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Bilateral carotid artery occlusion resulting from giant cell arteritis.

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Before the availability of C T and cranial ultrasound,
the extent of IVH and hydrocephalus among affected
neonates who survived was unknown, and the assessment of prognosis could not be made accurately.
Nevertheless, the prognosis for surviving children with
PHHC was thought to be poor. Published reports of
long-term outcome for such children have been scarce
{47, although a few have described a favorable shortterm outcome C2, 91.
In 1980, Chaplin and colleagues 141 described the
long-term neurodevelopmental outcome in a cohort of
20 survivors with PHHC. They found that 40% of
their subjects had significant motor deficits and that
only 33% had normal IQ scores (higher than 85). In
contrast, most of our subjects demonstrated a good
outcome for motor functions; all were ambulatory;
only one child had moderate motor impairment resulting from spastic diplegia. Moreover, most of our children showed normal intellectual development with
better IQ scores than those reported by Chaplin and
colleagues. The discrepancies in outcome might pertain
in part to differences in the severity of IVH between
our group and Chaplin's (severity was not documented
in Chaplin's report). The extent of IVH as indicated by
neonatal CT scans seems to be a useful prognostic indicator, with the presence of Grade I1 IVH on CT scan,
even with the development of PHHC, carrying a good
probability for normal neurodevelopmental outcome.
In our study, children with normal results on
neuromotor examinations also had higher IQ scores.
Except for short attention span and strabismus, these
children generally were free of other abnormalities. As
anticipated, children with minor and moderate motor
disabilities had lower I Q scores, short attention span,
speech and language impairment, and perceptual and
visual motor problems.
We found no significant difference in neurological
morbidity between the shunt and nonshunt group. On
the contrary, even children who required shunting
(presumably those more severely affected as a result of
progressive hydrocephalus) have done well. Nevertheless, the functional importance of minor motor dysfunctions, as well as the observed perceptual and attentional problems, should not be underestimated, as they
may lead to future academic failure and social
difficulties. More definitive predictions about the potential social and vocational outcome of this cohort can
be made only after further follow-up of a larger group
of affected children.
References
1. Ahmann PA, Lazzara A, Dykes FD, et al: Intraventricular
hemorrhage in the high-risk preterm infant: incidence and outcome. Ann Neurol 7:118-124, 1980
2. Bada HS, Salmon JH, Pearson DH: Early surgical intervention
in post-hemorrhagic hydrocephalus. Child's Brain 5: 109-1 13,
1979
204
3. Bayley N: Bayley Scales of Lfant Development Manual. New
York, Psychological Corp, 1969
4. Chaplin ER, Goldstein AW, Meyerberg DZ: Post-hemorrhagic
5.
6
7
8
9
10
hydrocephalus in the preterm infant. Pediatrics 65901-909,
1980
Krishnamoorthy KS, Shannon DC, DeLong GR, et al:
Neurologic sequelae in survivors of neonatal intraventricular
hemorrhage. Pediatrics 64:233-237, 1979
McCarthy D: McCarthy Scales of Children's Abilities Manual.
New York, Psychological Corp, 1972
Paine RS, Oppe TE (eds): Neurological Examination of Children. Clinics in Developmental Medicine, Nos 21, 22. London,
Spastics Society with Heinemann, 1966
Papille LA, Burstein J, Burstein R, Koffler H: Incidence and
evolution of subependymd and intraventricular hemorrhage. A
study of infants with birthweight less than 1500 gms. J Pediatr
92:529-534, 1978
Shankaran S, Slovis TL, Bedard MP, Poland RL:Sonographic
classification of intracranial hemorrhage. A prognostic indicator
of mortality, morbidity, and short-term neurologic outcome. J
Pediatr 100:469-475, 1982
Tarby TJ, Volpe JJ: Intraventricular hemorrhage in the premature infant. Pediatr Clin North Am 29:1077-1104, 1982
Bilateral Carotid Artery
Occlusion Resultinn from
Giant Cell Arteriti;
George F. Howard 111, MD,"? Sam U. Ho, MD,"
Kwang S. Kim, MD,S and Jami Wallach, MDS
~
~
~
~~~~~
A 65-year-old woman with subacute global deterioration
of neurological function had bilateral occlusion of the
internal carotid arteries demonstrated by angiography.
Postmortem examination showed isolated giant cell arteritis involving the carotid siphon bilaterally.
Howard GF 111, Ho SU, IQm KS, Wallach J
Bilateral carotid artery occlusion resulting from
giant cell arteritis. Ann Neurol 15:204-207, 1984
Clinical involvement of the internal carotid artery in
giant cell arteritis (GCA) is rare. In most large series
the incidence of stroke resulting from GCA confirmed
postmortem is less than 357 13-5, 7 ) . Most strokes
attributed to GCA are referable to the vertebrobasilar
circulation, and almost never are they the initial manifestation of the disease. We report here a patient with
From the Departments of *Neurology, $Radiology, and 4Pathology,
Northwestern University Medical School, Chicago, IL 606 1 1.
tPresent address: Department of Neurology, Boston Universii:y
School of Medicine, Boston, MA 02 118.
Received Apr 5, 1983, and in revised form Aug 2. Accepted for
publication Aug 3, 1983.
Address reprint requests to D r Ho, Departmenr o f Neurology, 103
E Chicago Ave, Chicago, IL 6061 1.
GCA who showed bilateral occlusion of the internal
carotid artery (ICA) as initial symptoms.
Case Report
A 65-year-old woman with chronic paranoid schizophrenia
developed left arm and facial weakness. She had not had
hypertension, heart disease, or diabetes and did not smoke or
drink. She had not complained of headache, visual disturbance, muscle aches, or weight loss. She was receiving
haloperidol 2.5 mg at bedtime and trihexyphenidyl 2 mg
twice a day.
About ten days prior to her hospital admission, her daughter observed difficulty in walking, slowness of speech, and
neglect of personal hygiene in the patient. Several days later a
neurologist noted dementia and rigidity, and scheduled hospital admission. The following morning her daughter noticed
the sudden onset of left facial drooping, left-sided weakness,
and slurring of speech.
H e r blood pressure was 140/90 mm Hg, pulse 76, and
temperature 37.6”C. She was oriented except for the exact
date. She was able to name the past three presidents and
mayors but was unable to calculate or remember three objects. Perseveration was noted. There was a gaze preference
to the right and facial weakness on the left. Oral-lingual dyskinesias were present. Paratonic rigidity was found in all
limbs. There was little spontaneous movement, but with
stimulation she moved her right side better than her left.
Muscle stretch reflexes were exaggerated, more so on the
right. Grasp, snout, and suck reflexes could be elicited, and
Babinski’s sign was present bilaterally. There were no arterial
bruits or prominence of the temporal arteries. Within two
days her gaze preference and focal weakness subsided, but
she remained demented and apathetic.
The following were normal: complete blood count, results
of blood chemistries and VDRL testing, prothrombin time,
partial thromboplastin time, platelet count, thyroxin, Biz, and
folate levels, and results of urinalysis, electrocardiography,
chest roentgenography, computed tomographic scanning of
the brain with contrast infusion, and spinal fluid examination.
O n the seventh day of hospitalization, the patient became
briefly unresponsive and developed slurred speech. In the
next three to four days, she was lethargic and unable to eat.
She startled easily and showed occasional myoclonic jerks.
Westergren sedimentation rate was 67 mm per hour. Results
of antinuclear antibody testing were normal, and serum protein electrophoresis showed no abnormalities except hypoalbuminemia.
She remained apathetic, hypokinetic, and verbally quiet
over the next three weeks. On day 30 she suddenly became
less responsive and developed a right facial droop. A computed tomographic scan for the first time showed multiple
areas of infarction bilaterally, more on the right. O n day 33
cerebral angiography was performed. Shortly afterward the
patient developed signs of right temporal lobe herniation and
she died 18 hours later.
Radiological Findings
Both common carotid arteries were normal. Two centimeters
distal to its origin, the right ICA tapered to a complete occlusion. The left ICA was markedly narrowed and occluded 1.5
cm distal to its origin. The left vertebral and basilar arteries
appeared normal, and the right vertebral artery was judged to
be patent on the basis of contrast washout from the basilar
artery during left vertebral injection. The temporal arteries
were normal.
Pathological Findings
The brain weighed 1,540 gm. The right cerebral hemisphere
was edematous, and uncal herniation was evident. Horizontal
sections of the brain revealed recent infarction within the
territory of the right middle and posterior cerebral arteries.
Small, old infarctions were seen within the territory of the
right anterior cerebral artery and the left middle cerebral
artery.
Microscopic examination revealed cortical, basal ganglionic, and thalamic infarcts ranging in age from several
hours to weeks. No intrinsic vascular disease was identified in
the leptomeningeal or parenchymal blood vessels or in the
circle of Willis. The basilar artery and the terminal 2.5 cm
segments of both vertebral arteries were also not involved.
The media and adventitia of the cavernous segment of both
ICAs revealed a mononuclear cell infiltrate with numerous
multinucleated giant cells of both the foreign body and Langhans’s type, fragmentation and destruction of the elastica, and
proliferation of the intima (Figure). Organizing and recanalizing thrombi occluded both vessels.
Serial sections of the cervical segments of the ICAs
showed mild intimal proliferation bilaterally but no inflammation. There was no evidence of dissection in either vessel. No
vasculitis was seen in the aorta or in the common carotid,
subclavian, innominate, or major coronary arteries. The cervical portions of the vertebral arteries and the external
carotid artery systems were not examined.
Discussion
This patient illustrates three important points about
GCA: (1) it is potentially a lethal disease; (2) the
carotid arteries may be affected selectively and early,
before typical symptoms have developed; and (3)
carotid occlusion resulting from GCA may be
evidenced not by a stroke b u t by a global, progressive
deterioration of neurological function.
The term giant cell arteritis covers a spectrum of clinical illness characterized by a specific histopathological
picture within affected arteries. Because of the usually
severe and clinically obvious involvement of the
superficial temporal arteries, the disease has often been
called “temporal arteritis.” This term, however, neglects the potentially serious involvement of other
medium-size or large arteries. Blindness d u e to
ophthalmic artery lesions is the most frequently recognized complication of GCA, but deaths resulting from
coronary occlusion [b},aortic dissection [ 5 ] , or cerebral infarction [S] have also been reported. W h e n the
carotid artery is involved [I, 2, 81, t h e pattern is similar
to that seen in o u r patient. The carotid siphon is most
severely affected, and t h e cervical segment is only
minimally involved, except for retrograde thrombosis.
Case Report: Howard et al: Carotid Artery Occlusion in GCA
205
The carotid branches in the circle of Willis are spared.
The histological changes within the siphon include typical destruction of mural architecture by an inflammatory infiltrate of mononuclear cells and multinucleated
giant cells, disruption of the internal elastic lamina, and
narrowing of the lumen caused by intimal proliferation.
Why these lesions did not produce a typical strokelike
illness in our patient is uncertain, but the relatively
gradual occlusive process may have allowed for the
development of collateral flow.
More noteworthy than the carotid occlusions them-
206 Annals of Neurology
Vol 15 N o 2
February 1984
Wall ofthe left internal carotid artery at the lwel of the ca~ie~nous sinus. The media and adimtitia rnJeala mononuclear cell
infiltrate with multinucleated giant cells (arrows). ( H &- E;
x 100.1
selves is the absence in our patient of involvement of
other vessels. The pathological study of Wilkinson and
Russell [8] found that whenever the ICA was affected
by GCA, the superficial temporal and vertebral arteries
were equally or even more severely involved. Although these vessels were not examined pathologically
in the present case, angiographically they were normal.
The absence of widespread disease explains why our
patient did not evidence such typical symptoms as
headache and jaw claudication.
The authors thank Dr Donald H. Harter for reviewing the manuscript.
References
1. Cardell BS, Hanley T: A fatal cate of giant-cell or temporal arreritis. J Pathol Bacteriol 63:587-597, 1951
2. Gilmour JR: Giant-cell chronic arteritis. J Pathol Bacteriol
53:263-277, 1941
3. Graham E, Holland A, Avery A, Russell RWR Prognosis in
giant-cell arteritis. Br Med J 282:269-271, 1981
4. Hollenhorst RW, Brown JR, Wagener HP, Shick RM:
Neurologic aspects of temporal arteritis. Neurology (Minneap)
10:490-498, 1960
5. Klein RG, Hunder GG, Stanson WA, Sheps SG: Large artery
involvement in giant cell (temporal) arteritis. Ann Intern Med
83:806-812, 1975
6. Martin JF, Kittas C, Triger DR Giant cell arteritis of coronary
arteries causing myocardial infarction. Br Heart J 43:487-489,
1980
7. Meadows SP: Temporal or giant cell arteritis. Proc R SOCMed
591329-333, 1966
8. Wilkinson IMS, Russell RWR: Arteries of the head and neck in
giant cell arteritis. Arch Neurol 27378-391, 1972
Case Report: Howard et al: Carotid Artery Occlusion in GCA
207
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