peroneal and tibial neuropathies (presumably ischaemic) persisted. Comment These two patients developed occlusion of major arteries while taking methysergide and parenteral ergotamine for cluster headache. Arteriograms showed arterial spasm and collateral vessels, which are features of ergotism.' These signs have been described in both ergotamine and methysergide toxicity in many areas of the arterial circulation. Thrombosis may also occur.2 Ergotamine is a direct vascular smooth-muscle stimulant.3 Parenteral administration increases potency tenfold through faster and more complete absorption and raises the risk ofarterial spasm.3 Methysergide is a derivative of methylergonovine,3 independently capable of producing arterial spasm.4 Arterial spasm persisted after withdrawal of the drugs in both cases. This is typical of ergotism and presumably represents tissue binding of the drugs, since the half lives of methysergide and ergotamine are only 2-75 and 2 03 hours respectively. Accumulation in tissue also explains the delay between introduction of the drugs and the development of toxicity in these patients. Neither patient was predisposed to ergotism through fever, sepsis, hepatic disease, thyrotoxicosis, or atherosclerosis.3 Flow studies using xenon-133 indicate increased cerebral blood flow during headache.1 Pizotifen, which was also taken by the second patient, is not known to produce arterial spasm. It appears, therefore, that methysergide and parenteral ergotamine together create a particularly high risk of arterial spasm. The combination should be avoided.
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