Chronic Paroxysmal Hemicrania and Cluster Seymour Jotkowitz, MD In the February 1978 issue of the Annals, Price and Posner [4] reported a fourth case of chronic paroxysmal hemicrania (CPH). They and the original investigators, Sjaastad and Dale [ 5 ] , stress its distinct temporal profile and pharmacology in distinguishing it from typical cluster headache. The following case may represent a transitional form in that the patient initially had typical cluster and subsequently developed a pattern consistent with CPH. A 41-year-old man was originally seen in 1973 with recurrent headaches occurring in clusters two to three times a year, each lasting four to six weeks. During a cluster he would have one to three headaches per day, each lasting 45 to 60 minutes, typically awakening him from sleep. The headaches were invariably right-sided, mainly right orbital and temporal, and were accompanied by right conjunctival hyperemia and lacrimation and right nasal stuffiness and rhinorrhea. There were never any associated visual or gastrointestinal symptoms. During the attack he would pace the floor. Alcohol invariably triggered a headache during a cluster period. Analgesics, including aspirin, were of no benefit. When originally seen in the midst of a cluster, he had a right ocular Horner syndrome. After 45 minutes, sublingually administered nitroglycerin [I] precipitated a typical headache that was almost immediately relieved by intramuscular ergotamine. Over the subsequent four years he did well on intermittent methysergide and sublingual ergot therapy. In 1977 the headaches seemed to change in temporal profile. They no longer occurred in clusters but remained continuous over many months. T h e frequency increased to “one every three hours, like clockwork.” T h e duration shortened to approximately 20 to 30 minutes. Methysergide and ergot were no longer effective. Inhalation of 100% oxygen remained mildly effective, and aspirin had some benefit. The location of the headache, the associated symptoms, and the severity remained unchanged. At about the time of this apparent transition, the patient had an upper respiratory infection with documented acute maxillary sinusitis and bilateral air-fluid levels. (Prior and subsequent sinus roentgenograms were normal.) Treatment of the respiratory infection with antibiotics and local decongestants, while resolving the sinusitis, did not influence the headaches. I t is of interest that both Horton 121 in cluster headache and Sjaastad and Dale [ 5 ] in C P H noted deterioration during upper respiratory infections Late in 1077 the patient was started on indomethacin, initially 75 and then 150 mg pcr day. O n this regimen h e showed a marked amelioration in the frequency and severity of the headaches ~

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From the Neurology Section, Hackensack Hospital, Hackensack, NJ .

Address reprint requests to Dr Jotkowitz, 90 Prospect Ave, Hackensack, NJ 07601.

O n e can only speculate as to the mechanism of this apparent change. Perhaps the contiguous infection and inflammation altered the reactivity of the symptomatic vascular bed from being primarily responsive to monoaminergic stimuli to prostaglandins. In view of the dramatic clinical response, it may be proper to extend the recommendation set forth by Price and Posner and suggest that patients with otherwise typical cluster headaches who do not respond to the usual therapy b e given a trial of indomethacin. However, in view of the high incidence of peptic ulcer disease [31 in individuals with cluster headache (including our patient), the usual precautions, including administering the dose after meals and perhaps with antacids, should be observed.

References 1. Ekbom K Nitroglycerin as a provocative agent in cluster. Arch

Neurol 19:487-493, 1968 2. Horton BT: Histaminic cephalgia; differential diagnosis and treatment. Proc Mayo Clin 31:325-333, 1956 3. Kudrow J: Prevalence of migraine, peptic ulcer, coronary hearc disease and hypertension in cluster headache. Headache 1666-69, 1976 4. Price RW, Posner JB: Chronic paroxysmal hemicrania: a disabling headache syndrome responding to indomethacin. Ann

Neurol 3:183-184, 1978 5. Sjaastad 0,Dale I: A new (?) clinical headache entity “chronic paroxysmal hemicrania” 2. Acta Neurol Scand 54: 140-159, 1976

Prognosis of Nonoperated Cerebellar Hemorrhage Jerome W. Freeman, MD, Robert M. Kennedy, MD, and Scott S. Petty, MD In their article “Benign Cerebellar Hemorrhages,” Heiman and Satya-Murti [ 11 stress the good functional recovery seen in 2 nonsurgically treated patients with spontaneous cerebellar hemorrhage. T h e following case emphasizes that a “benign” acute phase after cerebellar hemorrhage docs not necessarily anticipate full recovery.

A 59-year-old man experienced the sudden onset of diplopia, vertigo, and inability to walk. Lumbar puncture revealed bloody spinal fluid. When examined initially eight days later, he had marked truncal ataxia, left arm dysmetria, skew deviation of the eyes with spontaneous nystagnus, left sixth nerve palsy, and right face weakness. CAT scan revealed a large midline cerebellar hemorrhage. Because his condition had remained stable over eight days, the From the Department of Neurology, Veterans Administration Hospital, Kansas City, MO, and the University of Kansas Medical Center, Kansas City, KS. Address reprint requests to Dr Freeman, Department of Neurology, the University of Kansas Medical Center, Kansas City, KS 66103.

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