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Chronic paroxysmal hemicrania and cluster.

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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
~
~
~~
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.
Notes and Letters
389
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