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Cerebral infarction in young adults.

A B Grindal, R J Cohen, R F Saul and J R Taylor

Stroke. 1978;9:39-42
doi: 10.1161/01.STR.9.1.39
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Copyright © 1978 American Heart Association, Inc. All rights reserved.
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39
Cerebral Infarction in Young Adults
ALAN B. GRINDAL, M.D., ROBERT J. COHEN, M.D.,
ROBERT F. SAUL, M.D, AND JOHN R. TAYLOR, M.D.

SUMMARY The etiologic and prognostic features which tifiable etiology for their cerebral infarction, with nearly half of these
characterize cerebrovascular disease in the later decades of life are suffering from embolic infarction of cardiac origin. In 45% no clear
not applicable in younger patients. The records of 58 patients who etiology could be established but hypertension was prevalent in those
had suffered cerebral infarction between the ages of 15 and 40 were patients between 31 and 40 years of age.
reviewed in order to study these features. Follow up data were obtained on 68% of the hospital survivors;
Fifty-five percent of the patients were found to have had an iden- nearly V* of them had completely recovered or had improved.

CEREBROVASCULAR DISEASE occurs predominately Patient data collected included family history, predispos-
in the later decades of life. However, the occurrence of ing factors, past diseases, history of present neurologic
stroke in young adults is not an insignificant problem. The deficit, and outcome. When available, data were obtained in
annual incidence of stroke in the 35 to 45 age group is es- reference to brain scan, electroencephalogram, cerebral
timated at 25 per 100,000.' Aring and Merritt, 2 in an age in- arteriogram, lumbar puncture, and autopsy findings. On the
cidence tabulation of autopsied cases of cerebrovascular basis of available clinical and laboratory data, patients were
lesions, found that 5% of strokes occur in individuals under placed into one of several etiologic categories.
40. It has been pointed out that this figure relates to necrop- Hypertension was defined as a diastolic pressure greater
sied cases, and that the actual incidence may be greater. 3 than 95 mm Hg. recorded on at least 3 separate occasions
Two large studies of cerebrovascular disease originating during hospitalization. Diabetes mellitus was defined as an
from India4 and Ceylon5 estimate that 27.2% and 32% abnormal glucose tolerance test or an abnormal fasting
respectively of all strokes occur in adults under 40. These blood sugar (greater than 110 mg%). Hyperlipidemia was
findings may not be applicable to other world populations said to exist when serum cholesterol was greater than 270
because of differences in culture, diet, genetics, or other un- mg% or serum triglyceride was greater than 140 mg%.
identified factors. Follow up information regarding course of deficit, func-
The etiologic and prognostic features which characterize tional recovery and recurrence of cerebral infarction was ob-
cerebral infarction among older patients may not be tained either by correspondence or telephone.
applicable to young adults. Because of the relatively low
prevalence of degenerative arterial disease in the young, Results
potentially treatable non-atheromatous conditions may exist
A total of 58 patients fulfilled our criteria. Arteriography
in the young adult with stroke.7 Despite careful investiga-
was performed on 35 patients (60.3%) and autopsy on 3
tion, among young patients many cases of ischemic
(5.2%).
cerebrovascular disease emerge in which the etiology is un-
Table 1 provides a summary of the sex, age, and racial
clear and the role of established risk factors is uncertain.8"12
characteristics of the 58 patients. The number of females
In order to examine these factors, the records of young
was almost equal to the number of males. Over the age of
adults with cerebral infarction who had been hospitalized at
30, males were predominant whereas, between the ages of 21
the Medical College of Virginia hospitals were reviewed.
and 30, females outnumbered the males 10 to 1. The in-
cidence of cerebral infarction was greater in the older age
Methods groups, with nearly % of the patients being over 30 years of
The Medical College of Virginia Hospital is a large urban age. Fifty-seven percent of the patients were Negro and 43%
teaching center with a population of referral as well as com- were Caucasian.
munity care patients. The medical records of all inpatients The causes of cerebral infarction in these patients are
age 15 to 40 with cerebrovascular disease admitted to the summarized in table 2. Fifty-five percent of the patients had
Medical College of Virginia Hospitals between August 1, an identifiable etiology for their cerebral infarction, and of
1970 and July 31, 1975 were reviewed retrospectively. these, nearly one-half were embolic of cardiac origin. The
Patients included in the study had suffered cerebral infarc- majority of these latter patients suffered from rheumatic
tion just prior to admission or while in the hospital. Patients heart disease. Hematologic and inflammatory vascular dis-
with hemorrhagic strokes were not included. If a patient had orders together accounted for 9 cases, and angiographically
more than one cerebral infarct during the period of the demonstrated extracranial vascular disease was present in 4
study, only the first was included. others. Post-partum hypercoagulability and cranial trauma
were each thought to be responsible for 2 cases of cerebral
infarction.
From the Department of Neurology, Medical College of Virginia, 1200 The characteristics of the group of patients in whom no
East Broad St., Richmond, VA 23298.
Reprint requests to Dr. Grindal, Dept. of Neurology, Box 698, MCV Sta-
clear etiology was determined are shown in table 3. Twenty-
tion, Richmond, VA 23298. one of the 26 patients were over the age of 31. Ten of
This paper was presented at the 2nd Joint Meeting on Stroke and Cerebral these 21 were hypertensive and 3 diabetic. None had
Circulation, Miami, FL, Feb. 25, 26, 1977.
This study was supported in part by the Student Clerkship in stroke spon- hyperlipidemia. Of the 5 patients under 31, all were women
sored by the American Heart Association. and 3 of the 5 were taking oral contraceptives. Moreover, of

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40 STROKE VOL 9, No 1, JANUARY-FEBRUARY, 1978

TABLE 1 Population Characteristics TABLE 3 Unknown Etiology Group


Caucasian Negro Caucasian Negro
Age Male Female Male Female Total Age Male Female Male Female Total

15-20 3 1 1 1 6 15-20 0 0 0 1 1
21-25 0 2 0 2 4 21-25 0 1 0 1 2
26-30 1 2 0 4 7 26-30 0 1 0 1 2
31-35 5 1 6 3 15 31-35 2 0 4 3 9
36-40 5 5 9 7 26 36-40 1 3 5 3 12
Total 14 11 16 17 58 Total 3 5 9 9 26

the 8 females under 35 in this group, 5 were taking oral con- creased risk of cerebrovascular disease among women of
traceptives and none of the 5 had any other predisposing fac- childbearing age associated with oral contraceptive use,
tor for stroke. pregnancy, and the puerperium. Among women in Ceylon
Eight patients died during the initial hospitalization. Of age 15 to 45, the majority of ischemic strokes occur during
the remaining 50 patients, follow-up information was ob- pregnancy or the puerperium." Jolly et al. reported that a
tained on 34 (table 4). Mean follow-up was 31 months with a little over half of the young women with cerebral infarction
range of 7 to 69 months. Thirteen (38%) of these patients in their series from India suffered from puerperal venous
were followed for more than 3 years and 4 (12%) for less sinus thrombosis.4 Of our 16 female patients between the
than 1 year. Three patients died during the follow up period. ages of 15 and 35, 2 suffered cerebral infarction in the
All had a cardiac source for the initial cerebral infarct; 1 puerperium and 5 were taking oral contraceptives. None,
suffered a cardiac death and 2 died of recurrent cerebral in- however, experienced venous sinus thrombosis.
farction. Of the 31 survivors, 74% were recovered or im- Levine and Swanson emphasized the frequency of non-
proved and 71% were fully independent functionally. There atheromatous potentially treatable conditions in young
did not appear to be any relationship between sex, age, race, patients.7 Cerebral emboli of cardiac origin was the most
or hypertension and prognosis in these patients. common cause of cerebral ischemia in our study, as well as
Seven of the 34 hospital survivors with follow up informa- in Levine and Swanson's, with more than half the patients
tion had subsequent cerebral ischemic events and 6 of them within this group having rheumatic heart disease. The search
had a clear etiology for the initial event (3 cardiac, 1 inflam- for a cardiac embolic source is important since the value of
matory vascular, 1 hematologic and 1 extracranial athero- anticoagulation in decreasing mortality and preventing
thrombotic disease). Only 1 patient in the unknown category recurrent embolism has been established.14'16
had a recurrent cerebral infarction. A number of hematologic abnormalities including
polycythemia, sickle cell anemia, and coagulation abnor-
malities were found in this study. These disorders are well
Discussion recognized causes of cerebral ischemia in the young adult. 8 ''
Recently, Kalendovsky et al. demonstrated that platelet
The incidence of cerebral infarction was noted to increase
hypercoagulability may underlie many of the strokes in
with age in our young adult population, a finding that has
young patients.16 Unfortunately, special coagulation studies
been observed by others. 6 ' 8"10' " Although there is a male
were not performed on our cases.
predominance in cerebral ischemia after age 40, the sex ratio
Various vasculitides are known to produce focal ischemia.
is equal below this age both in our series, as well as in
In Ford and Siekert's series of 114 patients with periarteritis
others.8' " One explanation for this trend may be an in-
nodosa, 17 13% experienced cerebral infarction or
hemorrhage during the course of their illness. Systemic
TABLE 2 Etiology of Cerebral Infarction lupus erythematosus may involve the central nervous system
in as many as 75% of the cases,18 although as in periarteritis,
Unknown 26
Cardiac it is uncommon for neurologic signs to occur in isolation
15
Rheumatic heart disease with or without without other evidence of systemic disease. The diagnosis of
Atrial fibrillation collagen vascular disease was made prior to the episode of
Atrial fibrillation without rheumatic heart cerebral infarction in 2 of the 3 cases in this study. Other
disease types of cerebral arteritis, such as granulomatous angiitis,
Subacute bacterial endocarditis
Myocardial infarction
Hematologic TABLE 4 Outcome—34 Patients—Si Month Mean FolUwup
Polycythemia
Sickle cell disease 1 Initial deficit
Disseminated intravascular coagulation 1 Completely recovered or improved 23
Thrombocytosis 1 Unchanged 5
Inflammatory 4 Worse 3
Systemic lupus erythematosus 2 Died 3
Periarteritis nodosa 1 Functional recovery in survivors
Syphilis 1 Independent 22
Occlusive extracranial vascular disease 4 Some assistance 7
Post partum 2 Much supervision 1
Trauma 2 Fully dependent 1

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CI IN YOUNG ADULTS/Grindal et al. 41

and that which occurs with rheumatoid arthritis and farction showed progressive improvement of their initial
scleroderma are rare and were not seen in this series. deficit.10 In David's series of patients with cerebral infarc-
Occlusive extracranial vascular disease was found in 4 of tion, in which the mean age was 55 years, only 36 of 67 had
our patients in this study. All were over the age of 35 and, improved after 2 years and only one-half were able to take
except for one, had either hypertension, diabetes or both. It care of themselves.23
appears that premature atheromatous disease was responsi- Seven (21%) of the hospital survivors who were followed
ble for the occlusive process and ischemic symptoms in these up suffered recurrent cerebral infarction during the follow
patients. Two patients, aged 18 and 21, suffered internal up period. Three of these patients had underlying cardiac
carotid artery occlusion following head and neck trauma disease. The probability of recurrence of cerebral embolism
during automobile accidents. Humphrey and Newton,12 in associated with cardiac disease appears to be higher than for
their review of 117 patients under the age of 40 with internal cerebral infarction of any other etiology and partly account
carotid occlusion, reported that trauma was the most fre- for relatively high recurrence rate among our patients.
quent contributing factor and that atherosclerotic involve-
ment in these younger patients was uncommon.
Conclusions
The largest category of patients was that with no clear
etiology for cerebral infarction. Louis and McDowell,8 1) In our series 55% of young adults suffering cerebral in-
reviewed 56 cases of non-embolic cerebral infarction oc- farction had an identifiable etiology for the event; cerebral
curring under the age of 50 and concluded that after the age embolism of cardiac origin appeared to be the most fre-
of 30 cerebral infarction is most likely to be caused by quent cause.
atherosclerosis. Sprofkin and Blakely3 with Berlin et al.10 2) Among our patients suffering cerebral infarction under
also concluded that premature atherosclerosis constitutes an the age of 30, the predominance of females may be partly ex-
important pathogenic factor in the development of cerebral plained by an increased risk of thromboembolic disease
infarction among young adults. The frequency of known associated with the puerperium and oral contraceptive use.
precursors of atherogenesis, such as hypertension and dia- 3) Among our patients 31 to 40 years of age in whom no
betes, were prominent in some studies8-" and uncommon in eitology could be established, hypertension was prevalent
others.*• "• " The majority of patients in our unknown and cerebral infarction presumably resulted from premature
category were hypertensive Negroes aged 31-40. Of the 21 atherosclerotic disease.
patients over age 31, 10 were hypertensive and 3 diabetic. 4) Our study indicated that the prognosis for recovery
Moreover, if the 4 patients with extracranial vascular among young adults suffering cerebral infarction is favor-
occlusive disease were added to this group, we would able. Nearly % of hospital survivors improved and became
presume that atherosclerosis was the primary pathogenic functionally independent.
factor for cerebral infarction in at least 17 patients.
The role of oral contraceptives as a cause oP cerebral in- References
farction in women is controversial. Some studies 19 ' 20 sup-
port the theory that there is an increased risk of thromboem- 1. Report of Joint Committee for Stroke Facilities, I Epidemiology for
Stroke Facilities Planning. Stroke 3: 359-371, 1972
bolic cerebrovascular disease in young women taking birth 2. Aring CD, Merrit HH: Differential diagnosis between cerebral hemor-
control pills, while others21 feel that it is premature to in- rhage and cerebral thrombosis: Clinical and pathological study of 245
criminate these drugs. It is of interest that 5 of the 8 female cases. Arch Intern Med 56: 435-456, 1935
3. Sprofkin BE, Blakely HL: Acute spontaneous cerebral vascular acci-
patients under age 35 in the unknown category were taking dents in young normotensive adults. Arch Intern Med 98: 617-630, 1956
oral contraceptives. None of these 5 had any other 4. Jolly SS et al: Cerebrovascular accidents in young adults, (15-40) Indian
J Med Sci 25: 518-523, 1971
predisposing factor for stroke. These data, however, are not 5. Abraham J, Shefly G, Jose CJ: Strokes in the young. Stroke 2:258-267,
conclusive. 1971
The initial hospital mortality of 14% among our patients 6. Haerer AF, Smith RR: Cerebrovascular disease of young adults in a
Mississippi teaching hospital, Stroke 1: 466-475, 1970
was higher than expected and contrary to reports that acute 7. Levine J, Swanson PD: Non-atherosclerotic causes of stroke. Ann Intern
stroke mortality is less with younger patients.22 These find- Med 70: 807-816, 1969
ings might be explained by the severity of deficit as 8. Louis S, McDowell F: Stroke in young adults. Ann Intern Med 66:
932-938, 1967
evidenced by a disturbed level of consciousness in 7 of the 8 9. Wells CF, Timberger RJ: Cerebral thrombosis in patients under fifty
patients on admission, and the presence of serious concomi- years of age. Arch Neurol 4: 268-271, 1961
10. Berlin L, Tumarkin B, Martin HC: Cerebral thombosis in young adults.
tant disease in most cases. Of the 34 hospital survivors in N Engl J Med 252: 162-166, 1955
whom follow up was obtained, 3 (9%) died during the 31 11. Seneviratne B, Ameratunga B: Strokes in young adults, Br Med J 3:
month mean follow up period. Studies on cerebral throm- 791-793, 1972
12. Humphrey JG, Newton TH: Internal carotid artery occlusion in young
bosis in all age groups report mortality figures of 25-26% adults. Brain 83: 565-578, 1960
after 2 years among patients who survive the initial infarc- 13. Frithz G, Werner I: Stroke before fifty: Experiences from a five year
tion. 2325 The better long term prognosis among younger study. Ups J Med Sci 80: 156-160, 1975
14. Szekely PS: Systemic embolism and anticoagulant prophylaxis in
patients with cerebral infarction has been also noted by rheumatic heart disease. Br Med J 1: 1209-1212, 1964
others.'' 10 15. Wells CE: Cerebral embolus. Arch Neurol Psychiat 81: 667-677, 1959
16. Kalendovksy Z, Austin J, Steele P: Increased platelet aggregability in
The quality of survival also appears to be better among young patients with stroke. Arch Neurol 32: 13-20, 1975
younger patients. Of our hospital survivors who were 17. Ford RG, Siekert RG: Central nervous system manifestations of
followed up nearly % had completely recovered or improved periarteritis nodosa, Neurology (Minneap) 15: 114-122, 1965
18. Johnson RT, Richardson EP: Neurologic manifestations of systemic
and a similar proportion was functionally independent. All lupus erythematosus. Medicine 47: 337-365, 1968
but 1 of Berlin's 13 patients age 18 to 37 with cerebral in- 19. Collaborative Group for the Study of Stroke in Young Women: Oral

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contraceptives and increased risk of cerebral ischemia or thrombosis. N 23. David NJ, Heyman A: Factors influencing the prognosis of cerebral
Engl J Med. 288: 871-878, 1973 thrombosis and infarction due to atherosclerosis. J Chron Dis 11:
20. Masi AT, Dugdale M: Cerebrovascular diseases associated with the use 394^03, 1960
of oral contraceptives, Ann Intern Med 72: 111-120, 1970 24. Lindgren SO: Course and prognosis in spontaneous occlusions of cerebral
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Dilated Episcleral Arteries — A Significant


Physical Finding in Assessment of Patients
With Cerebrovascular Insufficiency
ROGER W. COUNTEE, M.D., A GNANADEV, M.D.,
AND PAMELA CHAVIS, M.D.

SUMMARY Dilated episcleral vessels associated with ipsilateral retrograde flow through markedly enlarged ophthalmic arteries filled
internal carotid artery occlusions have been previously reported in retrograde fashion from dilated external carotid collateral
though not widely appreciated. These ocular changes have been channels in the orbit. This association of dilated episcleral arteries as
presumed to be manifestations of ocular ischemia. The authors have a sign of increased orbital blood flow and the major source of
recently encountered this sign in seven patients and in none was there collateral blood supply to the homolateral cerebral hemisphere has
evidence of ocular ischemia. In addition to an ipsilateral internal not been previously reported. We reemphasize the importance of a
carotid artery occlusion, arteriograms demonstrated that the major careful examination of the episcleral vessels in patients suspected of
source of blood supply to the homolateral cerebral hemisphere was by having internal carotid artery occlusions.

A GREAT VARIETY of ocular signs have been described Jersey, Vetejans Administration Hospital in January, 1977,
in patients with cerebrovascular occlusive disease. Among with a history of several episodes of transient weakness of
these, dilated episcleral vessels associated with ipsilateral his left side for three months prior to his admission. Fre-
carotid artery occlusion, presumably a sign of ocular quently the episodes were accompanied by fleeting sensa-
ischemia, have been previously reported.1'2 This associa- tions of giddiness and on one occasion with a complete loss
tion, however, has not been widely appreciated. The authors of consciousness reported to have lasted 24 hours. The left-
have recently encountered seven instances of internal carotid sided weakness on this occasion is said to have lasted about
artery occlusion associated with ipsilateral dilated episcleral 48 hours. However, the subsequent attacks lasted no more
arteries in six patients in whom no signs of ocular ischemia than a "few minutes" to 2 to 3 hours. The patient was a
were present. In addition, however, angiograms revealed known hypertensive who had had two previous admissions
that the major source of blood to the affected hemispheres for uncontrolled blood pressure elevations.
was by way of markedly dilated ophthalmic arteries filling Upon hospital admission he was found to be generally
retrograde from external carotid orbital collateral channels. healthy but aesthenic with normal blood pressure, mild left-
This ocular sign, we believe, may imply increased orbital sided weakness, and a right carotid bruit. Ophthalmologic
blood flow and, therefore, carries additional physiological examination revealed markedly dilated and tortuous epi-
significance for the clinician in that it emphasizes the impor- scleral vessels in both eyes, which on slit lamp examination
tance of maintaining a patent external carotid artery. proved to be dilated arteries (fig. 1). Fundoscopic and formal
Two representative cases are described. field examinations were normal and vision was correctable
to 20/20 bilaterally. Intraocular pressures were normal.
Case Reports Ophthalmodynamometry pressures were 40/20 in both eyes.
While in the hospital, the patient experienced several fleet-
Case I (H.L.) ing episodes of transient right upper extremity weakness
A 57 year old, right-handed, hypertensive, white male was which often seemed to be related to postural changes.
admitted to the Neurology Service of the East Orange, New However, he reported no frank syncope or giddiness. Aortic
arch angiography with selective catheterization of both com-
mon carotids and the left vertebral arteries demonstrated
From the College of Medicine and Dentistry of New Jersey, New Jersey complete occlusions of both internal carotid arteries and the
Medical School, Newark, NJ, and East Orange Veterans Administration right vertebral artery. There was modest stenosis at the
Hospital, East Orange, NJ.
Reprint requests to Dr. Countee, College of Medicine and Dentistry of NJ,
origins of both external carotid arteries which were
NJ Medical School, Martland Hospital, 65 Bergen St., Newark, NJ 07107. markedly dilated and filled in retrograde fashion the

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