pressure ischemia and not to the specific effects of carbon monoxide."1 In a review, Penn et al proposed a similar cause for muscle necrosis in a variety of drug-induced comas inde¬ pendent of any specific myopathie effect of the drug.-' Our patient had no areas of red, blistered, or necrotic skin, ecchymoses, or tenderness from

tight compartmental swelling—signs and



seen with described in the

most often



Although no seizures were observed, no signs of prior seizure activity were present, and no epilep¬ togenic foci were seen on subsequent EEG tracings, prior hypoxic-induced literature.

convulsions cannot be excluded. Ma¬

jor-motor seizures can be followed by myalgia, but usually only by eleva¬ tions in the are


CPK level, which

considerably less than 100,000

IU/L. Most

probably, the patient was subjected to CO intoxication followed by hypoxia from methane inhalation. It is my belief that the


of his

myoglobinuria was a generalized, COinduced rhabdomyolysis.

John Slevin, MD Department of Neurology University of Virginia School of Medicine Charlottesville, VA 22908

1. Adams RD, Denny-Brown D, Pearson CM: Diseases of Muscle, ed 2. New York, Paul Hoeber Inc, 1962. 2. Penn AS, Rowland LP, Fraser DW: Drugs, coma and myoglobinuria. Arch Neurol 26:336\x=req-\ 343, 1972.


Voluntary Nystagmus

To the Editor.\p=m-\Wehave studied a patient with unusual voluntary nystagmus characterized by exceptionally long duration.

Report of a Case.\p=m-\A 23-year-old engineer produce nystagmus at will. He had possessed this unusual ability ever since he could

could remember and he had never needed to practice either to learn or to maintain it. Neither his parents, his grandparents, nor his siblings could produce nystagmus voluntarily. Visual acuity was right 20/20, left 16/20. Fundi were normal. The pupils were normal and reacted promptly to light and to accommodation. Convergence was normal. He had slight strabismus, convergent and sursumvergent. There was no spontaneous horizontal nystagmus, except that when the patient was excited fine horizontal spontaneous nystagmus appeared on forward gaze. Hearing and caloric-induced nystagmus were normal. There were no other neurological abnormalities. He could initiate and terminate nystagmus voluntarily at any time, with eyes opened, closed, or covered. The nystagmus was jerking and at a frequency of 3.5 to 4.5 cps. The patient could sustain it as long as

he wished and was only slightly tired after an hour's continuation. Optokinetic nys¬ tagmus was present and showed the partial inversion that is often observed in congen¬ ital nystagmus. Results of eye tracking showed almost smooth pursuit and was considered normal. Comment.—There have been at least 100 reports on voluntary nystagmus

Although the mean age of AcostaRua's patients was 48 years, the mean age of patients with familial aneurysm is probably ten to 15 years less than that of nonfamilial patients (mean age of 39 years, compared with 52 years for patients with aneurysm in general).3,4,6 Regarding location, two earlier reviews of familial aneurysms2,4 have shown anterior communicating artery

ment of the

half as frequently in familial cases as in cases of aneurysm in general (15% vs 30%). In siblings, identical-site aneurysms (eg, left internal carotid\p=m-\ posterior communicating junction in both cases) and mirror-image aneu¬ rysms (ie, side of occurrence ignored) are twice as common as in pairs of patients with aneurysm randomly selected from a general aneurysm

published since Williams first re¬ ported it in 1865.' Voluntary nystag¬ mus is usually described as being a high frequency, low amplitude move¬ eyes.2 The duration is 3

brief, being limited by fatigue. Usual¬ ly, the patient can sustain it for no longer than 30 s. Unusual variations have been reported, but there have been none of long duration. In addi¬ tion, the amplitude at 20° to 30° is quite large, and the frequency is somewhat lower than usual. Ordinary voluntary nystagmus is said to be composed of normal saccades,4 but the mechanism is poorly understood. Be¬

the nystagmus is similar to congenital nystagmus of the jerking type, we believe that this patient has a latent congenital nystagmus com¬ pounded by an inherent ability to produce voluntary nystagmus. This opinion is supported by the inversion of optokinetic nystagmus. cause

KUNIO Takahashi, MD Department of Neurosurgery Juntendo University School of Medicine

Tokyo Eiji Sakata, MD Department of Neurotology Saitama Medical School

Saitama, Japan Kimitaka Kaga, MD Department of Otorhinolaryngology Teikyo University School of Medicine


1. Williams HW, quoted by Luhr AF, Eckel JL: Fixation and voluntary nystagmus. Arch Ophthalmol 9:625-634, 1933. 2. Blair CJ, Goldberg MF, Von Noorden GK: Voluntary nystagmus. Arch Ophthalmol 77:349\x=req-\ 354, 1967. 3. Blumenthal H: Voluntary nystagmus. Neurology 23:223-225, 1973. 4. Shults WT, Stark L, Hoyt WF, et al: Normal saccadic structure of voluntary nystagmus. Arch

Ophthalmol 95:1399-1404,


Familial Intracranial


To the Editor.\p=m-\DrAcosta-Rua's article on familial intracranial aneurysms

(Archives 35:675-677, 1978) indicates the value of

family history in the of intracranial aneurysms.1-4 Several points may be made. The prevalence of hypertension in cases of familial aneurysm is not known. The notion that long-standing hypertension is present in the majority of patients with aneurysm seems to be unsupported.5 assessment

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aneurysms to



population.48 Possibly characteristic features of

gross7 and fine8

aneurysms have

structure of familial yet to be explored.

The implications for management could be important. If more observers would report cases of familial aneurysm, statistical analyses could be used, as has been done in the classic Cooperative Study." Dr Acosta-Rua's final comment with regard to cerebral angiography in symptomatic relatives of patients with subarachnoid hemorrhage may prove valuable. Observers have also suggested that angiography in a symptomatic relative (particularly a sibling) of a patient with aneurysm (especially one in the late 20s to early

40s) might permit diagnosis prior rupture.4·9


Andrews, MD Department of Surgery Walter Reed Army Medical Center Washington, DC 20012 R. J.

1. Jain KK: Familial intracranial aneurysms: Review of literature and presentation of six new cases. Acta Neurochir 30:129-137, 1974. 2. Sakai N, Sakata K, Yamada H, et al: Familial occurrence of intracranial aneurysms. Surg Neurol 2:25-29, 1974. 3. Hashimoto I: Familial intracranial aneurysms and cerebral vascular anomalies. J Neurosurg 46:419-427, 1977. 4. Andrews RJ: Intracranial aneurysms: Characteristics of aneurysms in siblings. New Engl J Med 297:115, 1977. 5. McCormick WF, Schmalstieg EJ: The relationship of arterial hypertension to intracranial aneurysms. Arch Neurol 34:285-287, 1977. 6. Sahs AL, Perret G, Locksley HB, et al (eds): Intracranial Aneurysms and Subarachnoid Hemorrhage: A Cooperative Study. Philadelphia, JB Lippincott Co, 1969. 7. du Boulay GH: The significance of loculation of intracranial aneurysms. Bull Schweiz Akad Med Wiss 24:480-486, 1968. 8. Stehbens WE: Ultrastructure of aneurysms. Arch Neurol 32:798-807, 1975. 9. Wilson PJE, Cast IP: "Twin" intracranial aneurysms. Br Med J 1:484, 1973.

Familial intracranial aneurysms.

pressure ischemia and not to the specific effects of carbon monoxide."1 In a review, Penn et al proposed a similar cause for muscle necrosis in a vari...
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