Cerebral Dissecting Aneurysms

Wolman, Lionel

doi:10.1093/brain/82.2.276

Cited by 135 publications

(37 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The diagnosis may be suggested by angiography when an irregular, thin column of dye (the string sign is seen as part of the occlusive process, but often only an intracranial occlusion, which may be indistinguishable from embolism, 4 -9 is noted. Pathologic documentation is usually required to establish the diagnosis of dissection and to clarify its pathogenesis.…”

Section: S Pontaneous (Nontraumatic) Intracranial Inter-mentioning

confidence: 99%

“…Histologic examinations of intracranial dissection have frequently identified defects, presumably congenital, in the internal elastic lamina. 4 ' 6 -12 Gaps in, fragmentation of, or disruption of the internal elastic lamina have been the usual findings implicated in the pathogenesis of dissection. In some cases there has been an association with other conditions such as fibromuscular dysplasia, moyamoya disease, and migraine.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Spontaneous intracranial carotid artery dissection.

Pessin

Adelman

Barbas

1989

Stroke

View full text Add to dashboard Cite

is seen as part of the occlusive process, but often only an intracranial occlusion, which may be indistinguishable from embolism, 4 -9 is noted. Pathologic documentation is usually required to establish the diagnosis of dissection and to clarify its pathogenesis.Several conditions have been implicated in the pathogenesis of spontaneous intracranial dissection. These include congenital defects in the media or internal elastic lamina, fibromuscular dysplasia, cystic medial necrosis, trivial trauma, and migraine. - -12 In a few patients, no preexisting abnormalities have been discovered, adding further to the mystery of this condition.-> The present patient falls in the latter category, in which no cause for the dissection was identified.Case Report A 46-year-old woman arose and prepared for work at 6:00 AM and was found on the floor shortly thereafter by her husband. She was vomiting but awake and mute, not moving her right side. She was taken to a local hospital and then to New England Medial Center. On examination, her blood pressure was 130/80 mm Hg and her pulse was 58 beats/min. She was lethargic and followed no verbal instructions. A left gaze preference was noted, but her eyes moved fully to the right with oculocephalic maneuvers. She had right lower face weakness, and her right arm and leg moved poorly to painful stimulation compared with her left arm and leg. Bilateral extensor plantar responses were present. There were no carotid or ocular bruits.There was no history of transient ischemic attacks, migraine, or neck or head trauma. She did not have hypertension, diabetes, or heart disease, and she was not taking oral contraceptives. She smoked cigarettes.Results of computed tomography (CT scan) and lumbar puncture were normal. Eight hours later she was comatose, with bilateral decorticate posturing and pupils poorly reactive to light. CT scan ( Figure 1) at that time showed a large infarct in the territories of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Despite medical measures to control her increased intracranial pressure, she died on the second hospital day.Gross examination of the brain revealed massive swelling and softening of the left cerebral hemisphere involving the territories of the ACA, MCA, and PCA. There was a medial temporal lobe herniation on the left. The left posterior communicating artery was large; the PI segment of the PCA was small. The anterior communicating artery (AComA) was of average size. The left ICA, as it entered the cavernous sinus, had a hematoma in its wall, without significant narrowing of the lumen. The distal intracavernous ICA was grossly normal. Redbrown, granular material obstructed the lumen of the left ICA in its most proximal intracranial portion. It was not possible to tell grossly if this material was in the lumen of the vessel or in its wall. This process extended along the ICA, past the orifice of the ACA, and involved the proximal MCA in the sylvian fissure (Figure 2). The carotid arteries in the n...

show abstract

Section: S Pontaneous (Nontraumatic) Intracranial Inter-mentioning

confidence: 99%

mentioning

confidence: 99%

Spontaneous intracranial carotid artery dissection.

Pessin

Adelman

Barbas

1989

Stroke

View full text Add to dashboard Cite

show abstract

“…Harvey and Alvord, 2 in a classification of cerebral arterial lesions associated with "acute hemiplegia of childhood," cite several examples of cerebral arterial dysplasia including intimal hyperplasia, 8 medial hypoplasia or atrophy, 9 and elastic hypoplasia or atrophy. 10 Fibromuscular dysplasia and Moyamoya disease also have been described as causes of cerebral ischemia, but we have found no reports of dramatic reduplication of the internal elastic lamina of the carotid arteries resulting in stenosis such as was seen in the case reported here.…”

Section: Discussionmentioning

confidence: 99%

Carotid Arterial Elastic Hyperplasia in a Newborn

Thompson

Grunnet

Anderson

1975

Stroke

View full text Add to dashboard Cite

Abstract:Carotid A rterial Elastic Hyperplasia in a Newborn• Cerebrovascular insufficiency in infancy and childhood is well documented and has a diverse and often unknown etiology. Reported here is a polycythemic, microcephalic infant girl of 43 weeks' gestation with bilateral cerebral infarction occurring in the perinatal period. Infarction was the result of bilateral carotid artery stenosis produced by massive reduplication of the internal elastic lamina. Review of the literature failed to reveal any reports of similar arterial lesions. The angiographical picture was also unique.The etiology of this unusual defect is not known, but we believe the problem was congenital perhaps due to an intrauterine infectious process. Additional Key Wordscerebral infarction congenital vascular disease• Numerous reports of cerebrovascular insufficiency in infancy and childhood have been recorded, and this problem has been the subject of comprehensive evaluation by the Joint Committee for Stroke Facilities in its recent report. 1The etiology of congenital cerebrovascular insufficiency is obscure in many cases, since mortality rates are relatively low and tissue specimens, therefore, are usually unavailable.The following is a report of bilateral cerebral infarction in a polycythemic newborn infant with stenosis of the carotid arteries resulting from massive reduplication of the internal elastic lamina. Case ReportThe patient was a 2,830 gm, 43-week gestation, infant girl (small for gestational age), who was the product of an uncomplicated pregnancy and delivery. The 33-year-old mother had two living children and four prior miscarriages. There was no maternal history of infection or ingestion of teratogenic agents during the pregnancy.The infant was in no acute distress at birth, although meconium staining of the skin and fingernails was noted. Within five minutes of birth the patient developed generalized tonic-clonic seizures, which were controlled with intramuscular phenobarbital (5 mg per kilogram). A bulging fontanelle was noted. The initial head circumference (OFC) was 32.2 cm, greater than two standard deviations below the mean for an infant girl of 43 weeks' gestation. No focal neurological deficit was present.At one day of age the fontanelle was still bulging, and intermittent, generalized seizure activity persisted. The , respirations of 50 per minute, and a pulse of 120 per minute. The head transilluminated normally. The right pupil was dilated and fixed to light, and there was a left sixth nerve palsy. The latter findings were interpreted as signs of transtentorial uncal herniation. Hyperactive, symmetrical deep tendon reflexes and intermittent decorticate posturing were noted as well.On admission the hematocrit was 75, polycythemic for a child of this age. Skull x-rays revealed diastasis of the sutures but no intracranial calcification. Serum calcium, phosphorus, glucose and electrolytes, urine amino acid screen, serum immunoglobulin-M, chest x-ray, karyotype, and cultures of the blood, cerebrospinal fluid and urine ...

show abstract

“…До этого времени диагноз под-тверждался только при патоморфологическом ис-следовании, и диссекция считалась достаточно ред-кой патологией, поскольку случаи с летальным ис-ходом нечасты [5][6][7][8][9][10]. Хотя нейровизуализация сыграла решающую роль в расширении наших зна-ний о диссекции и в выработке клинических диа-гностических критериев, только патоморфологиче-ское исследование позволяет приблизиться к пони-манию причин развития этого заболевания.…”

Section: Abstract: Internal Carotid Artery Dissection Ischemic Strokunclassified